NCI Drug Dictionary

2594 results found for: A

A-101 topical solution

A proprietary topical formulation consisting of a high-concentration of hydrogen peroxide (H2O2), with potential keratolytic activity. Upon administration of the A-101 topical solution to an affected area of skin, the hydrogen peroxide penetrates into the cells, increases oxygen content, produces reactive oxygen species (ROS), causes oxidative stress and induces apoptosis through oxidative damage. This may clear the affected skin cells and remove common warts (verruca vulgaris) or seborrheic keratosis (SK).

A-Hydrocort

(Other name for: hydrocortisone sodium succinate)

A2A/A2B adenosine receptor antagonist INCB106385

An orally bioavailable antagonist of both the immunomodulatory checkpoint molecules adenosine A2A receptor (A2AR; ADORA2A) and A2B receptor (A2BR; ADORA2B), with potential immunomodulating and antineoplastic activities. Upon oral administration, A2A/A2B adenosine receptor antagonist INCB106385 competes with tumor-released adenosine for binding to A2AR and A2BR expressed on numerous intra-tumoral immune cells, such as dendritic cells (DCs), natural killer (NK) cells, macrophages and T-lymphocytes. The binding of INCB106385 to A2AR and A2BR inhibits A2AR/A2BR activity and prevents adenosine-A2AR/A2BR-mediated signaling. A2AR/A2BR inhibition activates and enhances the proliferation of various immune cells, abrogates the adenosine-mediated immunosuppression in the tumor microenvironment (TME) and activates the immune system to exert anti-tumor immune responses against cancer cells, which leads to tumor cell killing. A2AR and A2BR, G protein-coupled signaling receptors, are expressed on the cell surfaces of numerous immune cells. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation.

A2A/A2B adenosine receptor antagonist YZJ-5053

An orally bioavailable antagonist of both the immunomodulatory checkpoint molecules adenosine A2A receptor (A2AR; ADORA2A) and A2B receptor (A2BR; ADORA2B), with potential immunomodulating and antineoplastic activities. Upon oral administration, A2A/A2B adenosine receptor antagonist YZJ-5053 competes with tumor-released adenosine for binding to A2AR and A2BR expressed on numerous intra-tumoral immune cells, such as dendritic cells (DCs), natural killer (NK) cells, macrophages and T lymphocytes. The binding of YZJ-5053 to A2AR and A2BR inhibits A2AR/A2BR activity and prevents adenosine-A2AR/A2BR-mediated signaling. A2AR/A2BR inhibition activates and enhances the proliferation of various immune cells, abrogates the adenosine-mediated immunosuppression in the tumor microenvironment (TME) and activates the immune system to exert anti-tumor immune responses against cancer cells, which leads to tumor cell killing. A2AR and A2BR, G protein-coupled signaling receptors, are expressed on the cell surfaces of numerous immune cells. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation.

A2AR antagonist EXS21546

An orally bioavailable immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon oral administration, A2AR antagonist EXS21546 selectively targets, binds to and inhibits A2AR expressed on T-lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T-lymphocytes. This results in the proliferation and activation of T-lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression in the tumor microenvironment (TME). EXS21546 does not penetrate the central nervous system (CNS).

Aacifemine

(Other name for: estriol)

abacavir sulfate

A sulfate salt form of abacavir, a nucleoside reverse transcriptase inhibitor analog of guanosine. This agent decreases HIV viral loads, retards or prevents the damage to the immune system, and reduces the risk of developing AIDS.

abagovomab

A murine IgG1 monoclonal anti-idiotype antibody, containing a variable antigen-binding region that functionally mimics the three-dimensional structure of a specific epitope on the ovarian cancer tumor-associated antigen CA-125, with potential antineoplastic activity. With a variable antigen-binding region that acts as a surrogate antigen for CA-125, abagovomab may stimulate the host immune system to elicit humoral and cellular immune responses against CA-125-positive tumor cells, resulting in inhibition of tumor cell proliferation.

abaloparatide

A 34 amino acid synthetic analog of human parathyroid hormone-related protein (PTHrP) (PTHrP(1-34) analog), with bone-growing and bone density conserving activities. Upon subcutaneous administration, abaloparatide acts similar to PTHrP and targets, binds to and activates parathyroid hormone 1 (PTH1) receptor (PTH1R), a G protein-coupled receptor (GPCR) expressed in osteoblasts and bone stromal cells. PTH1R activates the cyclic AMP (cAMP) signaling pathway and the bone anabolic signaling pathway, leading to bone growth, increased bone mineral density (BMD) and volume. This correlates with increased bone mass and strength and prevents or treats osteoporosis and decreases fractures.

abarelix

A synthetic decapeptide and antagonist of naturally occurring gonadotropin-releasing hormone (GnRH). Abarelix directly and competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. As a result, this may relieve symptoms associated with prostate hypertrophy or prostate cancer, since testosterone is required to sustain prostate growth.

abatacept

A soluble fusion protein consisting of the extracellular domain of human cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) linked to a modified Fc (hinge, CH2, and CH3 domains) portion of human immunoglobulin G1 (IgG1) with immunosuppressive activity. Abatacept binds CD80 and CD86 on antigen presenting cells (APCs), blocking interaction with CD28 on T lymphocytes, which initiates a co-stimulatory signal required for full activation of T lymphocytes.

abazistobart

A recombinant immunoglobulin G4 (IgG4) kappa monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, abazistobart targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

ABBV-221

An intravenously-administered agent capable of modulating the activity of epidermal growth factor receptor (EGFR), with potential antineoplastic activity.

ABCG2 substrate

Any substance that is subjected to cellular efflux by the ABC family transport protein, broad substrate specificity ATP-binding cassette transporter ABCG2.

Abecma

(Other name for: idecabtagene vicleucel)

Abegrin

(Other name for: etaracizumab)

abelacimab

A human anti-factor XI (FXI) monoclonal antibody, with potential anti-thrombotic activity. Upon administration, abelacimab targets and binds to the catalytic domain of FXI, thereby inactivating FXI, and also inhibits the activated form of FXI factor XIa. This prevents the activation of factor XIIa (FXIIa). The abrogation of FXI activation prolongs the activated partial thromboplastin time (aPTT) and reduces platelet and fibrin accumulation. This results in the inhibition of contact activation-initiated blood coagulation and prevents thrombus formation. FXI contributes to thrombotic disease while playing a limited role in normal hemostasis. Activation of FXI is essential for thrombus growth and stabilization.

Abelcet

(Other name for: liposomal amphotericin B)

abemaciclib

An orally available cyclin-dependent kinase (CDK) inhibitor that targets the CDK4 (cyclin D1) and CDK6 (cyclin D3) cell cycle pathway, with potential antineoplastic activity. Abemaciclib specifically inhibits CDK4 and 6, thereby inhibiting retinoblastoma (Rb) protein phosphorylation in early G1. Inhibition of Rb phosphorylation prevents CDK-mediated G1-S phase transition, thereby arresting the cell cycle in the G1 phase, suppressing DNA synthesis and inhibiting cancer cell growth. Overexpression of the serine/threonine kinases CDK4/6, as seen in certain types of cancer, causes cell cycle deregulation.

abequolixron

An orally bioavailable agonist of the nuclear receptor liver X receptor beta (LXRbeta; NR1H2; LXR-b), with potential immunomodulating and antineoplastic activities. Upon oral administration, abequolixron selectively targets and binds to LXRbeta, thereby activating LXRbeta-mediated signaling, leading to the transcription of certain tumor suppressor genes and the downregulation of certain tumor promoter genes. This particularly activates the expression of apolipoprotein E (ApoE), a tumor suppressor protein, in tumor cells and certain immune cells. This activates the innate immune system, resulting in depletion of immunosuppressive myeloid-derived suppressor cells (MDSCs), tumor cells and endothelial cells in the tumor microenvironment. This reverses immune evasion, enhances anti-tumor immune responses and inhibits proliferation of tumor cells. LXRbeta, a member of the oxysterol receptor family, which is in the nuclear receptor family of transcription factors, plays a key role in cholesterol transport, glucose metabolism and the modulation of inflammatory responses; activation of LXRbeta suppresses tumor cell invasion, angiogenesis, tumor progression, and metastasis in a variety of tumor cell types. The expression of the ApoE protein becomes silenced in human cancers as they grow, become invasive, and metastasize; ApoE silencing is related to reduced survival in cancer patients. The LXR-ApoE pathway regulates the ability of cancers to evade the immune system and recruit blood vessels.

Aberel

(Other name for: tretinoin)

abexinostat tosylate

The tosylate salt form of abexinostat, an orally bioavailable hydroxamate-based pan-inhibitor of histone deacetylase (HDAC), with potential antineoplastic and radiosensitizing activities. Upon administration, abexinostat inhibits HDAC, resulting in an accumulation of highly acetylated histones, followed by the induction of chromatin remodeling; the selective transcription of tumor suppressor genes; and the tumor suppressor protein-mediated inhibition of tumor cell division and induction of tumor cell apoptosis. In addition, abexinostat decreases the expression of the DNA-repair protein RAD51, thereby reducing the RAD51 protein, preventing repair of DNA double-strand breaks and increasing sensitivity of tumor cells to DNA damaging agents. HDAC, upregulated in many tumor types, is an enzyme that is responsible for the deacetylation of chromatin histone proteins.

abipapogene suvaplasmid

A therapeutic DNA vaccine composed of three parts, one encodes the E6/E7 fusion protein of human papillomavirus (HPV) type 16 (HPV16), the second is a dimerization entity and the third part encodes a protein that specifically binds to antigen presenting cells (APCs), with potential immunostimulating and antineoplastic activities. Upon intramuscular administration, abipapogene suvaplasmid expresses HPV16 E6/7 and a protein that targets receptors on APCs. Upon binding to APCs and subsequent internalization, the APCs mature and the HPV16 E6/7 antigenic protein is presented by the APCs. This attracts and stimulates B-lymphocytes, CD4-positive T-lymphocytes and elicits a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing HPV16-associated E6 and E7 oncoproteins, which result in tumor cell lysis. HPV16 E6/7, a viral antigen, plays a key role in the development of certain types of cancer.

abiraterone

A steroidal compound with antiandrogen activity. Abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex; CYP17A1), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. Administration of this agent may suppress testosterone production by both the testes and the adrenals to castrate-range levels.

abiraterone acetate

An orally active acetate ester form of the steroidal compound abiraterone with antiandrogen activity. Abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. Administration of this agent may suppress testosterone production by both the testes and the adrenals to castrate-range levels.

abiraterone amorphous solid dispersion formulation DST-2970

An orally bioavailable, amorphous solid dispersion formulation of the steroidal compound abiraterone, with potential antiandrogen activity. Upon oral administration, abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex; CYP17A1), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. This may suppress testosterone production by both the testes and the adrenals to castrate-range levels.

abiraterone decanoate depot

A depot formulation containing the decanoate ester of abiraterone, a steroidal compound with antiandrogen activity. Upon administration, abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex; CYP17A1), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. This suppresses testosterone production by both the testes and the adrenals to castrate-range levels. This may decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells.

abiraterone/prednisone regimen

A regimen consisting of abiraterone and prednisone that can be used for the treatment of prostate cancer and salivary gland tumors.

abituzumab

A humanized monoclonal antibody directed against the human alpha v integrin subunit with potential antiangiogenic and antineoplastic activities. Abituzumab, a chimeric antibody which includes the antigen binding sites of the anti-integrin mouse antibody 17E6, binds to and inhibits the activity of alphaVbeta3 integrin (vitronectin receptor); this may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in alphavbeta3-expressing tumor cells. AlphaVbeta3 integrin, a cell adhesion and signaling receptor, is expressed on the surface of tumor vessel endothelial cells and plays a crucial role in endothelial cell adhesion and migration.

abivertinib

An orally available, irreversible, epidermal growth factor receptor (EGFR) mutant-selective inhibitor, with potential antineoplastic activity. Upon oral administration, abivertinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the drug-resistant T790M EGFR mutant, which prevents signaling mediated by mutant forms of EGFR. This may both induce cell death and inhibit tumor growth in EGFR-mutated tumor cells. EGFR, a receptor tyrosine kinase that is mutated in a variety of cancers, plays a key role in tumor cell proliferation and tumor vascularization. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors, which also inhibit wild-type EGFR.

abivertinib maleate anhydrous

The maleate salt form of abivertinib, an orally available, irreversible, epidermal growth factor receptor (EGFR) mutant-selective inhibitor, with potential antineoplastic activity. Upon oral administration, abivertinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the drug-resistant T790M EGFR mutant, which prevents signaling mediated by mutant forms of EGFR. This may both induce cell death and inhibit tumor growth in EGFR-mutated tumor cells. EGFR, a receptor tyrosine kinase that is mutated in a variety of cancers, plays a key role in tumor cell proliferation and tumor vascularization. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors, which also inhibit wild-type EGFR.

Ablavar

(Other name for: gadofosveset trisodium)

Abraxane

(Other name for: nab-paclitaxel)

absorbable adhesion barrier gel

An isotonic, sterile, absorbable adhesion barrier gel composed of polyethylene oxide and sodium carboxymethylcellulose, with protective activity. Upon application of a single layer into the uterine cavity at the end of any hysteroscopic surgery, the absorbable adhesion barrier gel may provide a protective barrier which protects the traumatized tissue and allows for healing. This gel may therefore prevent the formation of post-surgical intrauterine adhesions.

absorbable fibrin sealant patch

A sterile, absorbable surgical sealing patch composed of an equine collagen sponge coated with the coagulation factors human fibrinogen and human thrombin, with potential hemostatic activity. Applied on the wound tissue, the absorbable fibrin sealant patch adheres to the tissue and the solid fibrinogen and thrombin dissolve upon contact with the physiological fluid. In turn, fibrinogen is converted to fibrin monomers by thrombin, and polymerize to form a fibrin clot at the wound surface. This causes the patch to adhere to the wound surface and promotes tissue sealing. This may reduce lymphatic drainage and prevent seroma formation.

absorbable gelatin sponge

A sterile hemostatic agent composed of purified porcine-derived gelatin. In regional chemotherapy, absorbable gelatin sponge may be used to embolize arteries in the region of a tumor in order to block or retard blood flow; this blockage results in a locally increased concentration of chemotherapeutic agents delivered to the tumor when chemotherapeutic agents are infused into the embolized arterial circulation upstream of the blockage.

absorbable modified polymer hemostatic powder

A hemostatic powder composed of hydrophilic, absorbable modified polymers (AMPs) derived from plant starch, with potential anti-hemorrhagic activity. Upon local administration of the AMP hemostatic powder directly sprayed over the bleeding surface, this powder adheres to the bleeding area, and the AMPs are able to absorb fluid and therefore soak up blood at the bleeding site. This leads to the formation of a gelled matrix that seals the affected site, and allows platelets, red blood cells and clotting factors in the blood to concentrate at the wound. In turn, this promotes the coagulation cascade, helps to stop or control bleeding, and prevents further blood loss. The AMP particles are naturally degraded by human enzymes over time.

ABT-510

A synthetic peptide that mimics the anti-angiogenic activity of the endogenous protein thrombospondin-1 (TSP-1). ABT-510 inhibits the actions of several pro-angiogenic growth factors important to tumor neovascularization; these pro-angiogenic growth factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)), hepatocyte growth factor (HGF), and interleukin 8 (IL-8).

ABT-751

An orally bioavailable antimitotic sulfonamide. ABT-751 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of microtubules, thereby preventing tumor cell replication. This agent also disrupts tumor neovascularization, reducing tumor blood flow and so inducing a cytotoxic effect.

ABVD regimen

A regimen consisting of doxorubicin, bleomycin, vinblastine and dacarbazine that can be used in the treatment of Hodgkin lymphoma (HL).

ABVE regimen

A regimen containing doxorubicin hydrochloride, bleomycin sulfate, vincristine sulfate and etoposide used in combination with radiation therapy for the treatment of low-risk, childhood Hodgkin lymphoma.

ABVE-PC regimen

A regimen consisting of doxorubicin, bleomycin, vincristine, etoposide, prednisone and cyclophosphamide, given in combination with radiation therapy and used for the treatment of high-risk, childhood Hodgkin's lymphoma.

AC regimen

A regimen consisting of cyclophosphamide and doxorubicin that can be used in the treatment for breast cancer. Cyclophosphamide/doxorubicin every 21 days regimen may be used for the treatment of breast cancer.

AC-T regimen

A regimen consisting of cyclophosphamide and doxorubicin followed by paclitaxel, used as a neoadjuvant or adjuvant treatment for breast cancer.

acadesine

A 5-aminoimidazole-4-carboxamide (AICA) riboside, a purine nucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria.

Acai Berry Juice

A juice product obtained from the fruit of the acai palm tree (Euterpe oleracea) with anti-inflammatory, antioxidant and potential chemopreventive activities. Besides high amounts of vitamins, minerals and fatty acids, acai berry is rich in phytonutrients such as anthocyanins and flavones which are potent scavengers of reactive oxygen species. The fruit also contains high amounts of the flavone velutin which exhibits potent anti-inflammatory properties. Velutin is able to inhibit the degradation of the inhibitor of nuclear factor kappa-B (NF-kB), thereby blocking the activation of NF-kB, as well as inhibiting phosphorylation of mitogen-activated protein kinase p38 and JNK. Inhibition of these processes results in suppression of the production of proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin 6.

acalabrutinib

An orally available inhibitor of Bruton tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, acalabrutinib inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.

acalabrutinib maleate monohydrate

The maleate monohydrate form of acalabrutinib, an orally available inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, acalabrutinib inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.

acalisib

An inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities. Acalisib inhibits the activity of PI3K, thereby preventing the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), which decreases tumor cell proliferation and induces cell death. PI3K-mediated signaling is often dysregulated in cancer cells; the targeted inhibition of PI3K is designed to preserve PI3K signaling in normal, non-neoplastic cells.

acapatamab

A half-life extended (HLE), bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA), fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration acapatamab binds to both CD3 on cytotoxic T lymphocytes (CTLs) and PSMA found on PSMA-expressing tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA, a tumor associated antigen, is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

Acapodene

(Other name for: toremifene citrate)

acarbose

A pseudotetrasaccharide and inhibitor of alpha-glucosidase and pancreatic alpha-amylase with antihyperglycemic activity. Acarbose binds to and inhibits alpha-glucosidase, an enteric enzyme found in the brush border of the small intestines that hydrolyzes oligosaccharides and disaccharides into glucose and other monosaccharides. This prevents the breakdown of larger carbohydrates into glucose and decreases the rise in postprandial blood glucose levels. In addition, acarbose inhibits pancreatic alpha-amylase which hydrolyzes complex starches to oligosaccharides in the small intestines.

Acasunlimab

A recombinant, Fc-silenced immunoglobulin G1 (IgG1) bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, acasunlimab simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. Through 4-1BB binding, acasunlimab acts as a conditional 4-1BB agonist, resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, acasunlimab prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

Accolate

(Other name for: zafirlukast)

Accutane

(Other name for: isotretinoin)

acebilustat

An orally bioavailable, small molecule inhibitor of the enzyme leukotriene A4 hydrolase (LTA4H), with potential anti-inflammatory activity. Upon oral administration, acebilustat targets and inhibits the activity of LTA4H, thereby inhibiting the synthesis of the pro-inflammatory mediator leukotriene B4 (LTB4). This may reduce inflammation in various inflammatory disorders including cystic fibrosis and serious pulmonary inflammatory diseases. LTA4H catalyzes a major and rate-limiting step in LTB4 production, and LTB4 plays an important role in pulmonary and systemic inflammation.

Acelarin

(Other name for: fosgemcitabine palabenamide)

acellular cadaveric dermal matrix

A human dermis-derived allograft material. Acellular cadaveric dermal matrix (ACDM) is derived from human cadaveric dermis from which the epidermis, all viable cells and major histocompatibility class (MHC) II antigens have been removed to minimize alloimmunogenicity, while the dermal collagen matrix is preserved. ACDM may placed over wounds to aid as a substitute for skin when necessary such as for surgical reconstruction or for protection against wound exposure and breakdown and wound infection.

acellular dermal matrix

An allograft composed of sterile, decellularized regenerative dermal tissue matrix with soft tissue reconstructive, regenerative and transplantation purposes. The acellular dermal matrix (ADM) is composed of the dermal layer and extracellular matrix of human or animal skin and in which the epidermal layer is removed, The ADM retains native growth factors, collagen and elastin. The ADM supports tissue expanders or implants for soft tissue reconstruction or to aid in wound healing, and allows for rapid cellular proliferation and infiltration, integration of mesenchymal cells into the matrix and re-vascularization. This facilitates surgical reconstruction and protects against wound exposure and wound infection.

acenocoumarol

A 4-hydroxycoumarin derivative with anticoagulant activity. As a vitamin K antagonist, acenocoumarol inhibits vitamin K epoxide reductase, thereby inhibiting the reduction of vitamin K and the availability of vitamin KH2. This prevents gamma carboxylation of glutamic acid residues near the N-terminals of the vitamin K-dependent clotting factors, including factor II, VII, IX, and X and anticoagulant proteins C and S. This prevents their activity and thus thrombin formation. Compared to other coumarin derivatives, acenocoumarol has a short half-life.

Aceon

(Other name for: perindopril erbumine)

Acetadote

(Other name for: acetylcysteine)

acetaminophen

A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.

acetazolamide

A sulfonamide derivative with diuretic, antiglaucoma, and anticonvulsant properties. Acetazolamide is a non-competitive inhibitor of carbonic anhydrase, an enzyme found in cells in the proximal tube of the kidney, the eye, and glial cells. Inhibition of this enzyme in the kidney prevents excretion of hydrogen, leading to increased bicarbonate and cation excretion and increased urinary volume, which results in an alkaline diuresis. Acetazolamide reduces the concentration of bicarbonate, resulting in a decreased synthesis of aqueous humor in the eye, thereby lowering intraocular pressure. Although its mechanism of action is unknown, acetazolamide has anti-convulsant properties resulting from indirect effects secondary to metabolic acidosis or direct effects on neuronal transmission. Acetazolamide also produces respiratory stimulant effects in response to changes to both carbon dioxide and oxygen tension levels within the lungs.

acetazolamide sodium

The sodium salt of acetazolamide, a nonbacteriostatic sulfonamide derivative with diuretic and anticonvulsant properties. Acetazolamide is a potent inhibitor of carbonic anhydrase that plays an important role in the control of fluid secretion. Inhibition of this enzyme in the kidney results in a reduction in the availability of hydrogen ions for active transport in the renal tubule lumen, thereby leading to increased bicarbonate and cation excretion, and increased urinary volume. Reduced bicarbonate level in circulation induces reduction of intraocular pressure via osmotic mechanism. The anticonvulsant activity of acetazolamide may contribute to inhibition of carbonic anhydrase in the CNS, which decreases carbon dioxide tension in the pulmonary alveoli, thus increasing arterial oxygen tension.

acetic acid

A synthetic carboxylic acid with antibacterial and antifungal properties. Although its mechanism of action is not fully known, undissociated acetic acid may enhance lipid solubility allowing increased fatty acid accumulation on the cell membrane or in other cell wall structures. Acetic acid, as a weak acid, can inhibit carbohydrate metabolism resulting in subsequent death of the organism.

acetohexamide

An intermediate-acting, first-generation sulfonylurea with hypoglycemic activity. Acetohexamide is metabolized in the liver to its active metabolite hydroxyhexamide.

acetyl-L-carnitine hydrochloride

A nutritional supplement composed of the hydrochloride salt form of the acetylated form of the endogenously produced L-carnitine, with potential neuroprotective, cognitive-enhancing, anti-depressive and immunomodulating activities. L-carnitine is responsible for the transport of fatty acids into the mitochondria for breakdown. It may also relieve peripheral neuropathy induced by chemotherapy, diabetes or other diseases. In addition, acetyl-L-carnitine may modulate the immune response by increasing T lymphocytes maturation and may downregulate pro-inflammatory cytokines in response to viruses, such as SARS-CoV-2. It may also disrupt the ACE2 signaling pathway and inhibit the production of reactive oxygen species (ROS).

acetylcysteine

A synthetic N-acetyl derivative and prodrug of the endogenous amino acid L-cysteine, a precursor of the antioxidant glutathione (GSH), with mucolytic, antioxidant, and potential cytoprotective, cancer-preventive, and anti-inflammatory activities. Upon administration, acetylcysteine exerts its mucolytic activity by reducing disulfide bonds in mucoproteins, resulting in liquification of mucus and reducing its viscosity. It is also used for the treatment of acetaminophen overdose as it can restore the depleted GSH reserves in the hepatocytes during the process of detoxification. The antioxidant activity is attributed to the ability of GSH to scavenge reactive oxygen species (ROS), thereby preventing ROS-mediated cell damage, decreasing oxidative stress, protecting cells against the damaging effects of free radicals and preventing apoptosis in these cells. In addition, this may inhibit tumor cell proliferation, progression and survival, in susceptible tumor cells that rely on ROS-mediated signaling for their proliferation and malignant behavior. Under certain circumstances, acetylcysteine is able to induce apoptosis in susceptible cells, including certain tumor cells, via the intrinsic mitochondria-dependent pathway but not involving endoplasmic reticulum stress. Also, acetylcysteine may also be able to degrade Notch2, thereby preventing proliferation, migration, and invasion in Notch2-overexpressing glioblastoma cells. In addition, acetylcysteine may inhibit viral stimulation by reactive oxygen intermediates, thereby producing antiviral activity in HIV patients. Acetylcysteine also possesses anti-inflammatory activity through modulation of the nuclear factor-kappa B (NF-kB) pathway and the modulation of cytokine synthesis.

acetylglucosaminyltransferase V inhibitor PhOx430

An inhibitor of the glycosyltransferase N-Acetylglucosaminyltransferase V (GnT-V), with potential antineoplastic activity. Upon administration, GnT-V inhibitor PhOx430 targets, binds to and inhibits the activity of GnT-V, a glycosylation enzyme that synthesizes the beta1, 6-GlcNAc branch in N-glycans. This inhibits the glycosylation of tumor cells and downregulates cell surface receptors implicated in tumor cell growth and metastasis. GnT-V and its product N-glycans, upregulated in various types of cancer cells, are associated with cancer proliferation and metastasis.

Achromycin

(Other name for: tetracycline hydrochloride)

acimtamig

A tetravalent bispecific antibody directed against human CD30 and the human low affinity IgG Fc region receptor (FCGR3A; CD16A), with potential immunomodulating and antineoplastic activities. Upon administration, acimtamig binds to the CD16A expressed on natural killer (NK) cells with two of its binding sites and to CD30 on CD30-expressing tumor cells with the other two binding sites, thereby selectively cross-linking tumor and NK cells. This may result in NK cell activation, antibody-dependent cellular cytotoxicity (ADCC) and eventually tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is overexpressed in hematologic malignancies; CD16A is specifically expressed on the surface of NK cells.

acinterferon alfa

A proprietary recombinant protein highly resembling human interferon alpha 2b (IFN-a2b), with potential anti-tumor, anti-inflammatory, immunomodulating and antiviral activities. Upon injection, acinterferon alfa binds to specific IFN alpha cell surface receptors. This activates interferon-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-specific response elements (ISREs). This may activate the immune system, including the activation of natural killer cells (NKs) and may result in an inhibition of tumor cell proliferation, tumor angiogenesis, metastasis and an induction of apoptosis. Compared to human IFN-a2b (HuINF-a2b), this agent exhibits enhanced antiviral and antiproliferative activities. In addition, this agent exhibits antiviral activity against a variety of viruses, including hepatitis B and C viruses, human immunodeficiency virus (HIV) and Avian Influenza.

Aciphex

(Other name for: rabeprazole sodium)

acitretin

An orally-active metabolite of the synthetic aromatic retinoic acid agent etretinate with potential antineoplastic, chemopreventive, anti-psoratic, and embryotoxic properties. Acitretin activates nuclear retinoic acid receptors (RAR), resulting in induction of cell differentiation, inhibition of cell proliferation, and inhibition of tissue infiltration by inflammatory cells. This agent may also inhibit tumor angiogenesis.

acivicin

A modified amino acid and structural analog of glutamine. Acivicin inhibits glutamine amidotransferases in the purine and pyrimidine biosynthetic pathways, thereby inhibiting tumor growth in cell lines dependent on glutamine metabolism.

aclarubicin

An oligosaccharide anthracycline antineoplastic antibiotic isolated from the bacterium Streptomyces galilaeus. Aclarubicin intercalates into DNA and interacts with topoisomerases I and II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Aclarubicin is antagonistic to other agents that inhibit topoisomerase II, such as etoposide, teniposide and amsacrine. This agent is less cardiotoxic than doxorubicin and daunorubicin.

Acnestrol

(Other name for: diethylstilbestrol)

ACNU 50

(Other name for: nimustine)

acodazole

A synthetic imidazoquinoline with antineoplastic activity. Acodazole intercalates into DNA, resulting in disruption of DNA replication. Use of this agent has been associated with significant cardiotoxicity.

Acolbifene Hydrochloride

The hydrochloride salt form of acolbifene, a fourth-generation estrogen receptor modulator (SERM) with potential lipid lowering and antineoplastic activity. Acolbifene specifically binds to estrogen receptors in responsive tissue, including liver, bone, breast, and endometrium. The resulting ligand-receptor complex is translocated to the nucleus where, depending on the tissue type, it promotes or suppresses the transcription of estrogen-regulated genes, thereby exerting its agonistic or antagonistic effects. Acolbifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the effects of estrogen in these tissues. This may inhibit tumor cell proliferation in ER-positive tumor cells. This agent functions as an estrogen agonist in lipid metabolism, thereby decreasing total and LDL cholesterol levels. In bone, it decreases bone resorption and bone turnover and increases bone mineral density.

acoramidis

A potent, highly selective, orally bioavailable transthyretin (TTR) stabilizer with potential disease-modifying activity. Upon oral administration, acoramidis binds to and stabilizes transthyretin (TTR), thereby preventing tetramer dissociation into monomers. This prevents misfolding of the TTR protein and inhibits the formation of TTR amyloid fibrils and the subsequent deposition of these insoluble protein clusters in the heart and peripheral nerves. TTR is a transport protein for thyroxine and retinol and is secreted by the liver into the blood. The accumulation of TTR amyloid fibrils may result in thickening and stiffening of the ventricular wall, leading to heart failure.

acoustic coupling fluid

A brain mimicking fluid with an attenuation coefficient similar to that found in the adult human brain, which can potentially improve the quality of an image acquired during intraoperative ultrasonography. Upon administration into the resection cavity during surgical removal of a brain tumor, the acoustic coupling fluid may both increase the quality of the ultrasound image and improve the visualization of the tumor. This may facilitate the surgical removal of residual tumor while sparing normal, healthy brain tissue.

acridine carboxamide

A tricyclic acridine-based (or carboxamide-based) drug with dual topoisomerase inhibitor and potential antineoplastic activities. Acridine carboxamide inhibits both topoisomerases I and II and intercalates into DNA, resulting in DNA damage, the disruption of DNA repair and replication, the inhibition of RNA and protein synthesis, and cell death.

ACSS2 inhibitor MTB-9655

An orally bioavailable small molecule inhibitor of the enzyme human acetyl coenzyme A synthetase short chain family member 2 (ACSS2; acetyl CoA synthetase 2), with potential antineoplastic activity. Upon oral administration, the ACSS2 inhibitor MTB-9655 selectively targets, binds to and inhibits the activity of ACSS2. This prevents acetate metabolism to acetyl-CoA which may lead to an inhibition of tumor cell proliferation. ACSS2, an enzyme that converts acetate to acetyl-CoA, is upregulated in cancer cells in response to low nutrient availability and hypoxia. Stressed cancer cells utilize acetate as an alternative nutrient source for cell growth.

Actemra

(Other name for: tocilizumab)

ACTH antagonist CRN04894

An orally bioavailable nonpeptide antagonist of the adrenocorticotropic hormone (ACTH) receptor (ACTHR; melanocortin receptor 2; MC2R), with potential steroid hormone production inhibitory activity. Upon oral administration, ACTH antagonist CRN04894 competes with ACTH for receptor binding to MC2R in the adrenal cortex and inhibits ACTH signaling. This may inhibit the synthesis and secretion of steroid hormones. MC2R, a member of the melanocortin receptor subfamily of type 1 G protein-coupled receptors, plays a key role in adrenal steroidogenesis.

ActHIB

(Other name for: Haemophilus influenzae b vaccine)

Acthrel

(Other name for: corticorelin ovine triflutate)

Actigall

(Other name for: ursodiol)

Actimab-A

(Other name for: actinium Ac 225 lintuzumab)

Actimid

(Other name for: pomalidomide)

Actimmune

(Other name for: interferon gamma-1b)

Actinex

(Other name for: masoprocol)

actinium Ac 225 DOTATATE RYZ101

A radioconjugate consisting of the somatostatin analog tyrosine-3-octreotate (Tyr3-octreotate or TATE) labeled, via the macrocyclic chelating agent 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra-acetic acid (DOTA), with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225 DOTATATE RYZ101, the TATE moiety targets and binds to SSTRs, with a much higher affinity for type 2 SSTR, present on the cell membranes of many types of neuroendocrine tumors (NETs). Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to SSTR-expressing tumor cells. SSTRs have been shown to be present in large numbers on NETs and their metastases, while most other normal tissues express low levels of SSTRs.

actinium Ac 225 FPI-2059

A radioconjugate consisting of a neurotensin receptor type 1 (NTSR1)-targeting small molecule antagonist labeled with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225 FPI-2059, the NTSR1-targeting moiety targets and binds to NTSR1 expressed on tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to NTSR1-expressing tumor cells. NTSR1, a G protein-coupled receptor for the tridecapeptide neurotensin (NTS), is overexpressed in certain types of cancers and plays a key role in tumor cell proliferation. 

actinium Ac 225 FPI-2068

A radioimmunoconjugate composed of FPI-2053, a humanized bispecific antibody targeting epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR; c-Met), chelated to the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and radiolabeled with the alpha-emitting radionuclide actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225 FPI-2068, the FPI-2053 moiety targets and binds to the extracellular domains of both EGFR and c-Met expressed on certain cancer cells, thereby delivering a cytotoxic dose of alpha radiation directly into EGFR- and c-Met-expressing tumor cells. Additionally, the induction of apoptosis and subsequent release of tumor-associated antigens (TAAs) from the tumor cells may induce an anti-tumor immune response, thereby further killing tumor cells. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation. EGFR and c-Met are co-expressed on the surface of various cancer cell types while co-expression on normal, healthy cells is minimal.

actinium Ac 225 lintuzumab

A radioimmunoconjugate consisting of the humanized monoclonal antibody lintuzumab conjugated to the alpha-emitting radioisotope actinium Ac 225 with potential antineoplastic activity. The monoclonal antibody moiety of actinium Ac 225 lintuzumab specifically binds to the cell surface antigen CD33 antigen, delivering a cytotoxic dose of alpha radiation to cells expressing CD33. CD33 is a cell surface antigen expressed on normal non-pluripotent hematopoietic stem cells and overexpressed on myeloid leukemia cells.

actinium Ac 225 PSMA-R2

A radioconjugate composed of PSMA-R2, a human prostate-specific membrane antigen (PSMA)-targeting ligand, conjugated to the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity against PSMA-expressing tumor cells. Upon intravenous administration of 225Ac-PSMA-R2, the PSMA-R2 moiety targets and binds to PSMA-expressing tumor cells. Upon binding, PSMA-expressing tumor cells are destroyed by a cytotoxic dose of alpha radiation. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on the majority of prostate tumor cells.

actinium Ac 225 rosopatamab tetraxetan

A radioimmunoconjugate consisting of a humanized monoclonal antibody directed against prostate specific membrane antigen (PSMA) labeled with the alpha particle-emitting radioisotope actinium Ac-225, with potential antineoplastic activity. Upon administration, actinium Ac 225 rosopatamab tetraxetan binds to the extracellular domain of PSMA with high affinity, thereby delivering alpha radiation to PSMA expressing cells. PSMA, a type II membrane protein expressed in all types of prostatic tissues, is often overexpressed in tumor cells.

actinium Ac 225 vofatamab

A radioimmunoconjugate containing vofatamab, a human immunoglobulin G1 (IgG1) monoclonal antibody directed against the fibroblast growth factor receptor type 3 (FGFR3) labeled, via a chelating agent, with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225 vofatamab, the vofatamab moiety specifically targets and binds to FGFR3. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to FGFR3-expressing tumor cells. FGFR3, a receptor tyrosine kinase upregulated or mutated in many tumor cell types, plays a key role in tumor cell proliferation.

actinium Ac 225 zadavotide guraxetan

A radioconjugate composed of zadavotide guraxetan, a human prostate-specific membrane antigen (PSMA)-targeting ligand linked to the bifunctional tmacrocyclic chelating agent 1,4,7,10-tetraazacyclododecane-1-(glutamic acid)-4,7,10-triacetic acid (DOTAGA; DOTA-GA), and conjugated to the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration, actinium Ac 225 zadavotide guraxetan targets and binds to PSMA-expressing tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to PSMA-expressing tumor cells. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.

actinium Ac 225-ABD147

A radioimmunoconjugate consisting of ABD147, an antibody fragment directed against the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) conjugated with a linker-chelator to the alpha-emitting radioisotope actinium Ac 225 (225Ac), with potential antineoplastic activity. Upon administration of actinium Ac 225-ABD147, ABD147 targets and binds to DLL3 on DLL3-expressing tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

actinium Ac 225-DOTA-anti-CEA monoclonal antibody M5A

A radioimmunoconjugate comprised of M5A, a humanized monoclonal antibody directed against carcinoembryonic antigen-related cell adhesion molecule 5 (CEA or CEACAM5), conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of actinium Ac 225-DOTA-anti-CEA monoclonal antibody M5A specifically targets and binds to CEA, thereby delivering a cytotoxic dose of alpha radiation to CEA-expressing tumor cells. CEA, a tumor-associated antigen (TAA) and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion and cell adhesion, and is overexpressed by a variety of cancer types.

Actinium Ac 225-DOTA-Daratumumab

A radioimmunoconjugate containing daratumumab, a human immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against the cell surface glycoprotein CD38, conjugated to the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225-DOTA-daratumumab, the monoclonal antibody moiety specifically targets and binds to cell surface antigen CD38. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to CD38-expressing tumor cells. CD38, a cell surface glycoprotein, is expressed on various hematopoietic cells and is overexpressed on multiple myeloma (MM) cells.

actinium Ac 225-DOTA-h11B6 JNJ-69086420

A radioimmunoconjugate containing h11B6, a humanized immunoglobulin G1 (IgG1) monoclonal antibody that targets human kallikrein-2 (hK2), conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225-DOTA-h11B6 JNJ-69086420, the monoclonal antibody moiety of JNJ-69086420 targets and binds to hK2, thereby delivering a cytotoxic dose of alpha radiation to hK2-expressing tumor cells. hK2 is overexpressed on a variety of cancer cells.

actinium Ac 225-DOTA-MTI-201

A radioconjugate composed of a melanocyte-stimulating hormone receptor (MSHR; melanocortin-1 receptor; MC1R; melanin-activating peptide receptor; melanotropin receptor)-targeting ligand conjugated to the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225-DOTA-MTI-201, MT-201 targets and binds to MC1R-expressing melanoma cells, thereby specifically delivering a cytotoxic dose of alpha radiation to cells expressing MC1R. MC1R, a G protein-coupled receptor expressed by melanocytes that binds to melanocortins, is involved in regulating mammalian skin and hair color. It is upregulated on the surface of on uveal and cutaneous melanoma cells, but not in healthy normal tissues.

actinium Ac 225-FL-020

A radioconjugate composed of FL-020, a human prostate-specific membrane antigen (PSMA)-targeting ligand, conjugated to the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225-FL-020, FL-020 targets and binds to PSMA-expressing tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to PSMA-expressing tumor cells. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.

actinium Ac 225-FPI-1434

A radioconjugate consisting of veligrotug, a humanized monoclonal antibody directed against insulin-like growth factor-1 receptor (IGF-1R) linked, via a bifunctional chelate, to the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration of actinium Ac 225-FPI-1434, the veligrotug moiety targets and binds to IGF-1R expressed on tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to IGF-1R-expressing tumor cells. Activation of IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily overexpressed by various cancer cell types, stimulates cell proliferation, promotes angiogenesis, enables oncogenic transformation, and suppresses apoptosis.

actinium Ac 225-PSMA-trillium

A radioconjugate composed of PSMA-trillium, a human prostate-specific membrane antigen (PSMA)-targeting small molecule that is linked to an albumin-binding moiety, and conjugated to the alpha-emitting radioisotope actinium Ac 225, with potential antineoplastic activity. Upon administration, actinium Ac 225-PSMA-trillium targets and binds to PSMA-expressing tumor cells. Upon binding, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to PSMA-expressing tumor cells. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors. The albumin-binding moiety targets and binds to albumin, which may improve therapeutic efficacy and reduce side effects in normal organs.

actinium Ac-225

An alpha-emitting radioisotope of actinium with a half-life of 10 days.

Actiq

(Other name for: fentanyl citrate)

Activase

(Other name for: alteplase)

activated charcoal

Carbon that has been treated to create small, low-volume pores that increase the surface area available for adsorption.

activated marrow infiltrating lymphocytes

A preparation of cells, which consists of autologous marrow infiltrating lymphocytes (MILs), that are manipulated in vitro, with potential antitumor and immune stimulating activities. MILs are harvested from autologous bone marrow from multiple myeloma patients and, in vitro, are exposed to and activated by anti-CD3/anti-CD28 monoclonal antibodies covalently attached to super-paramagnetic microbeads. After removal of the beads and expansion of the cells in culture, the activated MILs (aMILs) are re-introduced into the patient. The aMILs possess enhanced myeloma specificity, and are able to infiltrate the tumor microenvironment and initiate tumor cell lysis. CD3 and CD28, co-stimulatory molecules expressed on the surface of T-lymphocytes, play a key role in the activation of T-cells.

activated polyethylene glycol/polyethyleneimine-based surgical sealant

A surgical sealant composed of activated polyethylene glycol (PEG) and polyethyleneimine (PEI) that can be used to seal tears in the dura during spinal surgery in order to prevent cerebrospinal fluid (CSF) leakage. It may also minimize dural adhesions and scarring by providing a protective shield between the dura and surrounding tissue.

Activella

(Other name for: estradiol/norethindrone acetate tablet)

ActiVin

(Other name for: IH636 grape seed proanthocyanidin extract)

activin Type 2B receptor Fc fusion protein STM 434

A soluble fusion protein containing the extracellular domain of the activin receptor type 2B (ACVR2B or ActRIIB) fused to a human Fc domain, with potential antineoplastic activity. Upon intravenous administration, STM 434 selectively binds to the growth factor activin A, thereby preventing its binding to and the activation of endogenous ActRIIB. This prevents activin A/ActRIIB-mediated signaling and inhibits the proliferation of activin A-overexpressing tumor cells. Activin A, a member of the transforming growth factor beta (TGF-beta) superfamily, is overexpressed in a variety of cancers and plays a key role in promoting cancer cell proliferation, migration, and survival.

activin type IIA receptor Fc fusion protein KER-050

A recombinant fusion protein composed of a modified form of the ligand-binding domain of the human transforming growth factor beta (TGF-b) receptor activin receptor type IIA (ActRIIA) and linked to the Fc domain of human antibody, with red blood cell (RBC) and platelet stimulating activities. Upon subcutaneous administration, activin type IIA receptor Fc fusion protein KER-050 acts as a ligand trap, and binds to a subset of the TGF-b family of proteins. This inhibits the binding of these proteins to their receptors and blocks signaling mediated by this subset of TGF-b family of proteins and their receptors. This may promote hematopoiesis and increase RBC and platelet production.

ACTolog IMA101

(Other name for: ex vivo-expanded autologous T cells IMA101)

Actonel

(Other name for: risedronate sodium)

ACTOplus Met XR

(Other name for: metformide hydrochloride/pioglitazone hydrochloride extended-release tablet)

Actos

(Other name for: pioglitazone hydrochloride)

acyclic nucleoside phosphonate prodrug ABI-1968

A prodrug of an acyclic nucleoside phosphonate, with potential anti-viral and antineoplastic activities. Upon administration, acyclic nucleoside phosphonate prodrug ABI-1968 is taken up by viral-infected cells and converted to its active metabolite. The metabolite is incorporated into DNA chains by DNA polymerases, which results in the termination of DNA synthesis, inhibits viral replication and induces apoptosis and inhibits the proliferation of susceptible virally-infected tumor cells.

acyclovir

A synthetic analog of the purine nucleoside, guanosine, with potent antiviral activity against herpes simplex viruses type 1 and 2, varicella-zoster virus and other viruses of the herpesvirus family. After conversion in vivo to the active metabolite acyclovir triphosphate by viral thymidine kinase, acyclovir competitively inhibits viral DNA polymerase by incorporating into the growing viral DNA chain and terminating further polymerization.

Acyclovir Sodium

The sodium salt form of acyclovir, a synthetic analog of the purine nucleoside, guanosine, with potent antiviral activity against herpes simplex viruses type 1 and 2, varicella-zoster virus and other viruses of the herpesvirus family. After conversion in vivo to the active metabolite acyclovir triphosphate by viral thymidine kinase, acyclovir competitively inhibits viral DNA polymerase by incorporating into the growing viral DNA chain and terminating further polymerization.

acylfulvene-derived prodrug LP-184

A tumor-site activated acylfulvene-derived prodrug and alkylating agent, with potential antineoplastic activity. Upon administration, acylfulvene-derived prodrug LP-184 becomes activated by prostaglandin reductase 1 (PTGR1), an oxidoreductase that is specifically upregulated in certain tumor cell types. The active form of LP-184 covalently binds to and alkylates DNA at N3-adenine, thereby causing double strand breaks. As tumor cells often carry DNA damage repair (DDR) mutations and are therefore deficient in DDR pathways, the DNA damage cannot be repaired. In turn, the damaged DNA causes apoptosis and inhibits proliferation in susceptible DDR mutated tumor cells. PTGR1 is often elevated in solid tumors but not in normal tissues.

Aczone

(Other name for: dapsone)

Aczone Gel

(Other name for: dapsone gel, 5%)

Ad-hCMV-Flt3L

A human serotype 5, replication-defective, first generation adenoviral vector, with the viral E1a and E3 protein encoding regions deleted, which is engineered to express the soluble, immune-mediated stimulatory gene human fms-like tyrosine kinase 3 ligand (Flt3L), under the transcriptional control of the CMV promoter, with potential immunostimulating activity. Upon administration, Ad-hCMV-Flt3L is transduced into tumor cells and Flt3L is expressed. Flt3L stimulates both the proliferation of dendritic cells (DCs) and their migration to the tumor site. Upon exposure to the tumor-associated antigens (TAA) released from dying glioma cells, which were killed by thymidine kinase-mediated valacyclovir-induced tumor cell death, the DCs initiate a specific immune response against any remaining TAA-expressing tumor cells. Flt3L is a hematopoietic growth factor and ligand for the Flt3 tyrosine kinase receptor.

Ad-hCMV-TK

A human serotype 5, replication-defective, first generation adenoviral vector, with the viral E1a and E3 protein encoding regions deleted, which is engineered to express the herpes simplex virus thymidine kinase (HSV-tk) gene under the transcriptional control of the CMV promoter. This agent, when administered in conjunction with a synthetic acyclic guanosine analogue, possesses potential antineoplastic activity. Upon administration into the peritumoral region after tumor resection, adenoviral vector encoding HSV thymidine kinase is transduced into tumor cells, and HSV-tk is expressed. Tumor cells expressing HSV-tk are sensitive to synthetic acyclic guanosine analogues. Subsequent administration of a synthetic acyclic guanosine analogue, such as valacyclovir (VCV) or ganciclovir (GCV), kills the tumor cells expressing HSV-tk. The release of tumor-associated antigens (TAA) by dying tumor cells may then stimulate an antitumor cytotoxic T lymphocyte (CTL) response, directed aganst any remaining tumor cells.

Ad-ISF35

A replication-defective adenovirus vector (Ad-ISF35), which encodes a membrane-stabilized, chimeric human-mouse CD40 binding protein (CD40 ligand; CD40L; CD154), with potential immunomodulatory and antineoplastic activities. Upon intratumoral administration, Ad-ISF135 preferentially transduces tumor cells and immunoregulatory cells in the tumor microenvironment. This increases the expression of CD154 in tumor cells, activates CD40 and stimulates signaling and immunoactivation, which are both mediated by CD40. This increases the expression of co-stimulatory molecules on these cells, which enhances their ability to function as antigen presenting cells (APCs) and increases their apoptotic potential. This leads to an increase in the infiltration of macrophages and neutrophils, which promote direct cytotoxicity, enhances the production of pro-inflammatory cytokines in the tumor microenvironment, and induces a specific cytotoxic T-lymphocyte (CTL) response against the tumor cells. In addition, transduction with Ad-ISF35 induces direct tumor cell death, probably through an anti-viral immune response. Ad-ISF35 also exerts a strong bystander effect in non-transduced cells thereby further inducing tumor cell death. Altogether, this will eradicate tumor cells. CD154, the main ligand for CD40, plays a key role in the activation of APCs, promotes immunoactivation, and increases apoptotic potential. The protein encoded by Ad-ISF35 does not contain the mouse antibody binding domains and does not induce human neutralizing antibodies. The metalloprotease cleavage site is deleted in this chimeric CD154 and thus it resists cleavage; the encoded protein also contains amino acid substitutions within the carboxy-terminal. Both sets of engineered mutations promote cell surface expression.

Ad-RTS-hIL-12

An inducible adenoviral vector encoding human pro-inflammatory cytokine interleukin-12 (IL-12; IL12), which is under the transcriptional control of the RheoSwitch Therapeutic System (RTS) (Ad-RTS-hIL-12), with potential immunomodulating and antineoplastic activities. RTS consists of two fusion proteins: Gal4-EcR, which contains a modified ecdysone receptor (EcR) fused with the DNA binding domain of the yeast Gal4 transcription factor, and VP16-RXR, which contains a chimeric retinoid X receptor (RXR) fused with the transcription activation domain of the viral protein VP16 of herpes simplex virus type 1 (HSV1). Upon intratumoral administration of Ad-RTS-hIL-12, given in combination with the proprietary, diacylhydrazine-based activator ligand veledimex (INXN-1001), veledimex binds specifically to the EcR part of the RTS and stabilizes heterodimerization between the two fusion proteins, forming an active transcription factor, which induces the transcription of IL-12 under the control of an inducible promoter containing Gal4-binding sites. The expressed IL-12 activates the immune system by promoting the activation of natural killer cells (NK cells), inducing secretion of interferon-gamma (IFN-g) and inducing cytotoxic T-lymphocyte (CTL)-mediated responses against tumor cells, which may result in immune-mediated tumor cell lysis and inhibition of tumor cell proliferation. In the presence of veledimex, the protein heterodimer changes to a stable conformation and can bind to the inducible promoter, while without veledimex the two fusion proteins form unstable heterodimers; this allows the controlled, regulated intratumoral expression of the IL-12 gene.

Ad-sig-hMUC-1/ecdCD40L vaccine

A cancer vaccine consisting of a recombinant adenoviral vector encoding the tumor-associated antigen (TAA) human MUC-1 (hMUC-1) linked to the extracellular domain (ecd) of the co-stimulatory molecule CD40 ligand (CD40L) and an adenovirus signal sequence that encodes a secretory signal peptide (Ad-sig) with potential immunostimulating and antineoplastic activities. Due to the presence of the secretory signal peptide expressed by Ad-sig in the vaccine construct, transfected cells may secrete a fusion protein composed of hMUC-1 and the CD40L ecd. The CD40L moiety part of the fusion protein binds to CD40 receptors on dendritic cells (DCs). Subsequently, DCs may be activated and migrate, T cells may expand, and a cytotoxic T-lymphocyte (CTL) response against tumor cells that overexpress hMUC-1 may follow. MUC-1 is a hypoglycosylated TAA overexpressed by epithelial cancer cells.

Ad5 [E1-, E2b-]-HER2/Neu vaccine ETBX-021

A cancer vaccine composed of a genetically engineered, replication-defective oncolytic adenovirus serotype 5 (Ad5) vector, in which the E1, E2b and E3 genes are deleted, that encodes a modified version of the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (HER2/neu; ErbB-2; ERBB2), with potential antineoplastic activity. Upon administration of Ad5 [E1-, E2b-]-HER2/neu ETBX-021, the vector expresses HER2/neu and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing the HER2/neu antigen. This results in the immune-mediated induction of death in and inhibition of proliferation of HER2/neu-expressing tumor cells. HER2/neu, a member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumor cell types while expression is restricted and minimal in certain normal healthy cells. It plays a key role in cancer cell proliferation and survival. The gene deletions in Ad5 may circumvent pre-existing anti-adenovirus immunity, allow HER2 gene insertion and expression and induce a strong immune response.

Ad5-CMV-NIS

A recombinant type 5 adenovirus (Ad5), encoding the gene for the human sodium-iodide symporter (NIS) linked to the cytomegalovirus (CMV) promoter, with potential gene transfection activity. Upon intratumoral injection, Ad5-CMV-NIS is taken up by tumor cells, resulting in the cellular expression of NIS. Subsequently, orally administered iodine 131 is taken up by NIS-expressing tumor cells, which may result in the selective accumulation of a cytotoxic dose of beta and gamma radiation in non-thyroidal tumor cells, sparing adjacent normal tissue. NIS, an intrinsic membrane glycoprotein, is an ion pump that actively transports iodide into cells which concentrate iodine; in addition to thyroid epithelial cells, it is found in non-thyroidal tissues including the salivary glands, the gastric mucosa, and lactating mammary glands.

Ad5-encoding IFNg SP-002

A replication deficient adenovirus type 5 (Ad5) vector encoding for the cytokine human interferon gamma (IFNg; IFN-gamma), with potential antineoplastic and immunomodulating activities. Upon intratumoral administration, Ad5-encoding IFNg SP-002 expresses human IFNg, which binds to and activates the cell-surface IFN-gamma receptor and may stimulate an antiproliferative natural killer (NK) cell response against tumor cells and induce tumor cell apoptosis.

Ad5-SGE-REIC/Dkk-3 MTG-201

A replication incompetent adenoviral vector type 5 (Ad5) encoding the tumor suppressor gene dickkopf-3 (DKK3; reduced expression in immortalized cells; REIC; Dickkopf WNT signaling pathway inhibitor 3), and containing the super gene expression (SGE) system, composed of the triple tandem enhancer sequences of human telomerase reverse transcriptase (hTERT), simian virus 40 (SV40) and cytomegalovirus (CMV), with potential immunostimulating and antineoplastic activities. Upon intratumoral (IT) injection and transfection of Ad5-SGE-REIC/Dkk-3 MTG-201, tumor cells express REIC/DKK3 protein. This may result in the activation of c-Jun-NH2-kinase (JNK) and ultimately lead to apoptosis via B-cell lymphoma-2 (Bcl2) suppression and caspase-3 activation. Increased expression of REIC/DKK3 in cancer cells may lead to an induction of tumor cell apoptosis and a reduction in tumor cell growth, while sparing normal, healthy cells expressing endogenous REIC/DKK3. In addition, the tumor cell killing promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response, thereby further killing any remaining REIC-deficient, untransfected tumor cells. The SGE system, also called C-TSC (CMV promoter driving the triple tandem enhancer sequences of hTERT, SV40 and CMV), enhances gene expression compared to more conventional adenoviral vectors. REIC/DKK3 is expressed by healthy cells, but expression is reduced or absent in many cancer cells due to REIC/DKK3 gene defects. As REIC/DKK3 plays a key role in tumor cell apoptosis, the absence of the REIC protein in tumor cells prevents tumor cell apoptosis.

Ad5-SGE-REIC/Dkk-3 MTG-201

A replication incompetent adenoviral vector type 5 (Ad5) encoding the tumor suppressor gene dickkopf-3 (DKK3; reduced expression in immortalized cells; REIC; Dickkopf WNT signaling pathway inhibitor 3), and containing the super gene expression (SGE) system, composed of the triple tandem enhancer sequences of human telomerase reverse transcriptase (hTERT), simian virus 40 (SV40) and cytomegalovirus (CMV), with potential immunostimulating and antineoplastic activities. Upon intratumoral (IT) injection and transfection of Ad5-SGE-REIC/Dkk-3 MTG-201, tumor cells express REIC/DKK3 protein. This may result in the activation of c-Jun-NH2-kinase (JNK) and ultimately lead to apoptosis via B-cell lymphoma-2 (Bcl2) suppression and caspase-3 activation. Increased expression of REIC/DKK3 in cancer cells may lead to an induction of tumor cell apoptosis and a reduction in tumor cell growth, while sparing normal, healthy cells expressing endogenous REIC/DKK3. In addition, the tumor cell killing promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response, thereby further killing any remaining REIC-deficient, untransfected tumor cells. The SGE system, also called C-TSC (CMV promoter driving the triple tandem enhancer sequences of hTERT, SV40 and CMV), enhances gene expression compared to more conventional adenoviral vectors. REIC/DKK3 is expressed by healthy cells, but expression is reduced or absent in many cancer cells due to REIC/DKK3 gene defects. As REIC/DKK3 plays a key role in tumor cell apoptosis, the absence of the REIC protein in tumor cells prevents tumor cell apoptosis.

Ad5-survivin-transduced autologous dendritic cell vaccine

A cell-based cancer vaccine containing autologous dendritic cells (DCs) that are transduced with a replication-deficient adenovirus type 5 vector (Ad5) encoding a mutated form of the tumor-associated antigen (TAA) survivin, with potential immunostimulatory and antineoplastic activities. Upon administration, Ad5-survivin-transduced autologous DC vaccine may elicit an immune response against cancer cells expressing survivin by activating cytotoxic T cells (CTLs). This leads to an induction of cell death in survivin-positive tumor cells. Survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types and plays a key role in tumor cell growth and survival.

Ad5-yCD/mutTK(SR39)rep-ADP

A second generation, replication-competent adenovirus type 5 containing a yeast cytosine deaminase(yCD)/mutant sr39 herpes simplex virus thymidine kinase fusion (yCD/mutTKsr39) gene and the 11.6 kDa adenovirus death protein (ADP) gene with potential oncolytic activity. Upon intratumoral administration and transduction of Ad5-yCD/mutTK(SR39)rep-ADP into tumor cells and subsequent expression of cytosine deaminase and viral thymidine kinase, administered prodrugs 5-fluorocytosine (5-FC) and ganciclovir are converted into their respective metabolites 5-fluorouracil (5-FU) and ganciclovir-5-monophosphate (ganciclovir-MP); 5-FU is subsequently metabolized to cytotoxic active metabolites 5-fluoroxyuridine monophosphate (F-UMP) and 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP); ganciclovir-TP subsequently is converted by mammalian thymidine kinase to cytotoxic ganciclovir-triphosphate (ganciclovir -TP). Tumor cells adjacent to tumor cells transduced with this agent may be killed through a "bystander effect". ADP may enhance spread and oncolytic activity of replication-competent adenoviruses. In addition to its oncolytic activity, Ad5-yCD/mutTK(SR39)rep-ADP may exhibit radiosensitizing activity.

Ad5-yCD/mutTKSR39rep-hIL12

A replication-competent oncolytic adenovirus encoding the murine pro-inflammatory cytokine interleukin-12 (IL-12) gene and two suicide fusion genes, a yeast cytosine deaminase (yCD) and a mutant form of herpes simplex virus type 1 thymidine kinase (HSV-1 TKSR39), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of Ad5-yCD/mutTKSR39rep-hIL12, the adenovirus selectively infects and replicates in tumor cells, which results in direct tumor cell lysis. Synergistically, IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma (IFN-g) and inducing cytotoxic T-lymphocyte (CTL) responses against tumor cells, which may result in immune-mediated tumor cell death, inhibition of tumor cell proliferation and inhibition of tumor angiogenesis. In addition, Ad5-yCD/mutTKSR39rep-hIL12-infected cancer cells express yCD and TKSR39; upon administration of the prodrugs 5-fluorocytosine (5-FC) and valganciclovir (vGCV), the yCD and HSV-1 TKSR39 activate these prodrugs to form 5-fluorouracil (5-FU) and ganciclovir, respectively. 5-FU gets converted to 5-fluoro-uridine monophosphate (5-FUMP) and subsequently to 5-fluoro-deoxyuridine monophosphate (5-FdUMP); 5-FdUMP irreversible inhibits thymidylate synthase, inhibits deoxythymidine triphosphate (dTTP) formation and halts DNA synthesis. Once phosphorylated intracellularly, ganciclovir triphosphate competitively inhibits deoxyguanosine triphosphate (dGTP) incorporation into DNA and inhibits DNA synthesis.

Ad5.SSTR/TK.RGD

An RGD-4C-modified, infectivity-enhanced, bicistronic type 5 adenovirus expressing herpes simplex virus thymidine kinase (HSV-tk) gene, a therapeutic suicide gene, and the somatostatin receptor type 2 (SSTR2) gene with potential antineoplastic activity. Modification with the double cyclic peptide RGD-4C allows the virus to bind to cellular integrins, frequently expressed on the surfaces of ovarian cancer cells, instead of the coxsackie and adenovirus (CAR) receptor, which is often nonfunctional in ovarian cancer cells. Upon intratumoral administration, Ad5.SSTR/TK.RGD transfects tumor cells and expresses the HSV-tk gene. After subsequent administration of a synthetic acyclic guanosine analogue prodrug like ganciclovir (GCV), expressed HSV-tk phosphorylates and activates the prodrug, which may result in inhibition of DNA synthesis and apoptosis in HSV-tk-expressing cancer cells. Additionally, as a bystander effect, adjacent non-transfected cells may be killed by the activated antiviral drug. SSTR2 expression allows imaging of gene transfer into tumor cells using a radiolabeled somatostatin analogue.

Ad5F35-LMP1/LMP2-transduced autologous dendritic cells

Autologous dendritic cells (DCs) transduced with the replication-deficient adenoviral vector Ad5F53 encoding the Epstein-Barr virus (EBV) transmembrane latent membrane proteins 1 and 2 (LMP1/LMP2) with potential immunostimulatory activity. Vaccination with Ad5F35-LMP1/LMP2-transduced autologous dendritic cells may stimulate a specific cytotoxic T-lymphocyte (CTL) response against LMP1- and LMP2-expressing tumor positive cells, resulting in tumor cell lysis and inhibition of tumor cell proliferation. LMP1 and LMP2 are expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin disease.

Adacel

(Other name for: diphtheria toxoid/tetanus toxoid/acellular pertussis vaccine adsorbed)

adagloxad simolenin

A carbohydrate-based immunostimulant comprised of the Globo H hexasaccharide 1 (Globo H) epitope linked to the immunostimulant carrier protein keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration of adagloxad simolenin, the carbohydrate antigen Globo H may stimulate a cytotoxic T-lymphocyte (CTL) response against Globo H-expressing tumor cells, thereby decreasing tumor cell proliferation. Globo H is a tumor associated antigen (TAA) commonly found on a variety of tumor cells including breast cancer cells. KLH improves antigenic immune recognition and T-cell responses.

adagrasib

An orally available, small molecule inhibitor that targets the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration adagrasib covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.

adakitug

A human monoclonal antibody against the pro-inflammatory mediator interleukin-8 (IL-8; CXCL8), with potential antineoplastic activities. Upon administration, adakitug directly binds to IL-8, thereby inhibiting the binding of IL-8 to its receptors CXCR1 and CXCR2. This inhibits activation of IL-8-mediated signaling transduction pathways, which decreases proliferation of susceptible tumor cells. Also, BMS-986253 effectively blocks binding of IL-8 to neutrophils and inhibits neutrophil activation and recruitment towards sites of inflammation, which reduces inflammation. IL-8, a member of the CXC chemokine family, is upregulated in a variety of cancer cell types and inflammatory diseases; it plays a key role in tumor cell proliferation, endothelial cell proliferation, and cancer stem cell (CSC) renewal.

Adakveo

(Other name for: crizanlizumab)

adalimumab

A recombinant, human IgG1 monoclonal antibody directed against tumor necrosis factor-alpha (TNF-alpha), with immunomodulating activity. Upon administration, adalimumab binds to TNF-alpha, thereby preventing its binding to the p55 and p75 TNF cell surface receptors and inhibiting TNF-mediated immune responses. TNF-alpha, a pro-inflammatory cytokine, is upregulated in various autoimmune diseases.

Adanon

(Other name for: methadone hydrochloride)

adapalene

A topical retinoid-like compound, chemically similar to vitamin A. Although the exact mechanism of action is unknown, adapalene binds to specific retinoic acid receptors in the nucleus, leading to specific gene expression. This agent stimulates skin growth through modulation of cellular differentiation, inflammatory processes and keratinization of follicular epithelial cells. Adapalene may increase dermal sensitivity to ultraviolet radiation.

Adapin

(Other name for: doxepin hydrochloride)

adavosertib

A small molecule inhibitor of the tyrosine kinase WEE1 with potential antineoplastic sensitizing activity. Adavosertib selectively targets and inhibits WEE1, a tyrosine kinase that phosphorylates cyclin-dependent kinase 1 (CDK1, CDC2) to inactivate the CDC2/cyclin B complex. Inhibition of WEE1 activity prevents the phosphorylation of CDC2 and impairs the G2 DNA damage checkpoint. This may lead to apoptosis upon treatment with DNA damaging chemotherapeutic agents. Unlike normal cells, most p53 deficient or mutated human cancers lack the G1 checkpoint as p53 is the key regulator of the G1 checkpoint and these cells rely on the G2 checkpoint for DNA repair to damaged cells. Annulment of the G2 checkpoint may therefore make p53 deficient tumor cells more vulnerable to antineoplastic agents and enhance their cytotoxic effect.

AdC68 Expressing PSA/PSMA/PSCA Vaccine PF-06755992

A prime cancer vaccine comprised of a genetically engineered, replication-deficient chimpanzee adenovirus serotype-68 (AdC68) encoding the tumor-associated antigens (TAAs) human prostate-specific antigen (PSA), prostate-specific membrane antigen (PSMA) and prostate stem cell antigen (PSCA), with potential immunostimulating and antineoplastic activities. Upon administration of AdC68 expressing PSA/PSMA/PSCA priming vaccine PF-06755992, the adenovirus infects and expresses PSA, PSMA and PSCA. The expressed proteins may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing PSA, PSMA and PSCA, thereby inducing tumor cell lysis. PSA, PSMA and PSCA are overexpressed on a variety of cancer cell types.

Adcetris

(Other name for: brentuximab vedotin)

Adderall

(Other name for: dextroamphetamine-amphetamine)

Adderall XR

(Other name for: dextroamphetamine-amphetamine)

ADE regimen

A regimen consisting of high-dose cytarabine (Ara-C), daunorubicin and etoposide, that is used for the treatment of pediatric and adult acute myeloid leukemia (AML).

adebrelimab

An immunoglobulin G4 (IgG4), humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, adebrelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

adecatumumab

A recombinant human IgG1 monoclonal antibody (MoAb) directed against the tumor associated antigen (TAA) epithelial cell adhesion molecule (EpCAM) with potential antitumor activity. Adecatumumab binds to EpCAM, which may result in antibody-dependent cellular cytotoxicity (ADCC) directed against EpCAM-expressing tumor cells. EpCAM (CD326), a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells; for some cancers, overexpression has been correlated with decreased survival.

adefovir dipivoxil

A dipivoxil formulation of adefovir, a nucleoside reverse transcriptase inhibitor analog of adenosine with activity against hepatitis B virus (HBV), herpes virus, and human immunodeficiency virus (HIV).

adeno-associated virus encoding anti-CD19/anti-CD3 bispecific diabody VNX-101

An off-the-shelf preparation of adeno-associated virus (AAV) encoding the anti-CD19/anti-CD3 bispecific diabody GP101, with potential immunostimulating and antineoplastic activities. Upon administration, AAV encoding anti-CD19/anti-CD3 bispecific diabody VNX-101 induces the secretion of GP101 by hepatocytes and other cells into the bloodstream. GP101 binds to both the CD3 antigen on T cells and the CD19 antigen expressed on tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

adenosine A2A receptor antagonist AZD4635

An orally bioavailable antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist AZD4635 selectively binds to and inhibits A2AR expressed on T-lymphocytes. This blocks tumor-released adenosine from interacting with A2AR and prevents the adenosine/A2AR-mediated inhibition of T-lymphocytes. This results in the proliferation and activation of T-lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits T-cell proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist CS3005

An orally bioavailable immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist CS3005 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist DZD2269

An immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist DZD2269 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist ILB2109

An orally bioavailable immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon oral administration, A2AR antagonist ILB2109 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist JNJ-86974680

An immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist JNJ-86974680 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T-lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist NIR178

An orally bioavailable immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist NIR178 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist PBF-509

An orally bioavailable adenosine A2A receptor (A2AR) antagonist, with potential antineoplastic activity. Upon administration, A2AR antagonist PBF-509 selectively binds to and inhibits A2AR expressed on T lymphocytes. This abrogates the adenosine/A2AR-mediated inhibition of T-lymphocytes and activates a T-cell-mediated immune response against tumor cells, thereby reducing proliferation of susceptible tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often produced in excess by cancer cells.

adenosine A2A receptor antagonist TT-10

An immune checkpoint inhibitor and antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, A2AR antagonist TT-10 selectively binds to and inhibits A2AR expressed on T lymphocytes. This prevents tumor-released adenosine from interacting with the A2A receptors, thereby blocking the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.

adenosine A2A receptor antagonist/phosphodiesterase 10A PBF-999

An orally bioavailable inhibitor of both the adenosine A2A receptor (A2AR; ADORA2A) and phosphodiesterase 10A (PDE-10A), with potential immunomodulating and antineoplastic activities. Upon administration, A2A/PDE-10A inhibitor PBF-999 selectively binds to and inhibits A2AR expressed on T-lymphocytes. This blocks tumor-released adenosine from interacting with A2AR and prevents the adenosine/A2AR-mediated inhibition of T-lymphocytes. This results in the proliferation and activation of T-lymphocytes and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits T-cell proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression. In addition, PBF-999 binds to and inhibits the activity of PDE-10A, thereby preventing the degradation of cyclic guanosine monophosphate (cGMP) and activates cGMP/cGMP-dependent protein kinase G (PKG) signaling. This induces beta-catenin degradation and thereby prevents the translocation of beta-catenin into the nucleus, and the beta-catenin-mediated induction of transcription of survival proteins, such as cyclin D1 and survivin. It also suppresses RAS/RAF/mitogen-activated protein kinase (MAPK) signaling. This induces apoptosis and inhibits the growth of tumor cells in which PDE-10A is overexpressed. PDE-10A is a cGMP-degrading PDE isozyme that is highly expressed in the brain and overexpressed in certain types of tumor cells. Elevation of intracellular cGMP is known to inhibit tumor proliferation and induce apoptosis. cGMP levels are low in cancer cells resulting from the overexpression PDE-10A.

adenosine A2B receptor antagonist PBF-1129

An orally bioavailable antagonist of the immunomodulatory checkpoint molecule adenosine A2B receptor (A2BR; ADORA2B), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, A2BR antagonist PBF-1129 competes with adenosine for binding to A2BR expressed on various cancer cell types and numerous immune cells, such as dendritic cells (DCs), mast cells, macrophages and lymphocytes. This inhibits A2BR activity and prevents adenosine/A2BR-mediated signaling. The inhibition of A2BR in cancer cells prevents activation of downstream oncogenic pathways, which leads to an inhibition of cell proliferation and metastasis. A2BR inhibition also prevents the release of various growth factors, cytokines and chemokines, such as vascular endothelial growth factor (VEGF), interleukin-8 (IL-8) and angiopoietin-2 (Ang2) from immune cells, which may abrogate the adenosine-mediated immunosuppression in the tumor microenvironment (TME) and activate the immune system to exert anti-tumor immune responses against cancer cells leading to tumor cell killing. In addition, under non-cancerous inflammatory conditions, inhibition of A2BR leads to reduced activation and proliferation of various immune cells, which results in decreased pro-inflammatory cytokine production and may prevent inflammation. A2BR, a G protein-coupled signaling receptor, is expressed on the cell surfaces of numerous immune cells and is often overexpressed on a variety of cancer cell types; it plays a key role in their proliferation, progression and metastasis. Adenosine is overproduced under inflammatory conditions and plays a key role in pro-inflammatory actions. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation. The pro- and anti-inflammatory effects of adenosine and A2BR are cell type-specific and dependent on the extracellular microenvironment.

adenosine A2B receptor antagonist TT-4

An orally bioavailable antagonist of the immunomodulatory checkpoint molecule adenosine A2B receptor (A2BR; ADORA2B), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon oral administration, A2BR antagonist TT-4 competes with adenosine for binding to A2BR expressed on various cancer cell types and numerous immune cells, such as dendritic cells (DCs), mast cells, macrophages and lymphocytes. This inhibits A2BR activity and prevents adenosine/A2BR-mediated signaling. The inhibition of A2BR in cancer cells prevents activation of downstream oncogenic pathways, which leads to an inhibition of cell proliferation and metastasis. A2BR inhibition also prevents the release of various growth factors, cytokines and chemokines, such as vascular endothelial growth factor (VEGF), interleukin-8 (IL-8) and angiopoietin-2 (Ang2) from immune cells, which may abrogate the adenosine-mediated immunosuppression in the tumor microenvironment (TME) and activate the immune system to exert anti-tumor immune responses against cancer cells leading to tumor cell killing. In addition, under non-cancerous inflammatory conditions, inhibition of A2BR leads to reduced activation and proliferation of various immune cells, which results in decreased pro-inflammatory cytokine production and may prevent inflammation. A2BR, a G protein-coupled signaling receptor, is expressed on the cell surfaces of numerous immune cells and is often overexpressed on a variety of cancer cell types; it plays a key role in their proliferation, progression and metastasis. Adenosine is overproduced under inflammatory conditions and plays a key role in pro-inflammatory actions. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation. The pro- and anti-inflammatory effects of adenosine and A2BR are cell type-specific and dependent on the extracellular microenvironment.

adenosine A2B receptor antagonist TT-702

An orally bioavailable prodrug and selective antagonist of the immunomodulatory checkpoint molecule adenosine A2B receptor (A2BR; ADORA2B), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon oral administration, A2BR antagonist TT-702 is converted to its active metabolite TT-478. TT-478 selectively binds to and blocks A2BR expressed on various cancer cell types and numerous immune cells, such as dendritic cells (DCs), mast cells, macrophages and lymphocytes. This prevents the binding of adenosine to A2BR, inhibits A2BR activity and prevents adenosine/A2BR-mediated signaling. This abrogates adenosine/A2BR-mediated immunosuppression, activates immune stimulatory cell, such as DCs and cytotoxic T lymphocytes (CTLs), and reduces immunosuppressive cells myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). This suppresses cancer cell growth, which leads to an inhibition of cell proliferation and metastasis. A2BR inhibition also prevents the release of various growth factors, cytokines and chemokines, which may further abrogate the adenosine-mediated immunosuppression in the tumor microenvironment (TME). This further activates the immune system to exert anti-tumor immune responses against tumor cells leading to tumor cell killing. In addition, under non-cancerous inflammatory conditions, inhibition of A2BR leads to reduced activation and proliferation of various immune cells, which results in decreased pro-inflammatory cytokine production and may prevent inflammation. A2BR, a G protein-coupled signaling receptor, is expressed on the cell surfaces of numerous immune cells and is often overexpressed on a variety of cancer cell types, especially under hypoxic conditions; it plays a key role in their proliferation, progression and metastasis. Adenosine is overproduced under inflammatory conditions and plays a key role in pro-inflammatory actions. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation. The pro- and anti-inflammatory effects of adenosine and A2BR are cell type-specific and dependent on the extracellular microenvironment.

adenosine receptor A2A/A2B antagonist M1069

An orally bioavailable antagonist of both the immunomodulatory checkpoint molecules adenosine A2A receptor (A2AR; ADORA2A) and A2B receptor (A2BR; ADORA2B), with potential immunomodulating and antineoplastic activities. Upon oral administration, adenosine A2A/A2B receptor antagonist M1069 competes with tumor-released adenosine for binding to A2AR and A2BR expressed on numerous intratumoral immune cells, such as dendritic cells (DCs), natural killer (NK) cells, macrophages and T lymphocytes. The binding of M1069 to A2AR and A2BR inhibits A2AR/A2BR activity and prevents adenosine-A2AR/A2BR-mediated signaling. A2AR/A2BR inhibition activates and enhances the proliferation of various immune cells, abrogates the adenosine-mediated immunosuppression in the tumor microenvironment (TME) and activates the immune system to exert anti-tumor immune responses against cancer cells, which leads to tumor cell killing. A2AR and A2BR, G protein-coupled signaling receptors, are expressed on the cell surfaces of numerous immune cells. Adenosine is often overproduced by tumor cells and plays a key role in immunosuppression and tumor cell proliferation.

adenosine triphosphate

An adenine nucleotide comprised of three phosphate groups esterified to the sugar moiety, found in all living cells. Adenosine triphosphate is involved in energy production for metabolic processes and RNA synthesis. In addition, this substance acts as a neurotransmitter. In cancer studies, adenosine triphosphate is synthesized to examine its use to decrease weight loss and improve muscle strength.

adenovector encoding MDA7

A nonreplicating adenoviral vector (adenovector) encoding the melanoma differentiation-associated 7 gene (MDA7) with potential antineoplastic activity. After intratumoral injection and adenovector-mediated gene transfer of MDA7 into tumor cells, the expressed MDA7 transgene may inhibit tumor cell proliferation and induce tumor cell apoptosis.

adenovector-transduced AP1903-inducible MyD88/CD40-expressing autologous PSMA-specific prostate cancer vaccine BPX-201

A genetically-modified, dendritic cell (DC)-based vaccine in which the autologous cells are transduced with an adenoviral vector expressing the tumor antigen prostate-specific membrane antigen (PSMA) and a fusion protein composed of synthetic ligand inducible adjuvant iMC composed of a drug-inducible costimulatory CD40 receptor (iCD40) and the adaptor protein MyD88, with potential immunomodulating and antineoplastic activities. The iCD40 contains a membrane-localized cytoplasmic CD40 domain fused to the FK506 modified drug-binding protein 12 (FKBP12). Upon intradermal administration of BPX-201, these DCs accumulate in local draining lymph nodes. Twenty-four hours after vaccination, the dimerizing agent AP1903 is administered. AP1903 binds to the drug binding domain, leading to iMC oligomerization and activation of iCD40 and MyD88-mediated signaling in iMC-expressing DCs. This signaling pathway activates the DCs and stimulates a cytotoxic T-lymphocyte (CTL) response against host tumor cells that express PSMA. PSMA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed in prostate cancer cells and is used as a tumor marker for both diagnosis and treatment evaluation. MyD88 is involved in interleukin 1 receptor (IL1R) and toll-like receptor (TLR) signaling.

adenoviral brachyury vaccine ETBX-051

A therapeutic cancer vaccine composed of a replication-defective, serotype 5 adenovirus (Ad5) with the viral genes early 1 (E1), early 2b (E2b), and early 3 (E3) deleted, and the human transcription factor brachyury encoded, with potential immunostimulating and antineoplastic activities. Upon subcutaneous administration, the adenoviral brachyury vaccine ETBX-051 expresses the brachyury protein. The expressed brachyury may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing brachyury, thereby resulting in both immune-mediated inhibition of tumor cell proliferation and tumor cell death. Deletion of the E1, E2b and E3 genes from Ad5 prevents anti-adenovirus immune responses. Brachyury, a tumor-associated antigen (TAA) and member of the T-box family of transcription factors, is overexpressed in a variety of tumor types. It plays an important role in cancer progression and metastasis.

adenoviral cancer vaccine PF-06936308

A cancer vaccine composed of a replication-defective E1-deleted adenovirus vector based on chimpanzee adenovirus serotype 68 (AdC68) expressing three not yet disclosed tumor-associated antigens (TAAs), with potential immunostimulating and antineoplastic activities. Upon vaccination with the adenoviral cancer vaccine PF-06936308, the adenovirus infects cells and expresses the TAAs. In turn, the TAAs activate the immune system to produce a cytotoxic T-lymphocyte (CTL) response against cells expressing the TAAs.

adenoviral MUC1 vaccine ETBX-061

A therapeutic cancer vaccine composed of a replication-defective, serotype 5 adenovirus (Ad5) with the viral genes early 1 (E1), early 2b (E2b), and early 3 (E3) deleted, and the human glycoprotein mucin 1 (MUC1) encoded, with potential immunostimulating and antineoplastic activities. Upon subcutaneous administration, the adenoviral MUC1 vaccine ETBX-061 expresses the MUC1 protein. The expressed MUC1 may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing MUC1, thereby resulting in both immune-mediated inhibition of tumor cell proliferation and tumor cell death. Deletion of the E1, E2b and E3 genes from Ad5 prevents anti-adenovirus immune responses. MUC1, a tumor-associated antigen (TAA) and type I transmembrane protein, is overexpressed in a variety of tumor types. It plays an important role in cancer progression and metastasis.

adenoviral PSA vaccine ETBX-071

A cancer vaccine composed of a genetically engineered, replication-deficient adenovirus carrying the gene encoding human prostate-specific antigen (PSA), with potential immunostimulating and antineoplastic activities. Upon vaccination with the adenoviral-PSA vaccine ETBX-071, the adenovirus infects cells and expresses PSA. In turn, PSA activates the immune system and induces a cytotoxic T-lymphocyte (CTL) response against PSA-expressing tumor cells. PSA, a tumor associated antigen (TAA), is expressed by prostate epithelial cells and is overexpressed in prostate cancer.

adenoviral tumor-specific neoantigen priming vaccine GAd-209-FSP

An off-the-shelf neoantigen priming vaccine comprised of a great ape adenovirus (GAd) encoding tumor-specific neoantigens (TSNAs) derived from as of yet undisclosed frameshift peptides (FSPs) with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration of the adenoviral tumor-specific neoantigen priming vaccine GAd-209-FSP, the adenovirus infects cells and expresses the TSNAs. This stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the TSNAs, leading to tumor cell lysis. Adenoviral-TSNA priming vaccine GAd-209-FSP is followed by boosting with a vaccine that encodes the same target TSNAs.

adenoviral tumor-specific neoantigen priming vaccine GRT-C901

A personalized cancer vaccine comprised of a chimpanzee adenovirus vector (ChAdV) encoding twenty tumor-specific neoantigens (TSNAs) that have been identified through genetic sequencing of a patient’s tumor cells, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration of the adenoviral-TSNA priming vaccine GRT-C901, the adenovirus infects cells and expresses the TSNAs. This stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the TSNAs, leading to tumor cell lysis. Adenoviral-TSNA vaccine GRT-C901 is followed by monthly boosting with a self-amplifying mRNA (SAM) boosting vaccine that encodes the same 20 target TSNAs. The combined immunotherapy product, consisting of priming and boosting vaccines, is referred to as GRANITE-001.

adenoviral vector Ad5-CEA(6D) vaccine

A replication-defective, E1- and E2b-deleted oncolytic adenoviral serotype 5 (Ad5) encoding an epitope of human carcinoembryonic antigen (CEA) with potential antineoplastic activity. Adenoviral vector Ad5-CEA(6D) vaccine expresses a highly immunogenic analogue of CEA [CAP1-(6D)]. Upon administration, this vaccine may induce both humoral and cellular immune responses against tumor cells expressing the CEA antigen, thereby resulting in the immune-mediated inhibition of tumor cell proliferation and tumor cell death. CEA, a tumor-associated antigen, is overexpressed in various tumor cell types. Deletion of early genes E1 and E2b in Ad5 potentially circumvent pre-existing anti-adenovirus immunity and is capable of inducing strong immune responses.

adenoviral vector encoding VEGF-C LX-1101

A genetically engineered, replication-deficient adenovirus carrying the gene encoding for the human vascular endothelial growth factor C (VEGFC; VEGF-C; Flt4 ligand), with potential pro-angiogenic activity. Upon perinodal administration of the AdAptVEGF-C adenoviral vector LX-1101, the adenovirus infects cells and promotes expression of VEGF-C. In turn, VEGF-C induces vascular and lymphatic endothelial cell proliferation locally, and may help re-grow the lymphatic system and improve symptoms associated with lymphedema (LE). VEGF-C, a lymphatic growth factor, plays a key role in (lymph)angiogenesis and the functioning of the lymphatic system.

adenoviral-transduced hIL-12-expressing autologous dendritic cells INXN-3001 plus activator ligand INXN-1001

Autologous dendritic cells tranduced with a replication incompetent adenovirus encoding human pro-inflammatory cytokine interleukin-12 (IL-12) (INXN-3001) in combination with the proprietary orally bioavailable, small molecule activator ligand INXN-1001, with potential immunomodulating and antineoplastic activities. Production of IL-12 is controlled by an inducible DNA element that allows transcription initiation only in the presence of the ligand inducer INXN-1001. Upon intratumoral injection of INXN-3001 and subsequent oral administration of activator ligand, INXN-1001 is able to induce expression of IL-12 in INXN-3001. IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells, inducing the secretion of interferon-gamma and inducing a cytotoxic T lymphocyte response against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. As INXN-1001 regulates both the timing and the levels of IL-12 expression, IL-12 toxicity can be reduced.

adenovirus 5 CEA/MUC1/brachyury vaccine Tri-Ad5

A combination of three therapeutic cancer vaccines each containing a replication-defective, oncolytic adenoviral serotype 5 (Ad5) and each encoding a different tumor-associated antigen (TAA): human carcinoembryonic antigen (CEA), human glycoprotein mucin 1 (MUC1), and human transcription factor brachyury, with potential immunostimulating and antineoplastic activities. Upon subcutaneous administration, the Ad5 CEA/MUC1/brachyury vaccine Tri-Ad5 expresses the CEA, MUC1 and brachyury proteins. The expressed proteins may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing CEA, MUC1 and brachyury, thereby resulting in both immune-mediated inhibition of tumor cell proliferation and tumor cell death. CEA, MUC1 and brachyury are TAAs overexpressed in various tumor types. The Ad5 viral genes early 1 (E1), early 2b (E2b), and early 3 (E3) are deleted in Tri-Ad5, which prevents anti-adenovirus immune responses.

adenovirus 5-CD40 ligand

An adenovirus vector engineered to produce CD40 ligand. For use as a possible gene therapy agent. May induce apoptosis through the TNF pathway.

adenovirus 5-human guanylyl cyclase C-PADRE vaccine

A replication-defective, recombinant adenoviral serotype 5 (Ad5) encoding human guanylyl cyclase C (hGCC) and the synthetic Pan DR epitope (PADRE), with potential antineoplastic and immunomodulating activities. Upon intramuscular administration, the Ad5-hGCC-PADRE vaccine expresses hGCC, which may induce both humoral and cellular immune responses against tumor cells expressing the hGCC antigen. This results in the immune-mediated inhibition of tumor cell proliferation, and leads to tumor death. The hGCC protein is normally restricted to intestinal epithelial cells but is overexpressed by metastatic colorectal tumors. PADRE is a helper T-lymphocyte epitope that is able to augment the magnitude and duration of the cytotoxic T-lymphocyte (CTL) response.

adenovirus 5/F35-human guanylyl cyclase C-PADRE

A recombinant adenoviral serotype 5 (Ad5) in which the Ad5-based vector fiber is replaced by the fiber from the human B adenovirus serotype 35 (F35), encoding for the human guanylyl cyclase C (hGCC), and fused to the synthetic Pan DR epitope (PADRE), with potential antineoplastic and immunomodulating activities. Upon intramuscular administration of the Ad5/F35-hGCC-PADRE, the Ad5/F35 targets CD46, which is expressed widely on most tumor cells, and the virus is taken up by cells. Once inside the cells, the virus expresses hGCC. The expressed hGCC induces both humoral and cellular immune responses against tumor cells expressing the hGCC antigen. This results in the immune-mediated killing of tumor cells. The hGCC protein is normally restricted to intestinal epithelial cells but is overexpressed by metastatic colorectal tumors. PADRE is a helper T-lymphocyte epitope that is able to augment the magnitude and duration of the cytotoxic T-lymphocyte (CTL) response. The inclusion of the chimeric Ad5/F35 fiber increases viral uptake in cells through CD46.

adenovirus B7-1

A gene-viral vector complex comprised of an adenovirus vector and B7-1 gene targeting the CD80 antigen. Adenovirus B7-1 is used as a component in antineoplastic vaccines to elicit a cytotoxic T-cell response.

adenovirus encoding human aquaporin-1

A replication-deficient, recombinant adenovirus encoding human aquaporin-1 with potential membrane water channel activity. Upon transfection of salivary glands, adenovirus encoding human aquaporin-1 (AdhAQP1) directs human aquaporin-1 (hAQP1) expression in the apical and basolateral plasma membranes of salivary secretory cells, which may result in increased saliva production. hAQP1, a water channel protein, is one of several highly conserved water channel proteins that mediate water permeability in cells of water-transporting tissues.

adenovirus encoding rat Her-2/neu

A replication-defective oncolytic adenovirus, encoding rat Her-2/neu (ErbB-2), with potential antineoplastic activity. Upon administration, adenovirus encoding rat HER-2/neu may induce an immune response against tumor cells expressing the HER-2/neu antigen, which may result in the immune-mediated inhibition of tumor cell proliferation and tumor cell death. Her-2/neu, a tumor-associated antigen and member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumor cell types.

adenovirus encoding recombinant human endostatin

A replication-defective, recombinant oncolytic adenovirus encoding human endostatin with potential antineoplastic activity. Endostatin, a 20 kDa C-terminal proteolytic fragment of collagen XVIII, is an important angiogenesis inhibitor. Upon intratumoral administration, the adenovirus infects and replicates in tumor cells. The expressed endostatin may inhibit endothelial cell proliferation and angiogenesis which may result in a reduction of tumor growth.

adenovirus encoding tyrosinase/MART-1/MAGEA6-transduced autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) transduced with a recombinant adenoviral vector encoding three full length human melanoma associated antigens (MAAs), tyrosinase, melan-A (MART-1) and the melanoma antigen A6 (MAGEA6), with potential antineoplastic activity. Upon intradermal administration, adenovirus encoding tyrosinase/MART-1/MAGEA6-transduced autologous DC vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tyrosinase/MART-1/MAGEA6-positive tumor cells, which may result in tumor cell death and decreased tumor growth. Tyrosinase, a melanoma-specific differentiation antigen, catalyzes the first step of melanin synthesis in melanocytes. Vaccination with multi-antigen modified DC may improve the efficacy of the DC immunotherapy.

adenovirus expressing mutant HPV E6/E7

A cancer vaccine comprised of a genetically engineered, replication-deficient adenovirus encoding inactive, mutant forms of the human papillomavirus (HPV) transforming proteins E6 and E7, with potential immunostimulating and antineoplastic activities. Upon administration of adenovirus expressing mutant HPV E6/E7, the adenovirus infects and expresses the E6 and E7 proteins. The expressed E6 and E7 proteins stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing HPV E6 and E7, thereby inducing tumor cell lysis. Oncoproteins E6 and E7 play a key role in the development of cervical intraepithelial neoplasia (CIN) and cervical carcinoma.

adenovirus HER2-transduced autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) transduced with a replication-deficient adenovirus vector encoding HER-2 with potential antineoplastic activity. Upon administration, adenovirus HER2-transduced autologous dendritic cell vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against HER-2-positive tumor cells, which may result in tumor cell death and decreased tumor growth. HER-2, a tyrosine kinase receptor for epidermal growth factor (EGF) (also known as neu and ErbB2), is overexpressed by some breast, ovarian, and gastric cancers.

adenovirus RSV-TK

A gene viral vector complex comprised of a replication-defective adenovirus and a herpes simplex virus thymidine kinase gene that activates ganciclovir, causing inhibition of DNA synthesis and apoptosis.

adenovirus serotype 26-expressing HPV16 vaccine JNJ-63682918

A prime cancer vaccine comprised of a genetically engineered, replication-deficient adenovirus serotype 26 (Ad26) encoding the oncogenic human papillomavirus 16 (HPV16), with potential immunostimulating and antineoplastic activities. Upon intramuscular administration of Ad26-expressing HPV16 vaccine JNJ-63682918, the adenovirus infects and expresses HPV16. The expressed proteins stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing HPV16 antigens, thereby inducing tumor cell lysis. HPV16 infection plays a key role in the development of a variety of cancers.

adenovirus serotype 26-expressing HPV18 vaccine JNJ-63682931

A prime cancer vaccine comprised of a genetically engineered, replication-deficient adenovirus serotype 26 (Ad26) encoding the oncogenic human papillomavirus 18 (HPV18), with potential immunostimulating and antineoplastic activities. Upon intramuscular administration of Ad26-expressing HPV18 vaccine JNJ-63682931, the adenovirus infects and expresses HPV18. The expressed proteins stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing HPV18 antigens, thereby inducing tumor cell lysis. HPV18 infection plays a key role in the development of a variety of cancers.

adenovirus vector

One of a number of genetically-engineered adenoviruses designed to insert a gene of interest into a eukaryotic cell where the gene of interest is subsequently expressed. Unlike most other vectors, adenovirus vectors have the ability to infect post-mitotic cells. Thus, these agents are especially useful for gene transfer into neuronal cells.

adenovirus-encoding E.coli PNP

A replication-incompetent adenovirus encoding E. coli purine nucleoside phosphorylase (Ad/PNP) used as a prodrug activating agent. Administered intratumorally, Ad/PNP expresses the enzyme PNP, which may catalyze systematically administrated fludarabine phosphate prodrug into its active form 2-fluoroadenine (F-Ade). F-Ade inhibits DNA polymerase alpha, ribonucleotide reductase and DNA primase, thereby interrupting DNA synthesis and inhibiting tumor cell growth. Localized prodrug activation provides targeted chemotherapy, thereby potentially reducing systemic side effects.

adenovirus-expressing TLR5/TLR5 agonist nanoformulation M-VM3

A nanoparticle-based formulation containing a recombinant non-replicating adenovirus (Ad) encoding toll-like receptor 5 (TLR5) and its specific ligand protein 502S, with potential antineoplastic and immunomodulating activities. Upon administration, the Ad preferentially and specifically infects cells expressing the Coxsackievirus and adenovirus receptor (CAR), which is highly expressed in certain human tumors, and expresses both TLR5 and a specific agonistic ligand in the same cell. 502S binds to and activates TLR5, thereby allowing for continuous TLR5 signaling. This stimulates dendritic cells (DCs), monocytes, macrophages and the nuclear factor-kappa B (NF-kappaB) signaling cascade. This activation results in the production of pro-inflammatory cytokines, including interferon alpha, tumor necrosis factor-alpha and the interleukins (IL), IL-1 beta, -6 and -12. This may induce a T helper cell-1 (Th1) immune response and activate a cytotoxic T-lymphocyte (CTL) response against tumor associated antigens (TAAs). TLR5, a member of the TLR family, plays a key role in the activation of innate immunity.

adenovirus-mediated human interleukin-12

A replication-incompetent adenovirus encoding human pro-inflammatory cytokine interleukin-12 (IL-12) (Ad.hIL-12), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, the adenovirus selectively infects and replicates in tumor cells, which may result in tumor cell lysis. Synergistically, IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma and inducing cytotoxic T cell responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation.

adenovirus-mediated human interleukin-12 INXN-2001 plus activator ligand INXN-1001

A replication incompetent adenovirus encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) (INXN-2001) in combination with the proprietary activator ligand INXN-1001, with potential immunomodulating and antineoplastic activities. Production of IL-12 is controlled by an inducible DNA element that allows transcription initiation only in the presence of the ligand inducer. Upon intratumoral administration of INXN-2001 and oral administration of INXN-1001, INXN-1001 is able to induce expression of IL-12 from INXN-2001. IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma and inducing cytotoxic T cell responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation.

adenovirus-p53 transduced dendritic cell vaccine

A cancer vaccine consisting of autologous dendritic cells (DCs) transduced with a recombinant adenovirus encoding p53 peptide, with potential immunomodulating activity. Intradermal vaccination with adenoviral-p53 transduced dendritic cell vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing mutant p53, resulting in tumor cell lysis. p53, a tumor suppressor gene, is mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.

adenovirus-PSA prostate cancer vaccine

A cancer vaccine composed of a genetically engineered, replication-deficient type 5 adenovirus carrying the human prostate-specific antigen (PSA), with potential immunostimulating and antineoplastic activities. Upon subcutaneous vaccination with the adenovirus-PSA prostate cancer vaccine, the adenovirus infects cells and expresses PSA. In turn, PSA may activate the immune system and may induce a cytotoxic T-lymphocyte response against PSA-expressing tumor cells. PSA, a tumor associated antigen, is expressed by prostate epithelial cells and is overexpressed in prostate cancer.

adenovirus/cytomegalovirus/Epstein-Barr virus-specific allogeneic cytotoxic T lymphocytes

Allogeneic tri-viral specific, adenovirus, cytomegalovirus and Epstein-Barr virus (Adv, CMV and EBV or ACE), cytotoxic T-lymphocytes (CTLs) with potential antiviral activity. Donor-derived T-cells were exposed to dendritic cells nucelofected with DNA plasmids encoding Hexon and Penton (Adv), pp65 and IE1 (CMV), and LMP2, EBNA1 and BZLF1 (EBV), all are critical proteins for the proliferation of these viruses, and subsequently maintained in the presence of interleukins 4 and 7 with a novel culture device to expand and sustain the repertoire of CTLs. After an allogeneic hematopoietic stem cell transplant (HSCT), infusion of these CTLs primed towards Adv, CMV and EBV may prevent viral infection by these pathogens.

Adenuric

(Other name for: febuxostat)

AdGMCAIX-transduced autologous dendritic cells

Autologous dendritic cells (DCs) transduced with a recombinant, replication-defective adenoviral vector expressing the fusion gene granulocyte-macrophage colony-stimulating factor (GM-CSF) and carbonic anhydrase IX (CA-IX or CA9) (GMCA-9), with potential immunomodulating activity. The autologous DCs are transduced ex vivo and express the GMCA-9 fusion protein on the cell surface. Upon intradermal administration of the AdGMCAIX-transduced autologous DCs back into the patient, the DCs activate the immune system to both mount a cytotoxic T lymphocyte-mediated response against tumor cells positive for the CA9 antigen, and generate memory T cells. This may result in decreased tumor growth. CA9, also known as G250, is a renal cell carcinoma (RCC)-associated antigen and a member of the carbonic anhydrase family that contains a human leukocyte antigen (HLA)-A2.1-restricted epitope; it is found in a majority of renal cell carcinomas while absent in most normal tissues. The cytokine GM-CSF enhances the immunogenicity of CA9-based DC vaccines.

ADH-1

A small, cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis. N-cadherin, a cell- surface transmembrane glycoprotein of the cadherin superfamily of proteins involved in calcium-mediated cell-cell adhesion and signaling mechanisms; may be upregulated in some aggressive tumors and the endothelial cells and pericytes of some tumor blood vessels.

adipose-derived expanded mesenchymal stem cells SCM-010

A preparation of human adipose-derived mesenchymal stem cells (MSCs), that can potentially be used for engraftment purposes in certain autoimmune disorders. Upon intrathecal administration, adipose-derived expanded mesenchymal stem cells SCM-010 migrate to the bone marrow. These MSCs are pluripotent and capable of differentiating along specific lineages and may activate the immune system and repair damage to the nervous system.

adipose-derived regenerative cells

A population of cells derived from adipose tissue with stem cell and wound repair activities. Adipose-derived regenerative cells (ADRC) consists of several cell types, such as adult stem cells, vascular endothelial cells, and vascular smooth muscle cells, among others. These cells contribute to wound repair through a variety of mechanisms by promoting blood vessel growth and blocking apoptosis. In addition, ADRC can differentiate into several tissue types, such as bone, cartilage, fat, skeletal muscle, smooth muscle and cardiac muscle.

adipose-derived stromal vascular fraction cells

A population of stromal vascular fraction (SVF) cells derived from autologous adipose tissue, with potential tissue regenerative activity. SVF cells are obtained through liposuction and contain multiple cell types, including adipose-derived stem cells (ADSCs), mesenchymal and endothelial progenitor cells, leukocyte subtypes, lymphatic cells, pericytes, and vascular smooth muscle cells. The SVF cells are processed in such a way as to contain a reproducible and consistent composition of heterogeneous cells. Upon processing and administration, the adipose-derived SVF cells can differentiate into different tissue types, support neovascularization, replace cells and repair injured issue.

ado-trastuzumab emtansine

An antibody-drug conjugate (ADC) consisting of the recombinant anti-epidermal growth factor receptor 2 (HER2) monoclonal antibody trastuzumab conjugated to the maytansinoid DM1 via a nonreducible thioether linkage (MCC) with potential antineoplastic activity. The trastuzumab moiety of this ADC binds to HER2 on tumor cell surfaces; upon internalization, the DM1 moiety is released and binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting cell division and the proliferation of cancer cells that overexpress HER2. Linkage of antibody and drug through a nonreducible linker has been reported to contribute to the improved efficacy and reduced toxicity of this ADC compared to similar ADCs constructed with reducible linkers.

adoptive cell therapy agent

A preparation of allogeneic or autologous cells that is meant to be administered to a patient and may have an immunotherapeutic effect.

adozelesin

An alkylating agent that bind to the DNA minor groove in a sequence-specific manner and form covalent adducts with adenines, resulting in the inhibition of DNA replication and induction of apoptosis.

adrenocorticotropic hormone

A hormone secreted by the anterior portion of the pituitary gland and regulates hormone, primarily cortisol, secreted by the adrenal gland.

AdRTVP-1-transduced prostate cancer cell-based vaccine

A cell-based vaccine comprised of prostate cancer cells transduced with an adenoviral vector encoding human RTVP-1 (AdRTVP-1), with potential antineoplastic and immunostimulating activities. RTVP-1, also referred to as glioma pathogenesis-related protein 1 (GLIP1), is down-regulated in prostate tumors. Regulated by tumor suppressor p53, the expression of RTVP-1 functions as a tumor suppressor, and is abundant in normal human prostate epithelial cells as well as in differentiated macrophages. Administration of this vaccine leads to an induction of apoptosis through the expression of RTVP-1 and results in a reduction in cellular proliferation in prostate cancer cells. In addition, this cancer-cell based vaccine may induce a cytotoxic T lymphocyte (CTL) response against prostate specific tumor associated antigens, resulting in an immune-mediated prostate cancer cell death. Furthermore, RTVP-1 stimulates CTL and natural killer (NK) cell activities.

Adstiladrin

(Other name for: nadofaragene firadenovec-vncg)

ADVEXIN

(Other name for: contusugene ladenovec)

AE37 peptide/GM-CSF vaccine

A vaccine containing HER2/Neu-derived epitope (amino acids 776-790) linked to li-Key peptide (li-Key/HER2/neu hybrid peptide or AE37), and combined with granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunoadjuvant activities. Upon vaccination, AE37 may activate the immune system and stimulate T-helper cells against HER2/Neu expressing cancer cells. GM-CSF may potentiate the immune response against cancer cells expressing the HER2/Neu antigen. The Ii-Key moiety, a 4-amino acid (LRMK) epitope from the MHC class II-associated invariant chain (Ii protein), increases T-helper cell stimulation against HER2/neu antigen when compared to unmodified class II epitopes. HER2/neu, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types and is highly immunogenic.

AEE788

An orally bioavailable multiple-receptor tyrosine kinase inhibitor. AEE788 inhibits phosphorylation of the tyrosine kinases of epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), and vascular endothelial growth factor receptor 2 (VEGF2), resulting in receptor inhibition, the inhibition of cellular proliferation, and induction of tumor cell and tumor-associated endothelial cell apoptosis.

AEG35156

A second-generation synthetic antisense oligonucleotide with potential antineoplastic activity. AEG35156 selectively blocks the cellular expression of X-linked inhibitor of apoptosis protein (XIAP), a pivotal inhibitor of apoptosis that is overexpressed in many tumors. This agent reduces total levels of XIAP in tumor cells, working synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. XIAP interferes with both the intrinsic and extrinsic program-death signaling pathways, which may render tumor cells resistant to apoptosis.

aeneic multi-virus-specific T cells ALVR106

A preparation of off-the-shelf (OTS), donor-derived T lymphocytes that are specifically reactive towards four community acquired respiratory viruses: respiratory syncytial virus (RSV), influenza, parainfluenza virus (PIV), and human metapneumovirus (hMPV), with potential antiviral activity. Upon infusion into allogeneic hematopoietic stem cell transplant (HSCT), solid organ transplant (SOT) recipients or other immunocompromised patients, allogeneic multi-virus-specific T cells ALVR106 provides virus-specific cellular immunity and causes specific anti-viral effects against the four viruses RSV, influenza, PIV and hMPV. This may prevent RSV, influenza, PIV and hMPV infection, and inhibits viral-associated diseases.

Aeroseb-HC

(Other name for: therapeutic hydrocortisone)

aerosol gemcitabine

An aerosol inhalation formulation containing gemcitabine (GCB), a broad-spectrum antimetabolite and deoxycytidine analogue, with potential antineoplastic activity. Upon inhalation via a nebulizer, GCB is converted intracellularly by deoxycytidine kinase to its active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase (RNR), thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in DNA strand termination and the induction of apoptosis of lung tumor cells. GCB administration directly into the lungs via aerosol yields higher concentrations of GCB locally than can be achieved by systemic GCB administration, potentially reducing systemic toxicity.

aerosol sargramostim

An aerosol inhalation formulation containing a yeast-derived glycosylated recombinant form of human granulocyte macrophage colony stimulating factor (GM-CSF) with potential immunostimulating activity. Sargramostim binds to specific cell surface receptors, modulating the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production. This agent also activates neutrophils, monocytes, macrophages, and dendritic cells and promotes antigen presentation, upregulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated, lymphokine-activated killer cell function. Aerosol inhalation may help achieve high concentrations of sargramostim in the lung.

aerosolized aldesleukin

An aerosol formulation of aldesleukin, a recombinant form of interleukin-2 (IL-2), with potential immunostimulating activity. Upon IL-2 inhalation, this cytokine activates lymphokine-activated killer cells and natural killer cells, and induces expression of cytotoxic cytokines, such as interferon-gamma and transforming growth factor-beta. This may eventually halt tumor cell growth. Localized administration of IL-2 may decrease toxicity and increase efficacy.

aerosolized liposomal rubitecan

An aerosolized liposomal preparation of rubitecan, a water-insoluble derivative of camptothecin with potential antineoplastic activity. Rubitecan (or 9-nitro-20 (S)-camptothecin) and its active metabolite 9-aminocamptothecin (9-AC) selectively stabilize topoisomerase I-DNA covalent complexes during S-phase, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. This agent is formulated with dilauroylphosphatidylcholine and nebulized in particle sizes of 1.2-1.6 micrometer mass median aerodynamic diameter.

Aerrane

(Other name for: isoflurane)

Aezea

(Other name for: cenersen)

afamelanotide

A synthetic peptide analogue of the naturally occurring alpha-melanocyte stimulating hormone (a-MSH) with potential photoprotective activity. Mimicking the action of a-MSH, afamelanotide stimulates melanocytes to increase the production and release of melanin. Increased melanocyte melanin may protect against ultraviolet radiation (UVR)-initiated cellular DNA damage, oxidation of membrane proteins, and alterations in intracellular signaling processes in epidermal cells. Endogenously, a-MSH is released by skin cells in response to UVR exposure, stimulating melanocytes to produce and release melanin.

afamitresgene autoleucel

A preparation of autologous human T lymphocytes transduced with a lentiviral vector encoding an affinity-enhanced T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A2-restricted peptide human melanoma antigen A4 (MAGE-A4) C1032, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, afamitresgene autoleucel targets and binds to tumor cells expressing MAGE-A4. This results in cell death of MAGE-A4-expressing tumor cells. The tumor-associated antigen (TAA) MAGE-A4, a member of the MAGE-A family of cancer testis antigens, is overexpressed by a variety of cancer cell types.

afatinib dimaleate

The dimaleate salt form of afatinib, an orally bioavailable anilino-quinazoline derivative and inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with antineoplastic activity. Upon administration, afatinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4), and certain EGFR mutants, including those caused by EGFR exon 19 deletion mutations or exon 21 (L858R) mutations. This may result in the inhibition of tumor growth and angiogenesis in tumor cells overexpressing these RTKs. Additionally, afatinib inhibits the EGFR T790M gatekeeper mutation which is resistant to treatment with first-generation EGFR inhibitors. EGFR, HER2 and HER4 are RTKs that belong to the EGFR superfamily; they play major roles in both tumor cell proliferation and tumor vascularization and are overexpressed in many cancer cell types.

afeletecan hydrochloride

The hydrochloride salt form of afeletecan, a water-soluble camptothecin derivative conjugated to a carbohydrate moiety exhibiting antineoplastic activity. Afeletecan stabilizes the topoisomerase I-DNA covalent complex and forms an enzyme-drug-DNA ternary complex. As a consequence of the formation of this complex, both the initial cleavage reaction and religation steps are inhibited and subsequent collision of the replication fork with the cleaved strand of DNA results in inhibition of DNA replication, double strand DNA breakage and triggering of apoptosis. The peptide carbohydrate moiety of this agent stabilizes the lactone form of camptothecin in blood.

Affinitac

(Other name for: aprinocarsen)

Affinitak

(Other name for: aprinocarsen)

afimoxifene

A tamoxifen metabolite with both estrogenic and anti-estrogenic effects. Afimoxifene has a higher affinity for the estrogen receptor than tamoxifen, and functions as an antagonist in breast cancer cells.

Afinitor

(Other name for: everolimus)

Afinitor Disperz

(Other name for: everolimus tablets for oral suspension)

Aflodac

(Other name for: sulindac)

AFP gene hepatocellular carcinoma vaccine

A cancer vaccine composed of naked plasmid DNA of the gene for the tumor-associated antigen alpha-fetoprotein (AFP), a macromolecule that acts as a specific immunologic target for hepatocellular carcinoma. This agent exerts an antitumor effect by inducing cytotoxic T-lymphocytes to attack AFP-expressing tumor cells.

afuresertib

An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Afuresertib binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Agaricus blazei Murill extract

A dietary supplement containing an extract of the Basidiomycete fungus Agaricus blazei Murill with potential chemopreventive, antineoplastic and immunopotentiating activities. Agaricus blazei Murill extract contains high levels of phytochemicals, especially beta-D-glucans. Beta-D-glucans may promote dendritic cell (DC) maturation; increase interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) and immunoglobulin levels; and may enhance natural killer (NK) cell activity, potentially boosting anti-tumor host immune responses.

agatolimod sodium

The tricosasodium salt of a synthetic 24-mer oligonucleotide containing 3 CpG motifs with potential antineoplastic and immunostimulatory activity. Agatolimod selectively targets Toll-like receptor 9 (TLR9), thereby activating dendritic and B cells and stimulating cytotoxic T cell and antibody responses against tumor cells bearing tumor antigens.

agerafenib

An orally available v-raf murine sarcoma viral oncogene homolog B1 (B-raf) serine/threonine protein kinase inhibitor with potential antineoplastic activity. Agerafenib specifically and selectively inhibits the activity of the mutated form (V600E) of B-raf kinase. This inhibits the activation of the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway and may result in a decrease in the proliferation of tumor cells expressing the mutated B-raf gene. The Raf mutation BRAF V600E, in which valine is substituted for glutamic acid at residue 600, is frequently found in a variety of human tumors and results in the constitutive activation of the RAF/MEK/ERK signaling pathway that regulates cellular proliferation and survival.

agerafenib

An orally bioavailable selective multikinase inhibitor of mutant forms, fusions and rearrangements involving the proto-oncogene receptor tyrosine kinase rearranged during transfection (RET) as well as the serine/threonine-protein kinase B-raf (BRAF), with potential antineoplastic activity. Upon oral administration,agerafenib selectively and potently binds to and targets various RET- and BRAF-containing mutants, fusions and rearrangements. This results in inhibition of cell growth in tumors cells that exhibit increased RET and BRAF activity. RET overexpression, activating mutations, and fusions result in the upregulation and/or overactivation of RET tyrosine kinase activity in various cancer cell types; dysregulation of RET activity plays a key role in the development and progression of these cancers. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of MAP kinase/ERK signaling pathways, which may be constitutively activated in certain cancer cells with activating BRAF gene mutations.

aglatimagene besadenovec

An adenoviral vector engineered to express the herpes simplex virus thymidine kinase (HSV-tk) gene, which, when administered in conjunction with a synthetic acyclic guanosine analogue, possesses potential antineoplastic activity. Aglatimagene besadenovec is transduced into tumor cells, sensitizing tumor cells that overexpress HSV-tk to synthetic acyclic guanosine analogues. Subsequently, a low dose of a synthetic acyclic guanosine analogue such as valacyclovir (VCV) or ganciclovir (GCV) is given, which may preferentially kill tumor cells containing the adenoviral vector and overexpressing HSV-tk. Release of tumor-associated antigens (TAAs) by dying tumor cells may then stimulate an antitumor cytotoxic T lymphocyte (CTL) response.

agonistic anti-OX40 monoclonal antibody INCAGN01949

An agonistic human immunoglobulin G1 (IgG1) monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; TNFRSF4), with potential immunostimulatory and antineoplastic activities. Upon administration, agonistic anti-OX40 monoclonal antibody INCAGN01949 selectively binds to and activates OX40 on activated T cells, thereby potentiating T-cell receptor (TCR) signaling. OX40 activation inhibits regulatory T-cell (Treg)-mediated suppression of effector T cells, induces the proliferation of memory and effector T-lymphocytes and modulates cytokine production. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. In addition, the IgG1 Fc region of INCAGN01949 binds to and co-engages with the IgG Fc-gamma receptor III (FcgammaRIII; CD16) expressed by immune effector cells; thus, binding activates FcgammaRIII-mediated signaling and facilitates the selective depletion of intratumoral Tregs, thereby further enhancing the cytotoxic T-lymphocyte (CTL)-mediated tumor cell response. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells; OX40 stimulation abrogates the immunosuppressive tumor microenvironment.

agonistic anti-OX40 monoclonal antibody MEDI6469

An agonistic monoclonal antibody against the co-stimulatory receptor OX40 (CD134), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-OX40 monoclonal antibody MEDI6469 selectively binds to and activates OX40. OX40 activation induces proliferation of effector T lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on T lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells.

Agriflu

(Other name for: trivalent influenza vaccine)

Agrylin

(Other name for: Anagrelide Hydrochloride Anhydrous)

AhR inhibitor DA-4505

An orally bioavailable small molecule inhibitor of the aryl hydrocarbon receptor (AhR; class E basic helix-loop-helix protein 76; bHLHe76), with potential immunomodulating and antineoplastic activities. Upon oral administration, AhR inhibitor DA-4505 specifically targets and binds to AhR, inhibits AhR activation, prevents AhR-mediated signaling, and AhR-dependent tumor cell proliferation. Abrogation of AhR activation prevents the activation of immune-tolerant dendritic cells (DCs), regulatory T cells (Tregs) and decreases suppressive cytokines in the tumor microenvironment (TME). It stimulates cytotoxic T-cell activation and expansion. This may restore the immune response against tumor cells. AhR, a member of the basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) family of transcription factors, plays key roles in regulating immunity and cellular differentiation. It mediates the expression of multiple immune related and tumor cell signal transduction and proliferation genes.

AIE regimen

A regimen consisting of cytarabine (Ara-C), idarubicin and etoposide, used as an induction treatment for pediatric acute myeloid leukemia (AML). High-dose cytarabine/etoposide/idarubicin regimen may be used for the treatment of AML.

AIM2(-1)/HT001(-1)/TAF1B(-1) frameshift peptide vaccine

A cancer vaccine containing the three frame shift peptides (FSP) AIM2(-1), HT001(-1) and TAF1B(-1), with potential immunomodulating activity. Upon administration, the AIM2(-1)/HT001(-1)/TAF1B(-1) FSP vaccine may induce an immune response against microsatellite instability (MSI) colorectal cancer-associated antigens. Frame shift mutations of AIM2 (absent in melanoma 2, an interferon-inducible protein), HT001 (asteroid homolog 1 or ASTE1, with an unknown function) and TAF1B (TATA box-binding protein-associated RNA polymerase I B, a transcription factor) are seen in MSI-positive colorectal cancers and may be associated with malignant transformation, tumor progression and the presence of tumor-infiltrating lymphocytes. These FSPs all have one-base deletions.

Aimovig

(Other name for: erenumab)

AiRuiYi

(Other name for: fuzuloparib)

AK 3012

A proprietary topical formulation. Upon subcutaneous administration, the active ingredient in AK 3012 may inhibit actinic keratosis.

Akeega

(Other name for: niraparib tosylate monohydrate and abiraterone acetate)

Akkermansia muciniphila probiotic

An orally bioavailable, probiotic supplement containing Akkermansia muciniphila (A. muciniphila), a naturally occurring bacterium found in the healthy human gastrointestinal (GI) tract, with potential immunomodulating and mucosal protective activities. Upon oral administration of A. muciniphila probiotic, A. muciniphila may help maintain adequate colonization of the GI tract by modulating the composition of the normal microflora. During colonization in the GI tract, the bacteria may form a protective intestinal barrier that may help maintain gut lining and prevent both damage to the mucosal epithelia caused by toxins and attachment of potential pathogens, thereby protecting against bacterial translocation and infection. In addition, the probiotic bacteria may potentiate immunity and may improve response to certain cancer immunotherapies.

Aknoten

(Other name for: tretinoin)

AKR1C3-activated prodrug AST-3424

A small-molecule nitro-benzene, aldo-keto reductase 1C3 (AKR1C3)-activated prodrug of N,N'-bisethylenephosphoramidate, a DNA bis-alkylating agent, with potential antineoplastic activity. Upon intravenous administration, AKR1C3-activated prodrug AST-3424 is converted to its active form by AKR1C3, which is upregulated in certain tumor cell types while not expressed in normal healthy cells. The active metabolite selectively binds to and alkylates DNA in AKR1C3-overexpressing tumor cells, resulting in DNA base pair mismatching, interstrand crosslinking and inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis. As the expression of AKR1C3 is restricted to tumors, AST-3424 is selectively converted to its active metabolite in tumor cells only while its conversion in normal, healthy tissue is absent; this allows for an increased cytotoxic effect of the alkylating agent in tumor cells while decreasing its toxicity.

AKT 1/2 inhibitor BAY1125976

An orally bioavailable inhibitor of the serine/threonine protein kinase AKT (protein kinase B) isoforms 1 and 2 (AKT1/2) with potential antineoplastic activity. AKT1/2 inhibitor BAY1125976 selectively binds to and inhibits the phosphorylation and activity of AKT1/2 in a non-ATP competitive manner, which may result in the inhibition of the phosphatidylinositol 3 (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. This may lead to both the reduction of cell proliferation and the induction of cell apoptosis in AKT-overexpressing tumor cells. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.

AKT inhibitor

Any agent that inhibits protein kinase B (AKT).

Akt inhibitor GSK2141795

An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor GSK2141795 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Akt inhibitor LY2780301

An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor LY2780301 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway, thereby leading to inhibition of cell proliferation and the induction of apoptosis in tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Akt inhibitor MK2206

An orally bioavailable allosteric inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor MK2206 binds to and inhibits the activity of Akt in a non-ATP competitive manner, which may result in the inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Akt inhibitor NTQ1062

An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B), with potential antineoplastic activity. Upon oral administration, Akt inhibitor NTQ1062 targets, competitively binds to and inhibits the activity of Akt, which may result in the inhibition of the PI3K/Akt signaling pathway, thereby leading to the inhibition of cell proliferation and the induction of apoptosis in tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Akt inhibitor SR13668

An orally bioavailable indole-3-carbinol (I3C) analogue inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic and antiangiogenic activities. Akt inhibitor SR13668 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation, and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

AKT-1 antisense oligonucleotide WGI-0301

A lipid nanoparticle preparation of archexin, a 20-mer antisense (AS) oligodeoxynucleotide (ODN) against the proto-oncogene Akt, with potential antineoplastic activity. Upon administration of AS ODN WGI-0301, archexin binds to Akt-1 mRNA, inhibiting translation of the transcript. Suppression of Akt-1 expression may result in the inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt-mediated signaling. This may inhibit proliferation and induce apoptosis of tumor cells in which Akt-1 is overexpressed. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.

Akt-1/2 inhibitor-treated tumor infiltrating lymphocytes

Autologous tumor infiltrating lymphocytes (TILs) harvested directly from the infiltrate of a patient's tumor and treated with an inhibitor of the serine/threonine kinases Akt-1 and -2 (Akti-1/2) during ex vivo expansion, with potential antineoplastic activity. Upon reintroduction into the patient, the Akti-1/2-treated TILs recognize and kill cancer cells. Akt inhibition promotes the immunologic memory of the TILs and enhances their expansion, in vivo long-term persistence and antitumor activity.

AKT/RSK/S6K inhibitor TAS0612

An orally bioavailable inhibitor of the serine/threonine kinases AKT (protein kinase B), 90S ribosome S6 kinase (p90RSK; RSK) and 70S ribosome S6 kinase (p70S6K; S6K), with potential antineoplastic activity. Upon oral administration, AKT/RSK/S6K inhibitor TAS0612 targets, binds to, and inhibits the activity of AKT, p90RSK and p70S6K. This inhibits both the AKT/mTOR/p70S6K and RAS/RAF/MEK/p90RSK signaling pathways and prevents the phosphorylation, nuclear translocation, and activation of the transcription factor Y-box-binding protein 1 (YBX1; YB-1). This may lead to cell cycle arrest, an induction of apoptosis, and an inhibition of tumor cell proliferation in tumor cells that have overactivated AKT/mTOR/p70S6K and RAS/RAF/MEK/p90RSK signaling pathways. Nuclear expression of YBX1 is associated with drug resistance such as antiestrogen resistance. AKT, RSK and S6K play key roles in tumor cell proliferation, differentiation, survival, and metastasis.

AKT1 E17K inhibitor ALTA2618

An orally bioavailable covalent inhibitor of the serine/threonine protein kinase AKT (protein kinase B; v-akt murine thymoma viral oncogene homolog 1) isoform 1 mutation AKT1 E17K, with potential antineoplastic activity. Upon oral administration, AKT1 E17K inhibitor ALTA2618 targets, allosterically binds to and inhibits AKT1 E17K. This may inhibit growth of and induce apoptosis in AKT1 E17K-driven cancers. AKT1 E17K, overexpressed in a variety of cancer cell types, drives cancer cell proliferation. By specifically targeting the E17K mutant variant, ALTA2618 may avoid the toxicities associated with wild-type (WT) AKT inhibition.

Akten

(Other name for: lidocaine hydrochloride ophthalmic gel)

Akynzeo

(Other name for: netupitant/palonosetron hydrochloride)

alacizumab pegol

A pegylated, cross-linked, humanized divalent-Fab' antibody fragment directed against vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antiangiogenic and antitumor activities. Alacizumab pegol binds to and inhibits VEGFR-2, which may inhibit angiogenesis and tumor cell proliferation. Multivalent Fab' antibody fragments may exhibit improved retention and internalization properties compared to their parent IgGs.

alanosine

An amino acid analogue and antibiotic derived from the bacterium Streptomyces alanosinicus with antimetabolite and potential antineoplastic activities. L-alanosine inhibits adenylosuccinate synthetase, which converts inosine monophospate (IMP) into adenylosuccinate, an intermediate in purine metabolism. L-alanosine-induced disruption of de novo purine biosynthesis is potentiated by methylthioadenosine phosphorylase (MTAP) deficiency. The clinical use of this agent may be limited by its toxicity profile. MTAP is a key enzyme in the adenine and methionine salvage pathways.

Alantel

(Other name for: aloe vera/chamomile/thyme topical cream)

alanylglutamine

A nutritional supplement containing a stable, water-soluble dipeptide comprised of the amino acids L-glutamine and L-alanine, with potential protective and absorption enhancing activities. Upon oral or enteral administration, alanylglutamine works locally in the gastrointestinal (GI) tract to both protect the integrity of the intestinal mucosa and maintain intestinal barrier functions. This reduces bacterial translocation, the risk of infection, infection-induced inflammatory damage and infection-associated symptoms, such as diarrhea, dehydration, malabsorption and electrolyte imbalances. Alanylglutamine also increases absorption of other chemicals, enhances epithelial repair, and inhibits apoptosis due to cellular damage, and stimulates cellular proliferation. Altogether, this improves absorption of nutrients, decreases weight loss, reduces diarrhea, decreases the risk of GI-associated infections and improves recovery. Upon absorption, alanylglutamine may also help inhibit muscle protein catabolism.

Alba-Dex

(Other name for: dexamethasone)

albendazole

A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections.

Albenza

(Other name for: albendazole)

albumin

A family of globular proteins found in many plant and animal tissues that tend to bind a wide variety of ligands. Albumin is the main protein in blood plasma. Low serum levels occur in conditions associated with malnutrition, inflammation and liver and kidney diseases.

Albumin-binding Cisplatin Prodrug BTP-114

A proprietary, albumin-binding platinum (Pt)-based complex containing a prodrug form of the platinum compound cisplatin and a maleimide moiety, with an ability to strongly and selectively bind human serum albumin (HSA), and with potential antineoplastic activity. Upon intravenous administration, the maleimide group of BTP-114 rapidly conjugates with HSA in the bloodstream; this prolongs the blood circulation, enhances the half-life, and alters the biodistribution of BTP-114, as compared to cisplatin alone. Thus, BTP-114 demonstrates enhanced extravasation to the tumor, an increased accumulation in the tumor tissue and enhanced uptake by cancer cells. The prodrug form is reduced in the hypoxic tumor cell environment, which releases the highly cytotoxic active metabolite cisplatin. Once inside the tumor cell, cisplatin binds to nucleophilic groups, such as GC-rich sites, in DNA and induces intrastrand and interstrand DNA cross-links, resulting in apoptosis and cell growth inhibition. Compared to cisplatin alone, BTP-114 has improved selectivity towards tumor tissue, thereby enhancing efficacy while reducing systemic toxicities.

albuterol

A racemic mixture of the r-isomer levalbuterol and s-albuterol, a short-acting sympathomimetic agent with bronchodilator activity. Albuterol stimulates beta-2 adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP). Increased cAMP concentrations relax bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. Albuterol although to a lesser extent, also stimulates beta-1 adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

albuterol sulfate

The sulfate salt of the short-acting sympathomimetic agent albuterol, a 1:1 racemic mixture of (R)-albuterol and (S)-albuterol with bronchodilator activity. Albuterol stimulates beta2-adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of ATP to cyclic-3',5'-adenosine monophosphate (cAMP). Increased cAMP concentrations relax bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. To a lesser extent albuterol stimulates beta1-adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

ALC1 inhibitor EIS-12656

An orally bioavailable allosteric inhibitor of the chromatin remodeling enzyme chromodomain-helicase-DNA-binding protein 1-like (CHD1L; amplified in liver cancer 1; ALC1), with potential antineoplastic activity. Upon oral administration, ALC1 inhibitor EIS-12656 selectively targets, allosterically binds to and inhibits the activity of ALC1, thereby preventing ALC1/poly(ADP-ribose) polymerase (PARP)-mediated repair of DNA breaks in tumor cells. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. This inhibits tumor cell proliferation and may enhance the cytotoxicity of PARP inhibitors and DNA-damaging agents. ALC1, a SNF2 family ATPase that modulates the DNA retention of PARPs and other DNA repair enzymes, plays an important role in DNA damage repair. It is overexpressed in cancer cells with homologous recombination deficient (HRD) mutations. EIS-12656 is able to cross the blood-brain barrier (BBB).

alcohol

A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.

alcohol-free hypoallergenic barrier film solution

An alcohol-free, hypoallergenic, polymeric-cyanoacrylate-based solution that provides a barrier film, with potential skin protective and healing activities. Upon topical application of the barrier film solution to intact or damaged skin, the alcohol-free barrier film solution forms a breathable, transparent film over the skin and maintains and enhances skin integrity, provides long-lasting protection against skin injury, infection, and irritation, and maintains moisture to the skin.

Aldactone

(Other name for: spironolactone)

Aldara

(Other name for: imiquimod)

aldastotug

A humanized monoclonal antibody targeting the immune checkpoint molecule sialic acid-binding immunoglobulin (Ig)-like lectin 15 (Siglec-15; SIGLEC15; S15; CD33L3), with potential immune checkpoint inhibitory, antineoplastic and immunomodulatory activities. Upon administration, aldastotug targets and binds to S15 on the surface of tumor-associated macrophages (TAMs) and certain tumor cells. Binding to S15 may disrupt TAM-mediated activities such as promotion of tumor initiation and metastasis of tumor cells and inhibition of CD8-positive and CD4-positive T-cell responses. This leads to activation of the immune system and an inhibition of tumor cell growth. S15, a highly conserved type 1 cell surface protein, normally involved in osteoclast differentiation and bone remodeling, is overexpressed on and may play a key role in the survival and differentiation of TAMs and various tumor cells.

aldesleukin

A recombinant analog of the endogenous cytokine interleukin-2 (IL-2) with immunoregulatory and antineoplastic activities. Aldesleukin binds to and activates the IL-2 receptor, followed by heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma(c) chains; activation of the tyrosine kinase Jak3; and phosphorylation of tyrosine residues on the IL-2R beta chain, resulting in an activated receptor complex. Various cytoplasmic signaling molecules are recruited to the activated receptor complex and become substrates for regulatory enzymes that are associated with the receptor complex. This agent enhances lymphocyte mitogenesis; stimulates long-term growth of human IL-2 dependent cell lines; enhances lymphocyte cytotoxicity; induces lymphokine-activated killer (LAK) cell and natural killer (NK) cell activities; and induces expression of interferon-gamma. Aldesleukin may induce T cell-mediated tumor regression in some tumor types.

ALDH inhibitor NYH817G and mitochondrial complex 1 inhibitor NYH100P

An orally bioavailable combination agent composed of the aldehyde dehydrogenase (ALDH) inhibitor NYH817G and the mitochondrial complex 1 (NADH-ubiquinone oxidoreductase) inhibitor NYH100P, with potential antineoplastic activity. Upon oral administration of ALDH inhibitor NYH817G and mitochondrial complex 1 inhibitor NYH100P, NYH817G targets and binds to ALDH, and prevents the formation of NADH. It also inhibits lactate dehydrogenase A (LDH-A), thereby preventing lactate formation from pyruvate. NYH100P targets and binds to MC1. This all blocks the cancer cell energy production pathway, deprives tumor cells of nutrients, and energy, and inhibits nucleotide and amino acid production, which induces autophagy, causes tumor cell death and inhibits cell proliferation.

ALDH1/3 inhibitor ABD-3001

A suicidal inhibitor of aldehyde dehydrogenases 1 (ALDH1) and 3 (ALDH3), with potential antineoplastic activity. Upon administration, ALDH1/3 inhibitor ABD-3001 targets, binds to and irreversibly inhibits the activity of ALDH1 and ALDH3. This results in the accumulation of reactive aldehydes in tumor cells, which interferes with oncogenic signaling pathways and tumor cell proliferation. In addition, the inhibition of ALDH1 and ALDH3 disrupts glutathione redox balance in tumor cells, leading to oxidative stress which may further promote tumor cell death.

aldoxorubicin

A 6-maleimidocaproyl hydrazone derivative prodrug of the anthracycline antibiotic doxorubicin (DOXO-EMCH) with antineoplastic activity. Following intravenous administration, aldoxorubicin binds selectively to the cysteine-34 position of albumin via its maleimide moiety. Doxorubicin is released from the albumin carrier after cleavage of the acid-sensitive hydrazone linker within the acidic environment of tumors and, once located intracellularly, intercalates DNA, inhibits DNA synthesis, and induces apoptosis. Albumin tends to accumulate in solid tumors as a result of high metabolic turnover, rapid angiogenesis, hypervasculature, and impaired lymphatic drainage. Because of passive accumulation within tumors, this agent may improve the therapeutic effects of doxorubicin while minimizing systemic toxicity.

Alecensa

(Other name for: alectinib)

alectinib

An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, alectinib binds to and inhibits ALK kinase, ALK fusion proteins as well as the gatekeeper mutation ALKL1196M known as one of the mechanisms of acquired resistance to small-molecule kinase inhibitors. The inhibition leads to disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.

alefacept

A recombinant dimeric fusion protein consisting of the extracellular CD2-binding domain of the human leukocyte function-associated antigen 3 (LFA-3; CD58) linked to the Fc portion of human immunoglobulin G1 (IgG1) with potential immunosuppressive activity. Alefacept binds to the CD2 receptor expressed on the majority of T lymphocytes, blocking the binding of endogenous LFA-3, located on antigen-presenting cells (APCs), to the CD2 receptor; the activation and proliferation of T lymphocytes in response to LFA-3 binding is thus inhibited. In addition, binding of the IgG1 moiety of this agent to the Fc gamma receptor on the surface of natural killer (NK)cells may bridge NK cells and target T lymphocytes, initiating NK cell-mediated apoptosis of T lymphocytes.

alemtuzumab

A recombinant DNA-derived humanized monoclonal antibody directed against the cell surface glycoprotein, CD52. Alemtuzumab is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions derived from a rat monoclonal antibody. This agent selectively binds to CD52, thereby triggering a host immune response that results in lysis of CD52 + cells. CD52 is a glycoprotein expressed on the surface of essentially all normal and malignant B and T cells, a majority of monocytes, macrophages and natural killer (NK) cells, a subpopulation of granulocytes, and tissues of the male reproductive system.

alendronate sodium

The sodium salt of alendronate, a second generation bisphosphonate and synthetic analog of pyrophosphate with bone anti-resorption activity. Alendronate sodium binds to and inhibits the activity of geranyltranstransferase (farnesyl pyrophosphate synthetase), an enzyme involved in terpenoid biosynthesis. Inhibition of this enzyme prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are donor substrates of farnesylation and geranylgeranylation during the post-translational modification of small GTPase signalling proteins, which is important in the process of osteoclast turnover. As a result, osteoclast activity is inhibited and bone resorption and turnover are reduced.

Alesse

(Other name for: ethinyl estradiol/levonorgestrel)

Alfenta

(Other name for: alfentanil hydrochloride)

alfentanil hydrochloride

The hydrochloride salt of alfentanil, a synthetic short-acting opioid with analgesic and local anesthesia enhancing activity. Alfentanil primarily binds to mu-opioid receptor, a G-protein-coupled receptor, thereby mimicking the actions of morphine, the prototypical mu receptor agonist. This agent induces anti-nociception responses mediated through inhibiting the release of various neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline; in addition, the release of vasopressin, somatostatin, insulin and glucagon are also inhibited.

Alferon

(Other name for: recombinant interferon alfa)

alflutinib mesylate

The mesylate salt form of alflutinib, an orally available selective inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, alflutinib specifically binds to and inhibits the tyrosine kinase activity of EGFR T790M, a secondarily acquired resistance mutation. This prevents EGFR T790M-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. Compared to some other EGFR inhibitors, alflutinib may have therapeutic benefits in tumors with T790M-mediated drug resistance.

alfuzosin hydrochloride

The hydrochloride salt of alfuzosin, a quinazoline compound with smooth muscle-relaxing activity. Alfuzosin selectively binds to and antagonizes post-synaptic alpha-1-adrenoreceptors in smooth muscle of the prostate, bladder base, bladder neck, prostatic capsule, and prostatic urethra, initiating relaxation of smooth muscle and resulting in improvement of urine flow and the symptoms of benign prostatic hyperplasia (BPH). This agent also blocks alpha-1-adrenoreceptors in peripheral vascular smooth muscle, resulting in vasodilatation and a decrease in peripheral vascular resistance.

algenpantucel-L

A cancer vaccine comprised of irradiated allogeneic pancreatic cancer cells transfected to express murine alpha-1,3-galactosyltransferase with potential antitumor activity. Vaccination is associated with the expression of murine alpha-1,3-galactosyl (alpha-gal) carbohydrate residues on cell membrane glycoproteins and glycolipids of the vaccine pancreatic cancer cell allograft; murine alpha-gal epitopes, not present on human cells, then induce a hyperacute rejection of the vaccine pancreatic cancer cell allograft. The hyperacute rejection involves the binding of pre-existing human anti-alpha-gal antibodies (which naturally occur against gut flora) to murine alpha-gal epitopes, resulting in the rapid activation of antibody-dependent cell-mediated cytotoxicity (ADCC) towards allograft cells. The host immune system then attacks endogenous pancreatic cancer cells, resulting in ADCC towards endogenous pancreatic cancer cells.

Alimta

(Other name for: pemetrexed disodium)

Alinia

(Other name for: nitazoxanide)

alintegimod

An orally bioavailable, allosteric, small molecule activator of integrin cell adhesion receptors very late antigen-4 (VLA-4; integrin alpha4/beta1) and lymphocyte function-associated antigen-1 (LFA-1; integrin alphaL/beta2), with potential immunomodulatory and antineoplastic activities. Upon oral administration, alintegimod activates VLA-4 and LFA-1 expressed on the surface of leukocytes, thereby promoting the VLA-4- and LFA-1-mediated adhesion of leukocytes to counter-receptors vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1). This may promote VLA-4/VCAM-1- and LFA-1/ICAM-1-mediated cell-cell adhesion between naive T cells and antigen presenting cells (APCs) and enhance T-cell activation. The enhanced VCAM-1 and ICAM-1 binding by the activated integrins expressed on activated T cells may also promote intratumoral T-cell accumulation and infiltration. This may lead to enhanced T-cell-mediated killing of tumor cells. Integrins VLA-4 and LFA-1 are cellular adhesion molecules (CAMs) that play key roles in antigen presentation and leukocyte migration.

Aliqopa

(Other name for: copanlisib hydrochloride)

alirocumab

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against human proprotein convertase subtilisin/kexin type 9 (PCSK9), that can be used in the treatment of hypercholesterolemia. Upon administration, alirocumab targets, binds to and inhibits the activity of PCSK9. This prevents the binding of PCSK9 to low-density lipoprotein receptor (LDLR) on hepatocytes and prevents its degradation. This increases LDLR on hepatocytes and increases the liver's ability to remove LDL cholesterol (LDL-C) from the blood, thereby lowering LDL-C levels. PCSK9 binds to LDLR on the surface of hepatocytes to promote LDLR degradation within the liver.

alisertib

A second-generation, orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A kinase with potential antineoplastic activity. Alisertib binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers, including colon and breast cancers.

alisertib sodium

The sodium salt form of alisertib, a second-generation, orally bioavailable, selective inhibitor of the serine/threonine protein kinase Aurora A kinase, with potential antineoplastic activity. Upon oral administration, alisertib targets, binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation in susceptible cancer cells. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers and plays a key role in cancer cell proliferation.

alitretinoin

An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.

alizapride

A substituted benzamide that acts as a dopamine receptor antagonist with antiemetic properties.

ALK Inhibitor ASP3026

An orally available, small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, ASP3026 binds to and inhibits ALK tyrosine kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.

ALK inhibitor NVL-655

An orally bioavailable, brain-penetrant, selective small molecule inhibitor of the receptor tyrosine kinase (RTK) anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, ALK inhibitor NVL-655 specifically targets, binds to and inhibits ALK fusion proteins and activating mutations, including the acquired resistance mutations solvent front mutation (SFM) G1202R and the compound mutations G1202R/L1196M and G1202R/G1269A. The inhibition of ALK leads to the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types. NVL-655 is able to penetrate the blood-brain-barrier (BBB) and may therefore exert its activity against EGFR-driven central nervous system (CNS) primary tumors and CNS metastases.

ALK inhibitor PLB 1003

An orally available small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, PLB1003 selectively binds to and inhibits wild-type ALK, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and inhibits tumor cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.

ALK peptide vaccine

A peptide cancer vaccine directed against the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential immunostimulatory and antineoplastic activities. Upon administration, ALK peptide vaccine may elicit a cytotoxic T-lymphocyte (CTL) response against ALK-expressing tumor cells. ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types.

ALK-FAK inhibitor CEP-37440

An orally available dual kinase inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and focal adhesion kinase (FAK), with potential antineoplastic activity. Upon administration, ALK-FAK inhibitor CEP-37440 selectively binds to and inhibits ALK kinase and FAK kinase. The inhibition leads to disruption of ALK- and FAK-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK- and FAK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; its dysregulation and gene rearrangements are associated with a variety of tumors. The cytoplasmic tyrosine kinase FAK, a signal transducer for integrins, is upregulated and constitutively activated in various tumor types; it plays a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.

ALK/c-Met inhibitor TQ-B3139

An orally available, small molecule inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and hepatocyte growth factor receptor (c-Met; HGFR), with potential antineoplastic activity. Upon oral administration, TQ-B3139 binds to and inhibits the activity of ALK and c-Met, which leads to the disruption of ALK- and c-Met-mediated signaling and the inhibition of cell growth in ALK- and c-Met-expressing tumor cells. ALK and c-Met, overexpressed or mutated in many tumor cell types, play key roles in tumor cell proliferation, survival, invasion and metastasis.

ALK/FAK/Pyk2 inhibitor CT-707

An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), with potential antineoplastic activity. Upon administration, ALK/FAK/Pyk2 inhibitor CT-707 selectively binds to and inhibits ALK , FAK and Pyk2. The inhibition leads to disruption of ALK- , FAK- and Pyk2-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK-, FAK- and Pyk2-overexpressing tumor cells. Expression of these tyrosine kinases is dysregulated in various tumor types; they play a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.

ALK/ROS1 inhibitor XZP-3621

An orally bioavailable inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1), with potential antineoplastic activity. Upon oral administration, ALK/ROS1 inhibitor XZP-3621 targets, binds to and inhibits the activity of ALK and ROS1, which leads to the disruption of ALK- and ROS1-mediated signaling and the inhibition of cell growth in ALK- and ROS1-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types. XZP-3621 may be able to inhibit ALK resistance mutations associated with other ALK inhibitors. ROS1, overexpressed in certain cancer cells, plays a key role in cell growth and survival of cancer cells.

ALK/ROS1/Met inhibitor TQ-B3101

An orally available, small molecule inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK), C-ros oncogene 1 (ROS1) and Met (hepatocyte growth factor receptor; HGFR; c-Met), with potential antineoplastic activity. Upon oral administration, TQ-B3101 targets, binds to and inhibits the activity of ALK, ROS1 and c-Met, which leads to the disruption of ALK-, ROS1- and c-Met-mediated signaling and the inhibition of cell growth in ALK-, ROS1- and c-Met-expressing tumor cells. ALK, ROS1 and c-Met, overexpressed or mutated in many tumor cell types, play key roles in tumor cell proliferation, survival, invasion and metastasis.

ALK/TRK inhibitor TSR-011

An orally available inhibitor of both the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the tropomyosin-related kinases (TRK) TRKA, TRKB, and TRKC, with potential antineoplastic activity. Upon administration, ALK/TRK inhibitor TSR-011 binds to and inhibits both ALK and TRK kinases. The inhibition leads to disruption of ALK- and TRK-mediated signaling and impedes tumor cell growth in ALK/TRK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; ALK dysregulation and gene rearrangements are associated with a series of tumors. TRK, a family of receptor tyrosine kinases activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival.

ALK2 inhibitor INCB000928

An inhibitor of activin A receptor type 1 (activin receptor-like kinase 2; ALK2; ALK-2; ACVR1; ACTR-I), with potential anti-anemic and ossification suppressive activities. Upon administration, ALK2 inhibitor INCB000928 targets, binds to and inhibits the activity of ALK-2. This prevents ALK2-mediated signaling and ALK2-mediated excessive bone morphogenetic protein (BMP) signaling. This may suppress heterotopic ossification (HO). As ALK-2 enhances the secretion of hepcidin, a peptide liver hormone and a key modulator of iron homeostasis, INCB000928 is able to decrease hepcidin expression in the liver, thereby increasing and restoring plasma iron levels, enhancing erythropoiesis, and correcting anemia of chronic disease (ACD). ALK2, a serine/threonine receptor kinase and type I cell surface receptor for BMPs, is constitutively activated due to activating mutations in inflammatory conditions, various types of cancer, and in fibrodysplasia ossificans progressiva (FOP). Elevated serum hepcidin levels enhance storage of iron, reduce iron availability and causes iron deficiency anemia.

Alka Seltzer Gold

(Other name for: sodium bicarbonate/potassium bicarbonate/anhydrous citric acid)

Alkagin

(Other name for: zinc oxide/aluminum starch octenylsuccinate/glycyrrhetinic phytosome/vitamin E/botanical extracts-based skin protectant paste)

alkaline water

Water that has a pH above 7, that can be used to alter the conditions in the gastrointestinal (GI) tract and modify absorption of certain therapeutic agents. Upon oral administration, alkaline water provides alkaline conditions within the GI tract. This may decrease absorption of certain therapeutic agents, reduce epithelial damage and may alter bowel movements.

Alkeran

(Other name for: melphalan)

alkotinib

An orally available inhibitor of multiple kinases, including the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1), with potential antineoplastic activity. Upon oral administration, alkotinib binds to and inhibits the wild-type, point mutations and fusion proteins of ALK and ROS1. Inhibition of these kinases leads to the disruption of downstream signaling pathways and the inhibition of proliferation in tumor cells which these kinases are overexpressed, rearranged or mutated.

alkylglycerol/rosemary capsules

An orally available capsule containing alkylglycerols and Rosmarinus officinalis extracts standardized to diterpenes, including carnosic acid and carnosol, with potential antineoplastic and anti-inflammatory activities. Upon administration, carnosic acid and carnosol may induce apoptosis by decreasing apoptosis regulator B-cell lymphoma 2 (Bcl-2) expression, decrease tumor cell growth through inhibition of mammalian target of rapamycin (mTOR) phosphorylation, and inhibit metastatic activity by preventing the adhesion of tumor cells to type I collagen and fibronectin. Additionally, these diterpenes may decrease inflammation by downregulating cyclooxygenase (COX) type 2 (COX-2) protein synthesis. Alkylglycerols (alkyl-Gro) are bioactive ether lipids that may, through a not yet fully elucidated mechanism, inhibit tumor cell growth and metastases.

Allegra

(Other name for: fexofenadine hydrochloride)

AllerNaze

(Other name for: triamcinolone acetonide)

allitinib

An orally bioavailable and irreversible inhibitor of the receptor tyrosine kinases (RTKs) epidermal growth factor receptors 1 (EGFR; ErbB1) and 2 (ErbB2; HER2; HER-2), with potential antineoplastic activity. Upon oral administration, allitinib selectively and irreversibly binds to and inhibits the activity of both EGFR and HER2, which prevents signaling mediated by EGFR and HER2. This may inhibit tumor growth and angiogenesis in tumor cells overexpressing these RTKs. EGFR and HER2 are RTKs that belong to the EGFR superfamily; they play major roles in both tumor cell proliferation and tumor vascularization and are overexpressed in many cancer cell types.

alloantigen-specific allogeneic type 1 regulatory T cells T-allo10

A preparation of allogeneic CD4+ cells that were ex vivo stimulated with alloantigens, which involves exposing the cells to host antigen-presenting cells (APCs), in the presence of the immunomodulatory cytokine interleukin-10 (IL-10), with potential to prevent graft-versus-host disease (GvHD). The stimulation of the CD4+ cells by exposure to alloantigens plus IL-10 induces the differentiation of alloantigen-specific type 1 T regulatory (TR1) cells, which are hyporesponsive to the alloantigens. Upon infusion of T-allo10 and prior to donor hematopoietic stem cell transplantation (HSCT), the alloantigen-specific type 1 regulatory T cells are tolerant to the alloantigens and suppress alloreactive immune responses by donor CD4+ and CD8+ T cells. This may ultimately prevent GvHD. IL-10 plays a key role in controlling inflammation, down-regulating immune responses, and inducing immunological tolerance. IL-10 induces both a long lasting antigen specific T-cell anergy and the differentiation of TR1 cells.

Allocetra-OTS

(Other name for: allogeneic ex-vivo-treated peripheral blood mononuclear cells)

allodepleted haploidentical T cells expressing inducible Caspase 9

Allodepleted haploidentical T-lymphocytes transduced with the Gal-V pseudotyped retrovirus vector encoding SFG.iCasp9-2A-deltaCD19, with potential immune reconstitution property. SFG.iCasp9-2A-deltaCD19 contains the suicide gene inducible caspase 9 (iCasp9) linked with a 2A-like cleavable peptide to the selectable marker, truncated human CD19 (deltaCD19). iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9 using a short linker (SGGGS). Donor T cell therapy may help control transplant-related viral infections following allogeneic hematopoietic stem cell transplantation. However, even the addition of allodepleted donor T cells can lead to graft-versus-host disease (GVHD). In the event that GVHD begins to develop, the chemical homodimerizer AP1903 can be administered, which binds to the FKBP12-F36V domain activating caspase 9. This results in the death of T cells causing GVHD while sparing the virus reactive T-cells.

allodepleted T cell immunotherapeutic ATIR101

A cell-based immunotherapeutic product containing T-lymphocyte-enriched leukocytes that are devoid of alloreactive T-lymphocytes, that can potentially be used to restore lymphocyte levels after stem cell transplantations and are derived from partially matched (haploidentical) family donors for blood cancer patients who do not have a matching stem cell donor available. Host alloreactive T-cells, which can cause graft-versus-host disease (GVHD), are eliminated from the donor lymphocytes ex vivo using photodynamic therapy. After allogeneic hematopoietic stem cell transplantation (HSCT), allodepleted T cell immunotherapeutic ATIR101 is administered. This maintains a T-cell-mediated immune response against tumor cells and the donor T-cells can prevent opportunistic infections. ATIR101 does not cause severe, acute GVHD. In addition, administration of ATIR101 eliminates the need for immunosuppressants.

Allodepleted T-cell ImmunotheRapeutics

(Other name for: allodepleted T cell immunotherapeutic ATIR101)

AlloDerm

(Other name for: acellular cadaveric dermal matrix)

allogeneic adenovirus-specific cytotoxic T lymphocytes

A population of allogeneic cytotoxic T-lymphocytes (CTLs) specifically reactive to human adenovirus (Ad) with potential immunomodulating and anti-adenoviral activities. Upon immunoprophylactic adoptive cell therapy, infusion of allogeneic Ad-specific CTLs may help reconstitute Ad-specific CTL responses in patients at risk of developing Ad infections after allogeneic stem cell transplant or in Ad-infected immunocompromised hosts. These allogeneic Ad-specific CTLs are prepared by multiple rounds of stimulation with donor peripheral blood mononuclear cells and lymphoblastoid cell lines that have been transduced with Ad5f35, a recombinant adenoviral vector carrying no transgene.

allogeneic adipose-derived mesenchymal stem cells

A preparation of culture expanded human allogeneic adipose-derived mesenchymal stem cells (MSCs), that can potentially be used to restore the function of the salivary gland tissue. Upon intra-glandular administration of the allogeneic adipose-derived MSCs, these MSCs are pluripotent and capable of differentiating into functional cells of salivary tissues. This may help heal and restore the function of these glands that are damaged by chemo- and/or radio-therapy. This may reduce symptoms of hyposalivation and xerostomia.

allogeneic AdV/CMV/EBV-specific T lymphocytes

A preparation of human leukocyte antigen (HLA)-matched or HLA-mismatched, allogeneic CD4+ and CD8+ T lymphocytes, ex vivo incubated with synthetic peptides of the viral antigens of the three human viruses adenovirus (AdV), cytomegalovirus (CMV) and Epstein-Barr virus (EBV), with potential antiviral activity. Upon administration of the allogeneic AdV/CMV/EBV-specific T lymphocytes after allogeneic hematopoietic stem cell transplantation (HSCT), these T lymphocytes may kill AdV, CMV, and/or EBV-infected cells, and may prevent or reduce the severity of viral infections by these pathogens.

allogeneic AML antigen-expressing dendritic cell vaccine

A cancer vaccine consisting of allogeneic, immortalized dendritic precursor cells derived from a patient with acute myelogenous leukemia (AML), with potential immunostimulatory and antineoplastic activities. Upon ex vivo stimulation and expansion of the precursor cells into mature, fully functional dendritic cells (DCs) and subsequent administration, the allogeneic AML antigen-expressing DC vaccine may elicit a potent cytotoxic T-cell (CTL) and antibody response against AML antigen-expressing cells, resulting in tumor cell death.

allogeneic anti-B7-H3 CAR gamma delta T cells QH104

A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are engineered to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein and tumor-associated antigen (TAA) B7-homologue 3 (B7-H3, CD276), with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-B7-H3 CAR gamma delta T cells QH104 target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

allogeneic anti-BCMA CAR T cells ALLO-605

A preparation of allogeneic, transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T-lymphocytes that have been transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and engineered to express a constitutively active chimeric cytokine receptor (CACCR), with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain (TRAC) and CD52 genes are inactivated. Upon administration, the allogeneic anti-BCMA CAR T Cells ALLO-605 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. Inactivation of the CD52 gene makes the modified donor T-cells resistant to an anti-CD52 monoclonal antibody treatment, that is used during lymphodepletion. The knockout of TRAC eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells. The expression of CACCR allows for intracellular cytokine activation signaling, which may enhance expansion and persistence of the CAR T cells, thereby improving long-term anti-tumor activity. In addition, the incorporated CD20-based off-switch of ALLO-605 permits selective depletion of the ALLO-605 cells when the anti-CD20 monoclonal antibody rituximab is administered. ALLO-605 can also be inactivated with dasatinib.

allogeneic anti-BCMA CAR T cells P-BCMA-ALLO1

An off-the-shelf (OTS) preparation composed of human allogeneic T cells and containing primarily stem cell memory T cells (Tscm) that are transfected by electroporation with a proprietary transposon-based DNA plasmid vector (PiggyBac; PB) encoding for an undisclosed drug selection gene encoding for a selectable marker to generate close to 100% CAR-based product, a caspase-based safety switch to reduce or eliminate the product in vivo if needed, and a B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17)-specific single domain variable heavy chain (VH) chimeric antigen receptor (CAR) (VCAR), with potential immunostimulating and antineoplastic activities. The CAR T cells are also site specifically gene-edited with Cas-CLOVER (CC) to eliminate surface expression of both T-cell receptor (TCR) and beta-2 microglobulin (beta 2M) to decrease major histocompatibility complex (MHC) class I expression and further selected, by depletion of residual CD3-positive/TCR-positive cells, and expanded to yield Tscm enriched allogeneic transposed CAR T cells. Upon administration, allogeneic anti-BCMA CAR T cells P-BCMA-ALLO1 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a member of the tumor necrosis factor receptor superfamily (TNFRSF) that binds to both a proliferation-inducing ligand (APRIL; TNFSF13) and B-cell activating factor (BAFF; TNFSF13B), plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

allogeneic anti-BCMA CAR-transduced T cells ALLO-715

A preparation of allogeneic, ‘off-the-shelf’ (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T lymphocytes that have been transduced with a vector expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) derived from a monoclonal antibody specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain (TRAC) and CD52 genes are deleted from the CAR T cells. Upon administration, the allogeneic anti-BCMA CAR-transduced T cells ALLO-715 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. Deletion of the CD52 gene makes the modified donor T cells resistant to an anti-CD52 monoclonal antibody treatment, that is used during lymphodepletion. The knockout of TRAC eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells. The donor-derived, gene-edited CAR T cells have reduced production times and have increased availability when compared to autologous CAR-T cells, which use the patient's own cells and are produced on an individual basis. In addition, if the ALLO-715 cells cause unacceptable side effects, the incorporated CD20-based off-switch permits selective depletion of the ALLO-715 cells when the anti-CD20 monoclonal antibody rituximab is administered.

allogeneic anti-BCMA-CAR T cells PBCAR269A

A preparation of allogeneic, off-the-shelf Tlymphocytes that have been genetically modified using a proprietary synthetic nuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-BCMA-CAR T cells PBCAR269A specifically recognize and kill BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival.

allogeneic anti-BCMA/CS1 bispecific CAR-T cells

A preparation of allogeneic T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting both the tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; TNFRSF17) and human CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC), with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-BCMA/CS1 bispecific CAR-T cells target and bind to tumor cells expressing BCMA and/or CS1 and induce selective cytotoxicity in those cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells. Targeting the two different TAAs highly expressed on malignant plasma cells may improve coverage and protect against antigen escape and resistance as tumor cells would need to lose both antigens. 

allogeneic anti-CD123 CAR-NK cells JD123

A preparation of off-the-shelf (OTS), allogeneic natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human interleukin-3 receptor alpha chain (IL3RA; cluster of differentiation 123; CD123), with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD123 CAR-NK cells JD123 recognize, bind to and induce selective cytotoxicity in CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.

allogeneic anti-CD19 1XX-CAR T cells FT819

A preparation of off-the-shelf (OTS) T lymphocytes, generated from an induced pluripotent stem cell (iPSC) line, that have been genetically modified to express a CD19 1XX chimeric antigen receptor (CAR) that targets the tumor-associated antigen (TAA) CD19, linked to the co-stimulatory intracellular signaling domains of CD28 and the zeta chain of the TCR (T-cell receptor)/CD3 complex (CD3-zeta) (CD28zeta; CD28z), and inserted into the T-cell receptor alpha constant (TRAC) locus and edited for elimination of TCR expression, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD19 1XX-CAR T cells FT819 specifically recognize and bind to CD19-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B cells. The CD19 1XX CAR T-cells include a 1928zeta mutant, 1XX, which contains one instead of all three immunoreceptor tyrosine-based activation motifs (iTAMs). This may help prevent counterproductive T-cell differentiation and exhaustion, and may enhance the anti-tumor activity of the CAR T-cells. By nullifying the TCR, the possibility of graft versus host disease (GvHD) is eliminated.

allogeneic anti-CD19 CAR double-negative T cells RJMty19

An off-the-shelf (OTS) cell preparation composed of healthy, donor-derived CD4 and CD8 double-negative T lymphocytes (DNTs) that are transduced with a lentiviral vector expressing a humanized chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-CD19 CAR DNTs RJMty19 specifically targets and binds to tumor cells expressing CD19. This induces selective toxicity in tumor cells that express CD19. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. The DNTs contain a high proportion of stem cell-like memory T cells (Tscm).

allogeneic anti-CD19 CAR T cells ATA3219

A preparation of allogeneic human Epstein-Barr virus (EBV)-sensitized T lymphocytes that have been engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), with a modified CD3zeta signaling domain 1xx, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 CAR T cells ATA3219 recognize and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The use of allogeneic EBV T cells minimizes the risks for graft-versus-host disease (GvHD). The modified CD3zeta signaling domain 1xx retains signaling capacity in 1 of 3 immune-receptor-tyrosine-based-activation-motif (ITAM) regions, which may help prevent counterproductive T-cell differentiation and exhaustion, and may enhance the anti-tumor activity of the CAR T-cells.

allogeneic anti-CD19 CAR T cells PBCAR19B

A preparation of allogeneic T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 (cluster of differentiation 19), a single short hairpin RNA (shRNA) that disrupts the expression of beta-2 microglobulin (B2M) component of the class 1 major histocompatibility complex (MHC) molecules, and a HLA-E gene, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD19 CAR T cells PBCAR19B specifically recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-expressing tumor cells. The downregulation of the expression of the class 1 MHC molecule component B2M by shRNA and the HLA-E gene decrease the number of CAR T cells that are rejected and killed by natural killer (NK) and cytotoxic T cells. CD19 antigen is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies.

allogeneic anti-CD19 CAR-gamma/delta T cells QH103

A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 CAR-gamma/delta T cells QH103 target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. Gamma/delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. CD19 is overexpressed on certain tumor cell types.

allogeneic anti-CD19 CAR-NK cells QN-019a

A preparation of allogeneic natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-CD19 CAR-NK cells QN-019a recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

allogeneic anti-CD19 CAR-T cells ALLO-501A

A preparation of allogeneic, frozen, 'off-the-shelf', universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T-lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain and CD52 genes are deleted from the CAR19 T cells. Upon administration, allogeneic anti-CD19 CAR T cells ALLO-501A specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Deletion of the CD52 gene makes the modified donor T cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The knockout of the TCR alpha gene eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T cells. ALLO-501A lacks the rituximab recognition domains of ALLO-501.

allogeneic anti-CD19 gamma-delta CAR-T cells UTAA09

A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 gamma-delta CAR-T cells UTAA09 specifically target and bind to tumor cells expressing CD19, thereby inducing selective toxicity in CD19-expressing tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

allogeneic anti-CD19 T cells ThisCART19A

A preparation of allogeneic engineered T lymphocytes expressing a lentiviral vector encoding chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and an anti-CD3 single chain antibody with the KDEL peptide fused to its C-terminus, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 CAR T cells ThisCART19A specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. By eliminating TCR/CD3 expression, the potential induction of graft-versus-host disease (GvHD) by the donor T cells is abrogated.

allogeneic anti-CD19 universal CAR-T cells CTA101

A preparation of allogeneic, off-the-shelf (OTS), universal, gene-edited T lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD19 universal CAR-T cells CTA101 specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. CTA101 is genetically engineered to prevent graft-versus-host disease (GvHD) by the donor T cells. OTS CAR-T cells require reduced production times when compared to autologous CAR-T cells.

allogeneic anti-CD19-CAR-CD28-IL-15-expressing natural killer T cells

A preparation of allogeneic natural killer T lymphocytes (NKTs) that have been engineered to express a chimeric antigen receptor (CAR) specific for the human tumor associated antigen (TAA) CD19, interleukin 15 (IL-15) and the costimulatory T-cell-specific surface glycoprotein CD28, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD19-CAR-CD28-IL-15-expressing NKTs target, bind to, and induce selective toxicity in CD19-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. CD28 costimulatory molecule enhances activation and signaling after recognition of CD19, and may increase proliferation of T cells and antitumor activity. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

allogeneic anti-CD19/CD22 CAR-BBz T cells

A preparation of allogeneic T lymphocytes that have been transduced with a bivalent lentiviral vector encoding a chimeric antigen receptor (CAR) targeting the two tumor-associated antigens (TAAs) CD19 and CD22, linked to the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD19/CD22 CAR-BBz T cells bind to and induce selective toxicity in tumor cells expressing CD19 and CD22. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. By simultaneously targeting two B-cell antigens, this preparation may minimize relapse due to single antigen loss in patients with B-cell malignancies.

allogeneic anti-CD20 CAR T cells LUCAR-20S

A preparation of donor-derived T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD20 CAR T cells LUCAR-20S specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell-specific cell surface antigen expressed in B-cell lineage malignancies.

allogeneic anti-CD20 CAR T cells LUCAR-20SP

A preparation of donor-derived T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) cluster of differentiation 20 (CD20), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD20 CAR T cells LUCAR-20SP specifically recognize and kill CD20-expressing tumor cells. CD20, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.

allogeneic anti-CD20-CAR T cells PBCAR20A

A preparation of allogeneic, off-the-shelf (OTS), T lymphocytes, derived from healthy donors, that have been genetically modified using a proprietary synthetic endonuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD20-CAR T cells PBCAR20A specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.

allogeneic anti-CD20/CD22 universal CAR-expressing T lymphocytes UCART20x22

A preparation of allogeneic, off-the-shelf (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered T lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) specific for the tumor-associated antigens (TAAs) cluster of differentiation 20 (CD20) and CD22, with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain (TRAC) and CD52 genes are inactivated. Upon administration, the allogeneic anti-CD20/CD22 universal CAR-expressing T lymphocytes UCART20x22 specifically recognize and induce selective toxicity in CD20- and CD22-expressing tumor cells. CD20 and CD22 are overexpressed in certain hematologic malignancies. Inactivation of the CD52 gene makes the CAR-T cells UCART20x22 resistant to anti-CD52 monoclonal antibody treatment that is used during preconditioning regimen to enhance the expansion and persistence of the CAR-T cells. The knockout of TRAC eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the CAR-T cells.

allogeneic anti-CD30 CAR-Epstein-Barr virus-specific T lymphocytes

A preparation of allogeneic human Epstein-Barr virus (EBV)-specific T lymphocytes (EBVSTs) that have been genetically modified to express a chimeric antigen receptor (CAR) recognizing the tumor-associated antigen (TAA) cluster of differentiation 30 (CD30), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD30 CAR-EBVSTs specifically recognize and bind to CD30-expressing EBV-infected tumor cells, resulting in tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies. EBV, a ubiquitous human herpes virus, is associated with various malignancies, including nasopharyngeal carcinoma, Hodgkin disease, non-Hodgkin lymphoma, and other lymphomas.

allogeneic anti-CD33 CAR NK cells

A preparation of off-the-shelf natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the cluster of differentiation 33 (CD33) antigen, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD33 CAR NK cells target and bind to CD33 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and on myeloid leukemia cells.

allogeneic anti-CD33 CAR T cells VCAR33

A preparation of allogeneic T lymphocytes, derived from the same matched healthy donor who provided a stem cell transplant and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic anti-CD33 CAR T cells VCAR33 specifically recognize and kill CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.

allogeneic anti-CD38 DAR-T cells STI-1492

A preparation of human allogeneic T lymphocytes that are gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt the expression of endogenous T-cell receptor (TCR) alpha and to express a dimeric antigen receptor (DAR) composed of a fragment antigen-binding variable region (Fab) recognizing the tumor-associated antigen (TAA) cluster of differentiation 38 (CD38), linked to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, allogeneic anti-CD38 DAR-T cells STI-1492 are directed to and induce selective toxicity in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis. The disruption of endogenous TCR alpha prevents graft-versus-host disease (GvHD).

allogeneic anti-CD5 CAR T cells

A preparation of allogeneic T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for CD5, with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-CD5 CAR T cells target and bind to CD5-expressing tumor cells, thereby inducing selective cytotoxicity in CD5-expressing tumor cells. CD5 is a T-cell surface glycoprotein expressed on the surface of normal T cells and overexpressed on various B- and T-cell malignancies.

allogeneic anti-CD5-IL-15/IL-15sushi-safety switch CAR T cells

A preparation of allogeneic T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of a humanized anti-CD5 single chain variable fragment (scFv) domain linked to a interleukin (IL)-15/IL-15sushi domain and a safety switch, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD5-IL-15/IL-15sushi-safety switch CAR T cells target and bind to CD5-expressing tumor cells, thereby inducing selective cytotoxicity in CD5-expressing tumor cells. The IL-15/IL-15sushi domain activates and increases the levels of natural killer (NK) cells and memory CD8+ T cells. The memory T cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. The pro-survival cytokine IL-15 regulates CD8+ T- and NK-cell development, activation and proliferation. The safety switch, composed of two rituximab (RTX)-binding epitope sites, allows for the selective elimination of the CAR T cells through the administration of RTX. CD5, a T-cell associated antigen, is expressed in many T-cell lymphomas and leukemias.

allogeneic anti-CD6 CAR T-regulatory cells

A preparation of allogeneic T-regulatory cells (Tregs) that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the T-cell differentiation antigen CD6, with potential immunmodulating activity. Upon administration, the allogeneic anti-CD6 CAR Tregs may promote immunologic homeostasis and prevent autoimmunity. This may induce tolerance to allogeneic hematopoietic stem cell transplants, prevent graft-versus-host disease (GvHD), and suppress autoimmune pathology. The allogeneic anti-CD6 CAR Tregs also targets and binds to CD6, which may prevent CD6-mediated activation pathways, downregulate the activation and differentiation of T cells, and reduce the synthesis of pro-inflammatory cytokines. CD6, a co-stimulatory molecule predominantly expressed on lymphocytes, is involved in the adhesion and maturation of T cells.

allogeneic anti-CD7 CAR T cells

A preparation of donor-derived T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the allogeneic anti-CD7 CAR T cells specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

allogeneic anti-CD7 CAR T cells 4SCAR7U

A preparation of allogeneic, off-the-shelf (OTS), universal, gene-edited T lymphocytes expressing a fourth-generation chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD7 CAR T cells 4SCAR7U specifically target and kill CD7-expressing tumor cells. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

allogeneic anti-CD7 CAR T cells WU-CART-007

A preparation of off-the-shelf (OTS) donor-derived T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the allogeneic anti-CD7 CAR T cells WU-CART-007 specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

allogeneic anti-CD7 CAR-T cells BEAM-201

A preparation of off-the-shelf (OTS) donor-derived T lymphocytes that have been multiplex base-edited and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD7 CAR-T cells BEAM-201 specifically target and kill CD7-expressing tumor cells. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

allogeneic anti-CD70 CAR/dnTGF-BRII-expressing gamma delta T cells ADI-270

A preparation of allogeneic Vdelta1 gamma delta T lymphocytes engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70) and a dominant negative (dn) form of transforming growth factor-beta (TGF-beta; TGFb) receptor II (dnTGF-BRII), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic anti-CD70 CAR/dnTGF-BRII-expressing gamma delta T cells ADI-270 recognize and bind to CD70-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, a type II transmembrane glycoprotein and member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. The inclusion of dnTGF-BRII blocks the signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the ADI-270 T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

allogeneic anti-CD70-CAR T cells ALLO-316

An off-the-shelf (OTS) preparation of human allogeneic T lymphocytes obtained from healthy donors that are engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70) and gene-edited with transcription activator-like effector nuclease (TALEN) to inactivate the endogenous T-cell receptor alpha constant (TRAC) and CD52 loci, with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic anti-CD70-CAR T cells ALLO-316 recognize and bind to CD70-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, a type II transmembrane glycoprotein and member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. Deletion of the CD52 gene makes the modified donor T cells resistant to anti-CD52 monoclonal antibodies, which can be used during lymphodepletion. The deletion of the TRAC gene abrogates the potential induction of graft-versus-host disease (GvHD) by the donor T cells.

allogeneic anti-CD70-CAR-IL-15-transduced cord blood-derived natural killer cells

A preparation of allogeneic, umbilical cord blood (CB)-derived natural killer cells (NKs) that have been engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70) and interleukin-15 (IL-15), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-CD70-CAR-IL-15-transduced CB-derived NK cells target, bind to and induce selective cytotoxicity in CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27, is overexpressed on the surfaces of various cancer cell types. IL-15 is a pro-survival cytokine that promotes persistence of multiple lymphocyte lineages and potentiates the immune response against tumor cells.

allogeneic anti-EGFR CAR/HLA-A*02-gated inhibitory receptor-expressing T lymphocytes A2B395

A preparation of allogeneic T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the epidermal growth factor receptor (EGFR; HER1; ErbB1), and a leukocyte immunoglobulin-like receptor 1 (LIR-1)-based inhibitory receptor specific for human leukocyte antigen (HLA)-A*02 (HLA-A*02), with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic anti-EGFR CAR/HLA-A*02-gated inhibitory receptor-expressing T lymphocytes A2B395 target and bind to EGFR-expressing tumor cells, thereby killing EGFR-expressing tumor cells that have loss of heterozygosity (LOH) for HLA-A*02 protein. The inhibitory receptor specific for HLA-A*02 acts as a self-regulated safety switch that blocks the killing of HLA-A*02-positive EGFR-expressing normal, healthy cells. This may also protect the normal, healthy cells from graft versus host disease (GvHD) resulting from the administration of the allogeneic T cells. HLA-A*02 is expressed on normal cells but not on tumor cells due to LOH. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

allogeneic anti-HA-1 TCR-engineered T cells TSC-100

A preparation of donor-derived T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for HLA-A*02:01-restricted minor histocompatibility antigen HA-1 (HA1), with potential immunomodulating and antineoplastic activities. Following allogeneic haploidentical hematopoietic cell transplantation (HCT) in HLA-A*02:01 positive patients, allogeneic anti-HA-1 TCR-engineered T cells TSC-100 specifically recognize and bind to HA-1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing HA-1. HA-1 is a lineage-specific antigen found on leukemia cells.

allogeneic anti-HA-2 TCR-engineered T cells TSC-101

A preparation of donor-derived T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for HLA-A*02:01-restricted minor histocompatibility antigen HA-2 (HA2), with potential immunomodulating and antineoplastic activities. Following allogeneic haploidentical hematopoietic cell transplantation (HCT) in HLA-A*02:01 positive patients, allogeneic anti-HA-2 TCR-engineered T cells TSC-101 specifically recognize and bind to HA-2 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing HA-2. HA-2 is a lineage-specific antigen found on leukemia cells.

allogeneic anti-NY-ESO-1-TCR-IL-15-transduced cord blood-derived natural killer cells

A preparation of allogeneic, umbilical cord blood (CB)-derived natural killer cells (NKs) that have been engineered to express a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) human cancer-testis antigen NY-ESO-1 and interleukin-15 (IL-15), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic anti-NY-ESO-1-TCR-IL-15-transduced CB-derived NKs target, bind to and induce selective cytotoxicity in NY-ESO-1-expressing tumor cells. NY-ESO-1 is found in normal testis and on the surface of various tumor cell types. IL-15 is a pro-survival cytokine that promotes persistence of multiple lymphocyte lineages and potentiates the immune response against tumor cells.

allogeneic autophagosome-enriched vaccine DPV-001

An off-the-shelf (OTS) autophagosome-enriched tumor vaccine composed of dendritic cell (DC)-targeting microvesicles containing short lived proteins (SLiPs) and defective ribosomal products (DRiPs) derived from tumor cells, with potential immunostimulating and antineoplastic activities. The DriPs- and SLiPs-filled autophagosome microvesicles are made by treating two human non-small cell lung cancer (NSCLC) cell lines, UbiLT3 (non-specific histopathology) and UbiLT6 (adenocarcinoma-like) with both a proteasome inhibitor, to prevent protein degradation, and an autophagy inducer. DPV-001 contains a wide variety of NSCLC-derived TAAs, many as immunogenic altered-peptide ligands (APL), and numerous damage-associated molecular pattern molecules (DAMPs) with Toll-like receptor (TLR) 2, 3, 4, 7 and 9 agonist activities. Upon administration of allogeneic autophagosome-enriched vaccine DPV-001, the proteins in the vaccine target DCs and may stimulate the immune system to mount cytotoxic T-lymphocyte (CTL) and helper T-lymphocyte responses against the TAAs. The TAAs are overexpressed in a variety of cancer cell types other than NSCLC. The tumor-associated SLiPS and DRiPs are highly unstable and normally degraded by tumor cell proteasomes. They are typically not processed and cross-presented by antigen-presenting cells (APCs).

allogeneic B7.1/HLA-A1 transfected tumor cell vaccine

An allogeneic whole cell vaccine, derived from irradiated allogenic tumor cells manipulated to express human B7.1 (CD80 antigen) and human leukocyte antigen (HLA) A1, with potential antitumor activity. Vaccination with allogeneic B7.1/HLA-A1 transfected tumor cell vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor cell proliferation.

allogeneic BK-specific cytotoxic T lymphocytes

Allogeneic cytotoxic T lymphocytes (CTLs) that are specifically reactive to BK virus (BKV), with potential antiviral activity. Upon infusion of allogeneic BK-specific CTLs into immunocompromised patients who were infected with BKV after allogeneic stem cell transplantation, these cells exert a specific CTL response against BKV, thereby killing and eliminating the BKV-infected cells. BKV is a member of the polyomavirus family that may cause mild symptoms in normal, healthy people; however, BKV infection can lead to severe disease in immunocompromised patients.

allogeneic calibrated release IL-15-expressing logic-gated gene circuit anti-CD33/FLT3 CAR-NK cells SENTI-202

A preparation of off-the-shelf (OTS) natural killer (NK) cells engineered to express three chimeric proteins: 1) a bivalent activating chimeric antigen receptor (aCAR), controlled by OR logic gated gene circuit, specific for the tumor-associated antigens (TAAs) cluster of differentiation 33 (CD33) and FLT3 tyrosine kinase receptor (Fms-like tyrosine kinase 3; FLT3; FLT-3; CD135; fetal liver kinase-2; FLK2) (CD33 OR FLT3 (OR GATE) aCAR), 2) an inhibitory CAR (iCAR) recognizing endomucin (EMCN) and controlled by NOT logic gate (NOT EMCN (NOT GATE) iCAR), and 3) a calibrated release interleukin 15 (IL-15) (crIL15), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic crIL-15-expressing logic-gated gene circuit anti-CD33/FLT3 CAR-NK cells SENTI-202 targets and binds to CD33 and/or FLT3 expressed on the surface of tumor cells, such as primary acute myeloid leukemia (AML) blasts and leukemic stem cells (LSCs). This induces selective toxicity in tumor cells expressing CD33 and/or FLT3. To protect CD33/FLT3-expressing healthy hematopoietic stem cells (HSCs) from potential aCAR-mediated on-target/off-tumor toxicity, the iCAR recognizes and binds to the healthy cell surface protein EMCN, which is selectively expressed on healthy HSCs but absent on tumor cells. The crIL-15 allows for activation of the IL-15 receptor pathway, which increases the persistence, activation and killing activity of SENTI-202 and other immune cells. CD33 and FLT3 are expressed on healthy HSCs and on a variety of cancer cells.

allogeneic CAR T cells CT0594CP

A preparation of allogeneic T lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) specific for as of yet undisclosed tumor-associated antigens (TAAs), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic CAR T cells CT0594CP specifically targets and binds to tumor cells that express the undisclosed TAAs, resulting in tumor cell lysis.

allogeneic CD123-specific universal CAR123-expressing T lymphocytes

Allogeneic, off-the-shelf, universal transcription activator-like effector nuclease (TALEN)-engineered T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human interleukin-3 receptor alpha chain (IL3RA; cluster of differentiation 123; CD123), with potential immunomodulating and antineoplastic activities. Upon transfusion of allogeneic CD123-specific universal CAR123-expressing T lymphocytes (UCART123), these cells target and bind to cancer cells expressing CD123. This induces selective toxicity in and causes lysis of CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness. Using TALEN technology, the UCART123 cells no longer express the endogenous T-cell receptor (TCR) thereby abrogating the potential induction of graft-versus-host disease (GvHD) by the donor T cells.

allogeneic CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes

A preparation of genetically modified allogeneic T cells transduced with a replication-incompetent, self-inactivating lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR), comprised of a CD28 co-stimulatory signaling domain fused to CD3 zeta, the single-chain variable fragment of CD123 antigen (interleukin-3 receptor alpha chain or IL3RA), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, allogeneic CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes are directed to and induce selective toxicity in CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates detection of the administered T cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The costimulatory signaling domain enhances both proliferation of T cells and antitumor activity. Hinge optimization prevents recognition of the CAR by Fc receptors (FcRs).

allogeneic CD16-expressing natural killer cells CYNK-101

A population of cryopreserved, off-the-shelf (OTS) allogeneic natural killer (NK) cells derived from human placental hematopoietic stem cells (HSCs) expressing the CD34 surface antigen, and engineered to express a high-affinity, non-cleavable CD16 (hnCD16) Fc receptor, with potential antineoplastic and immunostimulatory activities. Upon infusion of CYNK-101, the allogeneic CD16-expressing NK cells bind to the Fc portion of tumor cell-bound monoclonal antibodies that were administered as induction therapy. This enhances NK cell activation, cytokine secretion, and antibody-dependent cellular cytotoxicity (ADCC) in the presence of certain antibody therapeutics. CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response. CYNK-101 NK cells' hnCD16 Fc receptor prevents downregulation and optimizes binding to tumor-targeting antibodies for enhanced ADCC.

allogeneic CD19-CAR CD45RA-negative T cells

A preparation of allogeneic T lymphocytes, depleted of CD45RA-positive cells, that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 (cluster of differentiation 19) fused to the co-stimulatory domain of 4-1BB (CD137) and the CD3-zeta (CD3z) T-cell signaling domain (4-1BBz), with potential immunostimulating and antineoplastic activities. CD45RA depletion results in a cellular product that contains a high amount of memory T cells (Tm). Upon administration, the allogeneic CD19-CAR CD45RA-negative T cells specifically recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. CD45RA is expressed on naive T cells (Tn), whereas Tm cells are CD45RA-negative. The depletion of the CD45RA-positive cells reduces the risk of graft-versus-host disease (GvHD) upon infusion. Tn cells have the potential to induce more severe graft-versus-host disease (GvHD) than Tm cells.

allogeneic CD19-OX40-CD3zeta-CAR-mbIL-15-expressing natural killer cells NKX019

A preparation of off-the-shelf (OTS), allogeneic and ex vivo expanded natural killer cells (NKs) that are engineered to express membrane-bound IL-15 (mbIL15) and a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 that is coupled to the co-stimulatory domain of OX40 (CD134), and to the zeta chain of the TCR/CD3 complex (CD3-zeta; CD3zeta), with potential immunomodulating and antineoplastic activities. Upon administration of allogeneic CD19-OX40-CD3zeta-CAR-mbIL-15-expressing NK cells NKX019, these cells specifically target and bind to tumor cells expressing CD19. This induces secretion of pro-inflammatory cytokines and results in the lysis of CD19-expressing tumor cells. IL-15 is a pro-survival cytokine that potentiates the immune response against tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

allogeneic CD19-specific CAR-modified CD8 plus central memory-derived virus-specific T cells

A preparation of allogeneic Epstein-Barr virus (EBV)- and human cytomegalovirus (CMV)-specific CD8+ central memory-derived T effector-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) anti-CD19/CD3 zeta chain fusion protein coupled to the intracellular signal domain of CD28 antigen, with potential immunostimulating, anti-viral and antineoplastic activities. Upon infusion, allogeneic CD19-specific CAR-modified CD8+ central memory-derived virus-specific T cells directs the T lymphocytes to CD19-expressing tumor cells, stimulating a selective toxicity to tumor cells which may eventually result in tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The viral specific T cells exert antiviral immunity.

allogeneic CD19-specific universal CAR19-expressing T lymphocytes

A preparation of allogeneic, frozen, ‘off-the-shelf’, universal transcription activator-like effector nuclease (TALEN)-engineered, gene-edited T lymphocytes expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, and containing a RQR8 transgene, with potential immunostimulating and antineoplastic activities. Using TALEN technology, the T-cell receptor (TCR) alpha chain and CD52 genes are deleted from the CAR19 T cells. Upon infusion, allogeneic universal CD19-specific CAR-modified T cells (UCART19) specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Deletion of the CD52 gene makes the modified donor T cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The knockout of the TCR alpha gene eliminates TCR expression and is intended to abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T cells. The gene-edited allogeneic, frozen UCART19 have reduced production times and provide off-the-shelf CAR-T cells when compared to autologous CAR-T cells, which use the patient's own cells and are produced on an individual basis. The protein expressed by the RQR8 transgene contains epitopes from CD34 and CD20, which allows tracking of the UCART19 cells with a clinically-approved anti-CD34 antibody. Additionally if the UCART19 cells cause unacceptable side effects, the CD20 portion of the protein permits selective depletion of the UCART19 cells when the anti-CD20 monoclonal antibody rituximab is administered.

allogeneic CD19/CD20-specific CAR-T cells P-CD19CD20-ALLO1

An off-the-shelf (OTS) preparation of human allogeneic T lymphocytes containing primarily stem cell memory T cells (Tscm) that have been genetically modified to express two chimeric antigen receptors (CARs) targeting the tumor-associated antigens (TAAs) CD19 and CD20, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic CD19/CD20-specific CAR-T cells P-CD19CD20-ALLO1 specifically recognize and induce selective toxicity in CD19- and/or CD20-expressing tumor cells. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD19 and CD20 may prevent tumor cell antigen escape and relapse.

allogeneic CD19CAR-CD28-CD3-zeta-expressing T lymphocytes

A preparation of allogeneic, donor-derived T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment), fused to the extracellular, transmembrane and intracellular signaling domains of the T-cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (19-28z), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic CD19CAR-CD28-CD3-zeta-expressing T lymphocytes are directed to CD19-expressing tumor cells, which induces selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. The inclusion of the CD28 signaling domain may increase proliferation of T cells and antitumor activity compared to the inclusion of the CD3-zeta chain alone.

allogeneic CD19CAR-transfected cytokine-induced killer cells

A preparation of allogeneic cytokine-induced killer (CIK) cells derived from peripheral blood mononuclear cells (PBMCs) transfected with the Sleeping Beauty (SB) transposon, CD19CAR (CARCIK-CD19), with potential immunomodulatory and antineoplastic activities. CIK cells are CD3- and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T lymphocytes. Upon infusion following an allogeneic stem cell transplantation, the CARCIK-CD19 cells bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CIK cells may have enhanced cytotoxic activity compared to lymphokine-activated killer (LAK) cells. CD19 is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

allogeneic CD22-specific universal CAR-expressing T lymphocytes UCART22

A preparation of allogeneic, off-the-shelf (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human CD22 with potential immunomodulating and antineoplastic activities. Upon transfusion, allogeneic CD22-specific universal CAR-expressing T lymphocytes UCART22 express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces, resulting in lysis of CD22-expressing tumor cells. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B cells.

allogeneic CD25/Treg-depleted donor lymphocytes

A preparation of allogeneic peripheral blood mononuclear cells (PBMCs) derived from an 8/8 HLA-matched donor that have been selectively depleted of CD4+CD25hiFoxp3+ regulatory T cells (Tregs; CD25hi Tregs) with potential to enhance graft-versus-tumor (GVT) immune responses in patients with myeloid relapse following a hematopoietic stem cell transplant (HSCT) from a matched donor. Following collection and ex-vivo depletion of CD25hi Tregs from PBMCs derived from the original donor, the CD25/Treg-depleted donor lymphocytes are infused into the patient. Upon administration, the CD25/Treg-depleted donor lymphocyte infusion (DLI) may enhance the proliferation of CD4+ and CD8+ effector T cells (Teffs) and potentially induce curative GVT immune responses in patients with myeloid relapse following HSCT.

allogeneic CD3- CD19- CD57+ NKG2C+ NK cells FATE-NK100

A preparation of pharmacologically-enriched, allogeneic natural killer (NK) cells derived from a related, but not completely matched, human leukocyte antigen (HLA)-haploidentical donor that is seropositive for cytomegalovirus (CMV+), with potential cytolytic and antineoplastic activities. Upon leukapheresis, the donor peripheral blood mononuclear cells (PBMCs) are treated to remove T lymphocytes (CD3+) and B lymphocytes (CD19+). The remaining leukocytes are cultured for 7 days with the cytokine interleukin-15 (IL-15) and a small molecule inhibitor of glycogen synthase kinase 3-beta (GSK3beta) to generate the adaptive, CD3- CD19- CD57+ NKG2C+ NK cells FATE-NK100 ex vivo. Upon infusion of the allogeneic CD3- CD19- CD57+ NKG2C+ NK cells FATE-NK100, these cells selectively recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which results in cancer cell lysis. Exposure to CMV induces the expression of the memory-like activating receptor NKG2C and the maturation marker CD57 in the isolated NK cells, making them more potent than those not pre-exposed to CMV. CD57 both enhances the effector function of NK cells and stimulates CD16-dependent signaling. Treatment with IL-15 enhances NK cell proliferation and survival. The GSK3beta inhibitor induces preferential expansion of CD57+ NK cells that exhibit enhanced interferon (IFN)-gamma production.

allogeneic CD3- CD19- selected natural killer cells

Human leukocyte antigen (HLA)-haploidentical donor-derived natural killer (NK) cells that are activated with the cytokine interleukin-15 (IL-15), with immunomodulating and antineoplastic activities. Upon leukapheresis, the HLA-haploidentical donor peripheral blood mononuclear cells (PBMCs) are treated to remove T lymphocytes (CD3+) and B-lymphocytes (CD19+) cells. In turn, NK cells are expanded and activated with IL-15. Upon infusion of the allogeneic CD3- CD19- selected NK cells, these cells recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which results in cancer cell lysis.

allogeneic CD33CAR-CD3zeta-4-1BB-expressing T lymphocytes

A preparation of allogeneic T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the CD33 antigen, coupled to the signaling domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon administration, allogeneic CD33CAR-CD3zeta-4-1BB-expressing T lymphocytes target and induce selective toxicity in CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and on myeloid leukemia cells.

allogeneic CD34+-enriched and CD45RA-depleted PBSCs

A preparation of donor-derived peripheral blood stem cells (PBSCs) that have been enriched with CD34-positive stem cells and have been depleted of CD45RA-positive cells, that can potentially be used for immune reconstitution purposes. CD45RA depletion results in a cellular product that contains a high amount of memory T cells (Tm). Upon infusion of the allogeneic CD34+-enriched and CD45RA-depleted PBSCs after a hematopoietic cell transplantation (HCT), these cells provide Tm recovery and are able to prevent viral infections. The depletion of the CD45RA-positive cells reduces the risk of graft-versus-host disease (GvHD) upon infusion. CD45RA is expressed on naive T cells (Tn), whereas Tm cells are CD45RA-negative. Tn cells have the potential to induce more severe GvHD than Tm cells.

allogeneic CD34-positive E-rosetted T-cell depleted peripheral blood stem cells

A preparation of CD34+ selected peripheral blood stem cells (PBSCs) that are depleted of T cells via erythrocyte rosetting (E-rosetting) and intended for allogeneic stem cell transplant. Administration of this particular preparation of CD34+E- T-cell depleted PBSCs may potentially reduce the occurrence of graft-versus-host disease (GvHD) without increasing the risk of graft failure or poor graft function.

allogeneic CD34-positive enriched peripheral blood stem cells

A preparation of allogeneic CD34+ selected peripheral blood stem cells (PBSCs) that can potentially be used for immune reconstitution purposes. Upon administration of the allogeneic CD34-positive enriched PBSCs after a hematopoietic cell transplantation (HCT), these cells may provide memory T-cell (Tm) recovery and potentially prevent viral infections. They potentially reduce the occurrence of graft-versus-host disease (GvHD) without increasing the risk of graft failure or poor graft function.

allogeneic CD4+ memory Th1-like T cells/microparticle-bound anti-CD3/anti-CD28

A preparation consisting of allogeneic, differentiated Th1-like T cells bound to T cell-stimulating monoclonal antibodies with potential antitumor activity. More specifically, allogeneic CD4+ memory Th1-like T cells/microparticle-bound anti-CD3/anti-CD28 are composed of a proprietary preparation of mismatched, allogeneic differentiated CD4+ memory Th1-like T cells bound to paramagnetic, epoxy-covered 4.5 micron microparticles with covalently bound anti-CD3/anti-CD28 monoclonal antibodies at a 2:1 bead:cell ratio. The CD4+ memory Th1-like T cells are derived from precursors found in the circulation of a normal donor. Stimulated by the microparticle-bound monoclonal antibodies, the infused T cells produce pro-inflammatory, anti-tumor cytokines such as like IFN-gamma, TNF-beta, and IL-2, disabling tumor immune avoidance mechanisms and stimulating the host immune system to both reject the infused T cells and kill tumor cells.

allogeneic CD56-positive CD3-negative natural killer cells CYNK-001

A population of cryopreserved, off-the-shelf (OTS) allogeneic natural killer (NK) cells derived from human placental hematopoietic stem cells (HSCs) and expressing the CD56 surface antigen and exhibiting a lack of CD3, with potential immunomodulating, antineoplastic and antiviral activities. Upon infusion of allogeneic CD56-positive CD3-negative NK cells CYNK-001, these cells are able to recognize tumor cells as well as virally-infected cells, secrete perforins, granzymes and cytokines, and induce apoptosis in tumor and virally-infected cells.

allogeneic CD8+ leukemia-associated antigens specific T cells NEXI-001

A preparation of allogeneic CD8+ T cells targeting multiple undisclosed leukemia-associated antigens, with potential immunomodulating and antineoplastic activities. Following peripheral blood mononuclear cell (PBMC) collection from the original stem cell donor and ex vivo priming and expansion, the allogeneic CD8+ leukemia-associated antigens specific T cells NEXI-001 are re-introduced into the leukemia patient, where they target and kill tumor cells expressing these leukemia-associated antigens.

allogeneic CD8+ memory T cells

A preparation of allogeneic CD8+ memory T cells from the same donor of hematopoietic cell transplantation (HCT), that can potentially be used for immune reconstitution purposes. Upon infusion of the allogeneic CD8+ memory T cells after HCT, these cells may provide recovery for CD8+ memory T cells and may prevent infections.

allogeneic cellular vaccine 1650-G

A pluripotent, allogeneic, tumor cell vaccine composed of irradiated tumor cells from the non-small cell lung cancer (NSCLC) cell line 1650 and the immunoadjuvant recombinant granulocyte-macrophage colony stimulating factor (GM-CSF) (1650-G), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic cellular vaccine 1650-G may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against tumor-associated antigens (TAAs) expressed on NSCLC cells. GM-CSF potentiates the antitumor immune response. The 1650 cell line is used as a source for TAAs.

allogeneic CMV antigen-specific CD4+/CD8+ T lymphocytes

A population of allogeneic T lymphocytes specifically reactive to cytomegalovirus (CMV) with potential antiviral activity. Allogeneic CMV antigen-specific T cells are prepared via ex vivo stimulation of donor-derived peripheral blood mononuclear cells (PBMCs) with major cytomegalovirus structural protein, pp65 (ppUL83). T cells that secrete interferon (IFN)-gamma in response to pp65 antigen exposure are selected and expanded for administration. Administration of the CMV antigen-specific CD4+ and CD8+T lymphocytes into hematopoietic stem cell transplant (HSCT) or immunocompromised patients infected with CMV may potentially reconstitute virus-specific responses, thereby controlling CMV infections

allogeneic CMV/AdV-specific cytotoxic T lymphocytes

A population of allogeneic cytotoxic T lymphocytes (CTLs) specifically reactive to cytomegalovirus (CMV) and adenovirus (AdV) with potential antiviral activity. Allogeneic CMV/AdV-specific cytotoxic T lymphocytes are prepared by exposing donor-derived CTLs to a lethally irradiated Epstein-Barr virus-positive lymphoblastoid B cell line (EBV-LCL) that has been transduced with a clinical-grade adenoviral vector (Ad5f35CMVpp65) as a source of CMV and AdV antigens. Infusion of these CTLs into stem cell transplant recipients may prevent CMV and AdV viral disease.

allogeneic CRISPR-Cas9 engineered anti-CD19 CAR T cells CTX110

A preparation of human allogeneic T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR, with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD19 CAR T-cells CTX110 recognize and bind to CD19-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. Removal of endogenous TCR reduces the risk of graft-versus-host disease (GvHD). CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

allogeneic CRISPR-Cas9 engineered anti-CD19 CAR T cells CTX112

A preparation of human allogeneic T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR, transforming growth factor-beta receptor II (TGFbRII), and Regnase-1, with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD19 CAR T cells CTX112 recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. Removal of endogenous TCR reduces the risk of graft-versus-host disease (GvHD). CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Incorporation of the Regnase-1 and TGFBR2 double knockout increases the potency, persistence and efficacy of the CAR-T cells and enhances anti-tumor activity.

allogeneic CRISPR-Cas9 engineered anti-CD70 CAR-T cells CTX131

A preparation of human allogeneic T lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD70 CAR T cells CTX131 recognize and bind to CD70-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. Disruption of endogenous TCR prevents graft-versus-host disease (GvHD); the disruption of MHC class I molecules increases the persistence of the CAR T cells.

allogeneic CRISPR-Cas9-engineered anti-CD70 CAR-T cells CTX130

A preparation of human allogeneic T lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD70 CAR-T cells CTX130 recognize and bind to CD70-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. Disruption of endogenous TCR prevents graft-versus-host disease (GvHD); the disruption of MHC class I molecules increases the persistence of the CAR-T cells.

allogeneic CRISPR-edited anti-BCMA CAR-T cells CB-011

A preparation of allogeneic, off-the-shelf T lymphocytes genetically modified and clustered regularly interspaced short palindromic repeats (CRISPR)-edited to contain a deletion of the TRAC gene, a site-specific insertion of a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) into the TRAC gene, a deletion of the B2M gene, and a site-specific insertion of a gene encoding a B2M-HLA-E-peptide fusion into the B2M gene, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic CRISPR-edited anti-BCMA CAR-T cells CB-011 recognize and bind to BCMA-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of BCMA-positive tumor cells. Knock out of the TRAC gene eliminates the endogenous T-cell receptors (TCRs), thereby preventing graft-versus-host disease (GvHD). The B2M protein is removed to eliminate endogenous HLA class I expression on the surface of the CB-011 CAR-T cells, which protects the CAR-T cells from host T-cell rejection. The B2M-HLA-E fusion protein is inserted to protect the CAR-T cells from host natural killer (NK) cell rejection. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival.

allogeneic CRISPR-edited anti-CD19 CAR T cells CB-010

A preparation of allogeneic, off-the-shelf T lymphocytes genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, and clustered regularly interspaced short palindromic repeats (CRISPR)-edited to eliminate endogenous T-cell receptor (TCR) and programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) expression, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic CRISPR-edited anti-CD19 CAR-T cells CB-010 recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the CD19-expressing tumor cells. The endogenous TCR is removed to prevent graft-versus-host disease (GvHD). CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

allogeneic CRISPR-edited anti-CD19 CAR T cells PACE CART19

An off-the-shelf (OTS) preparation of human allogeneic T lymphocytes transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), and electroporated with clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate the expression of endogenous TCR, HLA class I and HLA class II molecules, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic CRISPR-edited anti-CD19 CAR T cells PACE CART19 recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-expressing tumor cells. The removal of endogenous TCR, HLA class I and HLA class II molecules prevents allogeneic immune responses and reduces the risk of graft-versus-host disease (GvHD). The tumor-associated antigen (TAA) CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

Allogeneic CRISPR-edited Anti-CD19 CAR T Cells PBLTT52CAR19

A preparation of allogeneic T-lymphocytes transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with genetic modification of CD52 and T-cell receptor alpha constant (TRAC) loci via clustered regularly interspaced short palindromic repeats (CRISPR), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic CRISPR-edited anti-CD19 CAR T cells PBLTT52CAR19 recognize and bind to CD19-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The editing of the CD52 gene may make the modified donor T-cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The editing of the TRAC may eliminate TCR expression, which may abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells, and may also result in uniform CAR expression and enhanced T-cell potency.

allogeneic CRISPR-edited anti-CLL-1 CAR-T cells CB-012

A preparation of allogeneic, off-the-shelf T lymphocytes genetically modified and clustered regularly interspaced short palindromic repeats (CRISPR)-edited to contain the deletion of the TRAC gene, the site-specific insertion of a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) C-type-lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A; CD371) into the TRAC gene, the knockout of programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1), the deletion of the B2M gene, and the site-specific insertion of a gene encoding a B2M-HLA-E-peptide fusion into the B2M gene, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic CRISPR-edited anti-CLL-1 CAR-T cells CB-012 recognize and bind to CLL-1-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CLL-1-expressing tumor cells. Knock out of the TRAC gene eliminates the endogenous T-cell receptors (TCRs), thereby preventing graft-versus-host disease (GvHD). PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the CLL-1-expressing tumor cells. The B2M protein is removed to eliminate endogenous HLA class I expression on the surface of the CB-012 CAR-T cells, which protects the CAR-T cells from host T-cell rejection. The B2M-HLA-E fusion protein is inserted to protect the CAR-T cells from host natural killer (NK) cell rejection. CLL-1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

allogeneic CS1-specific universal CAR-expressing T lymphocytes UCARTCS1A

A preparation of allogeneic, off-the-shelf (OTS), universal transcription activator-like effector nuclease (TALEN)-engineered T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC), with potential immunomodulating and antineoplastic activities. Upon transfusion of allogeneic CS1-specific universal CAR-expressing T lymphocytes UCARTCS1A, these cells target and bind to cancer cells expressing CS1. This induces selective toxicity in and causes lysis of CS1-expressing tumor cells. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells.

allogeneic cytokine-induced memory-like NK cells WU-NK-101

A population of off-the-shelf (OTS) donor-derived cytokine-induced, memory-like, cytotoxic natural killer (NK) cells (CIML NKs) containing NK cell-activating surface receptors, with potential immunomodulating and antineoplastic activities. The allogeneic NK cells are pre-activated ex vivo using the human-derived cytokines interleukin (IL)-12, IL-15, and IL-18, which induces the differentiation of the NK cells into CIML NK cells, which contain more NK cell-activating surface receptors. The pretreated NK cells exhibit enhanced activation and increased production of the cytokine interferon-gamma (IFN-g), and may exert enhanced cytotoxicity against tumor cells, including enhanced antibody-dependent cellular cytotoxicity (ADCC). Upon administration, the CIML NKs WU-NK-101 may induce an anti-tumor immune response and kill tumor cells.

allogeneic cytomegalovirus-specific cytotoxic T lymphocytes

A population of allogeneic cytotoxic T lymphocytes (CTLs) specifically reactive to the herpes virus cytomegalovirus (CMV) with potential immunomodulating and antiviral activities. Upon immunoprophylactic adoptive cell therapy infusion with allogeneic cytomegalovirus-specific cytotoxic T lymphocytes, these CTLs may help reconstitute CMV-specific CTL responses in CMV-infected immunocompromised hosts after allogeneic hematopoietic stem cell transplant, thereby potentially preventing the occurrence of CMV viral disease or reducing the amount of antiviral drug therapy.

allogeneic dendritic cell vaccine COMBIG-DC

A cancer vaccine consisting of allogeneic, immortalized dendritic cells (DCs) loaded with tumor specific antigens and activated, with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration of the allogeneic dendritic cell vaccine COMBIG-DC, these activated DCs attract natural killer (NK) cells, induce an anti-inflammatory response leading to the induction of NK-cell-mediated tumor cell death. Upon release of tumor associated antigens (TAAs) from the lysed tumor cells, these antigens are taken up by antigen presenting cells which activate the immune system to elicit a potent cytotoxic T-cell (CTL) response against the TAAs, resulting in the death of TAAs-expressing tumor cells.

allogeneic dendritic cell-myeloma idiotype vaccine

A cell-based vaccine composed of allogeneic dendritic cells pulsed ex-vivo with an autologous myeloma idiotype with potential antineoplastic activity. Upon administration, allogeneic dendritic cell-myeloma idiotype vaccine may stimulate the host immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against myeloma cells, resulting in cell lysis.

allogeneic dendritic secretomes

A preparation of allogeneic dendritic cell (DC) secretomes, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic DC secretomes may help activate an anti-tumor immune response.

allogeneic DNT cells RC1012

A population of off-the-shelf (OTS) healthy, donor-derived CD4 and CD8 double-negative T lymphocytes (allo-DNTs), with potential immunomodulating and anti-leukemic activities. The DNTs are expanded ex vivo in order to enhance their tumor destroying potential. Upon administration of the allo-DNTs RC1012, the receptor type II integral membrane protein (KLRK1; NKG2D) and DNAX accessory molecule 1 (cluster of differentiation 226; CD226; DNAM-1) expressed on the DNTs recognize and bind to their cognate ligands expressed on leukemia cells. Upon binding, the DNTs release interferon-gamma (IFN-g), thereby destroying the tumor cells. NKG2D, a member of the CD94/NKG2 family of C-type lectin-like receptors, and DNAM-1, a member of the immunoglobulin superfamily containing 2 Ig-like domains of the V-set, play a key role in natural killer cell (NK)-mediated tumor cell killing. Certain tumor cells express higher levels of NKG2D and DNAM-1 ligands on their surfaces, thereby increasing their susceptibility to DNT-mediated cell lysis.

allogeneic double negative T cells

A population of healthy, donor-derived CD4 and CD8 double-negative T lymphocytes (DNTs), with potential immunomodulating and anti-leukemic activities. The DNTs are expanded ex vivo in order to enhance their tumor destroying potential. Upon administration of the allogeneic DNTs (DNT-UHN-1), the receptors NKG2-D type II integral membrane protein (KLRK1; NKG2D) and DNAX accessory molecule 1 (cluster of differentiation 226; CD226; DNAM-1) expressed on the DNTs recognize and bind to their cognate ligands expressed on leukemia cells. Upon binding, the DNTs release interferon-gamma (IFN-g), thereby destroying the tumor cells. DNTs derived from peripheral blood of healthy donors appear to be effective against certain types of tumor cells, including leukemia cells, and do not attack normal hematopoietic cells. NKG2D, a member of the CD94/NKG2 family of C-type lectin-like receptors, and DNAM-1, a member of the immunoglobulin superfamily containing 2 Ig-like domains of the V-set, play a key role in natural killer cell (NK)-mediated tumor cell killing. Certain tumor cells express higher levels of NKG2D and DNAM-1 ligands on their surfaces, thereby increasing their susceptibility to DNT-mediated cell lysis.

allogeneic EBV-transformed B-lymphoblastoid cell line lysate-pulsed autologous dendritic cell vaccine KSD-101

A cell-based cancer vaccine composed of autologous monocyte-derived dendritic cells (DCs) pulsed with allogeneic Epstein-Barr virus (EBV)-transformed B-lymphoblastoid cell line (BLCL) lysate, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, DCs are loaded with allogeneic EBV-transformed BLCL lysate. Upon re-administration of the allogeneic EBV-transformed BLCL lysate-pulsed autologous DC vaccine KSD-101, the immune system is exposed to EBV-specific antigens, which stimulates the induction of a specific cytotoxic T-lymphocyte (CTL) response against EBV-positive tumor cells or EBV-infected cells. This results in cell lysis and inhibition of cancer cell proliferation. EBV, a ubiquitous human herpes virus, is associated with various malignancies.

allogeneic Epstein-Barr virus-specific cytotoxic T lymphocytes

A preparation of allogeneic Epstein-Barr virus (EBV) specific cytotoxic T lymphocytes (CTL) with potential antineoplastic activity. Upon administration, the allogeneic EBV-specific CTLs are either harvested from a donor with an EBV-positive tumor or are donor CTLs activated against EBV-specific antigens ex vivo. Administration into a patient exerts a CTL response against EBV-positive tumor cells or EBV-infected cells. This results in cell lysis and inhibition of cancer cell proliferation. EBV, a ubiquitous human herpes virus, is associated with various malignancies, including nasopharyngeal carcinoma, Hodgkin disease, non-Hodgkin lymphoma, and other lymphomas.

allogeneic ex-vivo-treated peripheral blood mononuclear cells

A preparation of allogeneic peripheral blood mononuclear cells (PBMCs) treated and induced ex vivo to undergo early apoptosis, with potential immunomodulating and antineoplastic activities. Upon administration of allogeneic ex-vivo-treated PBMCs, the early apoptotic cells are engulfed by macrophages and immature dendritic cells (DCs). This leads to immune modulation, which may result in immune-mediated tumor cell death.

allogeneic gamma delta T cells GDKM-100

A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration of the allogeneic gamma delta T cells GDKM-100, these cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

allogeneic gamma-delta T lymphocytes KB-GDT-01

An off-the-shelf (OTS) preparation of unmodified, donor-derived T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration of the allogeneic gamma-delta T lymphocytes KB-GDT-01, these cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma-delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

allogeneic gamma-delta T lymphocytes TCB-008

A preparation of ex vivo-expanded, allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration of the allogeneic gamma-delta T lymphocytes TCB-008, these cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma-delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

allogeneic gene-edited CD33-knockout hematopoietic stem and progenitor cells

A preparation of human allogeneic hematopoietic stem and progenitor cells (HSPCs) that are ex-vivo gene-edited to remove the cluster of differentiation 33 (CD33) antigen, that can potentially be used to improve hematopoietic recovery after hematopoietic cell transplantation (HCT) and CD33-targeting therapy. Upon administration, allogeneic gene-edited CD33-knockout HSPCs increase and restore the number of HSPCs, which may prevent or decrease infection and other complications of HCT and chemotherapy-induced neutropenia (CIN). The removal of CD33 protects the agent from the cytotoxic effects of CD33-targeted agents administered after HCT.

allogeneic gene-modified gamma delta T cells

A preparation of genetically modified allogeneic gamma delta T lymphocytes, with potential immunomodulating and antineoplastic activities. Upon administration, the allogeneic gene-modified gamma delta T cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The genetic modification of the allogeneic gene-modified gamma delta T cells may confer resistance to alkylating chemotherapeutic agents including temozolomide and allow the use of the gamma delta T cells as an adjunct to these agents.

allogeneic glial progenitor cells

An allogeneic, off-the-shelf, preparation of purified human glial progenitor cells, with potential neuro-regenerative activity. Upon unilateral transplantation into spinal cord demyelinated lesions, the glial progenitor cells may integrate into the spinal cord lesion sites and differentiate into astrocytes and oligodendrocytes. Astrocytes are specialized neuroglial cells that perform many neuroprotective functions. Oligodendrocytes produce myelin and may repair damage in neurodegenerative diseases involving damaged or destroyed oligodendrocytes and myelin deficiency, such as transverse myelitis.

allogeneic glioblastoma stem-like cell line lysate-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from an allogeneic glioblastoma (GBM) stem-like cell line, with potential immunostimulatory and antineoplastic activities. Upon administration allogeneic glioblastoma stem-like cell line lysate-pulsed autologous dendritic cell vaccine exposes the immune system to GBM stem cell antigens, which may result in cytotoxic T lymphocyte (CTL) and antibody responses against GBM cells. This leads to GBM cell lysis. GBM stem-like cells contain a specific range of antigens that are essential for the neoplastic growth and survival of GBM cells.

allogeneic GM-CSF-based myeloma cell vaccine

An allogeneic tumor cell vaccine containing myeloma cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Upon vaccination, allogeneic GM-CSF-based myeloma cellular vaccine secretes GM-CSF, which may potentiate a tumor-specific cytotoxic T-lymphocyte (CTL) response against myeloma cancer cell-associated antigens.

allogeneic GM-CSF-secreting breast cancer vaccine

An allogenic vaccine consisting of irradiated breast cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene. Upon vaccination, the genetically modified cells secrete GM-CSF, thereby potentiating a tumor-specific T cell response against breast cancer cell-asociated antigens.

allogeneic GM-CSF-secreting breast cancer vaccine SV-BR-1-GM

A vaccine consisting of irradiated allogeneic breast cancer cells, derived from the breast cancer cell line SV-BR-1 that are transfected with the immunostimulant granulocyte-macrophage colony-stimulating factor (GM-CSF; CSF2) gene, with potential immunostimulating and antineoplastic activities. Upon intradermal administration of the allogeneic GM-CSF-secreting breast cancer vaccine SV-BR-1-GM, the genetically-modified cells secrete GM-CSF. This potentiates a tumor-specific cytotoxic T-lymphocyte (CTL) immune response against breast cancer cells.

allogeneic GM-CSF-secreting lethally irradiated pancreatic tumor cell vaccine

An allogeneic tumor vaccine composed of lethally irradiated allogeneic pancreatic tumor cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injection, allogeneic GM-CSF-secreting lethally irradiated pancreatic tumor cell vaccine secretes GM-CSF at the injection site. In turn, GM-CSF may stimulate the body's immune system against tumor cells by attracting and enhancing the activation of antigen-presenting cells (APCs), such as dendritic cells (DCs). This promotes antigen presentation to T lymphocytes and induces a cytotoxic T-lymphocyte (CTL) response against the pancreatic tumor cells expressing the pancreatic tumor-associated antigens (TAAs).

allogeneic GM-CSF-secreting lethally irradiated prostate cancer vaccine

An allogeneic whole cell vaccine expressing human granulocyte macrophage-colony stimulating factor (GM-CSF) with potential antineoplastic activity. Tumor cells from prostate cancer patients are harvested and then genetically modified to secrete GM-CSF, an immune stimulatory growth factor that plays a key role in stimulating the body's immune responses against tumor cells. Because the vaccine is derived from allogenic cells, it has demonstrated a favorable side effect profile than other approaches of delivering long-lasting GM-CSF.

allogeneic GM-CSF-secreting lethally irradiated whole melanoma cell vaccine

An allogeneic cancer vaccine composed of lethally irradiated whole melanoma cancer cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic GM-CSF-secreting lethally irradiated whole melanoma cell vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the body's immune system against tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B- and T-lymphocytes. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.

allogeneic GM-CSF-secreting myeloma vaccine

An allogeneic plasma cell myeloma vaccine consisting two multiple myeloma cell lines, H929 and U266, admixed with GM-CSF-secreting K562 cells, with potential antineoplastic and immunopotentiating activities. Upon administration, the secreted GM-CSF modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells, with some specificity towards stimulation of leukocyte production, and may reverse treatment-induced neutropenia. This agent also promotes antigen presentation, upregulates antibody-dependent cellular cytotoxicity (ADCC), increases interleukin-2-mediated lymphokine-activated killer cell (LAK) function and may augment host antitumoral immunity. For safety, the myeloma cells are irradiated prior to vaccination.

allogeneic GM-CSF-secreting tumor vaccine PANC 10.05 pcDNA-1/GM-Neo

An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF–secreting tumor vaccine PANC 10.05 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 10.05 tumor cell line.

allogeneic GM-CSF-secreting tumor vaccine PANC 6.03 pcDNA-1/GM-Neo

An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF–secreting tumor vaccine PANC 6.03 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 6.03 tumor cell line.

allogeneic HAdV antigen-specific T lymphocytes

A population of allogeneic T lymphocytes specifically reactive to human adenovirus (HAdV) with potential antiviral activity. Allogeneic HAdV antigen-specific T cells are prepared via ex vivo stimulation of donor-derived peripheral blood mononuclear cells (PBMCs) with HAdV hexon protein. T cells that secrete interferon (IFN)-gamma in response to HAdV antigen exposure are selected and expanded for administration. Infusion of the HAdV antigen-specific T lymphocytes into hematopoietic stem cell transplant (HSCT) patients infected with HAdV may potentially reconstitute virus-specific responses, thereby controlling HAdV infections.

allogeneic HLA A2/4-1BB ligand-expressing melanoma vaccine

An allogeneic melanoma cell vaccine derived from a cell line with high expression of melanoma associated antigens and genetically modified to express both HLA-A2 and 4-1BB ligand, with potential immunostimulating and antineoplastic activities. Upon administration, the 4-1BB ligand of the allogeneic HLA-A2/4-1BB ligand-expressing melanoma vaccine binds to 4-1BB on activated T-lymphocytes, which induces a strong immune response against HLA-A2 positive melanoma cells.

allogeneic HPV-specific CD4+ T lymphocytes

A preparation of allogeneic T lymphocytes, collected from a haploidentical donor of the patient after vaccination with human papillomavirus (HPV) vaccine series, and depleted of CD8+ lymphocytes, with potential antiviral and antineoplastic activities. Upon administration, allogeneic HPV-specific CD4+ T lymphocytes may induce selective toxicity in HPV-positive cancer cells and other HPV-infected cells. HPV is associated with various cancer cell types. The depletion of CD8+ lymphocytes from the donor cell preparation may lower the risk of graft-versus-host disease (GvHD).

allogeneic HPV-specific cytotoxic T lymphocytes

A population of allogeneic cytotoxic T lymphocytes (CTLs) that are specifically reactive to human papillomavirus (HPV), with potential antiviral and antineoplastic activities. Upon infusion of the allogeneic HPV-specific CTLs, these CTLs induce selective toxicity in HPV-positive cancer cells and other HPV-infected cells. HPV is associated with various cancer cell types.

allogeneic human stem cell-derived pancreatic islet cells VX-880

A preparation of allogeneic human stem cell-derived, fully differentiated functional pancreatic islet cells, that can be used for islet cell transplantation for the treatment of type 1 diabetes mellitus. Upon infusion into the hepatic portal vein, allogeneic human stem cell-derived pancreatic islet cells VX-880 may replace and restore pancreatic islet cells, which are destroyed in patients with type 1 diabetes. These cells may restore pancreatic islet cell function, produce insulin and may regulate blood glucose levels.

allogeneic human T-cell progenitors SMART 101

A preparation of allogeneic human T-cell progenitor cells, that can potentially be used for immune reconstitution purposes. Upon administration, the allogeneic human T-cell progenitors SMART 101 may accelerate immune reconstitution after T-cell-depleted allogeneic hematopoietic stem cell transplantation (HSCT) in patients with relapsed/refractory acute leukemia.

allogeneic hypoimmune anti-CD19 CAR T cells SC291

A preparation of human allogeneic T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, and modified ex vivo to disrupt the expression of major histocompatibility (MHC) class I and MHC class II molecules and to express CD47, with potential immunomodulating and antineoplastic activities. Upon introduction into the patient, the allogeneic hypoimmune anti-CD19 CAR T cells SC291 recognize and bind to CD19-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The disruption of MHC class I and MHC class II molecules and the expression of CD47 prevent immune response against the allogeneic CAR T cells, thereby increasing the persistence of the CAR T cells.

allogeneic hypoimmune anti-CD22 CAR T cells SC262

A preparation of human allogeneic CD4+ and CD8+ T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD22, and ex vivo modified to disrupt the expression of major histocompatibility (MHC) class I and MHC class II molecules and to express CD47, with potential immunomodulating and antineoplastic activities. Upon introduction into the patient, the allogeneic hypoimmune anti-CD22 CAR T cells SC262 recognize and bind to CD22-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD22-positive tumor cells. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells. The disruption of MHC class I and MHC class II molecules and the expression of CD47 prevent both innate and adaptive immune responses against the allogeneic CAR T cells, thereby increasing the persistence of the CAR T cells.

allogeneic iC9/CD19-CAR-CD28-zeta-2A-IL15-transduced cord blood-derived natural killer cells TAK-007

A preparation of allogeneic, umbilical cord blood (CB)-derived natural killer cells (NKs) transduced with a retroviral vector expressing interleukin-15 (IL-15) and encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 that is coupled to the co-stimulatory domains of CD28 and to the zeta chain of the TCR/CD3 complex (CD3-zeta), and is linked to the suicide gene inducible caspase 9 (iCasp9; iC9), with potential immunomodulating and antineoplastic activities. Upon transfusion, the allogeneic iC9/CD19-CAR-CD28-zeta-2A-IL15-transduced CB-NKs TAK-007 recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered NK cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered; AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9, and results in apoptosis of the administered NK cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies. IL-15 enhances the cytotoxic effect of the NK cells.

allogeneic IL13-zetakine/HyTK-expressing-glucocorticoid resistant cytotoxic T lymphocytes GRm13Z40-2

A preparation of glucocorticoid receptor (GR) negative, allogeneic cytotoxic T-lymphocytes (CTLs) expressing a membrane-tethered interleukin 13 (IL13) cytokine chimeric T-cell antigen receptor (zetakine), with potential antineoplastic activity. Upon transfection of donor T-lymphocytes with a plasmid encoding a fusion protein of the IL13-zetakine and the selection-suicide expression enzyme HyTK, these modified CTLs are expanded and introduced into a patient with glioblastoma multiforme (GBM). This agent specifically targets IL13 receptor alpha2, a glioma-restricted cell-surface epitope; the CTLs exert their cytolytic effect thereby killing IL13Ra2-expressing glioma cells. In addition, IL13-zetakine redirected CTLs induce production of certain cytokines. Furthermore, due to the fact that these CTLs are GR negative, they can be used concomitantly with glucocorticoid therapy. The IL13-zetakine consists of an extracellular IL-13 E13Y mutein-human IgG4 hinge-Fc chimera fused to human cytoplasmic CD3-zeta via the transmembrane domain of human CD4.

allogeneic interleukin-17-producing CD8-positive T cells

A preparation of allogeneic human cytotoxic T lymphocytes that express the pro-inflammatory cytokine interleukin-17 (IL-17; IL17), with potential immunomodulating and anti-tumor activities. Upon ex vivo stimulation, the IL-17-producing CD8-positive T cells (Tc17) convert to interferon-gamma (IFNg; IFN-g)-producing CD8-positive T cells (Tc1). Tc1 cells exert enhanced anti-tumor cytotoxicity. Human Tc17 cells may contribute to a number of human inflammatory and malignant diseases.

allogeneic invariant natural killer T cells agenT-797

A preparation of allogeneic, off-the shelf, natural killer T cells (NKTs) expressing an invariant (alpha, beta) T-cell receptor (iNKTs), with potential immunomodulating and antineoplastic activities. Upon administration of allogeneic iNKT agenT-797, the invariant T-cell receptor (TCR) and natural-killer group 2, member D receptor (NKG2D; KLRK1; natural killer cell activating receptor group 2D) expressed by these cells recognize CD1d-restricted lipid ligands and stress ligands, which are expressed on certain tumor cells. These receptor-ligand interactions may induce the secretion of large amounts of various pro-inflammatory cytokines, including interferon gamma (IFN-g), and activate the immune system against tumor cells. Additionally, iNKTs directly target and lyse tumor cells.

allogeneic iPSC-derived anti-CD19-CAR/IL-15-expressing NK cells CNTY-101

A preparation of allogeneic natural killer (NK) cells derived from a clonal master induced pluripotent stem cell (iPSC) line, and engineered to express a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) derived from the anti-CD19 monoclonal antibody FMC63 and coupled to the CD28 and zeta chain of the TCR/CD3 complex (CD3-zeta) costimulatory signaling domains, and interleukin 15 (IL-15), with potential immunostimulatory and antineoplastic activities. Upon administration, allogeneic iPSC-derived anti-CD19-CAR/IL-15-expressing NK cells CNTY-101 recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. The human tumor associated antigen (TAA) CD19 is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CNTY-101 is also engineered with a safety switch composed of a shorter version of the extracellular domain of human epidermal growth factor receptor (EGFR). This allows the elimination of CNTY-101 upon the administration of anti-EGFR antibodies such as cetuximab. In addition, CNTY-101 is gene-edited to prevent its elimination by the patient’s NK cells, CD4 and CD8 T cells.

allogeneic iPSC-derived anti-MICA/B CAR/CD16/IL-15RF-expressing CD38-eliminated NK cells FT536

A preparation of allogeneic, off-the-shelf (OTS), natural killer (NK) cells derived from a clonal master induced pluripotent stem cell (iPSC) line, and engineered and multiplex-edited to express a chimeric antigen receptor (CAR) specific for the alpha 3 domain of the natural-killer group 2, member D receptor protein (NKG2D or KLRK1) ligands MHC class I polypeptide-related sequence A (MICA) and B (MICB), a high-affinity, non-cleavable CD16 (hnCD16) Fc receptor and a recombinant fusion of IL-15 and IL-15 receptor alpha (IL-15RF), and to eliminate CD38 expression, with potential immunostimulatory and antineoplastic activities. Upon administration, allogeneic iPSC-derived anti-MICA/B CAR/CD16/IL-15RF-expressing CD38-eliminated NK cells FT536 recognize, bind to and induce selective cytotoxicity in MICA/B-expressing tumor cells, leading to tumor cell lysis and the release of tumor neoantigens. Additionally, FT536 NK cells secrete inflammatory cytokines and chemokines, thereby enhancing T-cell activity and recruitment to the tumor site. MICA and MICB are stress-induced NKG2D ligands overexpressed on infected cells and many cancer cell types, but are not expressed on most normal, healthy cells. The shedding of the alpha 1 and alpha 2 domains of MICA and MICB from tumor cell surface allows the tumor cells to evade NKG2D-expressing immune cells, and FT536 specifically targets the alpha 3 domain of MICA/B to overcome this shedding and tumor escape mechanism. IL-15RF promotes the survival of NK cells and enhances the cytotoxic effect of the NK cells and the activated anti-tumor T-cells. When used in combination with monoclonal antibodies, the hnCD16 Fc receptor of FT536 binds to the Fc portion of tumor cell-bound monoclonal antibodies, leading to NK cell activation, cytokine secretion and enhanced antibody-dependent cellular cytotoxicity (ADCC). CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response. The lack of CD38 in FT536 NK cells prevents NK cell fratricide upon co-administration with a CD38-targeting monoclonal antibody as CD38 is normally expressed on the surface of activated NK cells. This enhances ADCC mediated by CD38-targeting monoclonal antibodies.

allogeneic irradiated melanoma cell vaccine CSF470

An allogeneic cancer vaccine composed of a mixture of lethally irradiated whole melanoma cancer cells obtained from four different melanoma cell lines, with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic irradiated melanoma cell vaccine may stimulate the body's immune system to exert a cytotoxic T-lymphocyte response and antibody-dependent cellular cytotoxicity (ADCC) against the melanoma cancer cells.

allogeneic large multivalent immunogen breast cancer vaccine

A cancer vaccine, containing human-specific large multivalent immunogens (LMIs) isolated from the membrane fraction of cells from a breast cancer cell line, with potential immunostimulatory and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen breast cancer vaccine may stimulate a cytotoxic T lymphocyte (CTL) immune response against tumor cells that express the breast cancer cell-specific LMIs.

allogeneic large multivalent immunogen melanoma vaccine LP2307

A cancer vaccine, containing human-specific large multivalent immunogen (LMI) isolated from plasma membrane fractions of the melanoma cell lines MSM-M1 and MSM-M2, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen melanoma vaccine LP2307 may stimulate a CD8+ cytotoxic T lymphocyte (CTL) response against melanoma tumor cells that express melanoma-specific LMI.

allogeneic LMP1-/LMP2- specific cytotoxic T-lymphocytes

A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMC) are collected from a donor and are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding EBV LMP1/2 to generate LMP1/2-specific CTL which are subsequently expanded. Administration of allogeneic LMP1-/LMP2- specific CTL to patients with LMP1/2-positive tumors may result in a specific CTL response against tumor cells expressing LMP1 and LMP2, resulting in cell lysis and inhibition of tumor cell proliferation. As tumor associated antigens (TAAs), LMP1 and LMP2 are expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin lymphoma.

allogeneic melanoma vaccine AGI-101H

A cancer vaccine derived from two gentically modified human melanoma cell lines with potential antineoplastic activity. Allogeneic melanoma vaccine AGI-101H consists of a 1:1 mixture of cells from two genetically modified human melanoma cell lines, designated as Mich1H6 and Mich2H6, that have been gamma-irradiated to render the cells non-proliferative. Upon administration, this vaccine may stimulate a cytotoxic immune response against melanoma tumor cells.

allogeneic mesothelioma tumor lysate-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a mixture of lysates from five allogeneic mesothelioma tumor cell lines, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, DCs are loaded with allogeneic mesothelioma tumor cell lysates. Upon re-administration of the allogeneic mesothelioma tumor lysate-pulsed autologous DC vaccine, the immune system is exposed to an undefined amount of mesothelioma-associated antigens, which stimulates the induction of a specific cytotoxic T-lymphocyte (CTL) response against mesothelioma tumor cells and leads to tumor cell lysis.

allogeneic most closely HLA-matched adenovirus-specific cytotoxic T lymphocytes

A population of off the shelf, closely human leukocyte antigen (HLA)-matched allogeneic, ex vivo-expanded cytotoxic T lymphocytes (CTLs) specifically reactive to human adenovirus (Ad), with potential immunomodulating and anti-adenoviral activities. Upon administration, the allogeneic most closely HLA-matched Ad-specific CTLs may reconstitute Ad-specific CTL responses in patients at risk of developing Ad infections either following allogeneic stem cell transplantation or in Ad-infected immunocompromised hosts. The anti-adenoviral CTLs are provided by a third party donor and not by the allogeneic stem cell transplant donor.

allogeneic MUC1-C-specific CAR-T cells P-MUC1C-ALLO1

An off-the-shelf (OTS) preparation of human allogeneic T lymphocytes containing primarily stem cell memory T cells (Tscm) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the C-terminal subunit of the tumor-associated antigen (TAA) mucin-1 (MUC1-C) and gene-edited to knockout both the T-cell receptor (TCR) and major histocompatibility complex (MHC) class I proteins, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic MUC1-C-specific CAR-T cells P-MUC1C-ALLO1 specifically recognize and induce selective toxicity in MUC1-C-expressing tumor cells. MUC1, a glycoprotein normally expressed on epithelial cells and overexpressed on the surface of a variety of cancer cells, plays a key role in tumor cell survival and proliferation. The proteolytic cleavage of MUC1 in the tumor microenvironment (TME) leads to the overexpression of MUC1-C in the TME.

allogeneic multipotent adult progenitor cells

A biologic product that consists of undifferentiated stem cells, obtained from adult bone marrow or other non-embryonic tissue sources, that are expanded in vitro and deposited in master cell banks for "off-the-shelf" use, with potential hematopoiesis-inducing and immunomodulating activities. Allogeneic multipotent adult progenitor cells (MAPCs) are non-immunogenic due to the lack of major histocompatibility (MHC) molecule expression, and so elicit no immune response upon administration. In vivo, bone marrow-derived adult stem cells are capable of maturing into a broad range of cell types and may help restore the immune system by producing multiple therapeutic molecules in response to inflammation and tissue damage.

allogeneic multivirus-specific cytotoxic T lymphocytes

A population of closely human leukocyte antigen (HLA)-matched, donor-derived cytotoxic T lymphocytes (CTLs) that are specifically reactive towards five viruses, Epstein-Barr virus (EBV), cytomegalovirus (CMV), adenovirus (AdV), human herpesvirus 6 (HHV6), and human polyomavirus type I (BKV), with potential antiviral activity. Infusion of the multivirus-specific CTLs into allogeneic hematopoietic stem cell transplant (HSCT) recipients provides virus-specific cellular immunity and causes specific anti-viral effects against active viral infections. The administered CTLs also prevent EBV, CMV, AdV, HHV6, and BKV reactivation and infection as well as inhibiting viral-associated diseases in immunocompromised patients. The allogeneic multivirus-specific CTLs may also provide cellular immunity towards the human polyomavirus type II (JC virus; JCV), which is highly homologous to BKV.

allogeneic natural killer cell line MG4101

A population of allogeneic, cytotoxic natural killer (NK) cells with potential antitumor activity. Allogeneic natural killer cell line MG4101 is derived from cells of a normal, healthy donor upon leukapheresis and activation.

allogeneic natural killer cell line NK-92

A proprietary, human cytotoxic cell line composed of allogeneic, activated, interleukin-2 (IL-2) dependent-natural killer cells derived from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma, with potential antineoplastic activity. As NK-92 cells are devoid of killer inhibitory receptors (KIRs; also called killer cell immunoglobulin-like receptors), which are negative regulators of NK cell activity, cancer cells are unable to suppress the cancer cell killing ability of the NK-92 cells. Upon infusion of the allogeneic NK cell line NK-92, the NKs recognize and bind to tumor cells. This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, which results in cancer cell lysis and apoptosis. In addition, NK-92 cells express high affinity Fc receptors, which bind to therapeutic antibodies; therefore, this agent can enhance antibody dependent cellular cytotoxicity (ADCC) of co-administered therapeutic antibodies.

allogeneic natural killer cells CHM 0201

A preparation of off-the-shelf (OTS) allogeneic, natural killer (NK) cells that are activated and expanded ex vivo, with potential cytolytic and antineoplastic activities. Upon administration, allogeneic NK cells CHM 0201 recognize and lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response.

allogeneic natural killer cells DVX201

A preparation of allogeneic natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon administration, allogeneic NK cells DVX201 may directly lyse cancer cells. These cells also secrete pro-inflammatory cytokines and further stimulate a systemic immune response against cancer cells.

allogeneic natural killer cells IDP-023

A preparation of off-the-shelf (OTS) allogeneic, natural killer (NK) cells that contains g minus NK cells (G-NKs), with potential cytolytic and antineoplastic activities. Upon administration, allogeneic NK cells IDP-023 recognize and lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response. G-NKs are deficient in the FceR1g protein and show increased cytokine secretion, higher levels of cytolytic enzymes, increased persistence, and higher antibody dependent cell mediated cytotoxicity (ADCC) when combined with monoclonal antibody treatment.

allogeneic natural killer cells PB103

A preparation of allogeneic, natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon administration, allogeneic NK cells PB103 may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response.

allogeneic natural killer cells SAR445419

A preparation of allogeneic, off-the-shelf (OTS) ex vivo-expanded natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon infusion of the allogeneic NKs SAR445419, these cells may lyse cancer cells.

allogeneic nicotinamide-expanded natural killer cells

Allogeneic, nicotinamide (NAM)-expanded natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon administration, the allogeneic NAM-expanded NK cells may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response. Ex-vivo treatment with the vitamin B3 derivative NAM increases the in-vivo homing, retention and proliferation potential of the NK cells.

allogeneic nicotinamide-expanded natural killer cells GDA-201

A preparation of allogeneic, nicotinamide (NAM)-expanded natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon administration, the allogeneic NAM-expanded NK cells GDA-201 may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response. Ex-vivo treatment with the vitamin B3 derivative NAM increases the in-vivo homing, retention and proliferation potential of the NK cells.

allogeneic NK-like cells GAIA-102

A preparation of allogeneic, off-the-shelf (OTS), ex-vivo activated and expanded natural killer (NK)-like cells, with a CD3-negative/CD56bright/CD57-negative immature phenotype, with potential cytolytic and antineoplastic activities. Upon infusion, allogeneic NK-like cells GAIA-102 may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate anti-tumor immune responses.

allogeneic NKG2D CAR memory T cells

A preparation of donor-derived memory T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) encoding human natural-killer group 2, member D receptor protein (NKG2D or KLRK1), with potential antineoplastic activity. Upon administration, the allogeneic NKG2D CAR memory T cells specifically recognize and bind to tumor cells expressing NKG2D ligands (NKG2DLs), resulting in cytokine secretion and lysis of NKG2D ligand-expressing tumor cells. NKG2DLs, such as MICA, MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on a variety of cancer cell types, but are not expressed on most normal, healthy cells.

allogeneic NKG2D-OX40-CD3zeta-CAR-mbIL-15-expressing natural killer cells NKX101

A preparation of off-the-shelf (OTS), allogeneic and ex vivo expanded natural killer cells (NKs) that are engineered to express membrane-bound IL-15 (mbIL15) and a chimeric antigen receptor (CAR) encoding for human natural-killer group 2, member D receptor protein (NKG2D; KLRK1; natural killer cell activating receptor group 2D) that is coupled to the co-stimulatory domain of OX40 (CD134), and to the zeta chain of the TCR/CD3 complex (CD3-zeta; CD3zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion of the allogeneic NKG2D-OX40-CD3zeta-CAR-mbIL-15-expressing NKs NKX101, these cells specifically target and bind to tumor cells expressing NKG2D ligands (NKG2DL). This induces secretion of pro-inflammatory cytokines and results in the lysis of NKG2DL-expressing tumor cells. In addition, these cells target, bind to and kill NKG2DL-expressing tumor-associated endothelial cells in the neovasculature and immunosuppressive cells, such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) that express NKG2D ligands. IL-15 is a pro-survival cytokine that potentiates the immune response against tumor cells. NKG2D ligands are overexpressed in a variety of cancer cells.

allogeneic NKG2DL-targeting CAR-grafted gamma delta T cells

A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are engineered to express a chimeric antigen receptor (CAR) encoding for human natural-killer group 2, member D receptor protein (NKG2D or KLRK1; natural killer cell activating receptor group 2D), with potential immunomodulating and antineoplastic activities. Upon administration of the NKG2DL-targeting CAR-grafted gamma delta T cells, these cells specifically target and bind to tumor cells expressing NKG2D ligands (NKG2DL). This induces secretion of pro-inflammatory cytokines and results in the lysis of NKG2DL-expressing tumor cells. In addition, these cells target, bind to and kill NKG2DL-expressing tumor-associated endothelial cells in the neovasculature and immunosuppressive cells, such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) that express NKG2D ligands. Gamma/delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. Ligands for NKG2D, such as MHC class I chain-related protein A (MICA), MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on infected cells and most cancer cell types, but are not expressed on most normal, healthy cells.

allogeneic PD-L1 tumor-targeted high-affinity natural killer cells

A preparation of natural killer (NK) cells that are derived from NK-92 cells, a human cytotoxic cell line composed of allogeneic NK cells derived from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma (NHL), that are genetically engineered to express the high-affinity CD16/FcgammaRIIIa (158V) allele, endoplasmic reticulum (ER)-retained interleukin (IL)-2 and a chimeric antigen receptor (CAR) specific for programmed death-ligand 1 (PD-L1), with potential immunomodulating, cytolytic and antineoplastic activities. Upon infusion of the PD-L1 tumor-targeted high-affinity (ha) NK cells, the NK cells recognize and bind to tumor cells, preferentially to PD-L1-expressing tumor cells and human peripheral myeloid-derived suppressor cells (MDSCs). This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, and results in cancer cell lysis and apoptosis. In addition, the incorporation of the high-affinity CD16 allele allows the NK cells to lyse tumor cells via antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by tumor-antigen-specific immunoglobulin G1 (IgG1) antibodies through binding of CD16 with the Fc region of human IgG1 antibodies. IL-2 replenishes the granular stock of NK cells, leading to enhanced perforin- and granzyme-mediated lysis of tumor cells.

allogeneic plasmacytoid dendritic cells expressing lung tumor antigens PDC*lung01

An off-the-shelf (OTS) preparation composed of irradiated allogeneic plasmacytoid dendritic cells (pDCs) loaded with seven immunogenic, human leukocyte antigen (HLA)-A*02:01 serotype-restricted peptides derived from the lung tumor antigens cancer/testis antigen 1 (NY-ESO-1), melanoma antigen A3 (MAGE-A3), MAGE-A4, multi-MAGE, a peptide shared by multiple MAGE-A proteins, survivin, mucin1 (MUC1) and melanoma antigen recognized by T cells 1 (Mart-1; Melan-A), with potential immunostimulating and antineoplastic activities. Upon administration of the allogeneic pDCs expressing lung tumor antigens PDC*lung01, the pDCs may activate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against HLA-A*0201 positive lung cancer cells expressing the TAAs NY-ESO-1, MAGE-A3, MAGEA4, multi-MAGE, survivin, MUC1 and melan-A. The pDCs are derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology and express a characteristic set of surface markers and may increase the anti-tumor immune responses.

allogeneic polymer-encapsulated IL-2-secreting retinal pigmented epithelial cells AVB-001

A preparation of polymer-encapsulated cells, obtained from the human immortalized retinal pigment epithelia (RPE) cell line ARPE-19, that have been genetically engineered to express the human cytokine interleukin-2 (IL-2; IL2), with potential immunomodulatory and antineoplastic activities. Upon intraperitoneal administration, allogeneic polymer-encapsulated IL-2-secreting RPE cells AVB-001 produces IL-2 locally, which binds to the IL-2 receptor (IL-2R) and activates IL-2/IL-2R-mediated signaling. This activates cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). This leads to T-cell-mediated cytotoxic immune responses against tumor cells and inhibition of tumor cell proliferation. The local delivery of AVB-001 reduces systemic toxicities, and the polymer encapsulation allows for longer half-life.

allogeneic regulatory T cells TRX103

A preparation of off-the-shelf (OTS), allogeneic CD4+ cells engineered to mimic regulatory type 1 (Tr1) cells, with potential immunomodulating activity. Upon infusion of allogeneic regulatory T cells TRX103, these cells secrete the immunomodulatory cytokine interleukin-10 (IL-10) and other cytokines upon exposure to donor T cells, and may additionally stimulate the production of de novo Tr1 cells. This suppresses immune responses and resets the immune system. This may ultimately prevent or reduce graft versus host disease (GvHD). IL-10 plays a key role in controlling inflammation, downregulating immune responses, and inducing immunological tolerance. IL-10 induces both a long-lasting antigen specific T-cell anergy and the differentiation of Tr1 cells.

allogeneic renal cell carcinoma vaccine MGN1601

A whole cell vaccine comprised of irradiated allogeneic renal cell carcinoma (RCC) with potential immunostimulating and antineoplastic activities. Allogeneic renal cell carcinoma vaccine MGN1601 contains two active ingredients: 1) genetically modified allogeneic RCC cells that are transiently transfected with four different MIDGE (Minimalistic Immunogenically Defined Gene Expression) vectors encoding IL-7, GM-CSF, CD80 and CD154 and 2) the synthetic DNA-based immunomodulator dSLIM-30L1, a TLR9 agonist. Vaccination results in expression of IL-7, GM-CSF, CD80 and CD154, which all contribute to the activation or enhancement of immune responses. Furthermore, administration of this RCC vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth. TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate immunity.

allogeneic rituximab conjugated gamma delta T cells ACE1831

An off-the-shelf preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) conjugated to a DNA linker, attached via DNA hybridization to rituximab conjugated to another DNA linker, with potential immunomodulating and antineoplastic activities. Upon administration of the allogeneic rituximab conjugated gamma delta T cells ACE1831, rituximab targets and binds to CD20 expressed on tumor cells. The gamma delta T cells secrete interferon-gamma (IFN-g) and exert direct killing of the CD20-expressing tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

Allogeneic shRNA-based Anti-BCMA CAR T cells CYAD-211

A preparation of human allogeneic, 'off-the-shelf' (OTS), non-gene edited T lymphocytes that are engineered to co-express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and a single short hairpin RNA (shRNA) that disrupts the expression of the CD3zeta component of the T-cell receptor (TCR), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic shRNA-based anti-BCMA CAR T cells CYAD-211 recognize and bind to BCMA-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. The downregulation of the expression of the TCR CD3zeta subunit by shRNA prevents the potential induction of graft-versus-host disease (GvHD) by the donor T cells.

allogeneic skin-derived ABCB5-positive MSCs allo-APZ2-OTS

A preparation of off-the-shelf (OTS) allogeneic human dermal ex-vivo expanded mesenchymal stromal cells (MSCs) expressing the ATP-binding cassette (ABC) efflux transporter, subfamily B, member 5 (ABCB5) that can potentially be used in the treatment of various skin-related and systemic inflammatory and degenerative conditions, such as recessive dystrophic epidermolysis bullosa (RDEB). Upon administration of the allo-APZ2-OTS, the MSCs are able to differentiate into several lineages, provide immunomodulatory activity, interact with various immune cells, such as macrophages, neutrophils and regulatory T cells (Tregs), and are able to secrete various anti-inflammatory mediators and pro-angiogenic molecules. Altogether, allo-APZ2-OTS may contribute to inflammation control and tissue repair.

allogeneic T lymphocytes expressing NY-ESO-1-C259-specific TCR

Genetically engineered human allogeneic T lymphocytes that are transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the cancer/testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and introduction into the patient, the allogeneic T lymphocytes expressing NY-ESO-1-C259-specific TCR specifically target and bind to NY-ESO-1-overexpressing tumor cells. This may result in the specific cytotoxic T-lymphocyte (CTL) killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is expressed in normal testis and on the surface of various tumor cell types.

allogeneic TCR alpha/beta-positive T lymphocyte-depleted peripheral blood stem cells

A preparation of allogeneic T-cell receptor (TCR) alpha/beta-positive T cell-depleted peripheral blood stem cells (PBSCs), that can potentially be used for hematopoietic stem cell transplantation (HSCT). Allogeneic PBMCs are processed, using the proprietary CliniMACS device, to remove TCRalpha/beta T cells, while retaining other cells, such as donor-derived natural killer (NK) cells and gamma/delta T cells. As TCR alpha/beta-positive T cells appear to be related to the development of graft versus host disease (GvHD), depletion of these cells may lower the risk of the recipient developing GvHD. Upon infusion of the TCR alpha/beta-positive T cell-depleted PBSCs for allogeneic stem cell transplantation (allo SCT), the alpha/beta-positive T-cell depletion as well as the presence of allogeneic NK cells, and other cells, may facilitate engraftment, exert graft-versus-leukemia effects, enhance post-transplant immune recovery, and reduce the risk of infections and GvHD.

allogeneic TCR-CD3 complex/CD16/IL-15-expressing natural killer cells

A preparation of allogeneic natural killer (NK) cells that have been engineered to express a T-cell receptor (TCR)-CD3 complex, CD16 Fc receptor, and interleukin 15 (IL-15), with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic TCR-CD3 complex/CD16/IL-15-expressing NK cells lyse tumor cells. Upon coadministration with tumor-targeting and CD3-targeting bispecific antibodies, the tumor-targeting moiety binds to the tumor-associated antigens (TAAs) expressed on tumor cells and the anti-CD3 moiety binds to the TCR-CD3 complex expressed on the allogeneic NK cells. This may enhance NK cell-mediated lysis of the TAA-expressing tumor cells. Upon coadministration with certain tumor-targeting monoclonal antibodies, the Fab moiety of the antibodies binds to the TAAs expressed on tumor cells and the Fc moiety of the antibodies binds to CD16 expressed on the allogeneic NK cells. This leads to antibody-dependent cellular cytotoxicity (ADCC) of the antibody-bound tumor cells. CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response. IL-15 promotes the survival of NK cells and enhances the cytotoxic effect of NK cells and activated anti-tumor T cells.

allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001

A preparation of T-cell receptor (TCR) alpha and beta (TCRa/b)-depleted donor-derived T lymphocytes that have been transduced with a lentivirus vector encoding a TCR specific for HLA-A*02:01-restricted minor histocompatibility antigen HA-1 (HA1) and expressing RQR8, with potential immunomodulating and antineoplastic activities. Following HLA-matched allogeneic hematopoietic cell transplantation (HCT) in HLA-A*02:01 positive patients, allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001 specifically recognize and bind to HA-1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing HLA-A*02:01 HA-1. HA-1 is a lineage-specific antigen found on leukemia cells. BSB-1001 carries the universal RQR8 safety "off" switch, which allows selective removal of the T-cells through both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) following administration of rituximab if unacceptable side-effects occur. CRISPR-cas9 editing of the donor T cells deletes the endogenous TCRa/b chains. Depletion of TCRa/b increases expression of the transduced TCR and reduces risk of graft-versus-host disease (GVHD) caused by native TCRs.

allogeneic TGFBR2 KO CAR27/IL-15-expressing NK cells

A preparation of allogeneic, umbilical cord blood (CB)-derived natural killer cells (NKs) that have been engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70) and expressing the cytokine interleukin-15 (IL-15) and in which the gene transforming growth factor-beta receptor II (TGFbRII; TGFBR2) is deleted through clustered regularly interspaced short palindromic repeats (CRISPR)-Cas 9 gene editing, with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic TGFBR2 KO CAR27/IL-15-expressing NK cells target, bind to and induce selective cytotoxicity in CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27, is overexpressed on the surfaces of various cancer cell types. IL-15 is a pro-survival cytokine that promotes persistence of multiple lymphocyte lineages and potentiates the immune response against tumor cells. As TGF-beta activation and release leads to NK cell inactivation, deletion of the TGFBR2 gene increases the potency, persistence and efficacy of the NK cells and enhances anti-tumor activity.

allogeneic third-party suicide gene-transduced anti-HLA-DPB1*0401 CD4+ T cells CTL 19

A preparation of allogeneic, third-party, CD4+ T lymphocytes that specifically recognizes the human leukocyte antigen (HLA)-DPB1*0401 and transduced with a suicide gene, with potential antineoplastic activity. Upon administration, allogeneic third-party suicide gene-transduced anti-HLA-DPB1*0401 CD4+ T cells CTL 19 specifically target and kill HLA-DPB1*0401-positive leukemic cells. The suicide gene causes the destruction of the T-cell clone upon the administration and presence of ganciclovir, which enhances the safety of the agent. HLA-DP is expressed by many leukemic cells.

allogeneic tri-functional anti-CD19 CAR-NK cells

A preparation of allogeneic natural killer (NK) cells transduced with a retroviral vector expressing the immunostimulatory cytokine interleukin-15 (IL-15) and encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) that is coupled to the co-stimulatory domains cluster of differentiation 28 (CD28, T-cell-specific surface glycoprotein CD28), cluster of differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (TCRzeta; CD247; CD3zeta); and a blocker for the inhibitory T-cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immunomodulating and antineoplastic activities. Upon transfusion, the allogeneic tri-functional anti-CD19 CAR-NK cells recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. IL-15 enhances the cytotoxic effect of the NK cells and the activated anti-tumor T cells. The PD-1 inhibitory domain targets and binds to programmed cell death-1 ligand 1 (PD-L1) expressed on tumor cells, thereby preventing the binding of the PD-1 on T lymphocytes to its ligand, PD-L1 on tumor cells. This prevents PD-1/PD-L1-mediated inhibition of T lymphocytes and leads to the activation and expansion of T cells resulting in a cytotoxic T lymphocyte (CTL) response against tumor cells, thereby enhancing the elimination of tumor cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies. The co-stimulatory signaling domains enhance both proliferation of T cells and anti-tumor activity.

allogeneic tumor cell vaccine

A vaccine composed of tumor cells isolated from the tumor of one patient, killed and processed, and administered to another patient in order to stimulate cytotoxic immune responses to a similar tumor cell type. The cells found in this type of whole-cell vaccine express many cell-surface tumor-associated antigens. This vaccine is frequently administered with an adjuvant immunostimulant.

allogeneic umbilical cord blood-derived CXCR4-enriched T-regulatory cells CK0804

A preparation of allogeneic T-regulatory cells (Tregs) derived from umbilical cord blood (UCB) and enriched with C-X-C chemokine receptor type 4 (CXCR4), with potential immunomodulatory activity. Upon administration, allogeneic UCB-derived CXCR4-enriched Tregs CK0804 may promote immunologic homeostasis and modulate immune responses. CXCR4 enrichment promotes the traffic of the Tregs to the bone marrow and its retainment in the bone marrow, as bone marrow expresses the CXCR4 ligand stromal cell-derived factor 1 (CXCL12).

allogeneic umbilical cord blood-derived HSPCs NLA101

A preparation of universal, off-the-shelf, ex vivo expanded, allogeneic umbilical cord blood (UCB)-derived hematopoietic stem and progenitor cells (HSPCs) that can potentially be used to improve hematopoietic recovery after chemotherapy or hematopoietic cell transplantation (HCT). Upon administration of allogeneic HSPCs NLA101, these cells increase and restore the number of HSPCs, which may prevent or decrease infection and other complications of chemotherapy-induced neutropenia (CIN) or cord blood transplantation.

Allogeneic Variable Delta 1 Gamma-delta T-lymphocytes GDX012

An off-the-shelf (OTS) preparation of allogeneic variable delta 1 (Vd1) gamma-delta (gd) T-lymphocytes, with potential immunomodulating and antineoplastic activities. Upon administration of the allogeneic Vd1 gd T-lymphocytes GDX012, these cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. Vd1 gd T-cells, a subset of gamma delta T-cells, recognize and are activated by cancer cells, and may therefore have a stronger association with antitumor immune responses compared with other gamma delta T-cell subtypes.

allogeneic virus-specific T lymphocytes

A preparation of allogeneic donor-derived T lymphocytes that are specifically reactive to adenovirus (AdV), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and human polyomavirus type I (BKV), with potential antiviral activity. Upon administration, allogeneic VSTs may kill AdV, CMV, EBV and/or BKV-infected cells, thereby preventing or reducing the severity of viral infections by these pathogens.

allogeneic virus-specific T lymphocytes R-MVST

A preparation of allogeneic T lymphocytes generated from partially human leukocyte antigen (HLA)-matched healthy donors or from the original allogeneic hematopoietic stem cell transplantation (HSCT) donor, ex-vivo expanded, and specifically reactive to viruses that may include adenovirus (AdV), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and human polyomavirus type I (BKV), with potential antiviral activity. Upon administration, the allogeneic virus-specific T lymphocytes R-MVST may kill AdV, CMV, EBV and/or BKV-infected cells, and may prevent or reduce the severity of viral infections by these pathogens.

allopurinol

A structural isomer of hypoxanthine. Allopurinol inhibits xanthine oxidase, an enzyme that converts oxypurines to uric acid. By blocking the production of uric acid, this agent decreases serum and urine concentrations of uric acid, thereby providing protection against uric acid-mediated end organ damage in conditions associated with excessive production of uric acid, i.e. the massive cell lysis associated with the treatment of some malignancies.

allopurinol sodium

The sodium form of allopurinol, which is a structural isomer of hypoxanthine. Allopurinol inhibits xanthine oxidase, an enzyme that converts oxypurines to uric acid. By blocking the production of uric acid, this agent decreases serum and urine concentrations of uric acid, thereby providing protection against uric acid-mediated end organ damage in conditions associated with excessive production of uric acid, i.e. the massive cell lysis associated with the treatment of some malignancies.

allosteric ErbB inhibitor BDTX-189

An orally bioavailable, irreversible, selective, small-molecule inhibitor of certain oncogenic driver, allosteric mutations of the ErbB receptor tyrosine kinases epidermal growth factor receptor (EGFR/ErbB1) and human epidermal growth factor receptor 2 (HER2/neu or ErbB2), including extracellular domain allosteric mutations of HER2, and EGFR and HER2 exon 20 insertion mutations, with potential antineoplastic activity. Upon oral administration, the allosteric ErbB inhibitor BDTX-189 selectively binds to and inhibits these allosteric ErbB mutants while sparing wild-type EGFR, which may result in the selective inhibition of cellular proliferation and angiogenesis in tumor cells and tumors expressing these allosteric ErbB mutations. EGFR and HER2, ErbB receptor tyrosine kinases mutated or overexpressed in many tumor cell types, play a key role in tumor cell proliferation and tumor vascularization.

almond oil

The oil extracted from the seed fruits of Prunus amygdalus. Almond oil is typically used as a skin emollient and for massage.

almurtide

A synthetic muramyl dipeptide (MDP) H8analogue with potential immunostimulating and antineoplastic activity. As a derivative of the mycobacterial cell wall component MDP, almurtide activates both monocytes and macrophages. This results in the secretion of cytokines and induces the recruitment and activation of other immune cells, which may result in indirect tumoricidal or cytostatic effects.

alnodesertib

An orally bioavailable inhibitor of ataxia telangiectasia and Rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, alnodesertib selectively targets and inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This prevents ATR-mediated signaling, which results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress.

alnuctamab

A bispecific T-cell engager (BiTE) antibody directed against both the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; TNFRSF17) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, alnuctamab binds bivalently to BCMA expressed on tumor cells and monovalently to CD3 expressed on cytotoxic T-lymphocytes (CTLs). This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.

alobresib

An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, alobresib binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.

Alocrest

(Other name for: liposomal vinorelbine)

aloe vera gel

A preparation of leaf pulp from the parenchymal tissue of the plant Aloe vera (Liliaceae). Aloe vera gel contains carbohydrate polymers, such as glucomannans or pectic acid, and various vitamins and essential amino acids, as well as other organic and inorganic compounds. This agent has been used internally or externally for sunburn, skin problems, insect bites, ulcers, arthritis, constipation, and as an immune system enhancer.

aloe vera/chamomile/thyme topical cream

A topical skin cream containing aloe vera, chamomile, and thyme, with potential anti-inflammatory, soothing and protective activities. Upon application of the aloe vera/chamomile/thyme topical cream to the affected area(s), the ingredients in the cream may exert anti-inflammatory effects thereby reducing skin inflammation. The cream also soothes, protects irritated skin, and provides moisture.

aloe/anise/ascorbic acid/clove/peppermint/spearmint/thyme-based mouthwash

A herbal-based mouthrinse containing aloe, anise, ascorbic acid, clove, peppermint, spearmint and thyme, with potential anti-mucositic activity. When aloe/anise/ascorbic acid/clove/peppermint/spearmint/thyme-based mouthwash is used as a rinse, the ingredients in this agent may prevent or decrease inflammation and bacterial infections.This may prevent or inhibit radiotherapy- or chemotherapy-induced mucositis and decreases the pain associated with mucositis.

alofanib

An inhibitor of the fibroblast growth factor receptor (FGFR) type 2 (FGFR2), with potential antineoplastic and anti-angiogenic activities. Upon administration, alofanib targets, allosterically binds to the extracellular domain of FGFR2 and inhibits the activity of FGFR2, which may result in the inhibition of basic FGF (bFGF)/FGFR2-related signal transduction pathways. This inhibits FGF-induced endothelial cell proliferation and migration, and inhibits the proliferation of FGFR2-overexpressing tumor cells. FGFR2, a receptor tyrosine kinase upregulated in many tumor cell types, plays a key role in cellular proliferation, migration and survival.

alogliptin

A selective, orally bioavailable, pyrimidinedione-based inhibitor of dipeptidyl peptidase 4 (DPP-4), with hypoglycemic activity. In addition to its effect on glucose levels, alogliptin may inhibit inflammatory responses by preventing the toll-like receptor 4 (TLR-4)-mediated formation of proinflammatory cytokines.

alomfilimab

A human immunoglobulin G1 (IgG1) kappa monoclonal antibody that recognizes inducible T-cell co-stimulator (ICOS; CD278), with potential immunomodulating and antineoplastic activities. Upon administration, alomfilimab selectively binds to dimeric ICOS expressed on certain T cells. This prevents the interaction between ICOS-positive T cells and plasmacytoid dendritic cells (pDCs), which express the ICOS ligand (ICOSL). Blocking ICOS activation prevents the pDC-induced proliferation and accumulation of regulatory ICOS-positive T cells (ICOS+ Tregs) and inhibits interleukin-10 (IL-10) secretion by CD4+ infiltrating T cells. This may abrogate Treg-mediated immune suppression and may enhance cytotoxic T-lymphocyte (CTL)-mediated immune responses against tumor cells. Additionally, KY1044 may eliminate ICOS-positive T cells via antibody-dependent cellular cytotoxicity (ADCC). ICOS, a T-cell specific, CD28-superfamily costimulatory molecule and immune checkpoint protein, plays a key role in the proliferation and activation of T cells. It is normally expressed on both activated CD4+ T cells, which is a subset of memory T cells (Tm), and follicular helper T cells (Tfh). ICOS is highly expressed on Tregs infiltrating various tumors and its expression is associated with a poor prognosis; ICOS-positive Tregs play a key role in immune suppression and tumor immune evasion.

Aloprim

(Other name for: allopurinol sodium)

Aloxi

(Other name for: palonosetron hydrochloride)

alpelisib

An orally bioavailable phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Alpelisib specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.

alpha clash anti-IL-2 antibody fusion protein LAT010

An antibody fusion protein and interleukin-2 (IL-2) immunocytokine, with potential antineoplastic activity. Upon administration of the alpha-clash anti-IL-2 antibody fusion protein LAT010, the IL-2 moiety targets and binds to the intermediate-affinity IL-2 receptor beta,gamma (IL-2Rbg), thereby selectivity activating CD8+ T cells and natural killer (NK) cells against tumor cells. The alpha-clash anti-IL-2 antibody moiety of LAT010 prevents LAT010 from activating the high-affinity IL2Ralpha,beta,gamma receptor complex which may prevent severe IL-2-mediated systemic toxic effects.

alpha fetoprotein adenoviral vector vaccine

A vaccine consisting of a recombinant adenoviral vector encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis.

alpha fetoprotein plasmid DNA vaccine

A vaccine consisting of plasmid DNA encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis.

alpha galactosylceramide

A potent alpha galactosylceramide modified from marine-sponge that stimulates the immune system to exhibit antitumor activity.

alpha V beta 1 inhibitor ATN-161

A small peptide antagonist of integrin alpha5beta1 with potential antineoplastic activity. ATN-161 selectively binds to and blocks the receptor for integrin alpha5beta1, thereby preventing integrin alpha5beta1 binding. This receptor blockade may result in inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, angiogenesis, and tumor progression. Integrin alpha5beta1 is expressed on endothelial cells and plays a crucial role in endothelial cell adhesion and migration.

alpha V beta 8 antagonist PF-06940434

An antagonist of integrin alpha v beta 8, with potential antineoplastic activity. Upon administration, PF-06940434 selectively binds to and blocks the receptor for integrin alpha v beta 8, thereby preventing integrin alpha v beta 8 binding. This may result in the inhibition of cell adhesion in the tumor microenvironment (TME) and blocks the activation of the cytokine transforming growth factor-beta 1 (TGF-b1), preventing TGF-b1-mediated signal transduction. This abrogates TGF-b1-mediated immunosuppression, enhances anti-tumor immunity in the TME and promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGF-b1-dependent proliferation of cancer cells. Alpha v beta 8 integrin plays a key role in tumor initiation, growth, and progression through TGF-b1 activation. It is expressed in a variety of tumor cell types and is associated with poor prognosis.

alpha-1,3-galactosyltransferase-expressing allogeneic lung tumor cell vaccine

An allogeneic lung cancer vaccine with potential immunostimulating and antineoplastic activities. Derived from allogeneic lung tumor cells, alpha-1,3-galactosyltransferase-expressing allogeneic lung tumor cell vaccine is engineered to express the murine alpha-1,3-galactosyltransferase (GalT), an enzyme humans lack. GalT catalyzes the expression of foreign alpha-1,3-galactosyl (alpha-gal) carbohydrate epitopes in glycoproteins and in glycolipids on the cell membranes of the allogeneic lung tumor cells present in the vaccine, essentially producing a "xenograft". The hyperacute rejection involves pre-existing human anti-alpha-gal antibodies that bind the foreign alpha-gal epitopes expressed by the vaccine tumor cell “xenograft”, resulting in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) towards endogenous lung tumor cells with unmodified carbohydrate epitopes.

alpha-1,3-galactosyltransferase-expressing allogeneic renal cell carcinoma vaccine

An allogeneic renal cell cancer (RCC) vaccine composed of cell line-derived RCCs that are genetically engineered to express the murine alpha-1,3-galactosyltransferase (GalT), with potential immunostimulatory and antineoplastic activities. Not naturally occurring in humans, GalT catalyzes the expression of foreign alpha-1,3-galactosyl (alpha-gal) carbohydrate epitopes on the cell membranes of the allogeneic RCCs present in the vaccine. This induces a hyperacute rejection reaction involving pre-existing human anti-alpha-gal antibodies, which bind to the foreign alpha-gal epitopes expressed by the allogeneic RCCs. This results in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) towards endogenous RCCs with unmodified carbohydrate epitopes.

alpha-1-proteinase inhibitor human

Human serum-derived alpha-1 proteinase inhibitor (alpha-1-antitrypsin or AAT) with immunomodulating and anti-inflammatory activity. Upon administration, AAT reduces the production of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-32, IL-6, and proteinase 3, and induces the production of anti-inflammatory cytokines, such as IL-10 and the IL-1 receptor antagonist IL-1RN. This agent also downregulates heparan sulfate and reduces the expansion of cytotoxic effector T cells, interferes with the maturation of dendritic cells and increases T regulatory cells. Altogether, AAT may attenuate acute graft-versus-host disease (GvHD) and may facilitate graft acceptance and survival. In addition, AAT enhances levels of cAMP and activation of cAMP-dependent protein kinase A. AAT, a 52kD protein and serine protease inhibitor, belongs to the serpin superfamily.

alpha-fetoprotein peptide-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine comprised of autologous dendritic cells pulsed with four alpha-fetoprotein (AFP) peptides, with potential immunostimulatory and antineoplastic activities. Upon administration, AFP peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against AFP-expressing cancer cells, resulting in tumor cell lysis. AFP is overexpressed in a variety of cancer cells.

alpha-folate receptor-targeting thymidylate synthase inhibitor ONX-0801

An alpha-folate receptor (aFR)-mediated inhibitor of thymidylate synthase (TS), with potential antineoplastic activity. Upon intravenous infusion, ONX-0801 selectively targets and binds to aFR-expressing tumor cells. Upon uptake by aFR, this agent binds to and inhibits TS. This reduces thymine nucleotide synthesis, inhibits both DNA synthesis and cell division, and leads to tumor cell apoptosis. TS catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), an essential precursor for DNA synthesis, and plays a key role in cell growth and division. aFR, a cell-surface receptor glycoprotein, is overexpressed on various tumor cell types, but is minimally expressed by normal, healthy tissue.

alpha-Gal AGI-134

A synthetic alpha Gal (aGal) molecule, with potential immunomodulating and antineoplastic activities. Upon intratumoral injection of aGal AGI-134, aGal coats the cancer cell membranes and triggers an anti-aGal antibody-mediated immune response leading to an initial complement-dependent and antibody-dependent cellular cytotoxicity (ADCC). This cytotoxicity causes release from tumor cells and subsequent uptake of released tumor-associated antigens (TAAs) by antigen-presenting cells (APCs). This may activate a systemic immune response against the TAAs and may eradicate cancer cells. aGal is a cell-surface carbohydrate antigen not expressed by humans while being expressed by all other mammals and bacteria. Anti-aGal antibodies are continuously and abundantly produced by humans due to exposure to aGal present on intestinal bacteria in the digestive system.

alpha-Gal glycosphingolipids

A preparation of glycosphingolipids (GSL), containing the disaccharide epitope galactose-alpha-1,3-galactose (alpha-Gal), with potential antineoplastic activity. Upon intratumoral injection, alpha-Gal glycosphingolipids may stimulate the immune system to mount complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) responses against alpha-Gal GSL, which may result in tumor cell death; these responses involve natural anti-alpha-Gal immunoglobulins (Igs). As antibodies that occur naturally due to sensitization to alpha-Gal present on symbiotic bacterial flora, anti-alpha-Gal Igs are present in unusually high amounts in human sera. GSL represent a glycolipid subtype containing the amino alcohol sphingosine; tumor-associated GSL antigens contain various oligosaccharide residues.

alpha-galactosylceramide-pulsed autologous dendritic cells

A cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with the marine sponge glycolipid alpha-galactosylceramide (alpha-GalCer) with potential immunostimulatory and antimetastatic activities. Upon administration, alpha-galactosylceramide-pulsed autologous dendritic cells may result in the activation and proliferation of a subset of endogenous natural killer T ( NKT) cells, B cells, and CD4+ and CD8+ T cells, and the production of interferon-gamma and interleukin-12; these cascade events may result in a T helper-1 cell-biased proinflammatory antitumor immune response. The NKT cell ligand alpha-GalCer was originally isolated from the marine sponge Agelas mauritianusis.

alpha-lactalbumin breast cancer vaccine

A breast cancer vaccine consisting of recombinant human alpha-lactalbumin (aLA), with potential immunostimulatory and antineoplastic activities. Upon administration, aLA breast cancer vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells that express the aLA protein, resulting in tumor cell lysis. aLA is expressed in many types of breast cancer, including triple negative breast cancer (TNBC), while normally present in healthy breast tissues only during lactation.

alpha-lactalbumin-derived synthetic peptide-lipid complex alpha1H

A synthetic proteolipid complex comprised of the alpha-1 domain of alpha-lactalbumin (lactose synthase B protein) and oleic acid, with potential antineoplastic activity. Upon intravesical instillation, alpha1H selectively accumulates in the nuclei of tumor cells and binds to histones H3, H4, and H2B. By binding to histones, alpha1H disrupts chromatin assembly and interferes with intact chromatin, thereby preventing tumor cell transcription and replication. Additionally, alpha1H inhibits the phosphorylation of multiple kinases involved in cancer-associated pathways including the Ras/Raf/ERK, PI3K/AKT, p38 MAPK and JNK signaling pathways. This may inhibit tumor cell proliferation and induce apoptosis in tumor cells that are driven by the dysregulation of certain kinases and oncogenic GTPases.

alpha-lipoic acid

A naturally occurring micronutrient, synthesized in small amounts by plants and animals (including humans), with antioxidant and potential chemopreventive activities. Alpha-lipoic acid acts as a free radical scavenger and assists in repairing oxidative damage and regenerates endogenous antioxidants, including vitamins C and E and glutathione. This agent also promotes glutathione synthesis. In addition, alpha-lipoic acid exerts metal chelating capacities and functions as a cofactor in various mitochondrial enzyme complexes involved in the decarboxylation of alpha-keto acids.

alpha-lipoic acid-palladium/vitamin/mineral supplement

A proprietary water- and lipid-soluble polymer-based nutritional supplement composed of a complex mixture of alpha-lipoic acid bound to palladium (Palladium Lipoic Acid Complex (PdLA)) and other minerals, vitamins and amino acids, including vitamins B1, B2 and B12, formylmethionine, acetyl cysteine, and trace amounts of molybdinum, rhodium, and ruthenium, with potential anti-oxidant and cytoprotective activities. Upon oral administration, the alpha-lipoic acid-palladium/vitamin/mineral supplement acts as a free radical scavenger, crosses the cell membrane and is able to transfer electrons from fatty acids to DNA via the electron transport chain in mitochondria, which protects against DNA damage. This could protect non-cancerous cells from the oxidative damage caused by radiation and chemotherapy. In addition, in the hypoxic conditions found within tumors, the excess electrons can generate free radicals within mitochondria and could induce both cytochrome c release and apoptosis.

alpha-lipoic acid/Boswellia serrata extract/methylsulfonylmethane/bromelain dietary supplement

A dietary supplement composed of the fatty acid alpha-lipoic acid (ALA), a herbal extract from the tree Boswellia serrata, the sulfur-containing compound methylsulfonylmethane (MSM) and bromelain, which is a protein-digesting enzyme mixture derived from pineapple, with potential analgesic, antioxidant, and anti-inflammatory activities. Upon oral administration, the alpha-lipoic acid/Boswellia serrata extract/methylsulfonylmethane/bromelain dietary supplement may exert analgesic, antioxidant and anti-inflammatory effects and may relieve chemotherapy-induced peripheral neuropathy (CIPN).

alpha-methyl-4-deoxy-4-[(18)F]fluoro-D-glucopyranoside

A radioconjugate and sodium-dependent glucose transporter (SGLT)-specific tracer that is composed of a glucose analog labeled with the positron-emitting radioactive isotope fluorine F18, and can be used for tumor cell imaging upon positron emission tomography (PET). Upon administration, alpha-methyl-4-deoxy-4-[(18)F]fluoro-D-glucopyranoside (Me4FDG) is specifically taken up by SGLT-expressing tumor cells. The fluorine F 18 moiety can be visualized upon PET imaging and this agent can be used both as a tracer for sugar uptake by and for imaging and staging of certain tumor cell types. Glucose is a major metabolic substrate required for cancer cell survival and growth and is taken up by cancer cells at a much higher rate compared to normal cells. SGLTs, especially SGLT type 2 (SGLT2), are overexpressed on certain tumor cell types and play key roles in glucose transport in these cells. Me4FDG is not transported by glucose uniporter proteins (GLUTs). In contrast, Me4FDG is not transported by glucose transporters (GLUTs).

alpha-PD1/IL2 fusion protein AWT020

A bifunctional fusion protein comprised of a monoclonal antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) linked to an engineered, variant form of interleukin-2 (IL-2) and IL2c mutein (No-alpha-IL-2), with potential immunostimulating and antineoplastic activities. Upon administration of anti-PD-1-IL-2 fusion protein AWT020, the antibody moiety specifically targets, binds to and blocks PD-1 expressed on tumor-infiltrating lymphocytes (TILs) and thereby brings the IL-2 moiety to PD-1-expressing tumoral T cells. The IL-2 moiety binds to the interleukin-2 receptor (IL2R), activates pSTAT5, and may activate and expand tumor-infiltrating T cells. This may enhance the activity of cytotoxic T cells and potentiates T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity. No-alpha-IL-2 cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T cells (Tregs).

alpha-tocopherol

The orally bioavailable alpha form of the naturally-occurring fat-soluble vitamin E, with potent antioxidant and cytoprotective activities. Upon administration, alpha-tocopherol neutralizes free radicals, thereby protecting tissues and organs from oxidative damage. Alpha-tocopherol gets incorporated into biological membranes, prevents protein oxidation and inhibits lipid peroxidation, thereby maintaining cell membrane integrity and protecting the cell against damage. In addition, alpha-tocopherol inhibits the activity of protein kinase C (PKC) and PKC-mediated pathways. Alpha-tocopherol also modulates the expression of various genes, plays a key role in neurological function, inhibits platelet aggregation and enhances vasodilation. Compared with other forms of tocopherol, alpha-tocopherol is the most biologically active form and is the form that is preferentially absorbed and retained in the body.

Alpha-tocopheryloxyacetic Acid

An orally bioavailable vitamin E derivative with potential antineoplastic and immunostimulating activities. Upon administration, alpha-tocopheryloxyacetic acid (alpha-TEA) induces tumor autophagy; the autophagosomes formed, which carry tumor associated antigens (TAAs), allow for increased cross-presentation of TAAs by professional antigen-presenting cells (APCs). This activates a T cell-mediated T helper type 1 (TH1) response, generates a cytotoxic T-lymphocyte (CTL) response against cancer cells, and reduces the frequency of regulatory T-cell (Treg) differentiation. In addition, alpha-TEA modulates the release of various cytokines and chemokines and induces tumor cell apoptosis. Altogether, this results in decreased tumor cell proliferation.

alpha-type-1 polarized dendritic cells

A mature polarized dendritic cell with potent immunostimulating activity. Treating dendritic cells (DCs) with interferon-alpha (IFN-a) and polyinosinic:polycytidylic acid (p-I:C) in addition to a cytokine cocktail (tumor necrosis factor alpha/Interleukin-1beta/IFN-gamma) produces mature but not exhausted alpha type-1 polarized DCs (alphaDC1) that are capable of: 1) high responsiveness to other lymphoid chemokines, and 2) producing high level of interleukin-12p70 (IL-12p70). Therefore, alphaDC1 has a much more significant capability of inducing helper T-cell (CD4+ T-cell) responses in comparison with the "gold standard" DCs. When pulsed with specific tumor associated antigens (TAAs), alphaDC1 is able to induce a potent cytotoxic T-lymphocyte (CTL) response against TAAs; as a result it can be used as a cancer vaccine.

alpha/beta T-cell/CD19+ B-cell-depleted unrelated or partially matched donor-derived allogeneic peripheral blood stem cells

A preparation of allogeneic peripheral blood stem cells (PBSCs) from an unrelated or partially matched related donor that have been selectively depleted of alpha/beta T cells and CD19-positive (CD19+) B-cells with potential immune reconstituting activity. The alpha/beta T-cell/CD19+ B-cell-depleted stem cells contain high amounts of natural killer (NK) cells, gamma/delta T cells, CD34+ stem cells, and dendritic cells (DCs), while devoid of alpha/beta T-cells and CD19-positive B cells. Depletion of alpha/beta T cells, which are implicated in the adaptive immune response that mediates graft-versus-host disease (GvHD), may promote rapid and sustained engraftment, immune reconstitution, and may prevent or reduce the development of GvHD. The depletion of CD19+ B cells may reduce the risk of Epstein-Barr virus (EBV)-driven post-transplant lymphoproliferative disorders. The retained CD3+ gamma/delta T cells and NK cells may synergistically exert an anti-leukemic and antiviral effector function, which may further promote engraftment and immune reconstitution.

Alphagan

(Other name for: Brimonidine Tartrate)

alphaVbeta1/8 inhibitor PLN-101095

An orally bioavailable, small molecule dual inhibitor of the integrins alpha V beta 1 (aVb1) and 8 (aVb8), with potential immunomodulating and antineoplastic activities. Upon oral administration, alphaVbeta1/8 inhibitor PLN-101095 targets, binds to and inhibits the integrins aVb1 and aVb8 in the tumor microenvironment (TME). This blocks aVb1/8-mediated signaling and prevents the activation of tumor growth factor-beta (TGF-b). Inhibition of TGF-b promotes T-cell infiltration and the release of pro-inflammatory cytokines into the TME, and results in a cytotoxic T lymphocytes (CTLs)-mediated immune response against tumor cells. In addition, this may inhibit the TGF-beta-mediated resistance to checkpoint inhibitors and may sensitize tumors to checkpoint inhibitors. The integrins aVb1 and aVb8 are overexpressed in a variety of tumor types and play a key role in the activation and signaling of TGF-b.

ALPK1 agonist PTT-936

An orally bioavailable innate immune agonist and activator of the cytosolic alpha-protein kinase 1 (ALPK1) that is an ADP-heptose derived from bacteria, with potential immunomodulating and antineoplastic activities. Upon oral administration, ALPK1 agonist PTT-936, being a ADP-heptose, specifically targets and binds to ALPK1, thereby activating the ALPK1-mediated signal transduction pathway. This initiates the phosphorylation of TRAF-interacting protein with forkhead-associated domain (TIFA), leading to the activation of pro-inflammatory nuclear factor kappa-B (NF-kB) signaling, cytokine induction and the activation and recruitment of immune cells, such as natural killer (NK) cells and T cells. This leads to tumor cell eradication and inhibits tumor cell proliferation. ALPK1, a bacterial pattern recognition receptor (PPR), is involved in bacterial pathogen recognition and plays a key role in innate immune defenses against bacterial infection. It recognizes ADP-heptose, a metabolite released during the biosynthesis and degradation of lipopolysaccharides (LPS), which is present in bacteria but not present in mammalian cells.

alprazolam

A triazolobenzodiazepine agent with anxiolytic, sedative-hypnotic and anticonvulsant activities. Alprazolam binds to a specific site distinct from the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) binding site on the benzodiazepine-GABA-A-chloride ionophore receptor complex located in the limbic, thalamic and hypothalamic regions of the central nervous system (CNS). This binding causes an allosteric modification of the receptor and enhances the affinity of GABA to the receptor leading to an increase in the frequency of chloride-channel opening events. This leads to an increase in chloride ion conductance, neuronal hyperpolarization, inhibition of the action potential and leads to a decrease in neuronal excitability.

alprostadil

The naturally occuring prostaglandin E1 (PGE1) which displays a variety of pharmacologic actions. Alprostadil is a potent vasodilator agent that increases peripheral blood flow, inhibits platelet aggregation, and induces bronchodilation. Used in the treatment of erectile dysfunction, this agent produces corporal smooth muscle relaxation by binding to PGE receptors, resulting in the activation of adenylate cyclase and the subsequent accumulation of 3'5'-cAMP.

alrizomadlin

An orally available inhibitor of human homolog of double minute 2 (HDM2; mouse double minute 2 homolog; MDM2), with potential antineoplastic activity. Upon oral administration,alrizomadlin binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival.

alsevalimab

A fully human, glycoengineered monoclonal antibody targeting B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) with potential antineoplastic and immune checkpoint inhibitory activities. Upon intravenous administration, alsevalimab binds to B7-H4 on the surface of tumor cells, thereby preventing B7-H4 binding to T cells and abrogating the B7-H4-mediated negative regulation of T-cell activation. This increases a cytotoxic T-lymphocyte (CTL)-mediated immune response against B7-H4-expressing tumor cells. In addition, the afucosylated Fc region of the anti-B7-H4 monoclonal antibody FPA150 enhances its binding affinity for human FcgammaRIIIa receptors (CD16) on natural killer (NK) cells, resulting in enhanced antibody-dependent cellular cytotoxicity (ADCC) against B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses.

Altace

(Other name for: ramipril)

alteplase

A recombinant therapeutic agent which is chemically identical to or similar to endogenous tissue plasminogen activator (tPA). tPA is a serine protease which converts plasminogen to plasmin, a fibrinolytic enzyme. Upon administration, alteplase increases plasmin enzymatic activity, resulting in hyperfibrinolysis and potential dissolution of a thrombus or embolism.

Althose

(Other name for: methadone hydrochloride)

altiratinib

An orally bioavailable inhibitor of c-Met/hepatocyte growth factor receptor (HGFR), vascular endothelial growth factor receptor type 2 (VEGFR2), Tie2 receptor tyrosine kinase (TIE2), and tropomyosin receptor kinase (Trk), with potential antiangiogenic and antineoplastic activities. Upon administration, altiratinib selectively binds to c-Met, VEGFR2, Tie2 and Trk tyrosine kinases, which may lead to the inhibition of endothelial cell migration, proliferation and survival. This also results in both an inhibition of tumor cell proliferation and increased tumor cell death in c-Met/VEGFR2/Tie2/Trk-expressing cells. These receptor tyrosine kinases (RTKs), frequently overexpressed or mutated by a variety of tumor cell types, play crucial roles in the regulation of angiogenesis, tumor cell growth and survival.

Altretamine

A synthetic cytotoxic s-triazine derivative similar in structure to alkylating agent triethylenemelamin with antineoplastic activity. Although the precise mechanism by which altretamine exerts its cytotoxic effect is unknown, N-demethylation of altretamine may produce reactive intermediates which covalently bind to DNA, resulting in DNA damage.

Altuviiio

(Other name for: efanesoctocog alfa)

aluminum hydroxide

An inorganic compound containing aluminum. Used in various immunologic preparations to improve immunogenicity, aluminum hydroxide adjuvant consists of aluminum hydroxide gel in a saline solution. In vaccines, this agent binds to the protein conjugate, resulting in improved antigen processing by the immune system.

aluminum hydroxide/magnesium hydroxide

An oral suspension containing aluminum hydroxide and magnesium hydroxide, with antacid effects. Aluminum hydroxide and magnesium hydroxide neutralizes or reduces gastric acid, thereby relieving symptoms associated with indigestion, gastritis, and gastroesophageal disease (GERD). Combined with other liquid ingredients (such as lidocaine and diphenhydramine), this antacid provides relief for painful stomatitis, mucositis, and esophagitis associated with both chemotherapy and radiation therapy.

alunacedase alfa

A recombinant, soluble glycosylated form of human angiotensin converting enzyme 2 (rhACE2) with antihypertensive and potential antineoplastic activities. Alunacedase Alfa may normalize ACE2 levels, cleaving angiotensin II to create angiotensin-(1-7) and restoring the function of the renin-angiotensin system (RAS). ACE2, a homolog of ACE1, appears to function as a negative regulator of the RAS system by converting angiotensin II to angiotensin-(1-7), a peptide with actions that counteract the cardiovascular actions of angiotensin II. In addition, angiotensin-(1-7) may inhibit cyclooxygenase 2 (COX-2) and the production of proinflammatory prostaglandins and may activate the angiotensin-(1-7) G protein-coupled receptor Mas, resulting in diminished tumor cell proliferation. ACE2 levels may be reduced in malignancy and diabetes and in liver, cardiovascular and lung diseases.

Alunbrig

(Other name for: brigatinib)

ALVAC gp100 vaccine

A vaccine composed of the replication-defective plaque purified recombinant canarypox virus (ALVAC) that encodes the glycoprotein 100 (gp100) gene, with potential antineoplastic activity. Vaccination with ALVAC gp100 may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells positive for the gp100 melanoma antigen, resulting in decreased tumor growth.

ALVAC(2) melanoma multi-antigen vaccine

A therapeutic cancer vaccine, based on a replication-defective recombinant canarypox virus (ALVAC) encoding multiple melanoma antigens, with potential immunostimulatory and antineoplastic activities. Vaccination with ALVAC(2) melanoma multi-antigen therapeutic vaccine may stimulate the host immune system to mount an immune response against antigen-expressing melanoma cells, resulting in inhibition of tumor growth and/or metastasis.

ALVAC(2)-NY-ESO-1 (M)/TRICOM vaccine

A cancer vaccine consisting of a replication-defective recombinant canarypox virus [ALVAC(2)] encoding the cancer-testis antigen NY-ESO and the TRIad of COstimulatory Molecules (B7-1, ICAM-1 and LFA-3; also called TRICOM), with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC(2)/NY-ESO (M)/TRICOM vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells, including bladder, breast, hepatocellular, melanoma, and prostate tumor cells. TRICOM may enhance antigen presentation and activate cytotoxic T-cells. In addition, ALVAC(2) encodes the vaccinia virus (vv) E3L ad K3L genes, which may potentiate the translation of the NY-ESO and TRICOM genes.

ALVAC-CEA B7.1 vaccine

A cancer vaccine that uses a viral vector system derived from the canarypox virus engineered to target the carcinoembryonic antigen (CEA). It causes infected cells to temporarily display CEA and activates the immune system to attack the tumor cells.

ALVAC-CEA vaccine

A cancer vaccine consisting of ALVAC, a highly attenuated poxvirus strain derived from the canarypox virus, encoding for the tumor associated antigen (TAA) carcinoembryonic antigen (CEA), with potential antineoplastic activity. Upon administration, ALVAC-CEA vaccine expresses CEA and may stimulate a host immune response against tumor cells expressing CEA. This may result in the inhibition of tumor growth and/or metastasis. CEA is overexpressed in a variety of tumor cell types.

ALVAC-ESO-1 vaccine

A cancer vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) encoding the cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC-ESO-1 vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-1-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells.

ALVAC-hB7.1

A vaccine comprise of a canarypox viral vector that carries the gene for human B7.1 (CD80 antigen) with potential use as an autologous therapeutic cancer vaccine. Tumor cells harvested from a patient are infected with ALVAC-hB7 1, thereby producing an autologous cell line that exhibits increased expression of HLA class I and class II, CD54 (ICAM), and CD80. Increased expression of these proteins by this autologous cell line may activate an antitumor T-cell response when the modified cells are administered to the patient.

ALVAC-MART-1 vaccine

A cancer vaccine containing a replication-defective recombinant canarypox virus (ALVAC), encoding an epitope of MART-1 (melanoma antigen recognized by T-cells), with potential immunostimulatory and antineoplastic activities. Upon administration, the MART-1 epitope is expressed by the ALVAC vector in ALVAC-MART-1 vaccine; a host cytotoxic T lymphocyte (CTL) response against MART-1-expressing tumor cells may follow, resulting in tumor cell lysis and decreased tumor cell proliferation.

alvelestat

An orally bioavailable, selective and reversible inhibitor of human neutrophil elastase (NE), with potential anti-inflammatory activity. Upon administration, alvelestat binds to and inhibits the activity of human NE. This inhibits NE-mediated inflammatory responses, which may prevent lung inflammation and injury, and may improve lung function associated with NE-induced respiratory diseases. NE, a serine protease released by neutrophils during inflammation, is upregulated in a number of respiratory diseases.

alvespimycin hydrochloride

The hydrochloride salt of alvespimycin, an analogue of the antineoplastic benzoquinone antibiotic geldanamycin. Alvespimycin binds to HSP90, a chaperone protein that aids in the assembly, maturation and folding of proteins. Subsequently, the function of Hsp90 is inhibited, leading to the degradation and depletion of its client proteins such as kinases and transcription factors involved with cell cycle regulation and signal transduction.

alvimopan

A synthetic trans-3,4-dimethyl-4-(3-hydroxyphenyl) piperidine with peripherally selective opioid mu receptor antagonist activity. Alvimopan is a selective and competitive antagonist at mu-opioid receptors, found in myenteric and submucosal neurons and the immune cells of the lamina propria in the human gut. Upon administration, this agent binds to mu-opioid receptors in the gut, thereby reversing opioid-related disturbances in gut motility. Alvimopan is approximately three to nine times more potent than naloxone.

alvocidib hydrochloride

The hydrochloride salt form of alvocidib, a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.

alvocidib prodrug TP-1287

An orally bioavailable, highly soluble phosphate prodrug of alvocidib, a potent inhibitor of cyclin-dependent kinase-9 (CDK9), with potential antineoplastic activity. Upon administration of the phosphate prodrug TP-1287, the prodrug is enzymatically cleaved at the tumor site and the active moiety alvocidib is released. Alvocidib targets and binds to CDK9, thereby reducing the expression of CDK9 target genes such as the anti-apoptotic protein MCL-1, and inducing G1 cell cycle arrest and apoptosis in CDK9-overexpressing cancer cells.

Alymsys

(Other name for: bevacizumab)

amantadine hydrochloride

The hydrochloride salt of amantadine, a synthetic tricyclic amine with antiviral, antiparkinsonian, and antihyperalgesic activities. Amantadine appears to exert its antiviral effect against the influenza A virus by interfering with the function of the transmembrane domain of the viral M2 protein, thereby preventing the release of infectious viral nucleic acids into host cells; furthermore, this agent prevents virus assembly during virus replication. Amantadine exerts its antiparkinsonian effects by stimulating the release of dopamine from striatal dopaminergic nerve terminals and inhibiting its pre-synaptic reuptake. This agent may also exert some anticholinergic effect through inhibition of N-methyl-D-aspartic acid (NMDA) receptor-mediated stimulation of acetylcholine, resulting in antihyperalgesia.

Amaryl

(Other name for: glimepiride)

amatuximab

A chimeric IgG1 monoclonal antibody against human mesothelin with potential anti-tumor activity. Amatuximab specifically targets mesothelin, a cell surface glycoprotein involved in cell adhesion and overexpressed on many epithelial-derived cancer cells. Upon binding to the mesothelin antigen, amatuximab triggers an antibody dependent cellular cytotoxicity (ADCC)-mediated host immune response against mesothelin-expressing cells, resulting in cell lysis.

Ambien

(Other name for: zolpidem tartrate)

AmBisome

(Other name for: liposomal amphotericin B)

amblyomin-X

A recombinant form of a toxic protein derived from the salivary glands of the Amblyomma cajennense tick that inhibits Factor Xa and induces apoptosis, with potential antithrombotic and antineoplastic activities. Upon administration, amblyomin-X promotes endoplasmic reticulum (ER) stress, mitochondrial dysfunction, cytochrome-c release, poly(ADP-ribose) polymerase (PARP) cleavage, and activation of caspase. Additionally, this agent selectively induces apoptosis in tumor cells. It also affects endothelial cell functions, such as adhesion, and may inhibit angiogenesis. Amblyomin-X targets and binds to factor Xa, inhibits its activity and interrupts the blood coagulation cascade, thereby preventing thrombin formation and thrombus development. As cancer is associated with thrombosis, amblyomin-X could potentially exert its antineoplastic and antithrombotic effects in the cancer patient at the same time.

amcasertib

An orally available cancer cell stemness kinase inhibitor with potential antineoplastic activity. Even though the exact target has not been fully elucidated, amcasertib targets and inhibits one or more pathways involved in cancer stem cell survival. As a result, cancer stem cell (CSC) growth as well as heterogeneous cancer cell growth is inhibited. CSCs, self-replicating cells able to differentiate into heterogeneous cancer cells, appear to be responsible for both tumor relapse and metastasis.

amcenestrant

An orally available, nonsteroidal selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, SERD SAR439859 specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that promotes ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

amdizalisib

An orally bioavailable selective inhibitor of the delta isoform of phosphatidylinositide 3-kinase (phosphoinositide 3'-kinase delta; PI3Kd; PI3K-d), with potential antineoplastic activity. Upon oral administration, amdizalisib selectively binds to and inhibits PI3Kd, and prevents the activation of the PI3Kd/AKT signaling pathway, and B-cell activation. This both decreases proliferation and induces cell death in PI3Kd-overexpressing tumor cells. PI3Kd plays a key role in the B-cell receptor (BCR) signaling pathway and the proliferation of hematologic cancer cells. The targeted inhibition of PI3Kd is designed to preserve PI3K signaling in normal, non-neoplastic cells and thereby to minimize serious side effects. PI3Kd, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.

Amdray

(Other name for: valspodar)

Ameluz

(Other name for: aminolevulinic acid hydrochloride)

Amen

(Other name for: medroxyprogesterone acetate)

American Ginseng

The aromatic root of the perennial herb Panax quinquefolius, native to eastern North America. American ginseng, used in Chinese traditional medicine and available as a nutritional supplement, is classified as an adaptogenic herb with multiple effects, many of which are regulatory in nature. It contains a complex mixture of saponin glycosides, also known as ginsenosides or panaxosides. Although the mechanism of action is unclear, this agent is reported to enhance the immune system and reduce fatigue.

ametantrone

A topoisomerase II inhibitor of the anthrapyrazole family that causes covalent cross-links in DNA of tumor cells.

Amevive

(Other name for: alefacept)

amezalpat

An orally bioavailable, small molecule, selective and competitive antagonist of peroxisome proliferator activated receptor alpha (PPARa), with potential immunomodulating and antineoplastic activities. Upon oral administration, amezalpat targets, binds to and blocks the activity of PPARa, thereby blocking transcription of PPARa target genes leading to an intracellular metabolism shift from fatty acid oxidation (FAO) to glycolysis in FAO-dependent tumors and reducing the production of fatty acids in the tumor microenvironment (TME). As fatty acids are essential for tumor cell growth in FAO-dependent tumor cells and are needed for the metabolism of suppressive immune cells in the TME, including regulatory T-cells (Tregs), reducing the amount of fatty acids leads to a direct killing of FAO-dependent tumor cells. It also skews macrophages from the immune suppressive M2 phenotype to an effector M1 phenotype and facilitates the cytotoxicity of immune effector cells, thereby stimulating an anti-tumor immune response and further killing tumor cells. Amezalpat also restores the natural inhibitor of angiogenesis thrombospondin-1 (TSP-1) and stimulator of interferon genes (STING) in the TME. PPARa, a ligand-activated nuclear transcription factor and metabolic checkpoint, regulates the expression of FAO genes and lipid metabolism. It plays a key role in immunosuppression in the TME. FAO is a metabolic pathway essential to tumor growth, survival and immunosuppression.

Amfebutamone

(Other name for: bupropion hydrochloride)

Amicar

(Other name for: aminocaproic acid)

amifampridine

An organic compound derived from pyridine with potassium channel inhibition activity. Amifampridine inhibits potassium channel efflux, increasing the duration of the action potential, which results in an increase in the duration of calcium channel opening and enhanced acetylcholine (ACh) release. Increased ACh availability at the motor end plate allows muscles to contract.

Amifostine

The trihydrate form of a phosphorylated aminosulfhydryl compound. After dephosphorylation of amifostine by alkaline phosphatase to an active free sulfhydryl (thiol) metabolite, the thiol metabolite binds to and detoxifies cytotoxic platinum-containing metabolites of cisplatin and scavenges free radicals induced by cisplatin and ionizing radiation. The elevated activity of this agent in normal tissues results from both the relative abundance of alkaline phosphatase in normal tissues and the greater vascularity of normal tissues compared to tumor tissues.

amikacin inhalation solution

A solution for inhalation containing the aminoglycoside antibiotic amikacin, with anti-bacterial activity. Upon aerosolized administration using the Pulmonary Drug Delivery System (PDDS), amikacin irreversibly binds to the 30S ribosomal subunit of susceptible organisms, thereby interfering with the activity of the translation initiation complex, which leads to both the misreading of mRNA and the production of non-functional or toxic peptides, and prevents normal protein synthesis. This kills susceptible bacteria.

amikacin sulfate

The sulfate salt of amikacin, a broad-spectrum semi-synthetic aminoglycoside antibiotic, derived from kanamycin with antimicrobial property. Amikacin irreversibly binds to the bacterial 30S ribosomal subunit, specifically in contact with 16S rRNA and S12 protein within the 30S subunit. This leads to interference with translational initiation complex and misreading of mRNA, thereby hampering protein synthesis and resulting in bactericidal effect. This agent is usually used in short-term treatment of serious infections due to susceptible strains of Gram-negative bacteria.

Amikin

(Other name for: amikacin sulfate)

amilomer

A synthetic microsphere formulation with arterial occlusive properties. Amilomer, a product produced by partially hydrolyzing starch and epichlorohydrin, contains degradable starch microspheres (DSM) with a diameter size of 45 micrometers that are readily degraded by amylase. When used in transcatheter arterial chemoembolization (TACE) procedures, infusion leads to lodging of the microspheres in the precapillary vessels and, consequently, to the occlusion of the hepatic artery. Local occlusion of selected blood vessels in conjunction with intrahepatic chemotherapy administration, results in elevated intracellular hepatocyte drug concentrations and enhances localized cytotoxicity against hepatic tumor lesions.

Amino Acid Injection

A concentrated dietary supplement for injection containing the essential amino acids leucine, isoleucine, lysine, valine, phenylalanine, histidine, threonine, methionine and tryptophan as well as the non-essential amino acids alanine, arginine, glycine, proline, serine and tyrosine, with potential anabolic and anti-catabolic activities. Upon dilution and intravenous infusion of the amino acid nutritional supplement, the amino acids serve as protein building blocks, promote protein synthesis in muscle cells and prevent protein breakdown.

amino acid/electrolyte mixture-based dietary supplement

A nutritional supplement containing a proprietary mix of amino acids and electrolytes, with potential rehydrating and gastrointestinal (GI) supportive activities. Upon oral administration of the amino acid-electrolyte dietary supplement, the electrolytes are transported by amino acid-coupled transporters across the intestinal epithelial barriers. This helps rehydrate the intestinal epithelial cells, helps restore normal bowel function, prevents fluid loss and improves symptoms of diarrhea. In addition, the supplement helps restore the size and functioning of the damaged villi and facilitates the restoration of the intestinal cells, thereby helping to restore and increase nutrient absorption, restoring normal bowel function and supporting healthy immune function.

aminobenzoate potassium

The potassium salt form of aminobenzoate, with anti-inflammatory and antifibrotic activities. Aminobenzoate potassium increases oxygen uptake at the tissue level and may enhance monoamine oxidase (MAO) activity, which requires oxygen as a substrate. Enhanced MAO activity maybe accountable for the prevention or regression of fibrosis, which may occur due to too much serotonin or too little MAO activity.

aminocamptothecin

A water-insoluble camptothecin derivative. Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages. Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity.

aminocamptothecin colloidal dispersion

A colloidal dispersion formulation of 9-Aminocamptothecin, a water-insoluble camptothecin derivative. Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages. Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity.

aminocaproic acid

A synthetic lysine derivative with antifibrinolytic activity. Aminocaproic acid competitively inhibits activation of plasminogen, thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots as well as fibrinogen and other plasma proteins including the procoagulant factors V and VIII. Aminocaproic acid competitively reduces the conversion of plasminogen to plasmin by plasminogen activators. It directly inhibits proteolytic activity of plasmin, but higher doses are required than are needed to reduce plasmin formation. Aminocaproic acid is used in the treatment of hemorrhage and prophylactically against hemorrhage, including hyperfibrinolysis-induced hemorrhage and postsurgical hemorrhage.

aminoflavone prodrug AFP464

A synthetic lysyl prodrug of the amino-substituted flavone derivate aminoflavone with antiproliferative and antineoplastic activities. AFP464 is rapidly converted to aminoflavone in plasma. Aminoflavone activates the aryl hydrocarbon receptor (AhR) signaling pathway leading to an increase in cytochrome P450 1A1 (CYP1A1) and cytochrome P450 1A2 (CYP1A2) expression and, to a lesser extent, an increase in cytochrome P450 1B1 (CYP1B1) expression. Subsequently, aminoflavone is metabolized to toxic metabolites by the cytochromome P450 enzymes that it induces; these toxic metabolites covalently bind to DNA, resulting in the phosphorylation of p53, the induction of the p53 downstream target p21Waf1/Cip1, and apoptosis. Pulmonary toxicity may be dose-limiting.

aminoglutethimide

A synthetic derivative of the sedative and anticonvulsant glutethimide with anti-steroid properties. Originally used as an anticonvulsant, aminoglutethimide also blocks adrenal steroidogenesis by inhibiting the enzymatic conversion of cholesterol to pregnenolone. In addition, this agent blocks the peripheral aromatization of androgenic precursors to estrogens. Aminoglutethimide does not suppress ovarian estrogen production.

aminolevulinic acid

A topically administered metabolic precursor of protoporphyrin IX. After topical administration, aminolevulinic acid (ALA) is converted to protoporphyrin IX (PpIX) which is a photosensitizer. When the proper wavelength of light activates protoporphyrin IX, singlet oxygen is produced, resulting in a local cytotoxic effect.

aminolevulinic acid hydrochloride

The hydrochloride salt form of aminolevulinic acid, an aminoketone, used for local photosensitizing therapy. Aminolevulinic acid (ALA) is a metabolic pro-drug that is converted into the photosensitizer protoporphyrin IX (PpIX), which accumulates intracellularly. Upon exposure to light of appropriate wavelength (red, or blue), PpIX catalyzes oxygen to singlet oxygen, an intracellular toxin, which can further react to form superoxide and hydroxyl radicals. This leads to cellular cytotoxic effects.

aminolevulinic acid intravenous formulation SONALA-001

An intravenous formulation of aminolevulinic acid (ALA), a metabolic precursor of the photosensitizer protoporphyrin IX (PpIX), with potential antineoplastic activity upon magnetic resonance-guided focused ultrasound (MRgFUS). Upon intravenous administration of SONALA-001, ALA readily crosses the blood brain barrier (BBB) and accumulates intracellularly, where ALA is metabolized to the photosensitizer PpIX by enzymes in the heme biosynthesis pathway. Due to the distinct activity of these enzymes in tumor cells, there is a higher accumulation of PpIX in tumor cells. Upon MRgFUS, the energy of ultrasound produces light (sonoluminescence) within the brain and activates PpIX in tumor cells. Ultrasound-activated PpIX catalyzes molecular oxygen to singlet oxygen, an intracellular toxin, which can further react to form superoxide and hydroxyl radicals. This leads to cellular cytotoxic effects.

aminophylline

A methylxanthine and derivative of theophylline. Aminophylline relaxes smooth muscles, particularly bronchial muscles. This xanthine most likely exerts its effect by inhibiting cAMP or cGMP phosphodiesterases, thereby increasing levels of the second messenger cAMP or cGMP intracellularly. Other mode of actions include an adenosine antagonistic effect on the activity of CD4 lymphocytes and mediator release from mast cells thereby decreasing lung sensitivity to allergens and other substances that cause inflammation. Aminophylline also acts as a CNS stimulant and exerts a positive chronotropic and inotropic effect on the heart.

aminopterin

A synthetic derivative of pterins with antineoplastic and immunosuppressive properties. As a folate analogue, aminopterin competes for the folate binding site of the enzyme dihydrofolate reductase, thereby blocking tetrahydrofolate synthesis, and resulting in depletion of nucleotide precursors and inhibition of DNA, RNA and protein synthesis.

aminothiadiazole

A synthetic derivative of nicotinamide adenine dinucleotide (NAD). Aminothiadiazole competitively inhibits inosine 5-monophosphate dehydrogenase, thereby disrupting the regulation of cell proliferation and differentiation in a number of cells. This agent is also a selective human adenosine A3 receptor antagonist.

amiodarone hydrochloride

The hydrochloride salt of an iodine-rich benzofuran derivative with antiarrhythmic and vasodilatory activities. As a class III antiarrhythmic agent, amiodarone blocks the myocardial calcium, potassium and sodium channels in cardiac tissue, resulting in prolongation of the cardiac action potential and refractory period. In addition, this agent inhibits alpha- and beta-adrenergic receptors, resulting in a reduction in sympathetic stimulation of the heart, a negative chronotropic effect, and a decrease in myocardial oxygen demands. Amiodarone may cause vasodilation by stimulation of the release of nitric oxide and cyclooxygenase-dependent relaxing endothelial factors.

Amitiza

(Other name for: lubiprostone)

amitriptyline hydrochloride

The hydrochloride salt of the tricyclic dibenzocycloheptadiene amitriptyline with antidepressant and antinociceptive activities. Amitriptyline inhibits the re-uptake of norepinephrine and serotonin by the presynaptic neuronal membrane in the central nervous system (CNS), thereby increasing the synaptic concentration of norepinephrine and serotonin. Due to constant stimulation to these receptors, amitriptyline may produce a downregulation of adrenergic and serotonin receptors, which may contribute to the antidepressant activity. In the CNS the antinociceptive activity of this agent may involve high affinity binding to and inhibition of N-methyl-D-aspartate (NMDA) receptors and/or the enhancement of the action of serotonin at the spinal terminals of an opioid-mediated intrinsic analgesia system.

amivantamab and recombinant human hyaluronidase

A co-formulation composed of amivantamab, a human bispecific antibody targeting both epidermal growth factor receptor EGFR and hepatocyte growth factor receptor (HGFR; c-Met), and a recombinant form of human hyaluronidase, with potential antineoplastic activity. Upon subcutaneous administration of amivantamab and recombinant human hyaluronidase, the hyaluronidase reversibly depolymerizes the polysaccharide hyaluronan in the subcutaneous tissue. This increases the permeability of the subcutaneous tissue and enhances the absorption of amivantamab into the systemic circulation. In turn, amivantamab simultaneously targets and binds to wild-type or certain mutant forms of both EGFR and c-Met expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and c-Met-mediated signaling pathways. In addition, binding results in receptor degradation, which further inhibits EGFR- and c-Met-mediated signaling. Amivantamab also causes antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of tumor cell proliferation. When administered subcutaneously, hyaluronidase, an endoglycosidase, increases the dispersion and absorption of co-administered drugs. EGFR and c-Met, upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

amivantamab-vmjw

A human bispecific antibody targeting both epidermal growth factor receptor EGFR and hepatocyte growth factor receptor (HGFR; cMet), with potential antineoplastic activity. Upon administration, amivantamab simultaneously targets and binds to wild-type or certain mutant forms of both EGFR and cMet expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and cMet-mediated signaling pathways. In addition, binding results in receptor degradation, which further inhibits EGFR- and cMet-mediated signaling. JNJ-61186372 also causes antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of tumor cell proliferation. EGFR and cMet, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

AML mRNA positive lysate loaded autologous dendritic cell vaccine

A cancer vaccine consisting of autologous dendritic cells loaded with separate preparations of acute myelogenous leukemia (AML) cell lysate and AML-specific messenger RNA (mRNA) with potential immunostimulatory and antineoplastic activities. Upon administration, AML mRNA plus lysate loaded autologous dendritic cell vaccine may elicit a potent cytotoxic T-cell (CTL) response against AML cells, resulting in tumor cell death. Autologous dendritic cells doubly-loaded with AML cell lysate and AML-specific mRNA may elicit superior primary, recall, and effector lytic immune responses compared to autologous dendritic cells loaded with tumor lysate or tumor mRNA alone.

Ammoidin

(Other name for: methoxsalen)

ammonia N-13

A radiopharmaceutical composed of ammonia labeled with the radioisotope nitrogen N 13 that can be used, during positron emission tomography (PET), as a blood flow imaging agent and potentially as a tumor imaging agent. Upon intravenous administration, ammonia N 13 distributes to various organs in the body, such as the myocardium, liver, kidneys and brain. This agent is taken up by cells and is retained following conversion to glutamine N 13 by glutamine synthetase (GS). Upon PET, organ perfusion and the presence of cancer cells can be assessed. GS, an enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia, is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation.

Ammonium Trichlorotellurate

A synthetic non-toxic tellurium derivative, structurally similar to cisplatin, with immunostimulatory and anti-hair loss properties. Ammonium trichlorotellurate induces production of colony stimulating factor (CSF), interleukin-2 (IL-2), and IL-2 receptors by increasing the calcium ion influx through the cell membrane and subsequently exerts its immunostimulatory effects through the CSF-mediated increase in macrophage/granulocytes. This agent is also a potent inducer of interferon and a spectrum of cytokines such as IL-1, IL-6, and tumor necrosis factor (TNF). In animal studies, ammonium trichlorotellurate exerts its anti-hair loss effect by inducing anagen and obstructing spontaneous catagen via promoting follicular keratinocyte proliferation and interfering with terminal differentiation, respectively.

Amnesteem

(Other name for: isotretinoin)

AmnioFix

(Other name for: dehydrated human amnion/chorion membrane)

amnion-derived cellular cytokine solution

A topical cellular cytokine solution containing a distinct combination of growth factors and cytokines secreted by and released from amnion-derived multipotent progenitor (AMP) cells, with potential immunomodulating and skin healing activities. The amnion-derived cellular cytokine solution (ACCS) contains near physiological levels of transforming growth factor beta, tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2, as well as the angiogenesis factors platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and angiogenin that are normally found in healing wounds. Upon spraying the solution onto affected areas, the cytokines and growth factors in ACCS appear to increase the migration, proliferation and differentiation of both keratinocytes and fibroblasts; enhance the migration and phagocytosis of macrophages in wounds; and increase epithelialization. Together these processes may accelerate skin healing and tissue repair. Also, ACCS may be beneficial in the treatment of radiation burns of the skin.

Amoban

(Other name for: zopiclone)

amolimogene bepiplasmid

A plasmid DNA-based vaccine consisting of small biodegradable poly(lactide-co-glicolide) polymer microparticles encapsulating plasmid-DNA vector encoding a chimeric protein comprising epitopes derived from the E6 and E7 oncoproteins of the human papillomavirus (HPV) types 16 and 18, with potential antineoplastic activity. Upon intramuscular vaccination, amolimogene bepiplasmid may elicit the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells positive for HPV-16 and -18 E6 and E7 and may result in a reduction in tumor cell growth. HPV types 16 and 18 oncoproteins E6 and E7 are most commonly involved in cervical cancer.

amonafide dihydrochloride

The dihydrochloride salt of amonafide, an imide derivative of naphthalic acid. Amonafide intercalates into DNA and inhibits topoisomerase II, resulting in protein-associated strand breaks and impaired DNA and RNA synthesis.

amonafide L-malate

The malate salt of amonafide, an imide derivative of naphthalic acid, with potential antineoplastic activity. Amonafide intercalates into DNA and inhibits topoisomerase II, resulting in DNA double-strand breaks (DSB) and inhibition of DNA replication and RNA synthesis.

amorphous calcium carbonate

A nutritional supplement composed of a proprietary synthetic and amorphous form of calcium carbonate, that can potentially be used to replenish calcium. Upon administration of amorphous calcium carbonate (ACC), the mineral calcium may give calcium supplementary support, improve bone, muscle and heart strength, improve performance and decrease bone-associated pain.

amoxicillin

A broad-spectrum, semisynthetic aminopenicillin antibiotic with bactericidal activity. Amoxicillin binds to and inactivates penicillin-binding protein (PBP) 1A located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This interrupts bacterial cell wall synthesis and results in the weakening of the bacterial cell wall and causes cell lysis.

amoxicillin-clavulanate potassium

A combination of the semisynthetic broad-spectrum antibiotic amoxicillin and the beta-lactamase enzyme inhibitor clavulanate potassium. Clavulanate potassium increases the serum half-life of amoxicillin by inhibiting beta-lactamase-mediated metabolism of amoxicillin. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin binding proteins and inhibiting peptidoglycan synthesis, a critical component of bacterial cell walls.

Amoxil

(Other name for: amoxicillin)

AMP KRAS vaccine ELI-002

A peptide-based cancer vaccine composed of the adjuvant Amphiphile (Amph; AMP)-CpG-7909, which is a lipid-conjugated immune-stimulatory oligonucleotide, admixed with Amph modified Kirsten Rat Sarcoma (KRAS) mutated peptides, which contain a mixture of lipid-conjugated peptide-based antigens, with potential immunostimulatory and antitumor activities. Upon subcutaneous administration of the AMP KRAS vaccine ELI-002, the lipid moieties bind to tissue albumin and the complex is delivered to and accumulates in the lymph nodes where it is taken up by antigen presenting cells (APCs), primarily dendritic cells (DCs). This may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL)-mediated immune response against KRAS/neuroblastoma ras viral oncogene homolog (NRAS)-expressing tumor cells. KRAS and NRAS, tumor-associated antigens (TAAs) that are involved in the RAS/mitogen-activated protein kinase (MAPK) signaling pathway, are overexpressed on a variety of tumor cell types and play key role in tumor cell proliferation. The CpG-based adjuvant may enhance the mutated KRAS T cell-specific immune response. ELI-002 2P contains two KRAS mutated Amph-peptides, including Amph-G12D and Amph-G12R. ELI-002 (ELI-002 7P) contains seven KRAS mutated Amph-peptides (Amph-Peptide 7), including G12D, G12R, G12V, G12A, G12C, G12S and G13D.

amphotericin B deoxycholate

The deoxycholate salt of amphotericin B, a polyene antifungal antibiotic produced by Streptomyces nodosus, with antifungal activity. Amphotericin B binds to ergosterol, an essential component of the fungal cell membrane. This results in depolarization of the cell membrane, alterations in cell membrane permeability, leakage of important intracellular components, and cell rupture. This agent may also induce oxidative damage in fungal cells and has been reported to stimulate host immune cells.

ampicillin sodium/sulbactam sodium

A combination formulation of the sodium salts of the antibiotic ampicillin and the beta-lactamase inhibitor sulbactam with antibacterial activity. Ampicillin, a broad-spectrum, semisynthetic penicillin, binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall, thereby interfering with the cross-linking of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. As a result, the cell wall is weakened and the cell lyses. The sulbactam component irreversibly binds to bacterial beta-lactamase at or near its active site, thereby interfering with substrate binding and inhibiting bacterial metabolism of penicillin and cephalosporin beta-lactam antibiotics, effectively extending their antibiotic spectrum to include many beta-lactam-resistant bacteria.

Ampligen

(Other name for: rintatolimod)

Amplimexon

(Other name for: imexon)

amrecibart

An anti-factor XI (FXI) antibody, with potential anti-thrombotic activity. Upon administration, amrecibart targets and binds to the apple 2 (A2) domain of FXI and activated FXI (FXIa), thereby preventing the intrinsic pathway-triggered FXI activation. This prolongs the activated partial thromboplastin time (aPTT) and reduces platelet and fibrin accumulation. This results in the inhibition of contact activation-initiated blood coagulation and prevents thrombus formation. FXI contributes to thrombotic disease while playing a limited role in normal hemostasis. Activation of FXI is essential for thrombus growth and stabilization.

amredobresib

An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins with potential antineoplastic activity. Upon oral administration, amredobresib binds to bromodomain-containing proteins 2, 3, and 4 (BRD2, BRD3, and BRD4) as well as bromodomain testis-specific protein (BRDT), thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and suppresses the expression of certain oncogenes, including Myc and other transcriptional regulators. Preventing the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.

amrubicin

A synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.

amrubicin hydrochloride

The hydrochloride salt of a third-generation synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.

Amsa P-D

(Other name for: amsacrine)

amsacrine

An aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S/G2 phase of the cell cycle, and cell death. This agent's cytotoxicity is maximal during the S phase of the cell cycle when topoisomerase levels are greatest. In addition, amsacrine may induce transcription of tumor promoter p53 protein and block p53 ubiquitination and proteasomal degradation, resulting in p53-dependent tumor cell apoptosis.

amsilarotene

A retinobenzoic acid with potential antineoplastic activity. Amsilarotene inhibits retinoblastoma-gene product (RB) phosphorylation and increases the presence of 2 cyclin-dependent kinase (CDK) inhibitors, resulting in cell cycle arrest. This agent also causes a cytotoxic decline in cyclin A and thymidylate synthase expression.

amsulostat

An orally available, small-molecule, irreversible inhibitor of all lysyl oxidases (LOX) family members, with potential antifibrotic activity. Upon oral administration, amsulostat targets, binds to and inhibits the activity of all enzymes in the LOX family. This prevents the post-translational oxidative deamination of lysine residues on target proteins, including collagen and elastin, and reduces the formation of deaminated lysine (allysine), the formation of inter- and intramolecular cross-linkages and may prevent remodeling of the extracellular matrix (ECM), thereby reducing fibrotic tissue formation in certain chronic fibrotic diseases. LOX is often upregulated in fibrotic tissue and plays a key role in fibrosis.

Amtagvi

(Other name for: lifileucel)

amuvatinib

An orally bioavailable synthetic carbothioamide with potential antineoplastic activity. Multitargeted receptor tyrosine kinase inhibitor MP470 binds to mutant forms of the stem cell factor receptor (c-Kit; SCFR), inhibiting clinically relevant mutants of this receptor tyrosine kinase that may be associated with resistance to therapy. In addition, MP470 inhibits activities of other receptor tyrosine kinases, such as c-Met, Ret oncoprotein, and mutant forms of Flt3 and PDGFR alpha, which are frequently dysregulated in variety of tumors. This agent also suppresses the induction of DNA repair protein Rad51, thereby potentiating the activities of DNA damage-inducing agents. Mutant forms of c-Kit are often associated with tumor chemoresistance.

Amyvid

(Other name for: fluorine F 18 florbetapir)

anagrelide

A synthetic quinazoline derivative, anagrelide reduces platelet production through a decrease in megakaryocyte maturation. Anagrelide inhibits cyclic AMP phosphodiesterase, as well as ADP- and collagen-induced platelet aggregation. At therapeutic doses, it does not influence white cell counts or coagulation parameters. Anagrelide is used for treatment of essential thrombocythemia to reduce elevated platelet counts and the risk of thrombosis.

Anagrelide Hydrochloride Anhydrous

The hydrochloride salt of a synthetic quinazoline derivative, Anagrelide Hydrochloride reduces platelet production through a decrease in megakaryocyte maturation. Anagrelide inhibits cyclic AMP phosphodiesterase, as well as ADP- and collagen-induced platelet aggregation. At therapeutic doses, it does not influence white cell counts or coagulation parameters. Anagrelide is used for treatment of essential thrombocythemia to reduce elevated platelet counts and the risk of thrombosis.

anagrelide prolonged-release formulation

A prolonged-release tablet formulation containing the quinazoline anagrelide, with antiplatelet activity. Although the exact mechanism of action through which anagrelide exerts its effect has yet to be fully elucidated, this agent inhibits the maturation of megakaryocytes into platelets, which reduces platelet production. Anagrelide also inhibits cyclic AMP phosphodiesterase III (PDEIII), which prevents PDEIII-mediated platelet aggregation. This may prevent essential thrombocythemia and thrombosis.

anakinra

A recombinant human nonglycosylated interleukin-1 (IL-1) receptor antagonist with potential antineoplastic activity. Anakinra binds to the IL-1 receptor, thereby blocking the binding of the IL-1 to and activation of its receptor. Blockade of IL-1 activity may inhibit the cascade of downstream pro-angiogenic factors such as vascular endothelial cell growth factor, tumor necrosis factor-alpha, and IL-6, resulting in inhibition of tumor angiogenesis.

anamorelin hydrochloride

The orally bioavailable hydrochloride salt of a synthetic, small-molecule ghrelin mimetic with appetite-stimulating and anabolic activities. Anamorelin binds to and stimulates the growth hormone secretagogue receptor (GHSR) centrally, thereby mimicking the appetite-stimulating and growth hormone-releasing effects of grhelin. Stimulation of GHSR may also reduce the production of the pro-inflammatory cytokines TNF-alpha and interleukin-6, which may play a direct role in cancer-related loss of appetite.

anastrozole

A nonsteroidal inhibitor of estrogen synthesis that resembles paclitaxel in chemical structure. As a third-generation aromatase inhibitor, anastrozole selectively binds to and reversibly inhibits aromatase, a cytochrome P-450 enzyme complex found in many tissues including those of the premenopausal ovary, liver, and breast; aromatase catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis. In estrogen-dependent breast cancers, ananstrozole may inhibit tumor growth.

Anaxirone

A synthetic triepoxide alkylating agent with potential antineoplastic activity. Anaxirone alkylates DNA via actual or derived epoxide groups, resulting in inhibition of DNA synthesis. This agent has been shown to exhibit a broad spectrum of antineoplastic activity against experimental tumors, including those resistant to other alkylating agents.

anbalcabtagene autoleucel

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, anbalcabtagene autoleucel targets and binds to CD19-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and tumor cell lysis. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors.

anbenitamab

An engineered Fc-based heterodimeric bispecific monoclonal antibody, derived from trastuzumab and pertuzumab, directed against two distinct epitopes of the extracellular dimerization domain of the tumor-associated antigen (TAA) human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential immunomodulating and antineoplastic activities. Upon administration, anbenitamab simultaneously targets and binds to two separate, non-overlapping epitopes of HER-2, thereby inhibiting HER-2 heterodimerization and prevents the activation of HER-2 signaling pathways. By binding to HER-2, KN026 induces an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress HER-2. This results in tumor cell apoptosis and inhibits tumor cell proliferation of HER-2-overexpressing tumor cells. HER-2, overexpressed on a variety of tumor cell types, plays an important role in proliferation, differentiation and survival.

anbenitamab repodatecan

An antibody-drug conjugate (ADC) composed of the bispecific monoclonal antibody anbenitamab, directed against two distinct epitopes of the extracellular dimerization domain of the tumor-associated antigen (TAA) human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), site-specifically conjugated via N glycosylation site to a topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon administration of anti-HER2 ADC JSKN003, the anbenitamab moiety simultaneously targets and binds to two separate, non-overlapping epitopes of HER2 expressed on tumor cells. Upon binding and internalization, the topoisomerase-1 inhibitor moiety is released, binds to topoisomerase-1 and stabilizes cleaved DNA-topoisomerase-1 complexes. This prevents DNA re-ligation, induces irreversible DNA strand breaks, prevents DNA repair, and leads to cycle arrest and apoptosis specifically in tumor cells expressing HER2. HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

Ancef

(Other name for: cefazolin sodium)

ancient minerals magnesium lotion

(Other name for: magnesium chloride-based lotion)

ancitabine hydrochloride

The hydrochloride salt of a cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine. Subsequently, cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. Cytarabine agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.

Ancobon

(Other name for: flucytosine)

andamertinib

An orally bioavailable, mono-anilino-pyrimidine, mutant-selective epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, andamertinib targets, binds to and irreversibly inhibits the activity of various EGFR mutations, including exon 20 insertion (Ex20ins) activating mutations, the gatekeeper mutation T790M, ExDel19, and L858R. This prevents EGFR-mediated signaling, induces cell death and inhibits tumor growth in tumor cells expressing these EGFR mutations. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

andecaliximab

A humanized monoclonal antibody against matrix metalloproteinase 9 (MMP-9), with potential antineoplastic activity. Upon administration, andecaliximab binds to MMP-9 and inhibits its enzymatic activity. This results in an inhibition of extracellular matrix protein degradation and, potentially, the inhibition of angiogenesis, tumor growth, invasion, and metastasis. MMP-9, a protein belonging to the MMP family, plays a key role in the degradation of collagens and proteoglycans; increased activity of MMP-9 has been associated with increased invasion and metastasis of cancer.

Andro LA

(Other name for: testosterone enanthate)

AndroGel

(Other name for: testosterone gel)

androgen antagonist APC-100

An orally available, vitamin E derivative and androgen receptor (AR) antagonist with potential anti-oxidant, chemopreventative and antineoplastic activity. APC-100 binds to ARs in target tissues thereby inhibiting androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot be translocated to the nucleus. By inhibiting the formation of the complex between androgen activated AR- and the AP1 transcription factor JunD, the expression of androgen-responsive genes are blocked. One of such gene is spermidine/spermine N1-acetyl transferase gene (SSAT) that is responsible for the breakdown of polyamines, which are produced in high levels by prostatic epithelial cells, into reactive oxygen species (ROS) that cause cellular damage. APC-100 may ultimately lead to an inhibition of growth in both AR-dependent and AR-independent prostate tumor cells.

androgen receptor antagonist BAY 1161116

An orally bioavailable antagonist of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR antagonist BAY 1161116 specifically binds to AR, inhibits AR activation, and prevents AR-mediated signaling. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.

androgen receptor antagonist ONC1-0013B

An orally bioavailable antagonist of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR antagonist ONC1-13B specifically binds to AR, prevents AR activation, downregulates AR expression and prevents AR-mediated signaling. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.

androgen receptor antagonist SHR3680

An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon administration, SHR3680 competitively binds to AR in target tissues, which both prevents androgen-induced receptor activation and facilitates the formation of inactive complexes that cannot be translocated to the nucleus. This prevents binding to and transcription of AR-responsive genes, inhibits the expression of genes that regulate prostate cancer cell proliferation, and may lead to an inhibition of cell growth of AR-expressing tumor cells. ARs are overexpressed in prostate cancer and play a key role in prostate cancer cell proliferation.

androgen receptor antagonist TAS3681

An orally bioavailable inhibitor of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR inhibitor TAS3681 specifically binds to AR. This prevents AR activation, downregulates AR and prevents AR-mediated signaling. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.

androgen receptor antagonist TQB3720

An orally bioavailable antagonist of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR antagonist TQB3720 specifically targets and binds to the AR, thereby inhibiting both AR activation and the AR-mediated signaling pathway. This may inhibit cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in the proliferation, survival and chemoresistance of tumor cells.

androgen receptor antagonist TRC253

An orally bioavailable androgen receptor (AR) antagonist, with potential antineoplastic activity. Upon oral administration, AR antagonist TRC253 specifically binds to both wild-type and certain mutant forms of AR, thereby preventing androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes, inhibits the expression of genes that regulate prostate cancer cell proliferation, and may lead to an inhibition of growth of tumor cells in which AR is overexpressed and/or mutated. AR is often overexpressed and/or mutated in prostate cancers and plays a key role in proliferation, survival and chemoresistance of tumor cells.

androgen receptor antisense oligonucleotide AZD5312

An antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon intravenous administration, AZD5312 hybridizes with AR mRNA, which blocks translation of the AR protein. This both inhibits AR-induced tumor cell growth and promotes apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival.

Androgen Receptor Antisense Oligonucleotide EZN-4176

A locked nucleic acid (LNA)-based antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon administration, EZN-4176 is hybridized and releases the complementary sequences of AR mRNA, thereby blocking translation of the AR protein and inhibiting AR-induced tumor cell growth and promoting tumor cell apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival. LNAs contain a methylene bridge linking 2'-oxygen and 4'-carbon of ribose sugar rings, thereby increasing their thermal stability and decreasing degradation.

androgen receptor degrader AC176

An orally bioavailable androgen receptor (AR) chimeric degrader, with potential antineoplastic activity. Upon oral administration, AR degrader AC176 targets and degrades AR, thereby preventing AR-mediated signaling and inhibiting the proliferation of AR-overexpressing tumor cells. AR, a hormone-regulated transcription factor, plays a key role in tumor cell proliferation in castration-resistant prostate cancer (CRPC).

androgen receptor degrader ARV-766

An orally bioavailable androgen receptor (AR)-targeted protein degrader, composed of an AR ligand attached to an E3 ligase recognition moiety and utilizing the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. Upon oral administration, AR degrader ARV-766 targets and binds to the AR ligand binding domain on the AR. E3 ligase is then recruited to the AR by the E3 ligase recognition moiety of ARV-766 and the AR is tagged by ubiquitin. This causes ubiquitination and degradation of AR by the proteasome, and prevents the expression of AR target genes and halts AR-mediated signaling. This inhibits the proliferation of AR-overexpressing tumor cells. In addition, the degradation of the AR releases ARV-766, allowing it to bind to additional AR. AR plays a key role in the proliferation of castration-resistant prostate cancer cells (CRPC). ARV-766 may degrade resistance-driving point mutations of AR, including the L702H mutation associated with treatments including abiraterone.

androgen receptor degrader HP518

An orally available androgen receptor (AR)-targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. HP518 is composed of an AR ligand attached to an E3 ligase recognition moiety. Upon oral administration of AR degrader HP518, the AR-binding moiety specifically targets and binds to AR, particularly AR with AR ligand-binding domain (LBD) mutations. E3 ligase is recruited to the AR by the E3 ligase recognition moiety and the AR target protein is tagged by ubiquitin. This causes ubiquitination and degradation of AR by the proteasome. This prevents the expression of AR target genes and halts AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. AR, a hormone-regulated transcription factor, plays a key role in tumor cell proliferation in castration-resistant prostate cancer (CRPC).

androgen receptor degrader RO7656594

An orally bioavailable androgen receptor (AR) degrader, with potential antineoplastic activity. Upon oral administration, AR degrader RO7656594 targets, binds to and degrades AR, thereby preventing AR-mediated signaling and inhibiting the proliferation of AR-overexpressing tumor cells. AR, a hormone-regulated transcription factor, plays a key role in tumor cell proliferation in castration-resistant prostate cancer (CRPC).

androgen receptor downregulator AZD3514

An orally available selective androgen receptor (AR) downregulator (SARD), with potential antineoplastic activity. Upon oral administration, AZD3514 binds to the AR ligand binding domain and inhibits the binding of androgen, thereby preventing androgen-dependent AR signaling. AZD3514 also causes downregulation of AR expression, which further prevents AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. AR plays a key role in the proliferation of castration-resistant prostate cancer cells.

androgen receptor inhibitor EPI-506

An orally bioavailable, small molecule inhibitor of the N-terminal domain (NTD) of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR inhibitor EPI-506 specifically binds to the NTD of AR, thereby inhibiting both AR activation and the AR-mediated signaling pathway. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.

androgen receptor inhibitor ONCT-534

An orally bioavailable dual-action androgen receptor (AR) inhibitor, with potential antineoplastic activity. Upon oral administration, AR inhibitor ONCT-534 targets and binds to both the ligand-binding domain (LBD) and the N-terminal domain (NTD) of the AR, and inhibits AR-mediated signaling and induces the degradation of AR and AR splice variant (AR-SV) proteins. This may inhibit cell growth in AR-overexpressing tumor cells, including those with AR amplification, mutations in the AR LBD, and AR-SVs with loss of the AR LBD. AR is overexpressed in prostate cancers and is involved in the proliferation, survival and chemoresistance of tumor cells.

androgen receptor ligand-binding domain-encoding plasmid DNA vaccine MVI-118

A cancer vaccine containing pTVG4 plasmid DNA encoding the human androgen receptor (AR) ligand-binding domain (LBD) (pTVG-AR), with potential immunostimulating and antineoplastic activities. Upon intradermal administration of AR LBD-encoding plasmid DNA vaccine MVI-118, the plasmid DNA vaccine expresses AR LBD and may stimulate the host immune system to generate a cytotoxic T-lymphocyte (CTL) response against AR LBD-expressing prostate cancer cells. This reduces proliferation of AR-expressing tumor cells. AR, a tumor-associated antigen (TAA) overexpressed in prostate cancer cells, plays a key role in the development and progression of prostate cancer; its expression is correlated with poor prognosis.

androgen receptor/glucocorticoid receptor antagonist CB-03-10

An orally bioavailable steroidal cortexolone derivative and antagonist of the androgen receptor (AR) and glucocorticoid receptor (GR), with potential antineoplastic activity. Upon oral administration, AR/GR antagonist CB-03-10 specifically binds to AR and GR, inhibits AR and GR activation, and prevents AR- and GR-mediated signaling. This leads to an induction of both extrinsic and intrinsic apoptotic pathways and inhibits cell growth in AR- and GR-overexpressing tumor cells. AR and GR are overexpressed in certain types of cancer cells and are involved in proliferation, survival and chemoresistance of tumor cells.

Andrographolide

A labdane diterpenoid that is produced by the Andrographis paniculata plant, which has a broad range of therapeutic applications including anti-inflammatory and anti-platelet aggregation activities and potential antineoplastic properties. Since andrographolide has multiple therapeutic activities there are several proposed mechanisms of action for this agent. The anti-inflammatory effects of this agent appear to be related to the inhibition of nitric oxide (NO) production by macrophages. This agent may activate the NO/cyclic GMP pathway and inhibit both the phospholipase C gamma 2 (PLC gamma2)/protein kinase C (PKC) and PI3K/AKT-MAPK signaling pathways in activated platelets to inhibit platelet aggregation. In activated platelets, these three signaling pathways are downstream of integrin activation mediated by collagen binding and influence the association of fibrinogen with its receptors. Additionally, andrographolide may exert its anti-cancer activity through the induction of cell cycle arrest at G0/G1 phase and the stimulation of lymphocyte proliferation and activation. These processes could result in decreased proliferation of and increased immunocytotoxicity against tumor cells.

Android

(Other name for: methyltestosterone)

Android-F

(Other name for: fluoxymesterone)

Androstane Steroid HE3235

An orally bioavailable adrenal steroid analogue with potential antineoplastic activity. Androstane steroid HE3235 appears to bind the androgen receptor (AR), down-regulating anti-apoptotic genes, such as Bcl-2, while increasing the expression of pro-apoptotic genes, such as caspases. In vitro and in vivo studies indicate that this agent inhibits androstenediol-dependent LNCaP cell tumor growth. In addition, HE3235 may potentiate chemotherapeutic agents by down-regulating ABCG2, the gene encoding the multi-drug resistant (MDR) protein MDR2.

Anectine

(Other name for: succinylcholine chloride)

anetholtrithion

A substituted dithiolthione and analog of chemopreventive agent oltipraz. Anethole trithione is a bile secretion-stimulating drug that restores salivation and relieves the discomfort of dry mouth in chemotherapy-induced xerostomia. In addition, this agent has exhibited chemopreventive properties. The mechanism of action for the chemopreventive and xerostomia properties have not been fully elucidated.

anetumab ravtansine

A fully human IgG1 monoclonal antibody directed against the cell surface glycoprotein mesothelin and conjugated to the maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody moiety of anetumab ravtansine targets and binds to the tumor associated antigen mesothelin; upon internalization, the DM4 moiety binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of mesothelin-expressing tumor cells. Mesothelin is overexpressed on all mesotheliomas as well as many ovarian and pancreatic cancers while minimally expressed on normal tissue.

Aneustat

(Other name for: multifunctional/multitargeted anticancer agent OMN54)

ANF-Rho

(Other name for: pegfilgrastim anti-neutropenic factor)

Ang2/VEGF-binding peptides-antibody fusion protein CVX-241

A fusion protein containing angiopoietin-2 (Ang2) and vascular endothelial growth factor (VEGF) derived peptides covalently attached, via a proprietary diketone linker, to a proprietary humanized catalytic aldolase monoclonal antibody, with potential antiangiogenic and antineoplastic activities. The Ang2/VEGF peptide moieties of Ang2/VEGF-binding peptides-antibody fusion protein CVX-241 bind to Ang2 and VEGF receptors, which may inhibit tumor angiogenesis and tumor cell proliferation. The proprietary humanized catalytic IgG1 monoclonal aldolase antibody contains reactive lysine residues in its binding sites, which react covalently with compounds having a diketone function; the Ang2 and VEGFR peptide moieties are then covalently attached to the diketone linkers via a proprietary spacer. Both VEGF and Ang2 are upregulated in a variety of cancer cell types and play a crucial role in angiogenesis. This agent possesses an enhanced half-life compared to the naked peptides.

Angelica sinensis root extract

An herbal extract derived from the root of the plant Angelica sinensis with possible antiinflammatory, antispasmodic, vasodilatory, estrogenic, and antitumor activities. Angelica sinensis contains volatile oils, including safrole, isosafrole, and n-butylphthalide; coumarin derivatives, including psoralens, bergapten, osthol, imperatorin, and oxypeucedanin; and ferulic acid. The coumarin derivatives in this agent may vasodilate and relax smooth muscle and may exhibit additive anticoagulant effects. Ferulic acid, a phenolic phytochemical present in plant cell walls, may neutralize free radicals such as reactive oxygen species. In addition, Angelica sinensis extract has been shown to inhibit the growth and induce apoptosis of glioblastoma mutltiforme brain tumor cells through p53-dependent and p53-independent pathways.

Angiocept

(Other name for: pegdinetanib)

angiogenesis inhibitor JI-101

An orally active inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor beta (PDGFRb), and the ephrin B4 receptor B4 (EphB4) with potential antiangiogenic and antineoplastic activities. Angiogenesis inhibitor JI-101 binds to and inhibits VEGFR2, PDGFRb and EphB4, which may inhibit tumor angiogenesis and, so, cellular proliferation in tumor cells overexpressing VEGFR2, PDGFRb and EphB4. The receptor tyrosine kinases VEGFR2, PDGFRb and EphB4 may be overexpressed in a number of different cancer cell types and may play crucial roles in tumor angiogenesis.

angiopoietin-2-specific fusion protein PF-04856884

A humanized monoclonal antibody fused to two peptides that bind to angiopoietin 2 (Ang2; ANGPT2), with potential anti-angiogenic and antineoplastic activities. Upon intravenous administration, Ang2-targeting PF-04856884 CovX body specifically binds to Ang2 and prevents the binding of Ang2 to its receptor Tie2 expressed on endothelial cells. This inhibits Tie2-mediated signaling, prevents angiogenesis and inhibits tumor cell proliferation. Ang2, a proangiogenic cytokine and ligand for the Tie2 receptor, plays a key role in the regulation of tumor angiogenesis and tumor cell proliferation; its expression is upregulated by tumor endothelial cells.

angiostatin

Angiostatin (388, ~40 kDa) is encoded by the human PLG gene. This protein fragment is involved in the inhibition of blood vessel formation.

Angiozyme

(Other name for: anti-FLT-1 ribozyme)

anguidine

A trichothecene mycotoxin and potent teratogen. Anguidine inhibits initiation of protein synthesis, resulting in the death of rapidly proliferating cells. Anguidine also has been shown to both potentiate and protect against the cytotoxic effects of other drugs.

anhydrous enol-oxaloacetate

The anhydrous form of enol-oxaloacetate, a small molecule blood glutamate scavenger, that can be used to lower glutamate plasma levels, and has potential neuroprotective activity. Upon administration, enol-oxaloacetate targets and binds to glutamate in the bloodstream. This lowers glutamate plasma levels and lowers the free glutamate available to be picked up by cells, such as tumor brain cells, thereby preventing glutamate metabolism and glutamate-mediated signaling. This prevents the proliferation of rapidly growing cells, such as brain tumor cells. And by lowering glutamate plasma levels, a molecular imbalance is formed and glutamate is excreted across the blood-brain barrier, resulting in lower free brain glutamate. This may help protect the brain from excitotoxicity in conditions where there is a surge of glutamate production, such as traumatic brain injury, thereby protecting neuronal cells. Glutamate, a non-essential amino acid and the major excitatory neurotransmitter in the central nervous system (CNS), provides energy and generates building blocks for the production of macromolecules, which are needed for cellular growth and survival.

anhydrovinblastine

A semisynthetic derivative of the vinca alkaloid vinblastine, with potential antineoplastic activity. Like vinblastine, anhydrovinblastine targets and binds to tubulin and inhibits microtubule formation, resulting in disruption of mitotic spindle assembly and causing tumor cell cycle arrest in the M phase.

anidulafungin

A cyclic lipopeptide echinocandin derivative with antifungal activity. Anidulafungin inhibits 1,3 beta-D-glucan synthase, an enzyme involved in fungal cell wall synthesis, resulting in cell lysis and death. This agent is active against Candida species and Aspergillus.

aniline mustard

An alkylating mustard with antineoplastic activity. Aniline mustard forms covalent linkages with nucleophilic centers, resulting in depurination, base miscoding and strand scission, and crosslinking of DNA strands, all of which contribute to its cytotoxicity.

Anktiva

(Other name for: nogapendekin alfa inbakicept-pmln)

annamycin liposomal

A liposome-encapsulated form of the semi-synthetic doxorubicin analogue annamycin with antineoplastic activity. Annamycin intercalates into DNA and inhibits topoisomerase II, resulting in the inhibition of DNA replication and repair and RNA and protein synthesis. This agent circumvents multidrug-resistance (MDR) transporters, including P-glycoprotein (P-gp). Liposomal annamycin is less toxic and shows improved antitumor activity compared to annamycin.

Annonaceous acetogenins

A family of naturally occurring polyketides that consist of C32 or C34 long chain fatty acids and combined with a propan-2-ol unit at C-2 to form a gamma-lactone, which are isolated from various species of the plant family Annonaceae, with potential antineoplastic and antimicrobial activity. Annonaceous acetogenins bind to the ubiquinone catalytic site(s) within the mitochondrial NADH:ubiquinone oxidoreductase (complex I), and block the electron transport chain in mitochondria. In addition, the acetogenins bind to and block the activity of ubiquinone-linked NADH oxidase, an enzyme overexpressed in the plasma membranes of cancer cells. This inhibits adenosine triphosphate (ATP) production, decreases intracellular ATP levels, and induces tumor cell apoptosis. Compared to normal cells, cancer cells have higher ATP demands. The Annonaceous acetogenins also inhibit microbial glucose dehydrogenase 6.

anpocogin

An 85-amino acid recombinant peptide derived from protein c2 of the hemophagocytic hookworm Ancylostoma caninum (a common canine parasite) with anticoagulant activity. Anpocogin binds to circulating activated factor X (FXa) or zymogen factor X (FX) to form a binary complex which subsequently binds to and inhibits membrane-bound activated factor VII/tissue factor complex (FVIIa/TF). When administered prophylactically, this agent may reduce the incidence of deep venous thrombosis without hemostatic compromise. Because rNAPc2 inhibits the formation of the FVIIa/TF protease complex, which may play a role in the cellular signaling of both metastatic and angiogenic processes, it may impede tumor progression.

Ansaid

(Other name for: flurbiprofen)

anselamimab

A chimeric monoclonal antibody specifically targeting human immunoglobulin light chain (LC)-related fibrils, which may potentially be used in the treatment of light chain-associated (AL) amyloidosis. Upon administration, anselamimab targets and binds to the amyloid-related, conformational epitope on LC-related fibrils. This inhibits fibrillogenesis, induces an Fc-mediated cellular inflammatory response, increases degradation and elimination of AL amyloidomas, and prevents systemic LC-associated amyloid deposits. In AL amyloidosis the amyloid fibrils are composed of immunoglobulin light chain fragments.

Antabuse

(Other name for: disulfiram)

anthocyanin-rich corn extract

A corn-based, water-soluble extract rich in the polyphenol anthocyanin, with potential antioxidant, anti-inflammatory and chemoprotective activities. Upon administration of the anthocyanin-rich corn extract, the anthocyanins scavenge reactive oxygen species (ROS), which protects healthy cells from radiation-induced oxidative stress and DNA damage. In addition, anthocyanins modulate the expression of various genes and proteins involved in inflammation, tumor cell proliferation, angiogenesis, tumor cell invasion and differentiation. This agent also chelates metals and induces the expression of enzymes involved in Phase II antioxidant and detoxification pathways, which may further protect cells against oxidative stress induced by toxins and carcinogens.

anti c-KIT antibody-drug conjugate LOP628

An antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody against the stem cell factor receptor c-Kit (SCFR) and conjugated, via a non-cleavable linker, to the cytotoxic agent maytansine, with potential antineoplastic activity. The monoclonal antibody moiety of anti c-KIT ADC LOP628 targets and binds to the cell surface antigen c-Kit. After antibody-antigen interaction followed by internalization, the maytansine moiety binds to tubulin, inhibits microtubule assembly, and induces microtubule disassembly. This leads to a disruption of mitosis and the inhibition of cell proliferation in cancer cells expressing c-Kit. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.

anti LAG-3 monoclonal antibody HLX26

A recombinant monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody HLX26 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti PD1/IL-15 fusion protein SAR445877

A fusion protein composed of an antibody moiety targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a mutein of the immunostimulatory cytokine interleukin-15 (IL-15), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD1/IL-15 fusion protein SAR445877, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. The IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the tumor microenvironment (TME), and induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. The IL-15 mutein form lowers the systemic toxicity of IL-15.

anti-4-1BB Fab/TriCD40L fusion protein IMB071703

A bi-functional fusion protein consisting of a monovalent Fab fragment directed against 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) fused to a CD40 ligand (CD40L; CD154; TRAP; TNFSF5) trimer, triCD40L, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-4-1BB Fab/triCD40L fusion protein IMB071703 selectively targets and binds to both 4-1BB expressed on T cells and natural killer (NK) cells, and CD40 expressed on antigen-presenting cells (APCs), including dendritic cells (DC), B cells, T cells, and NKs. The trimeric binding of CD40L to CD40 (tumor necrosis factor receptor superfamily member 5; TNFRSF5) induces CD40 trimerization and crosslinking, activates CD40, increases CD40-mediated signaling and specifically induces proliferation and activation of DCs. The CD40 crosslinking leads to 4-1BB receptor clustering, and the Fab fragment binding to 4-1BB activates 4-1BB-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as NK-mediated tumor cell killing in the tumor microenvironment (TME). 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity, and T-cell memory formation. CD40, a costimulatory cell surface receptor that belongs to the TNF receptor family, plays a key role in DC maturation, and activation of antigen-specific T cells.

anti-4-1BB/5T4 bispecific Aantibody ALG.APV-527

A human bispecific antibody composed of a single-chain variable fragment (scFv) domain targeting the immune co-stimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) and a scFv domain targeting the tumor associated antigen (TAA) 5T4 (trophoblast glycoprotein; TPBG), that are linked through a mutated and silenced immunoglobulin G (IgG)-Fc domain, with potential immunomodulatory and antineoplastic activities. Upon administration of anti-4-1BB/5T4 bispecific antibody ALG.APV-527, the anti-5T4-specific scFv domain of ALG.APV-527 targets and binds to 5T4 expressed on tumor cells and the anti-4-1BB-specific scFv domain targets and binds to 4-1BB expressed on certain immune cells, such as T cells and natural killer cells (NK) cells within the tumor microenvironment (TME). This crosslinks T cells and tumor cells and allows for conditional 4-1BB activation, which stimulates the activation and proliferation of NKs and cytotoxic T lymphocytes (CTLs) in the TME leading to an anti-tumor immune response against the 5T4-expressing tumor cells. 5T4 is expressed on many different tumor cell types, including tumor-initiating cells, but expressed at low levels or not at all in normal tissue. ALG.APV-527 minimizes systemic immune activation and allows for tumor-specific responses that are localized to 5T4-positive tumors.

anti-4-1BB/anti-EGFR bispecific antibody HLX35

A recombinant human bispecific antibody targeting both the tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-EGFR/anti-4-1BB bispecific antibody HLX35 simultaneously targets and binds to the extracellular domain of EGFR, which is expressed on a variety of tumor cells and 4-1BB, which is expressed on activated T lymphocytes, natural killer (NK) cells and NK-T cells. This crosslinks EGFR-expressing tumor cells and 4-1BB-expressing T cells. The binding to EGFR inactivates EGFR and prevents EGFR-mediated signaling. Through 4-1BB binding, HLX35 acts as a conditional 4-1BB agonist, resulting in cytotoxic T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. It also activates memory T cells, NK cells and dendritic cells (DCs) in the tumor microenvironment (TME). This activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated lysis in EGFR-expressing tumor cells. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. EGFR, belonging to the receptor tyrosine kinases family and upregulated or mutated in a variety of tumor cell types, plays a key role in tumor cell proliferation.

anti-4-1BB/PD-L1 bispecific antibody BH3120

A heterodimeric immunoglobulin (IgG)-like bispecific antibody, with biased binding affinities, targeting human programmed death-ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-4-1BB/PD-L1 bispecific antibody BH3120 simultaneously targets and binds with its anti-4-1BB arm and with moderate affinity to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and, with its anti-PD-L1 arm with high affinity to PD-L1, which is expressed on tumor cells. Upon PD-L1 binding and PD-L1-mediated cross-linking, the 4-1BB activation signal is induced and BH3120 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, BH3120 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-5T4 antibody-drug conjugate ASN004

An antibody-drug conjugate (ADC) composed of an antibody directed against 5T4 and conjugated, via a non-cleavable linker, to a proprietary polymer carrying multiple auristatin analog molecules via a cleavable linker, with potential antineoplastic activity. Upon administration, the antibody moiety of ASN004 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and cleavage within the tumor cell cytosol, free auristatin analog molecules binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

anti-5T4 antibody-drug conjugate PF-06263507

An antibody-drug conjugate composed of an antibody directed against 5T4 and conjugated, via the stable linker maleimidocaproyl (mc), to the microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. Upon administration, the antibody moiety of PF-06263507 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAF binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

anti-5T4 antibody-drug conjugate SYD1875

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the oncofetal antigen 5T4 and site-specifically conjugated to a duocarmycin-based linker-drug valine-citrulline-seco-DUocarmycin-hydroxyBenzamide-Azaindole (vc-seco-DUBA), with potential antineoplastic activity. Upon administration, the antibody moiety of SYD1875 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and cleavage within the tumor cell by proteases, the free and activated duocarmycin payload binds to the minor groove of DNA and alkylates adenine at the N3 position, which eventually leads to tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

anti-5T4 CAR-NK cells

A preparation of allogeneic natural killer cells (NKs) expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) oncofetal trophoblast glycoprotein (5T4; TPBG; Wnt-activated inhibitory factor 1 or WAIF1), with potential immunomodulating and antineoplastic activities. Upon transfusion, the anti-5T4 CAR-NK cells recognize, bind to and induce selective cytotoxicity in 5T4-expressing tumor cells. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

anti-5T4/D-2102 antibody-drug conjugate ACR246

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the oncofetal antigen 5T4 and site-specifically conjugated, via a cleavable linker, to the cell penetrating cytotoxic agent and DNA topoisomerase I inhibitor D-2102, with potential antineoplastic activity. Upon administration of anti-5T4/D-2102 ADC ACR246, the anti-5T4 antibody moiety of ACR246 selectively binds to cells expressing 5T4. After internalization and cleavage within the tumor cell cytosol, the topoisomerase I inhibitor D-2102 is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in DNA damage, cell cycle arrest and apoptosis in tumor cells overexpressing 5T4. In addition, ACR246 induces a bystander effect, thereby killing neighboring tumor cells in the tumor environment (TME). 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types while its expression is limited in normal adult tissues; its expression is correlated with increased invasiveness.

anti-5T4/exatecan antibody-drug conjugate TUB-030

An antibody-drug conjugate (ADC) composed of a Fc-silenced, humanized, immunoglobulin G1 (IgG1) monoclonal antibody directed against the oncofetal antigen 5T4 and site-specifically conjugated, via a cleavable linker, to the cytotoxic agent and DNA topoisomerase I inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-5T4/exatecan ADC TUB-030, the anti-5T4 antibody moiety selectively targets and binds to cells expressing 5T4. After internalization and cleavage within the tumor cell, exatecan is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in DNA damage, cell cycle arrest and apoptosis in tumor cells overexpressing 5T4. In addition, TUB-030 induces a bystander effect, thereby killing neighboring tumor cells that don't necessarily express 5T4 in the tumor environment (TME). 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types while its expression is limited in normal adult tissues; its expression is correlated with increased invasiveness.

anti-5T4/MMAE antibody-drug conjugate XB010

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the oncofetal antigen 5T4 conjugated to the auristatin derivative and microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-5T4/MMAE ADC XB010, the anti-5T4 antibody moiety selectively binds to tumor cells expressing 5T4. Upon binding and internalization, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in 5T4-expressing tumor cells. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types while its expression is limited in normal adult tissues; its expression is correlated with increased invasiveness.

anti-A33 monoclonal antibody KRN330

A recombinant fully human monoclonal antibody directed against the human A33 antigen, with potential immunomodulatory and antineoplastic activity. Anti-A33 monoclonal antibody KRN330 recognizes and binds to the human A33 antigen, which may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against A33-positive colorectal cancers. A33 antigen, a 43 kDa transmembrane glycoprotein of the immunoglobulin superfamily, is highly and homogenously expressed in 95% of colorectal cancer cancers with only restricted expression in normal colonic mucosa and small bowel epithelia.

anti-A5B1 integrin monoclonal antibody PF-04605412

A monoclonal antibody directed against the human alpha5beta1 integrin with potential antiangiogenic and antineoplastic activities. Anti-alpha5beta1 integrin monoclonal antibody PF-04605412 selectively binds to alpha5beta1 integrin, preventing the binding of integrin ligands. This may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in alpha5beta1-expressing tumor cells. Alpha5beta1 integrin, a cell adhesion and signaling receptor, is often overexpressed on the surface of tumor vessel endothelial cells and plays a crucial role in endothelial cell adhesion and migration.

anti-ACTR/4-1BB/CD3zeta-viral vector-transduced autologous T lymphocytes ACTR087

Autologous T lymphocytes that are genetically modified and transfected with a viral vector expressing the ACTR gene, a proprietary gene encoding for an antibody-coupled T-cell receptor (ATCR), with potential antineoplastic activity. The ACTR contains the extracellular Fc receptor CD16 domain, normally found on certain immune cells, such as natural killer (NK) cells, coupled to the co-immunostimulatory signaling domain 4-1BB, normally expressed on T cells, and linked to the intracellular CD3 zeta domain (CD3z), which is needed for TCR signaling. Upon reintroduction into the patient and co-administration of a cancer-specific antibody, the co-administered antibody targets and binds to the tumor-associated antigen (TAA) expressed on the tumor cell. In turn, this induces the activation of the ACTR087 cells and destruction of the tumor cells by a) releasing cytotoxins that directly kill cancer cells; b) releasing cytokines that trigger an immune response and recruit other immune-mediated killer cells to kill the tumor cells; b) targeting and killing adjacent tumor cells that are not bound to the antibody; c) inducing T-cell proliferation and thereby further enhancing the T-cell mediated tumor cell attack. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it enhances the survival and persistence of T lymphocytes. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the TAA.

anti-ADAM9 ADC IMGC936

An immunoconjugate consisting of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) disintegrin and metalloproteinase domain-containing protein 9 (ADAM9) that is site-specifically conjugated, via a stable tri-peptide cleavable linker, to DM21, a cytotoxic maytansinoid microtubule-disrupting payload, with potential antineoplastic activity. Upon administration of anti-ADAM9 ADC IMGC936, the anti-ADAM9 monoclonal antibody moiety targets and binds to ADAM9 on tumor cells. Upon internalization, the maytansinoid moiety is released, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in the inhibition of cell division and cell growth of tumor cells. ADAM9, belonging to the disintegrin and metalloproteinase (ADAM) family of proteases, plays a key role in cytokine and growth factor shedding and cell migration. It is overexpressed on multiple solid tumors while minimally expressed on normal tissue. Dysregulation of ADAM9 has been implicated in tumor progression, migration and metastasis. Its expression is correlated with poor prognosis. The antibody is engineered to include a YTE mutation to improve pharmacokinetics.

anti-AG7 antibody drug conjugate AbGn-107

An antibody drug conjugate (ADC) composed of a monoclonal antibody that targets the tumor-associated antigen (TAA) AG7 and is linked, through a hydrophilic, self-immolative linker, to a proprietary cytotoxic payload, with potential antineoplastic activity. Upon administration of AbGn-107 the antibody moiety targets and binds to the AG7 antigen expressed on a variety of cancer cells. Upon binding and internalization, the linker is cleaved and the payload is released, binds to tubulin, inhibits tubulin polymerization and kills the AG7-expressing tumor cells.

anti-AGS-16 monoclonal antibody AGS-16M18

A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-16 with potential antineoplastic activity. Anti-AGS-16 monoclonal antibody AGS-16M18 selectively binds to AGS-16, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells expressing AGS-16. While normally expressed at low levels in the proximal tubules of the kidney, AGS-16 has been found to be overexpressed in more than 95% of kidney and 40% of liver neoplasms.

anti-AGS-5 antibody-drug conjugate ASG-5ME

An antibody drug conjugate (ADC) containing the fully human IgG2k monoclonal antibody targeting an epitope of SLC44A4 (AGS-5) linked, via a valine-citrulline (vc) maleimidocaproyl (mc) linker, to the antimicrotubulin drug monomethyl auristatin E (MMAE), with potential antineoplastic activity. The monoclonal antibody moiety of ASG-5ME selectively binds to AGS-5. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis. SLC44A4, potentially a sodium-dependent transmembrane transport protein, is overexpressed on more than 80 percent of samples derived from patients with pancreatic, prostate and gastric cancers.

anti-AGS-8 monoclonal antibody AGS-8M4

A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-8 with potential antineoplastic activity. Anti-AGS-8 monoclonal antibody AGS-8M4 selectively binds to AGS-8, triggering complement-dependent cell lysis and antibody-dependent cell-mediated cytotoxicity in tumor cells expressing AGS-8. While normally expressed at low levels in the heart in response to ischemia, AGS-8 has been found to be expressed in more than 70% of ovarian neoplasms.

anti-ALK-1 monoclonal antibody GT90001

A human immunoglobulin G2 (IgG2) monoclonal antibody against activin receptor-like kinase-1 (ALK-1; ALK1), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-ALK-1 monoclonal antibody GT90001 targets and binds to ALK-1, and prevents ALK-1 activation by its ligands bone morphogenetic protein 9 (BMP) 9 and BMP10. This prevents ALK-1-mediated endothelial cell signaling and the activation of transforming growth factor-beta (TGF-beta)/TGF-beta receptor I (ALK-5) signaling. This inhibits tumor blood vessel growth, reduces blood flow and angiogenesis and leads to an inhibition of tumor cell proliferation and modulation of the tumor microenvironment (TME). ALK-1 is a type I cell surface receptor and plays a key role in angiogenesis.

anti-ALPP/ALPPL2/MMAE ADC SGN-ALPV

An antibody-drug conjugate (ADC) composed of h12F3, a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the two oncofetal phosphatases alkaline phosphatase, placental type (ALPP; placental alkaline phosphatase; PLAP), and alkaline phosphatase, placental like 2 (ALPPL2; alkaline phosphatase, germ cell) conjugated, via a protease-cleavable peptide linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-ALPP/ALPPL2/MMAE ADC SGN-ALPV targets and binds to either ALPP or ALPPL2 or ALPP/ALPPL2 dimer on the surface of tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in ALPP and/or ALPPL2-expressing tumor cells. In addition, SGN-ALPV mediates antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). ALPP and ALPPL2, mainly expressed in placenta and testis, form homo- and heterodimers and play key roles in nucleotide recycling. They are overexpressed on certain tumor cell types while normal tissue expression of ALPP and ALPPL2 is restricted to placenta and reproductive tissue.

anti-AMHR2 monoclonal antibody GM102

An engineered, humanized, low fucose monoclonal antibody against mullerian hormone receptor II (Müllerian Inhibiting Substance Receptor II; AMHR2; AMHRII), with potential antineoplastic activity. Upon administration, anti-AMHR2 monoclonal antibody GM102 targets, binds to and inhibits AMHR2 and its downstream signaling pathways. GM102 primarily induces antibody dependent cellular cytotoxicity (ADCC) directed against AMHR2-expressing tumor cells through binding to CD16 (Fc-gammaRIIIa) that is present on immune effector cells. Decreased antibody fucosylation increases its affinity for binding to CD16 and ultimately enhances ADCC. AMHR2 is expressed in a subset of gynecological cancers.

anti-androgen siRNA SXL01

A small-interfering RNA (siRNA) directed against androgen receptor (AR), with potential antineoplastic activity. Upon administration of anti-AR siRNA SXL01, the siRNAs bind to AR mRNAs, which may result in the inhibition of translation of the AR protein. By preventing AR expression, AR-mediated signaling is decreased, which leads to growth inhibition for AR-expressing tumor cells. AR, overexpressed in a variety of cancers, is involved in cellular proliferation and survival.

anti-ANG2 monoclonal antibody MEDI-3617

A fully human IgG1 monoclonal antibody against angiopoietin 2 (ANG2), with potential antiangiogenic activity. Anti-ANG2 monoclonal antibody MEDI-3617 binds to Ang2 and interferes with the interaction between Ang2 and its receptor TEK tyrosine kinase (Tie2), thereby resulting in the disruption of vascular remodeling. This may inhibit angiogenesis and may eventually lead to an inhibition of tumor cell proliferation.

anti-angiopoietin monoclonal antibody AMG 780

An immunoglobulin (Ig) G2 monoclonal antibody targeting the proangiogenic cytokines angiopoietin 1 (Ang1) and 2 (Ang2), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-angiopoietin monoclonal antibody AMG 780 binds to Ang1 and Ang2. This prevents the binding of the angiopoietin ligands to their receptor Tie2 (TEK), an endothelial cell-specific receptor tyrosine kinase. This prevents Tie2-mediated signaling and results in an inhibition of Tie2-expressing, tumor-stimulated endothelial cell proliferation, which prevents angiogenesis and inhibits tumor cell proliferation.

anti-APRIL monoclonal antibody BION-1301

A humanized monoclonal antibody targeting a proliferation-inducing ligand (APRIL; tumor necrosis factor ligand superfamily member 13; TNFSF13), with potential antineoplastic and immune checkpoint inhibitory activities. Following administration, anti-APRIL monoclonal antibody BION-1301 binds to APRIL and inhibits its binding to both of its receptors, B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and transmembrane activator and CAML Interactor (TACI; tumor necrosis factor receptor superfamily member 13B; TNFRSF13B). This inhibits the activation of both BCMA and TACI, and their downstream signaling pathways, which prevents tumor growth, tumor cell adhesion to bone marrow cells and immune suppression. Additionally, BION-1301 may reduce APRIL-induced drug resistance which occurs in some tumors. APRIL, an extracellular protein and member of the tumor necrosis factor ligand superfamily (TNFSF), is expressed by bone marrow plasma cells and myeloid cells, and overexpressed in multiple myeloma (MM), chronic lymphocytic leukemia (CLL), and colorectal carcinoma. APRIL induces immune suppression and tumor progression through the activation of BCMA- and TACI-dependent signaling pathways.

anti-ASCT2 antibody-drug conjugate MEDI7247

An antibody-drug conjugate (ADC) consisting of a human monoclonal antibody against neutral amino acid transporter B(0) (ASCT2; SLC1A5) that is site-specifically conjugated, via a protease-cleavable linker, to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-ASCT2 ADC MEDI7247, the antibody moiety targets and binds to ASCT2 expressed on cancer cells. Upon antibody/antigen binding, internalization and linker cleavage, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of ASCT2-overexpressing tumor cells. ASCT2, a neutral amino acid transporter that mediates the uptake of glutamine, is overexpressed in a variety of cancer cell types.

anti-AXL monoclonal antibody-MMAE conjugate

An antibody-drug conjugate (ADC), consisting of a human monoclonal antibody directed against AXL receptor tyrosine kinase (AXL; UFO) and conjugated, through a protease-cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of HuMax-AXL-ADC binds to AXL, which is expressed on the surfaces of a variety of cancer cell types. Upon endocytosis and enzymatic cleavage, MMAE is released into the tumor cell cytosol, where it binds to tubulin and inhibits tubulin polymerization; this may result in G2/M phase arrest and apoptosis. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases and overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.

anti-B4 blocked ricin immunotoxin

An immunotoxin comprised of an anti-B4 (anti-CD19) murine monoclonal antibody linked to the modified plant-derived toxin blocked ricin. The antibody moiety of anti-B4 blocked ricin immunotoxin binds to B lymphocytes that express B4; after internalization of the immunotoxin by the B4-expressing B cell, the ricin moiety cleaves the N-glycosidic bond between the ribose and adenine base at position 4324 in the B lymphocyte 28S ribosomal RNA, resulting in ribosome inactivation, inhibition of protein synthesis, and cell death. Blocked ricin is ricin which has been chemically modified such that the lectin binding sites of the B chain (galactose-binding sites) have been blocked by covalent attachment of affinity ligands, leaving the ribosome-inactivating activity of the ricin A chain intact.

anti-B7-H3 antibody DS-5573a

An antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-B7-H3 antibody DS-5573a binds to the cell surface antigen B7-H3, thereby blocking B7-H3-mediated signaling. This abrogates the inhibitory effect on T-cell activation and may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate BAT8009

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) linked to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC BAT8009, the anti-B7-H3 antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate DB-1311

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) conjugated, via a cleavable linker, to the topoisomerase-1 inhibitor (TOP1i) P1021, with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC DB-1311, the anti-B7-H3 antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding, internalization and linker cleavage, P1021 is released, and inhibits DNA topoisomerase-1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate HS-20093

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the T-cell checkpoint ligand B7-homologue 3 (B7-H3, CD276) covalently linked to a topoisomerase inhibitor (TOPOi), with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC HS-20093, the anti-B7-H3 monoclonal antibody moiety targets and binds to B7-H3 expressed on tumor cells. Upon binding and internalization, the TOPOi is released, and inhibits DNA topoisomerase activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is an immunoregulatory protein overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate MGC026

An antibody-drug conjugate (ADC) composed of vobramitamab, a humanized monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), site-specifically conjugated, via a cleavable glycan-based linker, to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC MGC026, the anti-B7-H3 antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of B7-H3-expressing tumor cells. MGC026 also induces bystander killing activity. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells while its expression is limited on healthy cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate MHB088C

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) conjugated to an as of yet undisclosed topoisomerase-1 inhibitor via a cleavable linker, with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC MHB088C, the antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding, internalization and linker cleavage, the topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing B7-H3. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation, and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 antibody-drug conjugate YL201

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) site-specifically conjugated to an as of yet undisclosed topoisomerase-1 inhibitor via a tumor protease-cleavable linker, with potential antineoplastic activity. Upon administration of anti-B7-H3 ADC YL201, the antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding, internalization and linker cleavage, the topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing B7-H3. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation, and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H3 CAR T cells target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3 CAR T cells TAA06

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H3 CAR T cells TAA06 target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3/anti-EGFR bispecific antibody-drug conjugate IBI3001

An antibody-drug conjugate (ADC) composed of a bispecific antibody directed against the tumor associated antigens (TAAs) B7-homologue 3 (B7-H3, CD276) and human epidermal growth factor receptor (EGFR) that is site-specifically glycan-conjugated to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration, anti-B7-H3/anti-EGFR bispecific ADC IBI3001 targets and simultaneously binds to B7-H3 and EGFR expressed on tumor cells. This blocks EGFR activation by ligands and EGFR-mediated signaling. Upon binding, internalization and linker cleavage, exatecan is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis in B7-H3- and EGFR-expressing tumor cells. In addition, IBI3001 causes a bystander effect, thereby killing both EGFR- and B7-H3-positive cancer cells and EGFR- and B7-H3-negative cancer cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is an immunoregulatory protein and negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis. B7-H3 and EGFR are co-expressed in multiple solid tumors.

anti-B7-H3/CD28 bispecific antibody XmAb808

A bispecific antibody directed against the tumor-associated antigen (TAA) and immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and the co-stimulatory T-cell surface glycoprotein CD28, with potential immunostimulating and antineoplastic activities. Upon administration of anti-B7-H3/CD28 bispecific antibody XmAb808, this bispecific antibody binds to both B7-H3 on certain tumor cells and CD28 on cytotoxic T-lymphocytes (CTLs). This activates and redirects CTLs to B7-H3-expressing tumor cells, which may result in the CTL-mediated cell death of B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H3/topoisomerase-1 inhibitor antibody-drug conjugate BGB-C354

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) conjugated to an as of yet undisclosed topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon administration of anti-B7-H3/topoisomerase-1 inhibitor ADC BGB-C354, the antibody moiety targets and binds to B7-H3-expressing tumor cells. Upon binding and internalization, the topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing B7-H3. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation, and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-B7-H4 antibody drug conjugate BG-C9074

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the T-cell checkpoint ligand B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) linked to an as of yet unknown cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-B7-H4 ADC BG-C9074, the anti-B7-H4 monoclonal antibody moiety targets and binds to B7-H4 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent exerts an as of yet unknown mechanism of action (MoA) causing apoptosis in B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and tumor-associated macrophages (TAMs). It negatively regulates T-cell immune responses.

anti-B7-H4 antibody-drug conjugate XMT-1660

An antibody-drug conjugate (ADC) composed of XMT-1604, a human immunoglobulin G1 (IgG1) monoclonal antibody directed against the T-cell checkpoint ligand B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1), site-specifically conjugated to six cytotoxic auristatin derivative auristatin F-HPA (AF-HPA; auristatin F-hydroxypropylamide) payloads per antibody, with potential antineoplastic activity. Upon administration of anti-B7-H4 ADC XMT-1660, the anti-B7-H4 monoclonal antibody moiety targets and binds to B7-H4 expressed on tumor cells. Upon binding, internalization and linker cleavage, membrane permeating AF-HPA is metabolically converted to membrane non-permeating auristatin F, which binds to tubulin and inhibits microtubule polymerization. This results in G2/M phase arrest and the apoptosis of B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and tumor-associated macrophages (TAMs). It negatively regulates T-cell immune responses. The metabolic conversion of membrane permeating AF-HPA to membrane non-permeating auristatin F results in a controlled bystander effect, and prevents or lessens neutropenia as an adverse effect of auristatin.

anti-B7-H4 monoclonal antibody

Any monoclonal antibody directed against the T-cell checkpoint ligand B7-H4 (B7H4; V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1).

anti-B7-H4 monoclonal antibody NC762

A humanized immunoglobulin G1 kappa (IgG1k) monoclonal antibody targeting B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-B7-H4 monoclonal antibody NC762 binds to B7-H4 on the surface of tumor cells. This may induce antibody-dependent cellular cytotoxicity (ADCC) against B7-H4-expressing tumor cells, which leads to the inhibition of tumor cell proliferation. In addition, the Fc region of NC762 contains three point mutations. This enhances its binding affinity for human FcgammaRIIIa receptors (CD16a) on natural killer (NK) cells, resulting in enhanced ADCC against B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses. However, the anti-tumor activity of NC762 is not dependent upon T cells.

Anti-B7-H4/ TOP1i Antibody-drug Conjugate AZD8205

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) linked to a topoisomerase-1 inhibitor (TOP1i; TOP-Ii), with potential antineoplastic activity. Upon administration, the anti-B7-H4 monoclonal antibody moiety of ADC AZD8205 targets and binds to B7-H4 expressed on tumor cells. Upon binding and internalization, the TOP1i moiety is released, binds to TOP1 and stabilizes cleaved DNA-TOP1 complexes. This prevents DNA re-ligation, induces irreversible DNA strand breaks, prevents DNA repair, and leads to cycle arrest and apoptosis specifically in tumor cells expressing B7-H4. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and tumor-associated macrophages. It negatively regulates T-cell immune responses.

anti-B7-H4/anti-4-1BB bispecific antibody ABL103

A T-cell engaging (TCE) bispecific antibody against both the tumor-associated antigen (TAA) B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-B7-H4/anti-4-1BB bispecific antibody ABL103 targets and binds to both B7-H4 expressed on the surface of tumor cells and 4-1BB expressed on immune cells, including activated T lymphocytes, natural killer (NK) cells and NK-T cells. This crosslinks B7-H4-expressing tumor cells and 4-1BB-expressing T cells, NK cells and NK-T-cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME) only when in the presence of B7-H4 expressing cells. This induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response against tumor cells, induces NK-mediated tumor cell killing, and suppresses the immunosuppressive activity of regulatory T cells (Tregs). In addition, the blockage of B7-H4 by ABL103 directly prevents B7-H4-mediated inhibition of T cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses. B7-H4 expression in normal tissues is quite limited. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-B7-H4/anti-4-1BB bispecific antibody CLN-418

An Fc-silenced bispecific antibody against both the tumor-associated antigen (TAA) B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-B7-H4/anti-4-1BB bispecific antibody CLN-418 targets and binds to both B7-H4 expressed on the surface of tumor cells and 4-1BB expressed on activated T lymphocytes, natural killer (NK) cells and NK-T cells. This crosslinks B7-H4-expressing tumor cells and 4-1BB-expressing T cells, NK cells and NK-T cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response against tumor cells, induces NK-mediated tumor cell killing, and suppresses the immunosuppressive activity of regulatory T cells (Tregs). B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-B7-H4/anti-CD3 bispecific antibody GEN1047

A bispecific monoclonal antibody against both B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H4/anti-CD3 bispecific antibody GEN1047 targets and binds to both B7-H4 on the surface of tumor cells and CD3 on T cells. This results in the cross-linking of tumor cells and T cells, and induces a cytotoxic T-lymphocyte (CTL) response against B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses.

anti-B7-H4/anti-CD3 bispecific antibody PF-07260437

A bispecific monoclonal antibody against both B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H4/anti-CD3 bispecific antibody PF-07260437 targets and binds to both B7-H4 on the surface of tumor cells and CD3 on T cells. This results in the cross-linking of tumor cells and T cells, and induces a cytotoxic T-lymphocyte (CTL) response against B7-H4-expressing tumor cells. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and negatively regulates T-cell immune responses.

anti-B7-H4/MMAE ADC LNCB74

An antibody-drug conjugate (ADC) composed of a human immunoglobulin (Ig) G1 kappa monoclonal antibody directed against the T-cell checkpoint ligand B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) conjugated, via a beta-glucuronidase-cleavable linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic and immunomodulating activities. Upon administration of anti-B7-H4/MMAE ADC LNCB74, the anti-B7-H4 antibody targets and binds to B7-H4 expressed on tumor cells. Upon binding and internalization, MMAE is released upon cleavage by the cancer-associated lysosomal enzyme beta-glucuronidase. MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. This induces cell death in B7-H4-expressing cancer cells. LNCB74 also induces a bystander effect, thereby further killing neighboring tumor cells upon uptake of MMAE and induces an immune-mediated cell death. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and tumor-associated macrophages (TAMs) while minimally expressed in normal, healthy tissues. It negatively regulates T-cell immune responses. LNCB74 contains a LALA-hG1 Fc region to minimize uptake and toxicity to immune cells, thereby further improving the safety profile.

anti-B7-H4/TOP1i antibody-drug conjugate GSK5733584

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against B7-H4 (V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1) linked, via a protease-cleavable linker, to a topoisomerase-1 inhibitor (TOP1i; TOP-Ii), with potential antineoplastic activity. Upon administration of anti-B7-H4/ TOP1i ADC GSK5733584, the anti-B7-H4 monoclonal antibody moiety targets and binds to B7-H4 expressed on tumor cells. Upon binding and internalization, the TOP1i moiety binds to TOP1 and stabilizes cleaved DNA-TOP1 complexes. This prevents DNA re-ligation, induces irreversible DNA strand breaks, prevents DNA repair, and leads to cycle arrest and apoptosis specifically in tumor cells expressing B7-H4. B7-H4, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and tumor-associated macrophages. It negatively regulates T-cell immune responses.

anti-B7-H6/Anti-CD3 bispecific antibody BI 765049

An immunoglobulin G (IgG)-like bispecific T-cell engaging antibody directed against both natural cytotoxicity triggering receptor 3 ligand 1 (NCR3LG1; B7-H6) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H6/anti-CD3 bispecific antibody BI 765049 targets and binds to both B7-H6 on tumor cells and CD3 on T cells. This results in the cross-linking of B7-H6-expressing tumor cells and T-cells, redirects cytotoxic T lymphocytes (CTLs) to B7-H6-expressing tumor cells, which leads to the CTL-mediated cell death of B7-H6-expressing tumor cells. B7-H6, a member of the B7 family of immune modulators, is expressed in a variety of tumor cell types while minimally or not expressed in normal tissues. It is a specific ligand for the natural killer (NK) cell activating receptor NKp30, and may modulate NK cell function in certain cancers.

anti-B7-H6/anti-CD3 bispecific antibody TGI-6

A bispecific antibody directed against both natural cytotoxicity triggering receptor 3 ligand 1 (NCR3LG1; B7-H6) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H6/anti-CD3 bispecific antibody TGI-6 targets and binds to both B7-H6 on tumor cells and CD3 on T cells. This results in the cross-linking of B7-H6-expressing tumor cells and T cells, redirects cytotoxic T lymphocytes (CTLs) to B7-H6-expressing tumor cells, which leads to the CTL-mediated cell death of B7-H6-expressing tumor cells. B7-H6, a member of the B7 family of immune modulators, is expressed in a variety of tumor cell types while minimally or not expressed in normal tissues. It is a specific ligand for the natural killer (NK) cell activating receptor NKp30, and may modulate NK cell function in certain cancers.

anti-B7H7 monoclonal antibody HBM1020

A recombinant human monoclonal antibody directed against HERV-H LTR-associating protein 2 (HHLA2; B7 homolog 7; B7H7), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-B7H7 monoclonal antibody HBM1020 binds to B7H7 and blocks the interaction between B7H7 and its receptors. This abrogates the B7H7-mediated inhibition of T-cell and nature killer (NK) cell activation, which may lead to enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response and NK cell cytotoxicity against cancer cells. B7H7, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and a negative regulator of T-cell and NK-cell activation.

anti-BAFFR monoclonal antibody ESG206

A monoclonal antibody that is directed against the tumor-associated antigen (TAA) B-cell activating factor receptor (BAFFR; tumor necrosis factor receptor superfamily member 13C; TNFRSF13C; BLyS receptor 3; BR3), with potential antineoplastic activity. Upon administration, anti-BAFFR monoclonal antibody ESG206 binds to and blocks BAFFR. This prevents BAFFR-mediated signaling and may kill BAFFR-expressing tumor cells. BAFFR, a protein belonging to the TNF receptor superfamily, is expressed on the surface of certain types of cancer cells, including B-cell acute lymphoblastic leukemia. It plays a key role in the regulation of peripheral B-cell survival.

anti-BCMA antibody SEA-BCMA

A humanized, afucosylated monoclonal antibody created using the proprietary, sugar-engineered antibody (SEA) platform and directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; TNFRSF17), with potential immunoadjuvant activity. Upon administration, the anti-BCMA antibody SEA-BCMA targets and binds to BCMA expressed on tumor cells. When administered with antibody-coupled T-cell receptor (ACTR)-expressing T cells, the ACTR-expressing T cells bind, with high affinity, to the anti-BCMA antibody SEA-BCMA. This activates the ACTR T -cells and the T cells induce specific cytotoxic T-lymphocyte (CTL)-mediated cytotoxicity toward BCMA-expressing tumor cells. BCMA, a cell surface protein and member of the tumor necrosis factor (TNF) receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.

anti-BCMA antibody-drug conjugate AMG 224

An antibody-drug conjugate (ADC) comprised of an anti-human B-cell maturation antigen (BCMA) immunoglobulin G1 (IgG1) antibody conjugated via the noncleavable linker 4-(N-maleimidomethyl) cyclohexane-1-carboxylate (MCC), to the cytotoxic maytansine-derivative, DM1, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of AMG 224 selectively binds to BCMA expressed on the surface of tumor cells. Upon internalization, the DM1 moiety binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting both cell division and proliferation of tumor cells that express BCMA. BCMA, a receptor for a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF)and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

anti-BCMA antibody-drug conjugate CC-99712

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA, TNFRSF17), linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-BCMA ADC CC-99712, the antibody moiety targets and binds to the cell surface antigen BCMA expressed on certain cancer cells. Upon binding and internalization, the cytotoxic agent is released and kills the BCMA-expressing cancer cells through an as of yet unknown mechanism of action. BCMA, a receptor for a proliferation-inducing ligand (APRIL; tumor necrosis factor ligand superfamily member 13; TNFSF13), and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma survival. It is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

anti-BCMA CAR-NK cells

A preparation of umbilical cord blood (CB)-derived natural killer cells (NKs) expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunomodulating and antineoplastic activities. Upon transfusion, the anti-BCMA CAR-NK cells recognize, bind to and induce selective cytotoxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival.

anti-BCMA SparX protein plus BCMA-directed anti-TAAG ARC T cells CART-ddBCMA

An immunotherapeutic combination agent composed of antigen receptor complex T cells (ARC-T cells) which contain a proprietary binding domain specific for a universal TAG instead of a single chain variable fragment (scFv) binding domain, and a tumor-targeting antigen protein, soluble protein antigen-receptor X-linker (sparX) protein, containing a TAG moiety fused to two B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) binding domains, with potential antineoplastic activities. Upon administration of the anti-BCMA sparX protein plus BCMA-directed ARC T-cells CART-ddBCMA, the sparX protein, with its two BCMA binding domains, specifically targets and binds to two BCMA expressed on tumor cells. In turn, the ARC-T cells, with their anti-TAG domain, target and bind to the TAG domain on the sparX protein. This directly links the ARC-T cells to the BCMA-expressing tumor cells, through the ARC-T cell- sparX -tumor cell complex formation, thereby causing direct tumor cell killing. BCMA, a tumor-associated antigen (TAA), is found on the surfaces of plasma cells and is overexpressed on a variety of tumor cell types. Compared to anti-BCMA CAR-T cells, CART-ddBCMA, containing ARC-T cells that are re-programmed in vivo by the TAG sparX protein, shows enhanced efficiency and an improved safety profile. As ARC-T activity is dependent on the sparX dose administered, the rate of tumor cell killing, and related toxicities are also dependent on the sparX dose administered.

anti-BCMA/alpha-amanitin antibody-drug conjugate HDP-101

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA, TNFRSF17) conjugated, via a cleavable linker, to the cytotoxic, RNA polymerase II inhibitor alpha-amanitin, with potential antineoplastic activity. Upon administration of anti-BCMA/alpha-amanitin ADC HDP-101, the antibody moiety targets and binds to the cell surface antigen BCMA expressed on certain cancer cells. Upon antibody/antigen binding, internalization and cleavage, the cytotoxic alpha-amanitin is released. Alpha-amanitin binds to and inhibits RNA polymerase II, prevents RNA synthesis, induces apoptosis, and inhibits the proliferation of BCMA-overexpressing tumor cells. BCMA, a receptor for a proliferation-inducing ligand (APRIL; tumor necrosis factor ligand superfamily member 13; TNFSF13), and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma survival; it is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

anti-BCMA/anti-CD3 bispecific antibody EMB-06

A tetravalent, bispecific antibody directed against both the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-BCMA/anti-CD3 bispecific antibody EMB-06 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, leading to CTL-mediated killing of BCMA-expressing tumor cells. BCMA, a receptor for a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. In EMB-06, the two antigen-binding fragments (Fabs) are fused directly in a crisscross orientation resulting in four active and independent antigen binding sites.

anti-BCMA/anti-CD3 bispecific antibody REGN5459

A human bispecific antibody directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and another directed against the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-BCMA/anti-CD3 bispecific antibody REGN5459 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, leading to CTL-mediated killing of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.

anti-BCMA/anti-CD3 bispecific antibody WVT078

A bispecific antibody directed against both the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-BCMA/anti-CD3 bispecific antibody WVT078 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, leading to CTL-mediated killing of BCMA-expressing tumor cells. BCMA, a receptor for a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

anti-BCMA/anti-CD3 T-cell engaging bispecific antibody ABBV-383

A T-cell engaging, human, bispecific, immunoglobulin G4 (IgG4) monoclonal antibody (T-BsAb) directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-BCMA/anti-CD3 T-cell engaging bispecific antibody ABBV-383 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA found on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. Binding to low-activating CD3 preferentially activates effector over regulatory T cells and stimulates minimum cytokine release.

anti-BCMA/anti-GPRC5D CAR T cells OriC321

A preparation of T lymphocytes engineered to express chimeric antigen receptor(s) (CAR) targeting the human tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and G-protein coupled receptor family C group 5 member D (GPRC5D) and fused to as of yet not fully elucidated co-stimulatory domains, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-BCMA/anti-GPRC5D CAR T cells OriC321 specifically and simultaneously target and bind to tumor cells expressing BCMA and/or GPRC5D. This induces selective toxicity in tumor cells that express BCMA and/or GPRC5D. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation.

anti-BCMA/anti-GPRC5D CAR-T cells BMS-986453

A preparation of T lymphocytes engineered to express chimeric antigen receptor(s) (CAR) targeting the human tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and G-protein coupled receptor family C group 5 member D (GPRC5D), with potential immunostimulating and antineoplastic activities. Upon administration, anti-BCMA/anti-GPRC5D CAR-T cells BMS-986453 specifically and simultaneously target and bind to tumor cells expressing BCMA and/or GPRC5D. This induces selective toxicity in tumor cells that express BCMA and/or GPRC5D. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation.

anti-BCMA/CD38/CD3 trispecific antibody ISB 2001

A T-cell engager and trispecific antibody targeting the two tumor-associated antigens (TAAs) CD38 and human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-BCMA/CD38/CD3 trispecific antibody ISB 2001 simultaneously targets and binds to CD38 and BCMA expressed on tumor cells, and CD3 expressed on T cells. The resulting cross-linkage activates and redirects CTLs to CD38- and BCMA-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. Targeting both BCMA and CD38 increases binding and specificity to tumor cells, such as myeloma cells, and specifically increases death in tumors cells co-expressing CD38 and BCMA.

anti-BCMA/GPRC5D/CD3 trispecific antibody JNJ-79635322

A T-cell engager and trispecific antibody targeting the two tumor-associated antigens (TAAs) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and human G-protein coupled receptor family C group 5 member D (GPRC5D), and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-BCMA/GPRC5D/CD3 trispecific antibody JNJ-79635322 simultaneously targets and binds to BCMA and GPRC5D expressed on tumor cells, and CD3 expressed on T cells. The resulting cross-linkage activates and redirects CTLs to GPRC5D- and BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. GPRC5D is overexpressed on certain tumors, including multiple myeloma, while minimally expressed on normal, healthy cells, and plays a key role in tumor cell proliferation.

anti-BCMA/GPRC5D/CD3 trispecific antibody MBS314

A T-cell engager and trispecific antibody targeting the two tumor-associated antigens (TAAs) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and human G-protein coupled receptor family C group 5 member D (GPRC5D), and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-BCMA/GPRC5D/CD3 trispecific antibody MBS314 simultaneously targets and binds to BCMA and GPRC5D expressed on tumor cells, and CD3 expressed on T cells. The resulting cross-linkage activates and redirects CTLs to GPRC5D- and BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. GPRC5D is overexpressed on certain tumors, including multiple myeloma, while minimally expressed on normal, healthy cells, and plays a key role in tumor cell proliferation.

anti-BCMA/GPRC5D/CD3 trispecific antibody SIM0500

A humanized T-cell engager and trispecific antibody targeting the two tumor-associated antigens (TAAs) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and human G-protein coupled receptor family C group 5 member D (GPRC5D), and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-BCMA/GPRC5D/CD3 trispecific antibody SIM0500 simultaneously targets and binds to BCMA and GPRC5D expressed on tumor cells, and CD3 expressed on T cells. The resulting cross-linkage activates and redirects CTLs to GPRC5D- and BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival. GPRC5D is overexpressed on certain tumors, including multiple myeloma, while minimally expressed on normal, healthy cells, and plays a key role in tumor cell proliferation.

anti-BCMA/PBD ADC MEDI2228

An antibody-drug conjugate (ADC) consisting of a fully human monoclonal antibody against the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA, TNFRSF17) that is site-specifically conjugated, via a protease-cleavable linker, to a cytotoxic, DNA minor groove crosslinking agent and pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-BCMA/PBD ADC MEDI2228, the antibody moiety targets the cell surface antigen BCMA expressed on certain cancer cells. Upon antibody/antigen binding, internalization and lysosome-mediated cleavage, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of BCMA-overexpressing tumor cells. BCMA, a receptor for a proliferation-inducing ligand (APRIL; tumor necrosis factor ligand superfamily member 13; TNFSF13), and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma survival; it is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

anti-BTLA monoclonal antibody HFB200603

A monoclonal antibody directed against B- and T-lymphocyte attenuator (BTLA), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, anti-BTLA monoclonal antibody HFB200603 targets and binds to BTLA. This prevents BTLA-mediated inhibition of T-cell activation and induces the production of inflammatory cytokines in the tumor microenvironment (TME), leading to antigen specific T-cell proliferation and activation of a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. BTLA, an immunoglobulin (Ig) receptor family member expressed on activated T and B lymphocytes, subsets of dendritic cells (DCs), macrophages, and nature killer (NK) cells, is an immune checkpoint involved in suppressing immune responses. It mediates inhibition of human tumor-specific CTLs upon engagement by tumor expressed herpesvirus-entry mediator (HVEM).

anti-BTN1A1 monoclonal antibody hSTC810

A humanized monoclonal antibody directed against the immune checkpoint protein butyrophilin 1A1 (BTN1A1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti- BTN1A1 monoclonal antibody hSTC810 targets and binds to the extracellular domain of human BTN1A1, which prevents the formation of the BTN1A1-galectin-9 (Gal9)-programmed cell death protein 1 (PD-1) complex, and inhibits downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. The BTN1A1-Gal9-PD-1 axis suppresses T-cell receptor (TCR) signaling and T-cell activation. BTN1A1 does not bind to PD-1 directly but interacts with PD-1 through Gal9. BTN1A1, a member of the butyrophilin superfamily of immunomodulators, is upregulated in a variety of tumor cell types.

anti-BTN3A agonistic monoclonal antibody ICT01

A humanized agonistic monoclonal antibody directed against butyrophilin subfamily 3 member A (BTN3A; CD277), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-BTN3A agonistic monoclonal antibody ICT01 targets and binds to BTN3A present on epithelial and tumor cells. BTN3A binding may sensitize tumor cells to gamma 9 delta 2 (Vg9Vd2) T-cell killing. The Vg9Vd2 T cells secrete effector cytokines and exert a cytolytic effect on tumor cells. This may abrogate BTN3A-mediated tumor immunity and may enhance anti-tumor immune response. BTN3A, a member of the butyrophilin superfamily of immunomodulators, is upregulated in tumor cells.

anti-c-fms monoclonal antibody AMG 820

A fully human IgG2 monoclonal antibody against the colony-stimulating factor-1 (CSF-1 or M-CSF) receptor c-fms (or CSFR1), with potential antineoplastic activity. Upon administration, anti-c-fms monoclonal antibody AMG 820 binds to and blocks c-fms, thereby blocking CSF-1 binding to its receptor and suppressing CSF-1-induced c-fms signaling. This results in the suppression of recruitment and activation of tumor associated macrophages (TAM) within the tumor microenvironment. This eventually leads to a decrease in tumor growth. c-fms, a transmembrane protein belonging to the tyrosine kinase family, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation and regulation of cell proliferation. The presence of TAM is correlated with tumor proliferation, invasion and a poor prognosis.

Anti-c-KIT Monoclonal Antibody CDX 0158

A humanized immunoglobulin (Ig) G1 monoclonal antibody against the stem cell factor receptor c-Kit (SCFR; KIT; CD117), with potential antineoplastic and anti-allergic activities. Upon administration, the anti-c-KIT monoclonal antibody CDX 0158 binds to and inhibits the activation of the cell surface antigen c-Kit. This leads to an inhibition of the activation of c-KIT-mediated signal transduction pathways and inhibits cell proliferation in cancer cells expressing c-Kit. In mast cells, inhibition of c-KIT and c-KIT-mediated signaling prevents mast cell activation, degranulation and subsequent cytokine release. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in various cell types, including certain cancer cells and mast cells; it plays a key role in the regulation of cell differentiation and proliferation.

anti-c-Kit/MMAE antibody-drug conjugate NN3201

An antibody-drug conjugate (ADC) composed of 2G4, a human monoclonal antibody directed against the stem cell factor receptor c-Kit (SCFR; KIT; CD117), conjugated to the auristatin derivative and microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-c-Kit/MMAE ADC NN3201, the 2G4 antibody targets and binds to the cell surface antigen c-Kit. Upon binding and internalization, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in c-Kit-expressing tumor cells. c-Kit, a transmembrane protein and receptor tyrosine kinase (RTK) overexpressed in various solid tumors and hematological malignancies, plays a key role in the regulation of cell differentiation and proliferation.

anti-c-Met antibody-drug conjugate BYON3521

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody against the tumor-associated antigen (TAA) proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) site-specifically conjugated to a linker-duocarmycin payload, with potential antineoplastic activity. Upon intravenous administration of anti-c-Met ADC BYON3521, the monoclonal antibody moiety targets and binds to c-Met expressed on tumor cells. Upon binding, the linker is cleaved inside the tumor thereby releasing the duocarmycin payload. Duocarmycin binds to the minor groove of DNA, alkylates adenine at the N3 position, and induces cell death in c-Met-expressing cancer cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis.

anti-c-Met antibody-drug conjugate SHR-A1403

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against the tumor-associated antigen (TAA) the proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SHR-A1403 targets and binds to c-Met expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the c-Met-expressing cancer cells, through an as of yet unknown mechanism of action. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis.

anti-c-Met antibody-drug conjugate TR1801

An antibody-drug conjugate (ADC) consisting of a non-agonizing anti-c-Met humanized monoclonal antibody that is linked in a site-specific manner to a pyrrolobenzodiazepine dimer (PBD) toxin, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety targets and binds to the c-Met protein, which is overexpressed in certain tumor types. Upon antibody/antigen binding and internalization, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of tumor cell DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of c-Met-expressing cells. c-Met, also known as hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that is overexpressed or mutated in many tumor cell types and plays a key role in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.

anti-c-Met antibody-drug conjugate YL211

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) site-specifically conjugated, via a tumor microenvironment (TME) activable protease-cleavable linker, to a topoisomerase 1 inhibitor (TOP1i), with potential antineoplastic activity. Upon administration of anti-c-Met ADC YL211, the anti-c-Met antibody moiety targets and binds to c-Met expressed on tumor cells. Upon proteolytic cleavage in the TME and the release of the topoisomerase I inhibitor, the topoisomerase I inhibitor targets and binds to DNA topoisomerase I, thereby inhibiting DNA replication and killing the c-Met-expressing cancer cells. In addition, YL211 is able to induce a bystander effect on neighboring cells. This further inhibits tumor cell proliferation. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis.

anti-c-Met monoclonal antibody ARGX-111

A human monoclonal antibody targeting c-Met, with potential antineoplastic activity. Anti-c-Met monoclonal antibody ARGX-111 binds to c-Met, and blocks both ligand-dependent and -independent activation of c-Met-mediated signaling pathways. In addition, this agent enhances antibody-dependent cellular cytotoxicity (ADCC). This leads to a reduction in cell proliferation of c-Met-expressing cancer cells. c-Met, a receptor tyrosine kinase overexpressed in certain cancer cell types, is involved in cell proliferation, angiogenesis and metastasis in multiple solid tumors. Compared to other c-Met targeting monoclonal antibodies, ARGX-111 shows increased antibody circulation time, enhanced tissue distribution and increased efficacy. ARGX-111 is obtained through active immunization with C-met antigen in Camelids and utilizes the Camelid V-domains fused with human antibody backbones.

anti-c-MET monoclonal antibody HLX55

A humanized immunoglobulin (Ig) G2 monoclonal antibody directed against the human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Upon administration, anti-c-Met monoclonal antibody HLX55 specifically binds to the semaphorin (Sema)/Plexins-Semaphorins-Integrins (PSI) domain of c-Met, which prevents the binding of c-Met to its ligand HGF and the subsequent activation of the HGF/c-Met signaling pathway. In addition, HLX55 promotes c-Met degradation, which further inhibits c-Met-mediated signaling. This may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-c-MET monoclonal antibody LY2875358

A humanized IgG4 monoclonal antibody directed against human hepatocyte growth factor receptor (HGFR or c-MET) with potential antineoplastic activity. Anti-c-MET monoclonal antibody LY2875358 binds to c-MET, thereby preventing the binding of HGF to its receptor c-Met and subsequent activation of the HGF/c-Met signaling pathway. This may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-C-met monoclonal antibody SAIT301

A humanized monoclonal antibody targeting the alpha chain of the extracellular domain of human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Anti-c-Met monoclonal antibody SAIT301 binds to c-Met, thereby preventing both binding of its ligand, HGF, and the subsequent activation of the HGF/c-Met signaling pathway. In addition, SAIT301 induces c-Met internalization and subsequent degradation, which further inhibits c-Met-mediated signaling. This leads to a reduction in the proliferation of c-Met-expressing cancer cells. c-Met, a proto-oncogene receptor tyrosine kinase overexpressed in certain cancer cell types, is involved in various tumors.

anti-c-Met/anti-TROP2/anti-CD3/anti-CD28 tetra-specific antibody MDX2001

A tetra-specific antibody targeting the tumor-associated antigens (TAAs) proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) and trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1), the T-cell surface antigen CD3, and the T-cell specific surface glycoprotein and co-stimulatory molecule CD28, with potential immunostimulating and antineoplastic activities. Upon administration, anti-c-Met/anti-TROP2/anti-CD3/anti-CD28 tetra-specific antibody MDX2001 targets and binds to both CD3 and CD28 on T cells, and c-Met and TROP2 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against c-Met and/or TROP2-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival. The simultaneous binding of MDX2001 to two T-cell receptors (TCRs) and two TAAs may optimize T-cell function while preventing tumor antigen escape, and may result in an increased T-cell-mediated tumor cell killing as compared to antibodies that target one TCR and one TAA.

anti-c-Met/MMAE ADC MYTX-011

An antibody-drug conjugate (ADC) composed of an engineered pH-dependent humanized immunoglobulin G1 (IgG1) monoclonal antibody against the tumor-associated antigen (TAA) proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) and conjugated, via a valine-citrulline (VC) peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon intravenous administration of anti-c-Met/MMAE ADC MYTX-011, the monoclonal antibody moiety targets and binds to c-Met expressed on tumor cells. Upon binding, internalization, and proteolytic cleavage, MMAE is released. MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. This induces cell death in c-Met-expressing cancer cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis. The engineered pH-dependent anti-c-Met antibody allows enhanced binding and thus uptake into c-Met-expressing cancer cells while reducing binding to and uptake in healthy cells. This may increase efficacy and improve tolerability.

anti-c-Met/MMAE ADC RC108

An antibody-drug conjugate (ADC) consisting of an anti-c-Met monoclonal antibody that is conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-c-Met/MMAE ADC RC108, the monoclonal antibody moiety targets and binds to the c-Met protein, which is overexpressed in certain tumor types. After internalization of the agent, the MMAE moiety is released and binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and apoptosis. This inhibits the proliferation of c-Met-expressing tumor cells. c-Met, also known as hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that is overexpressed or mutated in many tumor cell types and plays a key role in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis. Its expression is associated with poor prognosis in many solid tumor types.

anti-C4.4a antibody-drug conjugate BAY1129980

An antibody-drug conjugate (ADC) composed of an antibody against a structural homolog of the urokinase-type plasminogen activator receptor (uPAR) and tumor-associated antigen, C4.4a, and conjugated with a cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, anti-C4.4a antibody-drug conjugate BAY1129980 targets and binds to C4.4a-expressing tumor cells. Upon binding and cell entry, the cytotoxic agent kills the tumor cell. C4.4a, a glycolipid-anchored membrane protein and a member of the Ly-6 family, is overexpressed by a variety of cancer cell types whereas it is minimally expressed on healthy cells.

anti-C5aR1 monoclonal antibody TJ210

A differentiated human monoclonal antibody targeting the complement component fragment 5a receptor (C5aR1, CD88), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-C5aR1 monoclonal antibody TJ210 specifically targets and binds to the N-terminus of C5aR1 expressed on subsets of tumor-promoting cells, such as myeloid-derived suppressor cells (MDSCs), neutrophils and M2 macrophages. This prevents the binding of its ligand complement factor 5a (C5a) to C5aR1 and prevents the C5aR1-mediated activation, migration and accumulation of the C5aR1-expressing cells in the tumor microenvironment (TME). This abrogates the secretion of inflammatory and angiogenic factors by these cells and restores the activation of T and natural killer (NK) cells. This results in the induction of anti-tumor immune responses and inhibits tumor cell proliferation. C5a, a factor in the complement cascade, is often overexpressed in the TME, where it attracts and activates C5aR1-expressing tumor-promoting immune cells, and contributes to tumor immune suppression.

anti-CA19-9 monoclonal antibody BNT321

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the carbohydrate antigen sialyl Lewis A (carbohydrate antigen 19-9; CA19-9), with potential antineoplastic activity. Upon administration, anti-CA19-9 monoclonal antibody BNT321 targets and binds to CA19-9, and kills CA19-9-expressing tumor cells through the induction of both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). CA19-9 is overexpressed on a number of different tumor cell types, and plays a key role in tumor cell survival and metastasis.

anti-CA6-DM4 immunoconjugate SAR566658

An immunoconjugate consisting of a humanized monoclonal antibody against the tumor-associated sialoglycotope CA6 (huDS6) conjugated to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. The anti-CA6 monoclonal antibody moiety of SAR566658 targets and binds to the cell surface antigen CA6. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CA6-expressing tumor cells. The CA6 epitope is found on a variety of solid tumors, including breast, ovarian, cervical, lung and pancreatic tumors.

anti-CAIX antibody-drug conjugate BAY79-4620

An antibody-drug conjugate (ADC) composed of 3ee9, a monoclonal antibody directed against the tumor-associated antigen (TAA) carbonic anhydrase IX (CAIX; carbonic anhydrase 9; CA9; G250), conjugated via a valine-citrulline (VC) peptide linker to the auristatin derivative and microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-CAIX ADC BAY79-4620, the monoclonal antibody moiety 3ee9 targets and binds to CAIX expressed on tumor cells. Upon internalization, proteolytic cleavage of linker, and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CAIX-expressing tumor cells. CAIX is a member of the carbonic anhydrase family that is found in a majority of renal cell carcinomas while absent in most normal tissues.

anti-CAIX CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) carbonic anhydrase IX (CAIX; carbonic anhydrase 9; CA9; G250), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CAIX CAR T cells target and bind to CAIX-expressing tumor cells, thereby inducing selective toxicity in CAIX-expressing tumor cells. CAIX is a member of the carbonic anhydrase family that is found in a majority of renal cell carcinomas while absent in most normal tissues.

anti-CALRmut/anti-CD3 bispecific antibody JNJ-88549968

A bispecific antibody directed against both the mutated form of calreticulin (CALRmut; mutCALR) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CALRmut/anti-CD3 bispecific antibody JNJ-88549968 targets and binds to both CALRmut expressed on CALR mutated CD34-positive hematopoietic stem cells (HSCs) and CD3 on T cells. This results in the cross-linking of CALRmut-expressing tumor cells and T cells, and induces a cytotoxic T-lymphocyte (CTL) response against CALRmut-expressing tumor cells. CALR mutations, either insertions or deletions in exon 9, result in a frameshift that causes the loss of the KDEL ER retention motif. CALR mutations drive a variety of myeloproliferative neoplasms (MPNs).

anti-Caprin-1 monoclonal antibody TRK-950

A humanized monoclonal antibody directed against cell cycle associated protein 1 (cytoplasmic activation- and proliferation-associated protein 1; Caprin-1; CAPRIN1; RNA granule protein 105; RNG105), with potential antineoplastic activity. Upon administration, anti-Caprin-1 monoclonal antibody TRK-950 targets and binds to Caprin-1 expressed on tumor cells. This may induce antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), thereby killing Caprin-1-expressing tumor cells. Caprin-1 is overexpressed on certain tumor cell types and plays a key role in tumor cell proliferation and metastasis.

anti-CCR7 antibody-drug conjugate JBH492

An antibody-drug conjugate (ADC) composed of an antibody targeting CC chemokine receptor 7 (CCR7) and conjugated to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. Upon administration of anti-CCR7 ADC JBH492, the antibody moiety targets and binds to CCR7 on tumor cells. Upon antibody/antigen binding and internalization, the ADC releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics. This results in the inhibition of cell division and cell growth of CCR7-expressing tumor cells. CCR7, a G-protein coupled receptor, is normally expressed by subsets of immune cells and overexpressed by various types of cancer cells. Its overexpression has been associated with lymph node metastasis and poor survival.

anti-CCR7 monoclonal antibody CAP-100

A humanized immunoglobulin G1 (IgG1) monoclonal antibody against C-C-chemokine receptor 7 (CCR7), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR7 monoclonal antibody CAP-100 targets and binds to CCR7 on tumor cells, and neutralizes ligand-mediated signaling through both ligands CCL19 and CCL21. This prevents the activity of CCR7 on tumor cells. CAP-100 is expected to prevent the migration of tumor cells to and their survival in lymphoid niches. In addition, CAP-100 eliminates CCR7-positive tumor cells via the induction of Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC). CCR7, a G-protein coupled receptor involved in trafficking of cells to lymph nodes, is normally expressed by subsets of immune cells and overexpressed in various types of cancer cells, such as in many hematological malignancies. Its overexpression has been associated with lymph node metastasis and poor survival.

anti-CCR8 monoclonal antibody ABBV-514

An afucosylated monoclonal antibody directed against human C-C motif chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody ABBV-514 targets and binds to CCR8 on CCR8-positive, immunosuppressive tumor-infiltrating T-regulatory (TITR) cells in the tumor microenvironment (TME). This depletes CCR8-positive TITR cells via antibody-dependent cell-mediated cytotoxicity (ADCC), which may reverse the suppression of CD8+ effector T cells and reactivate antitumor immune responses. CCR8 is specifically expressed by TITR cells in multiple types of cancer and plays a key role in immunosuppression.

anti-CCR8 monoclonal antibody AMG 355

A monoclonal antibody directed against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody AMG 355 targets and binds to CCR8 on CCR8-positive tumor-infiltrating regulatory T-cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.

anti-CCR8 monoclonal antibody BAY3375968

A human immunoglobulin G1 (IgG1) afucosylated monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody BAY3375968 targets, binds to and blocks the activity of CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. BAY3375968 eliminates CCR8-positive Tregs via the induction of Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody dependent cellular phagocytosis (ADCP), thereby depleting CCR8-positive Tregs. This may reactivate antitumor immune responses. CCR8 is specifically expressed on activated tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.

anti-CCR8 monoclonal antibody BGB-A3055

A monoclonal antibody directed against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody BGB-A3055 targets and binds to CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.

anti-CCR8 monoclonal antibody BMS-986340

A human immunoglobulin G1 (IgG1) nonfucosylated (NF) monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody BMS-986340 targets, binds to and blocks the activity of CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. BMS-986340 eliminates CCR8-positive Tregs via the induction of Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC), thereby depleting CCR8-positive Tregs. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.

anti-CCR8 monoclonal antibody CM369

A monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody CM369 targets and binds to CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME), and depletes CCR8-positive tumor-infiltrating Tregs via antibody-dependent cellular cytotoxicity (ADCC). This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression.

anti-CCR8 monoclonal antibody GS-1811

A humanized immunoglobulin G1 (IgG1) afucosylated monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody GS-1811 targets and binds to CCR8 on CCR8-positive, immunosuppressive tumor-infiltrating T-regulatory (TITR) cells in the tumor microenvironment (TME), and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. GS-1811 depletes CCR8-positive TITR cells via antibody-dependent cell-mediated cytotoxicity (ADCC), which may reactivate antitumor immune responses. CCR8 is specifically expressed by TITR cells in multiple types of cancer and plays a key role in immunosuppression.

anti-CCR8 monoclonal antibody HC006

A monoclonal antibody directed against human C-C motif chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody HC006 targets and binds to CCR8 on CCR8-positive, immunosuppressive tumor-infiltrating T regulatory (TITR) cells in the tumor microenvironment (TME). This depletes CCR8-positive TITR cells via antibody-dependent cell-mediated cytotoxicity (ADCC), which may reverse the suppression of CD8+ effector T cells and reactivate antitumor immune responses. CCR8 is specifically expressed by TITR cells in multiple types of cancer and plays a key role in immunosuppression.

anti-CCR8 monoclonal antibody RO7502175

A humanized immunoglobulin G1 (IgG1) afucosylated monoclonal antibody directed against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody RO7502175 targets and binds to the N-terminus of CCR8 on CCR8-positive, immunosuppressive tumor-infiltrating T regulatory (TITR) cells in the tumor microenvironment (TME). This depletes CCR8-positive TITR cells via antibody-dependent cell-mediated cytotoxicity (ADCC), which may reverse the suppression of CD8+ effector T cells and reactivate antitumor immune responses. CCR8 is specifically expressed by TITR cells in multiple types of cancer and plays a key role in immunosuppression.

anti-CCR8 monoclonal antibody S-531011

A human immunoglobulin G1 (IgG1) monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody S-531011 targets, binds to and blocks the activity of CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. S-531011 eliminates CCR8-positive Tregs via the induction of Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC), thereby depleting CCR8-positive Tregs. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.

anti-CCR8 monoclonal antibody ZL-1218

A humanized immunoglobulin G1 (IgG1) monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CCR8 monoclonal antibody ZL-1218 targets and binds to CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME), and depletes CCR8-positive tumor-infiltrating Tregs via antibody-dependent cellular cytotoxicity (ADCC). This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression.

anti-CD117/amanitin antibody-drug conjugate MGTA-117

An antibody-drug conjugate (ADC) consisting of a human monoclonal antibody directed against CD117 (tyrosine-protein kinase KIT; c-Kit; mast/stem cell growth factor receptor; SCFR), conjugated, via a cleavable linker, to the cytotoxic RNA polymerase II inhibitor amanitin, with potential antineoplastic activity and that can potentially be used as a conditioning agent to selectively deplete hematopoietic stem cells (HSCs) prior to allogeneic HSC transplants or other treatments for which HSCs need to be depleted. Upon administration of the anti-CD117/amanitin ADC MGTA-117, the antibody moiety targets and binds to the cell surface antigen CD117. Upon internalization and cleavage, the cytotoxic amanitin is released, binds to and inhibits RNA polymerase II. This prevents RNA synthesis and induces apoptosis of CD117-overexpressing HSCs and leukemic blasts. CD117, a transmembrane protein and receptor tyrosine kinase, is highly expressed on HSCs, progenitor cells and on leukemia cells. MGTA-117 is engineered to have a short half-life.

anti-CD11b monoclonal antibody ASD141

A monoclonal antibody directed against the CD11b (integrin alpha-M; ITGAM; integrin alpha M chain) subunit of MAC-1 (integrin alphaM/beta2; CD11b/CD18; CR3), with potential innate immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, anti-CD11b monoclonal antibody ASD141 targets, binds to and blocks the CD11b subunit of the Mac-1 receptor, thereby preventing TLT-1 (pro-T) binding to CD11b receptors on immature, innate myeloid cells in the tumor microenvironment (TME). This prevents CD11b-mediated signaling, abrogates the TLT-1-driven immunosuppressive nature of the TME and modulates the TME. This reduces infiltration of immunosuppressive tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), activates the innate immune system, and promotes infiltration of antigen-presenting cells (APCs). Specifically, the infiltration of mature interleukin-12 (IL-12)-producing dendritic cells (DCs) increases, and pro-inflammatory macrophage polarization is induced while immunosuppressive macrophage polarization is suppressed. The DC- and macrophage-driven anti-tumor immune responses along with the increase in cytotoxic T lymphocytes (CTLs) and production of interferon-gamma (IFN-g) kill tumor cells and suppress tumor growth. CD11b, a member of the integrin family of cell adhesion receptors and alpha-chain of the integrin receptor alphaMbeta2, is highly expressed on immune cells and is a negative regulator of immune suppression. TLT-1, a key regulatory protein released from platelets, plays a key role in the induction of the immune suppressive environment in the tumor and immune checkpoint blockade. Its expression in the TME is correlated with poor prognosis.

anti-CD122 humanized monoclonal antibody Mik-beta-1

A humanized version of the immunoglobulin (Ig) G1 monoclonal antibody Mik-Beta-1 (Hu-Mik-Beta-1) directed against CD122, the beta-subunit shared by the interleukin-2 (IL-2) and IL-15 receptor (IL-2/IL-15Rbeta). Upon intravenous infusion, Hu-Mik-Beta-1 binds to CD122 expressed on certain tumor cells. This blocks the binding of the inflammatory cytokines IL-2 and IL-15 to IL-2R and IL-15R, respectively, and prevents IL-2/IL-2R- and IL-15/IL-15R-mediated signaling. This may inhibit the proliferation of CD122-expressing tumor cells. In addition, blocking CD122 on T-lymphocytes prevents the over-activation of T lymphocytes in various T-cell mediated autoimmune diseases, which is predominantly mediated by IL-15/IL-15R signaling. CD122, involved in both IL-2 and IL-15 signaling, is overexpressed on certain cancer cells, such as those found in T-cell large granular lymphocyte (T-LGL) leukemia.

anti-CD123 ADC IMGN632

An antibody-drug conjugate (ADC) consisting of a humanized anti-CD123 (interleukin-3 (IL-3) receptor alpha chain; IL3RA) immunoglobulin G1 (IgG1) monoclonal antibody conjugated, via a cleavable linker, to a cytotoxic, DNA-alkylating payload, which is an indolino-benzodiazepine dimer containing an imine moiety, with potential antineoplastic activity. Upon administration of anti-CD123 ADC IMGN632, the antibody moiety targets the cell surface antigen CD123. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic moiety is released, and covalently binds to and alkylates DNA with its imine moiety. This results in cell cycle arrest in S-phase, which leads to apoptosis and inhibition of cell growth in cells overexpressing CD123. CD123, the alpha subunit of the IL-3 receptor, regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers.

anti-CD123 monoclonal antibody CSL360

A chimeric IgG1 monoclonal antibody against CD123 (Interleukin-3 receptor alpha chain) with potential antineoplastic activity. Derived from mouse monoclonal antibody 7G3, anti-CD123 monoclonal antibody CSL360 binds to and neutralizes CD123 which is upregulated on leukemic stem cells (LSC) in acute myeloid leukemia (AML). This may inhibit IL-3-dependent signalling and proliferation and may prevent the uncontrolled growth and differentiation of mutated LSC.

anti-CD123 monoclonal antibody KHK2823

A fully human monoclonal antibody against CD123 (interleukin-3 receptor alpha chain) with potential antineoplastic activity. Anti-CD123 monoclonal antibody KHK2823 binds to and neutralizes CD123, which is upregulated on leukemic stem cells (LSC) found in myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). This agent may inhibit IL-3-dependent signaling and proliferation and may prevent the uncontrolled growth and differentiation of mutated LSC.

anti-CD123 x anti-CD3 bispecific antibody XmAb14045

An anti-CD123/anti-CD3 bispecific monoclonal antibody, in which most of the naturally-occurring Fc domain is maintained, with potential immunostimulatory and antineoplastic activities. Anti-CD123/CD3 monoclonal antibody XmAb14045 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD123, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of XmAb14045, this bispecific antibody simultaneously binds to both CD3-expressing T cells and CD123-expressing cancer cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This may result in potent CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells. The Fc domain on the antibody prolongs the half-life of the bispecific antibody and enhances T-cell-mediated tumor cell killing through its binding to the Fc receptors.

anti-CD123-pyrrolobenzodiazepine dimer antibody drug conjugate SGN-CD123A

An antibody-drug conjugate (ADC) consisting of an anti-CD123 humanized monoclonal antibody conjugated, via a stable maleimidocaproyl-valine-alanine dipeptide protease-cleavable linker, to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-CD123 ADC SGN-CD123A, the antibody moiety targets the cell surface antigen CD123. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD123-overexpressing tumor cells. CD123, the alpha subunit of the IL-3 receptor, regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers, including myeloid leukemia, and increased expression of CD123 on leukemic stem cells is associated with poor prognosis. Cysteine engineering of the monoclonal antibody (EC-mAb) allows for a site-specific, stable conjugation and uniform loading of the PBD agent to the antibody.

anti-CD123/anti-CD16A bispecific antibody AFM28

A human, tetravalent, bispecific immunoglobulin G1 (IgG1)-single chain variable fragment (scFv) fusion antibody targeting both the tumor-associated antigen (TAA) CD123 and the human low affinity immunoglobulin G (IgG) Fc region receptor IIIA (FCGR3A; CD16A), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD123/CD16A bispecific antibody AFM28 simultaneously targets and binds to CD16A expressed on natural killer (NK) cells and macrophages, and to CD123 on CD123-expressing tumor cells, thereby selectively cross-linking CD123-expressing tumor cells with NK cells and macrophages. This may result in NK cell and macrophage activation, induce antibody-dependent cellular cytotoxicity (ADCC), and eventually causes tumor cell lysis. CD123 is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells. CD16A is specifically expressed on the surface of NK cells and macrophages.

anti-CD123/anti-CD3 bispecific DART molecule MGD024

An Fc-bearing, bispecific antibody-like protein directed against the tumor-associated antigen (TAA) CD123 and the human T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD123/anti-CD3 bispecific DART molecule MGD024 simultaneously binds to both CD123-expressing cancer cells and CD3-expressing T cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This results in the activation and proliferation of T cells and causes CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells. The Fc domain prolongs the half-life of the agent, and a reduced affinity of CD3-binding results in less cytokine release.

anti-CD123/CD3 bispecific antibody APVO436

An immunoglobulin Fc-modified bispecific monoclonal antibody against the tumor-associated antigen (TAA) CD123 and the human T-cell surface antigen CD3 bispecific monoclonal antibody, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD123/CD3 monoclonal antibody APVO436 simultaneously binds to both CD3-expressing T cells and CD123-expressing cancer cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This results in the activation and proliferation of T-cells and causes CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells. The Fc domain on the antibody prolongs the half-life of the bispecific antibody. Compared to some other CD123 x CD3 targeting bispecific antibodies, APVO436 causes less cytokine release upon T-cell stimulation.

anti-CD123/CD3 bispecific antibody JNJ-63709178

A humanized anti-CD123/anti-CD3 bispecific monoclonal antibody, with potential immunostimulating and antineoplastic activities. Anti-CD123/CD3 bispecific antibody JNJ-63709178 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD123, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of JNJ-63709178, this bispecific antibody simultaneously binds to both CD3-expressing T cells and CD123-expressing cancer cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This may result in potent CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of cancers; its expression is low or absent in normal, healthy cells.

anti-CD123/CD3 BiTE antibody SAR440234

A bispecific T-cell engager (BiTE) antibody comprised of a humanized Fc-silenced immunoglobulin G1 (IgG1) backbone and two single-chain variable fragments (scFvs): one directed against the CD3 antigen expressed on T lymphocytes and another directed against the alpha-chain of the interleukin-3 receptor (IL-3RA; CD123), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion, anti-CD123/CD3 BiTE antibody SAR440234 binds to both CD3 expressed on T cells and CD123 expressed on tumor cells. This activates and redirects cytotoxic T lymphocytes (CTLs) to CD123-expressing tumor cells, leading to enhanced CTL-mediated elimination of CD123-expressing tumor cells. CD123 is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells.

anti-CD123/duocarmazine ADC BYON4413

An antibody-drug conjugate (ADC) consisting of a humanized, immunoglobulin G1 (IgG1) monoclonal antibody against the interleukin-3 (IL3)-receptor alpha chain (CD123; IL-3RA) that is site-specifically conjugated to the cleavable linker-duocarmycin payload duocarmazine (valine-citrulline-seco duocarmycin hydroxybenzamide azaindole; vc-seco-DUBA; SYD980), with potential antineoplastic activity. Upon administration of anti-CD123/duocarmazine ADC BYON4413, the antibody moiety targets and binds to the cell surface antigen CD123 expressed on tumor cells. Upon binding, internalization and cleavage of the vc linker inside the tumor cell by proteases, duocarmycin is released and binds to the minor groove of DNA. This alkylates adenine at the N3 position, and induces cell death specifically in tumor cells expressing CD123. CD123 regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers, including myeloid leukemia, and increased expression of CD123 on leukemic stem cells is associated with poor prognosis.

anti-CD123/kinesin spindle protein inhibitor antibody-drug conjugate VIP943

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against the interleukin-3 (IL3)-receptor alpha chain (CD123; IL-3RA), conjugated, via a legumain-cleavable linker, to a physicochemically-modiffied payload composed of a kinesin spindle protein inhibitor (KSPi), with potential antineoplastic activity. Upon administration of anti-CD123/KSPi ADC VIP943, the antibody moiety targets the cell surface antigen CD123. Upon antibody/antigen binding, internalization, and transport to the lysosome, the KSPi moiety is released upon cleavage by the tumor-specific protease legumain, thereby accumulating the hydrophobic KSP (kinesin-5 or Eg5) inhibitor inside the tumor cell. In turn, KSPi inhibits KSP, thereby inhibiting mitotic spindle assembly, leading to an induction of cell cycle arrest during the mitotic phase, and cell death in CD123-overexpressing tumor cells that are actively dividing. This prevents proliferation of CD123-expressing tumor cells. KSP is an ATP-dependent microtubule motor protein that is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis. CD123 regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers, including myeloid leukemia, and increased expression of CD123 on leukemic stem cells is associated with poor prognosis. The modified KSPi payload is hydrophilic and thereby prevents diffusion out of the cell, allowing intracellular accumulation and reduces off-target toxicities by preventing membrane permeability into healthy cells.

anti-CD123/TOP1i antibody-drug conjugate AZD9829

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against the interleukin-3 (IL3)-receptor alpha chain (CD123; IL-3RA) conjugated to a topoisomerase-1 inhibitor (TOP1i), with potential antineoplastic activity. Upon administration of anti-CD123/TOP1i ADC AZD9829, the antibody moiety targets and binds to the cell surface antigen CD123 expressed on tumor cells. Upon binding and internalization, the TOP1i moiety is released, binds to TOP1 and stabilizes cleaved DNA-TOP1 complexes. This prevents DNA re-ligation, induces irreversible DNA strand breaks, prevents DNA repair, and leads to cycle arrest and apoptosis specifically in tumor cells expressing CD123. CD123 regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers, including myeloid leukemia, and increased expression of CD123 on leukemic stem cells is associated with poor prognosis.

anti-CD133-CAR vector-transduced allogeneic T lymphocytes

A preparation of allogeneic peripheral blood T lymphocytes (PBTL) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the chimeric CD (cluster of differentiation) 133 antigen receptor, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD133-CAR vector-transduced allogeneic T lymphocytes specifically recognize and kill CD133-expressing tumor cells. CD133, a tumor associated antigen (TAA), is overexpressed on a variety of tumor cell types.

anti-CD133-PE38-KDEL fusion protein

A fusion protein consisting of an anti-single-chain variable fragment (scFv) peptide sequence targeting the extracellular domain of human CD133 (prominin-1) (anti-CD133scFV) and a deimmunized truncated form of Pseudomonas exotoxin A (38-kDa derivative of PE; PE38) where the five C-terminal amino acid residues have been replaced with the endoplasmic reticulum (ER) retention signal, KDEL, with potential antineoplastic activity. Upon administration of the anti-CD133-PE38-KDEL fusion protein, the anti-CD133 scFV moiety targets and binds to CD133, which is expressed on a variety of tumor cells. Upon internalization of the receptor-fusion protein complex, the KDEL sequence targets the fusion protein to the ER, where the PE38 exotoxin portion then inhibits protein synthesis, which results in a reduction of proliferation of CD133-expressing tumor cells. CD133, a glycoprotein expressed by a variety of cancers and especially by cancer stem cells (CSCs), plays a key role in tumor initiation, proliferation and progression.

anti-CD137 agonistic monoclonal antibody ADG106

A human agonistic monoclonal antibody targeting CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating activity. Upon administration, anti-CD137 agonistic monoclonal antibody ADG106 binds to and activates CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytokine production and promotes T-cell mediated anti-tumor immune responses. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137 agonistic monoclonal antibody ADG206

An Fc-enhanced immunoglobulin G1 (IgG1) monoclonal antibody directed against the costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9) covalently linked to a peptide mask, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody ADG206 is selectively activated in the tumor microenvironment (TME), and targets, binds to, and activates CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytokine production and promotes T-cell mediated anti-tumor immuneresponses. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137 agonistic monoclonal antibody AGEN2373

A conditionally-active, fully human immunoglobulin G1 (IgG1) agonistic monoclonal antibody targeting the costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody AGEN2373 targets and binds to a non-ligand blocking epitope on CD137, thereby activating CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as induces NK-mediated tumor cell killing and suppresses the immunosuppressive activity of T-regulatory cells (Tregs). CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. In addition, as AGEN2373 engages with CD137 only in the presence of CD137 ligand and/or Fc gamma receptor-expressing antigen-presenting cells (APCs), this agent may have a decreased toxicity profile and improved tolerability compared to other agents that activate CD137 signaling beyond the tumor site in humans.

anti-CD137 agonistic monoclonal antibody ATOR-1017

A humanized agonistic immunoglobulin G4 (IgG4) monoclonal antibody targeting the costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody ATOR-1017 targets and binds to CD137 expressed on a variety of leukocyte subsets including activated T-lymphocytes and natural killer (NK) cells, and CD137 is activated upon crosslinking to Fc-gamma receptors (FcgRs) on macrophages. This enhances CD137-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as induces NK-mediated tumor cell killing and suppresses the immunosuppressive activity of T-regulatory cells (Tregs). CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. 4-1BB and FcgRs are both highly expressed in the tumor environment (TME) while their co-expression in non-tumor tissues is low. This may prevent systemic adverse effects.

anti-CD137 agonistic monoclonal antibody CTX-471

A fully human immunoglobulin G4 (IgG4) agonistic monoclonal antibody targeting CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody CTX-471 binds to and activates CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytokine production and promotes T-cell mediated anti-tumor immune responses. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137 agonistic monoclonal antibody EU101

A humanized agonistic monoclonal antibody targeting the costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody EU101 targets and binds to CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as induces NK-mediated tumor cell killing and suppresses the immunosuppressive activity of regulatory T cells (Tregs). CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137 agonistic monoclonal antibody YH004

A humanized immunoglobulin G1 (IgG1) agonistic monoclonal antibody targeting the costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 agonistic monoclonal antibody YH004 targets and binds to CD137, thereby activating CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as induces NK-mediated tumor cell killing and suppresses the immunosuppressive activity of T-regulatory cells (Tregs). CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137 monoclonal antibody PE0116

A human immunoglobulin G4 (IgG4) agonistic monoclonal antibody directed against the inducible T-cell costimulatory receptor CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD137 monoclonal antibody PE0116 is selectively activated in the tumor microenvironment (TME), and targets, binds to, crosslinks and activates CD137 expressed on a variety of leukocyte subsets including activated T lymphocytes and natural killer (NK) cells. This enhances CD137-mediated signaling, induces T-cell proliferation, cytokine production and promotes T-cell mediated anti-tumor immune responses. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity to promote anti-tumor immunity.

anti-CD137/anti-FAP bispecific antibody BI 765179

A bispecific antibody targeting both CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9) and fibroblast activation protein (FAP), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD137/anti-FAP bispecific antibody BI 765179 targets and binds to both FAP, expressed on cancer-associated fibroblasts (CAFs) in the tumor stroma, and CD137, expressed on the surface of immune cells including activated T-lymphocytes, natural killer (NK) cells and dendritic cells (DCs). The simultaneous binding of FAP and CD137 results in local clustering of FAP-expressing CAFs and CD137-expressing T cells in the tumor microenvironment (TME), local immune cell activation through the promotion of T-cell activation and cytokine release, and T-cell-mediated anti-tumor immune responses. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. FAP, a membrane-bound serine protease overexpressed on CAFs, is minimally expressed on normal, healthy cells.

anti-CD137/PD-L1 bispecific antibody AP203

A bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-CD137/PD-L1 bispecific antibody AP203 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T lymphocytes. Crosslinking of PD-L1-expressing tumor cells and activated T lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells. Through CD137 binding, AP203 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, AP203 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD137/PD-L1 bispecific monoclonal antibody FS222

A tetravalent immunoglobulin G1 (IgG1) bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-CD137/PD-L1 bispecific antibody FS222 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T lymphocytes. Through CD137 binding, FS222 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, FS222 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. Crosslinking of PD-L1-expressing tumor cells and activated T lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells.

anti-CD138 antibody-IFNalpha fusion protein QXL138AM

A masked immunocytokine (MIC) comprised of an immunoglobulin G1 (IgG1) antibody against the tumor-associated antigen (TAA) syndecan-1 (CD138) that is fused to the human cytokine interferon alpha (IFNalpha; IFN-alpha; IFNa) which is attached by a tumor-protease cleavable linker to a peptide mask, with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CD138 antibody-IFNalpha fusion protein QXL138AM targets and binds to CD138 expressed on tumor cells. In turn, the proteases on the cell surface cleave the linker and remove the peptide mask from IFNalpha, thereby enabling IFNalpha to attach to its IFN cell-surface receptor on tumor cells and immune cells within the tumor microenvironment (TME). This initiates direct tumor cell destruction through IFNalpha-induced apoptosis and activates IFN-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-stimulated response elements (ISREs), which activates both innate and adaptive anti-tumor immunity. Syndecan-1, a type 1 transmembrane proteoglycan, is overexpressed in a variety of cancer cells and plays a key role in the regulation of cell growth. The selective activation in the TME enhances the IFN-alpha-mediated cytolytic effect and immune responses against tumor cells while sparing the unwanted effects of systemic immune activation while in circulation.

Anti-CD147 Monoclonal Antibody DS-1471

A monoclonal antibody directed against the tumor-associated antigen (TAA) CD147 (Basigin; EMMPRIN; extracellular matrix metalloproteinase inducer; OX47; 5A11), with potential antineoplastic activity. Upon administration, anti-CD147 monoclonal antibody DS-1471 targets and binds to CD147, thereby inhibiting the binding of CD147 to its binding molecules and CD147 molecular chaperone functions. This inhibits CD147-mediated stabilization and recycling of various CD147-binding proteins, including CD44, integrins, and monocarboxylate transporter 1 (MCT1), and inhibits downstream signal transduction pathways mediated by these proteins. This may lead to cancer cell death. CD147, a cell-surface glycoprotein of the immunoglobulin G (IgG) superfamily, is overexpressed in certain human tumors and plays an important role in tumor cell proliferation, migration, progression, and metastasis.

anti-CD157 monoclonal antibody MEN1112

A humanized, Fc-engineered, de-fucosylated monoclonal immunoglobulin G1 (IgG1) antibody directed against the bone marrow stromal cell antigen 1 (BST1/CD157), with potential antineoplastic activity. Upon intravenous infusion, anti-CD157 monoclonal antibody MEN1112 specifically binds to and induces an antibody-dependent cell cytotoxic (ADCC) response against CD157-expressing tumor cells. CD157, also known as ADP-ribosyl cyclase 2, is a glycosyl-phosphatidylinositol (GPI)-anchored transmembrane protein belonging to the ADP-ribosyl-cyclase family and is overexpressed on certain cancer cell types. Fc-optimization of MEN1112, which involves the removal of fucose residues from its Fc domain, allows for enhanced Fc-gamma receptor binding on effector cells, such as natural killer (NK) cells, and further enhances tumor cell lysis.

anti-CD16/IL-15/anti-CD33 trispecific natural Killer cell engager GTB-3650

A trispecific natural killer (NK) cell engager comprised of an anti-cluster of differentiation 16 (CD16; FcgammaRIII) camelid nanobody, human interleukin-15 (IL-15), and an anti-CD33 single-chain variable fragment (scFv), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD16/IL-15/anti-CD33 trispecific NK cell engager GTB-3650 targets and binds to CD33 expressed on tumor cells and simultaneously binds to the activating CD16 Fc receptor expressed on NK cells, thereby bringing CD33-expressing tumor cells and NK cells together. This induces NK cell cytotoxicity specifically against CD33-expressing tumor cells. The cytokine IL-15 promotes NK cell proliferation, activity, survival and expansion. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.

anti-CD161 monoclonal antibody IMT-009

An Fc-attenuated human immunoglobulin G1 (IgG1) monoclonal antibody directed against the C-type lectin-like receptor cluster of differentiation 161 (CD161), with potential immunomodulatory and antineoplastic activities. Upon administration, anti-CD161 monoclonal antibody IMT-009 selectivity targets, binds to and blocks CD161. This disrupts the interaction of CD161 with its ligand lectin-like transcript-1 (CLEC2D; LLT1; OCIL), prevents CD161-mediated signaling, abrogates the CLEC2D/ CD161-mediated suppression of CD161-positive T and natural killer (NK) cells, and restores the activation of effector functions of both CD161-positive T and NK cells against tumor cells, thereby enhancing cytotoxicity towards tumor cells. CD161, an inhibitory immune checkpoint, is broadly expressed on NK and a subset of memory CD4+ and CD8+ T cells. It plays a key role in cancer immune surveillance and its expression is associated with many types of cancer. CLEC2D is expressed on the surface of both malignant cells and immune cells, including activated B cells and myeloid cells.

anti-CD163 monoclonal antibody OR2805

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the immunosuppressive receptor CD163 (scavenger receptor cysteine-rich type 1 protein M130), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD163 monoclonal antibody OR2805 targets and binds to CD163 expressed on immunosuppressive tumor-associated macrophages (TAMs) within the tumor microenvironment (TME), and prevents the binding of CD163 to its ligands. This inhibits CD163-mediated immunosuppression, including the secretion of immunosuppressive cytokines and the inhibition of T-cell activation. This enhances T-cell activation and proliferation and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. CD163, an immunosuppressive receptor highly expressed on TAMs, plays an important role in immunosuppression and the inhibition of anti-tumor T-cell immune responses.

anti-CD166 probody-drug conjugate CX-2009

A probody drug conjugate (PDC) composed of a recombinant antibody targeting the tumor-associated antigen (TAA) CD166, which is masked by a cleavable masking peptide, and conjugated to the cytotoxic agent maytansinoid DM4, with potential antineoplastic activity. Upon administration of CX-2009 and migration to the tumor microenvironment (TME), the cleavable masking peptide, which prevent anti-CD166 antibody binding to the CD166 expressed on both normal cells and tumor cells, is proteolytically cleaved by tumor-associated proteases that are specifically present in the TME. This enables the anti-CD166 antibody moiety of CX-2009 to selectively bind to, be internalized by, and deliver DM4 into CD166-expressing tumor cells. Following internalization, DM4 is released, binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD166-expressing tumor cells. The masking peptide prevents binding of the anti-CD166 antibody to CD166 in normal tissues, thereby minimizing toxicities.

anti-CD19 antibody-drug conjugate IKS03

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the tumor-associated antigen (TAA) CD19 (cluster of differentiation 19), that is site-specifically conjugated with a tumor-cleavable beta-glucuronide linker to a tumor-cleavable prodrug of pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-CD19 ADC IKS03 targets and binds to CD19 expressed on tumor cells. Upon binding and internalization, both the linker and prodrug are selectively cleaved by lysosomal b-glucuronidase overexpressed in tumor cells. Free PBD is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing CD19-expressing cancer cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19 antibody-drug conjugate SGN-CD19B

An antibody-drug conjugate (ADC) consisting of an anti-CD19 humanized monoclonal antibody (hBU12ec) with engineered cysteines (EC-mAb) conjugated, via a maleimidocaproyl-valine-alanine dipeptide protease-cleavable linker, to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer (SGD-1882), with potential antineoplastic activity. Upon administration of anti-CD19 ADC SGN-CD19B, the antibody moiety targets the cell surface antigen CD19, which is found on B-cell-derived cancers. Upon antibody/antigen binding, internalization and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD19-overexpressing tumor cells. CD19, a transmembrane receptor belonging to the immunoglobulin superfamily and a B-cell specific antigen, is expressed on B-cell-derived cancers. The cysteine engineering of the EC-mAb allows for a site-specific and stable conjugation of PBD to the antibody.

anti-CD19 antibody-T-cell receptor-expressing T cells ET019003

A preparation of T lymphocytes that have been engineered by incorporating an as of yet undisclosed co-stimulatory molecule into T cells expressing an anti-CD19 antibody T-cell receptor (AbTCR) structure (ET190L1), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19 AbTCR-expressing T cells ET019003 targets and binds to CD19-expressing tumor cells. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of CD19-positive tumor cells. The binding to CD19-expressing tumor cells may also activate the undisclosed costimulatory domain, leading to further T-cell proliferation. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. ET019003 is able to match the anticancer activity of chimeric antigen receptor (CAR) T cells, while they are less likely to stimulate cytokine release syndrome (CRS) and less likely to cause cytokine-related toxicities.

anti-CD19 CAR T cells AT101

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19 CAR T cells AT101 recognize and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

anti-CD19 CAR-IL-18-expressing autologous T lymphocytes

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), and expressing the pro-inflammatory cytokine interleukin 18 (IL-18), with potential antineoplastic activity. Upon intravenous administration, anti-CD19 CAR-IL-18-expressing autologous T lymphocytes target, bind to, and induce selective toxicity in CD19-expressing tumor cells. IL-18 promotes T-cell persistence and potentiates the immune response against tumor cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of costimulatory signaling domains increases human T-cell function, expansion, and survival.

anti-CD19 CAR-T cells XLCART001

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19 CAR-T cells XLCART001 targets and binds to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

anti-CD19 cord blood-derived CAR-NK cells

A preparation of cord blood (CB)-derived natural killer (NK) cells that have been genetically modified and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CD19 CB-derived CAR-NK cells recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19 iCAR NK cells

A preparation of natural killer (NK) cells engineered to express an inhibitory chimeric antigen receptor (iCAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19 iCAR-NK cells recognize, bind to and induce selective cytotoxicity in CD19-expressing tumor cells. The iCAR is designed to spare normal cells from NK cell actions by including an inhibitory receptor that is activated upon binding to antigens that are present on normal cells only. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

anti-CD19 monoclonal antibody DI-B4

A low-fucosylated, humanized, IgG1 isotype, monoclonal antibody directed against the B-cell-specific membrane protein CD19 with potential immunostimulating and antineoplastic activities. Anti-CD19 monoclonal antibody DI-B4 binds to CD19, which may result in a strong antibody-dependent cellular cytotoxicity (ADCC) directed at CD19-expressing B cells but with minimal complement dependent cytotoxicity. DI-B4 contains low levels of fucose, which contributes to its enhanced ADCC activity. CD19 is a B-cell specific membrane antigen that is widely expressed during B-cell development and in all B-cell lineage malignancies.

anti-CD19 monoclonal antibody MDX-1342

A fully human anti-CD19 monoclonal antibody directed against the B-cell-specific membrane protein CD-19 with potential antineoplastic activity. Anti-CD19 monoclonal antibody MDX-1342 binds to CD19, depleting and eliminating CD19-expressing B cells. CD19 is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.

anti-CD19-CAR CMV-specific T lymphocytes

A preparation of human cytomegalovirus (CMV)-specific T lymphocytes that have been engineered to express a chimeric antigen receptor (CAR) specific for the human tumor associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19-CAR CMV-specific T lymphocytes recognize, bind to, and induce selective toxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. The anti-CD19-CAR CMV-specific T lymphocytes may potentially be expanded in vivo through CMV vaccination.

anti-CD19-CAR FMC63-28Z retroviral vector-transduced allogeneic T lymphocytes

Allogeneic T-lymphocytes derived from peripheral blood mononuclear cells (PBMC) transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of both the light and heavy chain variable regions of anti-CD19 monoclonal antibody FMC63, coupled to the molecule CD28 and the signaling domain of the zeta chain of the T-cell receptor (TCR) (FMC63-28Z), with potential immunomodulating and antineoplastic activities. Upon transfusion, the anti-CD19-CAR FMC63-28Z retroviral vector-transduced allogeneic T lymphocytes specifically recognize and kill CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B-cells.

anti-CD19-CAR retroviral vector-transduced autologous T cells

A preparation of autologous peripheral blood T lymphocytes (PBTL) that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19-CAR retroviral vector-transduced autologous T cells direct the T lymphocytes to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex, which regulates both the assembly of complete TCR complexes and their expression on the cell surface. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.

anti-CD19-CAR-CD28/CD20-CAR-4-1BB-expressing autologous T lymphocytes Hu1928-Hu20BB

A preparation of autologous human T lymphocytes that have been genetically modified to express the CAR construct Hu1928-Hu20BB that consists of two chimeric antigen receptor (CAR) constructs: one encoding a fully-human anti-CD19 CAR with a co-stimulatory domain of CD28, Hu19-CD828, and one encoding a human anti-CD20 CAR with a co-stimulatory domain of 4-1BB (CD137), Hu20BB, with potential immunostimulating and antineoplastic activities. Upon re-infusion, the anti-CD19-CAR-CD28/CD20-CAR-4-1BB-expressing autologous T lymphocytes Hu1928-Hu20BB recognize and kill CD19- and/or CD20-expressing tumor B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19- and/or CD20-expressing tumor cells, thereby causing tumor cell lysis. Both the tumor-associated antigens (TAAs) CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies.

anti-CD19-CAR-CD3zeta-4-1BB-expressing natural killer cells

Allogeneic natural killer (NK) cells transduced with an mRNA expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. NK cells from haploidentical donors are expanded in culture and electroporated with the CAR mRNA. Upon transfusion of the transduced cultured cells, CD19CAR-CD3zeta-4-1BB-expressing allogeneic NK cells bind to and induce selective cytotoxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Its inclusion may also increase antitumor activity, when compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

anti-CD19-CD20-CAR-CD3zeta-4-1BB-expressing autologous T lymphocytes

Autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19 in tandem with an anti-CD20 scFv, and coupled to the cytoplasmic portion of the zeta chain of the human T-cell receptor (CD3zeta), and the co-stimulatory molecule 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon transfusion, anti-CD19-CD20-CAR-CD3zeta-4-1BB-expressing autologous T lymphocytes recognize and direct T cells to CD19- or CD20-expressing tumor B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19- or CD20-expressing tumor cells, and causes tumor cell lysis. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies.

anti-CD19-CD28-zeta modified CAR CD3+ T lymphocytes JCAR015

Genetically modified CD3-positive-enriched autologous T lymphocytes transduced with a replication incompetent gamma retroviral vector expressing a chimeric T-cell antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv), fused to the extracellular, transmembrane and intracellular signaling domains of the T-cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (CAR19-28z), with potential antineoplastic activities. Upon intravenous administration, autologous CD19-28z CAR-expressing CD3+ T lymphocytes are directed to CD19-expressing tumor cells, and, upon binding to the T cells, induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. The inclusion of the CD28 signaling domain may increase proliferation of T cells and antitumor activity compared to the inclusion of the CD3-zeta chain alone.

anti-CD19-glucosteroid receptor modulator ADC ABBV-31

An antibody drug conjugate (ADC) composed of an afucosylated immunoglobulin G1 (IgG1) monoclonal antibody directed against the B-cell-specific membrane protein CD19 conjugated to a glucocorticoid receptor (GR) modulator (GRM), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19-GRM ADC ABBV-319 targets and binds to CD19. thereby inducing antibody-dependent cellular cytotoxicity (ADCC). Additionally, by delivering the GRM payload directly to CD19-expressing tumor cells, ABBV-319 inhibits the activation of GR-dependent expression of proliferative and anti-apoptotic genes. This induces apoptosis and inhibits tumor cell proliferation in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies and drives B-cell proliferation. GRMs show robust anti-tumor activity against B-cell malignancies.

anti-CD19/anti-CD20/anti-CD22 CAR T cells LCAR-AIO

A preparation of human T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19), CD20 and CD22, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/anti-CD20/anti-CD22 CAR T cells LCAR-AIO target and bind to CD19, CD20 and CD22 expressed on the surface of certain tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. The TAAs are overexpressed in certain hematologic malignancies.

anti-CD19/anti-CD22 bispecific immunotoxin DT2219ARL

An immunotoxin consisting of two scFv ligands recognizing human CD19 and CD22 linked to the first 389 amino acids of diphtheria toxin (DT), DT 390, with potential antineoplastic activity. The VH and VL regions of anti-CD22 (sFv) and anti-CD19 are reversed and linked by an aggregration stabilizing linker (ARL) consisting of a 20 amino acid segment of human muscle aldolase (hma) and an Xho1-compatible restriction site; the CDR3 region of the VH of anti-CD22 sFv is mutated to enhance its affinity. The anti-CD19 and anti CD-22 portions of the immunotoxin specifically bind to CD19 and CD22 receptors on tumor B cells. Upon internalization, DT catalyzes ADP ribosylation of elongation factor 2 (EF-2) which may result in the irreversible inhibition of protein synthesis and cell death in CD19- and CD22-expressing tumor cells. CD19 and CD22 are transmembrane proteins upregulated on malignant B cells.

anti-CD19/anti-CD3/anti-CD2 trispecific antibody PIT565

A trispecific T-cell engager and antibody targeting the tumor-associated antigen (TAA) CD19, the T-cell surface antigen CD3, and the T-cell co-stimulatory receptor CD2, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/anti-CD3/anti-CD2 trispecific antibody PIT565 targets and binds to CD3 and CD2 on T cells and CD19 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19/anti-CD3/anti-CD28 trispecific antibody CC312

A trispecific T-cell engager and antibody targeting the tumor-associated antigen (TAA) CD19, the T-cell surface antigen CD3, and the T-cell specific surface glycoprotein and co-stimulatory molecule CD28, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/anti-CD3/anti-CD28 trispecific antibody CC312 targets and binds to CD3 and CD28 on T cells and CD19 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19/anti-CD70 4SCAR-expressing bispecific T cells

A preparation of T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) CD19 and CD70 (CD27 ligand; tumor necrosis factor superfamily member 7; TNFSF7), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/anti-CD70 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in CD19- and CD70-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD70, a cytokine belonging to the tumor necrosis superfamily (TNFSF) and the ligand for the costimulatory receptor CD27, is expressed on the surfaces of various types of cancer cells; its overexpression may play an important role in the evasion of immune surveillance. CD19 and CD70 are expressed at high levels on tumor cells but not at significant levels on normal tissues. Targeting two antigens may protect against antigen escape and may enhance CAR-T cell efficacy.

anti-CD19/anti-CD79b 4SCAR-expressing bispecific T cells

A preparation of T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) CD19 and B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/anti-CD79b 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in CD19- and CD79b-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD79b, a B-cell surface antigen and critical receptor for successful B-cell development, is part of the B-cell receptor (BCR) signaling complex. It is widely expressed in certain subtypes of B-cell lymphomas. CD19 and CD79b are expressed at high levels on tumor cells but not at significant levels on normal tissues. Targeting two antigens may protect against antigen escape and may enhance CAR-T cell efficacy.

anti-CD19/CD20 bicistronic CAR T cells

A preparation of T lymphocytes that have been transduced with a bicistronic vector encoding two distinct chimeric antigen receptors (CARs), one against the tumor-associated antigen (TAA) CD19 and the other one against the TAA CD20, with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CD19/CD20 bicistronic CAR T cells target, bind to and induce selective toxicity in tumor cells expressing CD19 and/or CD20. CD19 and CD20, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. By simultaneously targeting two B-cell antigens using two different CARs, this preparation may minimize relapse due to single antigen loss in patients with B-cell malignancies.

anti-CD19/CD20/CD22 CAR T cells

A preparation of human T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19), CD20 and CD22, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/CD20/CD22 CAR T cells target and bind to CD19, CD20 and CD22 expressed on the surface of certain tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. The TAAs are overexpressed in certain hematologic malignancies.

anti-CD19/CD20/CD22/CD30 CAR-T cells

A preparation of human T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19), CD20, CD22 and CD30, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/CD20/CD22/CD30 CAR-T cells target and bind to CD19, CD20, CD22 and CD30 expressed on the surface of certain tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. The TAAs are overexpressed in certain hematologic malignancies.

anti-CD19/CD22 CAR NK cells

A preparation of natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19) and CD22, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD19/CD22 CAR-NK cells target and bind to CD19 and CD22 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. By simultaneously targeting two B-cell antigens, this preparation may minimize relapse due to single antigen loss in patients with B-cell malignancies.

anti-CD19/CD28 bispecific antibody RO7443904

A bispecific antibody directed against both the tumor-associated antigen (TAA) CD19 and the co-stimulatory T-cell-specific surface glycoprotein CD28, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD28 bispecific antibody RO7443904 targets and binds to both CD28 expressed on T cells and CD19 expressed on tumor cells, which crosslinks the T cells to the tumor cells. This may result in a potent cytotoxic T-lymphocyte (CTL) response against the CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19/CD3 bispecific antibody CN201

A bispecific antibody and a T-cell engager targeting both the tumor-associated antigen (TAA) CD19, and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD3 bispecific antibody CN201 binds to both the CD3 antigen on T cells and the CD19 antigen expressed on tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19/CD3 bispecific antibody GNR-084

A bispecific antibody and a T-cell engager targeting both the tumor-associated antigen (TAA) CD19, and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD3 bispecific antibody GNR-084 binds to both the CD3 antigen on T cells and the CD19 antigen expressed on tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-CD19/CD3 bispecific antibody TNB-486

A human bispecific T-cell engager antibody composed of a fixed-light-chain (FLC) arm targeting the CD3 antigen found on T lymphocytes and a heavy-chain-only (HCO) arm targeting the B-cell-specific membrane protein CD19, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD3 bispecific antibody TNB-486 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD19 antigen expressed on malignant B cells. This activates and redirects CTLs to CD19-expressing tumor cells, resulting in CTL-mediated killing of tumor cells. CD19 is a membrane antigen that is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages. The FLC arm weakly activates CD3. The HCO arm has a high affinity anti-CD19 moiety.

anti-CD19/CD3 BiTE antibody AMG 562

A bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the B-cell-specific membrane protein CD19, and another that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD3 BiTE antibody AMG 562 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD19 antigen expressed on malignant B cells. This activates and redirects CTLs to CD19-expressing tumor cells, resulting in CTL-mediated killing of tumor cells. CD19 is a membrane antigen that is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.

anti-CD19/CD3 T-cell engaging bispecific antibody CLN-978

A half-life extended T-cell engaging bispecific antibody comprised of a single chain variable fragment (scFv) targeting the tumor-associated antigen (TAA) CD19, a scFv targeting the T-cell surface antigen CD3, and a single-domain heavy chain variable domain (VHH)-based antibody specific for human serum albumin (HSA), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19/CD3 T-cell engaging bispecific antibody CLN-978 targets and binds to both CD19 antigen expressed on tumor cells and CD3 antigen expressed on T cells. This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. The HSA binding domain prolongs the half-life of CLN-978.

anti-CD19/CD3 tetravalent antibody AFM11

An anti-CD19/anti-CD3 bispecific tetravalent antibody with potential immunostimulatory and antineoplastic activities. Anti-CD19/CD3 tetravalent antibody AFM11 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B-cells. Upon bolus infusion of AFM11, this bispecific antibody binds to CD3-expressing T cells and CD19-expressing cancer cells, thereby crosslinking CD19-expressing tumor B cells and cytotoxic T lymphocytes (CTLs). This may result in a potent CTL-mediated cell lysis of CD19-expressing B lymphocytes. CD19, a B-cell specific membrane antigen, is expressed during both B-cell development and B-cell malignant growth.

anti-CD1d/Vdelta2 gamma delta T-cell-engaging bispecific antibody LAVA-051

A humanized bispecific gamma delta T-cell engager (TCE) antibody directed against both CD1d and Vdelta2, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD1d gamma delta T-cell-engaging bispecific antibody LAVA-051 binds to both CD1d-expressing tumor cells and Vgamma9Vdelta2 T cells. This activates and redirects the Vgamma9Vdelta2 T cells to CD1d-expressing tumor cells, and the Vgamma9Vdelta2 T cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. The Vgamma9Vdelta2 T cells also activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. In addition, this activates invariant natural killer T cells (iNKTs). The iNKTs secrete large amounts of various cytokines, which may activate the immune system against tumor cells. Additionally, iNKTs directly target and lyse tumor cells. CD1d, an antigen-presenting glycoprotein, plays an important role in the presentation of glycolipid antigens to iNKTs; it is also expressed by various hematologic malignancies.

anti-CD20 antibody-drug conjugate MRG001

An antibody-drug conjugate (ADC) composed of a chimeric anti-CD20 monoclonal antibody conjugated via a valine citrulline linker to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-CD20 ADC MRG001, the monoclonal antibody moiety of MRG001 targets and binds to CD20 on the surfaces of tumor B cells and is rapidly internalized, thereby delivering MMAE intracellularly. Upon proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M checkpoint arrest and apoptosis in CD20-expressing tumor cells. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B-cells during most stages of B-cell development. It is often overexpressed in B-cell malignancies.

anti-CD20 antibody-drug conjugate TRS005

An antibody-drug conjugate (ADC) composed of an anti-CD20 monoclonal antibody conjugated via a valine-citrulline linker to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of anti-CD20 ADC TRS005 targets and binds to CD20 on the surfaces of tumor B cells. Upon internalization and cleavage, MMAE is released. MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M checkpoint arrest and apoptosis in CD20-expressing tumor cells. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B cells during most stages of B-cell development. It is often overexpressed in B-cell malignancies.

anti-CD20 B9E9 scFv-streptavidin fusion protein

An Escherichia coli periplasm-expressed tetrameric fusion protein composed of four single-chain variable regions (scFv) of the murine immunoglobulin (Ig) G2a anti-CD20 monoclonal antibody B9E9 fused to the streptavidin (SA) gene of Streptomyces avidinii (scFv-SA), with potential use in pretargeted radioimmunotherapy (PRIT). Upon intravenous administration of the anti-CD20 B9E9 scFv-SA fusion protein, this agent targets and binds to CD20-expressing tumor cells. Subsequently, a biotinylated N-acetylgalactosamine-containing clearing agent is administered, which binds to the streptavidin moiety of the unbound fusion protein and promotes its hepatic excretion. In turn, radiolabeled DOTA (1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid)-biotin is administered and, due to its small size, quickly distributes. The biotin moiety efficiently binds to the SA moiety of the bound fusion protein, which localizes the biotin-conjugated radionuclide to the tumor site. CD20, a tumor-associated antigen (TAA), is overexpressed on B-cell malignancies. PRIT increases both tumor uptake and renal elimination of the radionuclide conjugate as compared to conventional radioimmunotherapy (RIT), where the radioisotope is bound to the antibody before administration; this increases the dose of radionuclide delivered to the tumor while limiting radiation exposure for normal, healthy tissues.

anti-CD20 bispecific antibody DR-0201

A bispecific monoclonal antibody that targets the human tumor-associated antigen (TAA) CD20, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD20 bispecific antibody DR-0201 targets and binds to CD20 on B-cell surface. This results in CD20-mediated signaling blockade and may induce phagocytosis of CD20-overexpressing cells by tissue-resident and trafficking myeloid cells, such as macrophages. This results in a depletion of pathogenic B cells. CD20 is overexpressed by certain cancer cell types and in various autoimmune diseases.

anti-CD20 CAR T cells C-CAR066

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) cluster of differentiation 20 (CD20), with potential immunostimulating and antineoplastic activities. Upon administration, C-CAR066 specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies and certain melanoma cell subpopulations.

anti-CD20 monoclonal antibody B001

A recombinant humanized monoclonal antibody directed against human CD20 with potential antineoplastic activity. Upon intravenous administration, anti-CD20 monoclonal antibody B001 specifically binds to CD20 on the surfaces of B cells. Although the exact mechanisms through which B001 exert its effects have not been elucidated, B001 may induce a B-cell-directed cell-mediated immune response against CD20-expressing B cells and/or prevent CD20-medaited signaling. This induces tumor cell apoptosis and inhibits proliferation. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B cells during most stages of B-cell development and which is often overexpressed in B-cell malignancies.

anti-CD20 monoclonal antibody BAT4306F

A recombinant, glycosylation-modified monoclonal antibody directed against the human B-cell-specific cell surface antigen CD20, with potential antineoplastic and immunomodulating activities. Upon administration of anti-CD20 monoclonal antibody BAT4306F, the antibody specifically targets and binds to CD20. This induces antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B cells, which leads to B-cell apoptosis and the inhibition of tumor cell proliferation. CD20, a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B-cell development, is often overexpressed in B-cell malignancies. The complete defucosylation of BAT4306F may result in enhanced ADCC.

anti-CD20 monoclonal antibody MIL62

A glyco-engineered recombinant humanized monoclonal antibody directed against the human B-cell-specific cell surface antigen CD20, with potential antineoplastic and immunomodulating activities. Upon administration of anti-CD20 monoclonal antibody MIL62, the antibody specifically targets and binds to CD20. This induces antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B cells, which leads to B-cell apoptosis and the inhibition of tumor cell proliferation. In addition, MIL62 inhibits CD20-mediated signaling which further induces apoptosis in and inhibits proliferation of CD20-expressing tumor cells. CD20, a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B-cell development, is often overexpressed in B-cell malignancies.

anti-CD20 monoclonal antibody PRO131921

A third-generation, humanized monoclonal antibody directed against human CD20 with potential antineoplastic activity. Anti-CD20 monoclonal antibody PRO131921 specifically binds to the B cell-specific cell surface antigen CD20. This may result in the induction of a B cell-directed complement dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B cells leading to B cell apoptosis. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B cells during most stages of B cell development and which is often overexpressed in B-cell malignancies.

anti-CD20 monoclonal antibody SCT400

A chimeric monoclonal antibody directed against human CD20, with potential antineoplastic activity. Anti-CD20 monoclonal antibody SCT400 binds to the B cell-specific cell surface antigen CD20, which triggers an immune response against CD20-positive B-cells, leading to apoptosis. CD20, a non-glycosylated cell surface phosphoprotein, is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.

anti-CD20 monoclonal antibody TL011

A monoclonal antibody directed against human CD20 with potential antineoplastic activity. Anti-CD20 monoclonal antibody TL011 specifically binds to the B cell-specific cell surface antigen CD20 antigen (MS4A1; membrane-spanning 4-domains, subfamily A, member 1), thereby potentially triggering an immune response against CD20-positive B cells, leading to B cell apoptosis. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development and is often overexpressed in B-cell malignancies.

anti-CD20-CAR-CD3zeta-4-1BB-expressing autologous T lymphocytes

A preparation of autologous blood T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of an anti-CD20 scFv (single chain variable fragment); the cytoplasmic portion of the human TCR-[zeta] molecule; and the co-stimulatory molecule 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon transfusion, anti-CD20-CAR-CD3zeta-4-1BB-expressing autologous T-lymphocyte cells direct T-cells to CD20-expressing tumor cells. This results in cytotoxic T lymphocyte (CTL) and antibody responses against CD20-expressing tumor cells, causing tumor cell lysis. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the T-cell receptor (TCR)/CD3 complex and regulates the assembly of complete TCR complexes and their expression on the cell surface. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD20; the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone.

anti-CD20-engineered toxin body MT-3724

An engineered toxin body (ETB) composed of the single-chain variable fragment (ScFv) from an antibody targeting CD20 that is linked to a modified form of the ribosome-inactivating alpha subunit of Shiga-like toxin 1 (Shiga-like Toxin-1 A or SLT-1A), with antineoplastic activity. Upon administration, the ScFv moiety of anti-CD20-engineered toxin body MT-3724 targets and binds to the CD20 antigen expressed on tumor cells. Upon internalization, the SLT-1A moiety is released and acts as an N-glycosidase, which binds to and cleaves an adenine nucleobase in the 28S RNA component of the 60S subunit of ribosomes and prevents ribosome activity. This inhibits protein synthesis and eventually leads to apoptosis of CD20-expressing tumor cells. CD20, a B-cell specific transmembrane protein and tumor-associated antigen (TAA), is expressed during most stages of B-cell development and is often overexpressed in B-cell malignancies.

anti-CD20/anti-CD22 CAR T cells

A preparation of human T lymphocytes engineered to express chimeric antigen receptors (CARs) specific for the tumor-associated antigens (TAAs) cluster of differentiation 20 (CD20) and CD22, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD20/anti-CD22 CAR T cells target and bind to both CD20 and CD22 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. CD20 and CD22 are overexpressed in certain hematologic malignancies.

anti-CD20/anti-CD3 bispecific antibody CM355

A bispecific antibody and novel T-cell engager1 (nTCE) targeting both the tumor-associated antigen (TAA) CD20 and the CD3, a T-cell surface antigen, with potential immunomodulating and antineoplastic activities. Upon administration, anti-cd20/anti-cd3 bispecific antibody CM355 binds to both T cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B cells. CD20 is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.

anti-CD20/anti-CD3 bispecific antibody MBS303

A bispecific antibody and T-cell engager (TCE) targeting both the tumor-associated antigen (TAA) CD20 and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD20/anti-CD3 bispecific antibody MBS303 binds to both T cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B-cells. CD20 is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. MBS303, composed of a 2:1 bispecific antibody structure, binds to CD20 with two arms and CD3 molecule with one arm to increase affinity with tumor cells and decrease the off-target toxicity of T cells.

anti-CD20/anti-CD3 bispecific IgM antibody IGM2323

An engineered immunoglobulin M (IgM) bispecific antibody, with potential antineoplastic activity. Anti-CD20/CD3 bispecific IgM antibody IGM2323 contains ten high affinity binding domains for the tumor-associated antigen (TAA) CD20, and one binding domain for CD3, a T-cell surface antigen. Upon administration, IGM2323 binds to both T cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B cells. Additionally, IGM-2323 induces complement-dependent cytotoxicity (CDC) to a greater extent than anti-CD20/anti-CD3 IgG bispecific antibodies, thereby further enhancing the killing CD20-expressing tumor cells. The extra binding units of IGM-2323 may bind cancer cells that express relatively low amounts of CD20. Also, compared to IgG format bispecific T-cell engaging antibodies, IGM2323 appears to induce less cytokine release, which may reduce the risk of cytokine release syndrome (CRS). CD20 is exclusively expressed on B-cells during most stages of B cell development and is often overexpressed in B-cell malignancies.

anti-CD20/anti-CD3/anti-CD8 trispecific antibody AZD5492

A trispecific immunoglobulin G (IgG)-like T-cell engaging (TCE) antibody targeting the tumor-associated antigen (TAA) CD20 and the T-cell surface antigens CD3 and CD8, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD20/anti-CD3/anti-CD8 trispecific antibody AZD5492 targets and binds to CD20 on CD20-expressing tumor B-cell, and the CD3 and CD8 antigens on CD8-positive T lymphocytes. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor cells. CD20, a B-cell-specific cell surface antigen, is overexpressed in B-cell lineage malignancies.

anti-CD20/CD3 bispecific antibody JS203

A recombinant bispecific antibody targeting both the tumor-associated antigen (TAA) CD20 and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD20/CD3 bispecific antibody JS203 binds to both T cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B cells. CD20 is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.

anti-CD20/CD37 monoclonal antibody combination PSB202

A combination agent composed of two humanized monoclonal antibodies, PSB102, an Fc-enhanced immunoglobulin G1 (IgG1) monoclonal antibody directed against the human B-cell-specific cell surface antigen and tumor-associated antigen (TAA) CD20, and PSB107, an IgG1 monoclonal antibody directed against the TAA CD37, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD20/CD37 monoclonal antibody combination PSB202 specifically targets and binds to CD20 and CD37 expressed on tumor cells. This induces antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) against CD20- and CD37-expressing B cells, which leads to B-cell apoptosis and the inhibition of tumor cell proliferation. CD20, a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B-cell development, is often overexpressed in B-cell malignancies. CD37, a member of the tetraspanin superfamily of cell surface antigens, is overexpressed on a variety of cancer cell types and plays a key role in tumor cell proliferation.

anti-CD200R1 monoclonal antibody 23ME-00610

A humanized monoclonal antibody directed against the immune checkpoint cell surface transmembrane glycoprotein CD200 receptor 1 (CD200R1; CD200R; HCRTR2; MOX2R; OX2R; CD200 receptor 1), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CD200R1 monoclonal antibody 23ME-00610 targets and binds to CD200R1, thereby preventing the interaction of CD200R1 with its ligand CD200, which is highly expressed on certain tumor cell types, and preventing its activity. This inhibits CD200R1-mediated signaling pathways and may re-activate tumor-exhausted T cells and myeloid cells. This may lead to a T-cell mediated anti-tumor immune response and may kill cancer cells. CD200R1 is an inhibitory receptor expressed on T cells and myeloid cells and plays a key role in the maintenance of immune tolerance and immunosuppression.

anti-CD205 antibody-drug conjugate OBT076

An antibody-drug conjugate (ADC) comprised of an anti-CD205 (lymphocyte antigen 75; Ly75) humanized immunoglobin G1 (IgG1) monoclonal antibody conjugated to DM4, a maytansinoid microtubule disruptor, via a cleavable N-succinimidyl-4-(2-pyridyldithio) butanoate (SPDB) linker, with potential antineoplastic activity. Upon intravenous administration, anti-CD205 ADC OBT076 specifically targets and binds to CD205, a receptor involved in antigen capture and endocytosis, expressed on tumor cells. Following rapid internalization of the ADC/CD205 complex, OBT076 releases its DM4 payload due to cleavage of the SPDB linker by intracellular proteases. Then the DM4 binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of both cell division and cell growth of CD205-expressing tumor cells. CD205, a type I transmembrane surface glycoprotein belonging to the C-type lectin receptor family, is normally expressed on various antigen-presenting cells (APCs) and some leukocyte sub-populations but it is overexpressed in multiple cancer types where it plays a key role in facilitating metastatic invasion.

anti-CD22 ADC TRPH-222

An antibody-drug conjugate (ADC) composed of an anti-CD22 humanized monoclonal antibody site-specifically conjugated, via formylglycine (FG) residues and a protease insensitive 4AP linker, to a cytotoxic microtubule-targeting maytansinoid payload, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of TRPH-222 binds to B-cell-specific CD22 receptors and is rapidly internalized, thereby delivering the payload intracellularly. Upon proteolytic cleavage, the maytansinoid payload binds to tubulin, disrupting microtubule assembly/disassembly dynamics, inhibiting both cell division and tumor cell proliferation. CD22, a cell surface sialoglycoprotein, is expressed on mature B-cells and on most malignant B-cells. The site specific and stable conjugation to the payload allows for a higher drug-to-antibody ratio (DAR) and an enhanced therapeutic index.

anti-CD22 CAR T cells preparation

Any preparation of chimeric antigen receptor (CAR) expressing T lymphocytes that targets the tumor-associated antigen (TAA) CD22.

anti-CD22 CAR-expressing T lymphocytes

A preparation of human T lymphocytes transduced with a recombinant viral vector encoding a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of one or more binding domains targeting the tumor-associated antigen (TAA) CD22 and fused to one or more co-stimulatory, TCR-signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD22 CAR-expressing T lymphocytes, express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing B cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells.

anti-CD22 monoclonal antibody-MMAE conjugate DCDT2980S

An antibody-drug conjugate (ADC) composed of MCDT2219A , a humanized IgG1 anti-CD22 monoclonal antibody covalently linked, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DCDT2980S binds to B-cell-specific CD22 receptors and is rapidly internalized, thereby delivering MMAE intracellularly. Upon proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B-cells.

Anti-CD22 scFv TCRz:41BB-CAR Lentiviral Vector-transduced Autologous T-lymphocytes

Autologous human T-lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric T-cell receptor consisting of an anti-CD22 single chain variable fragment (scFv) and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with CD22-positive cancer are transduced with this lentiviral vector that encodes the CAR gene specific for CD22. After isolation, transduction, expansion in culture and reintroduction into the patient, the anti-CD22 scFv TCRz:41BB-CAR lentiviral vector-transduced autologous T-lymphocytes express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing tumor cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B-cells.

anti-CD22-CAR m971-BBz lentiviral vector-transduced autologous T lymphocytes

Autologous human T-lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of an anti-CD22 single chain variable fragment (scFv) derived from the monoclonal antibody (moAb) 971 (m971), and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with CD22-positive cancer are transduced with this lentiviral vector that encodes the CAR gene specific for CD22. After expansion in culture and reintroduction into the patient, the anti-CD22-CAR m971-BBz lentiviral vector-transduced autologous T-lymphocytes express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing tumor cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B-cells. m971 binds to a membrane proximal epitope on CD22 and has a higher binding affinity compared to any other anti-CD22 moAb.

anti-CD22-CAR m971-BBz lentiviral vector-transduced autologous T lymphocytes CRG-022

Autologous human T lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of an anti-CD22 single chain variable fragment (scFv) derived from the monoclonal antibody (moAb) 971 (m971), and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD22-CAR m971-BBz lentiviral vector-transduced autologous T lymphocytes CRG-022 express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing tumor cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells. m971 binds to a membrane proximal epitope on CD22 and has a higher binding affinity compared to other anti-CD22 moAb.

anti-CD22/anti-CD28 bispecific antibody REGN5837

A hinge-stabilized human immunoglobulin G4 (IgG4) bispecific antibody directed against both the tumor-associated antigen (TAA) CD22 and the co-stimulatory T-cell-specific surface glycoprotein CD28, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD22/anti-CD28 bispecific antibody REGN5837 targets and binds to both CD28 expressed on T cells and CD22 expressed on tumor cells, which crosslinks the T cells to the tumor cells. This may result in the activation of a cytotoxic T-lymphocyte (CTL) response against the CD22-expressing tumor cells. CD22 is exclusively expressed on B cells and is often overexpressed in B-lymphocytic malignancies. It negatively regulates the B-cell receptor.

anti-CD22/CD3 bispecific antibody JNJ-75348780

A human bispecific antibody, with potential antineoplastic activity. Anti-CD22/CD3 bispecific antibody JNJ-75348780 contains two binding sites, one for the tumor-associated antigen (TAA) CD22, and one for the T-cell surface antigen CD3. Upon administration, JNJ-75348780 binds to both CD3 on T cells and CD22-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD22-expressing tumor B cells. CD22 is exclusively expressed on B cells and is often overexpressed in B-lymphocytic malignancies. It negatively regulates the B-cell receptor.

anti-CD226 agonist antibody LY3435151

An agonistic antibody targeting the human cell surface glycoprotein CD226 (DNAX accessory molecule-1; DNAM-1), with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD226 agonist antibody LY3435151 targets and binds to CD226 on a variety of immune cell types, including T cells, natural killer (NK) cells, B cells and monocytes. This induces CD226-dependent signaling pathways, which may trigger the activation of antigen-presenting cells (APCs) and activate T cells and NK cells. This may result in an enhanced cytotoxic T-lymphocyte (CTL)-mediated and NK cell-mediated immune response against tumor cells. CD226, a cell surface glycoprotein that functions as an adhesion molecule, is expressed on various immune cells and plays an important role in the co-activation of T cells and NK cells upon interaction with its ligands CD155 and CD112.

anti-CD228/4-1BB bispecific agent SGN-BB228

A bispecific agent composed of a human immunoglobulin G4 (IgG4) monoclonal antibody targeting the cell surface antigen cluster of differentiation (CD228; melanotransferrin; MFI2; MELTF; p97) fused to a binding protein targeting the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD228/4-1BB bispecific agent SGN-BB228 simultaneously targets and binds to CD228 expressed on the surface of tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T-lymphocytes. This crosslinks CD228-expressing tumor cells and 4-1BB-expressing T-cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation, enhances T-lymphocyte-mediated anti-tumor activity and leads to cytotoxic T-cell-mediated lysis of CD228-expressing tumor cells. CD228, a cell-surfaced, glycosylphosphatidylinoitol (GPI)-anchored glycoprotein that belongs to the transferrin family of iron-binding proteins, is upregulated in certain tumor types including melanoma, mesothelioma and lung cancer. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD228/MMAE antibody-drug conjugate SGN-CD228A

An antibody-drug conjugate (ADC) composed of a humanized antibody targeting the cell surface antigen cluster of differentiation (CD228; melanotransferrin; MFI2; MELTF) that is conjugated, via a beta-glucuronidase-cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Following administration, the antibody moiety of anti-CD228/MMAE ADC SGN-CD228A targets and binds to CD228 on the surface of tumor cells. Following internalization of SGN-CD228A and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CD228-expressing tumor cells. CD228, a cell-surfaced, glycosylphosphatidylinoitol (GPI)-anchored glycoprotein, belongs to the transferrin family of iron-binding proteins.

anti-CD24 monoclonal antibody ATG-031

A humanized monoclonal antibody targeting the cell surface protein CD24, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD24 monoclonal antibody ATG-031 targets and binds to CD24 expressed on tumor cells, thereby blocking the interaction of CD24 with sialic acid-binding Ig-like lectin 10 (Siglec-10) expressed on innate immune cells including tumor-associated macrophages (TAMs) in the tumor microenvironment (TME). This prevents CD24/Siglec-10-mediated signaling and abrogates the CD24/Siglec-10-mediated inhibition of macrophage-mediated phagocytosis of tumor cells. This results in macrophage-dependent tumor cell phagocytosis, repolarization from the immunosuppressive M2 subtype macrophages to the anti-tumor M1 subtype in the TME, and the abrogation of the immunosuppressive TME. CD24, a glycophosphatidylinositol (GPI)-anchored, highly glycosylated cell adhesion protein, is overexpressed on the surface of a variety of cancer cells. Expression of CD24, and its interaction with Siglec-10, protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

anti-CD24 monoclonal antibody KH-801

A Fc-engineered humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the cell surface protein cluster of differentiation 24 (CD24), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD24 monoclonal antibody KH-801 selectively targets and binds to CD24 expressed on tumor cells, thereby blocking the interaction of CD24 with sialic acid-binding Ig-like lectin 10 (Siglec-10) expressed on innate immune cells including tumor-associated macrophages (TAMs) in the tumor microenvironment (TME). This prevents CD24/Siglec-10-mediated signaling and abrogates the CD24/Siglec-10-mediated inhibition of macrophage-mediated phagocytosis of tumor cells. This results in macrophage-dependent tumor cell phagocytosis, repolarization from the immunosuppressive M2 subtype macrophages to the anti-tumor M1 subtype in the TME, and the abrogation of the immunosuppressive TME. This causes immune activation and T-cell infiltration. In addition, KH-801 further induces antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) through its Fc-mediated immune effector function. CD24, a glycophosphatidylinositol (GPI)-anchored, highly glycosylated cell adhesion protein, is overexpressed on the surface of a variety of cancer cells. Expression of CD24, and its interaction with Siglec-10, protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

anti-CD24/anti-4-1BB bispecific monoclonal antibody IBD0333

A bispecific monoclonal antibody targeting the cell surface antigen cluster of differentiation 24 (CD24) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD24/anti-4-1BB bispecific monoclonal antibody IBD0333 simultaneously targets and binds to CD24 expressed on the surface of tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T lymphocytes. This crosslinks CD24-expressing tumor cells and 4-1BB-expressing T-cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation, enhances T-lymphocyte-mediated anti-tumor activity and leads to cytotoxic T-cell-mediated lysis of CD24-expressing tumor cells. CD24, a glycophosphatidylinositol (GPI)-anchored, highly glycosylated cell adhesion protein, is overexpressed on the surface of a variety of cancer cells. Expression of CD24, and its interaction with Siglec-10, protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate. Its expression is correlated with poor prognosis. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CD25 antibody-drug conjugate PF-08046032

An antibody-drug conjugate (ADC) composed of a detuned-affinity monoclonal antibody directed against CD25 (interleukin-2 receptor subunit alpha; IL-2R alpha; IL-2Ra), conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CD25 ADC PF-08046032 targets and binds to CD25 expressed on tumor-infiltrating regulatory T (Treg) cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in the Treg cells. This depletes Treg cells in the tumor microenvironment (TME) and prevents immunosuppression, thereby enhancing anti-tumor immune responses. CD25, the alpha chain of the IL-2 receptor, is highly expressed on Treg cells but not on effector T (Teff) cells in tumors.

anti-CD25 monoclonal antibody BA1106

A human monoclonal antibody directed against CD25 (interleukin-2 receptor subunit alpha; IL-2R alpha; IL-2Ra), with potential antineoplastic activity. Upon administration, anti-CD25 monoclonal antibody BA1106 targets and binds to CD25 expressed on tumor-infiltrating regulatory T (Treg) cells. This may deplete Treg cells in the tumor microenvironment (TME) through antibody-dependent cellular cytotoxicity (ADCC) and prevent immunosuppression, thereby increasing the number of effector T (Teff) cells and enhancing anti-tumor immune responses. CD25, the alpha chain of the IL-2 receptor, is highly expressed on Treg cells but not on Teff cells in tumors.

anti-CD25-IL-2 monoclonal antibody AU-007

A human immunoglobulin (Ig) G1 monoclonal antibody directed against the CD25 subunit-interacting domain of the cytokine interleukin-2 (IL-2; IL2), with potential immunomodulatory activity. Upon administration, anti-CD25-IL2 monoclonal antibody AU-007 targets, binds to and blocks the CD25 subunit-interacting domain of IL-2, thereby blocking the binding of IL-2 to the CD25 subunit (IL-2 receptor subunit alpha; IL-2Ralpha) of the human trimeric IL-2 receptor (IL-2R) expressed on the surface of regulatory T lymphocytes (Tregs), thereby inhibiting IL-2Ralpha-mediated Tregs activation. This may prevent Treg-mediated immunosuppression. As the ability of IL-2 to bind to dimeric CD122 (IL-2Rbeta)/CD132 receptor is preserved, AU-007 promotes immune effector activation by IL-2 via IL-2-mediated signaling through the dimeric IL-2R. This may active an anti-tumor immune response against tumor cells through activation of T lymphocytes, natural killer (NK) cells, and NK T cells, thereby killing cancer cells. In addition, by blocking the binding of IL-2 to CD25 expressed on vascular endothelium and smooth muscle cells and subsequent activation, exacerbation of vascular leak syndrome (VLS) is prevented. IL-2 binds to the IL-2R dimeric receptor expressed on CD8 T effector cells, memory T cells, NK cells and NKT cells and is composed of CD122 and CD132. The IL-2R trimeric receptor expressed on Tregs and vascular endothelium is composed of CD25, CD122 and CD132.

anti-CD26 monoclonal antibody YS110

A humanized, immunoglobulin G1 (IgG1) monoclonal antibody directed against the extracellular domain of dipeptidyl peptidase 4 (CD26; DPP4; DPP IV), with potential antineoplastic activity. Upon administration of anti-CD26 monoclonal antibody YS110, this antibody targets and binds to CD26 expressed on tumor cells. This inhibits CD26 activity and causes internalization of CD26-YS110. This leads to cell cycle arrest, lysis and inhibition of growth in CD26-positive tumor cells. YS110 also induces antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) against CD26-expressing tumor cells. CD26, a 110-kDa, type II transmembrane glycoprotein, is overexpressed in a variety of cancer cell types while absent in normal, healthy cells and plays a key role in tumor cell growth, migration, invasion and survival. It also plays a major role in the regulation of T-cell activity.

anti-CD27 monoclonal antibody

Any monoclonal antibody directed against the CD27 antigen (tumor necrosis factor receptor superfamily member 7; TNFRSF7).

anti-CD27L antibody-drug conjugate AMG 172

An immunoconjugate consisting of a human IgG1 monoclonal antibody directed against CD27L conjugated, via a non-cleavable linker, to the cytotoxic agent maytansinoid DM1, with potential antineoplastic activity. The monoclonal antibody moiety of this immunoconjugate binds to CD27L on tumor cell surfaces. After internalization, the DM1 moiety binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting both cell division and proliferation of cancer cells that express CD27L. CD27L, a type II transmembrane protein and member of the tumor necrosis factor family, is a co-stimulatory molecule constitutively expressed on a subset of activated T cells, B cells, and dendritic cells, which is overexpressed in certain tumor cell types.

anti-CD3 immunotoxin A-dmDT390-bisFv(UCHT1)

A bivalent recombinant fusion protein immunotoxin derived from the anti-CD3 monoclonal antibody UCHT1 with potential antineoplastic activity. Anti-CD3 immunotoxin A-dmDT390-bisFv(UCHT1) consists of 1-390 amino acid residues of chain A diphtheria toxin (DT) joined via a spacer to the Fv fragment of UCHT1, which is connected to a second UCHT1 Fv fragment via a disulfide bond (hence the "bisFv" designation); the addition of the second Fv fragment overcomes the steric hindrance of immunotoxin binding due to the large N-terminal DT domain. Once inside target T cells, the DT moiety catalyzes the transfer of the ADP-ribose moiety of NAD to diphthamide, a posttranslationally modified histidine residue found in elongation factor 2 (EF-2); inactivation of EF-2, disruption of polypeptide chain elongation, and cell death ensue. CD3 is a complex of five cell-surface polypeptides associated with the T cell receptor (TCR) complex.

anti-CD3 x anti-CD20 bispecific antibody-armed activated T cells

Autologous activated T cells that have been coated with bispecific antibodies (BiAb), with potential antineoplastic and immunomodulating activities. In vitro, T cells are activated through exposure to the anti-CD3 murine monoclonal antibody OKT3 and low-dose interleukin 2 (Il-2) for 6-14 days and then armed with anti-CD3 x anti-CD20 bispecific antibody (CD20Bi). Upon administration, anti-CD3 x anti-CD20 bispecific antibody-armed activated T cells (AATC) attach to CD3-expressing T cells and CD20-expressing tumor cells, selectively cross-linking T cells and tumor cells. This may result in the recruitment and activation of cytotoxic T lymphocyte (CTLs), CTL-mediated specific tumor cell lysis, and the secretion of antitumor cytokines and chemokines. CD20, a cell surface phosphoprotein, is found on normal B cells and most B-cell tumors.

anti-CD3/anti-5T4 bispecific antibody GEN1044

A recombinant immunoglobulin G1 (IgG1) bispecific antibody targeting both the human T-cell surface antigen CD3 and oncofetal antigen 5T4, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD3/anti-5T4 bispecific antibody GEN1044 simultaneously targets and binds to CD3 expressed on T cells and 5T4 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the 5T4-expressing tumor cells. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

anti-CD3/anti-BCMA bispecific antibody TQB2934

A T-cell engaging, human, bispecific, immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD3/anti-BCMA bispecific antibody TQB2934 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA found on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.

anti-CD3/anti-CD20 trifunctional bispecific monoclonal antibody FBTA05

A trifunctional bispecific monoclonal antibody with potential antineoplastic activity. FBTA05 contains two antigen-recognition sites: one for human CD3, a T cell surface antigen; and one for human CD20, a tumor-associated antigen that is exclusively expressed on B cells during most stages of B-cell development and often overexpressed in B-cell malignancies. In addition, the modified Fc portion of this antibody binds Fc receptors on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs). FBTA05 brings T cells, CD20-expressing tumor B-cells and APCs together into tricellular complexes, which may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B cells. Fc-mediated binding of APCs in the tricellular complex potentiates CD20 antigen presentation to T cells and the activation of anti-tumor cytotoxic T cells.

anti-CD3/anti-Claudin 18.2 bispecific antibody IBI389

A bispecific antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD3/anti-CLDN18.2 bispecific antibody IBI389 simultaneously binds to both CD3-expressing T cells and CLDN18.2-expressing cancer cells, thereby crosslinking CLDN18.2-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This results in the activation and proliferation of T cells and causes CTL-mediated cell lysis of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

Anti-CD3/Anti-EGFR-bispecific Monoclonal Antibody-armed Activated Autologous T-lymphocytes

Autologous activated T-cells that have been coated with bispecific antibodies (BiAb) comprised of an anti-CD3 monoclonal antibody heteroconjugated to an anti-epidermal growth factor receptor (EGFR) monoclonal antibody, with potential antineoplastic and immunomodulating activities. Upon administration, anti-CD3 x anti-EGFR bispecific antibody-armed activated T-cells (AATC) attach to and selectively cross-link CD3-expressing T-cells and EGFR-expressing tumor cells. This results in the activation of cytotoxic T-lymphocytes (CTLs) and selective cytotoxicity towards the EGFR-expressing tumor cells. In addition, cytokine and chemokine secretion by the T-cells further activates the immune system, which leads to the recruitment and activation of CTLs, and additional CTL-mediated tumor-specific cell lysis. CD3 is part of the functional T-cell receptor (TCR) complex, which is necessary for antigen recognition by T-cells, and is required for signal transduction. EGFR, a receptor tyrosine kinase, is overexpressed on the surfaces of various tumor cell types.

anti-CD3/anti-GUCY2C bispecific antibody PF-07062119

A bispecific antibody against human CD3, a T-cell surface antigen, and human guanylate cyclase 2C (GUCY2C; GCC; guanylyl cyclase C; heat-stable enterotoxin receptor; hSTAR), with potential antineoplastic activity. Upon administration, anti-CD3/anti-GUCY2C bispecific antibody PF-07062119 targets and binds to both CD3 on T cells and GUCY2C expressed on certain tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against GUCY2C-expressing tumor cells. GUCY2C, a transmembrane receptor expressed on intestinal epithelial cells, is overexpressed on certain tumors of the gastrointestinal (GI) tract.

anti-CD3/CD19/CD20 trispecific antibody 1A46

A trispecific immunoglobulin G (IgG)-like T-cell engaging antibody targeting the two tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19) and CD20, and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD3/CD19/CD20 trispecific antibody 1A46 binds to CD19- and/or CD20-expressing tumor B cell and CD3 antigen on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to CD19- and/or CD20-expressing tumor cells, resulting in CTL-mediated killing of tumor cells. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD19 and CD20 may prevent tumor cell antigen escape and relapse.

anti-CD3/CD38 bispecific monoclonal antibody AMG 424

A humanized, bispecific monoclonal antibody (BsAb) targeting CD3, a T-cell surface antigen, and CD38, a human cell surface glycoprotein and tumor-associated antigen (TAA), with potential antineoplastic activity. Upon intravenous administration, anti-CD3/CD38 bispecific monoclonal antibody AMG 424 binds to both CD3 on T cells and CD38 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD3/CD38 bispecific monoclonal antibody IGM-2644

An engineered bispecific, pentameric immunoglobulin M (IgM) monoclonal antibody directed against CD3, a T-cell surface antigen, and CD38, a human cell surface glycoprotein and tumor-associated antigen (TAA), with potential antineoplastic activity. IGM-2644 consists of ten CD38 binding sites and an anti-CD3epsilon single chain variable fragment (scFv) domain fused to a joining chain. Upon intravenous administration, anti-CD3/CD38 bispecific monoclonal antibody IGM-2644 targets and binds to both CD3 on T cells and CD38 expressed on tumor cells. The resulting cross-linkage may trigger T-cell dependent cellular cytotoxicity (TDCC) and complement-dependent cytotoxicity (CDC) against CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD3/CD7-ricin toxin A immunotoxin

An immunotoxin (IT) combination composed of two antibody-drug conjugates (ADCs), one containing a monoclonal antibody against CD3 and one against the CD7 antigen on activated T cells and natural killer (NK) cells, and both conjugated to ricin toxin A (RTA), the A-chain form of the potent plant toxin ricin, that can potentially be used to destroy activated T and NK cells. Upon administration of the anti-CD3/CD7-RTA immunotoxin, the anti-CD3 antibody moiety targets and binds to activated T-cells; the anti-CD7 antibody moiety targets and binds to CD7 on activated T cells and NK cells. Upon internalization and cleavage, the RTA moiety irreversibly inhibits protein synthesis and induces apoptosis in the activated T cells. This may eliminate activated T cells and may improve conditions such as graft-versus-host-disease (GvHD). In addition, the binding and blocking of the anti-CD3 antibody to the T-cell receptor/CD3 complex (TCR/CD3) results in activation-induced cell death (AICD) and immunosuppression.

anti-CD3/humanized 3F8 bispecific antibody-activated T lymphocytes

Autologous activated T cells that have been coated with bispecific antibodies (BiAb) comprised of anti-CD3 murine monoclonal antibody OKT3 heteroconjugated to anti-GD2 humanized monoclonal antibody 3F8 (hu3F8), with potential antineoplastic and immunomodulating activities. In vitro, T cells are exposed to OKT3, which binds to the T cell receptor-CD3 complex on the T cell surface, crosslinks the CD3 receptors and leads to T cell activation. In turn, the hu3F8 monoclonal antibody is heteroconjugated to OKT3. Upon administration, anti-CD3 x anti-GD2 bispecific antibody-armed activated T cells attach to GD2-expressing tumor cells, thereby selectively cross-linking T cells and tumor cells. This results in selective cytotoxicity towards the GD2-expressing tumor cells. In addition, cytokine and chemokine secretion by the T cells further activates the immune system, which leads to the recruitment and activation of cytotoxic T lymphocytes (CTLs), and additional CTL-mediated tumor-specific cell lysis. GD2, a disialoganglioside and tumor-associated antigen, is overexpressed in a variety of tumor cell types. CD3 is part of the functional T cell receptor (TCR) complex, which is necessary for antigen recognition by T cells, and is required for signal transduction.

anti-CD3/MUC1 antibody-armed PD-1 inhibitor-induced cytokine-induced killer cells

A preparation of cytokine-induced killer cells (CIKs), which have been exposed, ex vivo, to a specific set of cytokines and a programmed cell death protein 1 (PD-1) inhibitor, mixed with a bispecific anti-cluster of differentiation 3 (CD3)/anti-mucin-1 (MUC1) antibody, with potential anti-tumor cytotoxic activity. Upon administration of the anti-CD3/MUC1 antibody-armed PD-1 inhibitor-induced CIKs, the antibody moiety binds to both CD3 on the CIKs and MUC1 on cancer cells. This crosslinks the CIKs and tumor cells, which allows the CIKs to target and lyse MUC1-expressing cancer cells. PD-1 blockade activates the CIKs. The cytokines used, usually interferon-gamma (IFNg), interleukin 1 (IL-1), and IL-2, stimulate the proliferation and maturation of peripheral blood mononuclear cells (PBMCs) into CIK cells. Anti-CD3 stimulation allows for the CIKs' improved lytic activity.

anti-CD30 antibody-drug conjugate SGN-35C

An antibody-drug conjugate (ADC) composed of brentuximab (cAC10), a chimeric immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor necrosis factor (TNF) receptor CD30 (tumor necrosis factor receptor superfamily, member 8; TNFRSF8), conjugated to a camptothecin-derived topoisomerase 1 inhibitor (TOP1i), with potential antineoplastic activity. Upon administration, anti-CD30 ADC SGN-35C targets and binds to CD30 expressed on tumor cells. Upon binding and internalization, the TOP1i moiety is released, binds to TOP1 and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of CD30-expressing tumor cells. CD30 may be constitutively expressed in certain B- and T-cell lymphoma while expression is limited in normal, healthy cells.

anti-CD30 antibody-drug conjugate SGN-35T

An antibody-drug conjugate (ADC) composed of brentuximab (cAC10), a chimeric immunoglobuin G1 (IgG1) monoclonal antibody directed against the tumor necrosis factor (TNF) receptor CD30 (tumor necrosis factor receptor superfamily, member 8; TNFRSF8) conjugated, via a protease-cleavable tripeptide linker, comprised of D-leucine-alanine-glutamate (DLAE), to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CD30 ADC SGN-35T targets, binds to and is internalized by CD30-positive tumor cells. Upon enzymatic cleavage of the cleavable linker, MMAE is released into the cytosol. MMAE binds to tubulin and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis of CD30-expressing tumor cells. In addition, SGN-35T induces bystander effect in neighboring tumor cells and immunogenic cell death (ICD). CD30 may be constitutively expressed in certain B- and T-cell lymphoma while expression is limited in normal, healthy cells. The linkage system in is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells.

anti-CD30 monoclonal antibody MDX-1401

A fully human, second-generation, nonfucosylated monoclonal antibody directed against the cell surface receptor CD30 with potential immunomodulating and antineoplastic activities. Anti-CD30 monoclonal antibody MDX-1401 specifically binds to the CD30 antigen, which may result in a cytotoxic T lymphocyte (CTL) response against CD30-expressing tumor cells. CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on activated lymphocytes transiently and is constitutively expressed in hematologic malignancies including Hodgkin's disease and some T-cell non-Hodgkin's lymphomas. Compared to conventional antibodies, deletion of fucose molecules on the antibody backbone, as is done in MDX-1401, may result in an increased affinity for Fc receptors and an enhanced antibody-dependent cellular cytotoxicity (ADCC).

anti-CD30 monoclonal antibody XmAb2513

A humanized monoclonal antibody directed against the cell surface receptor CD30 with potential immunotherapeutic activity. Anti-CD30 monoclonal antibody XmAb2513 specifically binds to the CD30 antigen, which may result in a cytotoxic T lymphocyte (CTL) response against CD30-expressing tumor cells. CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on activated lymphocytes transiently and is constitutively expressed in hematologic malignancies including Hodgkin's disease and some T-cell non-Hodgkin's lymphomas.

anti-CD30/CD3 bispecific antibody GEN3017

An Fc-silenced immunoglobulin G1 (IgG1) bispecific monoclonal antibody against the tumor-associated antigen (TAA) CD30 (tumor necrosis factor receptor superfamily member 8; TNFRSF8) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD30/CD3 bispecific antibody GEN3017 targets and binds to both CD30 on the surface of tumor cells and CD3 on T cells. This results in the cross-linking of tumor cells and T cells, and induces a cytotoxic T-lymphocyte (CTL) response against CD30-expressing tumor cells. CD30, a member of the tumor necrosis factor receptor superfamily, is overexpressed on the surfaces of certain tumor cells.

anti-CD30/DM1 antibody-drug conjugate F0002

An antibody drug conjugate (ADC) consisting of a monoclonal antibody directed against the tumor necrosis factor (TNF) receptor CD30 conjugated, via a nonreducible thioether linker (succinimidyl trans-4-(maleimidylmethyl)cyclohexane-1-carboxylate or SMCC), to the cytotoxic agent maytansinoid mertansine (DM1), with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of F0002 targets and binds to CD30-expressing tumor cells. Upon cellular uptake and internalization, the mertansine moiety binds to tubulin and interferes with microtubule assembly and disassembly dynamics. This inhibits both cell division and the proliferation of tumor cells that express CD30. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8; TNFRSF8) may be constitutively expressed in some hematologic malignancies.

anti-CD32B monoclonal antibody BI-1206

A fully human monoclonal antibody targeting the Fc gamma receptor IIB (FcgRIIB; CD32B) with potential immunomodulatory and antineoplastic activities. Upon intravenous administration, anti-CD32B monoclonal antibody BI-1206 selectively binds to CD32B, a receptor expressed on the surface of B cells. This prevents CD32B-mediated internalization of anti-CD20 monoclonal antibodies, such as rituximab, which abrogates tumor cell resistance caused by CD32B-mediated monoclonal antibody internalization and degradation of CD32B-expressing B cells. By blocking CD32B, BI-1206 may recover and enhance the activity of rituximab and other anti CD20 monoclonal antibodies. In addition, BI-1206 itself activates the immune system to exert an immune-mediated tumor cell death of B cells. CD32B, an inhibitory member of the FcgammaR family, is implicated in immune cell desensitization and tumor cell resistance.

anti-CD32B monoclonal antibody BI-1607

A human immunoglobulin G1 (IgG1) monoclonal antibody targeting Fc gamma receptor IIB (FcgRIIB; CD32B), with potential immunomodulatory- and antineoplastic-enhancing activities. Upon administration, anti-CD32B monoclonal antibody BI-1607 selectively targets and binds to CD32B, an inhibitory Fc gamma receptor (FcgR) protein expressed on immune cells, including macrophages. This prevents both the binding of human epidermal growth factor receptor 2 (HER2; ErbB2; HER-2)-targeting monoclonal antibodies to CD32B, and CD32B-mediated inhibition of the activation of macrophages. By blocking CD32B, BI-1607 may enhance the activity of anti-HER2 monoclonal antibodies. CD32B, an inhibitory member of the FcgR family, is implicated in immune cell desensitization and tumor cell resistance.

anti-CD33 antibody-drug conjugate BL-M11D1

An antibody-drug conjugate (ADC) composed of gemtuzumab, an immunoglobulin G4 (IgG4) monoclonal antibody directed against the CD33 antigen, conjugated, via a cathepsin B-cleavable linker, to the camptothecin derivative and topoisomerase 1 inhibitor Ed-04, with potential antineoplastic activity. Upon administration of anti-CD33 ADC BL-M11D1, gemtuzumab specifically targets and binds to the cell surface antigen CD33 expressed on myeloid leukemia cells. Upon binding, internalization and linker cleavage, Ed-04 is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells that express CD33. Gemtuzumab may also induce an antibody-dependent cellular cytotoxicity (ADCC) against CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and myeloid leukemia cells.

anti-CD33 antibody-drug conjugate IMGN779

An antibody-drug conjugate (ADC) consisting of the humanized monoclonal antibody Z4681A conjugated, via a cleavable disulfide linker, to the cytotoxic DNA alkylating agent DGN462, which is an indolino-benzodiazepine dimer containing a mono-imine moiety, with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DGN462 conjugate IMGN779 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DGN462 moiety is released, and covalently binds to and alkylates DNA, thereby causing cell cycle arrest, apoptosis and inhibition of cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and myeloid leukemia cells.

anti-CD33 antigen/CD3 receptor bispecific monoclonal antibody AMV564

An anti-CD33/anti-CD3 bispecific tetravalent antibody, with potential immunostimulatory and antineoplastic activities. Anti-CD33/CD3 tetravalent bispecific monoclonal antibody AMV564 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD33, a tumor-associated antigen (TAA) overexpressed on the surface of a variety of tumor cell types. Upon infusion of AMV564, this bispecific antibody binds to CD3-expressing T cells and CD33-expressing tumor cells, thereby crosslinking CD33-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This may result in a potent CTL-mediated cell lysis of CD33-expressing cells. CD33, a glycoprotein expressed by a variety of cancers, including the majority of acute myeloid leukemias (AMLs), and normal non-pluripotent hematopoietic stem cells, plays a key role in tumor initiation, proliferation and progression.

anti-CD33 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD33 CAR T cells specifically recognize and kill CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.

anti-CD33 GSPT1 degrader BMS-986497

A targeted protein degrader (TPD) composed of OR000283, an antibody directed against the tumor-associated antigen (TAA) cluster of differentiation 33 (CD33), conjugated, via a cleavable beta-glucuronide linker, to SMol006, a membrane-permeable selective molecular glue degrader (MGD) of the translational termination factor GSPT1, with potential antineoplastic activity. Upon intravenous administration, anti-CD33 GSPT1 degrader BMS-986497 specifically targets and binds, with its antibody moiety, to CD33-expressing tumor cells. Upon internalization and cleavage, SMol006 specifically targets and binds to GSPT1, leading to GSPT1 degradation via the E3 ubiquitin ligase pathway. This disrupts oncogenic signaling, inhibits proliferation, and induces apoptosis in CD33-driven tumors. The translation termination factor GSPT1, a G-loop degron-containing protein, plays a key role in protein translation and is dysregulated in various tumor cell types. CD33, a cell surface antigen expressed on normal non-pluripotent hematopoietic stem cells, is overexpressed on myeloid leukemia cells.

anti-CD33 monoclonal antibody BI 836858

An engineered, fully human, immunoglobulin (Ig) G1 anti-CD33 monoclonal antibody, with potential antineoplastic activity. Upon administration, anti-CD33 monoclonal antibody BI 836858 induces an antibody-dependent cellular cytotoxicity (ADCC) against CD33-expressing tumor cells, leading to cell death. CD33, a cell surface antigen expressed on normal non-pluripotent hematopoietic stem cells, is overexpressed on myeloid leukemia cells.

anti-CD33 monoclonal antibody-DM4 conjugate AVE9633

An immunoconjugate consisting of the humanized monoclonal antibody huMy9-6 conjugated to the cytotoxic maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DM4 conjugate AVE9633 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DM4 moiety is released, binds tubulin, and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of cell division and cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells.

anti-CD33/BET degrader ADC ABBV-787

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody directed against the tumor-associated antigen (TAA) CD33 conjugated to a bromodomain and extra-terminal domain (BET) degrader payload, with potential antineoplastic activity. Upon administration of anti-CD33/BET degrader ADC ABBV-787, the monoclonal antibody portion of ABBV-787 specifically targets and binds to the cell surface antigen CD33 expressed on myeloid leukemia cells. Upon internalization, the BET degrader payload is released and leads, through an as of yet not fully elucidated mechanism, to the degradation of BET proteins by the ubiquitin-proteasome system. This dysregulates gene expression and specifically leads to the downregulation of the expression of certain growth-promoting genes, which may inhibit the proliferation of BET-overexpressing and CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and myeloid leukemia cells. BET family of proteins, comprised of bromodomain-containing proteins 2 (BRD2), 3 (BRD3), and 4 (BRD4) as well as bromodomain testis-specific protein (BRDT), are transcriptional regulators that are overexpressed in certain tumor cells and play important roles during cellular development and growth.

anti-CD33/CD123/CD70 DARPin CD3 engager MP0533

A multi-specific T-cell engaging designed ankyrin repeat proteins (DARPin) composed of a chain of six covalently linked DARPin domains of which three domains target the three tumor-associated antigens (TAAs) cluster of differentiation 33 (CD33), CD123 and CD70, one domain targets CD3 on T cells and two domains target human serum albumin (HSA) to prolong half-life, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD33/CD123/CD70 DARPin CD3 engager MP0533 selectively targets and binds to CD33, CD123 and CD70 that are expressed on a variety of tumor cells. The simultaneous binding of the CD3-targeting DARPin domain of MP0533 to T cells results in local clustering of the TAA-expressing tumor cells and T cells, and local immune cell activation through the promotion of T-cell activation, cytokine and chemokine release and T-cell-mediated anti-tumor immune responses. CD33, CD123 and CD70 are all present on acute myeloid leukemia (AML) cells and are more likely to be expressed together on AML blast cells and leukemic stem cells (LSCs) than on healthy cells, such as hematopoietic stem cells (HSCs), that may express a single TAA. The binding of MP0533 to either two or three TAAs enhances its selectivity for AML cells over healthy cells.

anti-CD33/CD3 bispecific antibody

A bispecific antibody directed against both the T-cell surface antigen CD3 and the tumor-associated antigen (TAA) CD33, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD33/CD3 bispecific antibody binds to both CD3 on cytotoxic T-lymphocytes (CTLs) and CD33 on CD33-expressing tumor cells, thereby crosslinking tumor cells and CTLs. This activates and redirects CTLs to CD33-expressing tumor cells, which results in the CTL-mediated cell death of CD33-expressing tumor cells. CD33, a myeloid differentiation antigen, is expressed on normal non-pluripotent hematopoietic stem and progenitor cells (HSPCs) and is overexpressed on a variety of cancer cell types, including acute myeloid leukemia (AML). It plays a key role in tumor initiation, proliferation and progression.

anti-CD33/CD3 bispecific antibody GEM 333

A bispecific antibody possessing two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for the tumor-associated antigen (TAA) CD33, with potential immunostimulating and antineoplastic activities. Upon administration of anti-CD33/CD3 bispecific antibody GEM 333, this bispecific antibody binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD33 antigen found on CD33-expressing tumor cells, thereby crosslinking tumor cells and CTLs. This activates and redirects CTLs to CD33-expressing tumor cells, which results in the CTL-mediated cell death of CD33-expressing tumor cells. CD33, a myeloid differentiation antigen, is expressed on normal non-pluripotent hematopoietic stem and progenitor cells (HSPCs) and is overexpressed on a variety of cancer cell types, including acute myeloid leukemia (AML). It plays a key role in tumor initiation, proliferation and progression.

anti-CD33/CD3 bispecific antibody JNJ-67571244

A bispecific antibody possessing two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for the tumor-associated antigen (TAA) CD33, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-CD33/CD3 bispecific antibody JNJ-67571244 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD33 antigen expressed on certain tumor cells, thereby crosslinking tumor cells and CTLs. This activates and redirects CTLs to CD33-expressing tumor cells, which results in CTL-mediated killing of CD33-expressing tumor cells. CD33, a myeloid differentiation antigen, is expressed on normal non-pluripotent hematopoietic stem and progenitor cells (HSPCs) and is overexpressed on a variety of cancer cell types, including acute myeloid leukemia (AML). It plays a key role in tumor initiation, proliferation and progression.

anti-CD352 antibody-drug conjugate SGN-CD352A

An antibody-drug conjugate (ADC) consisting of an engineered cysteine humanized monoclonal antibody (EC-mAb) targeting CD352 (SLAM family member 6; SLAM6) that is conjugated to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-CD352 ADC SGN-CD352A, the antibody moiety targets the cell surface antigen CD352. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD352-overexpressing tumor cells. CD352, a tumor-associated antigen (TAA), is overexpressed on a variety of cancers. Cysteine engineering of the monoclonal antibody allows for a site-specific, stable conjugation and uniform loading of the PBD agent to the antibody.

anti-CD37 bispecific monoclonal antibody GEN3009

An Fc-engineered, humanized, bispecific hexamer formation-enhanced immunoglobulin (Ig) G1 monoclonal antibody that targets two separate epitopes on the tumor-associated antigen (TAA) CD37, with the E430G hexamerization-enhancing mutation, with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CD37 bispecific monoclonal antibody GEN3009 specifically targets and binds to two non-overlapping CD37 epitopes, thereby inducing an assembly of antibody hexamers through intermolecular Fc-Fc interactions at the cell surface of CD37-overexpressing tumor cells. These hexamers recruit and activate C1, the first component of complement, thereby triggering the complement cascade which activates the immune system to induce complement-dependent cytotoxicity (CDC). In addition, GEN3009 binding to the CD37-overexpressing tumor cells also causes antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD37, a member of the tetraspanin superfamily of cell surface antigens, is expressed at high-levels on B cells and to a lesser extent on T cells and myeloid cells. The E430G mutation in the Fc domains enhances Fc-mediated IgG hexamerization upon cellular target binding, and enhances CDC.

anti-CD37 monoclonal antibody BI 836826

An Fc-engineered, chimeric immunoglobulin (Ig) G1 monoclonal antibody against the tumor-associated antigen (TAA) CD37, with potential antineoplastic activity. Upon administration, the anti-CD37 monoclonal antibody BI 836826 both activates the immune system to induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against CD37-overexpressing tumor cells and induces apoptosis in these tumor cells. BI 836826 is Fc-engineered to improve ADCC activity and enhance affinity for the receptor Fc-gamma-RIIIa, which is expressed on human natural killer (NK) cells. CD37, a member of the tetraspanin superfamily of cell surface antigens, is overexpressed on a variety of cancer cell types and plays a key role in tumor cell proliferation.

anti-CD37-CAR-expressing T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD37 (cluster of differentiation 37), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD37-CAR T-cells specifically recognize and kill CD37-expressing tumor cells. CD37, a member of the tetraspanin superfamily of cell surface antigens, is expressed in B-cell non-Hodgkin lymphomas (NHL), in chronic lymphocytic leukemia (CLL), and in some cases of cutaneous and peripheral T-cell lymphomas. It plays a key role in tumor cell proliferation.

anti-CD38 antibody-drug conjugate STI-6129

An antibody-drug conjugate (ADC) composed of STI-5171, a fully human monoclonal antibody targeting human cell surface glycoprotein and tumor-associated antigen (TAA) CD38, site-specifically conjugated, via a non-polyethylene glycol linker, to a monomethyl auristatin F (MMAF)-derived cytotoxic payload, with potential antineoplastic activity. Upon administration of anti-CD38 ADC STI-6129, the antibody moiety targets and binds to CD38 on tumor cells. Upon antibody/antigen binding and internalization, the MMAF derivative binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD38 monoclonal antibody CID-103

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the cell surface glycoprotein ADP-ribosyl cyclase 1 (CD38), with potential antineoplastic activity. Upon administration, anti-CD38 monoclonal antibody CID-103 specifically targets and binds to CD38 expressed on tumor cells. This may trigger antibody-dependent cellular cytotoxicity (ADCC), cell lysis and depletion of CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies.

anti-CD38 monoclonal antibody SAR442085

A preparation of Fc-engineered monoclonal antibody that targets the cell surface glycoprotein CD-38 with potential antineoplastic activity. Although the exact mechanisms(s) through which this agent exerts its effects have yet to be fully elucidated, upon administration, anti-CD38 monoclonal antibody SAR442085 targets and binds to CD38 on CD38-positive tumor cells. This may trigger, in addition to other possible responses, antitumoral antibody-dependent cellular cytotoxicity (ADCC) and may eventually lead to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies.

anti-CD38 monoclonal antibody SCTC21C

A monoclonal antibody that targets the cell surface glycoprotein CD38, with potential antineoplastic activity. Upon administration, anti-CD38 monoclonal antibody SCTC21C targets and binds to CD38 on CD38-positive tumor cells. This may kill, possiby through antibody-dependent cellular cytotoxicity (ADCC) or other responses, CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies.

anti-CD38 monoclonal antibody SG301

A human immunoglobulin G1 kappa (IgG1k) monoclonal antibody that targets the cell surface glycoprotein CD38, with potential antineoplastic activity. Although the exact mechanisms(s) through which this agent exerts its effects have yet to be fully elucidated, upon administration, anti-CD38 monoclonal antibody SG301 targets and binds to CD38 on CD38-positive tumor cells. This may trigger, in addition to other possible responses, antitumoral antibody-dependent cellular cytotoxicity (ADCC) and may eventually lead to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD38 monoclonal antibody TAK-079

A human, non-agonistic immunoglobulin G1 (IgG1) monoclonal antibody directed against the cell surface glycoprotein ADP-ribosyl cyclase 1 (CD38) with potential immunomodulating and antineoplastic activities. Anti-CD38 monoclonal antibody TAK-079 specifically binds to CD38 that is expressed on human plasmablasts, plasma cells, NK cells and activated T and B cells. This may trigger antibody-dependent cellular cytotoxicity (ADCC), cell lysis and depletion of CD38-expressing cells. Additionally, TAK-079 does not induce CD38-dependent signaling and does not promote cytokine activation in peripheral blood mononuclear cells (PMBCs). CD38, a type II transmembrane glycoprotein, is overexpressed on cells associated with autoimmune diseases and hematologic malignancies.

anti-CD38 monoclonal antibody TJ202/MOR202

A fully human monoclonal antibody directed against the cell surface glycoprotein CD-38 with potential antineoplastic activity. Anti-CD38 monoclonal antibody TJ202/MOR202 specifically binds to CD38 on CD38-positive tumor cells. This may trigger antitumoral antibody-dependent cellular cytotoxicity (ADCC) and may eventually lead to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.

anti-CD38 scFv/Anti-DOTA scFv fusion protein CD38-SADA

A fusion protein composed of a single chain variable fragment (scFv) targeting the human cell surface glycoprotein and tumor-associated antigen (TAA) CD38, an scFv targeting the chelating agent 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) and a self-assembling and disassembling (SADA) domain that can self-assemble from a monomeric polypeptide into tetrameric protein, that may be used as a pre-targeted radioimmunotherapeutic agent. Upon administration, anti-CD38 scFv/anti-DOTA scFv fusion protein CD38-SADA assembles in tetramers and the anti-CD38 scFv binds to CD38-expressing tumor cells. The unbound CD38-SADA is excreted. Upon administration of a DOTA-based radioactive payload, the anti-DOTA scFv binds to the DOTA moiety of the radioactive payload, and radiation is selectively delivered to tumor cells expressing CD38. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD38-CAR-TCRz/4-1BB-expressing T lymphocytes

A preparation of genetically modified T lymphocytes that have been transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 38 (CD38) that is linked to tandem costimulatory domains of the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3z) and 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD38-CAR-TCRz/4-1BB-expressing T lymphocytes are directed to and induce selective toxicity in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.

anti-CD38/anti-CD47 bispecific antibody ISB 1442

A human bispecific antibody directed against the human cell surface glycoproteins CD38 and CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, the biparatopic anti-CD38 moiety of anti-CD38/anti-CD47 bispecific antibody ISB 1442 targets and binds to different regions of CD38 on CD38-expressing tumor cells, and enables the binding of the anti-CD47 moiety to CD38/CD47-expressing tumor cells. The CD47 binding by ISB 1442 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD38/CD47-expressing tumor cells. In addition, the CD38 binding by ISB 1442 may trigger antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cell mediated phagocytosis (ADCP) and antibody-mediated complement dependent cytotoxicity (CDC) in CD38-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies. ISB 1442 enables CD47 binding only upon CD38 crosslinking. This may prevent side effects that would have resulted from the binding of the anti-CD47 moiety to CD47 expressed on healthy hematopoietic stem cells (HSCs).

anti-CD38/BCMA CAR T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a dual-targeted chimeric antigen receptor (CAR) recognizing the tumor-associated antigens (TAAs), cluster of differentiation 38 (CD38) and B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the anti-CD38/BCMA CAR T cells are directed to and induce selective toxicity in both CD38- and BCMA-expressing cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis. BCMA is found on the surfaces of plasma cells and is and overexpressed on malignant plasma cells.

anti-CD38/CD28xCD3 tri-specific monoclonal antibody SAR442257

A tri-specific T-cell engager and monoclonal antibody targeting CD38, a human cell surface glycoprotein and tumor-associated antigen (TAA), CD3, a T-cell surface antigen, and CD28, a T-cell specific surface glycoprotein and co-stimulatory molecule, with potential antineoplastic activity. Upon intravenous administration, anti-CD38/CD3/CD28 tri-specific monoclonal antibody SAR442257 targets and binds to CD3 and CD28 on T-cells and CD38 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD38-expressing tumor cells. In addition, SAR442257 can also directly target CD28 expressed on tumor cells, such as multiple myeloma cells, thereby enhancing the anti-tumor activity of this agent and allowing it to bind to tumor cells when CD38 is occupied by other antibodies. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD38/CD3 bispecific monoclonal antibody GBR 1342

A humanized, bispecific monoclonal antibody (BsAb) against human CD3, a T-cell surface antigen, and the human cell surface glycoprotein CD38, a tumor-associated antigen (TAA), with potential antineoplastic activity. Upon administration, anti-CD38/anti-CD3 bispecific monoclonal antibody GBR 1342 binds to both CD3 on T cells and CD38 expressed on certain tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a potent cytotoxic T-lymphocyte (CTL) response against CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis. GBR 1342 uses the proprietary bispecific engagement by antibodies based on the T-cell receptor (BEAT) platform.

anti-CD38/CD3 bispecific monoclonal antibody XmAb18968

A bispecific monoclonal antibody targeting CD3, a T-cell surface antigen, and CD38, a human cell surface glycoprotein and tumor-associated antigen (TAA), with potential antineoplastic activity. Upon administration, anti-CD3/CD38 bispecific monoclonal antibody XmAb18968 binds to both CD3 on T cells and CD38 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies; its expression has been correlated with poor prognosis.

anti-CD39 antibody/TGF-beta RII ectodomain fusion protein ES014

A fusion protein composed of a monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1) and fused to the transforming growth factor-beta receptor type II (TGF-beta RII) ectodomain, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39/TGF-beta RII ectodomain fusion protein ES014 specifically and simultaneously targets and binds to the CD39 antigen and TGF-beta in the tumor microenvironment (TME), thereby preventing CD39- and TGF-beta-mediated signaling. By preventing CD39 activation, the conversion and degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP) is abrogated as CD39 is the rate-limiting enzyme in the ATP-adenosine pathway. This leads to an increase in the extracellular levels of immunogenic ATP and a decrease in the levels of immunosuppressive adenosine within the TME. A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic and other myeloid-derived cells that are necessary for innate and adaptive immunity. The binding to TGF-beta prevents the activation of TGF-beta RII-mediated signaling pathways and also prevents the activation of CD39. This further reverses the immunosuppressive nature of the TME. This may further stimulate a T-cell-mediated anti-tumor immune response and may inhibit tumor cell proliferation. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy; blocking its action may improve anti-tumor immune responses. TGF-beta is expressed by a number of cancer cell types and is involved in cancer cell proliferation, tumor progression, and immunosuppression. It suppresses T-cell activation and induces CD39 expression.

anti-CD39 monoclonal antibody AB598

An immunoglobulin G1 (IgG1) Fc-silent human monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody AB598 specifically targets and binds to the CD39 antigen, thereby preventing the conversion and degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP). This leads to an increase in the extracellular levels of immunogenic ATP and a decrease in the levels of immunosuppressive adenosine within the tumor microenvironment (TME). A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic and other myeloid-derived cells that are necessary for innate and adaptive immunity. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy; blocking its action may improve anti-tumor immune responses.

anti-CD39 monoclonal antibody IPH5201

A monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody IPH5201 specifically targets and binds to the CD39 antigen, thereby preventing the conversion and degradation of the immune-stimulatory adenosine triphosphate (ATP) to adenosine monophosphate (AMP). This leads to an increase in the extracellular levels of ATP and a decrease in the levels of immunosuppressive adenosine within the tumor microenvironment (TME). A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic cells (DCs) and other myeloid-derived cells that are necessary for innate and adaptive immunity. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy. Blocking its action may improve anti-tumor immune responses.

anti-CD39 monoclonal antibody JS019

A recombinant, fully human monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody JS019 specifically targets and binds to the CD39 antigen, thereby preventing the conversion and degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP). This leads to an increase in the extracellular levels of immunogenic ATP and a decrease in the levels of immunosuppressive adenosine within the tumor microenvironment (TME). A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic and other myeloid-derived cells that are necessary for innate and adaptive immunity. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy; blocking its action may improve anti-tumor immune responses.

anti-CD39 monoclonal antibody PUR001

A monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody PUR001 specifically targets and binds to the CD39 antigen, thereby preventing the conversion and degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP). This leads to an increase in the extracellular levels of immunogenic ATP and a decrease in the levels of immunosuppressive adenosine within the tumor microenvironment (TME). A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic and other myeloid-derived cells that are necessary for innate and adaptive immunity. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy; blocking its action may improve anti-tumor immune responses.

anti-CD39 monoclonal antibody SRF617

A fully human monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody SRF617 specifically binds to the CD39 antigen, thereby preventing the conversion and degradation of adenosine triphosphate (ATP) to adenosine monophosphate (AMP). This leads to an increase in the extracellular levels of immunogenic ATP and a decrease in the levels of immunosuppressive adenosine within the tumor microenvironment (TME). A high level of ATP increases pro-inflammatory cytokine levels and promotes both T-cell proliferation and the stimulation of dendritic and other myeloid-derived cells that are necessary for innate and adaptive immunity. CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy. Blocking its action may improve anti-tumor immune responses.

anti-CD39 monoclonal antibody TTX-030

A fully human monoclonal antibody directed against the cell surface receptor CD39 (cluster of differentiation 39; ectonucleoside triphosphate diphosphohydrolase-1; NTPDase1; ENTPD1) with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD39 monoclonal antibody TTX-030 specifically binds to the CD39 antigen, which may inhibit both the conversion of adenosine triphosphate (ATP) to adenosine monophosphate (AMP) and the subsequent generation of immunosuppressive extracellular adenosine in the tumor microenvironment (TME). CD39, a cell surface ectonucleosidase, is upregulated on tumor cells as an immune evasion strategy; blocking its action may promote the stimulation of dendritic and other myeloid-derived cells that are necessary for both innate and adaptive immunity.

anti-CD4 CAR T cells

A preparation of T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD4 and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD4 CAR T cells target and bind to CD4-expressing tumor cells, thereby inducing selective toxicity in CD4-expressing tumor cells. CD4 antigen is expressed in CD4-positive T cell lymphomas.

anti-CD40 agonist monoclonal antibody ABBV-927

An agonistic monoclonal antibody directed against the B-cell surface antigen CD40, with potential antineoplastic activity. Upon administration, ABBV-927 binds to CD40 on a variety of immune cell types. This induces CD40-dependent signaling pathways, triggers the proliferation and activation of antigen-presenting cells (APCs), and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells and plays a key role in the activation of the immune system.

anti-CD40 agonist monoclonal antibody CDX-1140

A fully human immunoglobulin G2 (IgG2) agonistic monoclonal antibody targeting the B-cell surface antigen CD40, with potential immunostimulatory and antineoplastic activities. Upon administration, CDX-1140 targets and binds to CD40 on a variety of immune cell types. This induces CD40-dependent signaling pathways, triggers the proliferation and activation of antigen-presenting cells (APCs) and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as dendritic cells (DCs), macrophages and B cells, and plays a key role in the activation of the immune system.

anti-CD40 agonist monoclonal antibody MIL97

A recombinant, humanized, agonistic monoclonal antibody targeting the B-cell surface antigen CD40, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD40 agonist monoclonal antibody MIL97 targets and binds to CD40 on a variety of immune cell types. This induces CD40-dependent signaling pathways, triggers the proliferation and activation of antigen-presenting cells (APCs) and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as dendritic cells (DCs), macrophages and B-cells, and plays a key role in the activation of the immune system.

anti-CD40 agonistic monoclonal antibody LNF1901

A humanized, agonistic monoclonal antibody targeting the B-cell surface antigen CD40, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CD40 agonistic monoclonal antibody LNF1901 targets and binds to CD40 on a variety of immune cell types. This induces CD40-dependent signaling pathways, triggers the proliferation and activation of antigen-presenting cells (APCs) and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as dendritic cells (DCs), macrophages and B cells, and plays a key role in the activation of the immune system.

Anti-CD40 Monoclonal Antibody Chi Lob 7/4

An IgG1 chimeric monoclonal antibody agonist of the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-CD40 monoclonal antibody Chi Lob 7/4 binds to CD40 on a variety of immune cell types, triggering the cellular proliferation and activation of antigen-presenting cells (APCs), activating B cells and T cells, and enhancing the immune response; in addition, this agent binds to the CD40 antigen present on the surfaces of some solid tumor cells, resulting in complement-dependent cytotoxicity (CDC) and antibody-dependent cytotoxicity (ADCC) eventually resulting in decreased tumor growth. CD40, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, many B-cell malignancies, and many solid tumors, mediating both indirect tumor cell death through the activation of the immune system and direct tumor cell apoptosis.

anti-CD40/anti-TAA bispecific monoclonal antibody ABBV-428

A bispecific monoclonal antibody composed of a binding domain for an epitope found on the cell-surface receptor CD40 linked to a binding domain directed to an as of yet undisclosed tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. Upon administration of anti-CD40/anti-TAA bispecific monoclonal antibody ABBV-428, the anti-TAA moiety targets and binds to the TAA expressed on the tumor cells. The agonistic anti-CD40 moiety targets and binds to various CD40-expressing immune cells. This leads to the activation and proliferation of effector and memory T cells, and enhances the immune response against tumor cells, which kills and inhibits the proliferation of the TAA-expressing tumor cells. CD40, a stimulatory receptor and a member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as macrophages, B lymphocytes, and dendritic cells (DCs); it plays a key role in the activation of the immune system.

anti-CD40L Fc-fusion protein BMS-986004

A dimeric fusion protein composed of the C-terminus of the domain antibody (dAb) BMS2h-572-633 targeting the CD40 ligand (CD40L or CD154) linked to a modified Fc fragment of immunoglobulin G1 (IgG1), with potential immunomodulatory activity. Upon intravenous administration, the peptide moiety of anti-CD40L antibody BMS-986004 specifically targets and binds to CD40L expressed on T lymphocytes. This prevents the binding of CD40L to its cognate receptor CD40 expressed on B lymphocytes, macrophages, and dendritic cells (DCs). This prevents T-cell mediated proliferation and differentiation of B cells, and prevents the production of antibodies. By inhibiting both the production of anti-glycoprotein (GP) IIb/IIIa antibodies by B cells and GPIIb/IIIa-dependent T-cell proliferation, BMS-986004 may prevent platelet destruction and may increase platelet counts in idiopathic thrombocytopenic purpura (ITP). The direct binding of BMS-986004 to CD40L on platelets further prevents CD40L/CD40-mediated destruction by macrophages and DCs in ITP. The modified Fc domain prevents the binding of BMS-986004 to the Fc receptor FcgammaRIIA on platelets, thereby preventing FcgammaRIIA-dependent platelet activation and anti-CD40L-induced thromboembolism. CD40L, a transmembrane protein of the tumor necrosis factor (TNF) superfamily, is primarily expressed on activated T cells, but is also expressed on eosinophils, basophils, natural killer (NK) cells, mast cells, platelets and activated endothelial cells.

anti-CD44 monoclonal antibody RO5429083

A recombinant, humanized monoclonal antibody targeting the cancer stem cell (CSC) antigen CD44, with potential immunomodulating and antineoplastic activities. Upon administration, RO5429083 binds to the constant region of the extracellular domain of CD44, thereby preventing the activation of various CD44-mediated signal transduction pathways. This may lead to a reduction in the proliferation of CD44-expressing tumor stem cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types; it plays a key role in tumor cell proliferation, migration and survival.

anti-CD44v9 antibody-drug conjugate AMT-116

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) CD44 variant 9 (CD44v9), linked to the topoisomerase I inhibitor (TOP1i) and belotecan derivative KL610023 via a hydrolysable linker, with potential antineoplastic activity. Upon intravenous administration of anti-CD44v9 ADC AMT-116, the monoclonal antibody moiety targets and binds to CD44v9 expressed on tumor cells. Upon binding and internalization, KL610023 is released. KL610023 targets and binds to DNA topoisomerase I, thereby inhibiting DNA replication and killing the CD44v9-expressing cancer cells. CD44v9, a splicing variant of CD44 overexpressed in numerous cancer cell types, is associated with tumorigenicity and cancer treatment resistance.

anti-CD45 BC8 monoclonal antibody-streptavidin conjugate

An immunoconjugate containing a monoclonal antibody directed against the CD45 antigen BC8, conjugated to streptavidin, a nonglycosylated homotetrameric protein that has four high affinity binding sites for biotin. Anti-CD45 BC8 antibody-streptavidin conjugate binds to CD45, a transmembrane protein tyrosine phosphatase that is expressed on the surface of normal and malignant hematopoietic cells. Upon administration of a biotin-based radioconjugate, the biotin moiety of the radioconjugate binds to the streptavidin moiety of anti-CD45 BC8 antibody-streptavidin conjugate and, upon cellular internalization, specifically delivers cytotoxic radiation to CD45-expressing tumor cells.

anti-CD45 monoclonal antibody

A monoclonal antibody directed against the receptor-like leukocyte cell surface glycoprotein CD45 with leukocyte-depleting activity. Upon administration, anti-CD45 monoclonal antibody binds to leukocyte surface-expressed CD45, which may result in the transient depletion of circulating leukocytes including circulating T cell depletion (TCD). CD45, a receptor-like protein-tyrosine phosphatase that consists of several isoforms, is present on all differentiated hematopoietic cells except erythrocytes and plasma cells and is essential for T cell development and lymphocyte activation.

anti-CD45 monoclonal antibody AHN-12

A high affinity IgG1 monoclonal antibody with potential immunotherapeutic activity. Anti-CD45 monoclonal antibody AHN-12 recognizes CD45, a transmembrane protein tyrosine phosphatase that is expressed on the surface of normal and malignant hematopoietic cells.

anti-CD46 antibody-drug conjugate FOR46

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the cluster of differentiation 46 (CD46; membrane cofactor protein; MCP) and conjugated to an as of yet undisclosed cytotoxic payload, with potential antineoplastic activity. Upon administration, anti-CD46 ADC FOR46 specifically targets and binds to a specific conformational epitope on the immune modulatory receptor CD46 expressed on certain tumor cells. Upon binding and internalization, the cytotoxic payload kills the CD46-expressing tumor cells. The conformational epitope of CD46 is highly expressed in multiple tumor cell types while minimally expressed or absent in normal, healthy tissues. FOR46 does not interfere with other CD46-mediated pathways that naturally occur in normal, healthy tissues.

anti-CD46 monoclonal antibody YS5

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the cell surface antigen cluster of differentiation 46 (CD46; membrane cofactor protein; MCP) that can potentially be used as the antibody moiety of a radioimmunoconjugate and/or antibody-drug conjugate (ADC). Upon administration, anti-CD46 monoclonal antibody YS5 specifically targets and binds to a conformational epitope formed within Sushi domains (complement control protein repeats; CCPs) 1 and 2 on the immune modulatory receptor CD46 expressed on certain tumor cells, and is internalized. The conformational epitope on CD46 is highly expressed in multiple tumor cell types while minimally expressed or absent in normal, healthy tissues. CD46 plays a key role in the negative regulation of innate immunity.

anti-CD47 ADC SGN-CD47M

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody directed against human cell surface antigen CD47 conjugated to an as of yet not fully elucidated toxin, with potential antineoplastic activity. Upon administration of SGN-CD47M, the anti-CD47 monoclonal antibody moiety targets and binds to CD47 on tumor cell surfaces; upon internalization, the toxin moiety kills tumor cells through a mechanism of action that has not been elucidated. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells.

anti-CD47 monoclonal antibody AO-176

A humanized immunoglobulin G2 (IgG2) monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody AO-176 preferentially binds to CD47 on tumor cells because it exhibits enhanced binding at the acidic pH found in the tumor microenvironment (TME). This blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of tumor cells. Additionally, blocking CD47 signaling activates both an anti-tumor T lymphocyte immune response and T-cell-mediated killing of CD47-expressing tumor cells. In addition, AO-176 induces immunogenic cell death (ICD) and releases damage-associated molecular patterns (DAMPs) from tumor cells, thereby further stimulating immune responses. AO-176 is also able to induce direct cytotoxic cell death by a cell autonomous mechanism. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47 monoclonal antibody CC-90002

A monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody CC-90002 selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47 monoclonal antibody HMPL-A83

A humanized immunoglobulin G4 (IgG4) monoclonal antibody targeting leukocyte surface antigen CD47, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody HMPL-A83 targets and binds to CD47 expressed on tumor cells, blocking the interaction of CD47 with signal regulatory protein alpha (SIRPa) expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

anti-CD47 monoclonal antibody IBI188

A human immunoglobulin G4 (IgG4) monoclonal antibody targeting leukocyte surface antigen CD47 with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-CD47 monoclonal antibody IBI188 selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47 monoclonal antibody IMC-002

A human immunoglobulin G4 (IgG4) monoclonal antibody targeting leukocyte surface antigen CD47, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody IMC-002 targets and binds to CD47 expressed on tumor cells, blocking the interaction of CD47 with signal regulatory protein alpha (SIRPa) expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate. IMC-002 does not bind to red blood cells (RBCs). This may prevent adverse effects such as anemia that can result from the blockade of CD47 expressed on RBCs.

anti-CD47 monoclonal antibody MIL95

A humanized monoclonal antibody targeting leukocyte surface antigen CD47, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody MIL95 targets and binds to CD47 expressed on tumor cells, blocking the interaction of CD47 with signal regulatory protein alpha (SIRPa) expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

anti-CD47 monoclonal antibody SHR-1603

A monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody SHR-1603 preferentially binds to CD47 on tumor cells. This blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of tumor cells. Additionally, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47 monoclonal antibody SRF231

A human monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody SRF231 selectively binds to CD47 on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages. This prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47 monoclonal antibody STI-6643

A human monoclonal antibody targeting leukocyte surface antigen CD47, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody STI-6643 targets and binds to CD47 expressed on tumor cells, blocking the interaction of CD47 with signal regulatory protein alpha (SIRPa) expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) but is overexpressed on the surface of a variety of cancer cells and contributes to poor prognosis. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate. Compared to other anti-CD47 monoclonal antibodies, STI-6643 shows decreased binding to red blood cells (RBCs). This may prevent adverse effects such as anemia that can result from the blockade of CD47 expressed on RBCs. In addition, STI-6643 has a minimal effect on T-, B- or natural killer (NK) cell depletion which may further improve its efficacy by preserving infiltrating anti-tumor immune cells.

anti-CD47 monoclonal antibody ZL-1201

A humanized immunoglobulin G4 (IgG4) monoclonal antibody targeting leukocyte surface antigen CD47, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody ZL-1201 targets and binds to CD47 expressed on tumor cells, blocking the interaction of CD47 with signal regulatory protein alpha (SIRPa) expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.

anti-CD47/anti-HER2 bispecific antibody D3L-001

A bispecific antibody directed against both the human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/anti-HER2 bispecific antibody D3L-001, the anti-HER2 moiety selectively targets and binds to HER2 on HER2-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to the HER2-expressing tumor cells. The CD47 binding by D3L-001 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the HER2-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of HER2-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. HER-2, a tumor-associated antigen (TAA) overexpressed on a variety of tumor cell types, plays an important role in tumor cell proliferation, differentiation and survival. Co-targeting CD47 and HER2 may limit the binding of D3L-001 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize any associated adverse effects.

anti-CD47/anti-HER2 bispecific antibody IMM2902

A bispecific antibody directed against both the human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/anti-HER2 bispecific antibody IMM2902, the anti-HER2 moiety selectively targets and binds to the tumor-associated antigen (TAA) HER2 on HER2-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to the HER2-expressing tumor cells. The CD47 binding by IMM2902 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the HER2-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of HER2-expressing tumor cells. IMM2902 may also induce an anti-tumor activity through the induction of antibody-dependent cellular cytotoxicity (ADCC). CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. HER-2, overexpressed on a variety of tumor cell types, plays an important role in tumor cell proliferation, differentiation and survival. Co-targeting CD47 and HER2 may limit the binding of IMM2902 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize any associated adverse effects.

anti-CD47/anti-mesothelin bispecific antibody NI-1801

An immunoglobulin G1 (IgG1) bispecific human antibody directed against the human tumor-associated antigen (TAA) mesothelin (MSLN) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/anti-MSLN bispecific antibody NI-1801, the anti-MSLN arm selectively targets and binds to MSLN expressed on MSLN-positive cancer cells, thereby improving specific binding of the anti-CD47 arm to the MSLN-expressing cancer cells. The CD47 binding by NI-1801 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the MSLN/CD47-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of MSLN/CD47-expressing tumor cells. In addition, NI-1801 induces an anti-tumor activity through the induction of antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. By co-targeting CD47 and MSLN, NI-1801 has the potential to overcome the limitations of existing CD47-targeted therapies by possibly avoiding the side effects caused by binding to CD47 on healthy hematopoietic stem cells (HSCs) which causes unwanted macrophage-mediated phagocytosis. MSLN is overexpressed by a variety of cancer cell types.

anti-CD47/anti-PD-L1 bispecific antibody 6MW3211

A humanized bispecific antibody targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47/anti-PD-L1 bispecific antibody 6MW3211 targets and binds to both CD47 and PD-L1 expressed on tumor cells. The CD47 binding by 6MW3211 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of CD47-expressing tumor cells. The binding of 6MW3211 to PD-L1 blocks its binding to and activation of its receptor, programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation, which protects cancer cells from phagocytosis and allows proliferation of cancer cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) that is expressed on activated T cells, suppresses the immune system and results in immune evasion. By co-targeting CD47 and PD-L1, 6MW3211 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs).

anti-CD47/anti-PD-L1 bispecific antibody IBI322

A recombinant bispecific antibody targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47/anti-PD-L1 bispecific antibody IBI322 targets and binds to both CD47 and PD-L1 expressed on tumor cells, with a higher binding affinity to PD-L1 and a lower binding affinity to CD47. The CD47 binding by IBI322 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of CD47-expressing tumor cells. The binding of IBI322 to PD-L1 blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA), widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. By co-targeting CD47 and PD-L1 with a higher binding affinity to PD-L1, IBI322 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs). PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-CD47/anti-PD-L1 bispecific antibody PF-07257876

A bispecific antibody targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47/anti-PD-L1 bispecific antibody PF-07257876 targets and binds to both CD47 and PD-L1 expressed on tumor cells. The CD47 binding by PF-07257876 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of CD47-expressing tumor cells. The binding of PF-07257876 to PD-L1 blocks its binding to and activation of its receptor, programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation, which protects cancer cells from phagocytosis and allows proliferation of cancer cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) that is expressed on activated T cells, suppresses the immune system and results in immune evasion. By co-targeting CD47 and PD-L1, PF-07257876 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs).

anti-CD47/CD19 bispecific monoclonal antibody TG-1801

A bispecific monoclonal antibody composed of two single-chain variable fragments (scFv), one directed against the B-cell-specific membrane protein CD19, and another that is directed against the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/CD19 bispecific monoclonal antibody TG-1801, the anti-CD19 moiety selectively targets and binds to CD19 on CD19-positive B cells, thereby improving binding of the anti-CD47 moiety to the CD19+ malignant B cells. The CD47 binding by TG-1801 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD19/CD47-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD19/CD47-expressing tumor cells. In addition, TG-1801 induces an anti-tumor activity through the induction of antibody dependent cellular cytotoxicity (ADCC). CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA), widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CD19 is a membrane antigen that is widely expressed during B-cell development and in B-cell malignancies. By co-targeting CD47 and CD19, TG-1801 has the potential to overcome the limitations of existing CD47-targeted therapies by possibly avoiding the side effects caused by binding to CD47 on healthy hematopoietic stem cells (HSCs) which causes unwanted macrophage-mediated phagocytosis.

anti-CD47/CD20 bispecific antibody CC-96673

A humanized immunoglobulin G1 (IgG1) affinity-tuned bispecific antibody directed against both the B-cell-specific membrane protein and tumor-associated antigen (TAA) CD20, and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/CD20 bispecific antibody CC-96673, the anti-CD20 moiety selectively targets and binds with high affinity to CD20 on CD20-positive B cells, and the anti-CD47 moiety targets and binds with optimally lowered affinity to CD47 expressed on the CD20-positive malignant B-cells. The CD47 binding by CC-96673 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD20/CD47-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD20/CD47-expressing tumor cells. CC-96673 may also induce an anti-tumor activity through the induction of antibody dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) against CD20-positive tumor cells. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B cells during most stages of B-cell development. It is often overexpressed in B-cell malignancies. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-CD47/CD20 bispecific antibody IMM0306

A bispecific antibody directed against both the B-cell-specific membrane protein and tumor-associated antigen (TAA) CD20, and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/CD20 bispecific antibody IMM0306, the anti-CD20 moiety selectively targets and binds to CD20 on CD20-positive B cells, thereby improving the binding of the anti-CD47 moiety to the CD20-positive malignant B cells. The CD47 binding by IMM0306 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD20/CD47-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD20/CD47-expressing tumor cells. In addition, IMM0306 may induce an anti-tumor activity through the induction of antibody dependent cellular cytotoxicity (ADCC). CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CD20 is a membrane antigen that is overexpressed in B-cell malignancies. By co-targeting CD47 and CD20, IMM0306 has the potential to overcome the limitations of existing CD47-targeted therapies by possibly avoiding the side effects caused by binding to CD47 on healthy hematopoietic stem cells (HSCs) which causes unwanted macrophage-mediated phagocytosis.

anti-CD48/MMAE antibody-drug conjugate SGN-CD48A

An antibody-drug conjugate (ADC) composed of an antibody targeting the cell surface antigen CD48 that is conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), via a proprietary next-generation PEGylated glucuronide linker, with potential antineoplastic activity. Following intravenous administration, the antibody moiety of anti-CD48 ADC SGN-CD48A binds to CD48 on the surface of tumor cells. Following internalization of the ADC, the MMAE binds to tubulin and inhibits microtubule polymerization, which may result in G2/M phase cell cycle arrest and apoptosis in CD48-expressing tumor cells. CD48, a member of the signaling lymphocyte activation molecule (SLAM) family of immune cell receptors, is involved in T-cell activation and leukocyte trafficking. Additionally, CD48 is expressed on the surface of multiple myeloma cells at significantly higher levels than it is expressed on normal lymphocytes and monocytes. The linkage system in SGN-CD48A improves stability, reduces off-target uptake, and enables conjugation of larger numbers of MMAE/antibody than other systems, resulting in increased specificity against CD48-positive cells.

anti-CD52 monoclonal antibody ALLO-647

A monoclonal antibody directed against the cell surface glycoprotein CD52 (CAMPATH-1 antigen; Cambridge pathology 1 antigen), with potential immunodepleting activity. Upon administration, anti-CD52 monoclonal antibody ALLO-647 selectively targets and binds to CD52, thereby triggering a host immune response that results in the lysis of CD52-positive lymphocytes. This leads to immunodepletion and may prevent graft-versus-host disease (GvHD). CD52 is a glycoprotein expressed on the surface of many immune cells, including essentially all B and T lymphocytes.

anti-CD7 CAR T cells

A preparation of T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD7 CAR T cells specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

anti-CD7 CAR T cells BT-007

A preparation of T lymphocytes that have been genetically engineered and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, the co-immunostimulatory signaling domain 4-1BB (CD137) and the intracellular CD3 zeta domain (CD3z), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD7 CAR T cells BT-007 specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

anti-CD7 CAR T cells SenL-T7

A preparation of T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD7 CAR T cells SenL-T7 specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

anti-CD7 CAR-T cells RD13-02

A preparation of T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD7 CAR-T cells RD13-02 specifically target and kill CD7-expressing tumor cells. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

anti-CD7 immunotoxin

A toxin linked to an anti-CD7 antibody.

anti-CD70 antibody-drug conjugate MDX-1203

An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody, directed against the extracellular domain of the human CD70 molecule, conjugated to a prodrug of a CC-1065 (rachelmycin) analogue via a stable peptide-based linker, with potential antineoplastic activity. The anti-CD70 antibody moiety of the anti-CD70 antibody-drug conjugate MDX-1203 selectively binds to the extracellular domain of CD70 on tumor cell surfaces. Upon internalization, the prodrug moiety is released and activated and binds to double-stranded B-DNA within the minor groove, thereby alkylating the –3 position of adenine, which may result in the inhibition of cellular proliferation of tumor cells that overexpress CD70. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. The antitumor antibiotic CC-1065, a DNA minor-groove-binding alkylating agent, was originally isolated from the bacterium Streptomyces zelensis.

anti-CD70 antibody-drug conjugate PRO1160

An antibody-drug conjugate (ADC) consisting of a human monoclonal antibody directed against the tumor-associated antigen (TAA) cluster of differentiation 70 (CD70), conjugated via a cleavable, hydrophilic linker to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of anti-CD70 ADC PRO1160, the anti-CD70 antibody moiety targets and binds to CD70-expressing tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells.

anti-CD70 antibody-drug conjugate SGN-CD70A

An antibody-drug conjugate (ADC) containing an engineered cysteine monoclonal antibody (EC-mAb), directed against the extracellular domain of the human CD70 molecule, conjugated to the synthetic, cytotoxic, DNA minor-groove crosslinking agent, pyrrolobenzodiazepine (PBD) dimer, via a stable, protease-cleavable, peptide-based linker, with potential antineoplastic activity. The anti-CD70 antibody moiety of the anti-CD70 antibody-drug conjugate SGN-CD70A selectively binds to the extracellular domain of CD70 on tumor cell surfaces. Upon internalization, the PBD dimer moiety is released and covalently binds, through its imine moieties, to the N2 positions of guanines on opposite strands of DNA. This induces DNA double strand breaks and inhibits DNA replication, which lead to the inhibition of cell growth of tumor cells that overexpress CD70. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. The cysteine moiety of the EC-mAb allows for the stable conjugation of the PBD to the antibody.

anti-CD70 CAR-expressing T lymphocytes

A preparation of human T lymphocytes transduced with a recombinant viral vector encoding a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of one or more binding domains that target the tumor-associated antigen (TAA) CD70 (CD27 ligand; tumor necrosis factor superfamily member 7; TNFSF7) fused to one or more co-stimulatory TCR-signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CD70 CAR-expressing T lymphocytes, express anti-CD70-CAR on their cell surfaces and bind to the CD70 antigen on tumor cell surfaces thereby neutralizing the activity of CD70. This may induce antibody-dependent cellular cytotoxicity (ADCC) against CD70-expressing tumor cells. CD70, a cytokine belonging to the tumor necrosis superfamily (TNFSF) and the ligand for the costimulatory receptor CD27, is expressed on the surfaces of various types of cancer cells; its overexpression may play an important role in the evasion of immune surveillance.

anti-CD70 monoclonal antibody IMM40H

An immunoglobulin G1 (IgG1) monoclonal antibody directed against the human tumor-associated antigen (TAA) CD70, with potential immunomodulatory and antineoplastic activities. Upon administration, anti-CD70 monoclonal antibody IMM40H selectivity targets and binds to CD70, which blocks CD70-mediated signaling. This may inhibit cellular proliferation and survival of CD70-expressing tumor cells, and may modulate the immune system to inhibit inflammatory signals and increase antigen-specific T-cell responses in the tumor microenvironment (TME). In addition, IMM40H induces antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and complement-dependent cytotoxicity (CDC) against CD70-expressing tumor cells. CD70, a member of the tumor necrosis factor (TNF) family, is aberrantly expressed on malignant myeloid blasts while absent from healthy hematopoietic progenitor cells.

anti-CD70 monoclonal antibody MDX-1411

A glycoengineered, fully human IgG1 monoclonal antibody directed against the extracellular domain of the human CD70 molecule with potential antineoplastic activity. Anti-CD70 fully human monoclonal antibody MDX-1411 selectivity binds to the extracellular domain of CD70, which may induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on renal cell carcinoma (RCC) cells among other cancer cell types.

anti-CD70 monoclonal antibody SEA-CD70

A humanized, nonfucosylated monoclonal antibody directed against the human CD70 antigen, with potential immunomodulatory and antineoplastic activities. Upon administration, anti-CD70 monoclonal antibody sugar-engineered antibody (SEA)-CD70 selectivity targets and binds to the extracellular domain of CD70, which blocks CD70-mediated signaling. This may inhibit cellular proliferation and survival of CD70-expressing tumor cells, and may modulate the immune system to inhibit inflammatory signals and increase antigen-specific T-cell responses in the tumor microenvironment (TME). In addition, SEA-CD70 induces antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and complement-dependent cytotoxicity (CDC) against CD70-expressing tumor cells. CD70, a member of the tumor necrosis factor (TNF) family, is aberrantly expressed on malignant myeloid blasts while absent from healthy hematopoietic progenitor cells.

anti-CD71/vcMMAE probody-drug conjugate CX-2029

A probody-drug conjugate (PDC) composed of a monoclonal antibody directed against the transferrin receptor 1 (TFR1; TRP1; CD71), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, and conjugated, via a valine-citrulline (VC) peptide linker, to the potent cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of the anti-CD71/vcMMAE PDC CX-2029, the anti-CD71 moiety is unable to bind to CD71 antigen, which is highly expressed on both tumor and healthy dividing cells, until the masking peptide that is attached to the anti-CD71 probody is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Local protease-mediated removal of the linker and masking peptide enables specific binding of the unmasked anti-CD71 moiety to CD71 expressed on tumor cells. Upon internalization and proteolytic cleavage, MMAE is released into the cytosol of CD71-expressing tumor cells, binds to tubulin, and inhibits microtubule polymerization, which induces both G2/M phase arrest and tumor cell apoptosis. CD71, a transmembrane glycoprotein, is a highly expressed protein present in a number of solid and hematologic cancers, but is also expressed on normal, healthy tissues. The peptide masking of CX-2029 minimizes binding of the anti-CD71 antibody moiety to normal, healthy cells and may minimize systemic toxicity, when compared to other anti-CD71 antibody-drug conjugates (ADCs). Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.

anti-CD73 monoclonal antibody BMS-986179

A monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody BMS-986179 targets and binds to CD73, leading to clustering and internalization of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine. This prevents adenosine-mediated suppression of lymphocyte activity and increases the activity of CD8-positive effector cells. This also activates macrophages, and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.

anti-CD73 monoclonal antibody CPI-006

A type II humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-CD73 monoclonal antibody CPI-006 targets and binds to CD73 on tumor cells, leading to internalization of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine, thereby preventing adenosine-mediated suppression of lymphocyte activity and increasing the activity of cytotoxic T lymphocytes (CTLs). This also activates macrophages, and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.

anti-CD73 monoclonal antibody HB0045

A compound preparation composed of two monoclonal antibodies, HB0038 and HB0039, targeting different epitopes of human ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), in a 1:1 molar ratio, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody HB0045 targets and binds to two different epitopes of CD73 on tumor cells. HB0038 specifically binds to the catalytic domain composed of the N-terminus and C-terminus of CD73, thereby sterically blocking the CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine. HB0039 specifically and allosterically binds to the N-terminal region of CD73, thereby inhibiting the transition of CD73 from the inactive "open" conformation to a catalytically active "closed" conformation. This inhibits its enzymatic activity and further prevents adenosine formation from AMP. This prevents adenosine-mediated suppression of lymphocyte activity and increases the activity of cytotoxic T lymphocytes (CTLs). This also activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment (TME) and promotes tumor growth.

anti-CD73 monoclonal antibody HLX23

A recombinant, humanized monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody HLX23 targets and binds to CD73 on tumor cells, thereby inhibiting the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This increases the activity of cytotoxic T lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment (TME).

anti-CD73 monoclonal antibody IBI325

A monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody IBI325 targets and binds to CD73 on tumor cells, thereby inhibiting the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This attenuates the adenosine-induced immunosuppression in tumor microenvironment (TME), increases the activity of cytotoxic T lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the TME.

anti-CD73 monoclonal antibody INCA00186

A humanized monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody INCA00186 targets and binds to CD73 on tumor cells, thereby inhibiting the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This attenuates the adenosine-induced immunosuppression in tumor microenvironment (TME), increases the activity of cytotoxic T lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the TME.

anti-CD73 monoclonal antibody JAB-BX102

A humanized monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody JAB-BX102 targets and binds to CD73 on tumor cells, thereby inhibiting the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This attenuates the adenosine-induced immunosuppression in the tumor microenvironment (TME), increases the activity of cytotoxic T-lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the TME.

anti-CD73 monoclonal antibody NZV930

A fully human monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-CD73 monoclonal antibody NZV930 targets and binds to CD73 on tumor cells, leading to internalization of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine, thereby preventing adenosine-mediated suppression of lymphocyte activity and increasing the activity of cytotoxic T lymphocytes (CTLs). This also activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated in many cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.

anti-CD73 monoclonal antibody PT199

A humanized monoclonal antibody directed against the human ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody PT199 targets and directly binds to an epitope that is in or near the CD73 catalytic domain, thereby non-competitively and fully inhibiting both soluble shed CD73 and membrane-bound CD73 activity. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This attenuates the adenosine-induced immunosuppression in the tumor microenvironment (TME), increases the activity of cytotoxic T lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the TME. PT199 may inhibit the CD73 enzyme activity by preventing the transition of CD73 from the open to the closed conformation.

anti-CD73 monoclonal antibody Sym024

A monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CD73 monoclonal antibody Sym024 targets and binds to CD73 on tumor cells, thereby inhibiting CD73 activity. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine, preventing adenosine-mediated suppression of lymphocyte activity and increasing the activity of cytotoxic T lymphocytes (CTLs). This also activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment (TME).

anti-CD79b antibody-drug conjugate SHR-A1912

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against the tumor-associated antigen (TAA) B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29) conjugated to a topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-CD79b ADC SHR-A1912 targets and binds to CD79b expressed on tumor cells. Upon binding and internalization, the topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing CD79b. CD79b, a critical receptor for successful B-cell development and part of the B-cell receptor (BCR) signaling complex, is widely expressed in certain subtypes of B-cell lymphomas.

anti-CD79b CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD79b CAR T cells target and bind to CD79b-expressing tumor cells, thereby inducing selective toxicity in CD79b-expressing tumor cells. CD79b, a critical receptor for successful B cell development and part of the B-cell receptor (BCR) signaling complex, is widely expressed in certain subtypes of B-cell lymphomas.

anti-CD79b/CD20/CD3 trispecific antibody JNJ-80948543

A fully human effector-silent Fc immunoglobulin G1 (IgG1) trispecific antibody targeting the tumor-associated antigens (TAAs) B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29) and cluster of differentiation 20 (CD20), and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD79b/CD20/CD3 trispecific antibody JNJ-80948543 targets and binds to CD79b- and/or CD20-expressing tumor B-cells and CD3 antigen on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to CD79b- and/or CD20-expressing tumor B cells, resulting in CTL-mediated killing of tumor cells. CD79b, a critical receptor for successful B-cell development and part of the B-cell receptor (BCR) signaling complex, is widely expressed in certain subtypes of B-cell lymphomas. CD20 is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.

anti-CD8b antibody/IL-2 mutein fusion protein AB248

A recombinant fusion protein comprised of a humanized immunoglobulin G1 (IgG1) antibody targeting the T-cell surface glycoprotein CD8 beta chain (CD8b) linked to an affinity-attenuated interleukin-2 (IL-2) mutein, with potential immunostimulating and antineoplastic activities. Upon administration of anti-CD8b antibody/IL-2 mutein fusion protein AB248, the antibody moiety specifically targets and binds to CD8+ T cells, thereby allowing for the IL-2 mutein moiety to specifically bind to IL-2R and activate IL-2R-mediated signaling in CD8+ T cells. This enhances cytotoxic T lymphocytes (CTLs)-mediated cytotoxic immune responses against tumor cells. The IL-2 mutein has a reduced affinity to IL-2 receptor subunit alpha (IL-2Ralpha; CD25) and beta (IL-2Rbeta; CD122), which promotes the selective activation of CD8+ T cells over natural killer (NK) cells and immunosuppressive regulatory T cells (Tregs). The IL-2Ralpha/IL-2R beta-mediated activation of NK cells and immunosuppressive Tregs is associated with immunosuppression and adverse effects including vascular leak syndrome (VLS).

anti-CD93 monoclonal antibody DCBY02

A monoclonal antibody directed against a specific epitope of the insulin-like growth factor-binding protein 7 (IGFBP7) receptor complement component C1q receptor (C1QR1; CD93), with potential antineoplastic activity. Upon administration, anti-CD93 monoclonal antibody DCBY02 targets and binds to CD93 expressed on tumor-associated endothelial cells. This prevents the interaction of CD93 with its ligand IGFBP7, which improves tumor vascular function, reduces tumor hypoxia and increases tumor perfusion. This enhances immune cell infiltration into the tumor microenvironment (TME) and inhibits tumor cell proliferation. CD93 blockade and the normalization of tumor vasculature may also improve the delivery of other antineoplastic agents, thereby enhancing their antitumor effect. In addition, by increasing intratumoral effector T cells in the TME, DCSZ11 may enhance the efficacy of certain immunotherapeutic agents. CD93, a C-type lectin transmembrane protein, is upregulated in tumor-associated endothelial cells. Its expression is correlated with tumor vascular dysfunction and decreased immune cell infiltration.

anti-CD93 monoclonal antibody DCSZ11

A monoclonal antibody directed against a specific epitope of the insulin-like growth factor-binding protein 7 (IGFBP7) receptor complement component C1q receptor (C1QR1; CD93), with potential antineoplastic activity. Upon administration, anti-CD93 monoclonal antibody DCSZ11 targets and binds to CD93 expressed on tumor-associated endothelial cells. This prevents the interaction of CD93 with its ligand IGFBP7, which improves tumor vascular function, reduces tumor hypoxia and increases tumor perfusion. This enhances immune cell infiltration into the tumor microenvironment (TME) and inhibits tumor cell proliferation. CD93 blockade and the normalization of tumor vasculature may also improve the delivery of other antineoplastic agents, thereby enhancing their antitumor effect. In addition, by increasing intratumoral effector T cells in the TME, DCSZ11 may enhance the efficacy of certain immunotherapeutic agents. CD93, a C-type lectin transmembrane protein, is upregulated in tumor-associated endothelial cells. Its expression is correlated with tumor vascular dysfunction and decreased immune cell infiltration.

anti-CD98 monoclonal antibody IGN523

A humanized, monoclonal antibody targeting the CD98 (gp125) antigen, with potential immunomodulatory and antineoplastic activities. Upon intravenous administration, IGN523 binds to CD98 expressed on the tumor cell surface and elicits both natural killer (NK)-cell mediated antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity towards CD98-expressing tumor cells. In addition, IGN523 inhibits essential amino acid uptake by rapidly proliferating tumor cells. CD98, a type II transmembrane glycoprotein, is involved in both integrin signaling and amino acid transport processes; it is overexpressed in certain cancer cells and plays a key role in the proliferation, survival, and metastasis of tumor cells.

anti-CDH17/anti-CD3 bispecific antibody ARB202

A bispecific antibody directed against both the T-cell surface antigen CD3 and the tumor-associated antigen (TAA) cadherin-17 (CDH17), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CDH17/anti-CD3 bispecific antibody ARB202 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and CDH17 on CDH17-expressing tumor cells, thereby crosslinking tumor cells and CTLs. This activates and redirects CTLs to CDH17-expressing tumor cells, which results in the CTL-mediated cell death of CDH17-expressing tumor cells. CDH17, a cell surface adhesion protein, is overexpressed in a variety of cancer cell types.

anti-CDH3/MMAE antibody-drug conjugate BC3195

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the human tumor-associated antigen (TAA) cadherin-3 (CDH3; placental cadherin; P-cadherin), conjugated to the auristatin derivative and microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline (VC) peptide linker, with potential antineoplastic activity. Upon administration of anti-CDH3/MMAE ADC BC3195, the monoclonal antibody moiety targets and binds to CDH3 expressed on tumor cells. Upon internalization, proteolytic cleavage of linker, and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CDH3-expressing tumor cells. In addition, BC3195 is able to induce a bystander effect on neighboring tumor cells. CDH3 is a member of the cadherin family; it is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.

anti-CDH3/MSLN BiTE antibody AMG 305

A dual-targeting bispecific antibody and T-cell engager (BiTE) co-targeting both the human tumor-associated antigens (TAAs) cadherin-3 (CDH3; placental cadherin; P-cadherin) and mesothelin (MSLN) on tumor cells and CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CDH3/MSLN BiTE antibody AMG 305 binds with specificity to tumor cells co-expressing CDH3 and MSLN antigens and CD3 on cytotoxic T-lymphocytes (CTLs). This results in the cross-linking of T cells and tumor cells, and induces a cytotoxic T-lymphocyte (CTL) response against CDH3- and MSLN-co-expressing tumor cells. CDH3 is a member of the cadherin family; it is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. Binding of both CDH3 and MSLN allows for increased specificity in targeting these TAAs that may be expressed at low levels on the tumor surface while limiting activity against normal cells that express only one of the target antigens.

anti-CDH6 antibody-drug conjugate HKT288

An immunoconjugate consisting of a human monoclonal antibody directed against the tumor-associated antigen (TAA) cadherin-6 (CDH6; CDH-6) conjugated to a maytansine-based cytotoxic agent, with potential antineoplastic activity. The monoclonal antibody moiety of HKT288 targets and binds to CDH6 located on tumor cell surfaces. After internalization, the maytansine moiety binds to tubulin, which disrupts microtubule assembly/disassembly dynamics and inhibits both division and proliferation of CDH6-expressing tumor cells. CDH6, a member of the cadherin family and overexpressed by a variety of cancers, plays a key role in tumor cell proliferation.

anti-CDH6/exatecan ADC CUSP06

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) cadherin-6 (CDH6; CDH-6; K-cadherin) conjugated, via a protease cleavable linker, to the camptothecin analog and cytotoxic DNA topoisomerase I inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-CDH6/exatecan ADC CUSP06, the anti-CDH6 antibody moiety targets and binds to CDH6-expressing tumor cells. Upon uptake and cleavage of the linker by proteases, exatecan targets and binds to DNA topoisomerase I, thereby stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication and induction of apoptosis. This inhibits the proliferation of CDH6-expressing tumor cells. In addition, this may cause a bystander effect, thereby further killing CDH6-expressing tumor cells. CDH6, a member of the cadherin family and overexpressed by a variety of cancers, plays a key role in tumor cell proliferation.

anti-CEA BiTE monoclonal antibody AMG211

A recombinant, proprietary bispecific T-cell engagers (BiTE) antibody directed against human carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. Anti-CEA BiTE monoclonal antibody MEDI-565 possesses two antigen-recognition sites, one for CEA and one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR). This bispecific monoclonal antibody brings CEA-expressing tumor cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CEA-expressing cells. CEA, a tumor associated antigen, is overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers.

anti-CEA CAR T cells

A preparation of T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CEA CAR T cells specifically recognize and induce selective toxicity in CEA-expressing tumor cells. CEA, a member of the CEA family of proteins, plays a key role in cell migration, cell invasion and cell adhesion, and is overexpressed by a variety of cancer types.

anti-CEA IgCD28TCR-transduced autologous T cells

A population of autologous tumor infiltrating lymphocytes (TIL) transduced with a retroviral vector encoding the chimeric gene IgCD28TCR with potential immunostimulating and antineoplastic activities. The chimeric IgCD28TCR gene consists of portions of CD28, the zeta chain of the T-cell receptor (TCRzeta), and a single chain antibody domain (sFv) specific for the tumor-associated antigen CEA. Upon administration, these gene-modified TIL bind to tumor cells expressing CEA, which may result in activation and proliferation of TIL and an enhanced cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA may be overexpressed in various gastrointestinal and breast cancers. CD28, a T-cell surface-associated co-stimulatory molecule, is required for full T-cell activation, proliferation, and survival; expression of the CD28 fragment in this chimeric gene construct may impede activation-induced cell death (AICD) of TIL.

anti-CEA TCR retroviral vector-transduced autologous peripheral blood lymphocytes

Autologous human peripheral blood lymphocytes (PBLs), transduced with a retroviral vector encoding both the alpha and beta chains of a T-cell receptor (TCR) specific for the carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. After transduction, expansion in culture, and reintroduction into the patient, anti-CEA TCR retroviral vector-transduced autologous lymphocytes bind to tumor cells expressing CEA, which may result in cytokine expression, activation and proliferation of T cells, and a specific cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. The tumor-associated antigen (TAA) CEA is overexpressed by a variety of cancer cell types, including those of the gastrointestinal tract, lung , and breast.

anti-CEA-CAR autologous T lymphocytes

Autologous lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen human carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CEA-CAR autologous T-lymphocytes target and bind to tumor cells expressing CEA, which results in the cytotoxic T-lymphocyte (CTL)-mediated cell killing of CEA-expressing tumor cells. CEA is overexpressed in various tumor cell types.

anti-CEA/anti-4-1BB bispecific antibody

A bispecific antibody targeting both carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9).

anti-CEA/Anti-4-1BB bispecific antibody BGB-B167

A bispecific antibody targeting both the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CEA/anti-4-1BB bispecific antibody BGB-B167 simultaneously targets and binds to CEA expressed on tumor cells and 4-1BB expressed on activated T-lymphocytes and natural killer (NK) cells. This crosslinks CEA-expressing tumor cells and 4-1BB-expressing T-cells and NK cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation, enhances T-lymphocyte-mediated anti-tumor activity and leads to cytotoxic T-cell-mediated lysis of CEA-expressing tumor cells. The binding of BGB-B167 to CEA may also prevent CEA-mediated signaling. CEA is overexpressed by a variety of cancer cell types and plays a key role in cell migration, cell invasion, and cell adhesion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CEA/anti-4-1BB bispecific antibody LM-24C5

A bispecific antibody targeting both the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CEA/anti-4-1BB bispecific antibody LM-24C5 simultaneously targets and binds to CEA expressed on tumor cells and 4-1BB expressed on activated T lymphocytes and natural killer (NK) cells. This crosslinks CEA-expressing tumor cells and 4-1BB-expressing T cells and NK cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation, enhances T-lymphocyte-mediated anti-tumor activity and leads to cytotoxic T-cell-mediated lysis of CEA-expressing tumor cells. CEA is overexpressed by a variety of cancer cell types and plays a key role in cell migration, cell invasion, and cell adhesion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CEA/anti-CD3 bispecific antibody BA1202

A bispecific antibody targeting both the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA) and CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CEA/anti-CD3 bispecific antibody BA1202 targets and binds to both CEA expressed on tumor cells and CD3 on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to CEA-expressing tumor cells, which results in the CTL-mediated cell death of CEA-expressing tumor cells. CEA is overexpressed by a variety of cancer cell types and plays a key role in cell migration, cell invasion, and cell adhesion.

anti-CEA/anti-CEACAM6 antibody-drug conjugate EBC-129

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA; carcinoembryonic antigen-related cell adhesion molecule 5; CEACAM5) and the immune checkpoint regulator carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6; CEACAM-6; CD66c) and conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic and immune checkpoint inhibitory activities. Upon administration of anti-CEA/CEACAM6 ADC EBC-129, the monoclonal antibody moiety targets and binds to a specific glycosylation site that is conserved on both CEA and CEACAM6 expressed on tumor cells. Upon binding and internalization, MMAE is released where it targets and binds to tubulin and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CEA and/or CEACAM6-expressing tumor cells. CEA, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types. CEACAM6, an immune checkpoint receptor, is associated with tumor-mediated immune suppression. Elevated CEACAM6 expression is associated with advanced tumor stages and poor prognosis.

anti-CEA/anti-DR5 bispecific antibody IBI3004

A bispecific antibody targeting both the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA) and the pro-apoptotic death receptor tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAILR2; death receptor 5; DR5), with potential pro-apoptotic and antineoplastic activities. Upon administration, anti-CEA/anti-DR5 bispecific antibody IBI3004 targets and binds to both CEA and DR5 expressed on tumor cells. Receptor clustering and activation of DR5 induces apoptosis in CEA-expressing tumor cells. Activation of DR5 plays a key role in the induction of apoptosis. CEA-dependent clustering of DR5 allows IBI3004 to selectively induce apoptosis in CEA-expressing tumor cells thereby increasing efficacy and decreasing toxicity. CEA is overexpressed by a variety of cancer cell types and plays a key role in cell migration, cell invasion, and cell adhesion.

anti-CEA/anti-DTPA-In (F6-734) bispecific antibody

A bispecific monoclonal antibody (BsMAb) consisting of the Fab fragment of an anti-CEA monoclonal antibody (F6) coupled to the Fab fragment of an anti-DTPA-In monoclonal antibody (734) with potential radioimmunotherapeutic activity. In a two-step pretargeted radioimmunotherapeutic approach, this BsMAb, localizing to CEA-expressing tumor cells via the F6 Fab fragment, is introduced into patient first, followed by injection of indium 131-radiolabeled DTPA, which is recognized by the 734 Fab fragment of the BsMAb. Accordingly, a potentially lethal dose of indium 131 is delivered specifically to CEA-expressing tumor cells while minimizing radiotoxicity to normal tissues. CEA (carcinoembryonic antigen) is a tumor antigen overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers. DTPA (diethylenetriaminepentaacetic acid) is a bivalent hapten.

anti-CEA/anti-HSG bispecific monoclonal antibody TF2

A tri-Fab bispecific monoclonal antibody (BiMoAb) divalent for the carcinoembryonic antigen (CEA) and monovalent for histamine-succinyl-glycine (HSG) peptide-hapten. Anti-CEA/anti-HSG bispecific monoclonal antibody TF2 binds to the tumor associated antigen (TAA) CEA on CEA-expressing tumor cells. Subsequently, an HSG peptide-hapten carrying a radionuclide is administered, binding to the anti-HSG binding fragment on the BiMoAb. Depending on the characteristics of the radionuclide used, CEA-expressing tumor cells may then be radioimaged and/or treated radioimmunotherapeutically.

anti-CEACAM1 monoclonal antibody CM-24

A humanized monoclonal immunoglobulin G4 (IgG4) antibody targeting the anti-carcinoembryonic antigen (CEA)-related cell adhesion molecule 1 (CEACAM1; CD66a), with potential immunomodulating and antineoplastic activities. Upon administration of anti-CEACAM1 monoclonal antibody CM-24, this agent binds to CEACAM1 on cancer cells and certain immune cells. This blocks the binding of CEACAM1-expressing cancer cells to CEACAM1-expressing immune cells and abrogates CEACAM1-mediated immunosuppression. This enhances the activation of cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells and increases CTL- and NK-mediated killing of CEACAM1-overexpressing cancer cells. CEACAM1, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types. Its overexpression is correlated with both immunosuppression and poor prognosis.

anti-CEACAM5 ADC SGN-CEACAM5C

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA; carcinoembryonic antigen-related cell adhesion molecule 5; CEACAM5; CD66e) and conjugated to a cytotoxic camptothecin-based payload, with potential antineoplastic and immune checkpoint inhibitory activities. Upon administration of anti-CEACAM5 ADC SGN-CEACAM5C, the monoclonal antibody moiety targets and binds to CEA expressed on tumor cells. Upon binding and internalization, the payload is released. The camptothecin payload inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of CEA-expressing tumor cells. CEA, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types. Its expression is limited in normal. healthy, adult tissues, but is overexpressed in various cancers.

anti-CEACAM5 antibody-drug conjugate BG-C477

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; carcinoembryonic antigen; CEA; CD66e) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-CEACAM5 ADC BG-C477, the monoclonal antibody moiety targets and binds to CEACAM5 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the CEACAM5-expressing cancer cells through an as of yet unknown mechanism of action. This inhibits the proliferation of CEACAM5-expressing tumor cells. CEACAM5, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types. Its expression is limited in normal. healthy, adult tissues, but is overexpressed in various cancers.

anti-CEACAM5 antibody-drug conjugate M9140

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5; CEA), linked to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-CEACAM5 ADC M9140, the anti-CEACAM5 monoclonal antibody moiety targets and binds to CEACAM5 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills CEACAM5-expressing tumor cells through an as of yet undisclosed mechanism. CEACAM5, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types.

anti-CEACAM6 AFAIKL2 antibody fragment/Jack Bean urease immunoconjugate L-DOS47

A lyophilized formulation of DOS47, an immunoconjugate composed of AFAIKL2, a recombinant camelid single-domain antibody which recognizes carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6), and the enzyme urease derived from the plant Canavalia ensiformis (Jack bean), with potential antineoplastic activity. Upon intravenous administration, the AFAIKL2 antibody fragment moiety of L-DOS47 specifically targets and binds to CEACAM6 expressed on certain tumor cells. In turn, the urease moiety of L-DOS47 catalyzes the hydrolysis of urea into ammonia, which is further hydrolyzed to produce hydroxyl ions, and causes a locally increased concentration of the toxic waste product ammonia, which under normal conditions is converted into the nontoxic substance urea via the urea cycle. This increases the pH of the tumor microenvironment and alkalinizes the highly acidic environment that is needed for cancer cell survival and proliferation. In addition, the ammonia diffuses into cancer cells and exerts a cytotoxic effect. Altogether, this leads to cell death of CEACAM6-expressing cancer cells. The naturally-occurring enzyme urease catalyzes the hydrolysis of urea into ammonia and carbon dioxide. CEACAM6, a tumor-associated antigen and CEA family member, is overexpressed in a variety of tumor cells and plays a key role in tumor initiation, progression, metastasis and survival.

anti-CFH monoclonal antibody GT103

A recombinant human-derived monoclonal antibody targeting the tumor cell-protective protein complement factor H (CFH), with potential immunomodulatory and antineoplastic activities. Upon administration, the anti-CFH monoclonal antibody GT103 targets and binds specifically to a conformationally distinct epitope within a specific crucial functional domain of CFH bound on tumor cells. This activates the complement cascade, triggers complement dependent cytotoxicity and leads to the destruction of the tumor cells. In addition, GT103 modulates the adaptive anti-tumor immune response, thereby reducing the number of immune suppressive T-regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor. This may potentially provide long-term anti-tumor immunity and protection. CFH, the major regulator of the central complement protein C3b in the alternative pathway of complement activation, normally prevents cells from destruction by the immune system. CFH may play a key role in protection against complement-mediated lysis in various cancer cells.

anti-claudin 18.2 antibody-drug conjugate BL-M05D1

An antibody-drug conjugate (ADC) composed of a wild-type Fc-containing immunoglobulin (IgG) monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) (5103F3) conjugated, via a cathepsin B cleavable linker, to the camptothecin derivative and topoisomerase 1 inhibitor Ed-04, with potential antineoplastic activity. Upon administration of anti-CLDN18.2 ADC BL-M05D1, the anti-CLDN18.2 monoclonal antibody moiety specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon binding, internalization and linker cleavage, Ed-04 is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing CLDN18.2. In addition, BL-M05D1 may mediate antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is overexpressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin 18.2 antibody-drug conjugate CPO102

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated via a cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC CPO102 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin 18.2 antibody-drug conjugate EO-3021

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-CLDN18.2 ADC EO-3021, the anti-CLDN18.2 monoclonal antibody moiety specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin 18.2 antibody-drug conjugate JS107

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC JS107 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. In addition, JS107 kills tumor cells via antibody-dependent cellular cytotoxicity (ADCC) and complement dependent cytotoxicity (CDC). CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin 18.2 antibody-drug conjugate LM-302

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated via a cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC LM-302 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin 18.2 antibody-drug conjugate SKB315

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) that is site-specifically conjugated, via a stable linker, to a cytotoxic DNA topoisomerase I (Top I) inhibitor, with potential antineoplastic activity. Upon administration of anti-CLDN18.2 ADC MK-1200, the antibody moiety specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of the Top I inhibitor, the Top I inhibitor targets and binds to DNA topoisomerase I, thereby stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin 18.2 antibody-drug conjugate SOT102

An antibody-drug conjugate (ADC) composed of an immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) that is site-specifically conjugated, via a non-cleavable amide/peptide linker, to a derivative of the cytotoxic anthracycline PNU-159682, with potential antineoplastic activity. Upon administration of anti-CLDN18.2 ADC SOT102, the antibody moiety specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization, the anthracycline-based toxin intercalates into DNA and interacts with topoisomerase II. This leads to an inhibition of DNA replication and repair, and prevents RNA and protein synthesis. This kills the CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin 18.2 monoclonal antibody M108

A monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody M108 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. The binding induces antibody-dependent cellular cytotoxicity (ADCC) and may kill CLDN18.2-expressing tumor cells and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin 18.2 monoclonal antibody MIL93

A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody MIL93 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin-1 monoclonal antibody ALE.C04

A humanized monoclonal antibody directed against the tumor-associated antigen (TAA) claudin-1 (CLDN1; CLDN-1), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN1 monoclonal antibody ALE.C04 targets and binds to a specific extracellular loop epitope that is exposed in non-junctional (NJ) CLDN1 expressed on certain tumor cells. This prevents CLDN1-mediated signaling, which disrupts the stiff extracellular matrix (ECM) in tumors and, by disturbing the physical barrier, enhances the infiltration of immune cells, such as natural killer cells (NKs) and T cells. This abrogates immunosuppression in the tumor microenvironment (TME) and leads to NK- and T-cell-mediated tumor cell killing. In addition, ALE.C04 can directly kill CLDN1-expressing tumor cells via antibody-dependent cell mediated cytotoxicity (ADCC). CLDN1, which is normally confined within the tight junctions in epithelial tissues, is overexpressed on a variety of tumor cells in a non-junctional form. CLDN1 overexpression on tumor cells correlates with ECM remodeling and T-cell exclusion, and is associated with reduced efficacy of checkpoint inhibitors (CPIs).

anti-Claudin-18.2 monoclonal antibody NBL-015

A human monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody NBL-015 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may trigger antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cell mediated phagocytosis (ADCP) and antibody-mediated complement dependent cytotoxicity (CDC). This may kill CLDN18.2-expressing tumor cells and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin-18.2 monoclonal antibody SPX-101

A humanized monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody SPX-101 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill and inhibit proliferation of CLDN18.2-expressing tumor cells. SPX-101 may trigger antibody-dependent cellular cytotoxicity (ADCC). CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 ADC AZD0901

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated via a cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC AZD0901 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 antibody-drug conjugate IBI343

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC IBI343 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization, the cytotoxic agent induces apoptosis in CLDN18.2-expressing tumor cells through an as of yet unidentified mechanism of action (MoA). CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 CAR T cells IBI345

A preparation of T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 CAR T cells IBI345 specifically recognize and induce selective toxicity in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 CAR T cells IM92

A preparation of T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 CAR T cells IM92 specifically recognize and induce selective toxicity in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 CAR T cells LCAR-C18S

A preparation of T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-Claudin18.2 CAR T cells LCAR-C18S specifically recognize and induce selective toxicity in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin18.2 monoclonal antibody AB011

A recombinant humanized monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-claudin18.2 monoclonal antibody AB011 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin18.2 monoclonal antibody ASKB589

A monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-claudin18.2 monoclonal antibody ASKB589 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin18.2 monoclonal antibody LM-102

A recombinant humanized monoclonal antibody directed against the tumor-associated antigen (TAA) claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody LM-102 specifically targets and binds to CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells and inhibit tumor cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-Claudin18.2 monoclonal antibody TORL-2-307-MAB

A monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody TORL-2-307-MAB specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells and inhibit tumor cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin18.2/anti-4-1BB bispecific antibody TJ-CD4B

A bispecific antibody composed of a human, Fc-silenced immunoglobulin G1 (IgG1) monoclonal antibody targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) fused with a single chain variable fragment (scFv) targeting 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-4-1BB bispecific antibody TJ-CD4B simultaneously targets and binds to CLDN18.2 expressed on tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T lymphocytes. Upon CLDN18.2 binding, the 4-1BB activation signal is induced and TJ-CD4B acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and T-lymphocyte-mediated anti-tumor activity. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-claudin18.2/anti-CD3 bispecific antibody AZD5863

An affinity-optimized T-cell engaging (TCE) and human bispecific antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-CD3 bispecific antibody AZD5863 simultaneously targets and binds to both CLDN18.2-expressing tumor cells, with bivalent high affinity binding, and CD3-expressing T cells, with monovalent low affinity binding. This crosslinks CLDN18.2-expressing tumor cells and cytotoxic T lymphocytes (CTLs) and results in the activation and proliferation of T cells. This causes a CTL-mediated cell lysis of CLDN18.2-expressing tumor cells. Additionally, AZD5863 induces bystander killing of CLDN18.2-negative tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. The bivalent high-affinity binding to CLDN18.2 and monovalent low-affinity binding to CD3 of AZD5863 may reduce toxicities while optimizing specific anti-tumor activity.

anti-Claudin18.2/anti-CD3 bispecific antibody QLS31905

A bispecific antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-CD3 bispecific antibody QLS31905 simultaneously binds to both CLDN18.2-expressing tumor cells and CD3-expressing T cells, thereby crosslinking CLDN18.2-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This results in the activation and proliferation of T cells and causes CTL-mediated cell lysis of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-claudin18.2/anti-CD47 bispecific antibody PT886

A bispecific antibody directed against both the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CLDN18.2/anti-CD47 bispecific antibody PT886, the anti-CLDN18.2 moiety selectively targets and binds to the TAA CLDN18.2 on CLDN18.2-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to the CLDN18.2-expressing tumor cells. The CD47 binding by PT886 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CLDN18.2-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CLDN18.2-expressing tumor cells. PT886 may also induce an anti-tumor activity through the induction of antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells (RBCs) and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CLDN18.2, a tight junction protein and stomach-specific isoform of Claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. Co-targeting CD47 and CLDN18.2 may limit the binding of PT886 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize any associated adverse effects.

anti-Claudin18.2/MMAE antibody-drug conjugate TORL-2-307-ADC

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated, via a cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, anti-CLDN18.2/MMAE ADC TORL-2-307-ADC specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2 antibody-drug conjugate TQB2103

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) conjugated via a cleavable linker, to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration, anti-CLDN18.2 ADC TQB2103 specifically targets and binds to CLDN18.2 expressed on tumor cells. Upon endocytosis and the transfer to lysosomes, the payload is released via enzymatic cleavage of the linker. The cytotoxic agent causes DNA damage in and kills CLDN18.2-expressing tumor cells. Through bystander effect, TQB2103 is also able to kill adjacent tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2 CAR T cells LY011

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CLDN18.2 CAR T cells LY011 specifically recognize and bind to CLDN18.2-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is overexpressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2 CAR-T cells AZD6422

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 CAR-T cells AZD6422 specifically recognize and bind to CLDN18.2-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is overexpressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2 heavy chain antibody Fc fusion protein DR30303

A fusion protein composed of a recombinant humanized anti-Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) heavy chain antibody (VHH) fused to an engineered immunoglobulin gamma-1 (IgG1) Fc fragment, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 heavy chain antibody Fc fusion protein DR30303 specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. The binding induces antibody-dependent cellular cytotoxicity (ADCC) and may kill CLDN18.2-expressing tumor cells and inhibit tumor cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is overexpressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2 monoclonal antibody ZL-1211

An engineered monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2 monoclonal antibody ZL-1211 specifically targets and binds to CLDN18.2 expressed on tumor cells. The binding induces antibody-dependent cellular cytotoxicity (ADCC) and activates innate and adaptive immunity. This kills and inhibits proliferation of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2/anti-4-1BB bispecific antibody PM1032

A bispecific antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-4-1BB bispecific antibody PM1032 simultaneously targets and binds to CLDN18.2 expressed on tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T lymphocytes. Upon CLDN18.2 binding and CLDN18.2-mediated crosslinking of 4-1BB, the 4-1BB activation signal is induced and PM1032 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and T-lymphocyte-mediated anti-tumor activity. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CLDN18.2/anti-CD3 bispecific antibody ASP2138

A bispecific antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-CD3 bispecific antibody ASP2138 simultaneously binds to both CLDN18.2-expressing tumor cells and CD3-expressing T cells, thereby crosslinking CLDN18.2-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This results in the activation and proliferation of T cells and causes CTL-mediated cell lysis of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-CLDN18.2/anti-PD-L1 CAR-T cells

A preparation of T lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-PD-L1 CAR-T cells target and bind to CLDN18.2- and PD-L1-expressing tumor cells, thereby inducing selective toxicity in CLDN18.2- and PD-L1-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity.

anti-CLDN18.2/CD47 bispecific antibody AK132

A bispecific antibody directed against both the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CLDN18.2/CD47 bispecific antibody AK132, the anti-CLDN18.2 moiety selectively targets and binds to CLDN18.2 on CLDN18.2-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to the CLDN18.2-expressing tumor cells. The CD47 binding by AK132 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CLDN18.2-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CLDN18.2-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells (RBCs) and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CLDN18.2, a tight junction protein and stomach-specific isoform of Claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. Co-targeting CD47 and CLDN18.2 may limit the binding of AK132 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize any associated adverse effects.

anti-CLDN18.2/CD47 bispecific antibody SG1906

A recombinant, immunoglobulin G1 (IgG1) bispecific antibody directed against both the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CLDN18.2/CD47 bispecific antibody SG1906, the anti-CLDN18.2 moiety selectively targets and binds to CLDN18.2 on CLDN18.2-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to the CLDN18.2-expressing tumor cells. The CD47 binding by SG1906 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CLDN18.2-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CLDN18.2-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells (RBCs) and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CLDN18.2, a tight junction protein and stomach-specific isoform of Claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. Co-targeting CD47 and CLDN18.2 may limit the binding of SG1906 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize any associated adverse effects.

anti-CLDN4/anti-CD137 bispecific antibody ASP1002

A bispecific antibody directed against both claudin-4 (CLDN4) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN4/anti-CD137 bispecific antibody ASP1002 simultaneously targets and binds to CLDN4 expressed on tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T lymphocytes. The simultaneous binding to CLDN4 and CD137 allows for conditional stimulation of CD137 signaling within the tumor microenvironment (TME) only upon binding to CLDN4 on tumor cells. CD137 activation results in T-cell stimulation and enhances T-lymphocyte-mediated anti-tumor immune response against CLDN4-expressing tumor cells. CLDN4, a claudin protein family member that regulates tight junction formation, is overexpressed on a variety of tumor cells. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-CLDN6 antibody-drug conjugate DS-9606a

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin 6 (CLDN6; CLDN-6) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-CLDN6 ADC DS-9606a, the anti-CLDN6 antibody moiety targets and binds to CLDN6-expressing tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the CLDN6-expressing tumor cells, through an as of yet unknown mechanism of action. CLDN6, a transmembrane tight-junction protein and embryonic antigen, is overexpressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

anti-CLDN6 CAR T cells

A preparation of T lymphocytes expressing a chimeric antigen receptor (CAR) targeting the cell surface protein claudin 6 (CLDN6), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CLDN6 CAR T cells specifically target and bind to CLDN6-expressing tumor cells, thereby selectively lysing CLDN6-expressing tumor cells. CLDN-6, a transmembrane tight-junction protein and embryonic antigen, is overexpressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

anti-CLDN6 monoclonal antibody ASP1650

A monoclonal antibody directed against the cell surface protein claudin 6 (CLDN6), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CLDN6 monoclonal antibody ASP1650 binds to CLDN-6 and may stimulate the immune system to exert both an antibody-dependent cellular cytotoxicity (ADCC) and a complement-dependent cytotoxicity (CDC) mediated immune response against CLDN-6-expressing tumor cells. This may inhibit tumor cell growth. CLDN-6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

anti-CLDN6/9 antibody-drug conjugate SC-004

An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody directed against claudin-6 (CLDN6; CLDN-6) and claudin-9 (CLDN9; CLDN-9) linked to a cytotoxic pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-CLDN6/9 ADC SC-004 targets and binds to CLDN6/9 expressed on tumor cells, and the PBD moiety is released. Then the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CLDN6/9-overexpressing tumor cells. CLDN6, a transmembrane tight-junction protein and embryonic antigen, is overexpressed on a variety of tumor cells but is not expressed on normal, healthy adult cells. CLDN6 and CLDN9 differ at only 3 out of 76 residues in their extracellular loops, and CLDN9 is highly expressed in some normal tissues in addition to some tumors.

anti-CLDN6/CD3 bispecific antibody CTIM-76

An Fc-silenced humanized immunoglobulin G1 (IgG1) bispecific antibody targeting both the tumor-associated antigen (TAA) claudin 6 (CLDN6; CLDN-6) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-CLDN6/CD3 bispecific antibody CTIM-76 targets and binds to both CLDN6 expressed on tumor cells and CD3 expressed on T cells. This activates and redirects cytotoxic T lymphocytes (CTLs) to CLDN6-expressing tumor cells, which leads to enhanced CTL-mediated killing of CLDN6-expressing tumor cells. CLDN6, a tight-junction protein and embryonic antigen, is overexpressed on a variety of tumor cells but is not or minimally expressed on normal, healthy adult cells.

anti-CLDN6/CD3 bispecific antibody SAIL66

A bispecific antibody targeting both the tumor-associated antigen (TAA) Claudin 6 (CLDN6; CLDN-6) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-CLDN6/CD3 bispecific antibody SAIL66 targets and binds to both CLDN6 expressed on tumor cells and CD3 expressed on T-cells. This activates and redirects cytotoxic T lymphocytes (CTLs) to CLDN6-expressing tumor cells, which leads to enhanced CTL-mediated killing of CLDN6-expressing tumor cells. CLDN6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

anti-CLDN6/CD3 bispecific antibody XmAb541

A bispecific antibody directed against both the tumor-associated antigen (TAA) claudin 6 (CLDN6; CLDN-6) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN6/CD3 bispecific antibody XmAb541 bivalently binds to CLDN6 expressed on tumor cells and monovalently binds to CD3 expressed on T-cells. This activates and redirects cytotoxic T-lymphocytes (CTLs) to CLDN6-expressing tumor cells, which leads to enhanced CTL-mediated killing of CLDN6-expressing tumor cells. CLDN6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells. The bivalent binding to CLDN6 and monovalent binding to CD3 by XmAb541 may increase selective targeting of CLDN6-overexpressing tumor cells.

anti-CLDN6/CD3 BiTE antibody AMG 794

A half-life extended (HLE) human bispecific T-cell engager (BiTE) antibody targeting the CD3 antigen expressed on T lymphocytes and the cell surface protein claudin 6 (CLDN6; CLDN-6), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-CLDN6/CD3 BiTE antibody AMG 794 targets and binds to both CD3 expressed on T cells and CLDN6 expressed on tumor cells. This activates and redirects cytotoxic T lymphocytes (CTLs) to CLDN6-expressing tumor cells, produces cytokines and leads to enhanced CTL-mediated elimination of CLDN6-expressing tumor cells. CLDN6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

anti-CLEC12A/CD3 bispecific antibody MCLA117

An immunoglobulin G1 (IgG1) bispecific human monoclonal antibody against human CD3, a T-cell surface antigen, and human C-type lectin domain family 12 member A (CLEC12A), a tumor-associated antigen (TAA) overexpressed on certain tumor cells, with potential antineoplastic activity. Upon administration, anti-CLEC12A/CD3 bispecific antibody MCLA117 binds to both CD3 on T cells and CLEC12A expressed on malignant cells, such as myeloid blasts, atypical progenitor cells and leukemic stem cells (LSCs). This results in the cross-linking of T cells with tumor cells, and induces a potent cytotoxic T-lymphocyte (CTL) response against CLEC12A-expressing tumor cells. CLEC12A, a myeloid differentiation antigen and member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed on myeloid leukemia cells, but not on normal early hematopoietic progenitors, including hematopoietic stem cells (HSCs).

anti-CLL-1/anti-CD38 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) C-type-lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A) and CD38, with potential immunomodulating and antineoplastic activities. Upon administration, anti-CLL-1/anti-CD38 CAR T cells specifically and simultaneously target and bind to CD38- and CLL-1-expressing tumor cells. This induces selective toxicity in CD38- and CLL-1-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis. CLL-1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

anti-CLL1-PBD ADC DCLL9718S

An antibody-drug conjugate (ADC) consisting of MCLL0517A , an anti-C-type lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A) humanized immunoglobulin G1 (IgG1) monoclonal antibody, conjugated, via a cleavable disulfide linker, to two cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimers, with potential antineoplastic activity. Upon administration of anti-CLL1-PBD ADC DCLL9718S, the antibody moiety targets the cell surface tumor-associated antigen (TAA) CLL1. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic PBD moiety is released. The imine groups of the PBD moiety covalently bind to the N2 positions of guanines on opposite strands in the minor groove of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CLL1-overexpressing tumor cells. CLL1, a transmembrane glycoprotein and member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) while absent on normal hematopoietic stem cells (HSCs). It plays an important role in disease progression and relapse of myeloid malignancies.

anti-CLL1/anti-CD33 CAR-T cells LCAR-AMDR

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) C-type-lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A) and CD33, with potential immunomodulating and antineoplastic activities. Upon administration, the anti-CLL1/anti-CD33 CAR-T cells LCAR-AMDR specifically and simultaneously target and bind to CD33- and CLL1-expressing tumor cells. This induces selective toxicity in CD33- and CLL1-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells. CLL1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

anti-cMET/EGFR/VEGF trispecific antibody TAVO412

A trispecific antibody targeting hepatocyte growth factor receptor (HGFR; c-Met), epidermal growth factor receptor (EGFR), and vascular endothelial growth factor (VEGF), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-c-Met/EGFR/VEGF trispecific antibody TAVO412 simultaneously targets and binds to c-Met, EGFR and VEGF. The binding of TAVO412 to c-Met and EGFR expressed on tumor cells prevents receptor phosphorylation. This prevents the activation of both c-Met- and EGFR-mediated signaling pathways. The binding of TAVO412 to VEGF prevents both its binding to VEGF receptors (VEGFRs) and VEGF/VEGFR-mediated signaling. This inhibits the proliferation of vascular endothelial cells and prevents the growth and maintenance of tumor blood vessels, which leads to tumor cell death. In addition, TAVO412 induces Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP) and complement-dependent cytotoxicity (CDC). EGFR and c-Met, both upregulated and/or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation. VEGF is overexpressed in a variety of cancer cells, and VEGF/VEGFR signaling plays an essential role in angiogenesis and the proliferation, survival, migration and differentiation of endothelial cells.

anti-CNTN4 antibody GENA-104A16

An affinity-matured humanized monoclonal antibody directed against the inhibitory immune checkpoint protein contactin 4 (contactin-4; CNTN4), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CNTN4 monoclonal antibody GENA-104A16 targets and binds to CNTN4 expressed on cancer cells. This abrogates CNTN4-mediated immune suppression, decreases regulatory T cells (Tregs), and may restore and increase CD4+ and CD8+ T-cell proliferation and activation and the release of inflammatory cytokines. This may lead to a cytotoxic T-lymphocyte (CTL)-mediated killing of tumor cells that overexpress CNTN4. CNTN4 negatively regulates T-cell activity through binding with amyloid precursor protein (APP) on T cells. It is overexpressed on a variety of tumor cell types.

anti-CSF-1R monoclonal antibody IMC-CS4

A monoclonal antibody directed against colony stimulating factor 1 receptor (CSF1R) with potential antineoplastic activity. CSF1R monoclonal antibody IMC-CS4 binds to CSF1R which may trigger antitumoral antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells overexpressing CSF1R. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1); this receptor is overexpressed or mutated in certain tumor cell types and plays major roles in tumor cell proliferation and metastasis.

Anti-CSF1 Monoclonal Antibody PD-0360324

A humanized immunoglobulin (Ig) G2 monoclonal antibody (mAb) directed against the cytokine colony stimulating factor 1 (CSF1; CSF-1; macrophage colony-stimulating factor; M-CSF), with potential immunomodulating and antineoplastic activities. Upon administration, anti-CSF1 monoclonal antibody PD-0360324 targets, binds to and neutralizes CSF1. This prevents the binding of CSF1 to its receptor CSF1R (CD115; M-CSFR), which is expressed on various immune cells, such as monocytes and macrophages. This prevents CSF1R activation and CSF1R-mediated signaling in these cells; this inhibits monocyte differentiation, blocks the activity of macrophages, and reduces their production of inflammatory mediators, which reduces inflammation. By blocking the activity and proliferation of CSF1R-dependent tumor-associated macrophages (TAMs) in the tumor microenvironment, PD-0360324 reduces TAM-mediated immune suppression, decreases regulatory T-cells (Tregs), re-activates the immune system, and improves anti-tumor cell responses mediated by increasing infiltration by cytotoxic T-cells. TAMs play key roles in immune suppression, and tumor cell proliferation and survival. CSF-1 plays a key role in the regulation of the proliferation, differentiation and survival of monocytes and macrophages.

anti-CSF1R monoclonal antibody AMB-05X

A human immunoglobulin G2 (IgG2) monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; M-CSFR; c-fms), also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), with potential antineoplastic, anti-inflammatory, immunomodulating and anti-fibrotic activities. Upon administration, anti-CSF1R monoclonal antibody AMB-05X targets and binds to CSF1R expressed on tumor cells, monocytes and macrophages, and inhibits the binding of the CSF1R ligands and cytokines colony-stimulating factor-1 (CSF-1; CSF1) and interleukin-34 (IL-34) to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks tumor cell proliferation and the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment (TME) and activity of CSF1R-dependent tumor-associated macrophages (TAMs), AMB-05X enhances T-cell infiltration and antitumor T-cell immune responses, which further inhibits the proliferation of tumor cells. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival. In fibrosis, preventing CSF1R-mediated macrophage differentiation and fibroblast activation may prevent fibrosis. CSF1R, a cell-surface receptor overexpressed or mutated in certain tumor cell types, plays major roles in tumor cell proliferation, metastasis, inflammation, and idiopathic pulmonary fibrosis (IPF). CSF1 is overproduced in certain types of tumors.

anti-CSF1R monoclonal antibody IMC-CS4

A monoclonal antibody directed against colony stimulating factor 1 receptor (CSF1R) with potential antineoplastic activity. CSF1R monoclonal antibody IMC-CS4 binds to CSF1R which may trigger antitumoral antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells overexpressing CSF1R. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (Cluster of Differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1); this receptor is overexpressed or mutated in certain tumor cell types and plays major roles in tumor cell proliferation and metastasis.

anti-CTLA-4 monoclonal antibody ADU-1604

A humanized immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody ADU-1604 targets and binds to CTLA-4 expressed on T cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody BA3071

A conditionally active biologic (CAB) and monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration and specific activation in the tumor microenvironment (TME) due to the unique microphysical conditions that are present in the TME, anti-CTLA-4 monoclonal antibody BA3071 targets and binds to CTLA-4 expressed on T cells within the TME and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. By using a CAB anti-CTLA-4 antibody, systemic toxicity may be reduced.

anti-CTLA-4 monoclonal antibody IBI310

A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody IBI310 targets and binds to CTLA-4 expressed on T cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody KD6001

A monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody KD6001 targets and binds to CTLA-4 expressed on T cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody REGN4659

A fully human immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody REGN4659 targets and binds to CTLA-4 expressed on T cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody SHR-8068

A monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody SHR-8068 targets and binds to CTLA-4 expressed on T cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody XTX101

A fully humanized, Fc-engineered monoclonal antibody with masked antigen-binding regions directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration and the activation of the antigen-binding regions via cleavage by proteases that are upregulated in the tumor microenvironment (TME), anti-CTLA-4 monoclonal antibody XTX101 targets and binds to CTLA-4 expressed on T cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 monoclonal antibody-IL-15/IL-15Ra fusion protein JK08

A recombinant fusion protein consisting of a human monoclonal antibody directed against cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) fused to the immunostimulatory cytokine interleukin-15 (IL-15) cross-linked with the sushi domain of IL-15 receptor alpha (IL-15Ra), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 monoclonal antibody-IL-15/IL-15Ra fusion protein JK08, the monoclonal antibody domain targets and binds to CTLA-4 expressed on T cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. The IL-15/IL-15Ra complex targets and binds to CD8+ T and natural killer (NK) cells, thereby increasing their activation and proliferation. Altogether, this leads to an inhibition of regulatory T-cell (Tregs)-mediated immunosuppression, induces antibody-dependent cellular cytotoxicity (ADCC), increases memory T cells and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA-4 probody BMS-986288

A probody composed of a modified version of ipilimumab, a recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 probody BMS-986288, the masking peptide is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to CTLA-4, which is expressed on certain T cells. This inhibits the CTLA4-mediated downregulation of T-cell activation, and leads to both activation of tumor infiltrating T-effector cells and a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily expressed on activated effector T cells (Teffs) and regulatory T cells (Tregs), plays a key role in the inhibition of T-cell activity and downregulation of the immune system. The peptide masking of BMS-986288 minimizes binding to CTLA-4 in normal tissues and may reduce systemic toxicity, when compared to ipilimumab. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.

anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217

A fixed dose combination of two monoclonal antibodies of which one is directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the other one is directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217 targets and binds to both PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.

anti-CTLA-4/OX40 bispecific antibody ATOR-1015

A bispecific antibody consisting of a cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) inhibitory protein fused to an OX40 agonistic human immunoglobulin G1 (IgG1) antibody, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CTLA-4/OX40 bispecific antibody ATOR-1015 simultaneously binds to CTLA-4 and OX40, which may inhibit CTLA-4-mediated downregulation of T-cell activation and induce proliferation of memory and effector T lymphocytes via OX40 activation. Both CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), and OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), are overexpressed by regulatory T cells (Tregs) in the tumor microenvironment. ATOR-1015 may reduce the number of Tregs and promote the activation of effector T cells, thereby enhancing the immune-mediated anti-tumor response.

anti-CTLA4 antibody Fc fusion protein KN044

A recombinant, humanized fusion protein consisting of a cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) single domain antibody linked to a Fc domain, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA4 antibody Fc fusion protein KN044 targets and binds to CTLA4 expressed on T cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-CTLA4 mAb RNA/GITRL RNA-transfected autologous dendritic cell vaccine

An autologous dendritic cell (DC) cancer vaccine with potential immunostimulatory activity. Anti-CTLA4 MoAb RNA/GITRL RNA-transfected DC vaccine is prepared by transfecting DCs with RNAs encoding humanized heavy and light chains of the anti-CTLA4 (cytotoxic T-Lymphocyte-Associated Antigen 4) monoclonal antibody and tumor necrosis factor (ligand) superfamily, member 18 (TNFSF18 or GlTRL); expression of anti-CTLA4 blocks the inhibitory effect of CTLA4 on the activation of T lymphocytes, while expression of GlTRL modulates T-lymphocyte survival in peripheral tissues. Co-vaccination of this vaccine with melanoma antigen specific vaccine may eliminate the adverse effects associated with systemic administration of immune modulators, while also enhancing vaccine-induced immune responses.

anti-CTLA4 MoAb RNA-transfected autologous dendritic cell vaccine

An autologous dendritic cell (DC) cancer vaccine with potential immunostimulatory activity. Anti-CTLA4 MoAb RNA-transfected autologous DC vaccine is prepared by transfecting DCs with RNAs encoding humanized heavy and light chains of the anti-CTLA4 (cytotoxic T-Lymphocyte-Associated Antigen 4); expression of anti-CTLA4 blocks the inhibitory effect of CTLA4 on the activation of T lymphocytes. Co-vaccination of this vaccine with melanoma antigen specific vaccine may eliminate the adverse effects associated with systemic administration of immune modulators, while also enhancing vaccine-induced immune responses.

anti-CTLA4 monoclonal antibody BMS-986218

A Fc-modified monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA4 monoclonal antibody BMS-986218 targets and binds to CTLA4 expressed on T cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system. Removal of the fucose sugar units from the antibody's Fc region, enhances its activity and decreases the toxicity of BMS-986218.

anti-CTLA4 monoclonal antibody GIGA-564

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), with potential immunomodulatory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody GIGA-564 targets and binds to CTLA-4, and may induce Fc receptor (FcR) signaling. This may deplete regulatory T cells (Tregs) in the tumor microenvironment (TME), decrease the proliferation of the remaining Tregs in the TME, and reactivate antitumor immune responses. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. GIGA-564 has limited checkpoint inhibitory activity as it only weakly blocks the interaction between CTLA-4 and its B7 ligands CD80 and CD86.

anti-CTLA4 monoclonal antibody HBM4003

A recombinant human heavy chain only antibody (HCAb) directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody HBM4003 targets and binds to CTLA-4 expressed on T cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. In addition, HBM4003 induces an antibody-dependent cell cytotoxicity (ADCC). CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. HBM4003, being a HCAb, is smaller than conventional antibodies which may allow for increased tissue penetration.

anti-CXCR4 monoclonal antibody PF-06747143

A humanized immunoglobulin (Ig) G1 monoclonal antibody (mAb) against C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic activity. Upon administration, anti-CXCR4 mAb PF-06747143 binds to CXCR4, thereby preventing the binding of stromal cell-derived factor-1 (SDF-1 or CXCL12) to CXCR4 and inhibiting CXCR4 activation. This results in decreased proliferation and migration of CXCR4-expressing tumor cells. In addition, PF-06747143 promotes cell death through the induction of both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC). CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, is upregulated in several tumor cell types and plays an important role in cancer cell proliferation, survival, and chemotaxis, and in tumor angiogenesis.

anti-DDR1 monoclonal antibody PRTH-101

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against discoid domain receptor type 1 (DDR1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-DDR1 monoclonal antibody PRTH-101 specifically targets, binds to and blocks DDR1, a protein expressed on tumor cells that binds collagen to make a minimally permeable physical barrier that blocks immune cells in the tumor microenvironment (TME) from interacting with and attacking the tumor. By blocking DDR1, PRTH-101 causes the collagen fibers lose alignment and loosen. This creates gaps in the tumor barrier, thereby allowing cytotoxic T-cells to enter and attack the tumor.

anti-dectin-2 agonist monoclonal antibody BDC-3042

An agonistic monoclonal antibody targeting the immune-activating pattern recognition receptor (PRR) dectin-2 (C-type lectin domain family 6 member A; CLEC6A), with potential immunostimulatory and antineoplastic activities. Upon administration, anti-dectin-2 agonist monoclonal antibody BDC-3042 targets, binds to and activates dectin-2 expressed by tumor-associated macrophages (TAMs) in the tumor microenvironment (TME). This may lead to the secretion of pro-inflammatory cytokines and chemokines, repolarize TAMs into immunostimulatory macrophages, and enhance antigen processing and presentation, thereby promoting phagocytosis of tumor cells and T-cell-mediated anti-tumor immune response. Dectin-2, an activating C-type lectin receptor (CLR), is expressed by TAMs in various tumor types.

anti-denatured collagen monoclonal antibody TRC093

A humanized, affinity-matured IgG1k antibody directed against denatured collagens (I-IV) with potential antiangiogenic and antineoplastic activities. Anti-denatured collagen recombinant monoclonal antibody TRC093 binds to multiple epitopes on denatured collagens, inhibiting proteolytic collagen-mediated signaling in the extracellular matrix (ECM) that is important to tumor angiogenesis, tumor growth, and metastasis. The epitopes on denatured collagen bound by this antibody are considered cryptic because, in vivo, they are accessible only on the subendothelial basement membrane of tumors or in normal tissues undergoing neovascularization.

anti-DKK1 monoclonal antibody BHQ880

A humanized monoclonal antibody directed against Wnt antagonist Dickkopf-1 (DKK1) with potential anti-osteolytic activity. Anti-DKK1 monoclonal antibody BHQ880 binds to and inhibits DKK1, enhancing signaling through the Wnt pathway, which may result in osteoblast differentiation and activation within the bone matrix and the reversal of tumor-induced osteolytic disease. DKK! is a potent Wnt signaling pathway antagonist.

anti-DKK1 monoclonal antibody JS015

A humanized monoclonal antibody directed against Dickkopf-related protein 1 (Dickkopf-1; DKK1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-DKK1 monoclonal antibody JS015 binds to DKK1 and blocks the interaction between DKK1 and its ligands low-density lipoprotein receptor-related proteins (LRP) 5 and 6. This restores signaling through the Wnt/beta-catenin-dependent (canonical) pathway, and may decrease DKK1-mediated immunosuppressive effects in the tumor microenvironment (TME) and enhance anti-tumor immune responses. DKK1, an inhibitor of the Wnt/beta-catenin-dependent (canonical) signaling pathway, is overexpressed by and dysregulated in some cancers, as well as other diseases including osteoporosis, Alzheimer's disease and diabetes. 

anti-DLK-1 antibody-drug conjugate ADCT-701

An antibody-drug conjugate (ADC) composed of HuBa-1-3D, a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against human delta-like 1 homolog protein (DLK-1; DLK1) and site-specifically conjugated to PL1601, which contains a valine-alanine cleavable linker and SG3199, a cytotoxic pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-DLK-1 ADC ADCT-701, the antibody moiety targets and binds to DLK-1, which is expressed on the surfaces of a variety of cancer cell types. Upon endocytosis and enzymatic cleavage by cathepsin, free PBD is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing DLK-1-expressing cancer cells. DLK-1, an epidermal growth factor (EGF)-like membrane bound protein overexpressed by certain tumor cell types and on certain cancer stem cells (CSCs), plays a key role in tumor cell proliferation. Its expression is widely expressed during fetal development but in adult healthy tissue it is very restricted.

anti-DLK-1/MMAE antibody-drug conjugate TORL-4-500

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against human delta-like 1 homolog protein (DLK-1; DLK1) conjugated, via a cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-DLK-1/MMAE ADC TORL-4-500, the anti-DLK-1 antibody moiety targets and binds to DLK-1 expressed on tumor cells. Upon binding, internalization, and linker cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in DLK-1-expressing tumor cells. DLK-1, an epidermal growth factor (EGF)-like membrane bound protein overexpressed by certain tumor cell types and on certain cancer stem cells (CSCs), plays a key role in tumor cell proliferation. Its expression is widely expressed during fetal development but in adult healthy tissue it is very restricted.

anti-DLL3 ADC ZL-1310

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and linked to an as of yet unelucidated cytotoxic agent, with potential immunostimulating and antineoplastic activities. Upon administration, anti-DLL3 ADC ZL-1310 targets and binds to DLL3 found on DLL3-expressing tumor cells. Upon internalization, the cytotoxic agent causes cell death in DLL3-expressing tumor cells through an as of yet unknown mechanism of action. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3 antibody-drug conjugate FZ-AD005

An antibody-drug conjugate (ADC) composed of FZ-A038, a monoclonal antibody directed against the tumor-associated antigen (TAA) delta-like protein 3 (DLL3), conjugated, via a valine-alanine (Val-Ala) dipeptide linker, to the cytotoxic DNA topoisomerase I inhibitor and exatecan derivative DXd (MAAA-1181a; MAAA-1181), with potential antineoplastic activity. Upon administration, anti-DLL3 ADC FZ-AD005 targets and binds to DLL3-expressing tumor cells. Upon binding and internalization, DXd is released. DXd inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of DLL3-expressing tumor cells. FZ-AD005 is also able to induce a bystander effect on neighboring cells in the tumor environment. This further inhibits the proliferation of tumor cells. In addition, FZ-AD005 is Fc-silenced, which may prevent Fc gamma receptor (FcgR)-mediated toxicities. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development, tumor initiation and proliferation.

anti-DLL3 antibody-drug conjugate SC-002

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) delta-like protein 3 (DLL3), site-specifically conjugated to the cytotoxic pyrrolobenzodiazepine (PBD) dimer SC-DR002 via a plasma-stable valine-alanine dipeptide linker, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-DLL3 ADC SC-002 targets and binds to DLL3 expressed on tumor cells. Upon binding and internalization, the dipeptide linker is cleaved upon cathepsin-mediated proteolysis and SC-DR002 is released. Then the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of DLL3-overexpressing tumor cells. DLL3, a membrane protein that binds to Notch receptors and regulates Notch-mediated signaling and gene transcription, is overexpressed by certain cancers but is rarely expressed by normal, healthy cells.

anti-DLL3 bispecific antibody RO7616789

A bispecific T-cell engager antibody directed against both the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and an as of yet unspecified antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-DLL3 bispecific antibody RO7616789 binds to both the antigen on cytotoxic T lymphocytes (CTLs) and the DLL3 antigen on DLL3-expressing tumor cells. This activates and redirects CTLs to DLL3-expressing tumor cells, which results in the CTL-mediated cell death of DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3 CAR-NK cells

A preparation of natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) delta-like protein 3 (DLL3), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-DLL3 CAR-NK cells recognize, bind to and induce selective cytotoxicity in DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3 CAR-NK cells SNC-115

A preparation of natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) delta-like protein 3 (DLL3), with potential immunomodulating and antineoplastic activities. Upon administration, anti-DLL3 CAR-NK cells SNC-115 recognize, bind to and induce selective cytotoxicity in DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3/anti-CD47 bispecific antibody PT217

A bispecific antibody directed against both the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-DLL3/anti-CD47 bispecific antibody PT217, the anti-DLL3 moiety selectively targets and binds to DLL3 on DLL3-expressing tumor cells, thereby improving the binding of the anti-CD47 moiety to DLL3-expressing tumor cells. The CD47 binding by PT217 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of DLL3-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of DLL3-expressing tumor cells. PT217 may also induce an anti-tumor activity through the induction of antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells (RBCs) and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation. Co-targeting CD47 and DLL3 may limit the binding of PT217 to CD47 on healthy hematopoietic stem cells (HSCs) and may minimize the associated adverse effects.

anti-DLL3/CD3 bispecific antibody BI 764532

A bispecific T-cell engager antibody directed against both the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-DLL3/CD3 bispecific antibody BI 764532 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the DLL3 antigen on DLL3-expressing tumor cells. This activates and redirects CTLs to DLL3-expressing tumor cells, which results in the CTL-mediated cell death of DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3/CD3 bispecific antibody QLS31904

A bispecific antibody directed against both the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-DLL3/CD3 bispecific antibody QLS31904 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the DLL3 antigen on DLL3-expressing tumor cells. This activates and redirects CTLs to DLL3-expressing tumor cells, which results in the CTL-mediated cell death of DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL3/DLL3/CD3 trispecific antibody ZG006

A trispecific T-cell engaging (TCE) antibody directed against two different epitopes of the tumor-associated antigen (TAA) delta-like protein 3 (DLL3) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-DLL3/DLL3/CD3 trispecific antibody ZG006 binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the DLL3 antigen on DLL3-expressing tumor cells. This activates and redirects CTLs to DLL3-expressing tumor cells, which results in the CTL-mediated cell death of DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

anti-DLL4 monoclonal antibody MEDI0639

An immunoglobulin G1 lambda monoclonal antibody directed against the Notch ligand delta-like 4 (DLL4) with potential antineoplastic activity. Anti-DLL4 monoclonal antibody MEDI0639 specifically binds to DLL4 and prevents its interaction with Notch receptors, thereby inhibiting Notch-mediated signaling and gene transcription, which may block tumor angiogenesis and eventually the inhibition of tumor cell growth. Activation of Notch receptors by DLL4 stimulates proteolytic cleavage of the Notch intracellular domain (NICD); after cleavage, NICD is translocated to the nucleus and mediates the transcriptional regulation of a variety of genes involved in vascular development. The expression of DLL4 is highly restricted to the vascular endothelium; DLL4/Notch signaling is required for the development of functional tumor blood vessels.

anti-DLL4 monoclonal antibody REGN421

A human monoclonal antibody directed against Delta-like ligand-4 (DLL4) with potential antineoplastic activity. Anti-DLL4 monoclonal antibody REGN421 specifically binds to human DLL4, preventing its binding to Notch receptors and inhibiting Notch signaling, which may result in defective tumor vascularization and, so, the inhibition of tumor cell growth. DLL4 is the only Notch ligand selectively expressed on endothelial cells; DLL4/Notch signaling is required for the development of functional tumor blood vessels.

anti-DLL4/anti-VEGF-A bispecific antibody CTX-009

A bispecific antibody targeting Delta-like ligand 4 (DLL4) and vascular endothelial growth factor A (VEGF-A), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-DLL4/anti-VEGF-A bispecific antibody CTX-009 simultaneously targets, binds to and blocks DLL4 and VEGF-A. This prevents the activation of DLL-4/Notch- and VEGF-A/VEGF receptor (VEGFR)-mediated signaling pathways, which play key roles in angiogenesis and tumor vascularization. This prevents angiogenesis and may halt tumor cell proliferation. Activation of Notch receptors by DLL4 stimulates proteolytic cleavage of the Notch intracellular domain (NICD); after cleavage, NICD is translocated to the nucleus and mediates the transcriptional regulation of a variety of genes involved in vascular development. The expression of DLL4 is highly restricted to the vascular endothelium; DLL4/Notch signaling is required for the development of functional tumor blood vessels. VEGF-A is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis.

anti-DR5 agonist monoclonal antibody TRA-8

An agonist mouse monoclonal antibody directed against TRAIL death receptor type 5 (DR5) with potential antineoplastic activity. Anti-DR5 agonist monoclonal antibody TRA-8 binds DR5, which may induce apoptosis in DR5-expressing tumor cells. DR5 is a tumor cell surface ligand that crosslinks with death receptor type 4 (DR4) when bound by TRAIL [Tumor necrosis (TNF)-related apoptosis-inducing ligand], triggering apoptosis via a death receptor signaling pathway. The apoptotic activity of this antibody may not require DR4/DR5 crosslinking.

anti-DR5 agonistic monoclonal antibody INBRX-109

A recombinant, humanized, agonistic, tetravalent monoclonal antibody directed against human death receptor type 5 (DR5), also called tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAILR2), with potential pro-apoptotic and antineoplastic activities. Upon administration, INBRX-109 specifically binds to exactly four DR5 receptors per molecule, which mimics the interaction of DR5 with its natural ligand TRAIL. This activates DR5 and the death receptor signaling pathway, which results in the activation of caspase cascades, the induction of tumor cell apoptosis and a reduction in proliferation of DR5-expressing tumor cells. Utilizing a tetravalent monoclonal antibody may overcome the challenge of generating effective DR5 clustering while avoiding toxicities associated with anti-drug antibody (ADA) hyper-clustering. DR5, a member of the TNF receptor superfamily (TNFRSF), is expressed on the surfaces of a variety of tumor cells and plays a key role in the induction of tumor cell apoptosis.

anti-EDB antibody-drug conjugate PYX-201

An antibody-drug conjugate (ADC) composed of a fully human immunoglobulin G1 (IgG1) antibody against extra domain B (EDB) splice variant of fibronectin (EDB-FN; EDB+ FN), conjugated via the cleavable linker mc-Val-Cit-PABC, to the cytotoxic auristatin derivative Aur0101, with potential antineoplastic activity. Upon administration of anti-EDB ADC PYX-201, the antibody moiety targets and binds to EDB in the tumor stroma. Upon binding, the cell-permeable auristatin derivative payload is released, and diffuses across the cell membranes of nearby tumor cells, fibroblasts and tumor vasculature. The auristatin derivative binds to tubulin and inhibits microtubule polymerization, which results in G2/M phase arrest and apoptosis of these cells. Upon tumor cell death, the auristatin derivative is re-released, further killing nearby tumor cells. Tumor cell death may also promote dendritic cell (DC) maturation and anti-tumor immune responses. ED-B splice variant of fibronectin, a marker of tissue remodeling and angiogenesis, is overexpressed in the extracellular matrix in many tumors.

anti-EGFR antibody-drug conjugate ABBV-637

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated to an inhibitor of Bcl-extra large (Bcl-XL), with potential antineoplastic activity. Upon administration of anti-EGFR ADC ABBV-637, the monoclonal antibody moiety targets and binds to EGFR on tumor cell surfaces. Following receptor internalization, the Bcl-XL inhibitor is released, which targets, binds to and inhibits the activity of Bcl-XL. This restores apoptotic processes in EGFR-expressing tumor cells and inhibits the proliferation of EGFR-expressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-EGFR antibody-drug conjugate CPO301

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody directed against the epidermal growth factor receptor (EGFR; HER1; ErbB1) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-EGFR ADC CPO301, the monoclonal antibody moiety binds to EGFR on tumor cell surfaces. Upon binding and internalization, the cytotoxic agent is released and kills the EGFR-expressing cancer cells, through an as of yet unknown mechanism of action. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

anti-EGFR antibody-drug conjugate MRG003

An antibody-drug conjugate (ADC) consisting of a human immunoglobulin G1 (IgG1) monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-EGFR ADC MRG003, the monoclonal antibody moiety binds to EGFR on tumor cell surfaces. Following receptor internalization, the MMAE moiety is released and binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and apoptosis. This inhibits the proliferation of EGFR-expressing tumor cells. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

anti-EGFR CAR-transduced IL-12-expressing T lymphocytes

A preparation of human T lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) chimeric antigen receptor (CAR) gene coupled to the signaling domains from CD28, 4-1BB (CD137) and CD3 zeta, and modified to express the cytokine interleukin-12 (IL-12), with potential immunostimulatory and antineoplastic activities. Upon administration, the anti-EGFR CAR-transduced IL-12-expressing T lymphocytes target and bind to the EGFR antigen on tumor cell surfaces; subsequently, EGFR-expressing tumor cells may be lysed. IL-12 expression activates the immune system by promoting the secretion of interferon-gamma (IFNg), activating natural killer cells (NKs), and inducing cytotoxic T-cell responses, which may result in both decreased cell proliferation and increased cell death for the EGFR-overexpressing tumor cells. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.

anti-EGFR fluorescence imaging agent ABY-029

A fluorescence imaging and contrast agent composed of an epidermal growth factor receptor (EGFR)-targeting affibody tracer molecule and labeled, through maleimide, with a near-infrared (NIR) fluorescent probe, IRDye 800CW, with potential use in the imaging of EGFR-overexpressing cells. Upon administration, ABY-029 targets and binds to EGFR-overexpressing tumor cells. Upon fluorescent imaging, the fluorescent dye can be visualized and EGFR-positive tumor cells can be detected.

anti-EGFR gamma delta T-cell engaging bispecific antibody SGN-EGFRd2

A bispecific gamma delta T-cell engager (TCE) antibody targeting both the tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR; HER1; ErbB1) and Vdelta2-T-cell receptor (TCR) chain of Vgamma9Vdelta2 T cells, with potential immunostimulating and antineoplastic activities. Upon administration, anti-EGFR gamma delta T-cell engaging bispecific antibody SGN-EGFRd2 binds to both EGFR-expressing tumor cells and Vgamma9Vdelta2 T cells. This activates and redirects the Vgamma9Vdelta2 T cells to EGFR-expressing tumor cells, and the Vgamma9Vdelta2 T-cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, the Vgamma9Vdelta2 T-cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The Vdelta2 gamma delta T-cell subset is one of the two major gamma delta T-cell subsets that is almost exclusively paired with the Vgamma9 chain. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

anti-EGFR monoclonal antibody ABT-806

A humanized monoclonal antibody (MoAb) against human epidermal growth factor receptor (EGFR) with antineoplastic activity. MoAb ABT-806 targets the EGFR deletion variant, de2-7 EGFR as well as wild-type EGFR expressed in cells overexpressing the receptor, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization result in an inhibition in signal transduction and anti-proliferative effects. This MoAb targets cells expressing aberrant EGFR, hence making it an ideal candidate for generation of radioisotope or toxin conjugates.

anti-EGFR monoclonal antibody CPGJ 602

A recombinant, human-mouse chimeric monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Upon intravenous administration, anti-EGFR monoclonal antibody CPGJ 602 targets and binds to EGFR, which prevents receptor dimerization and activation. This leads to an inhibition of EGFR-dependent downstream pathways and EGFR-dependent tumor cell proliferation and metastasis. EGFR, a receptor tyrosine kinase, may be overexpressed on the surfaces of various tumor cell types.

anti-EGFR monoclonal antibody GC1118

A recombinant, human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Upon intravenous administration, GC1118 binds to and blocks the ligand binding site of EGFR, which prevents receptor dimerization and activation. This may lead to an inhibition of both EGFR-dependent downstream pathways and EGFR-dependent tumor cell proliferation and metastasis. EGFR, a receptor tyrosine kinase, may be overexpressed on the surfaces of various tumor cell types.

anti-EGFR monoclonal antibody mixture MM-151

An oligoclonal therapeutic composed of three fully human monoclonal antibodies targeting epidermal growth factor receptor (EGFR or ErbB1), with potential antineoplastic activity. Upon administration of MM-151, the three antibodies bind to distinct, non-overlapping epitopes of EGFR, thereby preventing the binding of a full range of both high and low affinity EGFR ligands and inhibiting EGFR-ERK-mediated signaling. This eventually inhibits tumor cell proliferation in EGFR-overexpressing tumor cells. Furthermore, multi antibody-antigen bindings cause crosslinking of EGFR and downregulate receptor signalings that are mediated via heterodimerization of EGFR with other members of the EGFR family. EGFR, a receptor tyrosine kinase overexpressed in a variety of cancer cell types, is a key regulator of cancer cell proliferation, apoptosis, invasion, and metastasis.

anti-EGFR monoclonal antibody SYN004

A glyco-engineered monoclonal antibody directed against the receptor tyrosine kinase epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon administration, anti-EGFR monoclonal antibody SYN004 binds to the extracellular domain of EGFR, which prevents ligand binding and the subsequent activation and dimerization of the receptor. This inhibits the activation of EGFR-mediated signaling pathways and inhibits EGFR-dependent tumor cell proliferation. EGFR, a member of the EGFR receptor tyrosine kinase family, may be overexpressed on the cell surfaces of various tumor cell types.

anti-EGFR monoclonal antibody ZZ06

A monoclonal antibody directed against human epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Upon administration, anti-EGFR monoclonal antibody ZZ06 targets, binds and prevents the activation of EGFR. This inhibits EGFR-mediated signaling and proliferation of EGFR-expressing tumor cells. EGFR, a member of the epidermal growth factor receptor family, is overexpressed on various tumor cell types.

anti-EGFR TAP antibody-drug conjugate IMGN289

A targeted antibody payload (TAP)-based immunoconjugate consisting of a human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated, via a nonreducible thioether linker (succinimidyl trans-4-(maleimidylmethyl)cyclohexane-1-carboxylate or SMCC), to the cytotoxic agent maytansinoid mertansine (DM1), with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of immunoconjugate IMGN289 binds to and inhibits EGFR on tumor cell surfaces. Inhibition of EGFR prevents EGFR-mediated signaling and may inhibit tumor cell proliferation. After internalization, the mertansine moiety binds to tubulin and interferes with microtubule assembly/disassembly dynamics. This inhibits both cell division and the proliferation of cancer cells that express EGFR. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival. Linkage of the antibody and drug, through a nonreducible linker, appears to contribute to the improved efficacy and reduced toxicity of this antibody-drug conjugate (ADC) compared to similar ADCs constructed with reducible linkers.

anti-EGFR/anti-B7-H3 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the epidermal growth factor receptor (EGFR) and the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-EGFR/anti-B7-H3 CAR T cells target and bind to EGFR-expressing tumor cells and B7-H3-expressing immune and tumor cells, thereby inducing selective toxicity in these cells. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

anti-EGFR/anti-c-Met monoclonal antibody FPI-2053

A humanized bispecific monoclonal antibody targeting epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR; c-Met), that can potentially be used as a ligand in radiotherapy. Upon administration, anti-EGFR/anti-c-Met monoclonal antibody FPI-2053 simultaneously targets and binds to the extracellular domains of both EGFR and c-Met expressed on cancer cells. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/anti-CD3 tumor protease-activated T-cell engager JANX008

A protease-activated, double masked tumor activated T-cell engager (TCE) composed of a tumor-associated antigen (TAA) binding domain that targets epidermal growth factor receptor (EGFR) and a T-cell binding domain that targets CD3, that are both conjugated, via a tumor protease-cleavable linker, to a peptide mask that prevents binding of the EGFR-binding domain to EGFR-expressing tumor cells and binding of the CD3-binding domain to T cells, respectively, and an albumin-binding domain that extends circulating half-life, with potential immunomodulating and antineoplastic activities. Upon intravenous administration of anti-EGFR/anti-CD3 tumor protease-activated TCE JANX008, the tumor protease-cleavable linkers are proteolytically cleaved in the tumor microenvironment (TME), which separates both the EGFR-binding domain and the CD3-binding domain of JANX008 from their respective peptide masks, thereby allowing the binding domains to bind to their respective targets. The EGFR-binding domain targets and binds to EGFR expressed on tumor cells. The CD3-binding domain targets and binds to T cells. The resulting cross-linkage triggers a cytotoxic T-lymphocyte (CTL) response against EGFR-expressing tumor cells in the TME. EGFR, a receptor tyrosine kinase, is overexpressed on the surfaces of various tumor cell types. The albumin-binding domain, which is attached to the CD3-binding domain mask, binds to albumin in the circulation, thereby extending the half-life of JANX008. While in circulation, the two tumor protease-cleavable peptide masks inhibit EGFR and CD3 binding and may prevent cytokine release syndrome (CRS) and on-target EGFR healthy tissue toxicity while increasing its efficacy when activated in the TME.

anti-EGFR/anti-HER3 bispecific antibody-drug conjugate IBI3005

An antibody-drug conjugate (ADC) composed of a bispecific antibody directed against the tumor associated antigens (TAAs) human epidermal growth factor receptor (EGFR; HER1; ErbB1), and human epidermal growth factor receptor 3 (HER3; ErbB3) conjugated to a camptothecin derivative, with potential antineoplastic activity. Upon administration, anti-EGFR/anti-HER3 bispecific ADC IBI3005 targets and simultaneously binds to EGFR and HER3 expressed on tumor cells. This blocks EGFR activation by ligands and EGFR-mediated signaling. Upon binding and internalization, the camptothecin derivative is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis in EGFR- and HER3-expressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. HER3, a member of the EGFR family of receptor tyrosine kinases, is frequently overexpressed in tumors.

anti-EGFR/c-Met bispecific antibody CKD-702

A tetravalent, bispecific antibody composed of a single-chain variable fragment (scFv) targeting epidermal growth factor receptor (EGFR) fused to the c-terminus of an immunoglobulin G1 (IgG1) antibody targeting hepatocyte growth factor receptor (HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met bispecific antibody CKD-702 simultaneously targets and binds to the extracellular domains of wild-type or certain mutant forms of both EGFR and c-Met expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and c-Met-mediated signaling pathways. In addition, binding results in receptor degradation, which further inhibits EGFR- and c-Met-mediated signaling, thereby inhibiting tumor cell proliferation. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/c-Met bispecific antibody MCLA-129

A human bispecific immunoglobulin G1 (IgG1) antibody targeting the tumor-associated antigens (TAAs) epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met bispecific antibody MCLA-129 simultaneously targets and binds to the extracellular domains of both EGFR and c-Met expressed on cancer cells. This prevents the activation of both EGFR- and c-Met-mediated signaling pathways. The binding results in antibody-dependent cellular cytotoxicity (ADCC), thereby inhibiting tumor cell proliferation and survival. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/c-Met/c-Met trispecific antibody BG-T187

A trispecific antibody targeting epidermal growth factor receptor (EGFR) and two different epitopes of hepatocyte growth factor receptor (HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met/c-Met trispecific antibody BG-T187 simultaneously targets and binds to the extracellular domain of both EGFR and two different epitopes of c-Met expressed on tumor cells, thereby preventing receptor phosphorylation and activation of both EGFR- and c-Met-mediated signaling pathways. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/c-MET/c-MET trispecific antibody GB263T

A Fc-enhanced trispecific antibody targeting epidermal growth factor receptor (EGFR) and two different epitopes of hepatocyte growth factor receptor (HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met/c-met trispecific antibody GB263T simultaneously targets and binds to the extracellular domain of both EGFR and two different epitopes on c-Met expressed on tumor cells, thereby preventing receptor phosphorylation and inducing internalization of EGFR and c-Met. This downregulates the expression levels of both EGFR and c-Met proteins and prevents the activation of both EGFR- and c-Met-mediated signaling pathways. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/c-Met/TOP1i ADC AZD9592

An antibody-drug conjugate (ADC) composed of a bispecific antibody targeting both epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (HGFR; c-Met) and conjugated to a topoisomerase-1 inhibitor (TOP1i), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met/TOP1i ADC AZD9592 simultaneously targets and binds to the extracellular domains of wild-type (WT) or certain mutant forms of both EGFR and c-Met expressed on cancer cells. Upon binding and internalization, the TOP1i moiety is released, binds to TOP1 and stabilizes cleaved DNA-TOP1 complexes. This prevents DNA re-ligation, induces irreversible DNA strand breaks, prevents DNA repair, and leads to cycle arrest and apoptosis specifically in tumor cells expressing EGFR and c-Met. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.

anti-EGFR/CD16A bispecific antibody AFM24

A human, tetravalent, bispecific antibody targeting both the epidermal growth factor receptor (EGFR) and the human low affinity IgG Fc region receptor IIIA (FCGR3A; CD16A), with potential immunomodulating and antineoplastic activities. Upon administration, anti-EGFR/CD16A bispecific antibody AFM24 simultaneously targets and binds to the CD16A expressed on natural killer (NK) cells and macrophages, and to EGFR on EGFR-expressing tumor cells, thereby selectively cross-linking EGFR-expressing tumor cells with NK cells and macrophages. This may result in NK cell and macrophage activation, antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and eventually tumor cell lysis. EGFR, a receptor tyrosine kinase upregulated or mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. CD16A is specifically expressed on the surface of NK cells and macrophages.

anti-EGFR/CD3 bispecific antibody SMET12

A bispecific antibody and T-cell engager (TCE) targeting both the tumor-associated antigen (TAA) human epidermal growth factor receptor (EGFR) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-EGFR/CD3 bispecific antibody SMET12 binds to both CD3 expressed on T cells and EGFR expressed on tumor cells. This crosslinks cytotoxic T lymphocytes (CTLs) and EGFR-expressing tumor cells, and activates and redirects CTLs to EGFR-expressing tumor cells. This leads to CTL-mediated killing of EGFR-expressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-EGFR/DM1 antibody-drug conjugate AVID100

A targeted antibody drug conjugate (ADC) consisting of a human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated to the cytotoxic agent maytansinoid mertansine (DM1), with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of AVID100 binds to and inhibits EGFR on tumor cell surfaces. Inhibition of EGFR prevents EGFR-mediated signaling and may inhibit tumor cell proliferation. Following receptor internalization, the mertansine moiety binds to tubulin and interferes with microtubule assembly/disassembly dynamics. This inhibits both cell division and proliferation of cancer cells that express EGFR. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

anti-EGFR/HER2/HER3 monoclonal antibody mixture Sym013

An antibody mixture composed of six humanized, immunoglobulin G1 (IgG1) monoclonal antibodies directed against three members of the human epidermal growth factor receptor (EGFR; HER) family: EGFR (HER1; ErbB1), HER2 (ErbB2) and HER3 (ErbB3), with potential antineoplastic activity. Upon administration of anti-EGFR/HER2/HER3 monoclonal antibody mixture Sym013, the six antibodies bind to non-overlapping epitopes on EGFR, HER2 and HER3, which prevents both ligand binding and receptor activation, and induce simultaneous down-modulation of EGFR, HER2 and HER3. This inhibits the activation of HER-dependent signaling pathways and HER-dependent tumor cell proliferation. Overexpression of the HER family plays a key role in many cancers; targeting multiple HER family members simultaneously may increase therapeutic efficacy.

anti-EGFR/HER3 monoclonal antibody MEHD7945A

An immunoglobulin (Ig) G1 monoclonal antibody directed against both human epidermal growth factor receptor 3 (HER3 or ERBB3) and human epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Anti-EGFR/HER3 Monoclonal Antibody MEHD7945A binds to both EGFR and HER3 and inhibits their activation. This may prevent EGFR/HER3-mediated signaling and inhibit EGFR/HER3-dependent tumor cell proliferation. In addition, MEHD7945A induces antibody-dependent cell-mediated cytotoxicity (ADCC) against EGR/HER3-expressing tumor cells. EGFR and HER3, members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in tumors; their expression is associated with both poor prognosis and drug resistance.

anti-EGFR/LGR5 bispecific antibody MCLA-158

An immunoglobulin G1 (IgG1) bispecific antibody targeting both epidermal growth factor receptor (EGFR; HER1; ErbB1) and leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5), with potential antineoplastic activity. Upon administration, anti-EGFR/LGR5 bispecific antibody MCLA-158 simultaneously targets and binds to both EGFR and LGR5, thereby inhibiting the activation of both EGFR- and LGR5-mediated signaling pathways. This results in the inhibition of tumor cell proliferation. EGFR, a receptor tyrosine kinase (RTK) upregulated and/or mutated in a variety of tumor cell types, plays an important role in tumor cell proliferation. LGR5, a member of the Wnt signaling pathway, is a cancer stem cell (CSC) receptor overexpressed on certain cancer cells; it plays a key role in CSC proliferation and survival.

anti-EGFR/PBD antibody-drug conjugate ABBV-321

An antibody drug conjugate (ADC) consisting of ABT-806 AM1, an affinity-matured humanized monoclonal antibody directed against the epidermal growth factor receptor (EGFR), and conjugated to the cytotoxic, DNA minor groove crosslinking agent, pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration of anti-EGFR/PBD ADC ABBV-321, the monoclonal antibody moiety of ABBV-321 targets and binds to EGFR on tumor cell surfaces. Following receptor internalization and lysosome-mediated cleavage, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death and inhibits the proliferation of EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase (RTK) that is overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.

anti-EGFR/topoisomerase I inhibitor antibody-drug conjugate HLX42

An antibody-drug conjugate (ADC) composed of an immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR) conjugated, via a cleavable linker, to a topoisomerase I inhibitor (TOP1i), with potential antineoplastic activity. Upon administration of anti-EGFR/TOP1i ADC HLX42, the anti-EGFR monoclonal antibody moiety targets and binds to EGFR expressed on tumor cells. Upon binding and cleavage in the tumor microenvironment (TME), the TOP1i moiety inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication which results in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of EGFR-expressing tumor cells. HLX42 also induces bystander killing activity. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-EGFRvIII antibody drug conjugate AMG 595

An immunoconjugate consisting of a human monoclonal antibody directed against the deletion-mutant of epidermal growth factor receptor, EGFRvIII, conjugated via a non-cleavable linker to the cytotoxic agent maytansinoid DM1, with potential antineoplastic activity. The monoclonal antibody moiety of this immunoconjugate binds to EGFRvIII on tumor cell surfaces. After internalization, the DM1 moiety binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting cell division and the proliferation of cancer cells that express the EGFRvIII mutant. EGFRvIII, a deletion mutation of exons 2-7 in the epidermal growth factor receptor gene, is overexpressed by a variety of cancers, including glioblastoma multiforme, non-small cell lung carcinoma, and breast carcinoma.

anti-EGFRvIII CAR-transduced allogeneic T lymphocytes

Allogeneic human T lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) variant III (EGFRvIII) mutant chimeric T-cell receptor (chimeric antigen receptor or CAR) gene coupled to the signaling domains from CD8, CD28, 4-1BB (CD137) and CD3 zeta, with potential immunostimulatory and antineoplastic activities. Upon administration, the anti-EGFRvIII CAR-transduced allogeneic T lymphocytes bind to the EGFRvIII antigen on tumor cell surfaces; subsequently, EGFRvIII-expressing tumor cells may be lysed. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types and absent in normal, healthy cells; it plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.

anti-EGFRvIII immunotoxin MR1-1

A recombinant immunotoxin consisting of single-chain variable domain fragment antibody directed against the tumor-specific antigen EGFRvIII (MR1scFv) fused to domains II and III of the Pseudomonas exotoxin (PE38KDEL), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-EGFRvIII immunotoxin MR1-1 binds to EGFRvIII; upon internalization, the exotoxin portion inhibits protein synthesis, resulting in a reduction in tumor cell proliferation of EGFRvIII- expressing tumor cells. EGFRvIII, a type III in-frame deletion mutation of the epidermal growth factor receptor (EGFR) gene, is expressed by a variety of cancers, including glioblastoma multiforme, non-small lung carcinoma, and breast carcinoma. Compared to intact IgG antibodies, single-chain antibodies such as MR1scFv are smaller and may penetrate tumors better. Pseudomonas exotoxin PE38KDEL was modified to remove the natural cell binding domain.

anti-EGFRvIII-CAR-CD3/EGFR BiTE-transduced autologous T lymphocytes CARv3-TEAM-E

A preparation of autologous human T lymphocytes transduced with a CARv3-TEAM-E lentiviral vector encoding for an anti-epidermal growth factor receptor (EGFR) variant III (EGFRvIII) mutant chimeric T-cell receptor (chimeric antigen receptor or CAR) and a T-cell-engaging antibody molecule (TEAM) which comprises a bispecific T-cell engager (BiTE) against EGFR and the T-cell signaling domain CD3, with potential immunostimulatory and antineoplastic activities. Upon administration via Ommaya reservoir of the anti-EGFRvIII CAR-CD3/EGFR BiTE-transduced autologous T lymphocytes CARv3-TEAM-E, the lymphocytes bind to the EGFRvIII antigen on tumor cell surfaces and the BiTE binds to CD3 on bystander T cells; thereby killing EGFRvIII-expressing tumor cells through the administered CAR-T cells and wild-type (WT) EGFR-expressing tumor cells by bystander T cells, respectively. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types and absent in normal, healthy cells; it plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.

anti-EGFRvIII/CD3 bispecific antibody hEGFRvIII:CD3 bi-scFv

A bispecific antibody and T-cell engager composed of two single chain variable fragments (bi-scFvs) directed against both a mutant form of the human epidermal growth factor receptor (EGFR), EGFR variant III (EGFRvIII), and the epsilon subunit of the human T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-EGFRvIII/CD3 bispecific antibody hEGFRvIII:CD3 bi-scFv specifically binds to both CD3 on cytotoxic T lymphocytes (CTLs) and hEGFRvIII on hEGFRvIII-expressing tumor cells. This crosslinks T cells and tumor cells, and activates and redirects CTLs to hEGFRvIII-expressing tumor cells. This leads to CTL-mediated killing of hEGFRvIII-expressing tumor cells. hEGFRvIII, a mutant form of EGFR expressed in certain tumor cell types and frequently seen in malignant glioma, plays a key role in tumor cell proliferation and survival.

anti-EGFRvIII/CD3 bispecific antibody RO7428731

A bispecific antibody directed against both a mutant form of the human epidermal growth factor receptor (EGFR), EGFR variant III (EGFRvIII), and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-EGFRvIII/CD3 bispecific antibody RO7428731 specifically binds to both CD3 on cytotoxic T-lymphocytes (CTLs) and EGFRvIII on EGFRvIII-expressing tumor cells. This crosslinks T-cells and tumor cells, and activates and redirects CTLs to EGFRvIII-expressing tumor cells. This leads to CTL-mediated killing of EGFRvIII-expressing tumor cells. EGFRvIII, a mutant form of EGFR expressed in certain tumor cell types and frequently seen in malignant glioma, plays a key role in tumor cell proliferation and survival.

anti-EGFRvIII/CD3 BiTE antibody AMG 596

A proprietary recombinant bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one that is directed against a tumor-associated antigen (TAA), the epidermal growth factor receptor (EGFR) deletion-mutant form, EGFR variant III (EGFRvIII), and one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of anti-EGFRvIII/CD3 BiTE antibody AMG 596, the bispecific antibody binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and EGFRvIII found on EGFRvIII-expressing tumor cells. This activates and crosslinks CTLs with EGFRvIII-expressing tumor cells, which results in the CTL-mediated cell death of EGFRvIII-expressing tumor cells. EGFRvIII, a mutation in the EGFR gene where exons 2-7 have been deleted, is overexpressed by a variety of cancers, but is absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy.

anti-EGFRvIII/CD3/PD-L1/4-1BB tetra-specific antibody GNC-039

A tetra-specific antibody directed against the tumor-associated antigen (TAA) and epidermal growth factor receptor (EGFR) mutant EGFR variant III (EGFRvIII), the T-cell surface antigen CD3, the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), and the immune co-stimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulatory and antineoplastic activities. Upon administration, anti-EGFRvIII/CD3/PD-L1/4-1BB tetra-specific antibody GNC-039 targets and binds to EGFRvIII, CD3, 4-1BB and PD-L1. The binding of GNC-039 to EGFRvIII expressed on tumor cells and CD3 expressed on T-cells may crosslink EGFRvIII-expressing tumor cells and cytotoxic T-lymphocytes (CTLs) and result in a potent CTL-mediated cell lysis of EGFRvIII-expressing tumor cells. In addition, the binding of GNC-039 to 4-1BB expressed on a variety of leukocyte subsets including activated T-lymphocytes results in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, GNC-039 binds to PD-L1 and prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances CTL-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. EGFRvIII, a mutant form of EGFR expressed in certain tumor cell types, plays a key role in tumor cell proliferation and survival.

anti-EGP-2 immunotoxin MOC31-PE

An immunotoxin consisting of a monoclonal antibody directed against epithelial glycoprotein-2 (EP-2, or epithelial cell adhesion molecule (EpCAM)) conjugated to the bacterial toxin Pseudomonas exotoxin A (PE) with potential antineoplastic activity. Upon administration of anti-EGP-2 immunotoxin MOC31-PE, the monoclonal antibody moiety targets and binds to EP-2. Upon internalization, the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in EP-2-expressing cells. EP-2, a tumor-associated antigen, is overexpressed in a variety of cancer cell types.

anti-emetic agent HR20013

An injectable anti-emetic agent, with anti-emetic activity. Upon administration, anti-emetic agent HR20013 may suppress chemotherapy-induced nausea and vomiting through an as of yet not elucidated mechanism of action (MoA).

anti-endosialin/TEM1 monoclonal antibody MORAb-004

A humanized IgG1 monoclonal antibody directed against human endosialin/TEM1 (tumor endothelial marker;CD248) with potential anti-angiogenic and antineoplastic activities. Anti-endosialin/TEM1 monoclonal antibody MORAb-004 binds to and inhibits the activity of cell surface protein endosialin/TEM1, which may result in the inhibition of angiogenesis, tumor cell proliferation and metastasis. Endosialin/TEM1 plays a key role in angiogenesis and may be overexpressed on tumor stromal cells and endothelial cells.

anti-ENPP3 antibody-drug conjugate AGS-16C3F

An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody (AGS-16C) directed to the ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3), conjugated via a non-cleavable linker to monomethyl auristatin F (MMAF), an auristatin derivative and a potent microtubule inhibitor, that has potential antineoplastic activity. Upon intravenous administration of ADC AGS-16C3F, the monoclonal antibody moiety of this conjugate selectively binds to ENPP3 then is internalized and undergoes proteolytic cleavage to release MMAF. MMAF binds to and inhibits tubulin polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. While normally expressed at low levels in the proximal tubules of the kidney, the type II transmembrane glycoprotein ENPP3 has been found to be overexpressed in renal neoplasms.

anti-ENPP3/anti-CD3 bispecific antibody JNJ-87890387

A human bispecific antibody directed against both ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3; NPP3; B10; PDNP3; CD203c; PD-IBETA) and the T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-ENPP3/anti-CD3 bispecific antibody JNJ-87890387 targets and binds to ENPP3 expressed on tumor cells and CD3 expressed on T cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against ENPP3-expressing tumor cells. While normally expressed at low levels on tubules of the kidney cortex and by some cells in gastrointestinal, adrenal, and endometrial tissues, the type II transmembrane glycoprotein ENPP3 is overexpressed in various cancers including most renal neoplasms and some liver cancers.

anti-ENPP3/anti-CD3 bispecific antibody XmAb819

A bispecific antibody directed against both ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3, NPP3, B10, PDNP3 CD203c, or PD-IBETA) and the T-cell surface antigen CD3, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-ENPP3/anti-CD3 bispecific antibody XmAb819 bivalently binds to ENPP3 expressed on tumor cells and monovalently binds to CD3 expressed on T-cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against ENPP3-expressing tumor cells. While normally expressed at low levels on tubules of the kidney cortex and by some cells in gastrointestinal, adrenal, and endometrial tissues, the type II transmembrane glycoprotein ENPP3 is overexpressed in various cancers including most renal neoplasms and some liver cancers. The bivalent binding to ENPP3 and monovalent binding to CD3 by XmAb819 may allow selective targeting of ENPP3-overexpressing tumor cells.

anti-ENPP3/MMAF antibody-drug conjugate AGS-16M8F

An antibody-drug conjugate (ADC) containing a human immunoglobulin (Ig) G2k monoclonal antibody (AGS-16C) directed against the ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3, NPP3, B10, PDNP3 CD203c, or PD-IBETA ), conjugated, via the non-cleavable maleimidocaproyl (mc) linker, to monomethyl auristatin F (MMAF), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. Upon intravenous administration of anti-ENPP3/MMAF ADC AGS-16M8F, the monoclonal antibody moiety selectively binds to ENPP3 expressed on tumor cells; upon internalization, the ADC is degraded by lysosomal proteases and MMAF is released. In turn, MMAF binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. While normally expressed at low levels in the proximal tubules of the kidney, the type II transmembrane glycoprotein ENPP3 is overexpressed in most renal neoplasms and some liver cancers.

anti-ENTPD2 monoclonal antibody KAZ954

A monoclonal antibody directed against ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ENTPD2 monoclonal antibody KAZ954 targets and binds to ENTPD2 expressed on a variety of tumor cells and inhibits its hydrolase activity, thereby preventing the conversion of adenosine triphosphate (ATP) to adenosine diphosphate (ADP). This leads to an increased intra-tumoral ATP:ADP ratio, an increase in intra-tumoral monocytes, natural killer (NK) cells, peripheral CD8+ T cells, macrophages, and CD11b+ dendritic cells (DCs), and results in a systemic pro-inflammatory response in the tumor microenvironment (TME). In addition, KAZ954 induces antibody-dependent cellular cytotoxicity (ADCC) in ENTPD2-overexpressing tumor cells. ENTPD2 catalyzes the hydrolysis of ATP, reduces the cytotoxic antitumor immune response, enhances the proliferation and polarization of immunosuppressive cells, and increases neovascularization. It plays a key role in the creation of an immunosuppressive TME.

anti-Ep-CAM monoclonal antibody ING-1

An engineered monoclonal antibody (MAb) directed against the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326), with potential antitumor activity. Upon administration, anti-Ep-CAM monoclonal antibody ING-1 binds to Ep-CAM, which may result in a cytotoxic T-lymphocyte (CTL)-mediated immune response against Ep-CAM-expressing tumor cells. Ep-CAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.

anti-EpCAM monoclonal antibody AM-928

A humanized monoclonal antibody directed against the tumor-associated antigen (TAA) epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326), with potential antineoplastic activity. Upon administration, anti-EpCAM monoclonal antibody AM-928 targets and binds to EpCAM on EpCAM-expressing tumor cells. This inhibits EpCAM-mediated signaling and the proliferation of EpCAM-expressing tumor cells. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.

anti-EpCAM/anti-4-1BB bispecific antibody BNT314

An Fc-inert bispecific antibody directed against the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-EpCAM/anti-4-1BB bispecific antibody BNT314 simultaneously targets and binds to both EpCAM expressed on tumor cells and 4-1BB expressed on a variety of leukocyte subsets including activated T lymphocytes. This crosslinks EpCAM-expressing tumor cells and 4-1BB-expressing T cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily (TNFRSF), is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-EpCAM/anti-CD3 bispecific antibody A-337

A T-cell engager (TCE) and bispecific antibody composed of two fragments targeting the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326) and one targeting the T-cell surface glycoprotein CD3, with potential immunomodulating and antineoplastic activities. Upon administration, anti-EpCAM/anti-CD3 bispecific antibody A-337 targets and binds to EpCAM on EpCAM-expressing tumor cells and CD3 on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to EpCAM-expressing tumor cells, which results in the CTL-mediated cell death of EpCAM-expressing tumor cells. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.

anti-EpCAM/anti-CD3 bispecific antibody BA3182

A conditionally active biologic (CAB) and bispecific antibody directed against both the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326) and T-cell surface glycoprotein CD3 epsilon chain (CD3E), with potential immunomodulating and antineoplastic activities. Upon administration and specific activation in the tumor microenvironment (TME), anti-EpCAM/anti-CD3 bispecific antibody BA3182 targets and binds to both EpCAM on EpCAM-expressing tumor cells and CD3E on cytotoxic T lymphocytes (CTLs) within the TME. This activates and redirects CTLs to EpCAM-expressing tumor cells, which results in the CTL-mediated cell death of EpCAM-expressing tumor cells. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells. Negatively charged, physiologically-occurring molecules interact with positively charged areas on the protein surface to prevent the activation of BA3182 outside the TME. In the acidic TME, the negatively charged molecules are neutralized and released, allowing the binding to EpCAM and CD3E. This may reduce systemic toxicity.

anti-EpCAM/anti-CD3 bispecific antibody M701

A human-mouse chimeric bispecific antibody directed against both CD3 and epithelial cell adhesion molecule (EpCAM), with potential immunomodulating and antineoplastic activities. Upon administration, anti-EpCAM/anti-CD3 bispecific antibody M701 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and EpCAM on EpCAM-expressing tumor cells. This activates and redirects CTLs to EpCAM-expressing tumor cells, which results in the CTL-mediated cell death of EpCAM-expressing tumor cells. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.

anti-EpCAM/anti-CD40 bispecific antibody KK2269

A bispecific antibody directed against both the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326) and the cell surface receptor CD40, with potential immunostimulatory and antineoplastic activities. Upon administration of anti-EpCAM/anti-CD40 bispecific antibody KK2269, the anti-EpCAM moiety targets and binds to EpCAM expressed on tumor cells, and the agonistic anti-CD40 moiety targets and binds to various CD40-expressing immune cells in the tumor microenvironment (TME). This induces EpCAM-dependent activation of CD40-mediated signaling pathways, and triggers the proliferation and activation of antigen-presenting cells (APCs) and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a stimulatory receptor and a member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as macrophages, B lymphocytes, and dendritic cells (DCs); it plays a key role in the activation of the immune system. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.

anti-EphA2 antibody-directed liposomal docetaxel prodrug MM-310

A formulation containing nanoparticles composed of liposomes that are conjugated to scFv antibody fragments directed against the ephrin receptor A2 (EphA2; Ephrin A2) and a proprietary prodrug of docetaxel, a poorly water-soluble, second-generation taxane analog, with potential antineoplastic activity. Upon intravenous administration of the anti-EphA2 antibody-directed liposomal docetaxel prodrug MM-310, the anti-EphA2 moiety selectively targets and binds to cells expressing EphI3:I12A2. Following accumulation of MM-310, docetaxel is slowly released from MM-310 and accumulates at the tumor site due to the unique characteristics of the tumor vasculature. In turn, docetaxel is taken up by tumor cells, where it binds to and stabilizes the beta-subunit of tubulin, thereby stabilizing microtubules and inhibiting microtubule disassembly. This results in cell cycle arrest and the induction of cell death. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of cancer cell types and plays an important role in tumor growth; its expression is associated with poor prognosis. Compared to free docetaxel, MM-310 increases docetaxel's half-life, and provides enhanced and specific accumulation in EphA2-expressing tumors, thereby increasing docetaxel's efficacy while lowering its systemic toxicity.

anti-EphA2 monoclonal antibody DS-8895a

A monoclonal antibody directed against the ephrin receptor A2 (EphA2), with potential antineoplastic activity. Upon administration, anti-EphA2 monoclonal antibody DS-8895a selectively binds to cells expressing the EphA2 receptor. This blocks EphA2 activation and EphA2-mediated signaling. In addition, DS-8895a may activate an immune response against EphA2-expressing tumor cells. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of cancer cell types and plays an important role in tumor growth.

anti-EphA2 monoclonal antibody-MMAF immunoconjugate MEDI-547

An auristatin analogue immunoconjugate directed against Eph receptor A2 (EphA2)-positive cancer cells with potential antineoplastic activity. Anti-EphA2 monoclonal antibody-MMAF immunoconjugate MEDI-547 is generated by conjugating the fully human IgG1 anti-EphA2 monoclonal antibody (1C1) to the small-molecule microtubule inhibitor monomethyl auristatin phenylalanine (MMAF) via the stable linker maleimidocaproyl (mc) (1C1-mcMMAF). The monoclonal antibody moiety of this agent selectively binds to cells expressing the EphA2 receptor. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAF binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types.

anti-EphA3 monoclonal antibody KB004

A non-fucosylated monoclonal antibody directed against the ephrin receptor A3 (EphA3), with potential antineoplastic activity. Upon administration, anti-EphA3 monoclonal antibody KB004 selectively binds to tumor cells expressing EphA3. This blocks both EphA3 activation and EphA3-mediated signaling, and induces apoptosis in EphA3-expressing tumor cells. In addition, KB004 can stimulate antibody dependent cell-mediated cytotoxicity (ADCC) against EphA3-expressing tumor cells. This agent also prevents tumor cell proliferation by inhibiting both EphA3 signaling and proliferation of endothelial cells in the tumor vasculature. The cell-surface receptor EphA3, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of tumor types but is not expressed in normal healthy adult tissues. It plays an important role in tumor cell proliferation. Non-fucosylation of the antibody enhances its ADCC activity.

anti-EphA5/MMAE antibody-drug conjugate MBRC-101

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody against the tyrosine kinase receptor ephrin type-A receptor 5 (EPH receptor A5; EphA5) and conjugated, via a protease-cleavable linker, to the auristatin derivative and microtubule disrupting agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-EphA5/MMAE ADC MBRC-101, the monoclonal antibody moiety targets and binds to EphA5 expressed on tumor cells. Upon binding, internalization, and proteolytic cleavage, MMAE is released. MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. This induces cell death in EphA5-expressing cancer cells. EphA5, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in axonal guidance during embryonic development, is overexpressed by a variety of cancer cell types.

anti-epidermal growth factor receptor 2 antibody expressing pluripotent killer T lymphocytes

A specific population of pluripotent killer (PIK) T cells that have been induced to express high levels of antibodies against human epidermal growth factor receptor 2 (ERBB2; HER2), with potential antitumor activity. Although the exact mechanism(s) of action through which PIK-HER2 cells exert their effects has yet to be elucidated, upon infusion, these cells secrete antibodies targeting HER2 expressed on the surface of tumor cells. This may inhibit HER2-dependent signaling, which may lead to inhibition of cellular proliferation and differentiation. Additionally, these cells may stimulate the host immune system to mount both a highly-specific cytotoxic T-lymphocyte (CTL) response and antibody-dependent cell cytotoxicity (ADCC) directed against HER2-overexpressing tumors, which leads to tumor cell lysis. HER2 is a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases and is frequently overexpressed in solid tumors.

anti-ErbB2/anti-ErbB3 bispecific monoclonal antibody MM-111

A bispecific monoclonal antibody directed against the human epidermal growth factor receptors ErbB2 (Her2) and ErbB3 (Her3) with potential antineoplastic activity. The anti-ErB2 targeting arm of anti-ErbB2/anti-ErbB3 bispecific monoclonal antibody MM-111 binds to ErbB2 on tumor cells with high affinity while the anti-Erb3 therapeutic arm binds to ErbB3, which may result in the inhibition of cellular proliferation and differentiation in ErbB2-overexpressing tumor cells via inhibition of ErbB3-dependent signal transduction pathways. ErbB2 and ErB3 are members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases and are frequently overexpressed in solid tumors.

anti-ErbB3 monoclonal antibody AV-203

A humanized monoclonal antibody (MoAb) directed against the human receptor tyrosine-protein kinase ErbB-3 (HER3) with potential antineoplastic activity. Anti-ErbB3 MoAb AV-203 binds to and inhibits both ligand neuregulin-1 (NRG-1)-dependent and ligand-independent ErbB3 activation, which may result in inhibition of ErbB3-dependent PI3K/Akt signaling and may lead to inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family, is frequently overexpressed in solid tumors and its overexpression generally correlates with poor prognosis and tumor resistance; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.

anti-ErbB3 monoclonal antibody CDX-3379

A human monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (HER3), with potential antineoplastic activity. Upon administration, the anti-ErbB3 monoclonal antibody CDX-3379 targets and binds to a unique epitope on ErbB3, thereby preventing ErbB3 phosphorylation and both ligand-dependent and ligand-independent ErbB3 signaling. This inhibits cellular proliferation and survival of ErbB3-expressing tumor cells. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in a variety of tumors and its overexpression generally correlates with poor prognosis and tumor resistance.

anti-ErbB3 monoclonal antibody REGN1400

A human monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) with potential antineoplastic activity. Upon administration, anti-ErbB3 monoclonal antibody REGN1400 binds to ErbB3 and prevents neuregulin 1 ligand binding to ErbB3, which may result in an inhibition of ErbB3-dependent phosphatidylinositol-3 kinase (PI3K)/Akt signaling. This eventually leads to the inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in a variety of solid tumors and its overexpression generally correlates with poor prognosis and tumor resistance.

anti-ErbB3/anti-IGF-1R bispecific monoclonal antibody MM-141

A bispecific monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) and the human insulin-like growth factor-1 receptor (IGF-1R), with potential antineoplastic activity. The anti-IGF-1R targeting arm of anti-IGF-1R/anti-ErbB3 bispecific monoclonal antibody MM-141 binds to IGF-1R on tumor cells thereby preventing the binding of the natural ligands IGF-1, 2 and heregulin (HRG) to IGF-1R; the anti-ErbB3 therapeutic arm prevents the binding of neuregulin (NRG) to ErbB3. This prevents the activation of the PI3K/AKT signal transduction pathway and may result in both the induction of apoptosis and a decrease in cellular proliferation in IGF-1R and ErbB3-overexpressing tumor cells. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily, and ErB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in solid tumors.

anti-ETBR/MMAE antibody-drug conjugate DEDN6526A

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin (Ig) G1 monoclonal antibody against anti-endothelin B receptor (ETBR) and covalently linked to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DEDN6526A binds to ETBR-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. ETBR, a G-protein coupled receptor that can activate RAF/MEK signaling, is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and angiogenesis.

anti-factor Bb monoclonal antibody NM8074

A humanized monoclonal antibody directed against complement factor Bb (FBb; Bb) that can be used to treat various alternate pathway (AP)-mediated diseases. Upon administration, anti-factor Bb monoclonal antibody NM8074 selectively targets, binds to and neutralizes Bb. This prevents the binding of Bb to C3 and prevents the formation of protease C3 convertase (C3Bb). This prevents the conversion of C3 into the fragments C3a and C3b, thereby preventing C3b deposition and C3b-mediated extravascular hemolysis. Also, by preventing the formation of C3Bb, C3Bb is unable to bind to C3b to form the protease C5 convertase (C3BbC3b). As C5 convertase is responsible for the conversion of C5 to C5a/C5b and initiation of membrane attack complex (MAC), NM8074 is able to prevent MAC-mediated tissue damage. Altogether, NM8074 inhibits the activation of the alternative complement pathway (ACP). Overactivation of AP plays a key role in the initiation and propagation of C3b deposition, inflammation and tissue destruction. Bb is created when complement factor D, a serine protease, cleaves complement factor B into 2 fragments, Ba and Bb, in the AP of the complement cascade. NM8074 does not block the classical pathway (CP) which is critical for host defense against infections.

anti-FAP antibody-drug conjugate OMTX705

An antibody-drug conjugate (ADC) composed of OMTX005, a humanized monoclonal antibody directed against fibroblast activation protein (FAP), conjugated to the cytotoxic tubulysin TAM470, with potential antineoplastic activity. Upon administration of anti-FAP ADC OMTX705, the anti-FAP monoclonal antibody moiety targets and binds to FAP expressed on cancer-associated fibroblasts (CAFs) in the tumor stroma. Upon binding, internalization and linker cleavage, the cytotoxic moiety is released, which binds to tubulin and inhibits microtubule polymerization. This results in G2/M phase arrest and the apoptosis of FAP-expressing CAFs. FAP, a membrane-bound serine protease overexpressed on CAFs, is minimally expressed on normal, healthy cells.

anti-FcRH5 antibody-drug conjugate DFRF4539A

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) Fc receptor-like protein 5 (FcRH5; CD307; FCRL5; IRTA2; BXMAS1) and conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, via the protease-labile linker maleimidocaproyl-valine-citrulline-p-aminobenzyloxycarbonyl (MC-VC-PABC), with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of anti-FcRH5 ADC DFRF4539A selectively binds to FcRH5 expressed on the surface of myeloma cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis. FcRH5, an immune receptor translocation-associated protein/Fc receptor homolog (IRTA/FCRH) family member and a B-cell lineage marker, is overexpressed on myeloma cells.

anti-FcRn monoclonal antibody SYNT001

A monoclonal antibody that targets the neonatal crystallizable fragment receptor (FcRn), with potential immunomodulating activity. Upon administration, SYNT001 targets and binds to FcRn at the immunoglobulin G (IgG) binding site, thereby preventing the interaction between FcRn and the serum protein IgG. By preventing FcRn/IgG binding, SYNT001 blocks the FcRn-mediated rescue of IgG, enables IgG degradation and prevents IgG-mediated inflammation. IgG plays a key role in many autoimmune diseases and is an important factor in inflammatory processes.

anti-FGFR2b/topoisomerase-1 inhibitor antibody-drug conjugate BG-C137

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the fibroblast growth factor receptor 2b (FGFR2b; fibroblast growth factor receptor 2 isoform IIIb; FGFR2 IIIb) conjugated to an as of yet undisclosed topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon administration of anti-FGFR2b/topoisomerase-1 inhibitor ADC BG-C137, the antibody moiety targets and binds to FGFR2b-expressing tumor cells. Upon binding and internalization, the topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing FGFR2b. FGFR2b is overexpressed on certain tumor cell types.

anti-FGFR3 antibody-drug conjugate LY3076226

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody against the fibroblast growth factor receptor type 3 (FGFR3) that is conjugated to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration, the antibody moiety of anti-FGFR3 ADC LY3076226 binds to FGFR3. Upon internalization, the cytotoxic moiety causes cell death in FGFR3-expressing tumor cells. FGFR3, a receptor tyrosine kinase upregulated or mutated in many tumor cell types, plays a key role in tumor cell proliferation.

anti-FGFR3 monoclonal antibody MFGR1877S

A human monoclonal antibody against the fibroblast growth factor receptor type 3 (FGFR3), with potential antineoplastic activity. Upon administration, the anti-FGFR3 antibody MFGR1877S binds to and inhibits FGFR3, which may result in the inhibition of both FGFR3 phosphorylation and FGFR3-mediated signal transduction pathways. This results in the inhibition of cell proliferation and the induction of cell death in FGFR3-expressing tumor cells. FGFR3, upregulated or mutated in many tumor cell types, is a receptor tyrosine kinase, and plays a key role in tumor cell proliferation.

anti-FGFR4 monoclonal antibody U3-1784

A human monoclonal antibody against human fibroblast growth factor receptor 4 (FGFR4), with potential antineoplastic activity. Upon administration, U3-1784 specifically binds to and blocks FGFR4. This prevents the activation of FGFR4, inhibits FGFR4-mediated signaling and leads to an inhibition of cell proliferation in FGFR4-overexpressing tumor cells. FGFR4, a receptor tyrosine kinase overexpressed by certain tumor cell types, is involved in tumor cell proliferation, differentiation, angiogenesis, and survival.

anti-FL(FITC-E2) CAR-T cells

A preparation of genetically modified T cells transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a second generation chimeric antigen receptor (CAR) consisting of an anti-fluorescein (anti-FL) fluorescein isothiocyanate (FITC)-E2 single chain variable fragment (scFv), that is coupled, via an immunoglobulin G4 (IgG4) hinge-CH2(L295D)-CH3 spacer, to the costimulatory signaling molecules CD28, CD137 (4-1BB), and CD3 zeta, and linked to a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Prior to the administration of anti-FL(FITC-E2) CAR-T cells, the CAR-T adaptor molecule (CAM) EC17 is administered. EC17 is a bispecific molecule that is composed of folic acid conjugated to FITC (folate-FITC). EC17 targets and binds with its folate moiety with high affinity to folate receptor (FR)-expressing tumor cells. Upon administration of the anti-FL(FITC-E2) CAR-T cells, these cells are attracted by and bind to the FITC antigen moiety of EC17. Upon binding to EC17, the T cells induce specific tumor cell lysis, cytokine secretion, and proliferation, and activate a robust immune response against the EC17-bound, FR-expressing tumor cells. FR is overexpressed in various tumor cell types and is associated with increased leukemic cell proliferation and aggressiveness. The co-stimulatory molecules are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity. EGFRt both facilitates detection of the administered T cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The reactivity of the anti-FL(FITC-E2) CAR-T cells is dependent on dosing of EC17, and therefore allows CAR-T-cell activity to be controlled by dosing of EC17.

anti-FLT-1 ribozyme

A nuclease-stabilized synthetic ribozyme (ribonucleic acid enzyme) with potential anti-angiogenesis activity. Ribozyme RPI.4610 specifically recognizes the mRNA for FLT1 (vascular endothelial growth factor receptor 1; VEGFR1), and hydrolyzes the mRNA, thereby preventing VEGFR1 proteins from being made. This may prevent VEGF-stimulated angiogenesis in cancerous tissue and metastasis.

anti-FLT3 antibody-drug conjugate AGS62P1

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the extracellular domain of receptor-type tyrosine-protein kinase FLT3 (FLT-3; FMS-like tyrosine kinase 3; CD135; fetal-liver kinase 2; FLK2) and conjugated, via an oxime linker and the site-directed non-natural amino acid linker para-acetyl-phenylalanine (pAcF), to a microtubule-disrupting cytotoxic agent, with potential antineoplastic activity. Upon administration of ADC AGS62P1, the antibody moiety targets and binds to FLT3. Upon antibody/antigen binding and internalization, the microtubule-targeting agent binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. The site-specific conjugation of the cytotoxic agent to the antibody, through pAcF, improves the biophysical properties of AGS62P1, increases payload distribution and stability, and optimizes its efficacy. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B-lineage, acute lymphoblastic leukemias and acute myeloid leukemias.

anti-FLT3 monoclonal antibody 4G8-SDIEM

A human, Fc-optimized, immunoglobulin G1 (IgG1) monoclonal antibody directed against the FLT3 tyrosine kinase receptor (CD135), with potential antineoplastic activity. Upon binding to FLT3, anti-FLT3 monoclonal antibody 4G8-SDIEM blocks FLT3 ligand binding to FLT3 and subsequent phosphorylation of FLT3, which may result in the inhibition of FLT3-mediated signal transduction pathways. In addition, this agent may stimulate an anti-FLT3 antibody-dependent cell-mediated cytotoxicity (ADCC) against FLT3-expressing tumor cells, which may lead to the inhibition of cellular proliferation and decreased survival in FLT3-expressing cells. FLT3 (FLK2), a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.

anti-FLT3 monoclonal antibody IMC-EB10

A fully human, IgG1 monoclonal antibody directed against the FLT3 tyrosine kinase receptor (CD135) with potential antineoplastic activity. Upon binding to FLT3, anti-FLT3 monoclonal antibody IMC-EB10 blocks FLT3 ligand binding to FLT3 and subsequent FLT3 phosphorylation, which may result in the inhibition of FLT3-mediated signal transduction pathways. In addition, this agent may stimulate an anti-FLT3 antibody-dependent cell-mediated cytotoxicity (ADCC) against FLT3-expressing tumor cells, which may result in the inhibition of cellular proliferation and survival in FLT3-expressing cells. FLT3 (FLK2), a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.

anti-FLT3/CD3 bispecific antibody CLN-049

A T-cell-engaging, humanized, Fc-silenced immunoglobulin G1 (IgG1)-based bispecific antibody directed against both the tumor-associated antigen (TAA) FLT3 tyrosine kinase receptor (Fms-like tyrosine kinase 3; FLT3; FLT-3; CD135; fetal liver kinase-2; FLK2) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-FLT3/CD3 bispecific antibody CLN-049 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and FLT3 found on FLT3-expressing tumor cells. This activates and redirects CTLs to FLT3-expressing tumor cells, which results in the CTL-mediated cell death of FLT3-expressing tumor cells. FLT3, a cytokine receptor belonging to the class III tyrosine kinase receptors, is overexpressed or mutated in most B-lineage and acute myeloid leukemias (AMLs).

anti-FLT3/CD3 BiTE antibody AMG 427

A bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) FLT3 tyrosine kinase receptor (Fms-like tyrosine kinase 3; FLT3; FLT-3; CD135; fetal liver kinase-2; FLK2), fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of anti-FLT3/CD3 BiTE antibody AMG 427, this bispecific antibody binds to both CD3 on cytotoxic T lymphocytes (CTLs) and FLT3 found on FLT3-expressing tumor cells. This activates and redirects CTLs to FLT3-expressing tumor cells, which results in the CTL-mediated cell death of FLT3-expressing tumor cells. FLT3, a cytokine receptor belonging to the class III tyrosine kinase receptors, is overexpressed or mutated in most B-lineage and acute myeloid leukemias (AMLs).

anti-folate receptor alpha antibody-drug conjugate AMT-151

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting folate receptor alpha (FRa; FolRa; FOLR1) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-FRa ADC AMT-151, the antibody moiety targets and binds to FRa expressed on tumor cells. Upon cellular uptake and internalization, the cytotoxic agent inhibits tumor cell proliferation through an as of yet undisclosed mechanism of action (MoA). FRa is a glycosylphosphatidylinositol linked cell-surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-FOLR1 antibody-drug conjugate

Any antibody-drug conjugate (ADC) that is directed against folate receptor alpha (FRa; FolRa; FOLR1).

anti-FOLR1 CAR T cells

A preparation of T lymphocytes that have been engineered to express a chimeric antigen receptor (CAR) specific for folate receptor alpha (FolRa; FOLR1), with potential immunostimulating and antineoplastic activities. Upon administration, anti-FOLR1 CAR T cells specifically recognize and bind to FOLR1-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. FOLR1 is a glycosylphosphatidylinositol linked cell surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-FOLR1 CoStAR-expressing autologous tumor-infiltrating lymphocytes ITIL-306

A preparation of autologous tumor infiltrating lymphocytes (TILs) genetically engineered to express a co-stimulatory antigen receptor (CoStAR) specific for folate receptor alpha (FolRa; FOLR1) and linked to the co-stimulatory domains CD28 and CD40, with potential immunomodulating and antineoplastic activities. Upon administration, the anti-FOLR1 CoStAR-expressing autologous TILs ITIL-306 specifically target, bind to and kill the FOLR1-expressing tumor cells. In addition, ITIL-306, by binding to FOLR1, is able to activate the TILs through the costimulatory signals. This increases T-cell proliferation and activation in the tumor microenvironment (TME), thereby enhancing the T-cell-mediated anti-tumor immune response against the FOLR1-expressing tumor cells. FOLR1 is a glycosylphosphatidylinositol linked cell-surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues. CoStAR provides synthetic costimulation in the TME and increases T-cell proliferation and survival, and improves the effector function of T cells, which may boost the efficacy of TILs.

anti-FOXP3 antisense oligonucleotide AZD8701

An antisense oligonucleotide (ASO) targeting the Forkhead Box P3 (FOXP3) mRNA, with potential immunomodulating and antineoplastic activities. Upon administration, anti-FOXP3 ASO AZD8701 blocks the translation of the FOXP3 protein. Reduction of FOXP3 levels may lessen the immunosuppressive functions of regulatory T cells (Tregs). This may lead to an enhanced immune response and antitumor activity. FOXP3, a transcription factor, plays an important role in the functioning of immunosuppressive Tregs. Tregs are overexpressed in various cancers and are associated with poor response to immune checkpoint inhibitors and poor survival.

anti-FRa/DM21 ADC IMGN151

An antibody-drug conjugate (ADC) composed of an asymmetric, bivalent, biparatopic antibody targeting two independent epitopes of folate receptor alpha (FRa; FolRa; FOLR1) that is conjugated, via a cleavable peptide linker, to the cytotoxic maytansinoid derivative DM21, with potential antineoplastic activity. Upon administration of anti-FRa/DM21 ADC IMGN151, the antibody moiety targets and binds to FRa expressed on tumor cells. Upon cellular uptake and internalization, DM21 is released, binds to tubulin and disrupts microtubule assembly/disassembly dynamics, which results in the inhibition of both cell division and cell growth of tumor cells. FRa is a glycosylphosphatidylinositol-linked cell surface glycoprotein, that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-FRalpha antibody-drug conjugate ZW191

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting folate receptor alpha (FRa; FolRa; FOLR1) conjugated, via a maleimidocaproyl (MC) anchor and a glycyl glycyl phenylalanyl glycine (GGFG)-aminomethyl (AM) protease-cleavable linker, to the camptothecin-based topoisomerase 1 inhibitor ZD06519, with potential antineoplastic activity. Upon administration of anti-FRalpha ADC ZW191, the antibody moiety targets and binds to FRa expressed on tumor cells. Upon binding, cellular uptake and linker cleavage, ZD06519 is released. ZD06519 inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and generating DNA single- and double-strand breaks. This leads to cell cycle arrest and tumor cell apoptosis. In addition, ZD06519 is able to induce a bystander effect on neighboring cells in the tumor environment. This inhibits the proliferation of tumor cells. FRa is a glycosylphosphatidylinositol linked cell-surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-FRalpha/exatecan ADC LY4170156

An antibody-drug conjugate (ADC) composed of a Fc-silenced, humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting folate receptor alpha (FRa; FolRa; FOLR1) linked, via a dipeptide cleavable linker and a polysarcosine hydrophobicity masking agent, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-FRalpha/exatecan ADC LY4170156, the antibody moiety targets and binds to FRa expressed on tumor cells. Upon binding, cellular uptake and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and generating DNA single- and double-strand breaks. This leads to cell cycle arrest and tumor cell apoptosis. In addition, exatecan is able to induce a bystander effect on neighboring cells in the tumor environment. This inhibits the proliferation of FRa-expressing tumor cells. FRa is a glycosylphosphatidylinositol linked cell-surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-FRalpha/exatecan ADC PRO1184

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody targeting folate receptor alpha (FRa; FolRa; FOLR1) conjugated, via a cleavable hydrophilic linker, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-FRalpha/exatecan ADC PRO1184, the antibody moiety targets and binds to FRa expressed on tumor cells. Upon binding, cellular uptake and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and generating DNA single- and double-strand breaks, and leading to cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of FRa-expressing tumor cells. FRa is a glycosylphosphatidylinositol linked cell-surface glycoprotein that is widely expressed in certain cancers while its expression is limited in normal tissues.

anti-fucosyl-GM1 monoclonal antibody BMS-986012

A monoclonal antibody directed against the ganglioside fucosyl-GM1, with potential antineoplastic and immunomodulating activities. Upon administration, anti-fucosyl-GM1 monoclonal antibody BMS-986012 binds to fucosyl-GM1 on cancer cells and may activate both antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity against the bound tumor cells. This may inhibit the proliferation of GM1-expressing tumor cells. Fucosyl-GM1, a sphingolipid monosialoganglioside and tumor-associated antigen (TAA), is overexpressed on the surface of many cancer cells while its expression is minimal or non-existent in normal tissues.

anti-galectin-9 monoclonal antibody LYT-200

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the immunosuppressive protein galectin-9, with potential immunostimulating and antineoplastic activities. Upon administration, the anti-galectin-9 monoclonal antibody LYT-200 targets, binds to and blocks galectin-9 on tumor cells which prevents galectin-9-mediated signaling. This may abrogate activation of immunosuppressive signaling pathways in the tumor microenvironment (TME) and may activate a cytotoxic T-lymphocyte (CTL)-mediated immune response against the galectin-9-expressing tumor cells. Galectin-9, overexpressed on a variety of tumor cells, plays a key role in cancer cell proliferation and evasion of immune responses. Its expression is correlated with decreased patient survival.

anti-ganglioside GM2 monoclonal antibody BIW-8962

A humanized anti-ganglioside GM2 (GM2) monoclonal antibody with potential antineoplastic and immunomodulating activities. Upon administration, anti-ganglioside GM2 monoclonal antibody BIW-8962 may activate an antibody dependent cellular cytotoxicity (ADCC) against GM2-expressing tumor cells. GM2 is a tumor associated antigen (TAA) overexpressed on the surface of many cancer cells, such as multiple myeloma (MM) cells and neuroblastoma cells.

anti-GARP monoclonal antibody DS-1055a

An afucosylated human monoclonal antibody directed against the transforming growth factor beta (TGFbeta) activator glycoprotein A repetitions predominant (GARP; leucine-rich repeat-containing protein 32; LRRC32), with potential immunomodulating and antineoplastic activities. Upon administration, anti-GARP monoclonal antibody DS-1055a selectively targets and binds to GARP and depletes GARP-positive regulatory T cells (Tregs). This leads to a reversal of immunosuppression mediated by GARP-positive Tregs and enhances the immune response to tumor cells. GARP, a transmembrane protein highly expressed on activated, immunosuppressive Tregs in the tumor microenvironment (TME), is essential for the expression of TGFbeta on the cell surface of activated Tregs; it plays an important role in regulation of the immune cell function and the immunosuppressive nature of Tregs.

anti-GARP monoclonal antibody HLX60

A monoclonal antibody directed against the transforming growth factor beta (TGFbeta) activator glycoprotein A repetitions predominant (GARP; leucine-rich repeat-containing protein 32; LRRC32), with potential immunomodulating and antineoplastic activities. Upon administration, anti-GARP monoclonal antibody HLX60 selectively targets and binds to GARP. This specifically blocks the GARP-mediated release of the cytokine transforming growth factor-beta 1 (TGF-b1), thereby relieving the immunosuppression caused by TGF-b1, reversing the immunosuppressive nature in the tumor microenvironment (TME), and improving anti-tumor immune responses. In addition, HLX60 induces antibody dependent cell-mediated cytotoxicity (ADCC), which leads to a depletion of GARP-positive tumor cells and immunosuppressive regulatory T cells (Tregs). The depletion of Tregs further leads to a reversal of immunosuppression mediated by GARP-positive Tregs and enhances the immune response to tumor cells. GARP, a transmembrane protein highly expressed on activated, immunosuppressive Tregs in the TME, is essential for the expression of TGF-b1 on the cell surface of activated Tregs; it plays an important role in regulation of the immune cell function and the immunosuppressive nature of Tregs.

anti-GARP monoclonal antibody JYB 1907

A humanized monoclonal antibody directed against the transforming growth factor beta (TGFbeta) activator glycoprotein A repetitions predominant (GARP; leucine-rich repeat-containing protein 32; LRRC32), with potential immunomodulating and antineoplastic activities. Upon administration, anti-GARP monoclonal antibody JYB1907 selectively targets and binds to GARP. This specifically blocks the GARP-mediated release of the cytokine transforming growth factor-beta 1 (TGF-b1), thereby relieving the immunosuppression caused by TGF-b1 and reversing the immunosuppressive nature in the tumor microenvironment (TME). This improves anti-tumor immune responses GARP, a transmembrane protein highly expressed on activated, immunosuppressive regulatory T cells (Tregs) in the TME, is essential for the expression of TGF-b1 on the cell surface of activated Tregs; it plays an important role in regulation of the immune cell function and the immunosuppressive nature of Tregs. TGF-b1 stimulates stromal cell proliferation, neovascularization, cancer cell metastasis, and inhibits immune cell infiltration.

anti-GARP/PD-L1 bispecific antibody BPB-101

An immunoglobulin G1 (IgG1) humanized bispecific antibody directed against the transforming growth factor beta (TGFbeta) activator glycoprotein A repetitions predominant (GARP; leucine-rich repeat-containing protein 32; LRRC32) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; PDL1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, anti-GARP/PD-L1 bispecific antibody BPB-101 selectively targets and binds to GARP. This specifically blocks the GARP-mediated release of the cytokine transforming growth factor-beta 1 (TGF-b1) from the GARP-TGFbeta complex (small latent complex; SLC) and neutralizes free/mature TGF-beta, thereby relieving the immunosuppression caused by TGF-b1 and reversing the immunosuppressive nature in the tumor microenvironment (TME). This improves anti-tumor immune responses. BPB-101 simultaneously targets, binds to, and inhibits the activity of PD-L1 on tumor cells, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. This prevents both TGF-beta- and PD-L1-mediated immuno-suppressive pathways signaling, inhibits the negative regulatory function of regulatory T cells (Tregs) and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. GARP, a transmembrane protein highly expressed on activated, immunosuppressive Tregs in the TME, is essential for the expression of TGF-b1 on the cell surface of activated Tregs; it plays an important role in regulation of the immune cell function and the immunosuppressive nature of Tregs. TGF-b1 stimulates stromal cell proliferation, neovascularization, cancer cell metastasis, and inhibits immune cell infiltration. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-GCC antibody-drug conjugate MLN0264

An antibody-drug conjugate (ADC) containing a monoclonal antibody directed against guanylyl cyclase C (GCC or GUCY2C) conjugated to monomethylauristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. The monoclonal antibody moiety of MLN0264 selectively binds to GCC, a transmembrane receptor normally found on intestinal cells and dopamine neurons in the brain, but is also overexpressed on the surface of gastrointestinal cancers. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis in GCC-expressing tumor cells.

anti-GCC antibody-drug conjugate TAK-164

An antibody-drug conjugate (ADC) comprised of a full-length, fully-human immunoglobulin G1 (IgG1) monoclonal antibody (mAb) directed against the extracellular domain of guanylyl cyclase C (GCC; GUCY2C), conjugated using the peptide-linked indolino-benzodiazepine DNA alkylator DGN549 (IGN-P1), with potential antineoplastic activity. Upon intravenous administration of TAK-164, the antibody moiety selectively binds to GCC-expressing cells. Upon antibody/antigen binding and internalization, the cytotoxic DGN549 payload is released and binds to guanine residues on opposing strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of GCC-expressing cells. GCC, a transmembrane receptor normally found on intestinal cells and dopamine neurons in the brain, is overexpressed on the surface of certain tumor cells.

anti-GD2 antibody-drug conjugate M3554

An antibody-drug conjugate (ADC) composed of the humanized monoclonal antibody dinutuximab (ch14.18) directed against the tumor-associated antigen (TAA) disialoganglioside (GD2; GD-2) conjugated, via a cleavable beta-glucuronide linker, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-GD2 ADC M3554, dinutuximab targets and binds to GD2 expressed on tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase 1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of GD2-expressing tumor cells. GD2 is overexpressed in certain tumor types including neuroblastoma, osteosarcoma, glioma and soft tissue sarcoma.

anti-GD2 monoclonal antibody BCD-245

A monoclonal antibody directed against the tumor-associated antigen (TAA) disialoganglioside (GD2; GD-2), with potential antineoplastic activity. Upon administration, anti-GD2 monoclonal antibody BCD-245 may induce cytotoxicity in GD2-expressing tumor cells by antibody-dependent cell-mediated cytotoxicity (ADCC). GD2 is overexpressed on the surface of neuroblastoma (NB) cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells.

anti-GD2 monoclonal antibody hu14.18K322A

A monoclonal antibody directed against human glycosphingolipid GD2 with potential antineoplastic activity. Upon binding to the GD2 antigen, anti-GD2 monoclonal antibody hu14.18K322A triggers a host immune response against GD2-expressing tumor cells, which may result in tumor cell death. GD2, an O-acetylated disialoganglioside with expression in normal tissues restricted primarily to the cerebellum and peripheral nerves, is commonly expressed at high levels on tumors of neuroectodermal origins such as melanomas and neuroblastomas.

anti-GD2 monoclonal antibody MORAb-028

A human IgM monoclonal antibody directed against disialoganglioside GD2 with potential immunomodulating activity. Upon administration, anti-GD2 monoclonal antibody MORAb-028 may stimulate the immune system to exert a complement-mediated cytotoxic response against GD2-expressing tumor cells. The glycosphingolipid GD2 is a tumor associated antigen (TAA) overexpressed on the surface of many cancer cells.

anti-GD2 scFv/anti-DOTA scFv fusion protein GD2-SADA

A fusion protein composed of a single chain variable fragment (scFv) targeting the tumor-associated antigen (TAA) and disialoganglioside GD2, an scFv targeting the chelating agent 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) and a self-assembling and disassembling (SADA) domain that can self-assemble from a monomeric polypeptide into tetrameric protein, that may be used as a pre-targeted radioimmunotherapeutic agent. Upon administration, anti-GD2 scFv/anti-DOTA scFv fusion protein GD2-SADA assembles in tetramers and the anti-GD2 scFv binds to GD2-expressing tumor cells. The unbound GD2-SADA is excreted. Upon administration of a DOTA-based radioactive payload, the anti-DOTA scFv binds to the DOTA moiety of the radioactive payload, and radiation is selectively delivered to tumor cells expressing GD2. GD2, a disialoganglioside with expression in normal tissues restricted primarily to the cerebellum and peripheral nerves, is commonly expressed at high levels on tumors of neuroectodermal origins such as melanomas and neuroblastomas.

anti-GD2/anti-CD56 4SCAR-expressing bispecific T cells

A preparation of T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) disialoganglioside (GD2) and CD56 (neural cell adhesion molecule 1; NCAM-1), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-GD2/anti-CD56 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in GD2- and CD56-expressing tumor cells. GD2 is overexpressed on the surface of neuroblastoma cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells. CD56 is overexpressed on the surface of various types of cancer cells, including small cell lung cancer (SCLC) and other neuroendocrine tumors (NETs).

anti-GD2/anti-CD70 4SCAR-expressing bispecific T cells

A preparation of T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) disialoganglioside (GD2) and CD70 (CD27 ligand; tumor necrosis factor superfamily member 7; TNFSF7), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-GD2/anti-CD70 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in GD2- and CD70-expressing tumor cells. GD2 is overexpressed on the surface of neuroblastoma cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells. CD70, a cytokine belonging to the tumor necrosis superfamily (TNFSF) and the ligand for the costimulatory receptor CD27, is expressed on the surfaces of various types of cancer cells; its overexpression may play an important role in the evasion of immune surveillance.

anti-GD2/PSMA/CD276 4SCAR-expressing T cells

A preparation of T cells that are genetically engineered to express fourth generation chimeric antigen receptors (4SCARs) targeting the three tumor-associated antigens (TAAs) prostate-specific membrane antigen (PSMA), disialoganglioside (GD2), and the immune checkpoint molecule protein B7-homologue 3 (B7-H3, CD276), coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (CD3zeta; CD3z), and fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-GD2/PSMA/CD276-4SCAR-expressing T cells are directed to and induce selective toxicity in GD2-, PSMA- and CD276-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. PSMA, a type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors, including brain tumor, neuroblastoma (NB) and some lymphoma tumor tissues. CD276, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is highly expressed on many solid tumors including NB. It is a negative regulator of the T-cell activation and plays a key role in tumor evasion. GD2 is overexpressed on the surface of NB cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

anti-GD3 antibody-drug conjugate PF-06688992

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against the ganglioside GD3, a surface antigen expressed on many malignant melanoma cells, and linked to an as of yet not fully elucidated chemotherapeutic agent, with potential antineoplastic activity. Upon administration of the ADC PF-06688992, the antibody moiety targets and binds to GD3 expressed on melanoma cells. Upon internalization, the chemotherapeutic agent specifically kills the GD3-positive cells. GD3 represents a major surface marker on most human melanoma cells and is not expressed on most other types of normal, healthy cells.

anti-GDF-15 monoclonal antibody AZD8853

A monoclonal antibody directed against growth/differentiation factor 15 (GDF-15; macrophage inhibitory cytokine-1; MIC-1; non-steroidal anti-inflammatory drug-inducible gene-1; NAG-1; placental transforming growth factor-beta; pTGFB; prostate-derived factor; PDF; placental bone morphogenetic protein; PLAB), with potential antineoplastic activity. Upon administration, anti-GDF-15 monoclonal antibody AZD8853 specifically targets, binds to and inhibits the activity of GDF-15, thereby preventing the GDF-15-mediated inhibition of differentiation and activation of human monocyte-derived dendritic cells (DCs) and T-cells. This may restore immune cell infiltration into the tumor, leading to increases in T cells and activated DCs in the tumor microenvironment (TME). This enhances tumor cell killing and inhibits tumor cell proliferation. GDF-15, a divergent member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is upregulated in tissue injuries and is secreted by various tumors. Upregulation of GDF-15 is associated with immunosuppression in the TME, drug resistance and poor prognosis.

anti-GDF-15 monoclonal antibody CTL-002

A humanized, hinge-stabilized immunoglobulin G4 (IgG4) monoclonal antibody directed against growth/differentiation factor 15 (GDF-15; macrophage inhibitory cytokine-1; MIC-1; non-steroidal anti-inflammatory drug-inducible gene-1; NAG-1; placental transforming growth factor-beta; pTGFB; prostate-derived factor; PDF; placental bone morphogenetic protein; PLAB), with potential antineoplastic activity. Upon administration, anti-GDF-15 monoclonal antibody CTL-002 specifically targets, binds to and inhibits the activity of GDF-15, which may include its inhibition of lymphocyte function-associated antigen 1 (LFA-1) activation on CD8+ T cells. This may restore immune cell infiltration into the tumor, leading to tumor cell killing and inhibition of tumor cell proliferation. GDF-15, a divergent member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is upregulated in tissue injuries and also secreted by various tumors. It has been linked to immunosuppression in the tumor microenvironment (TME) and is associated with drug resistance and poor prognosis.

anti-GDF15 monoclonal antibody AV-380

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against human growth/differentiation factor 15 (GDF-15; macrophage inhibitory cytokine-1; MIC-1; non-steroidal anti-inflammatory drug-inducible gene-1; NAG-1; placental transforming growth factor-beta; pTGFB; prostate-derived factor; PDF; placental bone morphogenetic protein; PLAB), with potential anti-cachexic activity. Upon administration, anti-GDF15 monoclonal antibody AV-380 specifically targets, binds to and inhibits the activity of GDF-15, a pro-inflammatory cytokine involved in cancer-induced cachexia. This may prevent or slow the effects of cachexia. GDF-15, a divergent member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is upregulated in cancer-associated cachexia and immunosuppression in the tumor microenvironment (TME). It is associated with poor prognosis.

anti-GFRAL monoclonal antibody NGM120

A long-acting monoclonal antibody directed against glial-cell-derived neurotrophic factor (GDNF) family receptor alpha-like (GFRAL), with potential anti-anorexia and anti-cachexia activities. Upon administration, NGM120 targets, binds to and blocks GFRAL. This prevents binding of growth differentiation factor 15 (GDF15; MIC-1) to its receptor GFRAL and prevents GDF15/GFRAL-mediated signaling. This may abrogate loss of appetite and uncontrolled weight loss associated with high serum levels of GDF15. GDF15, a stress response cytokine and divergent member of the TGF-beta superfamily, plays a key role in the regulation of body weight through central mechanisms. High GDF15 plasma levels, as seen in individuals with advanced cancers, are associated with loss of body mass.

anti-GITR agonistic monoclonal antibody ASP1951

A human, high-affinity, tetravalent monospecific agonistic monoclonal antibody targeting glucocorticoid-induced tumor necrosis factor receptor (GITR; tumor necrosis factor superfamily member 18; TNFRSF18; CD357), with potential immune checkpoint modulating activity. Upon administration, anti-GITR agonistic monoclonal antibody ASP1951 binds to and activates GITR, which is expressed on the cell surface of multiple types of T lymphocytes. This induces both the activation and proliferation of tumor antigen-specific T-effector cells (Teffs), and suppresses the function of activated T-regulatory cells (Tregs), which may promote the elimination of tumor cells. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress both Teffs and T-cell receptor (TCR) signaling.

anti-GITR agonistic monoclonal antibody MS-986156

An anti-human glucocorticoid-induced tumor necrosis factor receptor (GITR; tumor necrosis factor superfamily member 18; TNFRSF18; CD357) agonistic monoclonal antibody, with potential immune checkpoint modulating activity. Anti-GITR antibody BMS-986156 binds to and activates GITR, which is expressed on the cell surface of multiple types of T cells. This stimulates the immune system, induces both the activation and proliferation of tumor antigen-specific T-effector cells (Teffs), and suppresses the function of activated T-regulatory cells (Tregs). This leads to tumor cell eradication. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress both Teffs and T-cell receptor (TCR) signaling.

anti-GITR agonistic monoclonal antibody REGN6569

An agonistic monoclonal antibody targeting glucocorticoid-induced tumor necrosis factor receptor (GITR; tumor necrosis factor superfamily member 18; TNFRSF18; CD357), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-GITR agonistic monoclonal antibody REGN6569 targets, binds to and activates GITR, which is expressed on the cell surface of multiple types of T lymphocytes and other immune cells. This induces both the activation and proliferation of tumor antigen-specific T-effector cells (Teffs), and suppresses the function of activated T-regulatory cells (Tregs), which may promote the elimination of tumor cells. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B-cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress both Teffs and T-cell receptor (TCR) signaling.

anti-GITR monoclonal antibody GWN 323

An anti-human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor superfamily, member 18; TNFRSF18; GITR; CD357) agonistic monoclonal antibody, with potential immune checkpoint modulating activity. Anti-GITR antibody GWN 323 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system, induces both the activation and proliferation of tumor-antigen-specific T effector cells (Teff), and suppresses the function of activated T regulatory cells (Tregs). This leads to tumor cell eradication. GITR, a member of the TNF receptor superfamily and T-cell receptor-co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B-cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress both Teffs and T-cell receptor (TCR) signaling.

anti-GITR monoclonal antibody MK-4166

An anti-human glucocorticoid-induced tumor necrosis factor receptor (GITR) agonistic monoclonal antibody (MoAb) with potential immunomodulating activity. Anti-GITR monoclonal antibody MK-4166 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system and induces both the activation and proliferation of tumor-antigen-specific T effector cells, and suppresses the function of activated T regulatory cells. This leads to tumor cell eradication. Also, this agent is shown to act synergistically with chemotherapeutic drugs in multiple cancer models. GITR, a member of the TNF receptor superfamily, is expressed on the surface of multiple types of immune cells, including regulatory T-cells, effector T-cells, B-cells, and natural killer (NK) cells.

anti-globo H monoclonal antibody OBI-888

A monoclonal antibody targeting the hexasaccharide glycosphingolipid antigen Globo H with potential immunostimulating, anti-angiogenic and antineoplastic activities. Upon infusion, anti-Globo H monoclonal antibody OBI-888 may induce tumor cell destruction via the activation of antibody dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and complement-dependent cytotoxicity (CDC), and may reduce immunosuppression. Globo H is a tumor-associated antigen (TAA) expressed on the surface of various types of cancer cells.

anti-globo H/MMAE antibody-drug conjugate OBI 999

An antibody-drug conjugate (ADC) composed of OBI-888 (OBI 888), a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) globohexaosylceramide (globo H), covalently linked to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-globo H/MMAE ADC OBI 999, the antibody moiety of OBI 999, OBI 888, targets and binds to globo H on tumor cells and is rapidly internalized, thereby delivering MMAE intracellularly. Upon proteolytic cleavage, MMAE targets and binds to tubulin and inhibits its polymerization, resulting in G2/M checkpoint arrest and apoptosis in globo H-expressing tumor cells. Globo H, a hexasaccharide glycosphingolipid, is (over)expressed on the surface of many types of tumor cells. Globo H is minimally or not expressed on healthy, normal cells; its expression on cancer cells is associated with increased proliferation and poor prognosis.

anti-glypican 3-scFvGC33-CAR-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) derived from the anti-glypican-3 (GPC3) monoclonal antibody GC33 (scFvGC33), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3-scFvGC33-CAR autologous T lymphocytes specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells.. GPC3 plays an important role in cellular proliferation and differentiation.

anti-glypican 3/CD3 bispecific antibody ERY974

An anti-glypican 3 (GPC3; GPC-3)/anti-CD3 bispecific monoclonal antibody, with potential immunostimulating and antineoplastic activities. Anti-GPC3/CD3 bispecific antibody ERY974 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for GPC3, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of ERY974, this bispecific antibody simultaneously binds to both CD3-expressing and GPC3-expressing cells, thereby crosslinking GPC3-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This may result in potent CTL-mediated lysis of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and an oncofetal antigen protein, is overexpressed in a variety of cancers; it plays a role in cell division and growth regulation.

anti-GnRH vaccine PEP223

A peptide vaccine derived from the synthetic peptide pyroEHWSYGLRPG, corresponding to amino acids 22-31 of mouse gonadotropin releasing hormone (GnRH), with potential immunocastration activity. PEP223 is dimerized and contains a D-lysine (k) substitution at position 6 (pyroEHWSYkLRPG) to increase its immunogenicity. Anti-GnRH vaccine PEP223 may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against GnRH, neutralizing its activity. In turn, testosterone production and tumor cell growth may be inhibited in testosterone-sensitive tumors.

anti-gpA33/CD3 monoclonal antibody MGD007

An anti-glycoprotein A33 (gpA33)/anti-CD3 bispecific humanized monoclonal antibody with potential immunostimulatory and antineoplastic activities. Anti-gpA33/CD3 monoclonal antibody MGD007 possesses two antigen-recognition sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for gpA33, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of MGD007, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and gpA33-expressing cancer cells, thereby crosslinking cytotoxic T-lymphocytes (CTLs) to gpA33-expressing tumor cells. This may result in CTL-mediated cell lysis of the crosslinked tumor cells. The gpA33 antigen, a member of the immunoglobulin superfamily, is expressed in certain malignancies, including colon and gastrointestinal cancers.

anti-GPC3 T cell-engaging antibody AZD9793

A T-cell engaging (TCE) asymmetric trispecific immunoglobulin G1 (IgG1) antibody targeting the tumor-associated antigen (TAA) glypican-3 (GPC3; GPC-3) and the T-cell surface antigens CD3 and CD8, with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3 TCE antibody AZD9793 targets and binds to GPC3 expressed on tumor cells and to CD3 and CD8 antigens on CD8-positive T lymphocytes. This activates and redirects CTLs to GPC3-expressing tumor cells, which results in the CTL-mediated death of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells. GPC3 plays an important role in tumor cell proliferation in various tumor cell types.

anti-GPC3-CAR autologous T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3-CAR autologous T lymphocytes specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation.

anti-GPC3-CAR-T lymphocytes TAK-102

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3-CAR-T lymphocytes TAK-102 specifically targets and binds to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation.

anti-GPC3/anti-4-1BB bispecific antibody BGB-B2033

A bispecific antibody directed against both the tumor-associated antigen (TAA) glypican-3 (GPC3; GPC-3) and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3/anti-4-1BB bispecific antibody BGB-B2033 simultaneously targets and binds to GPC3 expressed on tumor cells and 4-1BB expressed on activated T lymphocytes and natural killer (NK) cells. This crosslinks GPC3-expressing tumor cells and 4-1BB-expressing T-cells and NK cells, and activates 4-1BB signaling locally in the tumor microenvironment (TME). This results in cytotoxic T-cell co-stimulation, enhances T-lymphocyte-mediated anti-tumor activity and leads to cytotoxic T-cell-mediated lysis of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells. GPC3 plays an important role in tumor cell proliferation in various tumor cell types.

anti-GPC3/anti-CD3 bispecific antibody CM350

A bispecific antibody directed against the tumor-associated antigen (TAA) glypican-3 (GPC3; GPC-3) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3/anti-CD3 bispecific antibody CM350 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and GPC3 on GPC3-expressing tumor cells. This activates and redirects CTLs to GPC3-expressing tumor cells, leading to CTL-mediated killing of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells. GPC3 plays an important role in tumor cell proliferation in various tumor cell types.

anti-GPC3/TCR nanobody SAR444200

A T-cell engaging (TCE) and heavy chain variable domain (VHH)-based nanobody targeting the tumor-associated antigen (TAA) glypican-3 (GPC3; GPC-3) and a T-cell surface antigen, with potential antineoplastic activity. Upon administration, anti-GPC3/TCR nanobody SAR444200 specifically targets and binds to GPC3 expressed on tumor cells and a T-cell surface antigen on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to GPC3-expressing tumor cells, leading to CTL-mediated killing of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells. GPC3 plays an important role in tumor cell proliferation in various tumor cell types.

anti-GPR20/DXd antibody-drug conjugate DS-6157a

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the G protein-coupled receptor 20 (GPR20) conjugated to the cytotoxic DNA topoisomerase I inhibitor and exatecan derivative DXd (MAAA-1181a; MAAA-1181), with potential antineoplastic activity. Upon administration of the anti-GPR20/DXd ADC DS-6157a, the anti-GPR20 antibody targets and binds to GPR20-expressing tumor cells. Upon cellular uptake, the DXd moiety targets and binds to DNA topoisomerase I, thereby stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication and apoptosis. This inhibits the proliferation of GPR20-expressing tumor cells. GPR20 is overexpressed on certain tumor cell types.

anti-GPRC5D monoclonal antibody SAR446523

A Fc-engineered immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) human G-protein coupled receptor family C group 5 member D (GPRC5D), with potential immunomodulating and antineoplastic activities. Upon administration, anti-GPRC5D monoclonal antibody SAR446523 targets and binds to GPRC5D expressed on certain tumor cells. This results in an antibody-dependent cell-mediated cytotoxicity (ADCC) against GPRC5D-expressing tumor cells, thereby killing the cancer cells. GPRC5D is overexpressed on certain tumors, such as multiple myeloma, while minimally expressed on normal, healthy cells, and plays a key role in tumor cell proliferation.

anti-GPRC5D/anti-CD19 CAR T cells

A preparation of T lymphocytes engineered to express chimeric antigen receptor(s) (CARs) targeting the human tumor-associated antigens (TAAs) G-protein coupled receptor family C group 5 member D (GPRC5D) and CD19, with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPRC5D/anti-CD19 CAR T cells specifically and simultaneously target and bind to tumor cells expressing GPRC5D and/or CD19. This induces selective toxicity in tumor cells that express GPRC5D and/or CD19. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies.

anti-GPRC5D/anti-CD3 bispecific antibody LBL-034

A humanized immunoglobulin G1 (IgG1) bispecific monoclonal antibody directed against human CD3, a T-cell surface antigen, and human G-protein coupled receptor family C group 5 member D (GPRC5D), a tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. Upon administration, anti-GPRC5D/anti-CD3 bispecific antibody LBL-034 binds to both CD3 on T cells and GPRC5D expressed on tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a potent cytotoxic T-lymphocyte (CTL) response against GPRC5D-expressing tumor cells. GPRC5D is overexpressed on certain tumors while minimally expressed on normal, healthy cells. It plays a key role in tumor cell proliferation.

anti-gremlin-1 monoclonal antibody TST003

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against gremlin-1 (gremlin1; GREM1; Drm), with potential antineoplastic activity. Upon administration, anti-gremlin-1 monoclonal antibody TST003 specifically targets and binds to gremlin-1, thereby neutralizing gremlin-1 expressed on tumor cells and cancer associated fibroblasts (CAFs). This prevents binding to bone morphogenetic proteins (BMP), specifically to BMP2 and 4, and blocks the gremlin-1-mediated inhibition of BMP signaling pathways. This may lead to increased infiltration of CD8 T-cells into the tumor and may inhibit tumor cell growth and proliferation. Gremlin-1, a BMP antagonist and a member of the tumor growth factor (TGF)-beta superfamily, is overexpressed in a variety of cancer cell types. It is involved in cancer cell growth and proliferation, and promotes epithelial to mesenchymal transition (EMT). Overexpression of gremlin-1 is often associated with poor prognosis.

anti-gremlin-1 monoclonal antibody UCB6114

A monoclonal antibody directed against gremlin-1 (GREM1; Drm), with potential antineoplastic activity. Upon administration, anti-gremlin-1 antibody UCB6114 specifically targets and binds to gremlin-1, thereby neutralizing Gremlin-1. This may block the gremlin-1-mediated inhibition of bone morphogenetic protein (BMP) signaling pathways, and may lead to the inhibition of tumor cell growth and proliferation. Gremlin-1, a BMP antagonist that is overexpressed in a variety of cancer cell types, is involved in cancer cell growth and proliferation as well as tissue fibrosis.

anti-GRP78 monoclonal antibody PAT-SM6

A IgM monoclonal antibody (MoAb) against 78-kDa glucose-regulated protein (GRP78; also called BiP or HSPA5), with potential proapoptotic and antineoplastic activities. Upon intravenous administration of the anti-GRP78 monoclonal antibody PAT-SM6, the MoAb strongly binds to GRP78, thereby preventing the activation of multiple GRP78-mediated pathways and blocking the GRP78-induced suppression of apoptotic pathways. This eventually leads to the induction of tumor cell apoptosis and a reduction in tumor cell proliferation. GRP78, the endoplasmic reticulum (ER) chaperone and unfolded protein response (UPR) regulator, is overexpressed on the surface of a variety of cancer cell types; its expression is associated with increased tumor cell survival and proliferation, as well as angiogenesis and resistance to chemotherapy.

anti-GUCY2C CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting human guanylate cyclase 2C (GUCY2C; GCC; guanylyl cyclase C; heat-stable enterotoxin receptor; hSTAR), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GUCY2C CAR T cells target and bind to GUCY2C-expressing tumor cells, thereby inducing selective toxicity in GUCY2C-expressing tumor cells. GUCY2C, a transmembrane receptor expressed on intestinal epithelial cells, is overexpressed on certain tumors of the gastrointestinal (GI) tract.

anti-HA epitope monoclonal antibody MEDI8852

A human immunoglobulin (Ig) G1 kappa monoclonal antibody (mAb) targeting a unique epitope in the stalk of the influenza A hemagglutinin (HA) protein, with broad influenza A virus neutralization activity. MEDI8852 was derived from an antibody isolated from human memory B cells from patients previously infected with influenza caused by type A strains that was further optimized to increase neutralization potential. Upon infusion, MEDI8852 targets and binds to a region within the stalk of the HA protein that is highly conserved amongst all influenza A virus subtypes. This neutralizes and prevents essential steps of the viral lifecycle, thereby blocking infectivity of all influenza A virus subtypes. HA, a glycoprotein found on the surface of the influenza virus, plays a key role in viral attachment and cell entry.

anti-HB-EGF monoclonal antibody KHK2866

A proprietary fucose-free monoclonal antibody directed against human heparin-binding EGF-like growth factor (HBEGF) with potential antineoplastic activity. Anti-HB-EGF monoclonal antibody KHK2866 binds to HBEGF, thereby blocking its binding to the EGF receptors. This prevents EGF receptor activation and the subsequent induction of cell growth signaling. HBEGF is mitogenic for fibroblasts and smooth muscle and may be involved in macrophage-mediated cellular proliferation. The fucose-free monoclonal antibodies enhance antigen dependent cellular cytotoxicity (ADCC), and increase binding affinity to the Fc receptor to overcome genetic polymorphism.

anti-HBEGF monoclonal antibody U3-1565

A humanized monoclonal antibody directed against human heparin-binding EGF-like growth factor (HBEGF) with potential antineoplastic activity. Anti-HBEGF monoclonal antibody U3-1565 binds to HBEGF and blocks the binding of HBEGF to the EGF receptors. This prevents EGF receptor activation and the subsequent induction of cell growth signaling. HBEGF is mitogenic for fibroblasts and smooth muscle and may be involved in macrophage-mediated cellular proliferation.

anti-hCD70-CAR retroviral vector-transduced autologous PBLs

A preparation of autologous human peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding for a T-cell chimeric antigen receptor (CAR) gene specific for the human cluster of differentiation 70 (CD70), with potential immunostimulatory and antineoplastic activities. Autologous PBLs from a patient with CD70-positive cancer are transduced with a retroviral vector that encodes the CAR gene specific for CD70. After expansion in culture and reintroduction into the patient, anti-hCD70-CAR retroviral vector-transduced autologous PBLs bind to the CD70 antigen on tumor cell surfaces; subsequently, CD70-expressing tumor cells are lysed. CD70, the ligand for the costimulatory receptor CD27, is overexpressed on the surfaces of various cancer cell types.

anti-HCV E2 monoclonal antibody MBL-HCV1

A neutralizing, human monoclonal antibody against the hepatitis C virus (HCV) E2 envelope glycoprotein, with potential immunomodulatory and antiviral activities against HCV. Upon administration, anti-HCV E2 monoclonal antibody MBL-HCV1 recognizes and binds to the E2 glycoprotein of HCV. This suppresses HCV load and provides passive immunization against HCV. This may prevent both infection by HCV in immunocompromised patients and hepatitis C-related liver disease. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family.

anti-hepcidin monoclonal antibody LY2787106

A humanized monoclonal antibody (MoAb) targeting the peptide hormone hepcidin, with potential anti-anemic activity. Upon intravenous administration, anti-hepcidin MoAb LY2787106 binds to hepcidin and prevents it from binding to the iron exporting protein ferroportin, which is expressed on both the basolateral surface of gastrointestinal (GI) enterocytes and the plasma membrane of macrophages. This prevents hepcidin-induced internalization and degradation of ferroportin and increases ferroportin-mediated iron export, thus increasing iron export from macrophages and iron absorption by enterocytes. This normalizes plasma iron levels, increases erythropoiesis and may inhibit anemia. Hepcidin, produced in hepatocytes, plays a key role in the homeostasis of systemic iron; it is upregulated during acute and chronic inflammation in response to cytokines and, in certain cancers, may contribute to cancer-associated anemia.

anti-Her-2-CAR retroviral vector-transduced autologous peripheral blood lymphocytes

Autologous human peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding an anti-Her-2 (epidermal growth factor receptor 2) chimeric T cell receptor (chimeric antigen receptor or CAR) gene with potential immunostimulatory and antineoplastic activities. Autologous PBLs from a patient with Her-2-positive cancer are pulsed with a retroviral vector that encodes the CAR gene specific for Her-2. After expansion in culture and reintroduction into the patient, anti-Her-2-CAR retroviral vector-transduced autologous peripheral blood lymphocytes, expressing anti-Her-2-CAR on their cell surfaces, bind to Her-2 antigen on tumor cell surfaces; subsequently, Her-2-expressing tumor cells may be lysed. Her-2 (ErbB-2), a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, belongs to the EGFR superfamily and plays key roles in tumor cell proliferation and tumor angiogenesis.

anti-HER2 ADC BB-1701

: An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated, through a cleavable linker, to the cytotoxic agent eribulin, a synthetic, macrocyclic ketone analogue of halichondrin B, with potential antineoplastic activity. Upon administration of anti-HER2 ADC BB-1701, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Upon binding and internalization, the linker is cleaved by the lysosomal protease cathepsin B. The unconjugated eribulin targets and binds to the vinca domain of tubulin and inhibits both the polymerization of tubulin and the assembly of microtubules. This inhibits mitotic spindle assembly, induces cell cycle arrest at G2/M phase, and results in apoptosis of HER2-expressing tumor cells. In addition, BB-1701 induces a potent bystander effect in neighboring tumor cells and immunogenic cell death (ICD). HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

anti-HER2 antibody conjugated natural killer cells ACE1702

An off-the-shelf preparation of natural killer (NK) cells conjugated to a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), with potential antineoplastic activity. Upon administration of anti-HER2 antibody conjugated natural killer cells ACE1702, the antibody moiety targets and binds to HER2 on tumor cells, which may lead to cell lysis of HER2-expressing tumor cells by the NK cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 antibody-drug conjugate BAT8001

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated via an uncleavable linker to an as of yet undisclosed maytansine derivative, with potential antineoplastic activity. Upon administration of the anti-HER2 ADC BAT8001, the anti-HER2 monoclonal antibody targets and binds to HER2 expressed on tumor cells. Upon cellular uptake, the cytotoxic maytansine derivative binds to tubulin, thereby affecting microtubule assembly and disassembly dynamics. This inhibits tumor cell proliferation and induces apoptosis in HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 antibody-drug conjugate BAT8010

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) linked to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of anti-HER2 ADC BAT8010, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER2-expressing tumor cells. HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

anti-HER2 antibody-drug conjugate BL-M07D1

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) linked to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-HER2 ADC BL-M07D1, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills HER2-expressing tumor cells through an as of yet undisclosed mechanism. HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

anti-HER2 antibody-drug conjugate DB-1303

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) and conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-HER2 ADC DB-1303, the antibody moiety targets and binds to HER2 on tumor cell surfaces. Upon cellular uptake and internalization, the cytotoxic agent inhibits tumor cell proliferation through an as of yet undisclosed mechanism of action (MoA). HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 antibody-drug conjugate DP303c

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) and conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-HER2 ADC DP303c, the antibody moiety targets and binds to HER2 on tumor cells. Upon antibody/antigen binding and internalization, the cytotoxic agent induces tumor cell apoptosis, through an as of yet not publicly known mechanism. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 antibody-drug conjugate FDA022-BB05

An antibody-drug conjugate (ADC) composed of trastuzumab, a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), conjugated, via a valine-alanine (Val-Ala)-based cathepsin B-cleavable linker, to the cytotoxic DNA topoisomerase I inhibitor and exatecan derivative DXd (MAAA-1181a; MAAA-1181), with potential antineoplastic activity. Upon administration, anti-HER2 ADC FDA022-BB05 targets and binds to HER2 expressed on tumor cells. Upon binding, internalization, and linker cleavage, DXd is released. DXd inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER2-expressing tumor cells. FDA022-BB05 is also able to induce a bystander effect on neighboring cells in the tumor environment. This further inhibits the proliferation of tumor cells. HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

anti-HER2 antibody-drug conjugate IBI354

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated to a camptothecin derivative, with potential antineoplastic activity. Upon administration of the anti-HER2 ADC IBI354, the anti-HER2 monoclonal antibody targets and binds to HER2 expressed on tumor cells. Upon cellular uptake, the camptothecin derivative inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 antibody-drug conjugate MEDI4276

An antibody-drug conjugate (ADC) composed of a bispecific antibody against the extracellular domain of human epidermal growth factor receptor 2 (HER2; ERBB2) comprised of the single-chain variable fragment (scFv) of the anti-HER2 monoclonal antibody trastuzumab, which binds to domain IV of HER2, fused to the heavy chains of the anti-HER2 monoclonal antibody 39S, which binds to domain II of HER2, and conjugated, via a cleavable linker, to the cytotoxic anti-microtubule agent tubulysin, with potential antineoplastic activity. Upon administration of MEDI4276, the anti-HER2 bispecific antibody specifically targets and binds to HER2 on the surface of certain cancer cells. Upon binding, crosslinking and internalization of antibody-HER2 complexes occurs and MEDI4276 is transported to the lysosome where the linker is cleaved, thereby delivering tubulysin inside HER2-expressing cancer cells. Tubulysin binds to tubulin and inhibits microtubule polymerization, which blocks cell division. This results in G2/M phase arrest, tumor cell apoptosis, and decreased proliferation of HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 bispecific antibody KM257

A bispecific antibody directed against two distinct domains of the tumor-associated antigen (TAA) human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential immunomodulating and antineoplastic activities. Upon administration, anti-HER2 bispecific antibody KM257 simultaneously targets and binds to two different domains of HER2. This prevents the activation of HER2 signaling pathways. In addition, by binding to HER2, KM257 induces an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that express HER2. This results in tumor cell apoptosis and inhibits the proliferation of HER2-expressing tumor cells. HER2, overexpressed on a variety of tumor cell types, plays an important role in tumor cell proliferation, differentiation and survival.

anti-HER2 bispecific antibody TQB2930

A bispecific antibody directed against two distinct domains of the tumor-associated antigen (TAA) human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential immunomodulating and antineoplastic activities. Upon administration, anti-HER2 bispecific antibody TQB2930 simultaneously targets and binds to two different domains of HER2. This prevents the activation of HER2 signaling pathways, resulting in tumor cell apoptosis and growth inhibition of HER2-expressing tumor cells. HER2, overexpressed on a variety of tumor cell types, plays an important role in tumor cell proliferation, differentiation and survival.

anti-HER2 bispecific antibody-drug conjugate ZW49

An antibody-drug conjugate (ADC) consisting of a bispecific monoclonal antibody (ZW25) directed against two different epitopes of the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (HER2, receptor tyrosine-protein kinase erbB-2) linked to an as of yet undisclosed cytotoxic payload, with potential antineoplastic activity. Upon intravenous administration, anti-HER2 bispecific ADC ZW49 targets and binds to HER2 expressed on tumor cells. Following receptor internalization, the cytotoxic payload is released and induces tumor cell death through an as of yet unknown mechanism of action. Additionally, binding of HER2 may inhibit HER2 activation, HER2 signaling and HER2-mediated tumor cell growth. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 dendritic cell vaccine

A type-1-polarized dendritic cell (DC1)-based cancer vaccine against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (HER2; EGFR2, ERBB2), with potential immunomodulatory and antineoplastic activities. Upon intratumoral administration of the anti-HER2 DC vaccine, the immune system gets exposed to HER2, which may stimulate a potent cytotoxic T-lymphocyte (CTL) response against HER2-positive tumor cells. This may result in tumor cell death and decreased tumor growth. HER2, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is overexpressed by a variety of cancers.

anti-HER2 GSPT1 degrader ORM-5029

A targeted protein degrader (TPD) composed of pertuzumab, an antibody directed against the tumor-associated antigen (TAA) human tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), conjugated, via a Val-Cit PABc cleavable linker, to SMol006, a membrane-permeable selective molecular glue degrader (MGD) of the translational termination factor GSPT1, with potential antineoplastic activity. Upon intravenous administration, anti-HER2 GSPT1 degrader ORM-5029 specifically targets and binds, with its pertuzumab moiety, to HER-2-expressing tumor cells. Upon internalization and cleavage, SMol006 specifically targets and binds to GSPT1, leading to GSPT1 degradation via the E3 ubiquitin ligase pathway. This disrupts oncogenic signaling, inhibits proliferation, and induces apoptosis in HER-2-driven tumors. The translation termination factor GSPT1, a G-loop degron-containing protein, plays a key role in protein translation and is dysregulated in various tumor cell types.

anti-HER2 immune stimulator-antibody conjugate NJH395

An immune stimulator-antibody conjugate (ISAC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated to a not yet disclosed immune stimulator, with potential antineoplastic and immunostimulating activities. Upon administration of the anti-HER2 immune stimulator-antibody conjugate NJH395, the antibody moiety targets and binds to HER2 expressed on tumor cells. Upon antibody/antigen binding, the immune-stimulating moiety may, through an as of yet undisclosed mechanism, enhance the immune-mediated killing of HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed in many cancer types and plays a key role in tumor cell proliferation and tumor vascularization.

anti-HER2 molecule AIP-303

A molecule targeting the tumor-associated antigen (TAA) epidermal growth factor receptor 2 (HER2, EGFR2, ERBB2), with potential antineoplastic activity. Upon administration, the anti-HER2 molecule AIP-303 targets and binds to HER2-expressing cells. This may inhibit HER2-mediated signaling and inhibit growth in HER2-overexpressing tumor cells. HER2, a tyrosine kinase, is overexpressed on the cell surfaces of various tumor cell types.

anti-HER2 monoclonal antibody

Any monoclonal antibody that is directed against human epidermal growth factor receptor 2 (HER2; HER-2; ERBB2).

anti-HER2 monoclonal antibody B002

A humanized monoclonal antibody directed against the human epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential antineoplastic activity. Upon administration, anti-HER2 monoclonal antibody B002 targets and binds to HER2 on HER2-expressing tumor cells. This prevents HER2-mediated signaling and may lead to antitumor activity. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 monoclonal antibody BAT1006

A glycosylation engineered recombinant humanized monoclonal antibody targeting the extracellular dimerization domain (subdomain II) of the tumor-associated antigen (TAA) and tyrosine kinase receptor epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential antineoplastic activity. Upon administration, anti-HER2 monoclonal antibody BAT1006 targets and binds to HER2 on tumor cells, thereby blocking HER2-mediated signaling. This may inhibit the proliferation of HER2-expressing tumor cells. In addition, BAT1006 induces antibody-dependent cell-mediated cytotoxicity (ADCC). HER2, overexpressed on a variety of tumor cell types, plays an important role in tumor cell proliferation, differentiation and survival.

anti-HER2 monoclonal antibody HLX22

A humanized immunoglobulin (lg) G1 monoclonal antibody directed against the human epidermal growth factor receptor 2 (HER2), with potential immunomodulating and antineoplastic activity. Upon administration, anti-HER2 monoclonal antibody HLX22 targets and binds to HER2 on tumor cell surface. This may induce a cytotoxic T-lymphocyte (CTL) response as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress HER2. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 monoclonal antibody QL1209

A humanized monoclonal antibody directed against the domain II of the extracellular domain of human epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential antineoplastic activity. Upon administration, anti-HER2 monoclonal antibody QL1209 targets and binds to HER2 on HER2-expressing tumor cells. This prevents HER2-mediated signaling and may lead to an inhibition of proliferation in HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2 protease-activated T-cell-engager AMX-818

A protease-activated prodrug T-cell-engager (TCE) composed of two tandem single chain variable fragments (scFvs) targeting the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) and CD3, a T-cell surface antigen, and conjugated, via a protease-cleavable linker, to two unstructured polypeptides (XTEN), with potential immunomodulating and antineoplastic activities. Double XTEN masking allows for universal masks that sterically hinder target binding of AMX-818 until cleaved by proteases; it also prolongs half-life. Upon intravenous administration of anti-HER2/CD3/XTEN protease-activated TCE AMX-818, the XTEN masks are proteolytically cleaved in the tumor microenvironment (TME) by dysregulated proteases at the base of the XTEN masks which releases the active TCE. The anti-HER2 scFv moiety targets and binds to HER2 expressed on tumor cells. The CD3 scFv moiety targets and binds to T cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against HER2-expressing tumor cells. HER2, a receptor tyrosine kinase (RTK) mutated or overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. The XTEN masks allows specific activation of AMX-818 in the TME and limits systemic unmasking; this minimizes systemic toxicity and increases efficacy. In healthy tissues, where protease activity is tightly regulated, the HER2-XTENylated protease-activated T-cell-engager (XPAT) AMX-818 remains predominantly inactive.

anti-HER2-CAR autologous CMV-specific cytotoxic T lymphocytes

Autologous human cytomegalovirus (CMV)-specific human cytotoxic T lymphocytes (CTLs) transduced with a retroviral vector encoding a human anti-HER2 (epidermal growth factor receptor 2) chimeric T cell receptor (CAR) gene with potential immunostimulatory and antineoplastic activities. Autologous CTLs from a patient with HER2- and CMV-positive glioblastoma multiforme (GBM) are genetically modified to express CAR gene specific for HER2 on their cell surfaces. After expansion in culture and reintroduction into the patient, the anti-HER2-CAR autologous CMV-specific CTLs bind to HER2 antigen on tumor cell surfaces; subsequently, HER2-positive tumor cells and stem cells may be lysed. HER2 (ErbB2), a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, plays key roles in tumor cell proliferation and tumor angiogenesis. CMV is present in the majority of GBM tumors.

anti-HER2-DM1 ADC B003

An antibody-drug conjugate (ADC) consisting of a recombinant humanized anti-epidermal growth factor receptor 2 (HER2) monoclonal antibody conjugated to the maytansinoid DM1 via a nonreducible thioether linkage (MCC), with potential antineoplastic activity. Upon administration of B003, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 on tumor cell surfaces; upon internalization, the DM1 moiety is released and binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics, inhibiting cell division and the proliferation of cancer cells that overexpress HER2.

anti-HER2-DM1 antibody-drug conjugate GQ1001

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) and conjugated, via a site-specific linker, to the cytotoxic maytansinoid mertansine (DM1), with potential antineoplastic activity. Upon administration of anti-HER2-DM1 ADC GQ1001, the antibody moiety targets and binds to HER2 on tumor cell surfaces. Upon cellular uptake and internalization, DM1 binds to tubulin and interferes with microtubule assembly and disassembly dynamics. This inhibits cell division and the proliferation of tumor cells that overexpress HER2. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2-STING agonist ADC XMT-2056

An antibody-drug conjugate (ADC) composed of HT-19, a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), linked to a payload composed of an agonist for the stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173), with potential immuno-activating and antineoplastic activities. Upon intravenous administration of anti-HER2 STING agonist ADC XMT-2056, the anti-HER2 antibody moiety targets and binds to HER2 while the STING agonist targets and binds to STING on immune cells in the tumor microenvironment (TME). This allows for specific activation of the STING pathway in the TME. This leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T lymphocyte (CTL)-mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system. The conjugation of the anti-HER2 antibody to the STING agonist improves targeted delivery of the STING agonist and increases tumor exposure and enhances the STING-mediated anti-tumor immune responses while limiting systemic toxicity.

anti-HER2-vc0101 ADC PF-06804103

A proprietary antibody-drug conjugate (ADC) composed of a monoclonal antibody against human epidermal growth factor receptor 2 (HER2) site-specifically linked, via a protease cleavable linker, to an analog of dolastatin 10, Auristatin-0101, with potential antineoplastic activity. Upon administration, anti-HER2-vc0101 ADC PF-06804103 targets HER2 expressed on tumor cells. Upon binding, internalization and cleavage, Auristatin-0101 binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and apoptosis of HER2-expressing tumor cells. HER2, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells.

anti-HER2/anti-CD3 bispecific antibody M802

A humanized bispecific antibody composed of a monovalent unit directed against the tumor-associated antigen (TAA) human epidermal growth factor 2 (HER2; ErbB2; HER-2) and a single chain unit directed against CD3 found on T lymphocytes, with potential immunostimulatory and antineoplastic activities. Upon administration, anti-HER2/anti-CD3 bispecific antibody M802 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and HER2 on HER2-expressing tumor cells. This activates and redirects CTLs to HER2-expressing tumor cells, which results in the CTL-mediated cell death of HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation.

Anti-HER2/Anti-CD3 Bispecific Monoclonal Antibody GBR 1302

An anti-human epidermal growth factor receptor 2 (HER2)/anti-CD3 bispecific monoclonal antibody with potential immunostimulatory and antineoplastic activities. Anti-HER2/Anti-CD3 bispecific monoclonal antibody GBR 1302 possesses two antigen recognition sites, one for HER2, a tyrosine kinase receptor overexpressed by many cancer cell types, and one for the CD3 complex, a group of T-cell surface glycoproteins that interact with the T-cell receptor (TCR). Upon administration of GBR 1302, this bispecific monoclonal antibody simultaneously binds to both CD3-expressing T cells and HER2-expressing cancer cells, thereby crosslinking HER2-expressing tumor cells and cytotoxic T lymphocytes (CTLs). This may result in potent CTL-mediated lysis of HER2-expressing tumor cells. HER2 plays a key role in tumor cell proliferation and tumor vascularization.

anti-HER2/anti-PD-1 bispecific antibody SSGJ-705

A bispecific antibody directed against the human epidermal growth factor receptor 2 (HER2; EGFR2, ERBB2) and the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-HER2/anti-PD-1 bispecific antibody SSGJ-705 simultaneously targets, binds to and inhibits HER2 and PD-1 and their downstream signaling pathways, and bridges PD-1-expressing T cells to HER2-expressing tumor cells. This may inhibit tumor cell proliferation of HER2-overexpressing cells. Inhibition of PD-1-mediated signaling may restore immune function through the activation of T cells and T-cell-mediated immune responses against the HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-HER2/anti-PD-L1 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) targeting the tumor-associated antigens (TAAs) human epidermal growth factor 2 (HER2; ErbB2; HER-2) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating and antineoplastic activities. Upon administration, anti-HER2/anti-PD-L1 CAR T cells target and bind to HER2- and PD-L1-expressing tumor cells, thereby inducing selective toxicity in HER2- and PD-L1-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation. PD-L1 is overexpressed by many human cancer cell types and plays a key role in the downregulation of the immune system and tumor evasion from host immunity.

anti-HER2/auristatin payload antibody-drug conjugate XMT-1522

An antibody-drug conjugate (ADC) composed of HT-19, a monoclonal antibody directed against the human epidermal growth factor receptor 2 (ERBB2; HER2), conjugated, via a proprietary biodegradable, hydrophilic polymer backbone and various linkers, to proprietary auristatin-derived payload molecules (about 15 per antibody), with potential antineoplastic activity. Upon administration of anti-HER2/auristatin payload ADC XMT-1522, the antibody moiety targets and binds to a unique epitope in the extracellular domain (ECD) of HER2. Upon internalization, cleavage and release of the cytotoxic molecules, the auristatin-derived molecules bind to tubulin and inhibit its polymerization, which results in G2/M phase arrest and induces apoptosis of HER2-expressing tumor cells. The attachment of multiple auristatin molecules to the backbone enables XMT-1522 to effectively kill tumors that express relatively low amounts of the HER2 protein; therefore, this agent shows increased therapeutic potential in tumors with low HER2 expression compared to other anti-HER2 antibody-based therapies. The polymer-based proprietary platform optimizes delivery of the cytotoxic drug payload and improves drug solubility.

anti-HER2/CD3 tri-specific antibody BR115

A tri-specific T-cell engager and monoclonal antibody targeting two separate epitopes of the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) and the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-HER2/CD3 tri-specific antibody BR115 targets and binds to two separate HER2 epitopes on HER2-expressing tumor cells and CD3 on T cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against HER2-expressing tumor cells. HER2, a receptor tyrosine kinase (RTK) mutated or overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-HER2/CD3/CD28 Tri-specific antibody SAR443216

A tri-specific T-cell engager and monoclonal antibody targeting the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), CD3, a T-cell surface antigen, and CD28, a T-cell specific surface glycoprotein and co-stimulatory molecule, with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-HER2/CD3/CD28 tri-specific antibody SAR443216 targets and binds to CD3 and CD28 on T cells and HER2 expressed on tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against HER2-expressing tumor cells. HER2, a receptor tyrosine kinase (RTK) mutated or overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-HER2/HER2 bispecific ADC KM501

A therapeutic cancer vaccine containing seven 17 amino acids long synthetic RAS oncogene-encoded peptides representing the most common codon 12 and 13 oncogenic mutations in Kirsten rat sarcoma viral oncogene homolog (KRAS), with potential immunomodulating and antineoplastic activities. Upon administration, RAS peptide cancer vaccine TG01 may stimulate a specific CD4-positive helper T-lymphocyte- and cytotoxic T-lymphocyte (CTL)-mediated immune response against RAS mutant-specific-expressing cancer cells, resulting in an inhibition of tumor cell proliferation and tumor cell death. Mutations in RAS genes are found in the majority of pancreatic cancers.

anti-HER2/HER3 dendritic cell vaccine

A dendritic cell (DC)-based cancer vaccine against the tumor-associated antigens (TAAs) human epidermal growth factor receptor 2 (HER2; EGFR2, ERBB2) and 3 (HER3; ErbB3), with potential immunomodulatory and antineoplastic activities. Upon administration of the anti-HER2/HER3 DC vaccine, the immune system gets exposed to HER2 and HER3, which may stimulate a potent cytotoxic T-lymphocyte (CTL) response against HER-2/3-positive tumor cells. This may result in tumor cell death and decreased tumor growth. HER-2/3, members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are overexpressed by a variety of cancers.

anti-HER2/PBD-MA antibody-drug conjugate DHES0815A

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody targeting human epidermal growth factor receptor 2 (ERBB2; EGFR2; HER2) linked to a DNA minor groove crosslinking agent pyrrolo[2,1- c][1,4]benzodiazepine monoamide (PBD-MA), with potential antineoplastic activity. Upon intravenous administration of ADC DHES0815A, the monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Following receptor internalization and lysosome-mediated cleavage, the cytotoxic PBD-MA moiety is released. In turn, the imine groups of the PBD-MA moiety bind to and crosslink specific sites of DNA, resulting in DNA strand breaks, cell cycle arrest, and cell death in HER2 expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2/topoisomerase I inhibitor ADC GQ1005

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated, via a cleavable open-ring linker, to a topoisomerase I (TopoI) inhibitor-based payload, with potential antineoplastic activity. Upon administration of the anti-HER2/topoisomerase I inhibitor ADC GQ1005, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Upon cellular uptake, the TopoI inhibitor inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication which results in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER2-expressing tumor cells. Also, GQ1005 induces an additional bystander effect, thereby further killing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER2/topoisomerase I inhibitor ADC TQB2102

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated, via an enzyme-cleavable linker, to a topoisomerase I (TopoI) inhibitor payload, with potential antineoplastic activity. Upon administration of the anti-HER2/topoisomerase I inhibitor ADC TQB2102, the anti-HER2 monoclonal antibody moiety targets and binds to HER2 expressed on tumor cells. Upon cellular uptake, the TopoI inhibitor inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication which results in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.

anti-HER3 antibody-drug conjugate YL202

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against human epidermal growth factor receptor 3 (HER3; ErbB3) conjugated via a tumor microenvironment (TME) activable protease-cleavable linker to a cytotoxic DNA topoisomerase I inhibitor, with potential antineoplastic activity. Upon administration of anti-HER3 ADC YL202, the anti-HER3 antibody moiety targets and binds to HER3 expressed on tumor cells. Upon proteolytic cleavage in the TME and the release of the topoisomerase I inhibitor, the topoisomerase I inhibitor targets and binds to DNA topoisomerase I, thereby stabilizing the cleavable complex between topoisomerase I and DNA and resulting in DNA breaks, inhibition of DNA replication and apoptosis in HER3-expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors.

anti-HER3 dendritic cell vaccine

A type-1-polarized dendritic cell (DC1)-based cancer vaccine against the tumor-associated antigen (TAA) human epidermal growth factor receptor 3 (HER3; ERBB3), with potential immunomodulatory and antineoplastic activities. Upon intratumoral administration of the anti-HER3 DC vaccine, the immune system gets exposed to HER3, which may stimulate a potent cytotoxic T-lymphocyte (CTL) response against HER3-positive tumor cells. This may result in tumor cell death and decreased tumor growth. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is overexpressed by a variety of cancers.

anti-HER3 monoclonal antibody GSK2849330

A monoclonal antibody directed against the human epidermal growth factor receptor 3 (HER3; ERBB3) with potential antineoplastic activity. Anti-HER3 monoclonal antibody GSK2849330 binds to HER3 and inhibits its activation. This may prevent HER3-mediated signaling and inhibit HER3-dependent tumor cell proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors and is associated with poor prognosis and drug resistance; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.

anti-HER3 monoclonal antibody LJM716

A human monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3) with potential antineoplastic activity. Anti-HER3 monoclonal antibody LJM716 possesses a novel mechanism of action; LJM716 binds to and locks HER3 in the inactive conformation and does not interfere with its interaction with neuregulin (NRG). The inactivated form of HER3 blocks the PI3K/Akt signaling pathway, thereby inhibiting cellular proliferation in HER2 or NRG expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.

anti-HER3 monoclonal antibody SIBP-03

A recombinant humanized monoclonal antibody directed against the human epidermal growth factor receptor 3 (HER3; ERBB3), with potential antineoplastic activity. Upon administration, anti-HER3 monoclonal antibody SIBP-03 targets and binds to HER3 and inhibits its activation. This may prevent HER3-mediated signaling and inhibit HER3-dependent tumor cell proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors and is associated with poor prognosis and drug resistance; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.

anti-HER3/topoisomerase I inhibitor antibody-drug conjugate

Any antibody-drug conjugate (ADC) that is composed of a monoclonal antibody directed against human epidermal growth factor receptor 3 (HER3; ErbB3) and conjugated to a cytotoxic DNA topoisomerase I inhibitor.

anti-HER3/topoisomerase I inhibitor antibody-drug conjugate DB-1310

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against human epidermal growth factor receptor 3 (HER3; ErbB3) conjugated, via a maleimide tetrapeptide-based cleavable linker, to a cytotoxic DNA topoisomerase I inhibitor, with potential antineoplastic activity. Upon administration of anti-HER3 ADC DB-1310, the anti-HER3 antibody moiety targets and binds to HER3 expressed on tumor cells. Upon internalization, the topoisomerase I inhibitor targets and binds to DNA topoisomerase I, thereby stabilizing the cleavable complex between topoisomerase I and DNA and resulting in DNA breaks, inhibition of DNA replication and apoptosis in HER3-expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors.

anti-HER3/topoisomerase I inhibitor antibody-drug conjugate IBI133

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against human epidermal growth factor receptor 3 (HER3; ErbB3) conjugated to a topoisomerase I (TopoI) inhibitor-based payload, with potential antineoplastic activity. Upon administration of anti-HER3/TopoI inhibitor ADC IBI133, the anti-HER3 antibody moiety targets and binds to HER3 expressed on tumor cells. Upon cellular uptake, the TopoI inhibitor inhibits DNA topoI activity, thereby inhibiting DNA replication which results in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of HER3-expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors.

anti-HGF monoclonal antibody TAK-701

A humanized monoclonal antibody directed against human hepatocyte growth factor (HGF) with potential antineoplastic activity. Anti-HGF monoclonal antibody TAK-701 binds to the soluble ligand HGF, preventing HGF binding to and activation of the HGF receptor c-Met and so the activation of the c-Met signaling pathway; this may result in the induction of cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in a variety of tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-HGF monoclonal antibody YYB101

A humanized monoclonal antibody directed against human hepatocyte growth factor (HGF), with potential antineoplastic activity. Upon administration, anti-HGF monoclonal antibody YYB101 targets and binds to HGF, preventing the binding of HGF to the HGF receptor c-Met and the activation of the c-Met signaling pathway. This may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-HHLA2 monoclonal antibody NPX887

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against HERV-H LTR-associating protein 2 (HHLA2; HHLA-2; B7 homolog 7; B7-H7), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-HHLA2 monoclonal antibody NPX887 targets and binds to HHLA2, and blocks the interaction between HHLA2 and its receptors. This abrogates the HHLA2-mediated inhibition of T-cell and nature killer (NK) cell activation, which may lead to enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response and NK cell cytotoxicity against cancer cells. HHLA2, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types and a negative regulator of T-cell and NK cell activation.

anti-HIF-1alpha LNA antisense oligonucleotide EZN-2968

A synthetic antisense oligodeoxynucleotide (AS ODN) targeting hypoxia-inducible factor-1alpha (HIF-1alpha) with potential antineoplastic activity. Anti-HIF-1alpha LNA antisense oligonucleotide EZN-2968 hybridizes with HIF-1alpha mRNA and blocks t HIF-1 alpha protein expression, which may result in the inhibition of angiogenesis, the inhibition of tumor cell proliferation, and apoptosis. HIF-1alpha, normally activated in response to hypoxia-induced stress, is a key transcription regulator of a large number of genes important in cellular adaptation to low-oxygen conditions, including angiogenesis, cell proliferation, apoptosis, and cell invasion.

anti-HIV-1 lentiviral vector-expressing sh5/C46 Cal-1

A gene transfer construct composed of a self-inactivating (SIN) lentiviral vector (LV) expressing a short hairpin RNA (shRNA) that targets the human C-C chemokine receptor type 5 (CCR5) mRNA (sh5) and expressing the HIV entry inhibitor C46, with potential anti-human immunodeficiency virus (HIV) type 1 (HIV-1) activity. Upon transduction of the anti-HIV-1 LVsh5/C46 Cal-1 in specified blood cell populations, such as peripheral blood mononuclear cells (PBMCs), hematopoietic stem/progenitor cells (HSPCs) and CD4+ T lymphocytes, the cells express shCCR5 and C46. shCCR5 targets and binds to CCR5 mRNA, which inhibits the expression of CCR5 and prevents binding of the virus to the cellular CCR5 co-receptor. The cell surface expression of the cell membrane-anchored C46 peptide blocks HIV-1 fusion to the cellular membrane. The removal of CCR5 from and the production of C46 in the bone marrow and white blood cells, make the transduced cells resistant to and protect them from HIV-1 entry, infection and replication. HIV-resistant HSPCs could provide long-term protection against latent HIV infection and against HIV-associated cancers. C46 is a membrane-anchored 46-amino acid sequence found in HIV-1 gp41. CCR5 is a HIV-1 co-receptor that mediates HIV attachment and cell entry.

anti-HJV monoclonal antibody DISC-0974

A humanized monoclonal antibody directed against the bone morphogenetic proteins (BMPs) co-receptor hemojuvelin (HJV), with potential to treat anemia of inflammation and other forms of anemia. Upon subcutaneous administration, anti-HJV monoclonal antibody DISC-0974 targets and binds to HJV, preventing it from binding to the hepcidin regulatory ligands BMPs and inhibiting the HJV-mediated signaling pathway. This suppresses hepcidin synthesis and increases iron availability, which may normalize plasma iron levels and increase erythropoiesis. HJV is required for hepcidin production. Hepcidin plays a key role in the homeostasis of systemic iron by restricting iron absorption and inhibiting ferroportin-mediated iron export; it is upregulated during acute and chronic inflammation in response to cytokines and, in certain cancers, may contribute to cancer-associated anemia.

anti-HLA-A*02/NY-ESO-1 bispecific T-cell engager DS-2243a

A T-cell engaging bispecific antibody directed against the tumor-associated antigen (TAA) NY-ESO-1 complexed with human leukocyte antigen (HLA)-A*02 (HLA-A*02) and an antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-HLA-A*02/NY-ESO-1 bispecific T-cell engager DS-2243a targets and binds to an antigen found on cytotoxic T lymphocytes (CTLs) and NY-ESO-1 presented by HLA-A*02 expressed on tumor cells. This activates and redirects CTLs to NY-ESO-1-expressing tumor cells, which results in the CTL-mediated cell death of NY-ESO-1-expressing tumor cells. NY-ESO-1, a cell surface protein expressed in normal fetal and adult testes, is upregulated in a variety of tumor cell types as a HLA-A*02/NY-ESO-1 complex.

anti-HLA-A*02:01/p53 R175H bispecific T-cell engager CLSP-1025

An asymmetric bispecific single-chain diabody (scDb) Fc fusion protein and T-cell engager (TCE) directed against the human TP53 (p53) R175H mutant peptide (p53(R175H)168-176) bound to human leukocyte antigen (HLA)-A*02:01 (HLA-A*02:01) and the T-cell-specific antigen CD3epsilon (CD3e), with potential immunostimulating and antineoplastic activities. Upon administration, anti-HLA-A*02:01/p53 R175H bispecific TCE CLSP-1025 specifically targets and binds to CD3 on cytotoxic T lymphocytes (CTLs) with its anti-CD3 domain and the p53(R175H)168-176 mutant peptide bound to HLA-A*02:01 expressed on tumor cells with its anti-peptide HLA (pHLA) domain. This activates and redirects CTLs to HLA-A*02:01/p53 R175H-expressing tumor cells, which results in the CTL-mediated cell death of these p53 R175H-expressing tumor cells. p53, a tumor suppressor gene, is mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.

Anti-HLA-A2-MAGE-A4/Anti-CD3 Bispecific Antibody RO7444973

A bispecific T-cell engaging antibody directed against both the tumor-associated antigen (TAA) human leukocyte antigen (HLA)-A2-restricted, melanoma-associated antigen A4 (MAGE-A4) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-HLA-A2-MAGE-A4/Anti-CD3 bispecific antibody RO7444973 simultaneously binds to both CD3 on cytotoxic T-lymphocytes (CTLs) and HLA-A2 MAGE-A4 on MAGE-A4-expressing tumor cells. This activates and redirects CTLs to MAGE-A4-expressing tumor cells, which results in the CTL-mediated cell death of MAGE-A4-expressing tumor cells. MAGE-A4 is overexpressed by a variety of cancer cell types.

anti-HLA-A2-WT1/anti-CD3 T-cell engaging bispecific antibody RO7283420

A T-cell receptor (TCR)-like T-cell engaging bispecific antibody (T-BsAb) targeting both the RMFPNAPYL nonapeptide (RMF peptide), which is derived from the intracellular Wilms tumor 1 (WT1; WT-1) and presented on human leukocyte antigen A2 (HLA-A2), and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-HLA-A2-WT1/anti-CD3 T-cell engaging bispecific antibody RO7283420 simultaneously binds to both CD3 on cytotoxic T lymphocytes (CTLs) and the HLA-A2 WT1 complex found on WT1-expressing tumor cells. This activates and redirects CTLs to WT1-expressing tumor cells, which results in the CTL-mediated cell death of WT1-expressing tumor cells. WT1, an intracellular oncoprotein and transcription factor, is overexpressed in a variety of tumor cell types.

anti-HLA-A2/NY-ESO-1 TCR-transduced autologous T lymphocytes

Autologous human peripheral blood T lymphocytes transduced with a lentiviral or retroviral vector encoding a human leukocyte antigen A2 (HLA-A2)-restricted anti-cancer-testis antigen 1 (NY-ESO-1) T-cell receptor (TCR) gene, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and re-introduction into the patient, the anti-HLA-A2/NY-ESO-1 TCR-transduced autologous T lymphocytes recognize and bind to NY-ESO-1/HLA-A2-positive tumor cells. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types.

anti-HLA-DR monoclonal antibody IMMU-114

A humanized IgG4 monoclonal antibody that targets the human leukocyte antigen HLA-DR, with potential antineoplastic activity. Upon administration, anti-HLA-DR monoclonal antibody IMMU-114 binds to HLA-DR on HLA-DR-expressing tumor cells and, although the exact mechanism has yet to be fully elucidated, appears to induce hyperactivation of ERK- and JNK-dependent mitogen activated protein kinase signaling pathways. This may lead to mitochondrial membrane depolarization and reactive oxygen species (ROS) generation. This eventually leads to an induction of tumor cell apoptosis and a reduction in tumor cell proliferation. IMMU-14 may be beneficial in the treatment of graft versus host disease (GVHD) as it appears to suppress T-lymphocyte proliferation and natural killer (NK) cell activation. As the Fc region of the orgnial IgG1 MoAb was replaced with the IgG4 isotype, IMMU-114 does not induce a complement cytotoxicity (CDC) or an antibody-dependent cell-mediated cytotoxicity (ADCC) . HLA-DR, a MHC class II molecule, is found on various B-cell hematologic malignancies and in autoimmune diseases as well as on normal cells.

anti-HLA-G antibody TTX-080

An antibody targeting HLA-G histocompatibility antigen, class I, G (human leukocyte antigen G; HLA-G), with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, the anti-HLA-G antibody TTX-080 targets and binds to HLA-G, thereby preventing the binding of HLA-G to its inhibitory receptors on a variety of immune cells, such as natural killer cells (NKs), T and B lymphocytes, and dendritic cells (DCs). This may prevent the HLA-G-mediated immune suppression, thereby activating both innate and adaptive immune responses. This may activate anti-tumor immune responses. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion.

anti-HLA-G monoclonal antibody UCB4594

An afucosylated humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting HLA-G histocompatibility antigen, class I, G (human leukocyte antigen G; HLA-G), with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, the anti-HLA-G monoclonal antibody UCB4594 targets and binds to HLA-G, thereby preventing the binding of HLA-G to its inhibitory receptors immunoglobin-like transcript (ILT) 2 and ILT4 on a variety of immune cells, such as natural killer cells (NKs), T and B lymphocytes, and dendritic cells (DCs). This may prevent HLA-G-mediated immune suppression, thereby activating both innate and adaptive immune responses. This may activate anti-tumor immune responses. In addition, UCB4594 induces direct NK cell-mediated killing of tumor cells, complement dependent lysis and antibody-dependent cellular phagocytosis (ADCP). HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion.

anti-HLA-G/CD3 bispecific antibody JNJ-78306358

A bispecific antibody targeting the tumor-associated antigen (TAA) HLA-G histocompatibility antigen, class I, G (human leukocyte antigen G; HLA-G) and the CD3 antigen found on T lymphocytes, with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, the anti-HLA-G/CD3 bispecific antibody JNJ-78306358 targets and binds to both CD3 on cytotoxic T lymphocytes (CTLs) and HLA-G found on HLA-G-expressing tumor cells. This activates and redirects CTLs to HLA-G-expressing tumor cells, which results in the CTL-mediated cell death of HLA-G-expressing tumor cells. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion. It inhibits immune responses by binding to its inhibitory receptors on a variety of immune cells, such as natural killer cells (NKs), T and B lymphocytes, and dendritic cells (DCs).

anti-HLA-G/CD3 bispecific antibody RO7515629

A bispecific antibody targeting the tumor-associated antigen (TAA) histocompatibility antigen, class I, G (human leukocyte antigen G; HLA-G) and the CD3 antigen found on T lymphocytes, with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, the anti-HLA-G/CD3 bispecific antibody RO7515629 targets and binds to both CD3 on cytotoxic T lymphocytes (CTLs) and HLA-G found on HLA-G-expressing tumor cells. This activates and redirects CTLs to HLA-G-expressing tumor cells, which results in the CTL-mediated cell death of HLA-G-expressing tumor cells. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor cell types and plays a key role in cancer immune evasion. It inhibits the immune responses by binding to its inhibitory receptors on a variety of immune cells, such as natural killer cells (NKs), T and B lymphocytes, and dendritic cells (DCs).

anti-HPV16 TCR-engineered T cells CRTE7A2-01

A preparation of T lymphocytes that has been genetically modified to express a T-cell receptor (TCR) specific for an as of yet not identified viral oncoprotein(s) of human papillomavirus type 16 (HPV16), with potential antineoplastic activity. Upon intravenous administration, the anti-HPV16 TCR-engineered T cells CRTE7A2-01 specifically recognize and bind to the HPV16 oncoprotein(s) expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing the HPV16 oncoprotein(s).

anti-human chorionic gonadotropin vaccine

A peptide vaccine consisting of the whole or partial beta subunit of human chorionic gonadotrophin hormone (hCG), linked to an adjuvant carrier of bacterial or viral origin, with anti-fertility activity. Anti-human chorionic gonadotropin vaccine blocks the activity of hCG which is naturally produced by the trophectoderm of the pre-implantation embryo within a few days of fertilization. hCG is required for the maintenance of the corpus luteum in the ovary thus ensuring its continued production of progesterone, which is required for the successful completion of implantation of the blastocyst. Without progesterone, the corpus luteum regresses, and menstruation is initiated.

anti-human cytomegalovirus monoclonal antibody combination CSJ-148

A combination agent composed of two human monoclonal antibodies against the human cytomegalovirus (HCMV), LJP538 and LJP539, with potential immunomodulating activity. Upon administration of CSJ-148, both LJP538 and LJP539 bind to and inhibit the function of viral HCMV glycoproteins that are essential for HCMV infection; LJP538 targets and binds to glycoprotein B (gB) and LJP539 targets and inhibits the pentameric complex, consisting of glycoproteins gH, gL, UL128, UL130, and UL131. Human cytomegalovirus (HCMV) can cause significant disease in immunocompromised patients.

anti-human GITR monoclonal antibody AMG 228

An agonistic anti-human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor receptor superfamily, member 18; TNFRSF18; GITR; CD357) humanized monoclonal antibody, with potential immune checkpoint modulating activity. Anti-human GITR monoclonal antibody AMG 228 binds to and activates GITRs found on multiple types of T cells. This stimulates the immune system, induces both the activation and proliferation of tumor-antigen-specific T-effector cells (Teffs), and suppresses the function of activated T-regulatory cells (Tregs). This leads to immune-mediated tumor cell eradication though a cytotoxic T-lymphocyte (CTL) response. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress Teffs and suppress T-cell receptor (TCR) signaling.

anti-human GITR monoclonal antibody TRX518

A humanized, Fc disabled anti-human glucocorticoid-induced tumor necrosis factor receptor (GITR) monoclonal antibody (MoAb) with immunomodulating activity. Anti-human GITR MoAb TRX518 blocks the interaction of GITR, found on multiple types of T cells, with its ligand, thereby inducing both the activation of tumor-antigen-specific T effector cells, as well as abrogating the suppression induced by inappropriately activated T-regulatory cells. This agent is shown to act synergistically with chemotherapeutic drugs in multiple cancer models.

anti-ICOS agonist monoclonal antibody BMS-986226

An agonistic monoclonal antibody that recognizes inducible T-cell co-stimulator (ICOS; CD278), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ICOS agonist monoclonal antibody BMS-986226 targets and binds to ICOS expressed on certain T cells. This stimulates ICOS-mediated signaling, induces proliferation of ICOS-positive T cells, enhances cytotoxic T lymphocyte (CTL) survival and augments the CTL-mediated immune response against tumor cells. ICOS, a T-cell-specific, CD28-superfamily co-stimulatory molecule and immune checkpoint protein, is normally expressed on certain activated T cells and plays a key role in the proliferation and activation of T cells.

anti-ICOS monoclonal antibody MEDI-570

An Fc-optimized humanized immunoglobulin (Ig) G1 monoclonal antibody (MoAb) directed against the inducible T-cell co-stimulator (ICOS, CD278), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-ICOS MoAb MEDI-570 targets and binds to ICOS expressed on tumor infiltrating CD4-positive T cells. This prevents the interaction between ICOS-positive T cells and plasmacytoid dendritic cells (pDCs), which express the ICOS ligand (ICOSL). Blocking ICOS activation prevents the pDC-induced proliferation and accumulation of regulatory ICOS-positive T cells (ICOS+ Tregs) and inhibits interleukin-10 (IL-10) secretion by CD4+ infiltrating T cells. This may abrogate Treg-mediated immune suppression and may enhance cytotoxic T-lymphocyte (CTL)-mediated immune responses against tumor cells. Fc optimization enhances antibody-dependent cellular cytotoxicity (ADCC). ICOS, a T-cell specific, CD28-superfamily costimulatory molecule and immune checkpoint protein, plays a key role in the proliferation and activation of T-cells. It is normally expressed on both activated CD4+ T cells, which is a subset of memory T cells (Tm), and follicular helper T cells (Tfh). ICOS is highly expressed on Tregs infiltrating various tumors and its expression is associated with a poor prognosis; ICOS-positive Tregs play a key role in immune suppression and tumor immune evasion.

anti-IGF-1R recombinant monoclonal antibody BIIB022

A recombinant, human monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. Anti-IGF-1R recombinant monoclonal antibody BIIB022 binds to membrane-bound IGF-1R, preventing binding of the ligand IGF-1 and the subsequent triggering of the PI3K/Akt signaling pathway; inhibition of this survival signaling pathway may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. The activation of IGF-1R, a tyrosine kinase and a member of the insulin receptor family, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been highly implicated in tumorigenesis and metastasis.

anti-IGF1/2 monoclonal antibody MEDI-573

A humanized monoclonal antibody directed against insulin-like growth factors 1 and 2 (IGF-1/2) with potential antineoplastic activity. Anti-IGF1/2 monoclonal antibody MEDI-573 inhibits IGF1- and IGF2-stimulated activation of membrane-bound IGF receptors and the subsequent triggering of proliferation and survival signaling pathways. This may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF1/2 ligands stimulate cell proliferation, enable oncogenic transformation, and suppress apoptosis; IGF1/2 signaling has been highly implicated in tumorigenesis and metastasis.

anti-IGFBP2 plasmid DNA vaccine AST-201

A polyepitope plasmid DNA therapeutic cancer vaccine containing the mammalian expression vector pUMVC3 encoding multiple epitopes derived from tumor-associated antigens (TAAs): human insulin-like growth factor-binding protein 2 (IGFBP2), with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination, anti-IGFBP2 plasmid DNA vaccine AST-201 enters cells which process the plasmid, and express the epitopes and present them to antigen-presenting cells (APCs). This activates the immune system to mount a combined response from specific T-helper type 1 (Th1) cells, memory T-cells and cytotoxic T lymphocytes (CTL) against IGFBP2-expressing tumor cells. IGFBP2, overexpressed in certain tumor cell types, plays a key role in cellular proliferation and survival.

anti-IGSF8 monoclonal antibody GV20-0251

A human, Fc-attenuated immunoglobulin G1 (IgG1) monoclonal antibody targeting the immune checkpoint immunoglobulin superfamily member 8 (IGSF8; PGRL; PG regulatory-like protein, KCT-4, CD81 partner 3; LIR-D1; KASP; KAI/CD82 associated protein; EWI-2; Glu-Trp-Ile EWI motif-containing protein 2), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-IGSF8 monoclonal antibody GV20-0251 targets and binds to IGSF8 expressed on various immune cells, thereby preventing the binding of IGSF8 to beta 1 integrins and various tetraspanins. This inhibits IGSF8-mediated signaling and abrogates the IGSF8-mediated inhibition on immune activation. This may stimulate a T-cell-mediated immune response against cancer cells. IGSF8, a transmembrane adhesion protein and member of the Ig super family (IgSF), is an immune inhibitory receptor that plays a key role in cancer cell motility and suppression of T-cell proliferation and activation. It is involved in tumor cell immune evasion and the inhibition of immune responses.

anti-IL-1 alpha monoclonal antibody XB2001

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the inflammatory cytokine interleukin-1 alpha (IL1a), with potential antineoplastic, anti-cachectic and anti-angiogenic activities. Upon administration, anti-IL1a monoclonal antibody XB2001 targets, binds to, and inhibits the activity of IL1a. This may inhibit IL1a-mediated tumorigenesis, angiogenesis and cachexia. IL1a, an inflammatory mediator expressed on monocytes, platelets and overexpressed by certain tumors, plays a key role in the promotion of tumor cell growth, metastasis and invasion. In addition, IL1a mediates metabolic activity, which may cause fatigue, anorexia, and anxiety.

anti-IL-11 monoclonal antibody 9MW3811

A humanized monoclonal antibody directed against interleukin-11 (IL-11), with potential anti-fibrotic and antineoplastic activities. Upon administration, anti-IL-11 monoclonal antibody 9MW3811 targets and binds to IL-11. This prevents the binding of IL-11 to interleukin-11 receptor subunit alpha (IL-11RA), and inhibits IL-11-mediated signaling via the gp130/IL-11RA receptor complex. This may decrease fibrosis and inhibit tumor cell proliferation. IL-11, a member of the IL-6 family of cytokines, is upregulated in some fibro-inflammatory diseases and cancers.

Anti-IL-4/IL-13 Combination Agent QBX258

A combination agent composed of the two human monoclonal antibodies VAK694 (VAK296), targeting interleukin-4 (IL-4), and QAX576, targeting IL-13, that can potentially be used to block signaling mediated by IL-4 and IL-13. Upon intravenous administration of the anti-IL-4/IL-13 co,mbination agent QBX258, the two antibodies VAK694 and QAX576 target and block the activity of the two cytokines IL-4 and IL-13, respectively, which prevents IL-4/IL-13-mediated signaling. In patients with breast cancer related lymphedema (BCRL), this agent may prevent lymphedema-associated effects, such as fibrosis, hyperkeratosis, the deposition of fibroadipose tissue, fluid accumulation, limb swelling, reduction of skin elasticity, and pain. By reducing the excess volume, QBX258 may improve lymphatic and arm functions. The development of lymphedema after lymphatic injury is associated with tissue inflammation, the infiltration of CD4-positive cells and their differentiation to the type 2 helper T-cell (Th2) phenotype. Th2 cells produce IL-4 and IL-13 that play a key role in the development of lymphedema-associated symptoms as well as other Th2-mediated diseases.

anti-IL17A monoclonal antibody CJM112

A human immunoglobulin G1 (IgG1) monoclonal antibody against the pro-inflammatory cytokine interleukin 17A (IL-17A; IL-17), with potential anti-inflammatory activity. Upon subcutaneous administration, anti-IL17A monoclonal antibody CJM112 selectively targets and binds to IL-17A, thereby neutralizing the IL-17A protein. This prevents binding of IL-17A to the IL-17 receptor (IL-17R), and inhibits IL-17A/IL-17R-mediated signaling and inflammation mediated by this pathway. IL-17A is mainly produced by inflammatory T helper 17 cells (Th17), and certain lymphocytes. IL-17A production is upregulated in many immune-mediated inflammatory diseases, such as psoriasis and multiple sclerosis (MS), and plays a key role in the development of inflammation and the immune response.

anti-ILT2 monoclonal antibody AGEN1571

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory immune checkpoint receptor Ig-like transcript 2 (ILT2; leukocyte immunoglobulin-like receptor subfamily B member 1; LILRB1; leukocyte immunoglobulin-like receptor 1; LIR1; monocyte/macrophage immunoglobulin-like receptor 7; MIR-7; CD85j), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-ILT2 monoclonal antibody AGEN1571 targets and binds to ILT2. This prevents the binding of ILT2 ligands, including the immunosuppressive MHC molecule HLA class I histocompatibility antigen, alpha chain G (HLA-G; human leukocyte antigen G), to the ILT2 receptor and prevents ILT2-mediated signaling. This inhibits ILT2-mediated immune suppression, thereby promoting both innate and adaptive immune responses and may result in the activation of anti-tumor immune responses. ILT2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed on both innate and adaptive immune cells. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion.

anti-ILT2 monoclonal antibody BND-22

A humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory immune checkpoint receptor Ig-like transcript 2 (ILT2; leukocyte immunoglobulin-like receptor subfamily B member 1; LILRB1; leukocyte immunoglobulin-like receptor 1; LIR1; monocyte/macrophage immunoglobulin-like receptor 7; MIR-7; CD85j), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ILT2 monoclonal antibody BND-22 targets and binds to ILT2. This prevents the binding of ILT2 ligands, including the immunosuppressive MHC molecule HLA class I histocompatibility antigen, alpha chain G (HLA-G; human leukocyte antigen G), to the ILT2 receptor and prevents ILT2-mediated signaling. This inhibits ILT2-mediated immune suppression, thereby activating both innate and adaptive immune responses. This may activate anti-tumor immune responses. ILT2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed on both innate and adaptive immune cells. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion.

anti-ILT2/anti-ILT4 bispecific antibody PF-07826390

A humanized immunoglobulin G1 (IgG1) bispecific antibody directed against the inhibitory immune checkpoint receptors immunoglobulin (Ig)-like transcript 2 (ILT2; leukocyte immunoglobulin-like receptor subfamily B member 1; LILRB1; leukocyte immunoglobulin-like receptor 1; LIR1; monocyte/macrophage immunoglobulin-like receptor 7; MIR-7; CD85j) and ILT4 (LILRB2; LIR2; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ILT2/anti-ILT4 bispecific antibody PF-07826390 targets and binds to both ILT2 and ILT4. This prevents the binding of ILT2 and ILT4 ligands, including the major histocompatibility complex class I (MHC I) molecules human leukocyte antigen (HLA)-A, HLA-B, HLA-C and HLA-G, to the ILT2 and ILT4 receptors and prevents ILT2- and ILT4-mediated signaling. This inhibits ILT2- and ILT4-mediated immune suppression and may activate both innate and adaptive immune responses, including natural killer (NK) and CD8+ T cell tumor cell killing, and macrophage phagocytosis of tumor cells. ILT2 and ILT4, expressed on myeloid cells in the tumor microenvironment (TME), are upregulated in various cancer types and play an important role in tumor immune evasion. ILT2 is also expressed on various innate and adaptive immune cells including NK cells, B cells and a subset of cytolytic T cells.

anti-ILT2/anti-ILT4 monoclonal antibody NGM707

A humanized, dual antagonist monoclonal antibody directed against the inhibitory immune checkpoint receptors immunoglobulin (Ig)-like transcript 2 (ILT2; leukocyte immunoglobulin-like receptor subfamily B member 1; LILRB1; leukocyte immunoglobulin-like receptor 1; LIR1; monocyte/macrophage immunoglobulin-like receptor 7; MIR-7; CD85j) and ILT4 (LILRB2; LIR2; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ILT2/anti-ILT4 monoclonal antibody NGM707 targets and binds to both ILT2 and ILT4. This prevents the binding of ILT2 and ILT4 ligands, including the major histocompatibility complex class I (MHC I) molecules human leukocyte antigen (HLA)-A, HLA-B, HLA-C and HLA-G, to the ILT2 and ILT4 receptors and prevents ILT2- and ILT4-mediated signaling. This inhibits ILT2- and ILT4-mediated immune suppression and may activate both innate and adaptive immune responses, including natural killer (NK) and CD8+ T-cell tumor cell killing, and macrophage phagocytosis of tumor cells. ILT2 and ILT4, expressed on myeloid cells in the tumor microenvironment (TME), are upregulated in various cancer types and play an important role in tumor immune evasion. ILT2 is also expressed on various innate and adaptive immune cells including NK cells, B cells and a subset of cytolytic T cells.

anti-ILT4 monoclonal antibody

Any monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; LILRB2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d).

anti-ILT4 monoclonal antibody CHS-1000

A Fc-modified humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (LILRB2; ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ILT4 monoclonal antibody CHS-1000 targets and binds to LILRB2. This prevents the binding of LILRB2 ligands HLA-A and HLA-G to their receptor and prevents LILRB2-mediated signaling. This abrogates the immunosuppressive activities of LILRB2 in the tumor microenvironment (TME), promotes re-polarization of suppressive myeloid cells to a pro-inflammatory phenotype, enhances activation of dendritic cells (DCs) and T cells, and increases pro-inflammatory cytokine secretion leading to tumor cell death. ILILRB2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, DCs and granulocytes, and in certain tumors. It plays a key role in tumor immune evasion.

anti-ILT4 monoclonal antibody MK-4830

A human monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; LILRB2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-ILT4 monoclonal antibody MK-4830 targets and binds to ILT4. This prevents the binding of ILT4 ligands to their receptor and prevents ILT4-mediated signaling. This abrogates the immunosuppressive activities of ILT4 in the tumor microenvironment (TME), activates the expression of pro-inflammatory cytokines, including GM-CSF and tumor necrosis factor alpha (TNFalpha), and enhances a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. ILT4, plays a key role in tumor immune evasion. ILT4, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and certain tumor cells.

anti-ILT4/anti-PD-L1 bispecific antibody SPX-303

A bispecific antibody directed against both the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; LILRB2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-ILT4/anti-PD-L1 bispecific antibody SPX-303 targets and binds to both ILT4 and PD-L1. The binding of SPX-303 to ILT4 prevents activation by its ligands, including the major histocompatibility complex class I (MHC I) molecules human leukocyte antigen (HLA)-A, HLA-B, HLA-C and HLA-G, and inhibits ILT4-mediated signaling. This abrogates the immunosuppressive activities of ILT4 in the tumor microenvironment (TME), activates the expression of pro-inflammatory cytokines, including GM-CSF and tumor necrosis factor alpha (TNFalpha), and enhances a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. The binding of SPX-303 to PD-L1 prevents the binding to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1/PD-L1-mediated signaling, and inhibits the PD-1/PD-L1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a CTL-mediated immune response against tumor cells. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity. ILT4, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and certain tumor cells; it also plays a role in tumor evasion.

anti-immunoglobulin-beta CAR T Cells

A preparation of T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) targeting immunoglobulin-beta (Igb), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-Igb CAR T cells are directed to, specifically bind to, and induce selective toxicity in Igb antigen-expressing tumor cells.

anti-inflammatory antibody ALXN1007

A proprietary antibody that targets the complement inflammatory pathway with potential immunomodulating and anti-inflammatory activities. Upon intravenous administration, anti-inflammatory antibody ALXN1007 modulates the complement inflammatory pathway through binding to an as of yet undisclosed target. This may help in the treatment of certain inflammatory-mediated disorders, such as antiphospholipid syndrome (APS). This agent may also influence the progression of graft-versus-host disease (GvHD).

anti-inflammatory/antimicrobial/analgesic aqueous mouth rinse

A water-based proprietary mouthwash with anti-inflammatory, antimicrobial and analgesic activities. Upon rinsing with this mouthwash, the unspecified ingredients may help prevent or reduce the symptoms and severity of mucositis.

anti-inhibitor coagulant complex

A sterile, freeze dried fraction of human plasma containing factor VIII coagulant antigen and both the inactive and active forms of coagulation factors II (prothrombin), VII, IX and X, with factor VIII (FVIII) inhibitor bypassing activity. Upon reconstitution and infusion, anti-inhibitor coagulant complex is able to, either directly or indirectly, activate thrombin, which facilitates the formation of fibrin from fibrinogen. This results in clot formation. In hemophilic patients, antibodies formed against factor VIII prevent factor VIII activation and impair thrombin formation; anti-inhibitor coagulant complex can both overcome the inhibitory activity of the antibodies and facilitate hemostasis in hemophilic patients.

anti-integrin alphaV/beta8 monoclonal antibody CRB-601

A humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against integrin alphaV/beta8 (aVb8), with potential antineoplastic activity. Upon administration, anti-integrin aVb8 monoclonal antibody CRB-601 targets and binds to integrin aVb8. This prevents the binding of integrin aVb8 to latent human transforming growth factor (TGF)-beta (L-TGFb) and inhibits the activation of L-TGFb complexes, thereby preventing TGFb-mediated signaling. This abrogates TGFb-mediated immunosuppression, enhances anti-tumor immunity in the tumor microenvironment (TME) and promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGFb-dependent proliferation of cancer cells. Integrin aVb8 plays a key role in tumor initiation, growth, and progression through TGF-b activation. It is expressed in a variety of tumor cell types and is associated with poor prognosis.

Anti-integrin Beta-1 Monoclonal Antibody OS2966

A humanized monoclonal antibody directed against the human integrin receptor beta-1 subunit (CD29), with potential antineoplastic activity. Upon administration, anti-integrin beta-1 monoclonal antibody OS2966 targets and binds to integrin beta-1 on the surface of tumor cells and macrophages in the tumor microenvironment (TME), thereby preventing integrin beta-1-mediated activation of downstream signaling pathways. This may include the blockade of the binding of integrin beta-1 to the effector kinase focal adhesion kinase (FAK), preventing FAK-mediated activation of Stat1 and Akt. This may inhibit tumor cell proliferation, invasion and migration in integrin beta-1-overexpressing tumor cells. Integrin beta-1, the dominant subunit in all four classes of integrin receptors, plays an important role in tumor cell proliferation, invasion, and drug resistance.

anti-integrin beta-6/MMAE antibody-drug conjugate SGN-B6A

An antibody-drug conjugate (ADC) composed of a humanized antibody targeting integrin beta-6 and conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-integrin beta-6/MMAE ADC SGN-B6A targets and binds to integrin beta-6 on the surface of tumor cells. Following internalization of SGN-B6A and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in integrin beta-6-expressing tumor cells. Integrin beta-6 is a subunit of integrin alpha-V beta-6 (aVb6). Integrin aVb6, a cell adhesion and signaling receptor, is upregulated in certain cancer cell types and has been associated with increased proliferation, migration and invasion of tumor cells.

anti-integrin monoclonal antibody-DM4 immunoconjugate IMGN388

An immunoconjugate consisting of an anti-integrin monoclonal antibody covalently attached to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Anti-integrin monoclonal antibody-DM4 immunoconjugate IMGN388 binds to tumor cell surface integrins; upon internalization, the DM4 moiety is released from the immunoconjugate, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in inhibition of cell division and cell growth of integrin-expressing tumor cells. Integrins, a class of transmembrane cell surface receptors, link the extracellular matrix (ECM) to intracellular signaling pathways that control cell proliferation and differentiation.

anti-interleukin 1 beta monoclonal antibody FL-101

A monoclonal antibody targeting the human proinflammatory cytokine interleukin-1 beta (IL-1b), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, anti-IL-1b monoclonal antibody FL-101 targets and binds to IL-1b and prevents the binding of IL-1b to the IL-1 receptor. This inhibits IL-1b-mediated signaling pathways, and suppresses inflammatory responses, tumorigenesis and angiogenesis mediated by IL-1b. IL-1b plays a key role in inflammation, which is present in various disease states including cancers. IL-1b-mediated signaling pathways include MAPK, cyclooxygenase and nuclear factor kappa B (NF-kB) pathways, which may lead to macrophage activation, intra-tumoral accumulation of immunosuppressive myeloid cells, and tumor growth, invasiveness, metastasis, and angiogenesis.

anti-interleukin-1 alpha monoclonal antibody MABp1

A human IgG1 monoclonal antibody targeting the inflammatory cytokine interleukin-1 alpha (IL1a) with potential antineoplastic, anti-cachectic and anti-angiogenic activities. Anti-IL1a monoclonal antibody MABp1 targets and binds to IL1a and prevents IL1a activity. This prevents IL1a-mediated tumorigenesis and angiogenesis. In addition, MABp1 abrogates IL1a-mediated cachexia. IL1a, an inflammatory mediator expressed on monocytes, platelets and overexpressed by certain tumors, plays a key role in the promotion of tumor cell growth, metastasis and invasion. In addition, IL1a stimulates metabolic activity in the central nervous system.

anti-interleukin-1 beta monoclonal antibody AK114

A monoclonal antibody targeting the human proinflammatory cytokine interleukin-1 beta (IL-1b), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, anti-IL-1b monoclonal antibody AK114 targets and binds to IL-1b and prevents the binding of IL-1b to the IL-1 receptor. This inhibits IL-1b-mediated signaling pathways, and suppresses inflammatory responses, tumorigenesis and angiogenesis mediated by IL-1b. IL-1b plays a key role in inflammation, which is present in various disease states including cancers. IL-1b-mediated signaling pathways include MAPK, cyclooxygenase and nuclear factor kappa B (NF-kB) pathways, which may lead to macrophage activation, intra-tumoral accumulation of immunosuppressive myeloid cells, and tumor growth, invasiveness, metastasis, and angiogenesis.

anti-interleukin-13 receptor alpha 2 allogeneic CAR T cells YYB-103

A preparation of T lymphocytes genetically modified to express a chimeric antigen receptors (CAR) specific for interleukin-13 receptor alpha 2 (IL13Ra2), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-IL13Ra2 CAR T cells YYB-103 target and bind to IL13Ra2 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing IL13Ra2. IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell types including glioblastoma multiforme (GBM); it is associated with increased invasiveness of tumor cells.

anti-interleukin-2 receptor subunit gamma monoclonal antibody REGN7257

A monoclonal antibody targeted against interleukin-2 (IL-2) receptor subunit gamma (IL2RG; CD132; cytokine receptor common subunit gamma; gamma chain; gc), with potential immunomodulatory activity. Upon administration, anti-IL2RG monoclonal antibody REGN7257 targets and binds to the gamma subunit of the human IL-2 receptor (IL-2R) expressed on the surface of activated T lymphocytes, thereby inhibiting IL-2 binding and IL-2-mediated T-cell activation. This may block T-cell-mediated immune responses. IL2RG plays a role in both immune responses and interleukin signaling.

anti-IRF4 antisense oligonucleotide ION251

An antisense oligonucleotide (ASO) targeting the interferon regulatory factor 4 (IRF4) mRNA, with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-IRF4 ASO ION251 hybridizes with IRF4 mRNA, which blocks translation of the IRF4 protein. Reduction of IRF4 levels prevents the expression of IRF4-controlled tumor promoter genes, and may enhance tumor cell apoptosis and prevent T-cell exhaustion. IRF4, a transcription factor expressed in lymphocytes and essential for plasma cell differentiation, is involved in immune cell development and plays a key role in T-cell functions. It is overexpressed in certain tumor cell types and is a key regulator of multiple genes controlling tumor cell survival.

anti-K-RAS G12D mTCR-transduced autologous peripheral blood lymphocytes

Autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding for an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine (Gly, G) to aspartic acid (Asp, D) point mutation at position 12 (G12D) variant of K-RAS (KRAS), with potential immunomodulating and antineoplastic activities. HLA-A1101-positive PBLs are harvested from a K-RAS G12D-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12D mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12D mTCR-expressing PBLs target and bind to K-RAS G12D-overexpressing tumor cells, which results in both cytokine secretion, including interferon-gamma (IFN-g), and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.

anti-K-RAS G12V mTCR-transduced autologous peripheral blood lymphocytes

Autologous peripheral blood lymphocytes (PBLs) transduced with an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine to valine point mutation at position 12 (G12V) variant of K-RAS, with potential antineoplastic activity. HLA-A1101 positive PBLs are harvested from a K-RAS G12V-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12V mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12V mTCR-expressing PBLs target and bind to K-RAS G12V-overexpressing tumor cells, which results in both cytokine secretion and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.

anti-KAAG1 antibody-drug conjugate ADCT-901

An antibody-drug conjugate (ADC) composed of 3A4, a humanized monoclonal antibody directed against human kidney associated antigen 1 (KAAG1; RU2) and conjugated, through a cathepsin-cleavable linker, to SG3199, a cytotoxic pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-KAAG1 ADC ADCT-901, the 3A4 moiety targets and binds to KAAG1, which is expressed on the surfaces of a variety of cancer cell types. Upon endocytosis and enzymatic cleavage by cathepsin, free PBD is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing KAAG1-expressing cancer cells. KAAG1, overexpressed by certain tumor cell types, plays a key role in tumor cell proliferation. Its expression on healthy tissue is very restricted.

anti-KIR monoclonal antibody IPH 2101

A human monoclonal antibody directed against the human inhibitory killer IgG-like receptor (KIR) with potential immunostimulating and antineoplastic activities. Anti-KIR monoclonal antibody IPH 2101 binds to the KIR receptor expressed on human natural killer (NK) cells, which may prevent KIR-mediated inhibition of NK cells and permit NK cell-mediated anti-tumor cytotoxicity. KIRs are surface glycoproteins that bind to major histocompatibility complex (MHC)/human leukocyte antigen (HLA) class I subtypes on target cells; binding of KIRs inhibits NK cell-mediated cytotoxicity.

anti-KIR3DL3 monoclonal antibody NPX267

A monoclonal antibody directed against human killer cell immunoglobulin-like receptor 3DL3 (killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 3; KIR3DL3), an inhibitory receptor for human endogenous retrovirus-H long terminal repeat-associating protein 2 (HHLA2; B7 homolog 7; B7-H7), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-KIR3DL3 monoclonal antibody NPX267 binds to KIR3DL3 expressed on T cells and natural killer (NK) cells and prevents the binding of KIR3DL3 to HHLA2 expressed on tumor cells. This abrogates the KIR3DL3/HHLA2-mediated inhibition of T-cell and NK-cell activation in the tumor microenvironment (TME), which may lead to enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response and NK cell cytotoxicity against cancer cells. HHLA2, a member of the B7 family of immune modulators, is upregulated in a variety of tumor cell types. The KIR3DL3-HHLA2 pathway is an immunosuppressive pathway and a negative regulator of T-cell and NK-cell activation.

anti-KLK2 CAR T cells JNJ-75229414

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting human kallikrein-2 (hK2; KLK2) expressed on tumor cells, with potential immunostimulating and antineoplastic activities. Upon administration, anti-KLK2 CAR T cells JNJ-75229414 target and bind to KLK2-expressing tumor cells, thereby inducing selective toxicity in KLK2-expressing tumor cells. KLK2 is overexpressed in certain tumors, including prostate adenocarcinoma.

anti-KLK2/CD3 bispecific antibody JNJ-78278343

A T-cell-redirecting agent and humanized immunoglobulin (Ig) G1 bispecific antibody targeting both human kallikrein-2 (hK2; KLK2) expressed on tumor cells and the CD3 receptor complex expressed on T cells, with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, anti-KLK2/CD3 bispecific antibody JNJ-78278343 binds to both CD3 on T cells and KLK2 on KLK2-expressing tumor cells. The resulting cross-linkage activates and redirects T cells to KLK2-expressing tumor cells. This results in T-cell-mediated lysis of KLK2-expressing tumor cells. KLK2 is overexpressed in certain tumors, including prostate adenocarcinoma.

anti-KSP/anti-VEGF siRNAs ALN-VSP02

A lipid nanoparticle formulation containing two small interfering RNAs (siRNAs) for kinesin spindle protein (KSP) and vascular endothelial growth factor (VEGF) with potential antitumor activity. Upon intravenous administration, the siRNAs in KSP/VEGF siRNAs ALN-VSP02ALN bind to both KSP and VEGF messenger RNAs (mRNAs), preventing translation of KSP and VEGF proteins; this may result in growth inhibition of tumor cells that overexpress KSP and VEGF. VEGF and KSP are upregulated in many tumor cells and play an important role in tumor proliferation and survival.

anti-LAG-3 monoclonal antibody

Any monoclonal antibody directed against the antigen lymphocyte-activation gene 3 (LAG-3; CD223).

anti-LAG-3 monoclonal antibody GLS-012

A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody GLS-012 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti-LAG-3 monoclonal antibody IBI-110

A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody IBI110 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti-LAG-3 monoclonal antibody LAG525

A humanized monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene-3 (LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-LAG-3 monoclonal antibody LAG525 binds to LAG-3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF) and expressed on various immune cells, negatively regulates cellular proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti-LAG-3 monoclonal antibody LBL-007

A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody LBL-007 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti-LAG-3 monoclonal antibody Sym022

A recombinant, human Fc-inert monoclonal antibody targeting lymphocyte-activation gene 3 protein (LAG-3; LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, monoclonal antibody Sym022 binds to human LAG-3 and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHCII) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHCII binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Additionally, Sym022 decreases LAG-3 surface levels through internalization and shredding. LAG-3 plays a key role in the activation of T cells and natural killer (NK) cells.

anti-LAG-3/anti-PD-L1 bispecific antibody IBI323

A recombinant, bispecific antibody directed against two immune checkpoint proteins, the inhibitory receptor lymphocyte activation gene 3 protein (LAG-3; LAG3) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3/anti-PD-L1 bispecific antibody IBI323 simultaneously targets and binds to LAG-3 expressed on T cells in the tumor microenvironment (TME) and PD-L1 expressed on tumor cells. This prevents LAG-3- and PD-L1-mediated signaling, reverses T-cell inactivation, activates the immune system and enhances cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune responses against PD-L1-expressing tumor cells, which together lead to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression is associated with tumor-mediated immune suppression. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to its receptor programmed death 1 (PD-1; PDCD1; CD279) on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-LAG-3/PD-1 bispecific antibody INCA32459

A human immunoglobulin G1 (IgG1) Fc-silenced bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279; programmed death 1) and lymphocyte activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3/PD-1 bispecific antibody INCA32459 targets and binds to both PD-1 and LAG-3 expressed on T cells and inhibits PD-1- and LAG-3-mediated downregulation of T-cell activation and proliferation. This may lead to cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1 and LAG-3 play key roles in suppressing T-cell activation and proliferation.

anti-LAG-3/PD-L1 bispecific antibody FS118

A bispecific antibody directed against two immune checkpoint proteins, the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. FS118 is generated by incorporating an anti-LAG-3 Fc-region with antigen binding (Fcab) into a PD-L1-specific antibody. Upon administration, FS118 simultaneously targets and binds to LAG3 expressed on T-cells in the tumor microenvironment (TME) and PD-L1 expressed on tumor cells. This prevents LAG3- and PD-L1-mediated signaling, reverses T-cell inactivation, activates the immune system and enhances cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune responses against PD-L1-expressing tumor cells, which together lead to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF) negatively regulates both proliferation and activation of T-cells. Its expression is associated with tumor-mediated immune suppression. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to its receptor programmed death 1 (PD-1; PDCD1; CD279) on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.

anti-LAG-3/TIGIT bispecific antibody ZGGS15

A bispecific antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223) and the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3/TIGIT bispecific antibody ZGGS15 targets, binds to and blocks LAG-3 expressed by tumor infiltrating lymphocytes (TILs), thereby preventing the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. In addition, ZGGS15 simultaneously targets and binds to TIGIT expressed on various immune cells, particularly on TILs, thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to further exert a T-cell-mediated immune response against cancer cells. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression on TILs is associated with tumor-mediated immune suppression. TIGIT, a member of the IgSF and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion.

anti-LAG3 monoclonal antibody TSR-033

A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-LAG3 monoclonal antibody TSR-033 binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.

anti-LAIR1 monoclonal antibody NC525

A humanized immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against leukocyte-associated immunoglobulin-like receptor 1 (LAIR1; LAIR-1; CD305), with potential antineoplastic activity. Upon administration, anti-LAIR1 monoclonal antibody NC525 targets, binds to and inhibits LAIR1-mediated downstream survival signaling. In addition, NC525 induces Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). This inhibits survival of LAIR1-expressing acute myeloid leukemia (AML) leukemic stem cells (LSCs) and blast cells, and decreases tumor cell proliferation. LAIR1, an immune inhibitory checkpoint receptor, is overexpressed in AML LSCs and blast cells while having a minimal expression on normal, healthy hematopoietic stem cells (HSCs.). LAIR1 plays a key role in mediating survival signaling in these tumor cells.

anti-LAIR1 monoclonal antibody NGM438

A monoclonal antibody directed against the collagen-binding immune inhibitory receptor leukocyte-associated immunoglobulin-like receptor 1 (LAIR1; LAIR-1; CD305), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAIR1 monoclonal antibody NGM438 targets, binds to and blocks LAIR1, thereby preventing its interaction with tumor-associated and stromal-derived collagens and the formation of the stromal checkpoint LAIR1-collagen complex. This may inhibit LAIR1-collagen complex-mediated downstream signaling pathways and abrogates LAIR1-collagen complex-mediated myeloid cell immune suppression and inhibition of antitumor immunity. This may also inhibit the physical exclusion of immune cells from the tumor by the LAIR1-collagen complex and enhance T-cell infiltration of the tumor. LAIR1, an immune inhibitory receptor expressed on immune cells and upregulated in various cancers along with stromal-derived collagens, plays an important role in tumor infiltration, immunosuppression and immune tolerance.

anti-LAMP1 antibody-drug conjugate SAR428926

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against lysosome-associated membrane protein 1 (LAMP1) conjugated, via the disulfide-containing cleavable linker N-succinimidyl-4-(2-pyridyldithio)butyrate (SPDB), to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. Upon administration of anti-LAMP1 ADC SAR428926, the anti-LAMP1 monoclonal antibody moiety targets and binds to the cell surface antigen LAMP1. After antibody-antigen interaction and internalization, the SPDB linker is selectively cleaved by proteases in the cytosol and the DM4 moiety is released. DM4 binds to tubulin and disrupts microtubule assembly/disassembly dynamics, thereby inhibiting both cell division and cell growth of LAMP1-expressing tumor cells. LAMP1, overexpressed on a variety of cancer cells, plays a key role in cell-cell adhesion and migration. The SPDB linker is resistant to cleavage in the bloodstream, which may increase stability and reduce toxicity.

anti-latent TGF-beta 1 monoclonal antibody SRK-181

A monoclonal antibody directed against latent human transforming growth factor (TGF)-beta 1 (TGFb1; TGF-b1), with potential antineoplastic activity. Upon administration, anti-latent TGFb1 monoclonal antibody SRK-181 specifically targets, binds to, and inhibits the activation of latent TGFb1 complexes, thereby preventing TGFb1-mediated signaling. This abrogates TGFb1-mediated immunosuppression, enhances anti-tumor immunity in the tumor microenvironment (TME) and promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGFb1-dependent proliferation of cancer cells. The TGF-beta signaling pathway is often deregulated in tumors and plays a key role in the regulation of cell growth, differentiation, apoptosis, motility, invasion, and angiogenesis. It plays a key role in immunosuppression in the TME. TGFb1 is the predominant isoform in many tumors.

anti-latent TGFb1 monoclonal antibody RO7496353

A monoclonal antibody directed against latent human transforming growth factor (TGF)-beta 1 (TGFb1; TGF-b1), with potential antineoplastic activity. Upon administration, anti-latent TGFb1 monoclonal antibody RO7496353 targets, binds to, and inhibits the activation of latent TGFb1 complexes, thereby preventing TGFb1-mediated signaling. This abrogates TGFb1-mediated immunosuppression, enhances anti-tumor immunity in the tumor microenvironment (TME) and promotes a cytotoxic T lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGFb1-dependent proliferation of cancer cells. The TGF-beta signaling pathway is often deregulated in tumors and plays a key role in the regulation of cell growth, differentiation, apoptosis, motility, invasion, and angiogenesis. It plays a key role in immunosuppression in the TME. TGFb1 is the predominant isoform in many tumors.

anti-Lewis B/Lewis Y monoclonal antibody GNX102

A humanized monoclonal antibody directed against human tumor-associated carbohydrate antigens (TACAs) Lewis B (LeB) and Lewis Y (LeY), with potential antineoplastic activity. Upon administration, anti-LeB/LeY monoclonal antibody GNX102 binds to branched LeB and LeY glycans, which may induce an antibody-dependent cellular cytotoxicity (ADCC) response against LeB- and LeY-expressing tumor cells. LeB and LeY antigens, tetrasaccharides with low to moderate expression in monomeric form in normal adult tissues, is overexpressed in branched form in multiple forms of cancers.

anti-LeY-CAR-transduced autologous T lymphocytes

Genetically modified, autologous T lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Lewis-Y (LeY), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-LeY-CAR-transduced autologous T lymphocytes specifically target and induce selective toxicity in LeY-expressing tumor cells. LeY, a difucosylated carbohydrate antigen, is overexpressed by a variety of cancer cell types.

anti-LGR5 monoclonal antibody BNC101

A humanized monoclonal antibody targeting leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5), with potential antineoplastic activity. Upon administration, the anti-LGR5 humanized monoclonal antibody BNC101 targets and binds to LGR5, thereby inhibiting LGR5-mediated signal transduction pathways. This prevents proliferation of LGR5-expressing tumor cells. LGR5, a member of the Wnt signaling pathway, is a cancer stem cell (CSC) receptor overexpressed on certain cancer cells; it plays a key role in CSC proliferation and survival.

anti-LILRB monoclonal antibody ADA-011

A monoclonal antibody targeting the leukocyte immunoglobulin-like receptors B (LILRB) immune checkpoint receptor family, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, anti-LILRB monoclonal antibody ADA-011 targets, binds to and inhibits LILRB family members and their downstream signaling pathways. This may restore immune function and anti-tumor immune responses. The LILRB receptor family is a family of inhibitory immune checkpoint receptors that negatively regulates immune activation and plays an important role in immune evasion. Various LILRBs are expressed on certain types of cancer cells and play a key role in cancer development.

anti-LILRB2 monoclonal antibody BMS-986406

A monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (LILRB2; ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-LILRB2 monoclonal antibody BMS-986406 targets and binds to LILRB2. This prevents the binding of LILRB2 ligands to their receptor and prevents LILRB2-mediated signaling. This abrogates the immunosuppressive activities of LILRB2 in the tumor microenvironment (TME), activates the expression of pro-inflammatory cytokines, including GM-CSF and tumor necrosis factor alpha (TNFalpha), and enhances a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. LILRB2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and in certain tumors, and plays a key role in tumor immune evasion.

anti-LILRB2 monoclonal antibody IO-108

A monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (LILRB2; ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti- LILRB2 monoclonal antibody IO-108 targets and binds to LILRB2. This prevents the binding of LILRB2 ligands to their receptor and prevents LILRB2-mediated signaling. This abrogates the immunosuppressive activities of LILRB2 in the tumor microenvironment (TME), activates the expression of pro-inflammatory cytokines, including GM-CSF and tumor necrosis factor alpha (TNFalpha), and enhances a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. LILRB2, plays a key role in tumor immune evasion. LILRB2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and in certain tumors.

anti-LILRB2 monoclonal antibody JTX-8064

A humanized monoclonal antibody directed against the inhibitory immune checkpoint receptor leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2; immunoglobulin-like transcript 4; ILT4; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-LILRB2 monoclonal antibody JTX-8064 targets and binds to LILRB2. This prevents the binding of LILRB2 ligands, including endogenous major histocompatibility complex class I (MHC I) molecules, to their receptor and prevents LILRB2-mediated signaling. This may abrogate the immunosuppressive activities of LILRB2 in the tumor microenvironment (TME), activate the expression of pro-inflammatory cytokines, including GM-CSF and tumor necrosis factor alpha (TNFalpha), and enhance a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. LILRB2, expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and certain tumor cells, plays a key role in tumor immune evasion.

anti-LILRB2 monoclonal antibody OR502

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the inhibitory immune checkpoint receptor immunoglobulin-like transcript 4 (LILRB2; ILT4; leukocyte immunoglobulin-like receptor subfamily B member 2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-LILRB2 monoclonal antibody OR502 targets and binds to LILRB2. This prevents the binding of LILRB2 ligands to their receptor and prevents LILRB2-mediated signaling. This abrogates the immunosuppressive activities of LILRB2 in the tumor microenvironment (TME), activates the expression of pro-inflammatory cytokines, including granulocyte macrophage-colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNFalpha), and enhances a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. LILRB2, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and in certain tumors. It plays a key role in tumor immune evasion.

anti-LILRB4 monoclonal antibody BND-35

A humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against the myeloid-enriched immune inhibitory receptor leukocyte immunoglobulin-like receptor B member 4 (LILRB4; ILT3; ILT-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LILRB4 monoclonal antibody BND-35 targets, binds to and blocks LILRB4, thereby preventing the interaction with its ligands, such as fibronectin, in the tumor microenvironment (TME). This prevents the activation of LILRB4-mediated downstream signaling pathways. This may abrogate LILRB4-mediated promotion of myeloid cell immunosuppression and inhibition of antitumor immunity. This may restore immune function by activating dendritic cells (DCs) and T cells, and may promote T-cell-mediated immune responses against tumor cells. LILRB4, an inhibitory immune receptor highly expressed on tumor-associated myeloid cells, primarily tolerogenic DCs, myeloid-derived suppressor cells (MDSCs) and M2 macrophages, functions as an immune checkpoint that negatively regulates DC- and T-cell activation. It is upregulated in several tumor types and plays an important role in tumor infiltration, immunosuppression and immune tolerance.

anti-LILRB4 monoclonal antibody IO-202

A monoclonal antibody directed against the immune inhibitory receptor leukocyte immunoglobulin-like receptor B4 (LILRB4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LILRB4 monoclonal antibody IO-202 targets, binds to and inhibits LILRB4 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells, and inhibit tumor infiltration. LILRB4, an immune inhibitory receptor normally expressed on monocytic cells and highly expressed on monocytic acute myeloid leukemia (AML) cells, functions as an immune checkpoint that negatively regulates T-cell activation as its extracellular domain inhibits T-cell activity. It plays an important role in tumor infiltration in leukemias through multiple signaling pathways.

anti-LILRB4 monoclonal antibody MK-0482

A humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against the myeloid-enriched immune inhibitory receptor leukocyte immunoglobulin-like receptor B member 4 (LILRB4; ILT3; ILT-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LILRB4 monoclonal antibody MK-0482 targets, binds to and blocks LILRB4, thereby preventing the interaction with its ligands, such as fibronectin, in the tumor microenvironment (TME). This prevents the activation of LILRB4-mediated downstream signaling pathways. This may abrogate LILRB4-mediated promotion of myeloid cell immunosuppression and inhibition of antitumor immunity. This may restore immune function by activating dendritic cells (DCs) and T-cells, and may promote T-cell-mediated immune responses against tumor cells. LILRB4, an inhibitory immune receptor highly expressed on tumor-associated myeloid cells, primarily tolerogenic DCs, myeloid-derived suppressor cells (MDSCs) and M2 macrophages, functions as an immune checkpoint that negatively regulates DC- and T-cell activation. It is upregulated in several tumor types and plays an important role in tumor infiltration, immunosuppression and immune tolerance.

anti-LILRB4 monoclonal antibody NGM831

A monoclonal antibody directed against the myeloid-enriched immune inhibitory receptor leukocyte immunoglobulin-like receptor B member 4 (LILRB4; ILT3; ILT-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LILRB4 monoclonal antibody NGM831 targets, binds to and blocks LILRB4, thereby preventing the interaction with its ligands, such as fibronectin, in the tumor microenvironment (TME). This prevents the activation of LILRB4-mediated downstream signaling pathways. This may abrogate LILRB4-mediated promotion of myeloid cell immunosuppression and inhibition of antitumor immunity. This may restore immune function by activating dendritic cells (DCs) and T cells, and may promote T-cell-mediated immune responses against tumor cells. LILRB4, an inhibitory immune receptor highly expressed on tumor-associated myeloid cells, primarily tolerogenic DCs, myeloid-derived suppressor cells (MDSCs) and M2 macrophages, functions as an immune checkpoint that negatively regulates DC- and T-cell activation. It is upregulated in several tumor types and plays an important role in tumor infiltration, immunosuppression and immune tolerance.

anti-LILRB4/MMAE ADC SG2918

An antibody-drug conjugate (ADC) consisting of a monoclonal antibody directed against leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4; ILT3; ILT-3) conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-LILRB4/MMAE ADC SG2918, the monoclonal antibody moiety targets and binds to LILRB4. After internalization of the agent, the MMAE moiety is released, binds to tubulin and inhibits its polymerization, which results in G2/M phase cell cycle arrest and apoptosis. This inhibits the proliferation of LILRB4-expressing tumor cells and may re-activate the immune system. LILRB4, an inhibitory immune receptor highly expressed on tumor-associated myeloid cells, primarily tolerogenic dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs) and M2 macrophages, functions as an immune checkpoint that negatively regulates DC- and T-cell activation. It is upregulated in several tumor types and plays an important role in tumor infiltration, immunosuppression and immune tolerance.

anti-LLT1 monoclonal antibody ZM008

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) lectin-like transcript-1 (LLT1; CLEC2D; OCIL), with potential immunomodulating and antineoplastic activities. Upon administration, anti-LLT1 monoclonal antibody ZM008 targets and binds to LLT1 expressed on a variety of tumor cells. This prevents the binding of LLT1 to its receptor C-type lectin-like receptor cluster of differentiation 161 (CD161) primarily expressed on CD161-positive natural killer (NK) cells. This prevents CD161-mediated signaling, abrogates the CLEC2D/CD161-mediated suppression of NK cells, leading to the activation and infiltration of NK cells and cytotoxic T cells in the tumor microenvironment (TME) and promotes anti-tumor immune response, thereby enhancing cytotoxicity towards tumor cells. CD161, an inhibitory immune checkpoint, is broadly expressed on NK and a subset of memory CD4+ and CD8+ T cells. LLT1 is expressed on the surface of both malignant cells and various immune cells, including activated B-cells and myeloid cells. The interaction between LLT1 and CD161 leads to immune repressive condition in the TME allowing tumor cells to bypass the human immune system.

anti-LOXL2 monoclonal antibody GS-6634

A humanized monoclonal antibody against lysyl oxidase-like 2 (LOXL2), with potential antineoplastic activity. Anti-LOXL2 monoclonal antibody AB0024 targets and specifically binds to the scavenger receptor cysteine rich domain 4 (SRCR-4) on LOXL2, thereby preventing the crosslinking of collagen and inhibiting the recruitment and activation of fibroblasts. Inhibiting fibroblast activation and the subsequent production of growth factors and chemokines may lead to an inhibition of tumor cell proliferation. LOXL2, a member of the lysyl oxidase (LO) gene family, is an extracellular, copper-dependent enzyme overexpressed in a variety of tumor cell types, and contributes to tumor cell invasion and metastasis.

anti-Ly6E antibody-drug conjugate RG 7841

An antibody-drug conjugate (ADC) composed of an antibody against the tumor-associated antigen (TAA) lymphocyte antigen 6 complex locus E (Ly6E) and linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the antibody moiety of RG 7841 targets and binds to Ly6E expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills, through an as of yet unknown mechanism of action, the Ly6E-expressing cancer cells. Ly6E, an interferon (IFN)-inducible glycosylphosphatidylinositol (GPI)-linked cell membrane protein, is expressed on a variety of tumor cell types.

Anti-M-CSF monoclonal antibody MCS110

A humanized monoclonal antibody directed against macrophage colony-stimulating factor (M-CSF) with potential anti-osteolytic activity. Anti-M-CSF monoclonal antibody MCS110 binds to M-CSF and blocks M-CSF-mediated signaling through the M-CSF receptor CD116 expressed on osteoclasts, which may result in inhibition of M-CSF-induced osteoclast differentiation and so osteoclastic bone resorption. Osteoclasts are derived through the fusion of cells of the monocyte/macrophage lineage. Osteoblasts and stromal cells may react to bone metastases by producing M-CSF and its osteoclastogenic cofactor RANKL (receptor activator of NF-kappaB ligand).

anti-MAGE-A4 T-cell receptor/anti-CD3 scFv fusion protein IMC-C103C

A T-cell re-directing bi-specific biologic composed of a modified form of human T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) human melanoma-associated antigen A4 (MAGE-A4) and fused to an anti-CD3 single-chain variable fragment (scFv), with potential antineoplastic activity. Upon intravenous administration of IMC-C103C, the TCR moiety of this agent targets and binds to MAGE-A4 on tumor cells and the anti-CD3 scFv moiety binds to CD3- expressing T lymphocytes. This selectively cross-links tumor cells and T lymphocytes and results in a CTL-mediated death of MAGE-A4-expressing tumor cells. MAGE-A4 is overexpressed by a variety of cancer cell types.

anti-MAGE-A4/anti-CD3 bispecific antibody RO7617991

A bispecific T-cell engaging antibody directed against both the tumor-associated antigen (TAA) melanoma-associated antigen A4 (MAGE-A4) and T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-MAGE-A4/anti-CD3 bispecific antibody RO7617991 simultaneously binds to both CD3 on cytotoxic T lymphocytes (CTLs) and MAGE-A4 on MAGE-A4-expressing tumor cells. This activates and redirects CTLs to MAGE-A4-expressing tumor cells, which results in the CTL-mediated cell death of MAGE-A4-expressing tumor cells. MAGE-A4 is overexpressed by a variety of cancer cell types.

anti-MART-1 TCR retroviral vector-transduced autologous TIL

Human tumor infiltrating lymphocytes (TIL) isolated from a melanoma patient and were engineered to react with the melanoma antigen MART-1 (Melanoma Antigen Recognized by T cells, also called Melan-A). These TILs are transfected with a retroviral vector encoding anti-MART-1 specific T-cell receptors, grown in culture, and then transferred back to the patient. These genetically modified TIL may recognize and halt the growth of MART-1-expressing melanoma cells.

anti-MASP-2 monoclonal antibody OMS721

A monoclonal antibody against mannan-binding lectin (MBL)-associated serine protease-2 (MASP-2), with potential anti-thrombotic and immunomodulating activities. Upon subcutaneous administration, OMS721 binds to and inhibits MASP-2. This prevents the activation of MASP-2, the cleavage of certain complement components, and the activation of the complement lectin pathway. This inhibits complement deposition and complement-induced thrombus formation. MASP-2, a pro-inflammatory protein, plays a key role in the activation of the lectin complement pathway, which is a key component in the immune system, and is associated with complement-mediated diseases, such as thrombotic microangiopathies (TMAs), which includes hematopoietic stem cell transplant (HSCT)-related TMA, atypical hemolytic uremic syndrome (aHUS), and thrombotic thrombocytopenic purpura (TTP).

anti-melanin monoclonal antibody PTI-6D2

A monoclonal antibody (MoAb) against extracellular melanin with tumor targeting activity. Anti-melanin monoclonal antibody PTI-6D2 binds to extracellular melanin, a melanocyte pigment which is released during tumor cell turnover from dead melanoma tumor cells, while avoiding the binding of melanin in normal, healthy tissue because of melanin's normal intracellular location. Upon labeling with the beta-emitting radioisotope rhenium Re 188 (PTI-188), this MoAb may target multiple melanoma (MM) cells, thereby delivering a cytotoxic dose of radiation specifically to the targeted tumor cells.

anti-mesothelin antibody-drug conjugate BMS-986148

An antibody-drug conjugate (ADC) composed of a human immunoglobulin G1 (IgG1) monoclonal antibody directed against the cell surface glycoprotein and tumor-associated antigen (TAA) mesothelin and conjugated, via a valine-citrulline linker, to the cytotoxic agent tubulysin, with potential antineoplastic activity. Upon administration of anti-mesothelin ADC BMS-986148, the monoclonal antibody moiety targets and binds to mesothelin. Upon internalization, the tubulysin moiety inhibits the polymerization of tubulin into microtubules. This leads to cell cycle arrest, induces tumor cell apoptosis, and may inhibit cellular proliferation of mesothelin-expressing tumor cells. Mesothelin is overexpressed by all mesotheliomas and a variety of other cancers, while it is minimally expressed in normal tissue.

anti-mesothelin CAR T cells UCMYM802

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. Upon administration, anti-MSLN CAR T cells UCMYM802 specifically target and kill MSLN-expressing tumor cells. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-mesothelin CAR vector-transduced autologous T lymphocytes

Genetically modified, autologous T lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) consisting of an anti-human tumor-associated antigen (TAA) mesothelin single chain variable fragment (scFv), the intracellular CD3 zeta T-cell receptor domain and the 4-1BB (cd137) costimulatory domain, with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the anti-mesothelin CAR vector-transduced autologous T lymphocytes specifically target and kill mesothelin-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-mesothelin CAR vector-transduced T lymphocytes

A preparation of genetically modified T lymphocytes transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-MSLN CAR vector-transduced T-lymphocytes specifically target and kill MSLN-expressing tumor cells. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-mesothelin CAR-CD40L-expressing T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), and CD40 ligand (CD40L; CD154; TRAP; TNFSF5), with potential immunomodulating and antineoplastic activities. Upon administration, anti-MSLN CAR-CD40L-expressing T lymphocytes specifically target and kill MSLN-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. CD40L binds to CD40 and activates CD40/CD40L-mediated signaling, which activates monocyte-derived dendritic cells (moDCs), increases the secretion of inflammatory cytokines and further stimulates cytotoxic T lymphocytes (CTLs). This enhances cytotoxicity and anti-tumor immune response.

anti-mesothelin CIR mRNA-electroporated autologous T cells

Autologous chimeric immune receptor (CIR) T cells transfected with anti-mesothelin chimeric T cell receptor mRNA, with potential antineoplastic activity. The anti-mesothelin mRNA encodes a single chain antibody variable fragment (ScFv), the intracellular CD 3 zeta T cell receptor domain and the 4-1BB (cd137) costimulatory domain. Upon intravenous administration, the anti-mesothelin CIR mRNA-electroporated autologous T cells may attach to cancer cells expressing mesothelin. This may stimulate the secretion of multiple cytokines and may result in cell lysis of mesothelin-expressing cancer cells. Mesothelin is a cell surface glycoprotein involved in cell adhesion and is overexpressed in many epithelial-derived cancers.

anti-mesothelin iCasp9M28z CAR-transduced autologous T lymphocytes

Genetically modified, autologous T lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for mesothelin linked to the signaling domains for the co-stimulatory molecules CD28 and CD3 zeta, as well as the suicide gene inducible caspase 9 (iCasp9 or iC9), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-mesothelin iCasp9M28z CAR-transduced autologous T lymphocytes specifically target and kill mesothelin-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T-cells lead to unacceptable side effects, a dimerizing agent can be administered, which binds to the FKBP12-F36V drug-binding domain and activates caspase 9, resulting in the apoptosis of the administered T cells. Mesothelin, a tumor-associated antigen, is overexpressed in a variety of cancer cell types.

anti-mesothelin T-cell engaging bispecific antibody JNJ-79032421

A bispecific T-cell engager (TCE) and bispecific antibody directed against both the tumor-associated antigen (TAA) mesothelin (MSLN) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-mesothelin T-cell engaging bispecific antibody JNJ-79032421 targets and binds to MSLN expressed on tumor cells and to CD3 expressed on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to MSLN-expressing tumor cells, which results in the CTL-mediated death of MSLN-expressing tumor cells. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-mesothelin-Pseudomonas exotoxin 24 cytolytic fusion protein LMB-100

An anti-mesothelin (MSLN) recombinant cytolytic fusion protein (cFP) composed of a humanized Fab fragment of anti-MSLN monoclonal antibody SS1 linked to a truncated and de-immunized 24 kDa fragment of the Pseudomonas exotoxin (PE) (PE24), with potential antineoplastic activity. Upon intravenous administration of anti-MSLN-PE24 cFP LMB-100, the anti-MSLN moiety targets and binds to MSLN-expressing tumor cells. Upon binding and internalization through endocytosis, the toxin moiety ADP-ribosylates and inactivates eukaryotic elongation factor 2 (eEF2), preventing the elongation step of protein synthesis and leading to both an inhibition of protein synthesis and an induction of MSLN-expressing tumor cell apoptosis. MSLN, a tumor-associated antigen overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation and migration. The engineered PE24 portion of LMB-100 does contain the targeting domain and furin cleavage site, which are needed for cytotoxicity, but most of the translocation domain II is deleted and the catalytic domain III contains point mutations, which result in the deletion and silencing of most T- and B-cell epitopes; therefore, the immunogenicity and toxicity is reduced compared to non-engineered PE toxin, which allows for the administration of larger doses of LMB-100.

anti-mesothelin/MMAE antibody-drug conjugate DMOT4039A

An antibody-drug conjugate (ADC) composed of MMOT0530A, a humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the cell surface glycoprotein mesothelin (MSLN), and covalently linked, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DMOT4039A binds to MSLN-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. MSLN, a tumor-associated antigen (TAA), is overexpressed by all mesotheliomas and a variety of other cancers, while it is minimally expressed in normal tissue.

anti-mesothelin/MMAE antibody-drug conjugate RC88

An antibody-drug conjugate (ADC) composed of an antibody directed against the human cell surface glycoprotein mesothelin and conjugated, via a cleavable linker, to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-mesothelin/MMAE ADC RC88 targets and binds to the tumor associated antigen (TAA) mesothelin on the surface of tumor cells. Upon internalization and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in mesothelin-expressing tumor cells. Mesothelin is overexpressed by all mesotheliomas and a variety of other cancers, while it is minimally expressed in normal tissue.

anti-Met monoclonal antibody mixture Sym015

A mixture of two humanized immunoglobulin G1 (IgG1) monoclonal antibodies, Hu9006 and Hu9338, which recognize non-overlapping epitopes in the extracellular domain of the human hepatocyte growth factor receptor (MET; HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-MET monoclonal antibody mixture Sym015 targets and binds to the extracellular domain of MET, thereby preventing the binding of its ligand, hepatocyte growth factor (HGF). This may prevent activation of the receptor and MET-mediated signal transduction pathways. This inhibits MET-dependent tumor cell proliferation. MET, a receptor tyrosine kinase, is overexpressed on the cell surfaces of various solid tumor cell types; it plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-MET x MET antibody drug conjugate REGN5093-M114

An antibody-drug conjugate (ADC) consisting of REGN5093, a biparatopic monoclonal antibody that targets two different epitopes of the human tumor-associated antigen (TAA) MET (c-MET; hepatocyte growth factor receptor; HGFR), and conjugated, via a protease cleavable linker, to the cytotoxic maytansine derivative M24, with potential antineoplastic activity. Upon administration of anti-MET x MET ADC REGN5093-M114, the REGN5093 moiety targets and binds to two different, non-overlapping epitopes on MET expressed on the tumor cell surface. After antibody-antigen interaction followed by internalization and protease cleavage, the maytansine M24 moiety binds to tubulin, inhibits microtubule assembly, and induces microtubule disassembly. This leads to a disruption of mitosis and the inhibition of cell proliferation in cancer cells expressing MET. MET, a receptor tyrosine kinase, is overexpressed on the cell surfaces of various solid tumor cell types where it is involved in epithelial-mesenchymal transition; it plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-Met/EGFR monoclonal antibody LY3164530

A monoclonal antibody (MoAb) against human epidermal growth factor receptor (EGFR) and human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Upon administration, anti-Met/EGFR MoAb LY3164530 targets and prevents the activation of EGFR and c-Met. This leads to a downstream inhibition of EGFR/c-Met-mediated signal transduction pathways, and prevents cellular proliferation in tumor cells overexpressing EGFR and c-Met. EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surface of various solid tumor cell types. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

anti-MICA/MICB monoclonal antibody DM919

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the natural-killer group 2, member D receptor protein (NKG2D or KLRK1) ligands MHC class I polypeptide-related sequence A (MICA) and B (MICB), with potential immunostimulating and antineoplastic activities. Upon administration, anti-MICA/MICB monoclonal antibody DM919 targets and binds to both MICA and MICB, and prevents the cleavage of MICA and MICB from the cell surface of tumor cells by proteases in the tumor microenvironment (TME), thereby stabilizing expression of surface MICA/B. This enhances the binding of NKG2D-expressing immune cells, including natural killer (NK) cells and T cells, to MICA- and MICB-expressing tumor cells, which leads to the activation of NK cells and the NK-mediated lysis of tumor cells. In addition, DM919 enhances antitumor response through antibody-dependent cell-mediated cytotoxicity (ADCC). MICA and MICB are stress-induced NKG2D ligands overexpressed on infected cells and many cancer cell types, but are not expressed on most normal, healthy cells. The shedding of MICA and MICB from tumor cell surface allows the tumor cells to evade NKG2D-expressing immune cells.

anti-minor histocompatibility complex donor T lymphocytes

A preparation of allogeneic, donor-derived T lymphocytes that are specific for a unique set of minor histocompatibility complex antigens (MiHA) exclusively found on the surface of malignant cells, with potential immunomodulating and antineoplastic activities. T lymphocytes are derived from an allogeneic hematopoietic cell transplant (AHCT) donor. Ex vivo, these T cells are exposed to and primed against a select set of host-specific hematopoietic tissue-restricted MiHAs that are expressed on leukemic cells. Then the cells are subsequently expanded. After AHCT and infusion of the anti-MiHA T lymphocytes, these cells target and bind to MiHA antigens expressed on the host's leukemia cells, thereby killing these cancer cells. MiHA are small, cell-surface peptides that are associated with graft-versus-host disease (GvHD). The selected set of MiHAs is expressed mainly, or only, by hematopoietic cells, and overexpressed on leukemic cells.

anti-MSLN CAR-T cells LCAR-M23

A preparation of Tl ymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-MSLN CAR-T cells LCAR-M23 specifically target and kill MSLN-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-MSLN/anti-CD3 bispecific antibody ZW171

A bispecific T-cell engager (TCE) and bispecific antibody directed against both the tumor-associated antigen (TAA) mesothelin (MSLN) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-MSLN/anti-CD3 bispecific antibody ZW171 bivalently binds to MSLN expressed on tumor cells and monovalently binds to CD3 expressed on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to MSLN-expressing tumor cells, which results in the CTL-mediated death of MSLN-expressing tumor cells. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

anti-MUC1 CAR-transduced autologous T lymphocytes

Autologous T lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) against the human tumor-associated epithelial antigen mucin 1 (MUC1), with potential immunomodulating and antineoplastic activities. Autologous PBLs from a patient with MUC1-positive cancer are transduced with a retroviral vector that encodes the CAR gene specific for MUC1. After expansion in culture and reintroduction into the patient, anti-MUC1 CAR-transduced autologous T lymphocytes target and induce selective toxicity in MUC1-expressing tumor cells. MUC-1 is a human, hypoglycosylated tumor-associated antigen (TAA) overexpressed by epithelial cancer cells.

anti-MUC1/EGFR bispecific antibody-drug conjugate M1231

An antibody drug conjugate (ADC) composed of a bispecific antibody directed against the tumor associated antigens (TAAs) mucin-1 (MUC1) and human epidermal growth factor receptor (EGFR), conjugated, via a cleavable valine-citruline-based linker, to the hemiasterlin-related toxic warhead, with potential antineoplastic activity. Upon intravenous administration, the antibody moiety of anti-MUC1/EGFR bispecific ADC M1231 targets and binds to MUC1 and EGFR expressed on certain tumor cells. Upon binding, internalization, and enzymatic cleavage, the cytotoxic hemiasterlin moiety of M1231 binds to the vinca domain on tubulin, resulting in inhibition of tubulin polymerization and microtubule assembly, depolymerization of existing microtubules, inhibition of mitosis, and inhibition of cellular proliferation. MUC1 and EGFR, overexpressed on the surface of a variety of cancer cells, play key roles in tumor cell survival and proliferation. MUC1 and EGFR are often co-localized due to loss of membrane polarization on tumor cells while co-expression in normal cells is limited.

anti-MUC16 CAR T cells 27T51

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human mucin-16 (MUC16, cancer antigen 125; CA125; FLJ14303), with potential immunostimulating and antineoplastic activities. Upon administration, anti-MUC16 CAR T cells 27T51 recognize and bind to MUC16-expressing tumor cells, thereby inducing selective toxicity in MUC16-expressing tumor cells. MUC16, a member of the mucin family of glycoproteins, is overexpressed on a variety of cancer cell types.

anti-MUC16/anti-CD3 bispecific antibody LBL-033

A bispecific monoclonal antibody containing one arm targeting human CD3, a T-cell surface antigen that is part of the T-cell receptor (TCR) complex, and two arms targeting the membrane-proximal domain of the tumor-associated antigen (TAA) human mucin 16 (MUC16, cancer antigen 125; CA125; FLJ14303), with potential antineoplastic activity. Upon administration, anti-MUC16/anti-CD3 bispecific antibody LBL-033 binds to both T-cells and MUC16-expressing tumor cells, which cross-links the T cells to the tumor cells, and may result in a potent cytotoxic T-lymphocyte (CTL) response against the MUC16-expressing tumor cells. MUC16, a member of the mucin family of glycoproteins, is overexpressed on a variety of cancer cell types. BY binding in a 2:1 ratio to MUC16 and CD3, LBL-033 improves aggregation in MUC16-overexpressing tumor cells while reducing the non-specific activation of CD3. This may improve efficacy and minimize potential systemic toxicity, such as cytokine release syndrome (CRS).

anti-MUC16/CD28 bispecific antibody REGN5668

A bispecific monoclonal antibody against both the tumor-associated antigen (TAA) human mucin 16 (MUC16, cancer antigen 125; CA125; FLJ14303) and the co-stimulatory T-cell-specific surface glycoprotein CD28, with potential antineoplastic and immunostimulating activities. Upon administration, anti-MUC16/CD28 bispecific antibody REGN5668 binds to both CD28 on T cells and MUC16-expressing tumor cells, which cross-links the T cells to the tumor cells. This may result in a potent cytotoxic T-lymphocyte (CTL) response against the MUC16-expressing tumor cells. MUC16, a member of the mucin family of glycoproteins, is overexpressed by several epithelial cancers, including ovarian cancer.

anti-MUC16/MMAE antibody-drug conjugate DMUC4064A

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against human mucin 16 (MUC16; cancer antigen 125; CA125; FLJ14303) conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, anti-MUC16/MMAE ADC DMUC4064A binds to MUC16 located on the tumor cell surface. After internalization of the agent, the MMAE moiety is released and binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and apoptosis. MUC16, a member of the mucin family glycoproteins, is overexpressed in a variety of tumor cells and plays a key role in tumor cell proliferation.

anti-MUC17/CD3 BiTE antibody AMG 199

A half-life extended (HLE), human bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human mucin 17 (MUC17), and one directed against human CD3, a T-cell surface antigen found on T lymphocytes, with potential antineoplastic activity. Upon administration, anti-MUC17/CD3 BiTE antibody AMG 199 binds to both CD3 on T cells and MUC17 expressed on tumor cells. This results in the cross-linking of T cells and tumor cells, and induces a potent cytotoxic T-lymphocyte (CTL) response against MUC17-expressing tumor cells. MUC17, a member of the mucin family of glycoproteins, is overexpressed in a variety of tumor cells of epithelial origin and plays a key role in tumor cell dissemination.

anti-mucin-1/CD16A bispecific antibody BGB-B3227

An immunoglobulin G1 (IgG1) humanized bispecific antibody directed against the tumor associated antigen (TAA) mucin-1 (MUC1) and the human low affinity IgG Fc region receptor IIIA (FCGR3A; CD16A), with potential immunomodulating and antineoplastic activities. Upon administration, anti-MUC1/CD16A bispecific antibody BGB-B3227 targets and binds to CD16A expressed on natural killer (NK) cells and MUC1 expressed on the surface of tumor cells, thereby selectively cross-linking tumor and NK cells. This may result in NK cell activation and eventually tumor cell lysis. CD16A is specifically expressed on the surface of NK cells. MUC1, a glycoprotein overexpressed on the surface of a variety of cancer cells, plays a key role in tumor cell survival and proliferation.

anti-mucin-1/PE immunoconjugate BM7PE

An immunoconjugate containing BM7, a murine monoclonal antibody directed against the human tumor-associated antigen (TAA) mucin-1 (MUC1; MUC-1) covalently linked to the bacterial toxin Pseudomonas exotoxin A (PE), with potential antitumor activity. Upon administration of BM7PE, the antibody moiety targets and binds to MUC1. In turn, the PE moiety inhibits protein synthesis via modifying translation elongation factor 2 (EF-2), thereby causing apoptosis and inhibiting tumor cell growth and proliferation in MUC1-overexressing cancer cells. MUC1, a type I transmembrane protein, is overexpressed in a variety of tumor types. It plays an important role in cancer progression and metastasis.

anti-mutant calreticulin monoclonal antibody INCA033989

A human immunoglobulin G1 (IgG1) monoclonal antibody targeting the mutated form of calreticulin (mutCALR), with potential antineoplastic activity. Upon administration, anti-mutCALR monoclonal antibody INCA033989 selectively targets and binds to mutCALR expressed on CALR mutated CD34-positive hematopoietic stem cells (HSCs) while not binding to normal wild-type (WT) CALR on healthy CD34-positive HSCs. This prevents the formation of a mutCALR complex with the thrombopoietin receptor (TPO-R) in the endoplasmic reticulum (ER), prevents the CALR mutant-dependent TPO-R dimerization and suppresses TPO-R signaling. This prevents the activation of the downstream Janus kinase 2 (JAK2)/signal transducer and activator of transcription (STAT) signaling pathway. This prevents mutCALR-driven oncogenic cell proliferation, causes cell cycle arrest and induces cell death. CALR mutations, either insertions or deletions in exon 9, result in a frameshift that causes the loss of the KDEL ER retention motif. CALR mutations drive a variety of myeloproliferative neoplasms (MPNs).

anti-myeloma monoclonal antibody-DM4 immunoconjugate BT-062

An immunoconjugate consisting of a monoclonal antibody directed against a highly-expressed myleoma cell surface antigen covalently attached to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Anti-myeloma monoclonal antibody-DM4 immunoconjugate BT-062 binds to an unspecified cell surface antigen highly expressed on myeloma cells; upon internaliization the DM4 moiety is released, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in the inhibition of cell division and cell growth of myeloma tumor cells.

anti-NaPi2b antibody-drug conjugate XMT-1592

An antibody-drug conjugate (ADC) composed of XMT-1535, a humanized monoclonal antibody against human sodium-dependent phosphate transport protein 2B (SLC34A2; NaPi2b), that is site-specifically bioconjugated to the cytotoxic aurastatin derivative auristatin F-HPA (AF-HPA; auristatin F-hydroxypropylamide), with potential antineoplastic activity. Upon administration of anti-NaPi2b ADC XMT-1592, the antibody moiety targets and binds to NaPi2b expressed on tumor cells. Following internalization of XMT-1592 and release of AF-HPA, the AF-HPA binds to tubulin and inhibits microtubule polymerization, which results in G2/M phase arrest and apoptosis of NaPi2b-expressing tumor cells. NaPi2b, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells and plays a key role in the transport of inorganic phosphate (Pi) and the maintenance of phosphate homeostasis.

anti-NaPi2b/exatecan antibody-drug conjugate TUB-040

An antibody-drug conjugate (ADC) composed of a Fc-silenced, humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against human sodium-dependent phosphate transport protein 2B (SLC34A2; NaPi2b), conjugated, via a cleavable linker, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-NaPi2b/exatecan ADC TUB-040, the antibody moiety targets and binds to NaPi2b expressed on tumor cells. Upon binding, cellular uptake and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and generating DNA single- and double-strand breaks. This leads to cell cycle arrest and tumor cell apoptosis. In addition, ADC TUB-040 is able to induce a bystander effect on neighboring tumor cells. This inhibits the proliferation of NaPi2b-expressing tumor cells. NaPi2b, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells and plays a key role in the transport of inorganic phosphate (Pi) and the maintenance of phosphate homeostasis.

anti-NaPi2b/MMAE antibody-drug conjugate DNIB0600A

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the sodium-dependent phosphate transport protein 2B (NaPi2b), and covalently linked to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DNIB0600A binds to NaPi2b-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. NaPi2b, a tumor-associated antigen (TAA), overexpressed in a variety of cancer cell types, plays a key role in transport of inorganic phosphate and the maintenance of phosphate homeostasis.

anti-nectin-4 antibody-drug conjugate 9MW2821

An antibody drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4), site-specifically conjugated, via a linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of the anti-nectin-4 ADC 9MW2821, the anti-nectin-4 antibody targets and binds to nectin-4 expressed on tumor cells. Upon binding and internalization, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4-expressing tumor cells. Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue.

anti-nectin-4 antibody-drug conjugate ADRX-0706

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4) that is conjugated to the tubulin inhibitor and cytotoxic agent AP052, with potential antineoplastic activity. Upon administration of the anti-nectin-4 ADC ADRX-0706, the anti-nectin-4 antibody targets and binds to nectin-4 expressed on tumor cells. Upon binding and internalization, AP052 targets and binds to tubulin, and inhibits its polymerization. This results in G2/M phase arrest and induces apoptosis in nectin-4-expressing tumor cells. Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue. It is associated with poor disease prognosis. ADRX-0706 has a drug-antibody ratio (DAR) of eight.

anti-nectin-4 antibody-drug conjugate IPH4502

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) Fc-competent monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4) conjugated, via a hydrophilic cleavable linker, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of anti-nectin-4 ADC IPH4502, the anti-nectin-4 antibody targets and binds to nectin-4 expressed on tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of nectin-4-expressing tumor cells. IPH4502 is also able to induce a bystander effect on neighboring cells in the tumor environment. This further inhibits the proliferation of tumor cells. In addition, the Fc-competent monoclonal antibody of IPH4502 may induce both antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) against nectin-4-expressing tumor cells. Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue.

anti-nectin-4 antibody-drug conjugate LY4052031

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4) conjugated, via a cleavable peptide linker, to the camptothecin analog and topoisomerase 1 inhibitor LSN3889710, with potential antineoplastic activity. Upon administration of the anti-nectin-4 ADC LY4052031, the anti-nectin-4 antibody moiety targets and binds to nectin-4 expressed on tumor cells. Upon binding, internalization and linker cleavage, LSN3889710 is released. LSN3889710 inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of nectin-4-expressing tumor cells. Nectin-4, an immunoglobulin-like protein belonging to the nectin family, is overexpressed in a variety of cancers.

anti-nectin-4 antibody-drug conjugate LY4101174

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) Fcg-silent monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4) conjugated, via maleimide-beta-glucuronide poly-sarcosine linkers, to the camptothecin analog and topoisomerase 1 inhibitor exatecan, with potential antineoplastic activity. Upon administration of the anti-nectin-4 ADC LY4101174, the anti-nectin-4 antibody targets and binds to nectin-4 expressed on tumor cells. Upon binding and internalization, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of nectin-4-expressing tumor cells. Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers.

anti-nectin-4 antibody-drug conjugate SHR-A2102

An antibody-drug conjugate (ADC) composed of an immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) nectin-4 (PVRL4) conjugated, via a cleavable linker, to a topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-nectin-4 ADC SHR-A2102 targets and binds to nectin-4 expressed on tumor cells. Upon binding, internalization and linker cleavage, topoisomerase-1 inhibitor is released and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and apoptosis in tumor cells expressing nectin-4. Nectin-4 is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue.

anti-Nectin-4 monoclonal antibody-drug conjugate AGS-22M6E

An antibody drug conjugate (ADC) containing a fully human monoclonal antibody AGS-22 targeting the cell adhesion molecule nectin-4 and conjugated, via a proprietary enzyme-cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE) (AGS-22M6E), with potential antineoplastic activity. The monoclonal antibody moiety of AGS-22M6E selectively binds to nectin-4. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4 overexpressing tumor cells. Nectin-4, a tumor associated antigen belonging to the nectin family, is overexpressed in a variety of cancers, including breast, bladder, lung and pancreatic cancer.

anti-nectin-4/MMAE antibody-drug conjugate CRB-701

An antibody-drug conjugate (ADC) composed of an immunoglobulin G1 (IgG1) monoclonal antibody directed against the cell surface adhesion molecule and tumor-associated antigen (TAA) nectin-4 (PVRL4), site-specifically conjugated, via a cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-nectin-4/MMAE ADC CRB-701, the anti-nectin-4 antibody moiety targets and binds to nectin-4 expressed on tumor cells. Upon binding, internalization, and linker cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4-expressing tumor cells. Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue. CRB-701 may also induce anti-tumor activity through the induction of antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) against nectin-4-expressing tumor cells.

anti-netrin-1 monoclonal antibody NP137

A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the laminin-related protein netrin-1 (NTN1), with potential antineoplastic activity. Upon administration, anti-NTN1 monoclonal antibody NP137 targets, binds to and neutralizes NTN1, thereby preventing its binding to and activation of NTN1 receptors. By blocking NTN1, NP137 is able to restore apoptosis in tumor cells. This inhibits tumor growth and metastasis. NTN1, overexpressed by a variety of cancers, plays a key role in promoting tumor initiation, progression, proliferation, adhesion, invasion, survival and modulation of tumor+F52:J54 plasticity and the tumor microenvironment (TME).

anti-neuropilin-1 monoclonal antibody MNRP1685A

A human IgG1 monoclonal antibody directed against neuropilin-1 (NRP1), with potential antiangiogenic and antineoplastic activities. Upon intravenous administration, MNRP1685A specifically targets and binds to NRP1; the antibody-NRP1 complex prevents the subsequent coupling of NRP1 to VEGFR2, thereby potentially inhibiting VEGF-mediated signaling and potentially preventing angiogenesis. In combination with other anti-VEGF therapies, MNRP1685A may enhance their anti-angiogenic effect. NRP1 is a membrane-bound co-receptor normally expressed by endothelial cells and overexpressed by certain tumor cells, and plays a role in angiogenesis, cell survival, migration, and invasion.

anti-nf-P2X7 antibody ointment BIL-010t

An ointment formulation composed of a purified sheep immunoglobulin G (IgG) antibody against the non-functional form of the purinergic P2X7 receptor (nf-P2X7), with potential antineoplastic activity. Upon topical application of the anti-nf-P2X7 antibody ointment BIL-010t, the antibody binds to nf-P2X7 and inhibits its antiapoptotic activity. This may induce apoptosis and inhibit the growth of nf-P2X7-overexpressing cancer cells. P2X7, an ATP-gated cation-selective channel, plays a role in the induction of apoptosis; nf-P2X7, is upregulated in a variety of cancer cell types while not expressed on normal, healthy cells and is unable to form a large transmembrane, apoptotic pore upon exposure to ATP and prevents apoptosis.

anti-NKG2A monoclonal antibody BMS-986315

A human monoclonal antibody against the human natural killer (NK) and T-lymphocyte cell checkpoint inhibitor killer cell lectin-like receptor subfamily C member 1 (NKG2A), with potential antineoplastic activity. Upon administration, anti-NKG2A monoclonal antibody BMS-986315 targets and binds to NKG2A, and prevents the binding of NKG2A to its ligand human leukocyte antigen-E (HLA-E), which is overexpressed on tumor cells. This blocks the HLA-E-mediated inhibition of NKG2A-positive infiltrating NK and cytotoxic T lymphocytes (CTLs) and induces a NK and CTL-mediated immune response against the cancer cells leading to their destruction. Human NKG2A, an inhibitory cell surface receptor covalently bound to CD94, is expressed by NK cells and CTLs. Stimulation of the CD94/NKG2A complex inhibits the cytotoxic activity of these cells. HLA-E, a nonclassical HLA class Ib molecule, is often overexpressed on tumor cells and is associated with poor prognosis.

anti-NKG2A monoclonal antibody BRY805

A humanized monoclonal antibody against the human natural killer (NK) and T-lymphocyte cell checkpoint inhibitor killer cell lectin-like receptor subfamily C member 1 (NKG2A; natural killer group 2 A), with potential antineoplastic activity. Upon administration, anti-NKG2A monoclonal antibody BRY805 targets and binds to NKG2A, thereby preventing the binding of NKG2A to its ligand human leukocyte antigen-E (HLA-E), which is overexpressed on tumor cells. This blocks the HLA-E-mediated inhibition of NKG2A-positive infiltrating NK and cytotoxic T lymphocytes (CTLs) and induces a NK and CTL-mediated immune response against cancer cells leading to their destruction. Human NKG2A, an inhibitory cell surface receptor covalently bound to CD94, is expressed by NK cells and CTLs. Stimulation of the CD94/NKG2A complex inhibits the cytotoxic activity of these cells. HLA-E, a nonclassical HLA class Ib molecule, is often overexpressed on tumor cells and is associated with poor prognosis.

anti-NKG2A monoclonal antibody Sym025

A monoclonal antibody against the human natural killer (NK) and T-lymphocyte cell checkpoint inhibitor killer cell lectin-like receptor subfamily C member 1 (NKG2A), with potential antineoplastic activity. Upon administration, anti-NKG2A monoclonal antibody Sym025 targets and binds to NKG2A, and prevents the binding of NKG2A to its ligand human leukocyte antigen-E (HLA-E), which is overexpressed on tumor cells. This blocks the HLA-E-mediated inhibition of NKG2A-positive infiltrating NK and cytotoxic T lymphocytes (CTLs) and induces a NK and CTL-mediated immune response against the cancer cells leading to their destruction. Human NKG2A, an inhibitory cell surface receptor covalently bound to CD94, is expressed by NK cells and CTLs. Stimulation of the CD94/NKG2A complex inhibits the cytotoxic activity of these cells. HLA-E, a nonclassical HLA class Ib molecule, is often overexpressed on tumor cells and is associated with poor prognosis.

anti-NRP1 antibody ASP1948

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against neuropilin-1 (NRP1; CD304; BDCA-4), with potential immunomodulatory and antineoplastic activities. Upon administration, anti-NRP1 antibody ASP1948 specifically targets and binds to NRP1. This prevents the binding of NRP1 to its ligand and may block the immune inhibitory actions of regulatory T cells (Tregs) mediated by the interaction of NRP1 with its ligand. This may enhance the immune response against tumor cells. NRP1 is a transmembrane co-receptor protein expressed in Tregs; it plays an important role in maintaining the stability and function of Tregs.

anti-nucleolin aptamer AS1411

A 26-base guanine-rich oligodeoxynucleotide aptamer with potential apoptotic induction activity. Upon administration, anti-nucleolin aptamer AS1411 targets and binds to nucleolin, a nucleolar phosphoprotein which is overexpressed on the surface of certain cancer cells. Via binding to cell surface nucleolin, AS1411 is internalized and may prevent nucleolin from binding to and stabilizing mRNA of the anti-apoptotic BCL2, thereby destabilizing BCL2 mRNA, leading to a reduction in BCL2 protein synthesis. This may lead to the induction of apoptosis.

anti-NY-ESO-1 TCR LV-transduced autologous T cells TAEST16001

A preparation of human autologous T lymphocytes that are transduced with a lentiviral vector (LV) encoding an affinity-enhanced T-cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential immunostimulating and antineoplastic activities. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the anti-NY-ESO-1 TCR LV-transduced autologous T cells TAEST16001 recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types, and is not, or is minimally, expressed in normal, healthy cells.

anti-NY-ESO1 TCR-transduced autologous CD62L+-derived T lymphocytes

Human autologous CD62L-positive T lymphocytes transduced with a retroviral vector encoding a T cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and reintroduction into the patient, the anti-NY-ESO1 TCR-transduced autologous CD62L+-derived T lymphocytes bind to NY-ESO-1-overexpressing tumor cells. This may result in cytotoxic T-lymphocyte (CTL)-mediated elimination of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. CD62L, also called L-selectin, is a lymphoid homing receptor and differentiation marker and is expressed on a subset of CD8-positive T-lymphocytes; it is involved in the migration of T-lymphocytes to lymph nodes and may improve the efficacy for ex vivo-expanded T-cells following adoptive cell therapy.

anti-NY-ESO1/LAGE-1A TCR/scFv anti-CD3 IMCnyeso

A bispecific molecule composed of a soluble, affinity-enhanced T-cell receptor (TCR) specific for human leukocyte antigen A2 (HLA-A2)-restricted cancer-testis antigens (CTAs) NY-ESO-1 and L antigen family member 1 isoform A (LAGE-1A; LAGE-A1; CT6.2a), fused to a single-chain variable fragment (scFv) specific for the T-cell surface antigen CD3, with potential immunomodulating and antineoplastic activities. Upon infusion, anti-NY-ESO1/LAGE-1A TCR/scFv anti-CD3 IMCnyeso specifically targets and binds with its TCR moiety to NY-ESO-1 and/or LAGE-1A expressed on tumor cells and with its scFv moiety to CD3 expressed on T-cells. This crosslinks tumor cells and T-cells, re-directs and activates T cells, and results in a cytotoxic T-lymphocyte (CTL)-mediated destruction of NY-ESO-1 and/or LAGE-1A-positive tumor cells. NY-ESO-1 and LAGE-1A, members of the cancer-testis antigen (CTA) family, are overexpressed on the surface of various tumor cell types; they share a specific HLA-A*0201 epitope, 157-165, which is expressed on certain tumor cell types while its expression is not found on normal, healthy cells.

anti-OX40 agonist monoclonal antibody ABBV-368

An agonistic humanized IgG1 monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory activity. Upon administration, anti-OX40 agonist monoclonal antibody ABBV-368 selectively binds to and activates OX40. This may induce the proliferation of memory and effector T-lymphocytes and inhibit the function of T-regulatory cells (Tregs) in the tumor microenvironment (TME). OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and plays an essential role in T-cell activation and differentiation.

anti-OX40 agonist monoclonal antibody BAT6026

An agonistic recombinant monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory activity. Upon administration, anti-OX40 agonist monoclonal antibody BAT6026 selectively targets, binds to and activates OX40. This may induce the proliferation of memory and effector T lymphocytes and inhibit the function of T-regulatory cells (Tregs) in the tumor microenvironment (TME). This enhances anti-tumor immune responses and prevents Tregs-mediated immune suppression. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and plays an essential role in T-cell activation and differentiation.

anti-OX40 agonist monoclonal antibody BGB-A445

An agonistic monoclonal antibody targeting the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory and antineoplastic activities. Upon administration, anti-OX40 agonist monoclonal antibody BGB-A445 selectively binds to OX40, thereby activating OX40. This induces the proliferation of memory and effector T-lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T cells.

anti-OX40 agonist monoclonal antibody GEN1055

An agonistic, hexabody-based monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory and antineoplastic activities. Upon administration, anti-OX40 agonist monoclonal antibody GEN1055 selectively targets and binds to OX40, thereby forming a hexamer and inducing OX40 clustering. This activates OX40 and induces the proliferation of memory and effector T lymphocytes and inhibits the function of T-regulatory cells (Tregs) in the tumor microenvironment (TME). This enhances anti-tumor immune responses and prevents Tregs-mediated immune suppression. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and plays an essential role in T-cell activation and differentiation.

anti-OX40 agonist monoclonal antibody HFB301001

An agonistic human immunoglobulin G1 (IgG1) monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunomodulatory and antineoplastic activities. Upon administration, anti-OX40 agonist monoclonal antibody HFB301001 selectively targets and binds to a unique epitope on OX40, and activates OX40 without competing with the endogenous OX40 ligand (OX40L; tumor necrosis factor ligand superfamily member 4; TNFSF4). This may induce the proliferation of memory and effector T lymphocytes and inhibit the function of T-regulatory cells (Tregs) in the tumor microenvironment (TME), thereby enhancing anti-tumor immune responses and preventing Tregs-mediated immune suppression. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and plays an essential role in T-cell activation and differentiation. HFB301001 does not lead to a downregulation of OX40 following the co-stimulation of T cells.

anti-OX40 antibody BMS 986178

An agonistic monoclonal antibody against the co-stimulatory receptor OX40 (CD134; TNFRSF4), with potential immunostimulatory activity. Upon administration, anti-OX40 monoclonal antibody BMS 986178 selectively binds to and activates the OX40 receptor, by mimicking the action of the endogenous OX40 ligand (OX40L). OX40 receptor activation induces proliferation of memory and effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor family (TNFRSF), is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T-cells.

anti-OX40 monoclonal antibody

An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Mimicking the natural OX4 ligand (OX40L), anti-OX40 monoclonal antibody selectively binds to and activates the OX40 receptor. Receptor activation induces proliferation of memory and effector T lymphocytes. In the presence of tumor associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed by CD4 T cells and provides a costimulatory signal for T cell activation.

anti-OX40 monoclonal antibody GSK3174998

An agonistic humanized immunoglobulin G1 (IgG1) monoclonal antibody against the cell surface receptor OX40 (CD134; TNFRSF4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-OX40 monoclonal antibody GSK3174998 selectively binds to and activates OX40. Receptor activation induces proliferation of memory and effector T lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T cells.

anti-OX40 monoclonal antibody MEDI0562

An agonistic, humanized monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Upon administration, anti-OX40 monoclonal antibody MEDI0562 selectively binds to and activates the OX40 receptor. OX40 receptor activation induces proliferation of memory and effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this agent may promote an immune response against TAAs-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T-cells.

anti-OX40 monoclonal antibody MOXR0916

An agonistic humanized monoclonal antibody against the receptor, OX40 (CD134), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-OX40 monoclonal antibody MOXR0916 selectively binds to and activates OX40, by mimicking the action of endogenous OX40 ligand (OX40L). OX40 activation induces proliferation of effector T lymphocytes and inhibits the activity of regulatory T cells. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on T lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells.

anti-p53 T-cell receptor-transduced peripheral blood lymphocytes

Human autologous peripheral blood lymphocytes (PBLs) transduced with an anti-p53 T cell receptor gene with potential antineoplastic activity. PBLs are harvested from a patient and pulsed with a retroviral vector that encodes the T-cell receptor gene specific for a mutated form of p53. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these modified PBLs express the anti-p53 T cell receptor which binds to mutant p53-overexpressing tumor cells; PBL-mediated tumor growth inhibition may follow. Many tumor cell types overexpress mutant p53 proteins, which are associated with the loss of apoptosis regulation and abnormal cell proliferation.

anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061

A 1:1 fixed dose combination formulation composed of the two monoclonal antibodies AI-025, a monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), and gotistobart, a pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061, AI-025 targets, binds to and inhibits PD-1 and ONC-392 targets, binds to and inhibits CTLA-4. This inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.

anti-PD-1 antibody-IL-15/IL-15Ra fusion protein IAP0971

A heterodimeric and bifunctional fusion protein composed of four chains: two heavy chains targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), one of which is fused to the cytokine interleukin-15 (IL-15) while the other one is fused to IL-15 receptor alpha (IL15Ralpha; IL15Ra) sushi domain, which fuses the IL-15/IL-15Ra sushi domain complex, and two anti-PD1 antibody light chains, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD-1 antibody-IL-15/IL-15Ra fusion protein IAP0971, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and induces a T-cell-mediated immune response against tumor cells. The IL-15 moiety specifically binds to the IL-2/15Rbeta,gamma receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the in the tumor microenvironment (TME), and further induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T- and NK-cell development, activation and proliferation. IL-15Ra complexed with IL-15 domain improves stability. IAP0971 increases specific signaling of IL-15 in the TME due to the high expression of PD-1 in the TME, thereby preventing systematic non-specific IL-15-mediated signaling.

anti-PD-1 antibody-interleukin-21 mutein fusion protein AMG 256

An antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a mutein of the cytokine interleukin-21 (IL-21), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD-1 antibody-IL-21 mutein fusion protein AMG 256, the antibody moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. The IL-21 mutein moiety binds to the IL-21 receptor and activates IL-21 cytokine signaling in PD-1-expressing cells. This may modulate the proliferation and/or differentiation, promote survival, and increase the cytolytic activity of PD-1-expressing T cells, thereby enhancing T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-21 plays an important role in the regulation of cellular immune responses.

anti-PD-1 fusion protein AMP-224

A recombinant B7-DC Fc-fusion protein composed of the extracellular domain of the PD-1 ligand programmed cell death ligand 2 (PD-L2, B7-DC) and the Fc region of human immunoglobulin (Ig) G1, with potential immune checkpoint inhibitory and antineoplastic activities. Anti-PD-1 fusion protein AMP-224 specifically binds to PD-1 on chronically stimulated T cells and reduces their proliferation. This may restore immune function and may result in the activation of cytotoxic T cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein of Ig superfamily and inhibitor receptor expressed on activated T cells, negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. AMP-224 does not bind normal activated T cells.

anti-PD-1 monoclonal antibody AMG 404

A human monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody AMG 404 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody BAT1306

A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1306 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody BAT1308

A humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1308 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody GNR-051

A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody GNR-051 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody JTX-4014

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody JTX-4014 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody LVGN3616

A humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody LVGN3616 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody LZM009

A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor, programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, LZM009 binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands, programmed cell death-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways, leading to the activation of both T cells and T-cell-mediated immune responses against tumor cells. PD-1 is a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T cells that negatively regulates T-cell activation and effector function when activated by its ligands. PD-1 plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody MEDI0680

A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MEDI0680 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody MW11

A recombinant humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MW11 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody OSE-279

A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody OSE-279 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody PE0105

A recombinant monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody PE0105 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody QL1604

A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody QL1604 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody SCT-I10A

A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SCT-I10A targets, binds to, and inhibits PD-1 and its downstream signaling pathways. This may restore immune functions through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody SHR-1901

A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1901 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2). PD-1 plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody Sym021

A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1 , PCD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody Sym021 binds to and inhibits PD-1 activation and its downstream signaling pathways. This may restore immune function through the activation of T cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF), is expressed on T cells and functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2). Activated PD-1 plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody SYN125

A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SYN125 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune functions through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 monoclonal antibody TY101

A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody TY101 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1 siRNA PH-762

A self-delivering small-interfering RNA (siRNA) targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, anti-PD-1 siRNA PH-762 binds to and destroys mRNA PD-1, thereby preventing the expression of PD-1. As PD1-mediates the downregulation of T-cell activation and proliferation, PH-762 is able to restore immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This may lead to an inhibition of tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 (cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.

anti-PD-1/anti-4-1BB bispecific antibody IBI-319

A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-4-1BB bispecific antibody IBI-319 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T lymphocytes in the tumor microenvironment (TME), and 4-1BB, which is expressed on activated T lymphocytes and natural killer (NK) cells. This crosslinks PD-1- and 4-1BB-expressing T cells. Through 4-1BB binding, IBI-319 acts as a conditional 4-1BB agonist, resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, PD-1 binding prevents PD-L1 from binding to and activating its receptor PD-1 and inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-PD-1/anti-CD73 bispecific antibody AK131

A bispecific antibody derived from penpulimab and dresbuxelimab and directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, anti-PD-1/anti-CD73 bispecific antibody AK131 simultaneously targets and binds to both PD-1 expressed on T cells and CD73 expressed on tumor cells. The binding of AK131 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of AK131 to CD73 inhibits the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This increases the activity of CTLs, activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. The binding of AK131 to CD73 may also promote B-cell activation and proliferation, thereby further enhancing anti-tumor immune responses. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment (TME).

anti-PD-1/anti-CTLA-4/anti-VEGF trispecific antibody HC010

A trispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-CTLA-4/anti-VEGF trispecific antibody HC010 simultaneously targets, binds to and blocks PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) in the tumor microenvironment (TME), thereby inhibiting the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of HC010 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. Both PD-1 and CTLA-4 negatively regulate the activation and effector functions of T cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-1/anti-HER2 bispecific antibody IBI315

A recombinant human immunoglobulin G1 (IgG1) bispecific antibody directed against the human epidermal growth factor receptor 2 (HER2) and the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-PD-1/anti-HER2 bispecific antibody IBI315 simultaneously targets, binds to and inhibits HER2 and PD-1 and their downstream signaling pathways, and bridges PD-1-expressing T cells to HER2-expressing tumor cells. This may inhibit tumor cell proliferation of HER2-overexpressing cells. Inhibition of PD-1-mediated signaling may restore immune function through the activation of T cells and T-cell-mediated immune responses against the HER2-expressing tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1/anti-ILT4 bispecific antibody CDX-585

A humanized, dual antagonist immunoglobulin G1 kappa (IgG1K) monoclonal antibody directed against the inhibitory immune checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and ILT4 (immunoglobulin-like transcript 4; leukocyte immunoglobulin-like receptor subfamily B member 2; LILRB2; lymphocyte immunoglobulin-like receptor 2; LIR2; monocyte/macrophage immunoglobulin-like receptor 10; MIR-10; CD85d), with potential immunomodulating and antineoplastic activities. Upon administration, anti-PD-1/anti-ILT4 bispecific antibody CDX-585 targets and binds to both PD-1 and ILT4. The binding of CDX-585 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and/or 2 (PD-L2). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of CDX-585 to ILT4 prevents activation by its ligands, including the major histocompatibility complex class I (MHC I) molecules human leukocyte antigen (HLA)-A, HLA-B, HLA-C and HLA-G, and inhibits ILT4-mediated signaling. Dual checkpoint blockade of PD-1 and ILT4 may enhance T-cell activation, activate expression of pro-inflammatory cytokines, including granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNFalpha), and augment cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune responses more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 or PD-L2; it plays an important role in tumor evasion from host immunity. ILT4, a transmembrane protein and inhibitory member of the immunoglobulin-like transcript (ILT) family of proteins, is expressed primarily by myeloid cells, including monocytes, macrophages, dendritic cells (DCs) and granulocytes, and certain tumor cells; it also plays a role in tumor evasion.

anti-PD-1/anti-PD-L1 bispecific antibody CTX-8371

A bispecific tetravalent antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and its ligand, human programmed death-ligand 1 (PD-L1; CD274), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-PD-L1 bispecific antibody CTX-8371 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes in the tumor microenvironment (TME), and PD-L1, which is expressed on tumor cells. This crosslinks PD-1-expressing T cells and PD-L1-expressing tumor cells, and prevents PD-L1 from binding to and activating its receptor PD-1, which inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-1/anti-PD-L1 bispecific antibody IBI318

A recombinant immunoglobulin G1 (IgG1) bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and its ligand, human programmed death-ligand 1 (PD-L1; CD274), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-PD-L1 bispecific antibody IBI318 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T lymphocytes in the tumor microenvironment (TME), and PD-L1, which is expressed on tumor cells. This crosslinks PD-1-expressing T cells and PD-L1-expressing tumor cells. This prevents PD-L1 from binding to and activating its receptor PD-1 and inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-1/anti-PD-L1 bispecific antibody LY3434172

A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and its ligand, human programmed death-ligand 1 (PD-L1; CD274), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-PD-L1 bispecific antibody LY3434172 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T lymphocytes in the tumor microenvironment (TME), and PD-L1 expressed on tumor cells. This prevents PD-L1 from binding to and activating its receptor PD-1 and inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-1/anti-TGF-beta bifunctional fusion protein TQB2868

A bifunctional fusion protein directed against both the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TGF-beta bifunctional fusion protein TQB2868 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.

anti-PD-1/anti-TGFbRII bispecific antibody INCA33890

A bispecific antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta) receptor II (TGFbRII), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/anti-TGFbRII bispecific antibody INCA33890 targets and binds to both PD-1 and TGFbRII and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). The binding of INCA33890 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of INCA33890 to TGFbRII prevents the binding of TGF-beta to TGFbRII, thereby preventing the activation of the TGF-beta-mediated signaling pathway. This abrogates TGF-beta-mediated immunosuppression in the TME, increases natural killer (NK) cell and CTL activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.

anti-PD-1/anti-TIGIT bispecific antibody IBI321

A bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-PD-1/anti-TIGIT bispecific antibody IBI321 simultaneously targets, binds to and inhibits PD-1 and TIGIT and their downstream signaling pathways. Inhibition of PD-1-mediated signaling may restore immune function through the activation of T cells and T-cell-mediated immune responses. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-PD-1/anti-TIGIT bispecific antibody ZG005

A humanized bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TIGIT bispecific antibody ZG005 simultaneously targets, binds to and inhibits PD-1 and TIGIT and their downstream signaling pathways. Inhibition of PD-1-mediated signaling may restore immune function through the activation of T cells and T-cell-mediated immune responses. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-PD-1/anti-TIM-3 bispecific antibody AZD7789

A bispecific antibody directed against both the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TIM-3 bispecific antibody AZD7789 simultaneously targets and binds to both TIM-3 and PD-1 expressed on certain T-cells. This blocks the interaction of TIM-3 with some of its physiologic ligands and prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is often co-expressed with PD-1 on tumor-antigen-specific T cells. Dual checkpoint blockade of PD-1 and TIM-3 may enhance T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.

anti-PD-1/anti-TIM-3 bispecific antibody LB1410

A recombinant humanized bispecific antibody directed against both the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TIM-3 bispecific antibody LB1410 simultaneously targets and binds to both TIM-3 and PD-1 expressed on certain T cells. This blocks the interaction of TIM-3 with some of its physiologic ligands and prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is often co-expressed with PD-1 on tumor-antigen-specific T cells. Dual checkpoint blockade of PD-1 and TIM-3 may enhance T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.

anti-PD-1/anti-VEGF bispecific antibody AI-081

A Fc-silenced, bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody AI-081 simultaneously targets and binds to both PD-1 expressed on T cells and VEGF expressed on tumor cells. The binding of AI-081 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of AI-081 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-1/anti-VEGF bispecific antibody JS207

A recombinant humanized bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody JS207 simultaneously targets and binds to both PD-1 expressed on T cells and VEGF expressed on tumor cells. The binding of JS207 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of JS207 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-1/anti-VEGF bispecific antibody MHB039A

A bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody MHB039A simultaneously targets and binds to both PD-1 expressed on T cells and VEGF expressed on tumor cells. The binding of MHB039A to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of MHB039A to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-1/anti-VEGF bispecific antibody SCTB14

A bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody SCTB14 simultaneously targets and binds to both PD-1 expressed on T cells and VEGF expressed on tumor cells. The binding of SCTB14 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of SCTB14 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-1/CD47 infusion protein HX009

A bispecific antibody fusion protein directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-PD-1/CD47 infusion protein HX009, the agent simultaneously and selectively targets and binds to PD-1 expressed on T lymphocytes and CD47 on tumor cells. The CD47 binding by HX009 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD47-expressing tumor cells. The binding of HX009 to PD-1 blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore effector T-cell functions and may further activate cytotoxic T-lymphocyte (CTL)-mediated tumor cell killing. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA), widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. By co-targeting CD47 and PD-1, HX009 has the potential to overcome the limitations of existing CD47-targeted therapies by possibly avoiding the side effects caused by binding to CD47 on healthy hematopoietic stem cells (HSCs), which causes unwanted macrophage-mediated phagocytosis. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.

anti-PD-1/CTLA-4 bispecific antibody SI-B003

A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD1/CTLA-4 bispecific antibody SI-B003 targets and binds to both PD-1 and CTLA4 expressed on tumor-infiltrating T lymphocytes (TILs), and inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD1 and CTLA4 with SI-B003 may enhance T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.

anti-PD-1/IL-2 bispecific antibody fusion protein IBI363

A bispecific antibody fusion protein composed of a monoclonal antibody targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and fused to a mutated form of the endogenous cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/IL-2 bispecific antibody fusion protein IBI363 targets and binds to PD-1 expressed on PD-1-expressing T cells, thereby inhibiting PD-1-mediated signaling. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. IL-2 targets and binds to the IL-2 receptor IL2R and activates IL-2/IL-2R-mediated signaling, which further activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). This further enhances T-cell-mediated cytotoxic immune responses against tumor cells. By selectively activating PD-1 positive T cells by IL-2, but not PD-1 negative bystander or naïve T cells, the activity of tumor-specific T cells is specifically enhanced while IL-2-induced systemic toxicity is decreased. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1/IL-2 fusion protein TEV-56278

A recombinant fusion protein composed of an antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to the cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon administration of anti-PD-1/IL-2 fusion protein TEV-56278, the antibody moiety targets and binds to PD-1 expressed on PD-1-expressing T cells in the tumor microenvironment (TME). The IL-2 moiety stimulates a local immune response and activates natural killer (NK) cells and cytotoxic T cells, which may enhance the activity of neoantigen specific T cells and potentiate T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

anti-PD-1/IL-2Ra/IL-2 fusion protein REGN10597

An antibody fusion protein composed of an antibody fragment targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and fused to the endogenous cytokine interleukin-2 (IL-2) and masked with an antibody fragment directed against the IL-2 receptor subunit alpha (IL2Ra; CD25) binding-site on IL-2, with potential immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/IL-2Ra/IL-2 fusion protein REGN10597 targets and binds to PD-1 expressed on PD-1-expressing T cells in the tumor microenvironment (TME), thereby specifically bringing IL-2 to the PD-1-positive T cells in the TME. The PD-1 binding specifically induces a confirmational change in REGN10597 that allows its IL-2 moiety to bind to the IL-2Ra expressed on PD-1-positive CD8+ T effector cells and natural killer (NK) cells, thereby activating IL2Ra-mediated signaling within these immune cells. The activation of cytotoxic T-lymphocytes (CTLs) and NK cells mediate cytolytic immune responses against tumor cells causing tumor cell destruction and inhibition of tumor cell proliferation. By selectively activating PD-1 positive T cells with IL-2, but not PD-1 negative bystander or naïve T cells, the activity of tumor specific T cells is specifically enhanced while IL-2-induced systemic toxicity is decreased. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. The receptor-masked IL-2 allows for specific activation of IL-2 in the presence of PD-1-positive cells in the TME.

anti-PD-1/LAG-3 bispecific antibody AK129

A humanized, immunoglobulin G1 (IgG1) bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279; programmed death 1) and lymphocyte activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/LAG-3 bispecific antibody AK129 targets and binds to both PD-1 and LAG-3 expressed on T cells, thereby blocking the interaction of PD-1 to its ligand programmed cell death-ligand 1 (PD-L1; cluster of differentiation 274; CD274) and of LAG-3 to its ligand major histocompatibility complex II (MHCII). This inhibits the PD-1- and LAG-3-mediated downregulation of T-cell activation and proliferation and abrogates downstream immune suppression. This may lead to a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1 and LAG-3 play key roles in suppressing T-cell activation and proliferation and promote tumor immune escape.

anti-PD-1/LAG-3 bispecific antibody EMB-02

A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279; Programmed Death 1) and lymphocyte activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/LAG-3 bispecific antibody EMB-02 targets and binds to both PD-1 and LAG-3 expressed on T cells and inhibits the PD-1- and LAG-3-mediated downregulation of T-cell activation and proliferation. This may lead to cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1 and LAG-3 play key roles in suppressing T-cell activation and proliferation.

anti-PD-1/TGF-beta RII bifunctional fusion protein JS201

A bifunctional fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating, immunomodulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta RII bifunctional fusion protein JS201 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression and the suppression of the immune response.

anti-PD-1/TGFbRII fusion protein LBL-015

A tetravalent bispecific fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta receptor II (TGFbRII) fusion protein LBL-015 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.

anti-PD-L-1/anti-OX-40 bispecific antibody EMB-09

A tetravalent, bispecific antibody directed against both the immunosuppressive ligand programmed cell death-1 (PD-L1; cluster of differentiation 274; CD274) and the co-stimulatory receptor OX40 (CD134; TNFRSF4), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PD-L1/anti-OX40 bispecific antibody EMB-09 binds to PD-L1 expressed on tumor cells, and simultaneously binds to and activates OX40 on activated T cells. The binding of EMB-09 to PD-L1 blocks its binding to and activation of its receptor, programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. The binding of EMB-09 to OX40 and the activation of OX40 induces the proliferation of memory and effector T lymphocytes, which also enhances the anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) that is expressed on activated T cells, suppresses the immune system and results in immune evasion. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor superfamily, is mainly expressed on activated T cells and provides a co-stimulatory signal for the proliferation and survival of activated T cells.

anti-PD-L1 antibody-drug conjugate HLX43

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), conjugated, via a cleavable linker, to a cytotoxic payload containing a camptothecin-based topoisomerase I (topo I) inhibitor, with potential antineoplastic activity. Upon administration of the anti-PD-L1 ADC HLX43, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressed on tumor cells. The linker is specifically cleaved in the tumor microenvironment (TME), thereby delivering the toxin into PD-L1-expressing malignant cells, while sparing the normal cells. The cytotoxic agent specifically inhibits DNA topoisomerase I activity, causes double-strand breaks (DSBs) of DNA, and thereby inhibiting DNA replication and resulting in tumor cell apoptosis. This inhibits the proliferation of PD-L1-expressing tumor cells. In addition, HLX43 induces bystander killing effects, thereby further decreasing PD-L1-expessing tumor cells. PD-L1, a transmembrane protein, is expressed on the surface of certain immune cells and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T cells, limits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1 antibody-drug conjugate SGN-PDL1V

An antibody-drug conjugate (ADC) composed of an antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), conjugated to the cytotoxic agent monomethyl auristatin E (MMAE) via a protease-cleavable peptide linker, with potential antineoplastic activity. Upon administration of the anti-PD-L1 ADC SGN-PDL1V, the anti-PD-L1 antibody specifically targets and binds to PD-L1 expressed on tumor cells. Following internalization, enzymatic cleavage and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on the surface of certain immune cells and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T cells, limits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1 antibody/IL-15 fusion protein IGM-7354

A fusion protein composed of a pentameric immunoglobulin M (IgM) antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1 antibody/IL-15 fusion protein IGM-7354, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cancer cells and antigen presenting cells (APCs) in the tumor microenvironment (TME), thereby delivering IL-15 to PD-L1-expressing tumor cells. In turn, the IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally, and reverses T-cell exhaustion. This induces an anti-tumor immune response in the TME against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on APCs and on various cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. The immunostimulatory cytokine IL-15 regulates CD8+ T and NK cell development, activation, and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. By binding to PD-L1-expressing cells in the TME, IGM-7354 enhances its IL-15-mediated activity on the immune system locally and increases its efficacy while reducing systemic toxicities.

anti-PD-L1 monoclonal antibody

A monoclonal antibody directed against programmed death-ligand 1 (PD-L1; CD274).

anti-PD-L1 monoclonal antibody BCD-135

A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody BCD-135 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody BGB-A333

A humanized immunoglobulin G1 (IgG1)-variant monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody BGB-A333 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, BGB-A333 blocks the interaction between PD-L1 and its other receptor, the immunostimulatory molecule cluster of differentiation 80 (CD80; B7-1). This prevents PD-L1/CD80 signaling and inhibits the induction of PD-L1-induced apoptosis of activated CD8+ T cells and increases T-cell proliferation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on activated T cells suppresses the immune system and results in immune evasion. PD-1 negatively regulates T-cell activation.

anti-PD-L1 monoclonal antibody FAZ053

A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1), with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody FAZ053 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated anti-tumor immune response and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.

anti-PD-L1 monoclonal antibody GR1405

A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody GR1405 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody HLX20

A recombinant human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody HLX20 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody IMC-001

A human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody IMC-001 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, anti-PD-L1 monoclonal antibody IMC-001 also induces antibody-dependent cell-mediated cytotoxicity (ADCC). PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody LP002

A humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody LP002 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, by binding to PD-L1, LP002 also prevents binding of this ligand to B7.1 expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody MDX-1105

A fully human monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Anti-PD-L1 monoclonal antibody MDX-1105 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.

anti-PD-L1 monoclonal antibody RC98

A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody RC98 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1 monoclonal antibody ZKAB001

A human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-PD-L1 monoclonal antibody ZKAB001 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.

anti-PD-L1/4-1BB bispecific antibody ATG-101

A bispecific antibody composed of a human immunoglobulin G1 (IgG1) monoclonal antibody targeting human programmed death-ligand 1 (PD-L1) fused with a single chain variable fragment (scFv) targeting 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/4-1BB bispecific antibody ATG-101 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells. Upon PD-L1 binding, the 4-1BB activation signal is induced and ATG-101 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, ATG-101 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-PD-L1/4-1BB bispecific antibody LBL-024

A tetravalent bispecific antibody targeting the immunosuppressive ligand programmed death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/4-1BB bispecific antibody LBL-024 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells. Upon 4-1BB binding, LBL-024 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, LBL-024 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-PD-L1/4-1BB bispecific antibody QLF31907

A bispecific antibody targeting the immunosuppressive ligand programmed death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/4-1BB bispecific antibody QLF31907 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells. Upon 4-1BB binding, QLF31907 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, QLF31907 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-PD-L1/anti-4-1BB bispecific antibody ABL503

A bispecific antibody composed of a Fc-silenced human immunoglobulin G1 (IgG1) monoclonal antibody targeting human programmed death-ligand 1 (PD-L1) fused with a single chain variable fragment (scFv) targeting 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/anti-4-1BB bispecific antibody ABL503 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells. Upon PD-L1 binding, the 4-1BB activation signal is induced and ABL503 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, ABL503 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.

anti-PD-L1/anti-CD47 bispecific antibody BAT7104

A symmetric immunoglobulin G (IgG)-like bispecific antibody targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-PD-L1/anti-CD47 bispecific antibody BAT7104 targets and binds to both CD47 and PD-L1 expressed on tumor cells. The CD47 binding by BAT7104 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of CD47-expressing tumor cells. The binding of BAT7104 to PD-L1 blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation, which protects cancer cells from phagocytosis and allows cancer cells to proliferate. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells. By co-targeting CD47 and PD-L1, BAT7104 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs).

anti-PD-L1/anti-CD47 bispecific monoclonal antibody LB101

A conditionally-activatable tetravalent bispecific antibody targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. LB101 contains two anti-CD47 domains blocked by two anti-PD-L1 domains, with human immunoglobulin (Ig) G-derived hinges linking the anti-CD47 and anti-PD-L1 domains. Upon administration of anti-PD-L1/anti-CD47 bispecific monoclonal antibody LB101, the PD-L1 targeting domains target and bind to PD-L1 expressed on tumor cells. The IgG-derived hinges are naturally degraded in the tumor microenvironment (TME) and, upon cleavage, unblock the CD47 domains. The CD47 domains target and bind to CD47, thereby blocking the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and induces antibody-dependent cellular phagocytosis (ADCP). The binding of LB101 to PD-L1 blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation, which protects cancer cells from phagocytosis and allows cancer cells to proliferate. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells. By co-targeting CD47 and PD-L1 and activating the CD47 domains within the TME, LB101 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs).

anti-PD-L1/anti-LAG-3 bispecific antibody ABL501

A bispecific antibody directed against two immune checkpoint proteins composed of an engineered immunoglobulin G4 (IgG4) monoclonal antibody targeting the inhibitory receptor lymphocyte activation gene 3 protein (LAG-3; LAG3) fused with a single chain variable fragment (scFv) targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1/anti-LAG-3 bispecific antibody ABL501 simultaneously targets and binds to LAG-3 expressed on T cells in the tumor microenvironment (TME) and PD-L1 expressed on tumor cells. This prevents LAG-3- and PD-L1-mediated signaling, reverses T-cell inactivation, activates the immune system and enhances cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune responses against PD-L1-expressing tumor cells, which together lead to a reduction in tumor growth. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to its receptor programmed death 1 (PD-1; PDCD1; CD279) on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T cells. Its expression is associated with tumor-mediated immune suppression.

anti-PD-L1/anti-TGF-beta bifunctional fusion protein TQB2858

A bifunctional fusion protein directed against both human programmed death ligand 1 (PD-L1) and transforming growth factor beta (TGF-beta), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, anti-PD-L1/anti-TGF-beta bifunctional fusion protein TQB2858 targets, binds to and neutralizes TGF-beta on tumor cells and simultaneously targets, binds to, and inhibits the activity of PD-L1 on the tumor cells. This prevents both TGF-beta- and PD-L1-mediated immunosuppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This also restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. TGF-beta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.

anti-PD-L1/anti-TIGIT bispecific antibody PM1022

A recombinant humanized bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-TIGIT/anti-PD-L1 bispecific antibody PM1022 simultaneously targets, binds to and inhibits TIGIT and PD-L1, thereby inhibiting their downstream signaling pathways. Inhibition of TIGIT, which is expressed on various immune cells and particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. Inhibition of PD-L1 prevents its binding to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1/anti-VEGF bispecific antibody

A bispecific antibody targeting both programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and vascular endothelial growth factor (VEGF).

anti-PD-L1/anti-VEGF bispecific antibody fusion protein B1962

A bispecific antibody fusion protein composed of an immunoglobulin G1 (IgG1) monoclonal antibody targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and fused to anti-vascular endothelial growth factor (VEGF) protein, with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF bispecific antibody fusion protein B1962 targets and simultaneously binds to both PD-L1 and VEGF expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against VEGF-expressing tumor cells. The binding of B1962 to VEGF prevents the binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.

anti-PD-L1/anti-VEGF-A bispecific antibody PM8002

A bispecific antibody targeting both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and vascular endothelial growth factor A (VEGF-A), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF-A bispecific antibody PM8002 targets and simultaneously binds to both PD-L1 and VEGF-A expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. The binding of PM8002 to VEGF-A prevents the binding of VEGF-A to VEGF receptor (VEGFR), thereby preventing the activation of VEGF-A/VEGFR-mediated signaling pathways. This prevents angiogenesis and may halt tumor cell proliferation. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF-A is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis.

anti-PD-L1/CD137 bispecific antibody MCLA-145

A full-length, Fc-silenced immunoglobulin G1 (IgG1) bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/CD137 bispecific antibody MCLA-145 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T lymphocytes. Through CD137 binding, MCLA-145 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, MCLA-145 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. Crosslinking of PD-L1-expressing tumor cells and activated T-lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells.

anti-PD-L1/CD27 bispecific antibody CDX-527

A bispecific antibody directed against both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the cell surface antigen CD27, with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PD-L1/CD27 bispecific antibody CDX-527 targets and binds to both PD-L1 expressed on tumor cells and CD27 expressed on a variety of immune cell types, including most T lymphocytes. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling and induces CD27-mediated signaling. This inhibits the PD-1-mediated downregulation of T-cell activation and proliferation, and enhances CD27-mediated responses, including the expansion of antigen-activated T cells and the cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity. CD27, a co-stimulatory molecule and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes, memory B cells and natural killer (NK) cells. It plays an important role in NK cell-mediated cytolytic activity and T- and B-lymphocyte proliferation and activation.

anti-PD-L1/Claudin18.2 bispecific antibody Q-1802

A bispecific antibody directed against both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PD-L1/Claudin18.2 bispecific antibody Q-1802 targets and simultaneously binds to both PD-L1 and CLDN18.2 expressed on certain types of tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against CLDN18.2-expressing tumor cells. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

anti-PD-L1/IL-15 fusion protein KD033

A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to the immunostimulatory cytokine interleukin-15 (IL-15), with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein KD033, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T cells, limits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1/IL-15 fusion protein SIM0237

A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), fused with potency reduced interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) sushi domain complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein SIM0237, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, the IL-15/IL-15Ra complex stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T cells, limits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. The attenuated IL-15 prevents the overstimulation of CD8+ T and NK cells.

anti-PD-L1/PD-L2 bispecific antibody IMGS-001

Fc-engineered bispecific monoclonal antibody targeting both immune checkpoint regulatory proteins human programmed death-ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/PD-L2 bispecific antibody IMGS-001 simultaneously targets and binds to PD-L1 and PD-L2 expressed on tumor cells, immunosuppressive stromal cells and endothelial cells. PD-L1 and PD-L2 binding by IMGS-001 prevents both PD-L1 and PD-L2 from binding to and activating their receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates PD-1-mediated signaling in T cells and PD-1-mediated T-cell inhibition. This activates cytotoxic T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. In addition, IMGS-001 induces antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), thereby killing PD-L1 and PD-L2-expressing cells in the tumor microenvironment (TME), and further abrogating the immunosuppressive nature of the TME. PD-L1 and PD-L2 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1/TGF-beta bispecific antibody Y101D

A recombinant bispecific antibody targeting both the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the human transforming growth factor beta (TGF-beta), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, the anti-PD-L1/TGF-beta bispecific antibody Y101D targets, binds to and neutralizes TGFbeta while simultaneously targets, binds to, and inhibits the activity of PD-L1 on tumor cells. This prevents both TGF-beta- and PD-L1-mediated immuno-suppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. TGF-beta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.

anti-PD-L1/TGFbetaRII fusion protein 6MW3511

A bifunctional fusion protein composed of a humanized anti-programmed death ligand 1 (PD-L1) nanobody fused to a mutant form of the human transforming growth factor beta (TGFbeta) receptor type II (TGFbetaRII), with potential antineoplastic and immune checkpoint modulating activities. Upon administration of anti-PD-L1/TGFbetaRII fusion protein 6MW3511, the TGFbetaRII moiety targets, binds to and neutralizes TGFbeta while the anti-PD-L1 nanobody moiety simultaneously targets, binds to, and inhibits the activity of PD-L1 on the tumor cell. This prevents both TGFbeta- and PD-L1-mediated immuno-suppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This restores and enhances anti-tumor immune responses and inhibits tumor cell proliferation in susceptible tumor cells. TGFbeta and PD-L1 are both upregulated in certain types of cancers and play key roles in tumor immune suppression; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis. The TGFbetaRII moiety is modified to enhance the stability of the agent.

anti-PD-L1/TGFbetaRII fusion protein BJ-005

A recombinant bifunctional fusion protein composed of a humanized immunoglobulin (Ig) G1 anti-programmed death ligand 1 (PD-L1) monoclonal antibody fused to the extracellular domain (ECD) of the human transforming growth factor beta (TGFbeta) receptor type II (TGFbetaRII), with potential antineoplastic and immune checkpoint modulating activities. Upon administration of anti-PD-L1/TGFbetaRII fusion protein BJ-005, the TGFbetaRII moiety targets, binds to and neutralizes TGFbeta while the antibody moiety simultaneously targets, binds to, and inhibits the activity of PD-L1 on the tumor cell. This prevents both TGFbeta- and PD-L1-mediated immuno-suppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. TGFbeta and PD-L1 are both upregulated in certain types of cancers and and play key roles in tumor immune suppression; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.

anti-PD-L1/TIM-3 bispecific antibody LY3415244

A bispecific antibody directed against the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, LY3415244 simultaneously targets and binds to TIM-3 expressed on certain T cells, including tumor-infiltrating lymphocytes (TILs), and PD-L1 expressed on tumor cells. This blocks the interaction of TIM-3 with some of its physiologic ligands and prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is often co-expressed with PD-1 on tumor-antigen-specific T cells. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-PD-L1/VEGF/TGF-beta trispecific antibody DR30206

A trispecific antibody targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), human vascular endothelial growth factor (VEGF) and human transforming growth factor beta (TGF-beta), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/VEGF/TGF-beta trispecific antibody DR30206 targets and simultaneously binds to both PD-L1 and VEGF expressed on tumor cells, and also neutralizes TGF-beta. This prevents both TGF-beta- and PD-L1-mediated immuno-suppressive pathways signaling, which increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, restores and enhances anti-tumor responses, and inhibits tumor cell proliferation in susceptible tumor cells. The binding of DR30206 to VEGF prevents the binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival. TGF-beta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.

anti-PDGFR alpha monoclonal antibody MEDI-575

A humanized monoclonal antibody directed against the platelet-derived growth factor receptor (PDGFR) alpha with potential antineoplastic activity. Anti-PDGFR alpha monoclonal antibody MEDI-575 inhibits activation of the cell-surface tyrosine kinase PDGFR alpha subunit and subsequent triggering of mitogenic signaling pathways, including the JAK/STAT, PI3K/Akt, and MAP kinase pathways. PDGFR alpha acts as a mitogenic signaling receptor for cells of mesenchymal origin and inhibition of receptor activity may inhibit tumor cell proliferation.

anti-PKN3 siRNA Atu027

A lipoplexed formulation consisting of short-interfering RNAs (siRNAs) directed against protein kinase N3 (PKN3) encapsulated in catiogenic and fusiogenic lipids with potential antineoplastic activity. Upon administration, catiogenic and fusiogenic lipids promote anti-PKN3 siRNA Atu02 uptake by tumor cells; the siRNAs moieties are subsequently released once inside the cell. The siRNAs bind to PKN3 mRNAs, which may result in the inhibition of translation and expression of the PKN3 protein and, so, growth inhibition of tumor cells that overexpress PKN3. The protein kinase C-related molecule PKN3, downstream in the phosphoinositide-3-kinase (PI3K) signaling pathway, is upregulated in many tumor cells and plays an important role in invasive cell growth and metastasis.

anti-plectin monoclonal antibody ZB131

A humanized monoclonal antibody directed against human plectin (plectin-1; plectin 1), with potential antineoplastic activity. Upon administration, anti-plectin monoclonal antibody ZB131 specifically binds to plectin expressed on the cell surface of cancer cells, thereby activating the immune system to induce an anti-tumor T-cell response against plectin-expressing cancer cells and inducing apoptosis in these cancer cells. Plectin, a pro-tumorigenic protein, is normally found inside the cytoplasm of healthy cells but is only selectively expressed on the cell surface of various cancer cells. Cancer-specific plectin (CSP), also known as cell surface plectin-1 (CSP1), plays an important role in cancer cell proliferation, migration and invasion.

anti-PLGF monoclonal antibody TB-403

A humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the placenta growth factor (PGF), with potential anti-angiogenic and antineoplastic activities. Anti-PGF monoclonal antibody TB-403 binds to both PGF-1 and -2, thereby inhibiting the binding of PGF-1 and -2 to the vascular endothelial growth factor receptor-1 (VEGFR-1) and subsequent VEGFR-1 phosphorylation. This may result in the inhibition of tumor angiogenesis and tumor cell proliferation. PGF, a member of the VEGF sub-family and a key molecule in angiogenesis and vasculogenesis, is upregulated in many cancers.

anti-PLVAP CSR02-Fab-tissue factor

A recombinant protein consisting of an antigen-binding fragment (Fab) of CSR02, a monoclonal antibody directed against plasmalemma vesicle associated protein (PLVAP), and linked to human tissue factor (TF), with potential antineoplastic activity. Upon intra-arterial (IA) infusion of CSR02-Fab-TF, the Fab moiety targets and binds to the vascular endothelial cell specific protein PLVAP that is present on the blood vessels of hepatocellular carcinoma (HCC) but that is not present on the blood vessels of normal liver tissue. In turn, TF initiates the clotting cascade, thereby blocking blood supply from the hepatic artery to the HCC. This deprives the HCC of its blood supply and leads to tumor cell death.

anti-poliovirus antibody

An antibody produced in response to exposure to poliovirus.

anti-PR1/HLA-A2 monoclonal antibody Hu8F4

A T-cell receptor (TCR)-like monoclonal antibody against PR1, a 9 amino-acid (VLQELNVTV) human leukocyte antigen (HLA)-A2-restricted leukemia-associated antigen (LAA) derived from the myeloid leukemia-associated antigens proteinase 3 (P3) and neutrophil elastase (NE), with potential immunostimulating and antineoplastic activities. Upon administration, anti-PR1/HLA-A2 monoclonal antibody Hu8F4 selectively binds to a combined epitope of the PR1/HLA-A2 complex expressed on acute myeloid leukemia (AML) blasts and leukemic stem cells (LSC), and prevents PR1/HLA-A2-mediated signaling. This induces complement-dependent cytotoxicity (CDC), to a lesser extent, antibody-dependent cell-mediated cytotoxicity (ADCC), and CDC/ADCC-independent cytolysis of myeloid leukemia cells. This results in a reduction of cellular proliferation in PR1/HLA-A2-overexpressing leukemic cells. PR1 in combination with the HLA-A2 molecule is highly expressed on AML blasts and LSCs.

anti-PRAME T-cell receptor/anti-CD3 scFv fusion protein IMC-F106C

A T-cell re-directing bi-specific biologic composed of a modified form of human T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) preferentially expressed antigen in melanoma (PRAME) and fused to an anti-CD3 single-chain variable fragment (scFv), with potential antineoplastic activity. Upon administration of IMC-F106C, the TCR moiety of this agent targets and binds to PRAME on tumor cells and the anti-CD3 scFv moiety binds to CD3- expressing T lymphocytes. This selectively cross-links tumor cells and T lymphocytes and results in a CTL-mediated death of PRAME-expressing tumor cells. The TAA PRAME is overexpressed by a variety of cancer cell types.

anti-PRL-3 monoclonal antibody PRL3-zumab

A humanized monoclonal antibody against phosphatase of regenerating liver 3 (PRL-3; PTP4A3), with potential immunomodulating and antineoplastic activities. Upon administration, anti-PRL-3 monoclonal antibody PRL3-zumab targets, binds to and blocks PRL-3 expressed on tumor cells. Although the exact mechanism of action through which this antibody kills tumor cells has yet to be fully elucidated, PRL3-zumab binds to PRL-3. This prevents PRL-3-mediated signaling in, inhibits the proliferation of and induces apoptosis in PRL-3-expressing tumor cells. PRL-3, a member of the PRL family of protein tyrosine kinases, is upregulated in a variety of tumor cells. Its expression is associated with increased invasiveness, higher metastatic potential, increased tumor cell survival and poor prognosis.

anti-programmed cell death protein 1 antibody expressing pluripotent killer T lymphocytes

A specific population of pluripotent killer (PIK) T cells that have been induced to express high levels of antibodies against the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential antitumor activity. Although the exact mechanism(s) of action through which PIK-PD-1 cells exert their effects has yet to be elucidated, upon infusion, these cells secrete antibodies that target PD-1 expressed on the surface of activated T cells and tumor cells. This may block the interaction of PD-1 with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) and PD-1 ligand 2 (PD-L2, PD-1L2; CD273). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation; PD-L1 is overexpressed on certain cancer cells, and PD-L2 is primarily expressed on antigen presenting cells (APCs).

anti-progranulin monoclonal antibody AG01

A monoclonal antibody targeting human progranulin (PGRN; glycoprotein 88; GP88), with potential antineoplastic activity. Upon administration, anti-PGRN monoclonal antibody AG01 targets and binds to PGRN expressed on tumor cells. This neutralizes PGRN and prevents the activation of downstream signaling pathways, which may include extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), phosphatidylinositol 3-kinase (PI3K), and focal adhesion kinase (FAK), thereby inhibiting tumor cell proliferation, migration and invasion. PGRN, an autocrine growth factor overexpressed in various types of cancers, plays an important role in tumorigenesis, tumor cell proliferation and invasiveness, and drug resistance.

anti-prolactin receptor antibody LFA102

A neutralizing antibody against the prolactin receptor (PRLR) with potential antineoplastic activity. Upon administration, anti-prolactin receptor antibody LFA102 binds to PRLR and prevents the binding of the peptide hormone prolactin (PRL) to its receptor. This binding induces an antibody-dependent cellular cytotoxicity (ADCC) and may eventually prevent tumor cell proliferation in PRLR-positive cancer cells. PRLR/PRL signaling pathway is frequently overexpressed in breast and prostate cancer.

anti-PSCA monoclonal antibody AGS-1C4D4

An IgG1k fully human monoclonal antibody directed against the human prostate stem cell antigen (PSCA) with potential antineoplastic activity. Anti-PSCA fully human monoclonal antibody MK4721 selectively targets and binds to PSCA, triggering complement-dependent cell lysis and antibody-dependent cell-mediated cytotoxicity in tumor cells expressing PSCA. PSCA is a glycosyl-phosphatidylinositol (GPI)-linked cell surface antigen found in cancers of the bladder, pancreas, and prostate.

anti-PSMA antibody-drug conjugate ARX517

An antibody-drug conjugate (ADC) containing a humanized immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against prostate-specific membrane antigen (PSMA) and site-specifically conjugated to two of the microtubule-disrupting toxin amberstatin (AS269), with potential antineoplastic activity. Upon administration of anti-PSMA ADC ARX517, the monoclonal antibody moiety selectively binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells. Upon internalization, amberstatin binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. The site-specific conjugation of the cytotoxic agent to the antibody improves the biophysical properties of ARX517, increases payload stability and optimizes its efficacy.

anti-PSMA gamma delta T-cell engaging bispecific antibody LAVA-1207

A bispecific gamma delta T-cell engager (TCE) antibody targeting both the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA) and Vdelta2 on Vgamma9Vdelta2 T cells, with potential immunostimulating and antineoplastic activities. Upon administration, anti-PSMA gamma delta T-cell engaging bispecific antibody LAVA-1207 binds to both PSMA-expressing tumor cells and Vgamma9Vdelta2 T cells. This activates and redirects the Vgamma9Vdelta2 T cells to PSMA-expressing tumor cells, and the Vgamma9Vdelta2 T cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, the Vgamma9Vdelta2 T cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The Vdelta2 gamma delta T-cell subset is one of the two major gamma delta T-cell subsets that is almost exclusively paired with the Vgamma9 chain. PSMA, a type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.

anti-PSMA monoclonal antibody MDX1201-A488

A recombinant, human monoclonal antibody targeting an extracellular epitope of human prostate specific membrane antigen (PSMA) that is conjugated with a fluorescent dye A488, with potential imaging activity. Upon intravenous administration, the MDX1201 moiety of anti-PSMA monoclonal antibody MDX1201-A488 targets PSMA expressed on cancer cells. Subsequently, the A488 moiety can then be visualized by fluorescence-based imaging and the amount of PSMA-expressing tumor cells can be assessed. A488 is a photostable fluorescent dye with a high quantum yield. PSMA, a tumor-associated antigen and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells.

anti-PSMA monoclonal antibody MLN591-DM1 immunoconjugate MLN2704

An immunoconjugate that consists of a humanized monoclonal antibody (MLN591), directed against prostate-specific membrane antigen linked to a maytansinoid (DM1). The monoclonal antibody moiety of MLN2704 binds to tumor cells expressing prostate-specific membrane antigen; MLN274 is then internalized into the tumor cell where the DM1 maytansinoid moiety binds to tubulin and inhibits tubulin polymerization and microtubule assembly, resulting in a disruption of microtubule activity and cell division, and cell death.

anti-PSMA monoclonal antibody-MMAE conjugate

An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody directed against prostate-specific membrane antigen (PSMA), conjugated via a stable, enzyme-cleavable linker to monomethylauristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. The monoclonal antibody moiety of this conjugate selectively binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis.

anti-PSMA/anti-CD28 bispecific antibody JNJ-87189401

A bispecific antibody directed against both the tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA) and the co-stimulatory T-cell-specific surface glycoprotein CD28, with potential immunostimulating and antineoplastic activities. Upon administration, anti-PSMA/anti-CD28 bispecific antibody JNJ-87189401 binds to both CD28 expressed on cytotoxic T lymphocytes (CTLs) and PSMA expressed on tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which may result in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

anti-PSMA/anti-CD3 T-cell engaging bispecific antibody TNB-585

A T-cell engaging bispecific antibody directed against the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-PSMA/anti-CD3 T-cell engaging bispecific antibody TNB-585 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and PSMA found on PSMA-expressing tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

anti-PSMA/anti-CD70 4SCAR-expressing bispecific T cells

A preparation of T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) prostate-specific membrane antigen (PSMA) and CD70 (CD27 ligand; tumor necrosis factor superfamily member 7; TNFSF7), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-PSMA/anti-CD70 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in PSMA- and CD70-expressing tumor cells. PSMA, a type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors, including brain tumor, neuroblastoma and some lymphoma tumor tissues. CD70, a cytokine belonging to the tumor necrosis superfamily (TNFSF) and the ligand for the costimulatory receptor CD27, is expressed on the surfaces of various types of cancer cells; its overexpression may play an important role in the evasion of immune surveillance.

anti-PSMA/CD3 bispecific antibody CCW702

A bispecific antibody that targets both the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA) and the CD3 antigen found on T lymphocytes, with potential immunostimulatory and antineoplastic activities. Upon administration of anti-PSMA/CD3 bispecific antibody CCW702, this bispecific antibody binds to both CD3 on cytotoxic T lymphocytes (CTLs) and PSMA found on PSMA-expressing tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

anti-PSMA/CD3 bispecific antibody JNJ-63898081

A bispecific antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA), fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of anti-PSMA/CD3 bispecific antibody JNJ-63898081, this bispecific antibody binds to both CD3 on cytotoxic T lymphocytes (CTLs) and PSMA found on PSMA-expressing tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA, a tumor associated antigen, is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

anti-PSMA/CD3 bispecific antibody REGN4336

A bispecific antibody that targets both the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA) and the CD3 antigen found on T lymphocytes, with potential immunostimulatory and antineoplastic activities. Upon administration of anti-PSMA/CD3 bispecific antibody REGN4336, this bispecific antibody binds to both CD3 on cytotoxic T lymphocytes (CTLs) and PSMA found on PSMA-expressing tumor cells. This activates and redirects CTLs to PSMA-expressing tumor cells, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

anti-PSMA/CD3 monoclonal antibody MOR209/ES414

An anti-prostate specific membrane antigen (PSMA)/anti-CD3 bispecific humanized monoclonal antibody, with potential immunostimulatory and antineoplastic activities. Anti-PSMA/CD3 monoclonal antibody MOR209/ES414 possesses two antigen-recognition sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for PSMA, a tumor-associated antigen (TAA) overexpressed on the surface of prostate tumor cells. Upon intravenous administration of MOR209/ES414, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and PSMA-expressing cancer cells, thereby crosslinking PSMA-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This results in CTL-mediated cancer cell lysis of prostate cancer cells expressing PSMA.

Anti-PSMA/CD3 Protease-activated T-cell Engager JANX007

A protease-activated, masked T-cell engager (TCE) composed of a prostate-specific membrane antigen (PSMA)-binding domain and a CD3-binding domain conjugated, via a tumor protease-cleavable linker, to a peptide mask that prevents CD3 engagement on T-cells and an albumin-binding domain that extends circulating half-life, with potential immunomodulating and antineoplastic activities. Upon intravenous administration of anti-PSMA/CD3 protease-activated TCE JANX007, the tumor protease-cleavable linker is proteolytically cleaved in the tumor microenvironment (TME), which separates the active PSMA-targeted TCE from the peptide mask and the albumin-binding domain. The PSMA-binding domain targets and binds to PSMA expressed on tumor cells. The CD3-binding domain targets and binds to T-cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against PSMA-expressing tumor cells in the TME. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors. The peptide mask allows specific activation of JANX007 in the TME, thereby minimizing systemic toxicity and increasing efficacy.

anti-PSMA/PBD ADC MEDI3726

An antibody-drug conjugate (ADC) consisting of an engineered version of anti-human prostate-specific membrane antigen (PSMA) monoclonal antibody J591 conjugated, via a valine-alanine dipeptide linker, to tesirine, a cytotoxic, DNA minor groove crosslinking agent and pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-PSMA/PBD ADC MEDI3726, the antibody moiety targets the cell surface antigen PSMA, which is found on prostate cancer cells. Upon antibody/antigen binding, internalization and lysosome-mediated cleavage of the dipeptide linker, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of PSMA-overexpressing tumor cells. PSMA is overexpressed by prostate cancers; its expression is associated with poor prognosis and metastasis.

anti-PSMA/STEAP1 antibody-drug conjugate ABBV-969

An antibody-drug conjugate (ADC) composed of an antibody targeting the tumor-associated antigens (TAAs) human prostate-specific membrane antigen (PSMA) and six transmembrane epithelial antigen of the prostate 1 (STEAP1), linked to an as of yet undisclosed cytotoxic payload, with potential antineoplastic activity. Upon administration of anti-PSMA/STEAP1 ADC ABBV-969, the antibody moiety targets and binds to PSMA and STEAP1 expressed on tumor cells. Following receptor internalization, the cytotoxic payload is released and induces tumor cell death through an as of yet unknown mechanism of action. PSMA is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors. STEAP1 is overexpressed in a variety of cancers including prostate cancer.

anti-PTK7/MMAE ADC PRO1107

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody against human inactive tyrosine-protein kinase 7 (protein tyrosine kinase 7; PTK7) linked to LD343, which is comprised of a protease-cleavable hydrophilic linker conjugated to the microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of anti-PTK7/MMAE ADC PRO1107, the anti-PTK7 antibody moiety targets and binds to PTK7 expressed on tumor cells. Upon binding, internalization and cleavage, MMAE is released and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in PTK7-expressing tumor cells. In addition, this may cause a bystander effect, thereby further killing PTK7-expressing tumor cells. PTK7, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells with limited expression in normal tissues. It is an integral player in cancer cell stemness and tumor progression. The highly hydrophilic stable, cleavable linker is used to mask the hydrophobicity of conjugated MMAE.

anti-PVR monoclonal antibody NTX-1088

An immunoglobulin G4 (IgG4) monoclonal antibody targeting the poliovirus receptor (PVR; CD155; nectin-like protein 5; NECL-5), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PVR monoclonal antibody NTX-1088 targets and binds to PVR expressed on tumor cells, thereby preventing its interactions with the human cell surface glycoprotein CD226 (DNAX accessory molecule-1; DNAM-1), the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the negative immunoregulatory human cell surface receptor CD96 (Tactile; T-cell activation increased late expression). The binding of NTX-1088 to CD226 prevents the internalization of CD226 and restores its expression on the surface of immune cells. This promotes CD226-dependent signaling pathways, which may trigger the activation of antigen-presenting cells (APCs) and activate T cells and natural killer (NK) cells, and result in an enhanced cytotoxic T-lymphocyte (CTL)-mediated and NK cell-mediated immune response against tumor cells. The binding of NTX-1088 to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands and promotes the interaction of its ligands with the costimulatory receptor CD226 expressed on immune cells. This leads to CD226 dimerization and further promotes CD226-mediated signaling and anti-tumor immune responses. The binding of NTX-1088 to CD96 expressed primarily on T cells and NK cells prevents its downstream signaling pathways. This may abrogate CD96-mediated inhibition of T-cell and NK-cell effector function and may further restore immune function and anti-tumor immune responses through the activation of T cells and NK cells. PVR, a key regulator of immune activation through multiple mechanisms, is overexpressed in a variety of tumor cell types while minimally or not expressed in normal tissues.

anti-PVRIG monoclonal antibody COM701

A humanized, hybridoma monoclonal antibody against the poliovirus receptor-related immunoglobulin (PVRIG; PVR Related Immunoglobulin Domain Containing Protein; CD112R), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PVRIG monoclonal antibody COM701 targets and binds to PVRIG expressed on cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells within the tumor microenvironment (TME). This blocks the interaction of PVRIG with its ligand nectin cell adhesion molecule 2 (poliovirus receptor-related 2; PVRL2; CD112), which is overexpressed on a variety of tumor cell types. Inhibiting the activation of PVRIG, abrogates the PVRIG-induced inhibition of T-lymphocyte and NK-cell activation. This activates CTLs and NK cells, enhances anti-tumor responses and immune-mediated tumor cell killing, and inhibits tumor cell proliferation. PVRIG, a member of the B7/CD28 family and immune checkpoint receptor that, upon activation, negatively regulates the activation of various immune cells. It plays a key role in immunosuppression.

anti-PVRIG monoclonal antibody JS009

A recombinant humanized immunoglobulin G4 (IgG4) monoclonal antibody against poliovirus receptor-related immunoglobulin (PVRIG; PVR related immunoglobulin domain containing protein; CD112R), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PVRIG monoclonal antibody JS009 targets and binds to PVRIG expressed on cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells within the tumor microenvironment (TME). This blocks the interaction of PVRIG with its ligand nectin cell adhesion molecule 2 (poliovirus receptor-related 2; PVRL2; CD112), which is overexpressed on a variety of tumor cell types. Inhibiting the activation of PVRIG abrogates the PVRIG-induced inhibition of T-lymphocyte and NK cell activation. This activates CTLs and NK cells, enhances anti-tumor responses and immune-mediated tumor cell killing, and inhibits tumor cell proliferation. PVRIG, a member of the B7/CD28 family and an immune checkpoint receptor that, upon activation, negatively regulates the activation of various immune cells. It plays a key role in immunosuppression.

anti-PVRIG monoclonal antibody NM1F

A humanized immunoglobulin G1 (IgG1) monoclonal antibody against poliovirus receptor-related immunoglobulin (PVRIG; PVR related immunoglobulin domain containing protein; CD112R), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PVRIG monoclonal antibody NM1F targets and binds to PVRIG expressed on cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells within the tumor microenvironment (TME). This blocks the interaction of PVRIG with its ligand nectin cell adhesion molecule 2 (poliovirus receptor-related 2; PVRL2; CD112), which is overexpressed on a variety of tumor cell types. Inhibiting the activation of PVRIG abrogates the PVRIG-induced inhibition of T-lymphocyte and NK cell activation. This activates CTLs and NK cells, enhances anti-tumor responses and immune-mediated tumor cell killing, and inhibits tumor cell proliferation. PVRIG, a member of the B7/CD28 family and an immune checkpoint receptor that, upon activation, negatively regulates the activation of various immune cells. It plays a key role in immunosuppression.

anti-RANKL monoclonal antibody GB-223

A monoclonal antibody directed against the receptor activator of nuclear factor kappa beta ligand (RANKL) with potential antiosteoclast and antineoplastic activities. Upon administration, anti-RANKL monoclonal antibody GB-223 specifically binds to RANKL and blocks the interaction of RANKL with RANK, a receptor located on osteoclast cell surfaces. This results in the inhibition of osteoclast activity, a decrease in bone resorption, and a potential increase in bone mineral density. By blocking the activation of the RANK/RANKL-mediated signaling pathway, GB-223 may also reduce tumor-associated bone destruction and may result in tumor regression in bone tumors with high RANK and RANKL expressions. RANKL, a protein expressed by osteoblastic cells, plays an important role in osteoclastic differentiation and activation. Both RANKL and RANK are overexpressed in certain bone tumors, and the RANK/RANKL-mediated signaling pathway plays an important role in certain bone tumors.

anti-RANKL monoclonal antibody HS-20090

An immunoglobulin G2 (IgG2) monoclonal antibody directed against the receptor activator of nuclear factor kappa beta ligand (RANKL), with antiosteoclast activity. Upon administration, anti-RANKL monoclonal antibody HS-20090 specifically binds to RANKL and blocks the interaction of RANKL with RANK, a receptor located on osteoclast cell surfaces. This results in an inhibition of osteoclast activity, a decrease in bone resorption, and a potential increase in bone mineral density. RANKL, a protein expressed by osteoblastic cells, plays an important role in osteoclastic differentiation and activation.

anti-ribonucleoprotein antibody ATRC-101

An engineered, human immunoglobulin (Ig) G1 monoclonal antibody directed against a ribonucleoprotein (RNP) complex, with potential immunostimulating and antineoplastic activities. Upon administration, anti-RNP antibody ATRC-101 targets and binds to its RNP complex antigen on tumor cells. This may activate the innate immune system, change the local tumor microenvironment (TME) and promote T-cell-mediated killing of tumor cells. The tumor-restricted RNP complex is expressed in a variety of tumor cells.

anti-RNF43 antibody-drug conjugate SC-006

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) ring finger protein 43 (RNF43), linked to a DNA crosslinking pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-RNF43 ADC SC-006 targets and binds to RNF43 expressed on tumor cells. Upon binding and internalization, the cytotoxic PBD moiety is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing RNF43-expressing cancer cells. RNF43, a single-span transmembrane E3 ubiquitin ligase, is overexpressed by certain tumor cell types and a negative regulator of the Wnt signaling pathway.

anti-ROR1 antibody-drug conjugate CS5001

An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1) that is site-specifically conjugated with a tumor-cleavable beta-glucuronide linker to a tumor-cleavable prodrug of pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of anti-ROR1 ADC CS5001 targets and binds to ROR1 expressed on tumor cells. Upon binding and internalization, both the linker and prodrug are selectively cleaved by lysosomal b-glucuronidase overexpressed in tumor cells. Free PBD is released and forms highly cytotoxic DNA interstrand cross-links, thereby blocking cell division and killing ROR1-expressing cancer cells. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in various hematological and solid malignancies. It plays key roles in tumor cell proliferation and survival.

anti-ROR1/anti-CD3 bispecific antibody EMB-07

A bispecific antibody directed against both the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon administration, anti-ROR1/anti-CD3 bispecific antibody EMB-07 binds to both ROR1 expressed on tumor cells and CD3 expressed on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to ROR1-expressing tumor cells, which results in the CTL-mediated death of ROR1-expressing tumor cells. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in many types of hematological malignancies. It plays key roles in tumor cell proliferation and survival.

anti-ROR1/anti-CD3/anti-HSA trispecific antibody NM32-2668

A trispecific antibody directed against the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1), the T-cell surface antigen CD3 and human serum albumin (HSA), with potential immunostimulating and antineoplastic activities. Upon administration, anti-ROR1/anti-CD3/anti-HSA trispecific antibody NM32-2668 binds to both ROR1 expressed on tumor cells and CD3 expressed on cytotoxic T lymphocytes (CTLs). This activates and redirects CTLs to ROR1-expressing tumor cells, which results in the CTL-mediated death of ROR1-expressing tumor cells. Anti-ROR1/anti-CD3/anti-HSA trispecific antibody NM32-2668 also binds to HSA, which prolongs the half-life of the agent. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in many types of hematological malignancies. It plays key roles in tumor cell proliferation and survival.

anti-ROR1/CD3 T-cell-engager NVG-111

A bispecific antibody and T-cell engager directed against the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-ROR1/CD3 T-cell engager NVG-111 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and ROR1 found on ROR1-expressing tumor cells. This activates and redirects CTLs to ROR1-expressing tumor cells, which results in the CTL-mediated death of ROR1-expressing tumor cells. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in many types of hematological malignancies. It plays key roles in tumor cell proliferation and survival.

anti-ROR1/PNU-159682 derivative antibody-drug conjugate NBE-002

An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody against the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1) site-specifically conjugated to a derivative of the highly potent anthracycline PNU-159682, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of NBE-002 targets and binds to ROR1 expressed on tumor cells. Upon binding and internalization, the anthracycline-based toxin intercalates into DNA and interacts with topoisomerase II. This leads to an inhibition of DNA replication and repair, and prevents RNA and protein synthesis. This kills the ROR1-expressing cancer cells. In addition, the PNU-159682 derivate may promote immunogenic cell death (ICD) and activate a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response, thereby further killing the ROR1-expressing tumor cells. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and by certain leukemias. It plays key roles in tumor cell proliferation and survival.

anti-RSPO3 monoclonal antibody OMP-131R10

An immunoglobulin (Ig) G1 humanized monoclonal antibody targeting human R-spondin 3 (RSPO3), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the anti-RSPO3 monoclonal antibody OMP-131R10 targets and binds to RSPO3 expressed on tumor cells. This prevents the activation of RSPO3, and inhibits both the binding of RSPO3 to leucine-rich repeat-containing G-coupled receptors (LGRs) and the activation of the RSPO-LGR pathway. This may result in an inhibition of both cancer stem cell (CSC) survival and the proliferation of cancer cells in which this pathway is overactivated. The RSPO-LGR pathway is a CSC pathway activated in a variety of cancer cell types.

anti-RSV nanobody ALX-0171

A trivalent nanobody composed of three monovalent Nb017 moieties linked with glycine-serine (GS) linkers, directed against the fusion protein (F protein) of human respiratory syncytial virus (RSV), with potential activity against RSV infections. Upon administration via nebulization and inhalation, the anti-RSV nanobody ALX-0171 targets and binds to RSV F protein, neutralizing the virus, and preventing viral entry into host cells. RSV F protein is a small envelope glycoprotein required for cytopathic syncytia formation that results from cell-to-cell fusion.

anti-S15 monoclonal antibody NC318

A humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting sialic acid binding Ig-like lectin 15 (Siglec-15; SIGLEC15; S15), a member of the sialic acid-binding immunoglobulin type lectins, with potential antineoplastic and immunomodulatory activities. Upon administration, anti-S15 monoclonal antibody NC318 targets and binds to S15 on the surface of tumor-associated macrophages (TAMs) and certain tumor cells. Binding to S15 may disrupt TAM-mediated activities such as promotion of tumor initiation and metastasis of tumor cells, inhibition of T-cell responses, and stimulation of tumor angiogenesis and disease progression. S15, a highly conserved type 1 cell surface protein, normally involved in osteoclast differentiation and bone remodeling, may play a role in the survival and differentiation of TAMs.

anti-SARS-CoV-2 monoclonal antibodies AZD5156

A combination of two neutralizing human monoclonal antibodies, cilgavimab, a neutralizing human monoclonal antibody directed against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spike (S) protein, and AZD3152, a long-acting neutralizing human monoclonal antibody directed against SARS-CoV-2, derived from B cells of convalescent patients with SARS-CoV-2 infection, that can potentially be used for passive immunization against Coronavirus disease 2019 (COVID-19). Upon administration of anti-SARS-CoV-2 monoclonal antibodies AZD5156, cilgavimab specifically targets and binds to the SARS-CoV-2 S protein, thereby blocking viral attachment and entry into human cells and may thereby neutralize SARS-CoV-2. Anti-SARS-CoV-2 monoclonal antibody AZD3152 also neutralizes SARS-CoV-2. This may slow the progression of the disease and accelerate recovery, and may potentially provide temporary protection against infection with SARS-CoV-2. S protein, usually found on the surface of SARS-CoV-2, plays an essential role in the infection pathway of the SARS-CoV-2 virus.

anti-SARS-CoV-2 monoclonal antibody AZD3152

A long-acting neutralizing human monoclonal antibody derived from B cells of convalescent patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and directed against SARS-CoV-2, that can potentially be used for passive immunization against Coronavirus disease 2019 (COVID-19). Upon administration, anti-SARS-CoV-2 monoclonal antibody AZD3152 neutralizes SARS-CoV-2. This may slow the progression of the disease and accelerate recovery, and may potentially provide temporary protection against infection with SARS-CoV-2.

anti-sCLU monoclonal antibody AB-16B5

A humanized, immunoglobulin (Ig) G2 monoclonal antibody against the secreted form of human clusterin (sCLU) expressed by tumor cells, with potential antineoplastic and anti-metastatic activities. Upon administration, anti-sCLU monoclonal antibody AB-16B5 specifically binds to tumor-associated sCLU and inhibits its activity. This inhibits both the sCLU-mediated signal transduction pathways and epithelial-to-mesenchymal transition (EMT), which leads to the inhibition of tumor cell migration and invasion. In addition, AB-16B5 enhances chemo-sensitivity. sCLU, a heterodimeric disulfide-linked glycoprotein overexpressed by various types of cancer cells, contributes to proliferation and survival of cancer cells, and stimulates tumor cell EMT.

anti-Senl-h19 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, anti-Senl-h19 CAR T cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

anti-SEZ6 antibody-drug conjugate ABBV-011

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against seizure protein 6 homolog (SEZ6) linked to the cytotoxic antitumor antibiotic calicheamicin, with potential antineoplastic activity. Upon administration of anti-SEZ6 ADC ABBV-011, the monoclonal antibody moiety targets and binds to SEZ6 expressed on tumor cells. Upon binding and internalization, calicheamicin is released. Calicheamicin binds to the minor groove of DNA, causing double strand DNA breaks and resulting in apoptosis of SEZ6-expressing tumor cells. SEZ6, overexpressed in certain cancers while minimally expressed in normal tissues, plays a role in cell-cell recognition and in neuronal membrane signaling.

anti-SEZ6 antibody-drug conjugate ABBV-706

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against seizure protein 6 homolog (SEZ6) linked to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration of anti-SEZ6 ADC ABBV-706, the monoclonal antibody moiety targets and binds to SEZ6 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills SEZ6-expressing tumor cells through an as of yet undisclosed mechanism. SEZ6, overexpressed in certain cancers while minimally expressed in normal tissues, may play a role in cell-cell recognition and in neuronal membrane signaling.

anti-Siglec-10 monoclonal antibody ONC-841

A humanized monoclonal antibody directed against the immune checkpoint molecule sialic acid-binding immunoglobulin (Ig)-like lectin 10 (Siglec-10; SIGLEC10), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-Siglec-10 monoclonal antibody ONC-841 targets and binds to Siglec-10 expressed on various immune cells, including tumor-associated macrophages (TAMs) and natural killer (NK) cells, in the tumor microenvironment (TME). This prevents Siglec-10-mediated signaling, and activates NK cells, macrophages, and T cells. This abrogates Siglec-10-mediated inhibition of phagocytosis of tumor cells and induces antibody-dependent cell-mediated cytotoxicity (ADCC), thereby killing tumor cells and inhibiting tumor cell growth. Siglec-10, an inhibitory receptor expressed on a variety of immune cells, plays an important role in tumor immune invasion through its interaction with the tumor-expressed co-stimulatory molecule CD24.

anti-SIRP monoclonal antibody ELA026

A human immunoglobulin G1 (IgG1) monoclonal antibody targeting certain specific proteins of the human signal-regulatory protein (SIRP) family, with potential immunoregulatory activity. Upon administration, anti-SIRP monoclonal antibody ELA026 targets and binds to SIRP, a cell surface protein expressed on myeloids and T lymphocytes. This depletes pathological myeloids and T lymphocytes that are circulating due to excessive immune activation and inflammation. This eradicates pathological immune cells that are driving inflammation. SIRP is a family of cell surface receptors expressed on various immune cell types. ELA026 does not inhibit the activity of the SIRPalpha/CD47 immune checkpoint.

anti-SIRP-alpha antibody BR105

An antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa antibody BR105 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPa antibody FSI-189

An antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa antibody FSI-189 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPa monoclonal antibody ADU-1805

A humanized immunoglobulin G2 (IgG2) monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa monoclonal antibody ADU-1805 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPa monoclonal antibody BI 765063

An immunoglobulin G4 (IgG4) monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa monoclonal antibody BI 765063 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPa monoclonal antibody BI 770371

An immunoglobulin G1 (IgG1) monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa monoclonal antibody BI 770371 targets and binds to SIRPa expressed on myeloid cells, including monocytes, macrophages, dendritic cells (DCs), and neutrophils, thereby blocking the interaction between SIRPa and its ligand cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis and the CD47/SIRPa-mediated suppression of the innate immune response. This induces pro-phagocytic signaling and the specific phagocytosis of tumor cells, and restores immune responses mediated by myeloid cells in the tumor microenvironment (TME). SIRPa, an innate immune checkpoint receptor expressed primarily on myeloid cells and neurons that is also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and DC activation. CD47, also known as integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of phagocytosis and the suppression of innate immunity, which allows cancer cells to proliferate. BI 770371 binds to both the V1 and V2 variants of SIRPa.

anti-SIRPa monoclonal antibody DS-1103

An immunoglobulin G4 (IgG4) monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa monoclonal antibody DS-1103 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPa monoclonal antibody LM-101

A monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa monoclonal antibody LM-101 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

anti-SIRPalpha monoclonal antibody BYON4228

A humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPalpha monoclonal antibody BYON4228 targets and binds to the two allelic variants of SIRPa v1 and v2 expressed on innate immune cells, including monocytes, macrophages, dendritic cells (DCs), and neutrophils, thereby blocking the interaction between SIRPa and its ligand cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis and the CD47/SIRPa-mediated suppression of the innate immune response. This induces pro-phagocytic signaling and the specific phagocytosis of tumor cells, and restores immune responses mediated by myeloid cells in the tumor microenvironment (TME). SIRPa, an innate immune checkpoint receptor expressed primarily on myeloid cells and neurons that is also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and DC activation. CD47, also known as integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of phagocytosis and the suppression of innate immunity, which allows cancer cells to proliferate.

anti-SSTR2/CD3 monoclonal antibody XmAb18087

A humanized, Fc domain-containing, bispecific monoclonal antibody targeting human CD3, a T-cell surface antigen, and somatostatin receptor 2 (SSTR2), a tumor-associated antigen (TAA) expressed on certain cancer cells, with potential antineoplastic activity. Upon administration, anti-SSTR2/CD3 monoclonal antibody XmAb18087 binds to both T cells and SSTR2-expressing cancer cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the SSTR2-expressing cancer cells. The inclusion of an Fc domain on the antibody prolongs the half-life of the bispecific antibody.

anti-STEAP1 antibody-drug conjugate ADRX-0405

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the tumor-associated antigen (TAA) six transmembrane epithelial antigen of the prostate 1 (STEAP1) conjugated, through a protease-cleavable linker, to a topoisomerase 1 (TOP1) inhibitor payload, with potential antineoplastic activity. Upon administration of anti-STEAP1 ADC ADRX-0405, the antibody moiety targets and binds to STEAP1 expressed on tumor cells. Following receptor internalization and linker cleavage, the TOP1 inhibitor targets and inhibits the activity of DNA topoisomerase 1, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis of STEAP1-overexpressing tumor cells. STEAP1 is overexpressed in a variety of cancers, including prostate cancer, while its expression in normal healthy tissue is limited.

anti-STEAP1 CAR T cells

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) six transmembrane epithelial antigen of the prostate 1 (STEAP1), with potential immunostimulating and antineoplastic activities. Upon administration, anti-STEAP1 CAR T cells recognize and bind to STEAP1-expressing tumor cells, thereby inducing selective toxicity in STEAP1-expressing tumor cells. STEAP1 is overexpressed in a variety of cancer cell types.

anti-STn antibody-drug conjugate SGN-STNV

An antibody-drug conjugate (ADC) composed of an antibody directed against the tumor-associated carbohydrate antigen Sialyl Thomsen-nouveau (STn) conjugated to the cytotoxic agent monomethyl auristatin E (MMAE) via the MC-vc-PAB linker, with potential antineoplastic activity. Upon administration of the anti-STn ADC SGN-STNV, the anti-STn antibody targets and binds to STn expressed on tumor cells. Following internalization of SGN-STNV and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in STn-expressing tumor cells. STn, a tumor-associated carbohydrate antigen that is present on various tumor-associated glycoproteins including CA-125 and mucin-1 (MUC1), is expressed in multiple tumor types.

anti-survivin T-cell receptor/anti-CD3 bispecific therapeutic ABBV-184

A T-cell redirecting bispecific therapeutic composed of a T-cell receptor (TCR) moiety specific for the tumor-associated antigen (TAA) survivin and a CD3 binding moiety, with potential immunostimulating and antineoplastic activities. Upon administration of anti-survivin TCR/anti-CD3 bispecific therapeutic ABBV-184, the TCR moiety of this agent targets and binds to survivin on tumor cells and the anti-CD3 moiety binds to CD3-expressing T lymphocytes. This selectively cross-links tumor cells and T lymphocytes and results in a CTL-mediated killing of survivin-expressing tumor cells. Survivin, a member of the inhibitor of apoptosis (IAP) family expressed during embryonic development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy.

anti-TAA monoclonal antibody-chelator conjugate BAY3547922

An immunoconjugate comprised of a monoclonal antibody directed against an as of yet undisclosed tumor-associated antigen (TAA) conjugated to an as of yet undisclosed chelator. When bound to the radioisotope zirconium Zr 89 (Zr89), the monoclonal antibody moiety of anti-TAA monoclonal antibody-chelator conjugate BAY3547922 specifically targets and binds to the TAA expressed on tumor cells, which may allow the tracing of TAA-expressing tumor cells upon positron emission tomography/computed tomography (PET/CT).

anti-TAG-72 monoclonal antibody CC49-streptavidin conjugate

An immunoconjugate containing CC49, a monoclonal antibody (MAb) directed against the tumor-associated antigen (TAA) tumor-associated glycoprotein 72 (TAG-72), conjugated to streptavidin, a nonglycosylated homotetrameric protein that has four high affinity binding sites for biotin, with potential use in pre-targeted radioimmunotherapy (PRIT). Upon administration of anti-TAG-72 MAb CC49-streptavidin conjugate, the MAb moiety targets and binds to TAG-72 expressed on cancer cells. Upon subsequent administration of a biotin-based radioconjugate, such as yttrium Y 90 DOTA-biotin, the biotin moiety of the radioconjugate binds to the streptavidin moiety of MAb CC49-streptavidin conjugate, which localizes the biotin-conjugated radionuclide to the tumor site. Upon cellular internalization, a cytotoxic does of radiation may be specifically delivered to TAG-72-expressing tumor cells. TAG-72, a human pancarcinoma antigen, is overexpressed on a variety of cancer cell types.

anti-TCR Vb6/Vb10/IL-2 antibody fusion protein STAR0602

A bifunctional antibody fusion protein composed of an agonist antibody targeting the variable (V) beta 6 (Vb6) and beta 10 (Vb10) regions of the T cell receptor (TCR) and fused to the cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon administration, anti-TCR Vb6/Vb10/IL-2 antibody fusion protein STAR0602 selectively targets and binds to the Vb6 and Vb10 regions of the TCR expressed on a subset of alpha/beta T cells, thereby activating and expanding these alpha/beta T-cells. This promotes T-cell-mediated immune responses against tumor cells. IL-2 targets and binds to the IL-2 receptor IL2R and activates IL-2/IL-2R-mediated signaling, which further activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). This further enhances T-cell-mediated cytotoxic immune responses against tumor cells. Alpha/beta T cells play an important role in the adaptive immune response.

anti-TF antibody-drug conjugate MRG004A

An antibody-drug conjugate (ADC) comprised of a monoclonal antibody against human tissue factor (TF) conjugated, via a protease-cleavable BCN-valyl-citrulline linker, with monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antiangiogenic, anticoagulant and antineoplastic activities. Upon administration of anti-TF ADC MRG004A, the monoclonal antibody moiety binds to cell surface TF and is internalized. After internalization of the agent, the MMAE moiety is released by proteolytic cleavage. It then binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and apoptosis. TF, a transmembrane protein and initiator of the coagulation cascade, is overexpressed in many tumor cells and tumor-resident endothelial cells. Expression of TF is correlated with metastasis, angiogenesis, tumor cell growth and tumor-associated thrombosis.

anti-TF monoclonal antibody ALT-836

A recombinant human-mouse chimeric monoclonal antibody against human tissue factor (TF), with potential antiangiogenic, anticoagulant and anti-inflammatory activities. Upon administration, anti-TF monoclonal antibody ALT-836 binds to TF or the TF-Factor VIIa (FVIIa) complex preventing binding and activation of Factor X (FX) and Factor IX (FIX). This may prevent thrombin formation and cancer-associated venous thromboembolism, and may inhibit angiogenesis and tumor cell proliferation. TF, a transmembrane protein and procoagulant, is overexpressed in many tumor cell types, and is correlated with metastasis, angiogenesis, tumor growth and tumor-associated thrombosis.

anti-TGF-beta 1/Anti-COX-2 siRNAs STP707

A polypeptide nanoparticle (PNP)-based therapeutic comprised of two small interfering RNA (siRNA) oligonucleotides directed against transforming growth factor-beta 1 (TGF-beta 1) and cyclo-oxygenase-2 (COX-2), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-TGF-beta 1/anti-COX-2 siRNAs STP707 binds to both TGF-beta 1 and COX-2 messenger RNAs (mRNAs), preventing the translation and expression of TGF-beta 1 and COX-2 proteins. This inhibits TGF-beta 1-mediated signaling and abrogates TGF-beta 1-mediated immunosuppression, which may enhance anti-tumor immunity in the tumor microenvironment (TME) and promote a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. The inhibition of COX-2 prevents COX-2-mediated signaling, which may result in apoptosis and a reduction in tumor cell proliferation, tumor angiogenesis and metastasis.

anti-TGF-beta monoclonal antibody SAR-439459

A monoclonal antibody (mAb) directed against human transforming growth factor beta (TGF-beta; TGFb), with potential antineoplastic activity. Upon administration, anti-TGF-beta monoclonal antibody SAR-439459 specifically targets and binds to TGF-beta, thereby preventing the activation of TGF-beta-mediated signaling pathways. This may inhibit the proliferation of tumor cells in which TGF-beta is overactivated. TGF-beta, a pro-inflammatory mediator that is mutated and/or overexpressed in a variety of cancer cell types, is involved in cancer cell proliferation and migration, and in tumor progression.

anti-TGF-beta RII monoclonal antibody IMC-TR1

A monoclonal antibody directed against transforming growth factor-beta receptor type II (TGF-beta RII) with potential antineoplastic activity. Anti-TGF-beta RII monoclonal antibody IMC-TR1 specifically targets and binds to TGF-beta R11, thereby preventing the activation of TGF-beta RII-mediated signaling pathways. TGF-beta RII is mutated in a number of cancer cell types and is involved in cancer cell proliferation and tumor progression.

anti-thymocyte globulin

Purified gamma globulin, with immunosuppressive activity. Obtained from animals that have been immunized with human thymocytes, antithymocyte globulin (ATG) specifically recognizes and destroys T lymphocytes. Although not completely understood, the mechanism of action appears to involve T lymphocyte clearance from the circulation and modulation of T lymphocyte activity. Administering ATG with chemotherapy prior to stem cell transplantation may reduce the risk of graft-versus-host (GVH) disease.

anti-thyroglobulin mTCR-transduced autologous peripheral blood lymphocytes

Peripheral blood lymphocytes (PBLs) transduced with a gene encoding for a thyroglobulin (TG)-specific murine T-cell receptor (mTCR), with potential antineoplastic activity. PBLs are harvested from a thyroid cancer patient, and transfected with a retroviral vector that encodes the mTCR gene specific for the human TG antigen. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-TG mTCR-expressing PBLs target and bind to TG-overexpressing tumor cells, which results in both cytokine secretion and tumor cell lysis. TG is a thyroid-specific protein.

anti-TIGIT antibody/TGFbeta-RII fusion protein AK130

A bifunctional fusion protein composed of a humanized Fc-mutant anti-T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains (TIGIT) antibody fused to transforming growth factor beta (TGF-beta) receptor type II (TGFbetaRII), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-TIGIT antibody/TGFbeta-RII fusion protein AK130, the TGFbetaRII moiety targets, binds to and neutralizes TGF-beta while the anti-TIGIT antibody moiety simultaneously targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs) and natural killer (NK) cells. The neutralization of TGF-beta prevents TGF-beta-mediated immunosuppressive signaling, thereby enhancing anti-tumor immunity in the tumor microenvironment (TME). The binding to TIGIT prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5), and enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1) expressed on immune cells, such as NK cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig superfamily (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion and the inhibition of antiviral immune responses. TGF-beta, dysregulated in many types of cancer, plays a key role in immunosuppression in the TME and is involved in tumor cell proliferation and tumor progression. The mutations in the Fc region of the anti-TIGIT antibody moiety prevent antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), and the resulting loss of lymphocytes.

anti-TIGIT bispecific antibody BMS-986442

A Fc-enhanced bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and an as of yet undisclosed receptor expressed specifically on T cells and natural killer (NK) cells, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, the anti-TIGIT bispecific antibody BMS-986442 simultaneously targets and binds to TIGIT and the undisclosed receptor. Upon binding to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), BMS-986442 blocks the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as NK cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. In addition, binding of BMS-986442 to the undisclosed target expressed on T cells and NK cells may further enhance anti-tumor immune responses. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody AB308

A FcR-enabled immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody AB308 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody AK127

A humanized immunoglobulin G1 kappa (IgG1k) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody AK127 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs) and natural killer (NK) cells, thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as NK cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody ASP8374

A fully human, immunoglobulin G4 (IgG4) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody ASP8374 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody BAT6005

An immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6005 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody BAT6021

A recombinant humanized monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody COM902

A fully human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody COM902 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody IBI939

A recombinant human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody IBI939 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody PM1021

A recombinant immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody PM1021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody SGN-TGT

A nonfucosylated human immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody SGN-TGT targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T-lymphocytes (TILs). This prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5), and enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This enhances depletion of TIGIT-positive regulatory T cells (Tregs) and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT monoclonal antibody TAB006

A recombinant humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody TAB006 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.

anti-TIGIT/anti-PD-L1 bispecific antibody HB0036

A bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-TIGIT/anti-PD-L1 bispecific antibody HB0036 simultaneously targets, binds to and inhibits TIGIT and PD-L1, thereby inhibiting their downstream signaling pathways. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. Inhibition of PD-L1 prevents its binding to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-TIGIT/anti-PD-L1 bispecific antibody HLX301

A bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIGIT/anti-PD-L1 bispecific antibody HLX301 simultaneously targets, binds to and inhibits TIGIT and PD-L1, thereby inhibiting their downstream signaling pathways. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. Inhibition of PD-L1 prevents its binding to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion.

anti-TIGIT/anti-PVRIG bispecific antibody PM1009

A bispecific antibody composed of a human immunoglobulin G1 (IgG1) monoclonal antibody directed against the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) with a single chain variable fragment (scFv) targeting poliovirus receptor-related immunoglobulin (PVRIG; PVR Related Immunoglobulin Domain Containing Protein; CD112R) fused to the c-terminus, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIGIT/anti-PVRIG bispecific antibody PM1009 simultaneously targets, binds to and inhibits TIGIT and PVRIG and their downstream signaling pathways. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. Inhibition of PVRIG expressed on cytotoxic T-lymphocytes (CTLs) and NK cells within the tumor microenvironment (TME) blocks the interaction of PVRIG with its ligand nectin cell adhesion molecule 2 (poliovirus receptor-related 2; PVRL2; CD112), which is overexpressed on a variety of tumor cell types. This abrogates the PVRIG-mediated inhibition of T-lymphocyte and NK cell activation. This activates CTLs and NK cells, enhances anti-tumor responses and immune-mediated tumor cell killing, and inhibits tumor cell proliferation. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses. PVRIG, a member of the B7/CD28 family and an immune checkpoint receptor, negatively regulates the activation of various immune cells upon activation and plays a key role in immunosuppression.

anti-TIGIT/anti-PVRIG bispecific antibody SIM0348

A humanized immunoglobulin G1 (IgG1)-based bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and poliovirus receptor-related immunoglobulin (PVRIG; PVR Related Immunoglobulin Domain Containing Protein; CD112R), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIGIT/anti-PVRIG bispecific antibody SIM0348 simultaneously targets, binds to and inhibits TIGIT and PVRIG and their downstream signaling pathways. Inhibition of TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. Inhibition of PVRIG expressed on cytotoxic T lymphocytes (CTLs) and NK cells within the tumor microenvironment (TME) blocks the interaction of PVRIG with its ligand CD112, which is overexpressed on a variety of tumor cell types. This abrogates the PVRIG-mediated inhibition of T-lymphocyte and NK cell activation. This activates CTLs and NK cells, enhances anti-tumor responses and immune-mediated tumor cell killing, and inhibits tumor cell proliferation. In addition, SIM0348 induces Fc-mediated killing of TIGIT-expressing immunosuppressive regulatory T cells (Tregs) and Tregs expressing TIGIT and PVRIG. TIGIT, a member of the immunoglobulin super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses. PVRIG, a member of the B7/CD28 family and an immune checkpoint receptor, negatively regulates the activation of various immune cells upon activation and plays a key role in immunosuppression.

anti-TIM-3 antibody BMS-986258

An antibody against the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Following administration, anti-TIM-3 antibody BMS-986258 binds to TIM-3 that is expressed on certain T cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which together result in decreased tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-TIM-3 monoclonal antibody

Any monoclonal antibody that targets the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2).

anti-TIM-3 monoclonal antibody BC3402

A monoclonal antibody against the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-TIM-3 monoclonal antibody BC3402 targets and binds to TIM-3 expressed on certain T cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-TIM-3 monoclonal antibody Sym023

A recombinant, fully human monoclonal antibody against the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIM-3 monoclonal antibody Sym023 binds to TIM-3 expressed on certain T cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor cell proliferation. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-TIM-3 monoclonal antibody TQB2618

A monoclonal antibody against the inhibitory T-cell receptor, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-TIM-3 monoclonal antibody TQB2618 targets and binds to TIM-3 expressed on certain T cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-TIM3 monoclonal antibody LY3321367

A monoclonal antibody against the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIM-3 monoclonal antibody LY3321367 binds to TIM-3 expressed on certain T cells, including tumor-infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-TIM3 monoclonal antibody SHR-1702

A monoclonal antibody against the inhibitory T-cell receptor, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-TIM3 monoclonal antibody SHR-1702 targets and binds to TIM-3 expressed on certain T-cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.

anti-tissue factor antibody-drug conjugate XB002

An antibody-drug conjugate (ADC) comprised of a monoclonal antibody against human tissue factor (TF) conjugated via a linker to an auristatin payload, with potential antineoplastic activity. Upon administration of anti-TF ADC XB002, the anti-TF antibody moiety binds to cell surface TF and is internalized. After internalization of the agent, the auristatin moiety is released. It then binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis of TF-expressing tumor cells. TF, a transmembrane protein and an initiator of the coagulation cascade, is overexpressed in many tumor cells and tumor-resident endothelial cells. Expression of TF is correlated with metastasis, angiogenesis, tumor cell growth and tumor-associated thrombosis. The anti-TF antibody in XB002 does not affect coagulation.

anti-tissue factor monoclonal antibody MORAb-066

A humanized monoclonal antibody against human tissue factor (TF), with potential antiangiogenic, anticoagulant and anti-inflammatory activities. Upon administration, anti-TF monoclonal antibody MORAb-066 binds to TF and prevents Factor VIIa (FVIIa) from binding, thereby interfering with the activation of Factor X (FX) into FXa. This may prevent thrombin formation and cancer-associated venous thromboembolism, and may inhibit angiogenesis and tumor cell proliferation. TF, a transmembrane protein and initiator of the coagulation cascade, is overexpressed in many tumor cells and tumor endothelial cells; its expression is correlated with metastasis, angiogenesis, tumor cell growth and tumor-associated thrombosis.

anti-TLR2 monoclonal antibody OPN-305

A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against toll-like receptor type 2 (TLR2), with potential anti-inflammatory and antineoplastic activities. Upon intravenous administration, OPN-305 binds to the ligand-binding site on the TLR2 receptor and blocks the activation of TLR2-mediated innate immunity signaling. This prevents the TLR2-mediated production of pro-inflammatory mediators and prevents inflammation. TLR2, a member of the TLR family primarily found on leukocytes, plays a key role in the activation of innate immunity; it is overexpressed in various inflammatory diseases and in certain types of cancer.

anti-TNFR2 monoclonal antibody BI-1808

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against tumor necrosis factor Receptor 2 (TNFR2; tumor necrosis factor receptor superfamily member 1B; TNFRSF1B), with potential antineoplastic activity. Upon administration, anti-TNFR2 monoclonal antibody BI-1808 targets and binds to TNFR2 on tumor-associated regulatory T cells (Tregs) in the tumor microenvironment (TME), thereby preventing TNFR2-mediated signaling. This depletes intra-tumoral Tregs, induces and expands intra-tumoral CD8+ T cells, thereby enhancing T-cell-mediated immune responses against tumor cells. TNFR2 plays a role in tumor necrosis factor signaling, tumor expansion and survival.

anti-TNFR2 monoclonal antibody BI-1910

An agonistic monoclonal antibody directed against tumor necrosis factor receptor 2 (TNFR2; tumor necrosis factor receptor superfamily member 1B; TNFRSF1B), with potential antineoplastic activity. Upon administration, anti-TNFR2 monoclonal antibody BI-1910 targets and binds to TNFR2 expressed on the surface of CD4+ T cells, CD8+ T cells and natural killer (NK) cells in the tumor microenvironment (TME), thereby activating CD4+ T cells, CD8+ T cells and NK cells. This may enhance cytotoxic T-cell- and NK cell-mediated immune responses against tumor cells. TNFR2, a member of the TNFR family of co-stimulatory molecules, plays an important role in T-cell co-stimulation.

anti-TNFR2 monoclonal antibody HFB200301

A humanized agonistic monoclonal antibody directed against tumor necrosis factor receptor 2 (TNFR2; tumor necrosis factor receptor superfamily member 1B; TNFRSF1B), with potential antineoplastic activity. Upon administration, anti-TNFR2 monoclonal antibody HFB200301 targets and binds to TNFR2 expressed on the surface of CD4+ T cells, CD8+ T cells and natural killer (NK) cells in the tumor micro-environment (TME), thereby activating CD4+ T cells, CD8+ T cells and NK cells. This may enhance T-cell- and NK cell- mediated immune responses against tumor cells. TNFR2, a member of the TNFR family of co-stimulatory molecules, plays an important role in T-cell co-stimulation.

anti-TNFR2 monoclonal antibody NBL-020

A fully human monoclonal antibody directed against tumor necrosis factor receptor 2 (TNFR2; tumor necrosis factor receptor superfamily member 1B; TNFRSF1B), with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, anti-TNFR2 monoclonal antibody NBL-020 targets and binds to TNFR2 expressed on immune suppressive cells, such as tumor-associated regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME). This prevents the activation of TNFR2 by endogenous tumor necrosis factor (TNF), inhibits TNFR2-mediated signaling, and blocks the activation of the nuclear factor kappa B (NF-kB) signaling pathway, which halts TNFR2-mediated immunosuppression, inhibits the proliferation and function of Tregs, induces and expands intra-tumoral CD8+ T cells, and enhances cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune responses. TNFR2 plays a role in tumor necrosis factor signaling, tumor expansion and survival.

anti-TNFR2 monoclonal antibody SIM1811-03

A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against tumor necrosis factor receptor 2 (TNFR2; tumor necrosis factor receptor superfamily member 1B; TNFRSF1B), with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities Upon administration, anti-TNFR2 monoclonal antibody SIM1811-03 targets and binds to TNFR2 expressed on immune suppressive cells, such as tumor-associated regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME). This induces antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), and depletes these TNFR2-expressing immune suppressive cells. Also, SIM1811-03 prevents the activation of TNFR2 by endogenous tumor necrosis factor (TNF) and TNFR2-mediated signaling, blocks the activation of the nuclear factor kappa B (NF-kB) signaling pathway, halts TNFR2-mediated immunosuppression, thereby inhibiting the proliferation and function of Tregs and enhancing cytotoxic T-cell-mediated anti-tumor immune responses. In addition, SIM0235 is able to bind to TNFR2 expressed on the surface of tumor cells, thereby killing TNFR2-expressing tumor cells directly. TNFR2, a member of the TNFR family of co-stimulatory molecules, plays a role in tumor necrosis factor signaling, tumor expansion and survival. It is primarily expressed on the surface of tumor cells and suppressive immune cells in the TME, but rarely in normal human tissues or peripheral immune cells.

anti-TRAILR2/CDH17 tetravalent bispecific antibody BI 905711

A tetravalent bispecific antibody targeting both the pro-apoptotic death receptor tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAILR2; death receptor 5; DR5) and cadherin-17 (CDH17), with potential pro-apoptotic and antineoplastic activities. Upon administration of anti-TRAILR2/CDH17 tetravalent bispecific antibody BI 905711, the antibody targets and binds to both TRAILR2 and CDH17, expressed on tumor cells. Receptor clustering and activation of TRAILR2 induces apoptosis in CDH17-positive cancer cells. Activation of TRAILR2 plays a key role in the induction of apoptosis. CDH17-dependent clustering of TRAILR2 allows BI 905711 to selectively induce apoptosis in CDH17-expressing tumor cells thereby increasing efficacy and decreasing liver toxicity. CDH17 is overexpressed in a variety of cancer cell types while its expression is restricted in normal liver tissue.

anti-transthyretin siRNA ALN-TTR02

A lipid nanoparticle (LNP)-based formulation consisting of small-interfering RNAs (siRNAs) directed against transthyretin (TTR)-encapsulated in lipids, which has potential use in the treatment of TTR-mediated amyloidosis (ATTR). Upon intravenous administration of ALN-TTR02, the lipid formulation promotes the uptake by cells. The siRNAs bind to TTR mRNAs, which may result in the inhibition of both the translation and expression of the TTR protein. ATTR is caused by mutations in the TTR gene and results in the formation of abnormal amyloid proteins that accumulate in and cause damage to various body organs and tissues.

anti-TRBC1-CAR-CD3zeta-4-1BB-RQR8-expressing autologous T lymphocytes AUTO4

Autologous human T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) containing an anti-T-cell receptor beta constant 1 (TRBC1; T-cell receptor beta-1 chain C region) single chain variable fragment (scFv) and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Upon administration, anti-TRBC1-CAR-CD3zeta-4-1BB-RQR8-expressing autologous T lymphocytes AUTO4 targets and binds to the TRBC1 expressed on tumor cell surfaces. Subsequently, TRBC1-expressing tumor cells are lysed. In addition, AUTO4 carries the universal RQR8 safety "off" switch, which allows selective removal of the T-cells through both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) following administration of rituximab if unacceptable side-effects occur.

anti-TREM1 agonistic monoclonal antibody PY159

A humanized agonistic monoclonal antibody targeting triggering receptor expressed on myeloid cells 1 (TREM1), with potential immunomodulating and antineoplastic activities. Upon administration, anti-TREM1 agonistic monoclonal antibody PY159 targets, binds to, crosslinks and activates TREM1 located on immunosuppressive tumor-associated myeloid cells within the tumor microenvironment (TME), including monocytic myeloid derived suppressor cells (mMDSCs), tumor associated neutrophils (TANs), and tumor associated macrophages (TAMs). This activates TREM1-mediated signaling through the TREM1/DNAX activating protein of 12kDa (DAP12) complex. This reprograms and repolarizes the immunosuppressive myeloid cells, thereby inducing a pro-inflammatory state in these cells and altering the TME. This stimulates anti-tumor immune responses leading to tumor cell destruction. TREM1, an immunoglobulin (Ig) superfamily transmembrane protein constitutively expressed on the cell surface of peripheral blood monocytes and neutrophils, is expressed within the TME and is associated with poorer patient outcomes. Activation of TREM1 may amplify immune responses.

anti-TREM2 monoclonal antibody PY314

A humanized monoclonal antibody targeting triggering receptor expressed on myeloid cells 2 (TREM2; TREM-2), with potential immunomodulating and antineoplastic activities. Upon administration, anti-TREM2 monoclonal antibody PY314 targets and binds to TREM2 located on immunosuppressive tumor-associated myeloid cells within the tumor microenvironment (TME), including tumor associated macrophages (TAMs). This induces antibody dependent cell mediated cytotoxicity (ADCC) and/or antibody dependent cell mediated phagocytosis (ADCP), thereby killing TREM2-positive cells, including TAMs. The depletion of TAMs alters the TME, activates cytotoxic T lymphocytes (CTLs), natural killer (NK) cells and M1-like macrophages, which stimulate anti-tumor immune responses, and leads to tumor cell destruction. TREM2, an immunoglobulin (Ig) superfamily transmembrane protein, is expressed within the TME and is associated with poorer patient outcomes.

anti-TROP-2 antibody-drug conjugate DB-1305

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) covalently linked, via a cleavable linker containing maleimide tetrapeptide, to the topoisomerase-1 inhibitor P1021, with potential antineoplastic activity. Upon administration of the anti-TROP-2 ADC DB-1305, the anti-TROP-2 antibody targets and binds to TROP-2 expressed on tumor cells. Upon binding and internalization, the topoisomerase-1 inhibitor P1021 is released, and inhibits DNA topoisomerase-1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP-2-expressing tumor cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP-2 antibody-drug conjugate HS-20105

An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) linked, via a cleavable linker, to a topoisomerase-1 inhibitor, with potential antineoplastic activity. Upon administration of anti-TROP-2 ADC HS-20105, the anti-TROP-2 antibody targets and binds to TROP-2 expressed on tumor cells. Upon binding, internalization and linker cleavage, the topoisomerase-1 inhibitor is released, and inhibits DNA topoisomerase-1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP-2-expressing tumor cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP-2 antibody-drug conjugate PBI-410

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; tumor-associated calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) site-specifically conjugated to a camptothecin analog via a cleavable linker, with potential antineoplastic activity. Upon administration of the anti-TROP-2 ADC PBI-410, the anti-TROP-2 antibody targets and binds to TROP-2 expressed on tumor cells. Upon binding and internalization, the camptothecin analog is released, and inhibits DNA topoisomerase-1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP-2-expressing tumor cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP-2 antibody-drug conjugate PF-06664178

An antibody-drug conjugate (ADC) composed of PF-06478924 (RN926), a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1), site-specifically conjugated via a valine-citrulline cleavable linker with the auristatin-based cytotoxic agent Aur0101 (PF-06380101), with potential antineoplastic activity. Upon administration of anti-TROP-2 ADC PF-06664178, the anti-TROP-2 monoclonal antibody moiety PF-06478924 targets and binds to TROP-2 expressed on tumor cells. Upon binding, internalization and linker cleavage, Aur0101 binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and apoptosis of TROP-2-expressing tumor cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP-2/MMAE antibody-drug conjugate LCB84

An antibody-drug conjugate (ADC) composed of Hu2G10, a humanized immunoglobulin G1 (IgG1) monoclonal antibody that targets the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1), conjugated via a beta-glucuronidase-cleavable linker to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of anti-TROP-2/MMAE ADC LCB84, the anti-TROP-2 antibody targets and binds to TROP-2 expressed on tumor cells. Upon binding and internalization, MMAE is released upon cleavage by the cancer-associated lysosomal enzyme beta-glucuronidase. MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. This induces cell death in TROP-2-expressing cancer cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP-2/topoisomerase inhibitor ADC MHB036C

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) conjugated to an as of yet undisclosed topoisomerase inhibitor (TopoI), with potential antineoplastic activity. Upon administration of the anti-TROP-2/TopoI ADC MHB036C, the anti-TROP-2 antibody targets and binds to TROP-2 expressed on tumor cells. Upon binding, internalization and cleavage, TopoI is released, and inhibits DNA topoisomerase activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP-2-expressing tumor cells. TROP-2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 antibody-drug conjugate

Any antibody-drug conjugate (ADC) that is directed against trophoblast cell surface protein 2 (trophoblast antigen 2; tumor-associated calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1).

anti-TROP2 antibody-drug conjugate BAT8003

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) conjugated via an uncleavable linker to an as of yet undisclosed maytansine derivative toxin, with potential antineoplastic activity. Upon administration of the anti-TROP2 ADC BAT8003, the anti-TROP2 antibody targets and binds to TROP2 expressed on tumor cells. Upon cellular uptake, the cytotoxic maytansine derivative binds to tubulin, thereby affecting microtubule assembly and disassembly dynamics. This inhibits tumor cell proliferation of TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 antibody-drug conjugate BAT8008

An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) conjugated via a cleavable linker to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of the anti-TROP2 ADC BAT8008, the anti-TROP2 antibody targets and binds to TROP2 expressed on tumor cells. Upon binding, internalization and linker cleavage, exatecan is released. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 antibody-drug conjugate BIO-106

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) linked to an as of yet undisclosed tubulin inhibitor, with potential antineoplastic activity. Upon administration of anti-TROP2 ADC BIO-106, the anti-TROP2 antibody targets and binds to TROP2 expressed on tumor cells. Upon binding and internalization, the tubulin inhibitor is released, and binds to tubulin and inhibits its polymerization. This results in G2/M phase arrest and apoptosis, and inhibits the proliferation of TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 antibody-drug conjugate BL-M02D1

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-TROP2 ADC BL-M02D1, the anti-TROP2 antibody targets and binds to TROP2 expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TROP2-expressing tumor cells, through an as of yet unknown mechanism of action. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 antibody-drug conjugate OBI-992

An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1), conjugated to a topoisomerase-1 inhibitor (TOP1i; TOP-Ii) via a hydrophilic, enzyme-cleavable linker, with potential antineoplastic activity. Upon administration of anti-TROP2 ADC OBI-992, the anti-TROP2 antibody moiety targets and binds to TROP2 expressed on tumor cells. Upon binding, internalization and linker cleavage, the TOP1i moiety is released, binds to TOP1 and inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2 monoclonal antibody-Tub196 conjugate JS108

An antibody-drug conjugate (ADC) composed of a recombinant humanized monoclonal antibody against tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) conjugated, via a 2,3-disubstituted long side chain hydrolysis-resistant linker, to the tubulysin B analog Tub196, with potential antineoplastic activity. Upon administration of the anti-TROP2 monoclonal antibody-Tub196 conjugate JS108, the anti-TROP2 antibody targets and binds to TROP2 expressed on tumor cells. Upon cellular uptake, the cytotoxic tubulysin B analog binds to tubulin, thereby affecting microtubule assembly and disassembly dynamics. This inhibits microtubule polymerization, which blocks cell division and results in G2/M phase arrest, tumor cell apoptosis and a decrease in proliferation of TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance, increased tumor cell survival and poor prognosis.

anti-TROP2-CAR-IL-15-transduced Cord blood-derived natural killer cells

A preparation of umbilical cord blood (CB)-derived natural killer cells (NKs) that have been engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; tumor-associated calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) and interleukin-15 (IL-15), with potential immunostimulating and antineoplastic activities. Upon administration, anti-TROP2-CAR-IL-15-transduced CB-derived NK cells target, bind to and induce selective cytotoxicity in TROP2-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes persistence of multiple lymphocyte lineages and potentiates the immune response against tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

anti-TROP2/EGFR bispecific antibody-drug conjugate DM001

An antibody-drug conjugate (ADC) composed of a bispecific antibody directed against the tumor associated antigens (TAAs) trophoblast cell surface protein 2 (trophoblast antigen 2; calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1) and human epidermal growth factor receptor (EGFR), conjugated, via a protease-cleavable linker, to the auristatin derivative and microtubule-disrupting cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-TROP2/EGFR bispecific ADC DM001 targets and binds to TROP2 and EGFR expressed on tumor cells. Upon binding, internalization, proteolytic cleavage of linker, and the release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in TROP2 and EGFR-expressing tumor cells. TROP2 and EGFR are co-expressed in a variety of cancer cells. TROP2, a transmembrane protein overexpressed in various tumors, is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

anti-TWEAK monoclonal antibody RG7212

A humanized monoclonal antibody directed against the apoptotic ligand TNF-like weak inducer of apoptosis (TWEAK) with potential antineoplastic activity. Anti-TWEAK monoclonal antibody RG7212 binds to TWEAK and prevents the binding of TWEAK to its receptor, FGF-inducible molecule 14 (Fn14), thereby blocking the TWEAK/Fn14 signaling. This may prevent tumor cell proliferation, invasion, migration and angiogenesis. TWEAK has pleiotropic effects, mediating proinflammatory and pro-angiogenic activity as well as stimulation of invasion, migration, and survival mediated via its receptor Fn14; Fn14 is expressed at relatively low levels in normal tissues, but is elevated in tumor cells and locally in injured and diseased tissues.

anti-TYRP1/CD3 T-cell engager RO7293583

A bispecific T-cell engager directed against the tumor-associated antigen (TAA) tyrosinase-related protein 1 (TYRP1; TRP1; glycoprotein 75; gp75) and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, anti-TYRP1/CD3 T-cell engager RO7293583 binds to both CD3 on cytotoxic T lymphocytes (CTLs) and TYRP1 found on TYRP1-expressing tumor cells. This activates and redirects CTLs to TYRP1-expressing tumor cells, which results in the CTL-mediated death of TYRP1-expressing tumor cells. TYRP1, a transmembrane glycoprotein, is involved in melanin biosynthesis and is expressed in melanosomes of human melanocytes and melanomas.

anti-ULBP6 monoclonal antibody 23ME-01473

An Fc effector-enhanced, humanized afucosylated monoclonal antibody directed against the natural-killer group 2, member D receptor protein (NKG2D or KLRK1) ligand UL16-binding protein 6 (ULBP6), with potential immunostimulating and antineoplastic activities. Upon administration, anti-ULBP6 monoclonal antibody 23ME-01473 targets and binds to soluble form of ULBP6, thereby preventing the binding of soluble ULBP6 to NKG2D-expressing immune cells. This enhances the binding of NKG2D-expressing immune cells, including natural killer (NK) cells and subset of T cells, to ULBP6-expressing tumor cells, which leads to the activation of NK cells and T cells, the secretion of interferon-gamma (IFNg), and the lysis of tumor cells. In addition, the afucosylated Fc domain of 23ME-01473 binds to the activating Fc receptor low affinity immunoglobulin gamma Fc region receptor III-A (FcgammaRIIIA; CD16a) expressed on NK cells, which enhances antitumor response through antibody-dependent cell-mediated cytotoxicity (ADCC). ULBP6 is a stress-induced cell surface NKG2D ligand overexpressed on cancer cells. The shedding of ULBP6 from tumor cell surface to produce the soluble form allows tumor cells to evade NKG2D-expressing immune cells. 23ME-01473 also targets and binds to ULBP2 and ULBP5, blocking their interaction with NKG2D.

anti-uPARAP ADC ADCE-D01

An antibody-drug conjugate (ADC) composed of AB-004, a humanized monoclonal antibody directed against urokinase plasminogen activator receptor-associated protein (uPARAP; endocytic receptor 180; Endo180; C-type mannose receptor 2) conjugated, via a protease-cleavable tetra-peptide linker, to the topoisomerase-1 inhibitor (TOP1i) P1021, with potential antineoplastic activity. Upon administration of anti-uPARAP ADC ADCE-D01, AB-004 targets and binds to uPARAP-expressing tumor cells. Upon binding, internalization and linker cleavage, P1021 is released, and inhibits DNA topoisomerase-1 activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of uPARAP-expressing tumor cells. uPARAP, a recycling endocytic receptor involved in collagen homeostasis and turnover, is overexpressed on various tumor cell types while its expression is limited in healthy tissues.

anti-VEGF anticalin PRS-050-PEG40

A pegylated, proprietary lipocalin that targets human vascular endothelial growth factor (VEGF), with potential antineoplastic activity. Pegylated anti-VEGF anticalin PRS-050 specifically targets and binds to VEGF receptor 2 (VEGFR2 or KDR), thereby preventing its activity. This may inhibit angiogenesis and eventually reduce tumor cell growth.

anti-VEGF monoclonal antibody hPV19

A humanized monoclonal antibody directed against human vascular endothelial growth factor (VEGF), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-VEGF monoclonal antibody hPV19 targets and binds to VEGFR at a unique binding site and inhibits VEGF binding to its receptors, VEGFR1 and VEGFR2, thereby preventing VEGF/VEGFR-mediated signaling. This prevents the growth and maintenance of tumor blood vessels. This decreases nutrient supply to tumor cells, resulting in tumor cell death. Increased VEGF/VEGFR signaling is associated with increased invasiveness and decreased survival.

anti-VEGF/ANG2 nanobody BI 836880

A nanobody directed against angiopoietin-2 (Ang2; ANGPT2)- and vascular endothelial growth factor (VEGF)-derived peptides, with potential antiangiogenic and antineoplastic activities. Anti-VEGF/ANG2 nanobody BI 836880 binds to Ang2 and VEGF and inhibits receptor binding; this prevents Ang2- and VEGF-mediated signaling and inhibits both tumor angiogenesis and tumor cell proliferation. Both VEGF and Ang2 are upregulated in a variety of cancer cell types and each plays a crucial role in angiogenesis. The nanobody is based on functional fragments of single-chain antibodies.

Anti-VEGF/TGF-beta 1 Fusion Protein HB-002T

A recombinant, human immunoglobulin Fc fusion protein targeting both the transforming growth factor (TGF) beta 1 (TGF-beta 1; TGFb1) and the vascular endothelial growth factor (VEGF), with potential anti-angiogenic and antineoplastic activities. Upon administration of anti-VEGF/TGF-beta 1 fusion protein HB-002T, the fusion protein specifically and selectively targets, binds to and neutralizes both TGF-beta 1 and VEGF. This prevents TGFb1- and VEGF-mediated signaling and abrogates VEGF/VEGFR-induced angiogenesis and TGFb1-mediated induction of VEGF, which further inhibits angiogenesis. It also inhibits TGFb1-mediated immunosuppression, thereby enhancing anti-tumor immunity in the tumor microenvironment (TME) and promoting a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death.

anti-VEGF/TGF-beta bispecific antibody fusion protein ZGGS18

A bifunctional antibody fusion protein targeting both vascular endothelial growth factor (VEGF) and the pro-inflammatory cytokine human transforming growth factor beta (TGF-beta; TGFb), with potential antineoplastic activity. Upon administration, anti-VEGF/TGF-beta bispecific antibody fusion protein ZGGS18 targets, binds to and neutralizes both VEGF and TGF-beta. This prevents VEGF- and TGF-beta-mediated signaling and abrogates VEGF/VEGFR-induced angiogenesis and TGF-beta-mediated induction of VEGF, which further inhibits angiogenesis. It also inhibits TGF-beta-mediated immunosuppression, thereby enhancing anti-tumor immunity in the tumor microenvironment (TME) and promoting a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. VEGF is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis. TGF-beta, dysregulated in many types of cancer, plays a key role in immunosuppression in the TME, enhances tumor cell proliferation, and promotes cancer progression.

anti-VEGFC monoclonal antibody VGX-100

A fully human monoclonal antibody directed against the human vascular endothelial growth factor C (VEGFC or Flt4 ligand) with potential antiangiogenic activity. Anti-VEGFC monoclonal antibody VGX-100 specifically binds to and inhibits VEGFC protein, thereby preventing its binding to VEGFR3 (FLT4) or VEGFR2 (KDR or FLK1). This may prevent VEGFC-mediated signaling and may lead to the inhibition of vascular and lymphatic endothelial cell proliferation. The inhibition of tumor angiogenesis and lymphangiogenesis may eventually decrease tumor cell proliferation and prevent metastasis. VEGFC is overexpressed in a variety of cancer cells, and is associated with increased invasiveness and decreased survival.

anti-VEGFR-2 monoclonal antibody AK109

A human monoclonal antibody directed against human vascular endothelial growth factor receptor 2 (VEGFR-2; VEGFR2), with potential anti-angiogenesis and antineoplastic activities. Upon administration, anti-VEGFR-2 monoclonal antibody AK109 specifically binds to and inhibits VEGFR-2 on vascular endothelial cells, which may inhibit tumor angiogenesis and tumor cell proliferation. VEGFR-2, a tyrosine-protein kinase that plays an essential role in angiogenesis and the proliferation, survival, migration and differentiation of endothelial cells, is overexpressed in certain tumor types.

anti-VEGFR2 monoclonal antibody HLX06

A fully human monoclonal antibody directed against human vascular endothelial growth factor receptor 2 (VEGFR-2) with potential anti-angiogenesis and antineoplastic activities. Upon administration, anti-VEGFR2 monoclonal antibody HLX06 specifically binds to and inhibits VEGFR-2, which may inhibit tumor angiogenesis and tumor cell proliferation. VEGFR-2, a tyrosine-protein kinase that plays an essential role in angiogenesis and the proliferation, survival, migration and differentiation of endothelial cells, is overexpressed in certain tumor types.

anti-VEGFR2 monoclonal antibody MSB0254

A humanized monoclonal antibody directed against human vascular endothelial growth factor receptor 2 (VEGFR-2; VEGFR2) with potential anti-angiogenesis and antineoplastic activities. Upon administration, anti-VEGFR2 monoclonal antibody MSB0254 specifically binds to and inhibits VEGFR2, which may inhibit tumor angiogenesis and tumor cell proliferation. VEGFR2, a tyrosine-protein kinase that plays an essential role in angiogenesis and the proliferation, survival, migration and differentiation of endothelial cells, is overexpressed in certain tumor types.

anti-VEGFR2-CAR retroviral vector-transduced autologous T lymphocytes

Autologous human CD8-positive T-lymphocytes transduced with a recombinant retroviral vector encoding a chimeric T cell receptor (chimeric antigen receptor or CAR) consisting of an anti-vascular endothelial growth factor receptor type 2 (VEGFR2) scFv (single chain variable fragment), linked to the transmembrane domain of human CD8alpha and coupled to the costimulatory signaling domains of both CD28 and 4-1BB (CD137), and the CD3 zeta chain of the T-cell receptor (TCR), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with VEGFR2-positive cancer are pulsed with a retroviral vector that encodes the CAR gene specific for VEGFR2. After expansion in culture and reintroduction into the patient, the anti-VEGFR2 CAR-gene engineered CD8+ lymphocytes express anti-VEGFR2-CAR on their cell surfaces and bind to the VEGFR2 antigen on tumor cell surfaces. Subsequently, VEGFR2-expressing tumor cells are lysed. VEGFR2, a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, belongs to the VEGFR superfamily and plays key roles in tumor cell proliferation, survival, invasion and tumor angiogenesis. The co-stimulatory molecules are required for optimal T-cell activation.

anti-VEGFR3 monoclonal antibody IMC-3C5

A fully-human monoclonal antibody directed against human vascular endothelial growth factor receptor 3 (VEGFR-3; Flt-4) with antiangiogenic activity. Anti-VEGFR-3 monoclonal antibody IMC-3C5 specifically binds to and inhibits VEGFR-3, which may result in inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR-3 plays a critical role in the embryonic vascular system development but is restricted postnatally to endothelial cells of lymphatic vessels and found to be expressed in many solid and hematologic malignancies.

anti-VISTA monoclonal antibody HMBD-002

An immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immune checkpoint regulatory protein V-domain Ig suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon administration, anti-VISTA monoclonal antibody HMBD-002 targets and binds to VISTA on monocytes and T cells. This inhibits VISTA-mediated signaling, decreases the presence of monocytic myeloid-derived suppressor cells (MDSCs), increases the presence of activated dendritic cells (DCs) and abrogates VISTA-induced suppression of T-lymphocyte immune responses. This enhances cytotoxic T-cell infiltration, proliferation and activation within the tumor microenvironment (TME), increases cytokine production by T cells, and inhibits tumor cell growth. VISTA, a negative checkpoint molecule of immune activation, is highly expressed on myeloid cells, T cells and in several tumor types. It plays a key role in the suppression of T-cell function.

anti-VISTA monoclonal antibody SNS-101

A conditionally active, pH-sensitive human immunoglobulin (Ig) G1 monoclonal antibody directed against the negative immune checkpoint regulatory protein V-domain Ig suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon administration, anti-VISTA monoclonal antibody SNS-101 selectively targets, binds to and blocks the VISTA checkpoint within a low, acidic pH tumor microenvironment (TME). This prevents the interaction of VISTA with its receptor PSGL-1 on T cells, inhibits VISTA-mediated signaling, decreases the presence of monocytic myeloid-derived suppressor cells (MDSCs), increases the presence of natural killer cells (NKs), activates dendritic cells (DCs) and abrogates VISTA-induced suppression of T-lymphocyte immune responses. This enhances cytotoxic T-cell infiltration, proliferation, and activation within the TME, increases cytokine production by T cells, and inhibits tumor cell growth. VISTA, a negative checkpoint molecule of immune activation, is highly expressed on myeloid cells, T cells and in several tumor types. It plays a key role in the suppression of T-cell function and tumor immunosuppression.

anti-VISTA monoclonal antibody W0180

A humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the negative immune checkpoint regulatory protein V-domain Ig suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon administration, anti-VISTA monoclonal antibody W0180 targets and binds to the extracellular domain of VISTA on myeloid cells and T cells within the tumor microenvironment (TME). This inhibits VISTA-mediated signaling, decreases the presence of monocytic myeloid-derived suppressor cells (MDSCs), increases the presence of natural killer cells (NKs), activates dendritic cells (DCs) and abrogates VISTA-induced suppression of T-lymphocyte immune responses. This enhances cytotoxic T-cell infiltration, proliferation and activation within the TME, increases cytokine production by T cells, and inhibits tumor cell growth. VISTA, a negative checkpoint molecule of immune activation, is highly expressed on myeloid cells, T cells and in several tumor types. It plays a key role in the suppression of T-cell function.

anti-von Willebrand factor nanobody

A humanized, bivalent anti-von Willebrand factor (VWF) nanobody with potential anti-platelet activity. Anti-von Willebrand factor nanobody specifically binds to the A1 domain of the VWF molecule, thereby inhibiting and neutralizing VWF activity. This prevents the interaction of VWF with the platelet glycoprotein (Gp)Ib-IX-V receptor and prevents VWF-mediated platelet aggregation. VWF is a glycoprotein and plays a key role in blood coagulation. Increased VWF, which is seen in a number of diseases, is associated with an increased risk in thrombosis. The nanobody formulation allows for rapid distribution, onset of action and clearance. The nanobody is based on the smallest functional fragments of single-chain antibodies that naturally occur in the Camelidae family.

anti-VSIG4 monoclonal antibody EU103

A humanized immunoglobulin G1 kappa (IgG1kappa) monoclonal antibody directed against V-set and immunoglobulin domain-containing 4 (VSIG4), with potential immunomodulating and antineoplastic activities. Upon administration, anti-VSIG4 monoclonal antibody EU103 targets, binds to and inhibits the activity of VSIG4 expressed on immunosuppressive M2 macrophages. This induces repolarization of these tumor-associated macrophages (TAMs) and leads to macrophage conversion of M2 into M1 macrophages. This improves the tumor microenvironment (TME), blocks VSIG4-mediated T-cell suppression, and leads to a cytotoxic T-cell-mediated anti-tumor immune response. VSIG4, one of the B7 family-related proteins, is overexpressed in various tumor cell types. Its overexpression negatively regulates T-cell proliferation and is correlated with poor prognosis.

anti-Wolbachia agent AWZ1066S

An orally bioavailable synthetic compond that is active against the bacterium Wolbachia and that can potentially be used to treat diseases caused by namatodes of the family Filariodidea, such as lymphatic filariasis and onchocerciasis. Upon oral administration, the anti-Wolbachia agent AWZ1066S specifically kills Wolbachia through an as of yet not fully identified mechanism of action (MoA). In filarial nematodes-infected humans, adult worms need Wolbachia in order to grow, reproduce, and survive. Targeting Wolbachia may indirectly kill the adult parasitic worms and prevent filariasis.

antiangiogenic drug combination TL-118

A proprietary, oral suspension containing a combination of agents comprised of a nonsteroidal anti-inflammatory agent, an alkylating agent, a histamine H2 antagonist and a sulfonamide with potential anti-angiogenic and antineoplastic activities. Antiangiogenic drug combination TL-118 is administrated as a specific dosing regimen and may result in a synergistic effect and reduce angiogenesis and inhibit tumor cell proliferation.

antibiotic SQ109

An orally available, acid-stable diamine antibiotic, with potential antimicrobial activity against a variety of bacteria including Helicobacter pylori (H. pylori) and Mycobacterium tuberculosis (M. Tuberculosis). As an ethambutol analogue with asymmetric structure, SQ109 does not act on the same target as ethambutol. However, this agent interferes with cell wall synthesis, thereby causing weakening of the cell wall and ultimately cell lysis.

antibody receptor-Trap fusion protein IMM2520

An immunoglobulin G1 (IgG1) Fc-containing bispecific antibody-receptor fusion protein targeting both the human cell surface antigen CD47 and the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration, the antibody receptor-Trap fusion protein IMM2520 targets and binds to both CD47 and PD-L1 expressed on tumor cells. The CD47 binding by IMM2520 blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of CD47-expressing tumor cells. The binding of IMM2520 to PD-L1 blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, IMM2520 induces Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation, which protects cancer cells from phagocytosis and allows cancer cells to proliferate. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells. By co-targeting CD47 and PD-L1, IMM2520 may more selectively bind to tumor cells expressing both CD47 and PD-L1, reducing the side effects caused by the blockade of CD47 expressed on healthy hematopoietic stem cells (HSCs).

antibody ROSE12

An antibody directed against an as of yet undisclosed antigen, with potential antineoplastic activity. Upon administration, antibody ROSE12 binds to the undisclosed antigen, which may enhance anti-tumor immune response through an as of yet undisclosed mechanism of action (MoA).

antibody STING drug conjugate TAK-500

An antibody-drug conjugate (ADC) composed of an as of yet undisclosed antibody conjugated to TAK-676, an agonist for the stimulator of interferon genes (STING; transmembrane protein 173; TMEM173), with potential immuno-activating and antineoplastic activities. Upon intravenous administration, antibody STING drug conjugate TAK-500 targets and binds to the undisclosed target, thereby allowing TAK-676 to bind to STING. This activates the STING pathway in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system. The conjugation of the antibody to TAK-676 improves targeted delivery of the STNG agonist and increases tumor exposure to TAK-676 and enhances the STING-mediated anti-tumor immune responses.

antibody-drug conjugate ABBV-176

An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against the prolactin receptor (PRLR) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of ABBV-176 targets and binds to PRLR expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the PRLR-expressing tumor cells, through an as of yet unknown mechanism of action. PRLR, a tumor-associated antigen (TAA), is overexpressed by a variety of tumor cell types.

antibody-drug conjugate anti-TIM-1-vcMMAE CDX-014

A monoclonal antibody-drug conjugate (ADC) comprised of human immunoglobulin G1 (IgG1) clone CR014, which targets the extracellular domain of T-cell immunoglobulin mucin-1 (TIM-1; HAVCR1), that is linked, via a valine-citrulline (VC) peptide linker, to the potent cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of ADC anti-TIM-1-vcMMAE CDX-014, the monoclonal antibody moiety targets and binds to TIM-1. Upon internalization and proteolytic cleavage, MMAE is released into the cytosol of TIM-1-expressing tumor cells, binds to tubulin, and inhibits microtubule polymerization, which induces both G2/M phase arrest and tumor cell apoptosis. TIM-1 is upregulated in a variety of cancer cell types while only minimally expressed in healthy tissue. The linkage system in CDX-014 is highly stable in plasma, resulting in increased specificity and cytotoxic efficacy towards TIM-1-positive cells.

antibody-drug conjugate PHN-010

An antibody-drug conjugate (ADC) composed of an as of yet undisclosed monoclonal antibody directed against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of ADC PHN-010 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.

antibody-drug conjugate RC118

An antibody-drug conjugate (ADC) composed of an as of yet undisclosed monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of ADC RC118 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.

antibody-drug conjugate SC-003

An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SC-003 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.

antibody-drug conjugate SC-005

An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against a tumor-associated antigen (TAA) linked to a currently undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SC-005 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an unknown mechanism of action.

antibody-drug conjugate SC-007

An antibody-drug conjugate (ADC) composed of a monoclonal antibody against an undisclosed tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SC-007 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.

antibody/PNE-based biologic agent ABBV-461

A biologic agent composed of an antibody fragment targeting an as of yet unidentified tumor-associated antigen (TAA) that is linked to a 14 aa peptide epitope, or alpha-peptide neo-epitope (PNE), recognizable by autologous alpha-PNE switchable CAR-T cells CLBR001, that may be used to activate CLBR001. Upon administration of the antibody-based biologic agent ABBV-461, and upon co-administration of CLBR001, the antibody moiety targets and binds to tumor cells expressing the TAA. In turn, the PNE part of ABBV-461 binds to the binding domain of CLBR001, thereby activating CLBR001. This induces selective toxicity in and causes lysis of the TAA-expressing tumor cells to which ABBV-461 is bound.

anticachexia agent MT-102

A small molecule with potential anticachexia activity. The anticachexia agent MT-102 may increase protein synthesis and decrease muscle protein breakdown. This may result in improved body weight, muscle mass and may improve weakness and fatigue associated with cancer-related cachexia.

anticachexia agent OC514

A combination agent composed of two active ingredients, with potential anti-cachexia and anti-sarcopenia activities. Upon administration of OC514, the two active ingredients exert their mechanism of action (MoA) through an as of yet undisclosed manner to potentially prevent or decrease loss of skeletal muscle mass and strength.

antifungal agent VL-2397

A cyclic hexapeptide and natural compound isolated from the Malaysian leaf litter fungus, Acremonium persicinium MF-347833, with potential antifungal activity against various invasive fungal infections including invasive aspergillosis (IA). Upon administration, VL-2397, by resembling the siderophore ferrichrome, is specifically taken up by fungal cells through the membrane-bound transporter siderophore iron transporter 1 (Sit; Sit1). Upon fungal cell entry, VL-2397 targets and binds to an as of yet undisclosed intracellular site, thereby killing fungal cells. Since mammalian cells lack the Sit1 transporter, VL-2397 is not taken up by human cells.

antigen-presenting cells-expressing HPV16 E6/E7 SQZ-PBMC-HPV

A preparation of antigen presenting cells (APCs) specific for human papillomavirus (HPV) type 16 E6 and E7 proteins, with potential immunomodulating and antineoplastic activities. Autologous peripheral blood mononuclear cells (PBMCs) were ex vivo manipulated, using a technique involving membrane disruption to get the HPV16 E6 and E7 proteins into the cells; the resulting APCs present the antigens in a major histocompatibility type I (MHC-I) manner. Upon administration of the APCs-expressing HPV16 E6/E7 SQZ-PBMC-HPV, these cells activate the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing HPV16 E6 and E7. HPV16 E6 and E7 play an important role in the development of certain types of cancer.

antigen-presenting cells-expressing HPV16 E6/E7/CD86/mbIL-2/mbIL-12 SQZ-eAPC-HPV

A preparation of antigen presenting cells (APCs) specific for human papillomavirus (HPV) type 16 E6 and E7 proteins, and engineered to express the costimulatory molecule CD86 and the membrane-bound cytokines interleukin-2 (mbIL-2) and interleukin-12 (mbIL-12), with potential immunomodulating and antineoplastic activities. Autologous peripheral blood mononuclear cells (PBMCs) are ex vivo engineered with five mRNA encoding for HPV 16 E6/E7 antigens, CD86, mbIL-2 and mbIL-12; the resulting APCs present the antigens in a major histocompatibility type I (MHC-I) manner. Upon administration of the APCs-expressing HPV16 E6/E7/CD86/mbIL-2/mbIL-12 SQZ-eAPC-HPV, these cells activate the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing HPV16 E6 and E7. The costimulatory molecule CD86 and the cytokines mbIL-2 and mbIL-12 further activate the immune system by promoting the secretion of interferon-gamma (IFNg), activating natural killer cells (NKs), and inducing CTL responses, further killing tumor cells. HPV16 E6 and E7 play an important role in the development of certain types of cancer.

antigen-targeted personalized breast cancer vaccine

An individualized, therapeutic cancer vaccine (IVAC) composed of liposomes containing RNA encoding two or three tumor-associated antigens (TAAs) that are specifically expressed in the patient's individual cancer selected from a warehouse (“off the shelf”) and p53 RNA, with potential immunostimulatory and antineoplastic activities. Upon administration, the antigen-targeted personalized breast cancer vaccines are translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL) and memory T-cell immune responses against the TAAs. The RNAs in the vaccine are specifically selected for an individual patient after RNA profiling of the patient’s tumor.

antihemophilic factor, human recombinant

The recombinant form of human antihemophilic factor (AH) (Factor VIII) with coagulation promoting activity. Antihemophilic factor binds to factor IXa in the coagulation cascade along with calcium and phospholipid. This complex converts factor X to the activated form, factor Xa. In turn, factor Xa/Va complex activates thrombin, which cleaves fibrinogen into fibrin, eventually resulting in blood clot formation.

antimetabolite FF-10502

An antimetabolite with potential antineoplastic activity. Upon administration, FF-10502 is able to enter the nucleus where it inhibits DNA polymerases, thereby preventing DNA synthesis and halting tumor cell proliferation.

antimoniotungstate

A non-nucleoside reverse transcriptase inhibitor. Antimoniotungstate is a mineral condensed ion with a cryptic structure.

antineoplaston A10

A piperidinedione antineoplaston with potential antineoplastic activity. Antineoplaston A10 was originally isolated from human urine but is now synthetically derived. This agent intercalates into DNA, resulting in cell cycle arrest in G1 phase, reduction of mitosis, and decreased protein synthesis. Antineoplaston A10 may also inhibit ras-oncogene expression and activate tumor suppressor gene p53, leading to cell differentiation and apoptosis.

antineoplaston AS2-1

A 4:1 mixture of phenylacetate and phenylacetylgluatmine, degradation products of the antineoplaston agent A10. Antineoplaston AS2-1 inhibits the incorporation of L-glutamine into tumor-cell proteins, leading to cell cycle arrest in the G1 phase and inhibition of mitosis. This agent may also inhibit RAS oncogene expression and activate tumor suppressor gene p53, resulting in cell differentiation and apoptosis.

antiperspirant cream F511

A cream formulation containing aluminum chlorohydrate with astringent and antiperspirant activities. Upon topical application of F511 cream, aluminium chlorohydrate forms a gel matrix in the sweat gland which subsequently reduces, then stops the flow of water. In addition, this agent exerts an astringent effect, thereby further preventing sweat formation. Hyperhidrosis appears to play a role in the development of certain mucocutaneous reactions, such as palmar-plantar erythrodysesthesia (PPE), upon administration of chemotherapeutic agents such as doxorubicin, 5-fluorouracil, and capecitabine.

antisecretory factor-enriched egg yolk powder supplement

A dietary supplement composed of dried egg yolk powder that is highly enriched in the protein anti-secretory factor (AF), with anti-inflammatory, anti-diarrheal, immunomodulating and chemo-adjuvant activities. Upon intratumoral administration of the AF-enriched egg yolk powder supplement, AF is able to normalize fluid flow by regulating the ion and fluid balance across the cell membranes, and decreases high interstitial fluid pressure (IFP). As elevated IFP presents a barrier to drug uptake and poor perfusion in solid tumors, reducing IFP levels allows for increased uptake and an enhanced effect of chemotherapeutic agents. In addition, AF may be able to modulate the immune system and may have immunomodulatory effects on myeloid cells. It may also modulate the secretion of immunomodulatory agents from tumor cells. In addition, AF may affect the secretion of various pro-inflammatory mediators such as interleukin-6 (IL-6), IL-8, monocyte chemotactic protein-1 (MCP-1; monocyte chemoattractant protein-1; C-C Motif Chemokine Ligand 2; CCL2), macrophage inflammatory protein-1alpha (MIP-1a), and macrophage inflammatory protein-1beta (MIP-1b). AF, a 41 kilodalton (kDa) endogenous and essential protein secreted in plasma and other tissue fluids in mammals, is increased after exposure to bacterial toxins and endogenous triggers of inflammation.

antisense oligonucleotide GTI-2040

A 20-mer antisense oligonucleotide complementary to a coding region in the mRNA of the R2 small subunit component of human ribonucleotide reductase. GTI-2040 decreases mRNA and protein levels of R2 in vitro and may inhibit tumor cell proliferation in human tumors in vivo.

antisense oligonucleotide QR-313

A twenty-one nucleotide-containing antisense oligonucleotide (AON) with potential use in the treatment of recessive dystrophic epidermolysis bullosa (RDEB) due to mutations in exon 73 of the COL7A1 gene. Upon topical administration, QR-313 hybridizes to a specific sequence in COL7A1 pre-mRNA, resulting in exclusion of exon 73 from mRNA and translation of a functional type VII collagen protein. This may restore functionality of integument anchoring fibrils, prevent blistering, and improve wound healing in patients with DEB. Type VII collagen is a major component of anchoring fibrils, attachment structures that mediate dermal-epidermal adherence in human skin. DEB is an inherited mechano-bullous disorder caused by mutations in the COL7A1 gene, which lead to perturbations in anchoring fibrils.

Antitumor B Key Active Component-alpha

An orally available concentrated preparation of antitumor B (ATB, Zeng Sheng Ping), a Chinese herbal formula comprised of Sophora tonkinensis, Polygonum bistorta, Prunella vulgaris, Sonchus brachyotus, Dictamnus dasycarpus, and Dioscorea bulbifera, with potential antineoplastic activity. Upon administration, antitumor B key active component-alpha (ATB-KAC-alpha) may, through a not yet fully elucidated mechanism, inhibit tumorigenesis and prevent the development of certain cancers.

Antivert

(Other name for: meclizine hydrochloride)

antiviral agent TGN-S11

A small molecule agent, with potential antiviral and antineoplastic activities. Upon administration, antiviral agent TGN-S11 may exert its activity by as of yet not elucidated mechanisms of action.

Antrin

(Other name for: motexafin lutetium)

Antrodia cinnamomea supplement

A dietary supplement containing extract from the medicinal fungus Antrodia cinnamomea with potential antiangiogenic, hepatoprotective and antioxidant activities. The components in Antrodia cinnamomea supplement are rather complex, however, rich in triterpenoids, polysaccharides, nucleosides (adenosine) nucleic acids, superoxide dismutase, other small molecular weight proteins and steroid like compounds. Neutral sugars in this supplement show inhibitory activity on endothelial tube formation, while maleimide and maleic anhydride derivative components in the extract, such as antrodin B and antrodin C and their metabolites, exhibit significant cytotoxic effects on tumor cells and hepatitis C virus.

anvatabart opadotin

An antibody-drug conjugate (ADC) composed of anvatabart, a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2) site-specifically conjugated at two engineered residues of para-acetyl-phenylalanine (pAcF) via a stable oxime linker to the monomethyl auristatin F (MMAF) analog and potent microtubule inhibitor opadotin, with potential antineoplastic activity. Upon administration of anvatabart opadotin, the antibody moiety targets and binds to HER2 on tumor cells. Upon antibody/antigen binding and internalization, opadotin binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types. The site-specific conjugation of the cytotoxic agent to the antibody improves the biophysical properties of anvatabart opadotin, increases payload stability and optimizes its efficacy.

anvumetostat

An orally available small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, anvumetostat selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. Methylthioadenosine phosphorylase (MTAP) is deleted in certain cancer cells leading to an accumulation of methylthioadenosine (MTA). As MTA inhibits PRMT5, MTAP-null cancer cells are specifically sensitive to PRMT5 inhibitors.

anzurstobart

An immunoglobulin G1 (IgG1) monoclonal antibody targeting signal-regulatory protein alpha (SIRPa; CD172a) with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anzurstobart targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47/SIRPa-mediated signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.

AO+ Mist

(Other name for: topical ammonia-oxidizing bacteria-based probiotic solution)

apadamtase alfa

A recombinant human form of a disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS13) that may be used as a replacement therapy for ADAMTS13 with indirect anti-thrombotic and anti-thrombocytopenic activities. Upon administration, apadamtase alfa acts similarly as endogenous ADAMTS13 and mediates the cleavage of von Willebrand factor (VWF) at the Tyr1605-Met1606 bond in the A2 domain. The cleavage of ultralarge (UL) VWF multimers into smaller forms helps regulate the size of VWF multimers, preventing the binding of platelets to UL VWF and the resulting thrombotic thrombocytopenic purpura (TTP). ADAMTS13 plays a key role in the proteolysis of VWF multimers. VWF is involved in platelet adhesion and blood coagulation.

apalutamide

A small molecule and androgen receptor (AR) antagonist with potential antineoplastic activity. Apalutamide binds to AR in target tissues thereby preventing androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot be translocated to the nucleus. This prevents binding to and transcription of AR-responsive genes. This ultimately inhibits the expression of genes that regulate prostate cancer cell proliferation and may lead to an inhibition of cell growth in AR-expressing tumor cells.

apamistamab

A murine IgG1 anti-CD45 monoclonal antibody (MoAb) with immunotherapeutic activity. CD45 antigen, a receptor protein-tyrosine phosphatase essential for T cell development and lymphocyte activation, is expressed on virtually all leukocytes. Apamistamab has specificity for hematopoietic tissues and may be used in targeted immunotherapy.

Apatorsen

A second-generation antisense oligonucleotide targeting heat shock protein 27 (Hsp27) with potential antitumor and chemosensitizing activities. Apatorsen suppresses tumor cell expression of Hsp27, which may induce tumor cell apoptosis and enhance tumor cell sensitivity to cytotoxic agents. Hsp27, a chaperone belonging to the small heat shock protein (sHsp) group of proteins, is a cytoprotective protein that supports cell survival under conditions of stress; it has been found to be over-expressed in a variety of human cancers.

apaziquone

An indolequinone bioreductive prodrug and analog of mitomycin C with potential antineoplastic and radiosensitization activities. Apaziquone is converted to active metabolites in hypoxic cells by intracellular reductases, which are present in greater amounts in hypoxic tumor cells. The active metabolites alkylate DNA, resulting in apoptotic cell death. This agent displays activity towards both hypoxic solid tumors, which exhibits higher expression of cytochrome P450 reductase, and well-oxygenated malignant cells that overexpress the bioreductive enzyme NQO1 (NAD(P)H: quinone oxidoreductase). Apaziquone may selectively sensitize hypoxic tumor cells to radiocytotoxicity.

APC8015F

A cell-based vaccine composed of previously frozen autologous antigen-presenting peripheral blood mononuclear cells (enriched for a dendritic cell fraction) that have been exposed to a recombinant protein consisting of granulocyte-macrophage colony-stimulating factor (GM-CSF) fused to prostatic-acid phosphatase (PAP), a protein expressed by prostate cancer cells. Upon administration, the vaccine may stimulate an antitumor T-cell response against tumor cells expressing PAP.

APE1/Ref-1 redox inhibitor APX3330

An orally bioavailable inhibitor of apurinic/apyrimidinic endonuclease 1/reduction-oxidation (redox) effector factor-1 (APE1/Ref-1; APEX1), with potential anti-angiogenic and antineoplastic activities. Upon administration, the APE1/Ref-1 Inhibitor APX3330 selectively targets and binds to APE1/Ref-1. This inhibits the redox-dependent signaling activity of APE1/Ref-1, by preventing the reduction and activation of numerous APE1/Ref-1-dependent oncogenic transcription factors (TFs), such as nuclear factor kappa B (NF-kB), AP-1, STAT3, p53, NRF2 and HIF-1alpha, that are involved in signaling, cell proliferation, tumor progression and survival of cancer cells. Therefore, this agent inhibits the activation of multiple TF-mediated signaling pathways and inhibits tumor cell proliferation and survival. APE1/Ref-1, a multifunctional protein overexpressed in many cancer cell types, plays a key role as a redox regulator of transcription factor activation and in base excision repair upon DNA damage. It drives cancer cell proliferation, migration, drug resistance, angiogenesis and inflammation and its expression level correlates with increased tumor aggressiveness and decreased patient survival. APX3330 specifically blocks the redox activity of APE1/Ref-1 and does not affect its ability to act as a DNA repair endonuclease.

APF530

A controlled-release formulation of a biodegradable poly(ortho ester) polymer, encapsulating the indazole derivative granisetron, with antiemetic activity. Upon administration of APF530, the polymer slowly erodes and releases the active ingredient granisetron. As a selective serotonin receptor antagonist, granisetron competitively blocks the action of serotonin at 5-hydroxytryptamine3 (5-HT3) receptors, resulting in the suppression of nausea and vomiting over a sustained period of time.

apilimod dimesylate capsule

A capsule containing the dimesylate salt form of apilimod, an inhibitor of the class III PI kinase phosphatidylinositol-3-phosphate 5-kinase (PIKfyve), with potential antineoplastic and immunomodulatory activities. Upon oral administration of apilimod dimesylate capsule, apilimod selectively binds to and inhibits PIKfyve. The inhibition leads to disruption of PIKfyve-mediated signal transduction pathways and eventually inhibits tumor cell growth in PIKfyve-overexpressing tumor cells. Also, PIKfyve inhibition by apilimod inhibits the toll-like receptor (TLR)-induced production of various cytokines, including interleukin-12 (IL-12) and IL-23, thereby preventing IL-12/IL-23-mediated immune responses. PIKfyve, a lipid kinase dysregulated in various tumor types, plays a key role in TLR signaling and tumor cell migration, proliferation and survival.

APIM-containing peptide ATX-101

A cell-penetrating peptide comprised of the proliferating cell nuclear antigen (PCNA)-interacting motif AlkB homologue 2 PCNA interacting motif (APIM) and cell penetration and nuclear localization domains, with potential chemo-sensitizing and antineoplastic activities. Upon administration, APIM-containing peptide ATX-101 penetrates cells and targets and disrupts the interactions between PCNA and other APIM-containing proteins. This may result in the downregulation of oncogenic signaling pathways such as MAPK/AKT/ERBB2/EGFR signaling and the inhibition of DNA repair, thereby enhancing the efficacy of some antineoplastic agents and inducing apoptosis. PCNA is a scaffold protein involved in multiple cellular processes via its interactions with many proteins through PCNA-interacting motifs.

apitolisib

An orally available agent targeting phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. Apitolisib inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion.

apixaban

An orally active inhibitor of coagulation factor Xa with anticoagulant activity. Apixaban directly inhibits factor Xa, thereby interfering with the conversion of prothrombin to thrombin and preventing formation of cross-linked fibrin clots.

Aplenzin

(Other name for: bupropion hydrochloride controlled-release)

Aplidin

(Other name for: plitidepsin)

aplitabart

A recombinant agonistic pentameric immunoglobulin M (IgM) monoclonal antibody directed against human death receptor type 5 (DR5), also called tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAILR2), with potential pro-apoptotic and antineoplastic activities. Upon administration, aplitabart, containing ten binding sites specific for DR5, specifically targets and binds to DR5, which mimics the interaction of DR5 with its natural ligand TRAIL. This cross-links and activates DR5 receptors, and activates the death receptor signaling pathway. This results in the activation of caspase cascades, the induction of tumor cell apoptosis and a reduction in proliferation of DR5-expressing tumor cells. DR5, a member of the TNF receptor superfamily (TNFRSF), is expressed on the surfaces of a variety of tumor cells and plays a key role in the induction of tumor cell apoptosis.

apoaequorin/vitamin D supplement

A dietary supplement composed of synthetic form of the naturally-occurring protein apoaequorin and vitamin D, that may potentially be used to improve memory. Upon oral administration of apoaequorin/vitamin D supplement, apoaequorin, a calcium binding protein naturally found in luminescent jellyfish (Aequorea victoria), may potentially improve memory through the regulation of intracellular calcium in neuronal cells, though it has not been shown to be able to cross the blood brain barrier (BBB).

Apocept

(Other name for: asunercept)

apolizumab

A humanized monoclonal antibody directed against 1D10, a polymorphic determinant on the HLA-DR beta chain that is expressed on normal and neoplastic B cells. Apolizumab induces complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis of 1D10 antigen-positive B cells in vitro.

apomab

A fully human monoclonal antibody directed against human death receptor 5 (DR5; TRAIL-R2; TNFRSF10B) with potential proapoptotic and antineoplastic activities. Mimicking the natural ligand TRAIL (tumor necrosis factor-related apoptosis inducing ligand), apomab binds to DR5, which may directly activate the extrinsic apoptosis pathway and indirectly induce the intrinsic apoptosis pathway in tumor cells. DR5 is a cell surface receptor of the TNF-receptor superfamily and is expressed in a broad range of cancers.

apomine

A 1,1-bisphosphonate ester with potential antineoplastic and hypocholesterolemic activities. SR-45023A binds to hydroxyapatite crystals in the bone matrix where it inhibits enzymatic activity of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which is required for the formation of mevalonate, the precursor of cholesterol. Consequently, shortage of mevalonate impedes the synthesis of downstream isoprenoids that are essential for protein prenylation. This leads to the loss of activity of proteins involved in osteoclast function and cellular proliferation, such as Ras and Rho, leading to an inhibition of cellular proliferation, and induction of osteoclasts apoptosis. In addition, SR-45023A activates the farnesoid X activated receptor (FXR), a member of the nuclear hormone superfamily implicated in cholesterol metabolism and bile acid transport and may play a role in this agent's antineoplastic effect.

APOPTONE

(Other name for: Androstane Steroid HE3235)

apoptosis inducer BZL101

An orally active aqueuous extract derived from the plant Scutellaria barbata with potential antineoplastic activity. Sparing normal cells, apoptosis inducer BZL101 specifically facilitates translocation of the protein apoptosis-inducing factor (AIF) from the mitochondrial membrane into the nucleus in tumor cells, thereby causing tumor cell-specific chromatin condensation and DNA degradation followed by the induction of caspase-independent apoptosis. AIF is both a mitochondrial intermembrane flavoprotein with oxidoreductase activity and a caspase-independent death effector that, similar to cytochrome c, is released from mitochondria early in the apoptotic process.

apoptosis inducer GCS-100

A galectin-binding polysaccharide derived from citrus pectin with potential antineoplastic activity. Apoptosis inducer GCS-100 binds to the carbohydrate-binding domain of the lectin galectin-3, which may result in apoptosis mediated through mitochondria/caspase activation cascades; this agent may overcome tumor growth mediated through anti-apoptotic protein Bcl-2, heat shock protein-27 (Hsp-27), and nuclear factor-kappa B (NF-kB). Galectin-3, a chimeric molecule consisting of both carbohydrate recognition and collagen-like domains, interacts with a variety of carbohydrate and protein ligands to form pentamers with unique crosslinking abilities; this lectin also exhibits anti-apoptotic properties, perhaps, in part, through the regulation of intracellular signaling pathways.

apoptosis inducer MPC-2130

A broad-acting, apoptosis-inducing, small molecule with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, apoptosis inducer MPC-2130 exhibits proapoptotic activities in tumor cells, including membrane phosphatidylserine externalization, release of cytochrome C from mitochondria, caspase activation, cell condensation, and DNA fragmentation. In addition, because this agent is not a substrate for several types of multidrug resistance (MDR) ABC superfamily transporters, such as P-glycoprotein 1 (MDR-1), multidrug resistance-associated protein 1 (MRP1), and breast cancer resistance protein 1 (BCRP1/ABCG2), it may be useful in treating MDR tumors that express these particular MDR efflux pumps.

apoptotic autologous tumor cells-pulsed alpha-type-1 polarized dendritic cells

A cell-based cancer vaccine composed of mature polarized dendritic cells (DCs) and pulsed with apoptotic autologous tumor cells that has potential immunostimulating and antineoplatic activities. Dendritic cells (DCs) were treated with interleukin-1 beta, tumor necrosis factor alpha, interferon-alpha (IFN-a), IFN-gamma and polyinosinic:polycytidylic acid (p-I:C) to produce mature alpha type-1 polarized DCs (alphaDC1) that are capable of producing high levels of interleukin-12p70 (IL-12p70). The alphaDC1 are subsequently pulsed with apoptotic autologous tumor cells. Upon administration, these DCs are able to induce a potent cytotoxic T lymphocyte (CTL) response against tumor associated antigens (TAAs), resulting in tumor cell lysis and inhibition of tumor cell growth. Apoptotic tumor cells contain an array of TAAs.

Apra

(Other name for: CT2584)

apraglutide

A synthetic, long-acting glucagon-like peptide-2 (GLP-2) agonist, with intestinotrophic activity. Apraglutide is a synthetic 33 amino acid peptide with four amino acid substitutions as compared to the native protein: alanine (Ala) to glycine (Gly) at position 2 (A2G), methionine (Met) to the synthetic lysine analog, aminocaproic acid (Ahx) at position 10 (M10Ahx), asparagine (Asn) to D-phenylalanine (D-Phe) at position 11 (N11F), and asparagine (Asn) to leucine (Leu) at position 16 (N16L). Following subcutaneous administration, apraglutide, as an analog of natural GLP-2, selectively activates GLP-2 receptors in the gastrointestinal (GI) tract, which stimulates intestinal growth, increases intestinal fluid and nutrient absorption, promotes healing, and improves intestinal epithelial integrity and function. As apraglutide becomes highly bound to plasma protein and resistant to degradation by dipeptidyl peptidase-4 (DPP-4), this agent has a longer half-life as compared to other GLP-2 agonists, which allows for less frequent dosing.

apremilast

An orally bioavailable, small molecule inhibitor of phosphodiesterase 4 (PDE4), with potential anti-inflammatory activity. Upon oral administration, apremilast targets, binds to and inhibits the activity of PDE4, thereby blocking cyclic adenosine monophosphate (cAMP) degradation and increasing intracellular cAMP levels. This may decrease the production of the proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha). PDE4 is an enzyme that plays an important role in the degradation of cAMP and in cytokine production in inflammatory cells.

aprepitant

A small molecule, high-affinity substance P antagonist (SPA) with antiemetic activity. Crossing the blood brain barrier, aprepitant binds selectively to the human substance P/neurokinin 1 receptor in the central nervous system (CNS), thereby inhibiting receptor binding of endogenous substance P and substance P-induced emesis. This agent has little or no affinity for serotonin type 3 (5-HT3), dopamine, and corticosteroid receptors.

Apretude

(Other name for: cabotegravir)

apricoxib

An orally bioavailable nonsteroidal anti-inflammatory agent (NSAID) with potential antiangiogenic and antineoplastic activities. Apricoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), thereby inhibiting the conversion of arachidonic acid into prostaglandins. Apricoxib-mediated inhibition of COX-2 may induce tumor cell apoptosis and inhibit tumor cell proliferation and tumor angiogenesis. COX-related metabolic pathways may represent crucial regulators of cellular proliferation and angiogenesis.

aprinocarsen

A synthetic phosphorothioate oligodeoxynucleotide. As an antisense molecule, aprinocarsen hybridizes to the 3-untranslated region of the human protein kinase C (PKC-alpha) mRNA, thereby inhibiting PKC-alpha expression and growth of PKC-alpha-dependent tumor cells.

Apriso

(Other name for: mesalamine)

aprotinin

A single chain polypeptide isolated from bovine lung with antifibrinolytic and anti-inflammatory activities. As a broad-spectrum serine protease inhibitor, aprotinin bovine competitively and reversibly inhibits the activity of a number of different esterases and proteases, including trypsin, chymotrypsin, kallikrein, plasmin, tissue plasminogen activator, and tissue and leukocytic proteinases, resulting in attenuation of the systemic inflammatory response (SIR), fibrinolysis, and thrombin generation. This agent also inhibits pro-inflammatory cytokine release and maintains glycoprotein homeostasis.

aprutumab

An antibody against the fibroblast growth factor receptor type 2 (FGFR2), with potential antineoplastic activity. Upon administration, aprutumab binds to and inhibits FGFR2, which may result in the inhibition of both FGFR2 phosphorylation and FGFR2-mediated signal transduction pathways. This results in the inhibition of cell proliferation and the induction of cell death of FGFR2-expressing tumor cells. FGFR2, upregulated in many tumor cell types, is a receptor tyrosine kinase, which is essential to tumor cellular proliferation, differentiation and survival.

aprutumab ixadotin

An antibody-drug conjugate (ADC) directed against the fibroblast growth factor receptor type 2 (FGFR2) and conjugated to an as of yet unidentified toxin, with potential antineoplastic activity. Upon intravenous administration, aprutumab ixadotin binds to FGFR2. Upon binding, the toxin selectively induces cell death, through an as of yet undisclosed mechanism of action, in FGFR2-expressing tumor cells. FGFR2, a receptor tyrosine kinase upregulated in many tumor cell types, plays an essential role in tumor cell proliferation, differentiation and survival.

Aptosyn

(Other name for: exisulind)

Aquacel AG with Hydrofiber

(Other name for: ionic silver-impregnated sodium carboxymethyl cellulose antimicrobial dressing)

Aquadiol

(Other name for: therapeutic estradiol)

AquaMephyton

(Other name for: Phytonadione)

Aquaphor

(Other name for: petrolatum-mineral oil-lanolin-ceresin ointment)

Aquasol A

(Other name for: vitamin A compound)

AR antagonist BMS-641988

An androgen receptor (AR) antagonist with potential antineoplastic and anti-androgenic activities. BMS-641988 binds to the androgen receptor in target tissues, thereby preventing androgen-induced receptor activation, and facilitates the formation of inactive complexes that cannot be translocated to the nucleus. This may inhibit androgen-dependent gene expression, subsequently leading to an inhibition of cell growth and apoptosis in AR-expressing cells.

Aralast

(Other name for: alpha-1-proteinase inhibitor human)

Aranelle

(Other name for: ethinyl estradiol/norethindrone)

Aranesp

(Other name for: darbepoetin alfa)

Arava

(Other name for: leflunomide)

arazasetron besylate

The besylate salt form of the R-enantiomer of azasetron, a benzamide derivative and selective serotonin (5-hydroxytryptamine; 5-HT) receptor and calcineurin antagonist, with potential antinauseant and antiemetic, and otoprotective activities. Upon administration, arazasetron selectively binds to and inhibits 5-HT subtype 3 receptors (5-HT3R) located peripherally on vagus nerve terminals and centrally in the chemoreceptor trigger zone (CTZ) of the area postrema, which may result in suppression of nausea and vomiting. R-azasetron also targets and inhibits the activation of calcineurin, thereby preventing inner ear lesions, nerve degeneration, induction of apoptosis and sensory hair loss. This may prevent hearing loss. Calcineurin activation plays a key role in structural degeneration, swelling, synaptic uncoupling and the induction of apoptosis in the inner ear leading to hair cell loss and hearing loss.

ARC fusion protein SL-279252

An agonist redirected checkpoint (ARC) fusion protein consisting of the extracellular domains of human programmed cell death 1 (PD-1; PDCD1; CD279) and tumor necrosis factor ligand superfamily member 4 (TNFSF4; OX40 ligand; OX40L; CD252), linked by a central Fc domain (PD1-Fc-OX40L), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, ARC fusion protein SL-279252 simultaneously binds to both tumor necrosis factor receptor superfamily member 4 (TNFRSF4; OX40) and PD-1 expressed on T lymphocytes. Stimulation of OX40 may promote cytokine production and induce proliferation of memory and effector T lymphocytes against tumor cells, while PD-1 binding disrupts PD-1 signaling and may restore immune function through the activation of T cells. This may enhance the immune-mediated elimination of tumor cells more effectively than PD-1 blockade or OX40-agonism alone. OX40L, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) ligand family, provides a co-stimulatory signal for the proliferation and survival of activated T cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.

archexin

A 20-mer antisense oligodeoxynucleotide (ODN) against the proto-oncogene Akt with potential antineoplastic activity. Akt-1 antisense oligonucleotide RX-0201 binds to Akt-1 mRNA, inhibiting translation of the transcript; suppression of Akt-1 expression may result in the inhibition of cellular proliferation and the induction of apoptosis in tumor cells that overexpress Akt-1. Akt-1 is a serine-threonine protein kinase that stimulates proliferation and inhibits apoptosis of tumor cells.

arcitumomab

A murine IgG monoclonal Fab' fragment antibody directed against carcinoembryonic antigen (CEA), a protein that is overexpressed by many tumor cell types. For tumors that overexpress CEA, technetium-99m labeled arcitumomab may be used as an adjunct diagnostic imaging tool to obtain prognostic information following resection and to monitor for recurrent disease.

Arcoxia

(Other name for: etoricoxib)

Aredia

(Other name for: pamidronate disodium)

arfolitixorin

The R-isomer of folitixorin, a reduced folate-based biomodulator and active metabolite of folate drugs leucovorin (LV) and levoleucovorin (l-LV) that can be used to increase the efficacy of certain antimetabolites, such as the cytotoxic agent 5-fluorouracil (5-FU), and reduce as well as protect against certain antimetabolite-associated adverse effects, such as those seen with high-dose (HD) methotrexate. Upon administration of arfolitixorin, 5,10-methylenetetrahydrofolate (MTHF) is a reduced folate substrate for the enzyme thymidylate synthase (TS) and stabilizes, upon co-administration of 5-FU, the covalent binding of the 5-FU metabolite 5-fluoro-2'-deoxyuridine-5'-monophosphate (FdUMP), instead of deoxyuridine monophosphate (dUMP), to its target enzyme TS, which results in an inhibition of TS. This inhibits the synthesis of deoxythymidine monophosphate (dTMP) and leads to the depletion of thymidine triphosphate (TTP), which is a necessary constituent of DNA. This inhibits DNA synthesis, which leads to an inhibition of cellular proliferation and induces tumor cell death. As MTHF is able to stabilize and strengthen the ternary complex, co-administration of arfolitixorin enhances the inhibition of DNA synthesis and increases the cytotoxic effect of 5-FU. As MTHF is the active form of folate and the active metabolite of LV and l-LV, arfolitixorin does not need to be converted to an active metabolite to become activated. In DNA synthesis, a ternary complex is formed between the reduced folate substrate MTHF, the TS enzyme and dUMP in order to convert dUMP to the DNA building block dTMP, which is necessary for DNA synthesis.

ARG1/ARG2 inhibitor OATD-02

An orally bioavailable boronic acid derivative and inhibitor of arginase 1 (ARG1) and 2 (ARG2), with potential immunomodulating and antineoplastic activities. Upon oral administration, ARG1/ARG2 inhibitor OATD-02 selectively inhibits ARG1 and ARG2, thereby preventing the breakdown of arginine by arginase and restoring arginine levels. This allows arginine to stimulate the synthesis of nitric oxide (NO) and the secretion of pro-inflammatory cytokines and chemokines, which induces the proliferation and activation of T cells. Therefore, this agent may prevent the immunosuppressive effects of tumor-infiltrating myeloid cells, inhibit the immunomodulatory effect induced by regulatory T cells (Tregs), and promote lymphocyte-mediated immune responses against tumor cells. In addition, inhibition of ARG-mediated signaling may also kill tumor cells and decrease tumor cell growth by modulating tumor metabolism. Arginase, a manganese-dependent enzyme that hydrolyzes the amino acid arginine to form ornithine and urea, is produced by neutrophils, macrophages and myeloid-derived suppressor cells (MDSC). It plays a key role in inflammation-associated immunosuppression, tumor immunity, tumor cell growth and in metabolic pathways. Overexpressed in various types of tumors, its overexpression correlates with poor prognosis due to diminished arginine levels.

argatroban

A synthetic derivative of L-arginine with antithrombotic activity. Argatroban is a univalent and direct inhibitor of fibrin-bound thrombin. This agent reversibly binds to the thrombin active site thereby preventing the thrombin-dependent reactions, which include conversion of fibrinogen to fibrin; the activation of factors V, VIII and XI; the activation of protein C; and platelet aggregation. Argatroban is highly selective for thrombin and is able to inhibit the action of both free and clot-associated thrombin. As a result, stabilization of blood clots and coagulation is inhibited.

arginase-1 long peptide vaccine

A peptide cancer vaccine comprised of a long peptide, amino acid 169 through 206 (ISAKDIVYIGLRDVDPGEHYILKTLGIKYFSMTEVDRL), obtained from arginase-1, with potential immunomodulating and antineoplastic activities. Upon vaccination, the arginase-1 long peptide vaccine may activate the immune system to induce a cytotoxic T lymphocytes (CTLs)-mediated immune response against arginase-1-expressing cells. Arginase-1 is expressed by some cancer cells and by immune inhibitory cells, such as myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs); its expression is associated with poor prognosis.

arginase-1 peptide vaccine

A vaccine comprised of arginase-1 peptides, with potential antineoplastic activity. Upon vaccination, the arginase-1 peptide vaccine may activate the immune system to induce an immune response against arginase-1-expressing cells. Arginase-1 is expressed by some cancer cells and by immune inhibitory cells, such as myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs); its expression is associated with poor prognosis.

arginine butyrate

A compound composed of the short chain fatty acid (SCFA) butyrate combined with the amino acid arginine, with potential Epstein-Barr virus thymidine kinase gene (EBV-TK)-inducing activity. Upon administration, arginine butyrate induces the expression of thymidine kinase (TK). This activates a co-administered antiviral, such as ganciclovir, and results in the destruction of EBV-infected cancer cells. In addition, butyrate inhibits histone deacetylase (HDAC), which results in hyperacetylation of histones H3 and H4. Acetylated histones have a reduced affinity for chromatin; this reduced histone-chromatin affinity may allow chromosomal unfolding, potentially enhancing the expression of genes related to tumor cell growth arrest and apoptosis.

arginine hydrochloride

The hydrochloride salt form of arginine, an essential amino acid in juvenile humans. Arginine is a complex amino acid, often found at active sites in proteins and enzymes due to its amine-containing side chain. Arginine may prevent or treat heart and circulatory diseases, combat fatigue, and stimulate the immune system. It also boosts production of nitric oxide, relaxing blood vessels, and treating angina and other cardiovascular problems. Arginine is also an important intermediate in the urea cycle and in detoxification of nitrogenous wastes.

arginine/nucleotides/omega-3 fatty acids/olive oil polyphenols/antioxidants/L-carnitine oral supplement

A hypercaloric, hyperproteic, enteric nutritional supplement, enriched in arginine, nucleotides, omega-3 fatty acids, olive oil polyphenols, L-carnitine, and antioxidants, with potential immunomodulatory activity. Upon oral or tube administration of the arginine/nucleotides/omega-3 fatty acids/olive oil polyphenols/antioxidants/L-carnitine oral supplement, these immunonutrients may modulate the activity of key components of the immune system, including lymphocytes, antigen presenting cells (APC), and various cytokines.

arginine/omega-3 fatty acids/nucleotides oral supplement

A specialized enteric nutritional supplement, containing substantial amounts of polyunsaturated fatty acids, arginine, and nucleotides, with potential immunostimulating activity. Compared to traditional enteric nutritional supplements, the omega-3 fatty acids/arginine/nucleotides oral supplement may enhance the growth, development, and activity of key components of the immune system, including lymphocytes, antigen presenting cells, and various cytokines.

ArginMax

(Other name for: L-arginine/Korean ginseng/ Gingko biloba/damiana-based supplement)

argipressin

A synthetic peptide identical to the endogenous nonapeptide hormone with antidiuretic property. Synthesized in the hypothalamus and stored/released from the posterior lobe of the pituitary, argipressin's primary function is regulating extracellular fluid volume. This agent can also act as a vasoconstrictor, increasing blood pressure and systemic vascular resistance.

Aricept

(Other name for: donepezil hydrochloride)

Arimidex

(Other name for: anastrozole)

Aristocort

(Other name for: triamcinolone)

Aristocort A

(Other name for: triamcinolone acetonide)

Arixtra

(Other name for: fondaparinux sodium)

arlocabtagene autoleucel

A preparation of autologous T-lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human G-protein coupled receptor family C group 5 member D (GPRC5D), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, arlocabtagene autoleucel specifically recognize and induce selective toxicity in GPRC5D-expressing tumor cells. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation.

armodafinil

The R-enantiomer of the racemic synthetic agent modafinil with central nervous system (CNS) stimulant and wakefulness-promoting activities. Although the exact mechanism of action has yet to be fully elucidated, armodafinil appears to inhibit the reuptake of dopamine by binding to the dopamine-reuptake pump, which leads to an increase in extracellular dopamine levels in some brain regions. This agent does not bind to or inhibit several receptors and enzymes that may be involved in sleep/wake regulation and is not a direct- or indirect-acting dopamine receptor agonist. Armodafinil has a longer half-life than modafinil.

Arnebia Indigo Jade Pearl topical cream

A proprietary multiherbal topical cream based on Chinese herbal medicine with potential antineoplastic, antiviral, antibacterial and immunostimulatory activities. Arnebia Indigo Jade Pearl topical cream contains 12 ingredients including 9 herbs infused in sesame oil, with an additional three powdered ingredients and beeswax added to the infused oil to create the salve. The purported mechanism(s) of action is unclear due to the complexity of the herbal mixture.

Aromasin

(Other name for: exemestane)

Aroplatin

(Other name for: liposomal NDDP)

Arranon

(Other name for: nelarabine)

arsenic trioxide

A small-molecule arsenic compound with antineoplastic activity. The mechanism of action of arsenic trioxide is not completely understood. This agent causes damage to or degradation of the promyelocytic leukemia protein/retinoic acid receptor-alpha (PML/RARa) fusion protein; induces apoptosis in acute promyelocytic leukemia (APL) cells and in many other tumor cell types; promotes cell differentiation and suppresses cell proliferation in many different tumor cell types; and is pro-angiogenic.

arsenic trioxide capsule formulation ORH 2014

An orally bioavailable capsule formulation of the inorganic toxic compound arsenic trioxide (As2O3), with potential antineoplastic activity. Although the mechanism of action (MoA) of As2O3 is not well understood, upon oral administration of ORH 2014, As2O3 appears to bind to DNA, prevent DNA synthesis, and cause DNA fragmentation, which leads to an induction of apoptosis in proliferating cells, including tumor cells. In addition, As2O3 causes damage to and induces degradation of the promyelocytic leukemia protein/retinoic acid receptor-alpha (PML/RARa) fusion protein, and inhibits the activity of the enzyme thioredoxin reductase.

artemether sublingual spray

A sublingual spray containing artemether, a semisynthetic derivative of artemisinin, an endoperoxide extracted from the Chinese herb qinghaosu (Artemisia annua or annual wormwood), with antiparasitic and potential antineoplastic activity. Upon sublingual application of the spray, artemether exerts its antineoplastic activity through as of yet not fully elucidated mechanism(s) of action. This agent binds to heme molecules inside cells, thereby inducing reactive oxygen species (ROS)-mediated damage which selectively kills cancer cells. In addition, artemether appears to target and modulate the expression of various proteins involved in cancer cell proliferation, angiogenesis, invasion and metastasis. Also, this agent depletes T regulatory cells, and modulates the production of inflammatory cytokines, such as interleukin-4 and interferon-gamma. Altogether, this inhibits tumor cell proliferation. The sublingual spray allows faster absorption of a higher percentage of the artemether dose, when compared to the oral form, as it avoids first pass metabolism; this results in an increased efficacy.

Artemisia absinthium

An herbal remedy containing the leaves and/or flowering tops of a species of wormwood (Artemisia absinthium) with potential anticachexia activity. Upon oral consumption, Artemisia absinthium may decrease production of pro-inflammatory cytokines such as TNF-alpha. As increased levels of pro-inflammatory cytokines is correlated with decreased appetite and weight loss, Artemisia absinthium may increase appetite and improve weight gain.

Artemisia annua decaffeinated coffee

A decaffeinated coffee formulation containing Artemisia annua, with potential anti-inflammatory, antioxidant and chemopreventive activities. Artemisia annua contains specific sesquiterpene lactones, flavonoids, coumarins, phenolic acids, tannins, saponins, polyalkenes, phytosterols, fatty acids and proteins. The antioxidant compounds scavenge free radicals and inhibit cell damage due to reactive oxygen species (ROS). This inhibits oxidative stress and may protect against DNA damage.

artenimol

An active metabolite of artesunate, with anti-malarial activity, and potential insulin sensitivity-improving, anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration of artenimol and the hydrolysis of its active endoperoxide bridge moiety by liberated heme in parasite-infected red blood cells (RBCs), reactive oxygen species (ROS) and carbon-centered radicals form, which damage and kill parasitic organisms. Artenimol may also increase insulin sensitivity and improve insulin resistance. In addition, artenimol induces the 26S proteasome-mediated degradation of the androgen receptor (AR), thereby lowering AR expression, which may prevent androgen-responsive cellular proliferation. It also reduces luteinizing hormone LH) and testosterone levels, and may improve polycystic ovary syndrome (PCOS). In addition, artenimol may modulate the immune system and may inhibit tumor cell proliferation through various apoptotic and non-apoptotic pathways.

artesunate

A water-soluble, semi-synthetic derivative of the sesquiterpine lactone artemisinin with anti-malarial, anti-schistosomiasis, antiviral, and potential anti-neoplastic activities. Upon hydrolysis of artesunate's active endoperoxide bridge moiety by liberated heme in parasite-infected red blood cells, reactive oxygen species and carbon-centered radicals form, which have been shown to damage and kill parasitic organisms. Additionally, in vitro studies demonstrate that this agent induces DNA breakage in a dose-dependent manner. Artesunate has also been shown to stimulate cell differentiation, arrest the cell cycle in the G1 and G2/M phases, inhibit cell proliferation, and induce apoptosis through mitochondrial and caspase signaling pathways. Artemisinin is isolated from the plant Artemisia annua.

artichoke whole phytocomplex concentrate

A whole phytocomplex concentrate (W.P.C.) composed of a standardized extract of the Cynara scolymus (artichoke) leaf with potential antioxidant, protective and chemopreventive activities. The artichoke W.P.C. is high in flavonoids and polyphenols, such as caffeoylquinic acids, which are mainly responsible for the pharmacological effects of the extract. Artichoke W.P.C. also contains protein, fiber, vitamins, minerals, numerous enzymes, volatile oils, phytosterols and polyunsaturated fatty acids.

artificial saliva spray

A spray formulation containing a saliva substitute, composed of potassium chloride, sodium chloride, magnesium chloride, calcium chloride, dipotassium phosphate and monopotassium phosphate, that has potential anti-xerostomia activity. Upon direct oral application of the artificial saliva spray, a protective film of moisture is deposited over the mucous membranes of the mouth, which relieves dryness of the mucous membranes and increases salivary flow. In addition, artificial saliva may help prevent chemotherapy- or radiotherapy-induced oral mucositis.

arugula seed powder

A dietary supplement containing an extract powder derived from the seeds of the cruciferous vegetable arugula (Eruca sativa), with potential chemopreventive and antioxidant activities. Arugula seed powder contains numerous vitamins and minerals, and is rich in phytonutrients, such as sulforaphane and indole-3-carbinol. Although the exact mechanism of action through which arugula seed powder may exert its anti-tumor effect has yet to be fully elucidated, the effects of this powder on cancer cells may be attributable to the antioxidant and pro-apoptotic activities of the phytonutrients.

aryl hydrocarbon receptor antagonist BAY2416964

An orally available formulation containing a small molecule antagonist of the aryl hydrocarbon receptor (AhR; class E basic helix-loop-helix protein 76; bHLHe76) with potential immunomodulating and antineoplastic activities. Upon oral administration, AhR antagonist BAY2416964 specifically binds to AhR, inhibits AhR activation, and prevents AhR-mediated signaling. Abrogation of AhR activation prevents the activation of immune-tolerant dendritic cells (DCs) and regulatory T cells (Tregs) in the tumor microenvironment (TME). This may restore the immune response against tumor cells. AhR, a member of the basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) family of transcription factors, has important roles in regulating immunity and cellular differentiation. AhR can exhibit both pro-oncogenic and tumor suppressor-like functions depending on the tumor type; therefore, its expression may serve as a negative or positive prognostic factor.

aryl hydrocarbon receptor inhibitor IK-175

An orally bioavailable selective inhibitor of the aryl hydrocarbon receptor (AhR; class E basic helix-loop-helix protein 76; bHLHe76), with potential immunomodulating and antineoplastic activities. Upon oral administration, AhR inhibitor IK-175 specifically targets and binds to AhR, inhibits AhR activation, prevents AhR-mediated signaling, and AhR-dependent tumor cell proliferation. Abrogation of AhR activation prevents the activation of immune-tolerant dendritic cells (DCs), regulatory T cells (Tregs) and decreases suppressive cytokines in the tumor microenvironment (TME). It stimulates cytotoxic T-cell activation and expansion. This may restore the immune response against tumor cells. AhR, a member of the basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) family of transcription factors, plays key roles in regulating immunity and cellular differentiation. It mediates the expression of multiple immune related and tumor cell signal transduction and proliferation genes.

Arzerra

(Other name for: ofatumumab)

arzoxifene hydrochloride

The hydrochloride salt of arzoxifene, a synthetic aromatic derivative with anti-estrogenic properties. Arzoxifene binds to estrogen receptors as a mixed estrogen agonist/antagonist. In comparison to other selective estrogen receptor modulators (SERMs), arzoxifene exhibits greater bioavailability and higher anti-estrogenic potency in the breast than raloxifene; it exhibits reduced estrogenicity in the uterus compared with either tamoxifen or raloxifene. This agent may have beneficial effects on bone and the cardiovascular system.

AS03-adjuvanted H1N1 pandemic influenza vaccine

A split-virus, inactivated influenza A (H1N1) vaccine containing H1N1 immunizing antigen combined with the adjuvant AS03, with potential immunostimulating activity. Upon intramuscular vaccination, AS03-adjuvanted H1N1 influenza vaccine may elicit an immune response against the H1N1 virus and the production of anti-H1N1 antibodies. AS03 is a stabilized oil-in-water emulsion adjuvant containing DL-alpha-tocopherol, squalene and polysorbate 80 that non-specifically stimulates cell-mediated immune antigen responses.

Asacol

(Other name for: mesalamine)

asaley

An L-leucine derivative of melphalan with antineoplastic activity. Asaley alkylates and crosslinks DNA, resulting in disruption of DNA synthesis.

asaretoclax

An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, asaretoclax targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

asciminib hydrochloride

The hydrochloride salt form of asciminib, an orally bioavailable, allosteric Bcr-Abl1 tyrosine kinase inhibitor, with antineoplastic activity. Upon administration, asciminib targets and binds to the myristoyl pocket of the Bcr-Abl1 fusion protein at a location that is distinct from the ATP-binding domain, thereby inhibiting the activity of both wild-type Bcr-Abl and certain mutation forms, including the T315I mutation. This binding results in the inhibition of Bcr-Abl1-mediated proliferation and enhanced apoptosis of Philadelphia chromosome-positive (Ph+) hematological malignancies. The Bcr-Abl1 fusion protein tyrosine kinase is an abnormal enzyme produced by leukemia cells that contain the Philadelphia chromosome.

Asclera

(Other name for: polidocanol)

ascorbic acid

A natural water-soluble vitamin (vitamin C). Ascorbic acid is a potent reducing and antioxidant agent that functions in fighting bacterial infections, in detoxifying reactions, and in the formation of collagen in fibrous tissue, teeth, bones, connective tissue, skin, and capillaries. Found in citrus and other fruits, and in vegetables, vitamin C cannot be produced or stored by humans and must be obtained in the diet.

ascrinvacumab

A human immunoglobulin G2 (IgG2) monoclonal antibody against activin receptor-like kinase-1 (ALK-1; ALK1), with potential anti-angiogenic and antineoplastic activities. Upon administration, ascrinvacumab targets and binds to ALK-1, and prevents ALK-1 activation by its ligands bone morphogenetic protein 9 (BMP) 9 and BMP10. This prevents ALK-1-mediated endothelial cell signaling and the activation of transforming growth factor-beta (TGF-beta)/TGF-beta receptor I (ALK-5) signaling. This inhibits tumor blood vessel growth, reduces blood flow and angiogenesis and leads to an inhibition of tumor cell proliferation and modulation of the tumor microenvironment (TME). ALK-1, a member of the transforming growth factor beta (TGF-b) type I receptor family, is overexpressed on endothelial cells in a variety of tumor cell types and increases endothelial cell proliferation and migration.

ashwagandha root powder extract

A dietary supplement containing an extract powder derived from the root of the ashwagandha shrub with potential antineoplastic, antioxidant, immunostimulating and anti-angiogenic activities. Ashwagandha root powder extract contains numerous alkaloids, including withanine as the primary alkaloid, and steroidal lactone withanolides. The withanolides in this agent may suppress nuclear factor-kappaB activation and nuclear factor-kappaB-regulated gene expression, potentiating apoptosis and inhibiting tumor cell invasion. Cultivated in India and North America, ashwagandha (Withania somnifera Dunal or Indian ginseng) belongs to the Solanaceae (nightshade) family.

Asian ginseng

The aromatic root of perennial herbs of Panax ginseng. Ginseng, used in traditional Chinese medicine and available as a nutritional supplement, is classified as an adaptogenic herb with multiple effects, many of them are regulatory in nature. It contains a complex mixture of saponins, ginsenosides and panaxosides. Although the mechanism of action is unclear, ginseng is reported to enhance the immune system and reduce fatigue.

AsiDNA

(Other name for: DNA repair inhibiting oligonucleotide)

ASK1 inhibitor GS-4997

An orally bioavailable inhibitor of apoptosis signal-regulating kinase 1 (ASK1), with potential anti-inflammatory, antineoplastic and anti-fibrotic activities. Upon oral administration, ASK1 inhibitor GS-4997 targets and binds to the catalytic kinase domain of ASK1 in an ATP-competitive manner, thereby preventing its phosphorylation and activation. This prevents the phosphorylation of downstream kinases, such as c-Jun N-terminal kinases (JNKs) and p38 mitogen-activated protein kinase (p38 MAPK). By preventing the activation of ASK1-dependent signal transduction pathways, GS-4997 prevents the production of inflammatory cytokines, down-regulates the expression of genes involved in fibrosis, suppresses excessive apoptosis and inhibits cellular proliferation. ASK1, also called mitogen-activated protein kinase kinase kinase 5 (MAP3K5), is activated in response to oxidative and endoplasmic reticulum (ER) stress, calcium influx and infection. It plays a key role in the development of certain cardiovascular and neurodegenerative diseases, diabetes, as well as certain types of cancer.

ASO-STAT6-loaded PTGFRN-expressing exosomes CDK-004

A preparation of engineered cell-derived exosomes loaded with an antisense oligonucleotide (ASO) targeting the transcription factor signal transducer and activator of transcription (STAT) 6 (STAT6) on its surface and expressing high levels of the exosome surface glycoprotein prostaglandin F2 receptor negative regulator (PTGFRN; CD315), with potential immunoactivating and antineoplastic activities. Upon intravenous administration, ASO-STAT6-loaded PTGFRN-expressing exosomes CDK004 preferentially targets and binds to antigen-presenting cells (APCs), specifically M2 polarized tumor-associated macrophages (TAMs) in the tumor microenvironment (TME). The selective delivery of ASO STAT6 to the immunosuppressive TAMs with a M2 phenotype allows for selective reduction of STAT6 mRNA expression in these cells. By preventing the STAT6 expression in TAMs, the expression of STAT6 target genes, including the transcription of M2 signature genes, is halted. This increases the expression of M1 genes and leads to the reprogramming of TAMs toward a pro-inflammatory M1 phenotype in the TME, and leads to a cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. This may reduce tumor cell proliferation. STAT6 is a key regulator of the macrophage M2 transcriptional program and represses the activation of the M1 phenotype.

ASONEP

(Other name for: sonepcizumab)

Asorbicap

(Other name for: ascorbic acid)

ASP4132

A molecule with potential antineoplastic activity. Upon oral administration, ASP4132 affects oxidative phosphorylation in mitochondria of metabolically-active tumor cells, which reduces both energy production and tumor cell proliferation. Mitochondrial oxidative phosphorylation is hyperactivated in tumor cells and plays a key role in the promotion of tumor cell proliferation.

ASP9853

An orally bioavailable small molecule, with potential antineoplastic activity.

aspacytarabine

A small molecule pro-drug consisting of cytarabine, an antimetabolite analog of cytidine with a modified arabinose sugar moiety, covalently bonded to asparagine, with potential antineoplastic activity. Upon intravenous administration, aspacytarabine targets cancer cells, which often lack asparagine synthetase and are dependent on an external source of amino acids due to their high metabolic rate. Once the prodrug is inside target cells, the cytarabine component is cleaved and competes with cytidine for incorporation into DNA. The arabinose sugar moiety of cytarabine sterically hinders the rotation of the molecule within DNA, resulting in cell cycle arrest, specifically during the S phase of replication. Cytarabine also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Because BST-236 specifically targets cancer cells, it may spare normal tissues from cytarabine-related toxicities.

asparaginase

An enzyme isolated from the bacterium Escherichia coli or the bacterium Erwinia carotovora with antileukemic activity. Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia in leukemic cells, resulting in the depletion of asparagine, inhibition of protein synthesis, cell cycle arrest in the G1 phase, and apoptosis in susceptible leukemic cell populations. Asparagine is critical to protein synthesis in leukemic cells; some leukemic cells cannot synthesize this amino acid de novo due to the absent or deficient expression of the enzyme asparagine synthase. The E. carotovora-derived form of asparaginase is typically reserved for cases of asparaginase hypersensitivity.

asparaginase erwinia chrysanthemi (recombinant)-rywn

A recombinant form of asparaginase (Erwinia asparaginase; crisantaspase) derived from the bacterium Erwinia chrysanthemi, genetically engineered to be produced in Pseudomonas fluorescens, with potential antineoplastic activity. Upon administration of recombinant asparaginase Erwinia chrysanthemi-rywn, the recombinant asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia. This depletes cancer cells of asparagine, which blocks protein synthesis and tumor cell proliferation. Asparagine is critical to protein synthesis in cancer cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. It can be used as an alternative in patients who are hypersensitive to Escherichia (E.) coli-derived asparaginase products.

asparaginase Erwinia chrysanthemi-rywn

A recombinant form of asparaginase derived from the bacterium Erwinia chrysanthemi, genetically engineered to be produced in Pseudomonas fluorescens, with potential antineoplastic activity. Upon administration, asparaginase Erwinia chrysanthemi-rywn hydrolyzes L-asparagine to L-aspartic acid and ammonia. This depletes cancer cells of asparagine, which blocks protein synthesis and tumor cell proliferation. Asparagine is critical to protein synthesis in cancer cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Asparaginase Erwinia chrysanthemi can be used as an alternative in patients who are hypersensitive to Escherichia (E.) coli-derived asparaginase products.

Asparlas

(Other name for: calaspargase pegol-mknl)

Aspergum

(Other name for: aspirin)

aspirin

An orally administered non-steroidal antiinflammatory agent. Acetylsalicylic acid binds to and acetylates serine residues in cyclooxygenases, resulting in decreased synthesis of prostaglandin, platelet aggregation, and inflammation. This agent exhibits analgesic, antipyretic, and anticoagulant properties.

Aspirin/Simvastatin/Atenolol/Ramipril/Thiazide Capsule

An orally bioavailable combination pill containing aspirin, simvastatin, atenolol, ramipril and thiazide with preventive activity against cardiovascular disease (CVD). Aspirin is a cyclooxygenase inhibitor with antiplatelet, analgesic, antipyretic and anti-inflammatory activities; simvastatin is a statin with a cholesterol lowering effect; and the beta-blocker atenolol as well as the ACE inhibitor ramipril and the thiazide diuretic all have blood pressure lowering activity. Upon oral administration of aspirin/simvastatin/atenolol/ramipril/thiazide capsule, the combined effects of the active ingredients in this formulation lower the risk of CVD.

astatine At 211 anti-CD38 monoclonal antibody OKT10-B10

A radioimmunoconjugate composed of the anti-CD38 monoclonal antibody (MoAb) OKT10-B10 labeled with the alpha-emitting radionuclide astatine (At) 211 (211At), with potential antineoplastic activity. Upon administration of astatine At 211 anti-CD38 MoAb OKT10-B10, the MoAb moiety targets and binds to CD38-expressing tumor cells, thereby delivering a cytotoxic dose of alpha radiation directly to the CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein and tumor-associated antigen (TAA), is present on various immune cells and in hematologic malignancies; its expression has been correlated with poor prognosis.

astatine At 211 anti-CD45 monoclonal antibody BC8-B10

A radioimmunoconjugate containing the murine IgG1 anti-CD45 monoclonal antibody (MAb) BC8 where the lysine side groups have been conjugated with decaborate (closo-decaborate; B10) and labeled with astatine (At) 211, with potential immunotherapeutic activity. Astatine At 211 anti-CD45 monoclonal antibody BC8-B10 binds to CD45 antigen, a receptor protein-tyrosine phosphatase expressed on the surface of both normal and malignant hematopoietic cells. After binding and internalization by CD45-expressing tumor cells, this agent may deliver a cytotoxic dose of alpha radiation. Additionally, the radiolabel can be leveraged to assay the biodistribution and/or pharmacokinetics (absorption, distribution, metabolism and excretion) for this agent. The use of B10 rather than other labeling methods increases the therapeutic efficacy while decreasing the toxicity of the radioconjugate.

astatine At 211 F(ab')2 MX35

A radioimmunoconjugate composed of the F(ab')2 fragment of monoclonal antibody MX35 targeting the sodium-dependent phosphate transport protein 2b (NaPi2b; SLC34A2) labeled with the alpha-emitting radionuclide astatine (At) 211 (211At), with potential antineoplastic activity. Upon administration of astatine At 211 F(ab')2 MX35, the F(ab')2 MX35 moiety targets and binds to NaPi2b-expressing tumor cells, thereby delivering a cytotoxic dose of alpha radiation directly to the NaPi2b-expressing tumor cells. NaPi2b, a multi-transmembrane, sodium-dependent phosphate transporter, is highly expressed in certain types of tumor cells.

astaxanthin

A natural and synthetic xanthophyll and nonprovitamin A carotenoid, with potential antioxidant, anti-inflammatory and antineoplastic activities. Upon administration, astaxanthin may act as an antioxidant and reduce oxidative stress, thereby preventing protein and lipid oxidation and DNA damage. By decreasing the production of reactive oxygen species (ROS) and free radicals, it may also prevent ROS-induced activation of nuclear factor-kappa B (NF-kB) transcription factor and the production of inflammatory cytokines such as interleukin-1beta (IL-1b), IL-6 and tumor necrosis factor-alpha (TNF-a). In addition, astaxanthin may inhibit cyclooxygenase-1 (COX-1) and nitric oxide (NO) activities, thereby reducing inflammation. Oxidative stress and inflammation play key roles in the pathogenesis of many diseases, including cardiovascular, neurological, autoimmune and neoplastic diseases.

Astragalus membranaceus/Angelica gigas/Trichosanthes kirilowii Maximowicz mixed herbal extract SH003

A traditional Chinese medicine (TCM)-based herbal extract composed of Astragalus membranaceus (Am), Angelica gigas (Ag) and Trichosanthes kirilowii Maximowicz (Tk), with potential anti-angiogenic and antineoplastic activities. Upon administration, the active ingredients in Am/Ag/Tk mixed herbal extract SH003 work synergistically to exert a number of activities through various mechanisms of action (MOA); although, not all of the MOAs are fully elucidated. SH003 blocks the binding of vascular endothelial growth factor (VEGF) to its receptor VEGF receptor 2 (VEGFR2; KDR), thereby inhibiting VEGF/VEGFR2-mediated signaling and VEGF-induced tumor endothelial cell migration, invasion and tube formation. This inhibits tumor angiogenesis. In addition, SH003 inhibits signal transducer and activator of transcription 3 (STAT3) activation and STAT3-mediated signaling, decreases the production of the pro-inflammatory cytokine interleukin-6 (IL-6) and the expression of STAT3 target genes. This induces apoptosis in, and reduces proliferation and metastasis of, cancer cells in which STAT3 signaling is overactivated. STAT3 activation contributes to inflammation in the cancer environment and tumor cell proliferation.

Astragalus-based formulation Qing Shu Yi Qi Tang

An herbal remedy containing Astragalus membranaceus, Panax ginseng, Atractylodes chinensis Koidz, Cimicifuga foetida, A. macrocephala Koidz, Alisma orientale Juzep, and Citrus reticulata Blanco, with potential immunomodulating, anti-oxidant and anticachexia activities. Upon oral consumption, the ingredients in this herbal supplement may modulate the activity of the immune system through a decrease in both the expression of nuclear factor-kappa B (NF-kappa B) and he production of pro-inflammatory cytokines such as interleukin-1beta (Il-1b), IL-6, and tumor necrosis factor-alpha (TNF-alpha). Increased levels of pro-inflammatory cytokines are correlated with decreased appetite and weight loss; thus, this herbal remedy may improve immune function, appetite and weight gain, which could prevent cachexia.

astrovirus-derived peptide RLS-0071

A 15 amino acid-long peptide derived from the capsid protein of Astrovirus and a small 24-mer polyethylene glycol (PEG) tail on its C-terminus, with potential immunomodulating, anti-inflammatory and complement cascade inhibiting activities. Upon administration, Astrovirus-derived peptide RLS-0071 targets and binds to the hydrophobic pocket of the hinge region of C1q, which is part of the initiating component C1 of the classical complement pathway, thereby blocking and displacing the serine protease enzymatic core complex and preventing C1 cleavage. This inhibits the activation of C1 and the classical complement pathway. This reduces the infiltration of immune cells, thereby reducing complement-mediated inflammation and decreasing complement-mediated hemolysis. In addition, RLS-0071 also binds to and inhibits the initiating component of the lectin complement pathway mannose-binding lectin (MBL). In addition, RLS-0071 inhibits the activity of myeloperoxidase (MPO), thereby preventing the generation of hypochlorous acid by MPO. This modulates neutrophil activation and prevents neutrophil extracellular trap (NET) formation, and the induction of NETosis. This prevents neutrophil-associated and NETosis-induced host tissue damage in many inflammatory processes.

Astugenal

(Other name for: antineoplaston AS2-1)

astuprotimut-R

A cancer vaccine consisting of a recombinant form of human melanoma antigen A3 (MAGE-A3) combined with a proprietary adjuvant with potential immunostimulatory and antineoplastic activities. Upon administration, astuprotimut-R may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the MAGE-A3 antigen, resulting in tumor cell death. MAGE-A3, a tumor-associated antigen (TAA) originally discovered in melanoma cells, is expressed by various tumor types. The proprietary immunostimulating adjuvant in this agent is composed of a specific combination of immunostimulating compounds selected to increase the anti-tumor immune response to MAGE-A3.

asulacrine isethionate

The isethionate salt of an amsacrine analogue with antineoplastic properties. Asulacrine inhibits the enzyme topoisomerase ll, thereby blocking DNA replication and RNA and protein synthesis.

asunaprevir

An orally bioavailable inhibitor of the nonstructural protein 3 (NS3), with potential activity against hepatitis C virus (HCV). Upon administration, asunaprevir binds to the active center of the HCV NS3 and prevents NS3 protease-mediated polyprotein maturation. This disrupts the processing of viral proteins required for HCV replication. NS3, a serine protease, is essential for the proteolytic cleavages within the HCV polyprotein and plays a key role during HCV viral RNA replication. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family.

asunercept

A human, soluble fusion protein consisting of the extracellular domain of the CD95 receptor fused to the Fc-domain of the human IgG antibody, with potential antineoplastic activity. Upon administration, asunercept binds to the CD95 ligand (CD95L) and blocks the binding of CD95L to the CD95 receptor. In tumor cells, blockage of CD95L-mediated signaling pathways may prevent cell migration and invasive cell growth; in healthy cells, blockage of CD95L-mediated signaling pathways may prevent apoptosis and may protect cell damage. Activation of the CD95 receptor plays an important role in the initiation of apoptosis in healthy cells or the invasive growth of cancer cells.

At 211 monoclonal antibody 81C6

A radioimmunoconjugate of a human-murine chimeric IgG2 monoclonal antibody (MoAb) 81C6 labeled with an alpha-emitting radionuclide Astatine 211 (At-211), with imaging and radioimmunotherapeutic properties. MoAb 81C6 recognizes the extracellular matrix antigen tenascin (hexabrachion), which is up-regulated in gliomas and other cancers. Using MoAb 81C6 as a carrier for At-211 results in the targeted imaging and/or destruction of cells expressing tenascin.

Atacand

(Other name for: Candesartan Cilexetil)

atamestane

A synthetic steroidal substance with antineoplastic activity. Atamestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens.

atamparib

An orally available small molecule inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) 7, with potential immunomodulating and antineoplastic activities. Upon oral administration,atamparib selectively binds to PARP7 and restores interferon (type 1) signaling. This may lead to the induction of both innate and adaptive immune responses, and the inhibition of tumor growth and proliferation. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA.

atazanavir/ritonavir

A fixed combination of atazanavir, a human immunodeficiency virus type 1 (HIV-1) protease inhibitor, and ritonavir, a cytochrome P450 3A4 (CYP3A4) inhibitor, that may be used to treat HIV-1 infection. Upon oral administration of atazanavir/ritonavir, atazanavir selectively binds to the active site of HIV-1 protease and inhibits the proteolytic cleavage of viral Gag and Gag-Pol polyproteins in HIV-infected cells. This inhibition leads to the production of immature, non-infectious viral proteins that are unable to form mature virions. Ritonavir inhibits CYP3A4, thereby limiting the metabolism of atazanavir, which is a CYP3A4 substrate, and increasing its systemic exposure. This leads to an increased concentration and half-life of atazanavir as compared to the administration of atazanavir without ritonavir.

Atengenal

(Other name for: antineoplaston A10)

atenolol

A synthetic isopropylamino-propanol derivative used as an antihypertensive, hypotensive and antiarrhythmic Atenolol acts as a peripheral, cardioselective beta blocker specific for beta-1 adrenergic receptors, without intrinsic sympathomimetic effects. It reduces exercise heart rates and delays atrioventricular conduction, with overall oxygen requirements decreasing.

atezolizumab

A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).

atezolizumab and hyaluronidase-tqjs

A co-formulation composed of atezolizumab, a humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), and a recombinant form of human hyaluronidase (rHuPH20), with potential immune checkpoint inhibitory and antineoplastic activities. Upon subcutaneous administration of atezolizumab and hyaluronidase, atezolizumab targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC). Hyaluronidase hydrolyzes and degrades the glycosaminoglycan hyaluronic acid (HA), thereby decreasing interstitial viscosity and enhancing penetration of atezolizumab through the interstitial space. This facilitates the delivery of atezolizumab to PD-L1-expressing tumor cells.

ATGAM

(Other name for: anti-thymocyte globulin)

Atgam

(Other name for: horse anti-thymocyte globulin)

atibuclimab

A recombinant chimeric monoclonal antibody against human CD14, with potential anti-inflammatory and immunomodulating activities. Upon administration, atibuclimab binds to and neutralizes CD14, and prevents the interactions of CD14 with pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) resulting from bacterial and viral infection. This prevents membrane and soluble CD14-mediated signaling and inflammatory cascade, and prevents cytokine release, granulocyte activation, and the resulting tissue and organ injury. CD14, a protein involved in the innate recognition of many pathogens including bacteria and viruses, is expressed on the surface of monocytes and neutrophils and present in the blood and lung fluids as a soluble isoform. This allows CD14 to amplify inflammatory responses in multiple sites in the body which help fight infections, however, it may sometimes lead to overreaction and tissue and organ injury.

atiprimod

An orally bioavailable small molecule belonging to the azaspirane class of cationic amphiphilic agents with anti-inflammatory, antineoplastic, and antiangiogenic properties. Atiprimod inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3), blocking the signalling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1, thereby inhibiting cell proliferation, inducing cell cycle arrest, and inducing apoptosis.

Ativan

(Other name for: lorazepam)

ATM inhibitor M 3541

An orally bioavailable inhibitor of ataxia telangiectasia mutated kinase (ATM), with potential chemo-/radio-sensitizing and antineoplastic activities. Upon oral administration, M 3541 targets and binds to ATM, thereby inhibiting the kinase activity of ATM and ATM-mediated signaling. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, induces tumor cell apoptosis, and leads to cell death of ATM-overexpressing tumor cells. In addition, M 3541 sensitizes tumor cells to chemo- and radiotherapy. ATM, a serine/threonine protein kinase, is upregulated in a variety of cancer cell types; it is activated in response to DNA damage and plays a key role in DNA-strand repair.

ATM kinase inhibitor AZD0156

An orally bioavailable ataxia telangiectasia mutated (ATM) kinase inhibitor, with potential chemo-/radio-sensitizing and antineoplastic activities. Upon oral administration, AZD0156 targets and binds to ATM, thereby inhibiting the kinase activity of ATM and ATM-mediated signaling. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, induces tumor cell apoptosis, and leads to cell death of ATM-overexpressing tumor cells. In addition, AZD0156 sensitizes tumor cells to chemo- and radiotherapy. ATM, a serine/threonine protein kinase, is upregulated in a variety of cancer cell types; it is activated in response to DNA damage and plays a key role in DNA-strand repair.

ATM kinase inhibitor AZD1390

An orally bioavailable inhibitor of ataxia telangiectasia mutated (ATM) kinase, with potential antineoplastic activity. Upon oral administration, AZD1390 targets and binds to ATM, thereby inhibiting the kinase activity of ATM and ATM-mediated signaling. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, induces tumor cell apoptosis, and leads to cell death in ATM-overexpressing tumor cells. AZD1390 hypersensitizes tumors to chemo/radiotherapy. In addition, AZD1390 is able to cross the blood-brain barrier (BBB). ATM, a serine/threonine protein kinase belonging to the phosphatidylinositol 3-kinase-related kinase (PIKK) family of protein kinases, is upregulated in a variety of cancer cell types. It is activated in response to DNA double-strand breaks (DSB) and plays a key role in DNA repair.

ATM kinase inhibitor WSD-0628

An orally bioavailable, brain-penetrable inhibitor of ataxia telangiectasia mutated (ATM) kinase, with potential chemo-and radio-sensitizing and antineoplastic activities. Upon oral administration, ATM kinase inhibitor WSD-0628 selectively targets and binds to ATM, thereby inhibiting the kinase activity of ATM and ATM-mediated signaling. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, induces apoptosis in damaged tumor cells, and leads to cell death in ATM-overexpressing tumor cells. WSD-0628 hypersensitizes tumors to chemo/radiotherapy. In addition, WSD-0628 is able to cross the blood-brain barrier (BBB). ATM, a serine/threonine protein kinase belonging to the phosphatidylinositol 3-kinase-related kinase (PIKK) family of protein kinases, is upregulated in a variety of cancer cell types. It is activated in response to DNA double-strand breaks (DSB) and plays a key role in DNA repair.

ATM kinase/DNA-PK inhibitor XRD-0394

An orally bioavailable, small molecule, dual inhibitor of ataxia telangiectasia mutated kinase (ATM) and DNA-dependent protein kinase (DNA-PK), with potential radio-sensitizing and antineoplastic activities. Upon oral administration, ATM kinase/DNA-PK inhibitor XRD-0394 selectively targets, binds to and inhibits the activity of ATM and DNA-PK. This inhibits ATM-mediated signaling, which may prevent DNA damage checkpoint activation, disrupt DNA damage repair and induce tumor cell apoptosis. By disrupting DNA damage repair, this agent may sensitize tumor cells to radiotherapy and increase its anti-tumor activity. In addition, by inhibiting the activity of DNA-PK, this agent interferes with the non-homologous end joining (NHEJ) process which may prevent the repair of DNA double strand breaks (DSBs) caused by ionizing radiation. This may also increase radiotherapy cytotoxicity leading to enhanced tumor cell death. ATM, a serine/threonine protein kinase upregulated in a variety of cancer cell types, is activated in response to DNA damage and plays a key role in DNA-strand repair. DNA-PK plays a key role in the NHEJ pathway and DSB repair. The enhanced ability of tumor cells to repair DNA damage plays a major role in the resistance of tumor cells to radiotherapy.

atomoxetine hydrochloride

The hydrochloride salt of atomoxetine, a phenoxy-3-propylamine derivative and selective non-stimulant, norepinephrine reuptake inhibitor with cognitive-enhancing activity. Although its precise mechanism of action is unknown, atomoxetine appears to selectively inhibit the pre-synaptic norepinephrine transporter, resulting in inhibition of the presynaptic reabsorption of norepinephrine and prolongation of norepinephrine activity in the synaptic cleft; the effect on cognitive brain function may result in improved attention and decreased impulsivity and activity levels.

atorvastatin calcium

The calcium salt of atorvastatin, a synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent increases the number of LDL receptors on hepatic cell surfaces, enhancing the uptake and catabolism of LDL and reducing LDL production and the number of LDL particles, and lowers plasma cholesterol and lipoprotein levels. Like other statins, atorvastatin may also display direct antineoplastic activity, possibly by inhibiting farnesylation and geranylgeranylation of proteins such as small GTP-binding proteins, which may result in the arrest of cells in the G1 phase of the cell cycle. This agent may also sensitize tumor cells to cyctostatic drugs, possibly through the mTOR-dependent inhibition of Akt phosphorylation.

atovaquone

A synthetic hydroxynaphthoquinone with antiprotozoal activity. Atovoquone blocks the mitochondrial electron transport at complex III of the respiratory chain of protozoa, thereby inhibiting pyrimidine synthesis, preventing DNA synthesis and leading to protozoal death.

ATR inhibitor ATG-018

An orally bioavailable inhibitor of the DNA damage response (DDR) protein kinase ataxia telangiectasia and Rad3 related (ATR) kinase, with potential checkpoint inhibitory and antineoplastic activities. Upon oral administration, ATR inhibitor ATG-018 selectively targets and binds to ATR, and inhibits its activity and ATR-mediated signaling. This blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress.

ATR inhibitor ATRN-119

An orally bioavailable inhibitor of the DNA damage response (DDR) protein kinase ataxia telangiectasia and Rad3 related (ATR) kinase, with potential checkpoint inhibitory and antineoplastic activities. Upon oral administration, ATR inhibitor ATRN-119 selectively targets and binds to ATR, and inhibits its activity and ATR-mediated signaling. This blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress.

ATR inhibitor IMP9064

An orally bioavailable inhibitor of the DNA damage response (DDR) protein kinase ataxia telangiectasia and Rad3 related (ATR) kinase, with potential checkpoint inhibitory and antineoplastic activities. Upon oral administration, ATR inhibitor IMP9064 selectively targets and binds to ATR, and inhibits its activity and ATR-mediated signaling. This blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress. In addition, IMP9064 is selective against other as of yet undefined kinases.

ATR inhibitor TQB3015

An orally bioavailable small molecule inhibitor of the DNA damage response (DDR) protein kinase ataxia telangiectasia and Rad3 related (ATR) kinase, with potential checkpoint inhibitory and antineoplastic activities. Upon oral administration, ATR inhibitor TQB3015 selectively targets and binds to ATR, and inhibits its activity and ATR-mediated signaling. This blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress.

ATR kinase inhibitor VX-803

An orally available inhibitor of ataxia telangiectasia and Rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, ATR kinase inhibitor VX-803 selectively inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase CHK1. This prevents ATR-mediated signaling, which results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival; it is activated by DNA damage caused during DNA replication-associated stress.

ATR-101

An orally bioavailable agent that is selective towards adrenal cortex cells with potential antitumor activity. Upon administration, ATR-101 selectively kills adrenal and adrenal cancer cells, through an unknown mechanism.

Atragen

(Other name for: liposomal tretinoin)

atrasentan hydrochloride

The orally available hydrochloride salt of pyrrolidine-3-carboxylic acid with potential antineoplastic activity. As a selective antagonist of the endothelin-A (ETA) receptor, atrasentan binds selectively to the ETA receptor, which may result in inhibition of endothelin-induced angiogenesis and tumor cell proliferation.

Atripla

(Other name for: efavirenz/emtricitabine/tenofovir disoproxil fumarate)

Atromid-S

(Other name for: clofibrate)

atropine sulfate

The sulfate salt of atropine, a naturally-occurring alkaloid isolated from the plant Atropa belladonna. Atropine functions as a sympathetic, competitive antagonist of muscarinic cholinergic receptors, thereby abolishing the effects of parasympathetic stimulation. This agent may induce tachycardia, inhibit secretions, and relax smooth muscles.

attenuated chimpanzee adenovirus 5T4 vaccine

A cancer vaccine comprised of a recombinant, attenuated, replication-defective simian adenovirus vector (ChAdOx1) encoding the human 5T4 fetal oncoprotein (ChAdOx1.5T4), with potential immuno-activating and antineoplastic activities. Upon administration of the recombinant attenuated chimpanzee adenovirus 5T4 vaccine, the viral vector expresses 5T4 and stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing 5T4, which results in tumor cell lysis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.

attenuated corynebacterium parvum

A heat-inactivated preparation of Corynebacterium parvum with immunoadjuvant properties. Therapeutic Corynebacterium parvum may stimulate host antitumor immune responses when added to cancer vaccines.

attenuated Listeria monocytogenes ANZ-100

A live-attenuated strain of the Gram-positive bacterium Listeria monocytogenes (Lm) with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, attenuated Listeria monocytogenes ANZ-100 may accumulate in and infect liver cells where it may activate a potent innate immune response and an adaptive immune response involving the by recruitment and activation of T lymphocytes. This agent may potentiate the immune response to vaccines against various liver neoplasms.

attenuated live Listeria monocytogenes encoding KRAS G12D

An off-the-shelf, plasmid DNA-based cancer vaccine composed of a live-attenuated strain of the Gram-positive bacterium Listeria monocytogenes (Lm) carrying a plasmid vector encoding multiple, not yet disclosed, tumor associated antigens (TAAs) and sequence peptides associated with commonly occurring hotspot mutations, including the aspartic acid substitution for glycine at position 12 (G12D) in KRAS, with potential immunostimulatory and antineoplastic activities. Upon administration, ADXS-503 is taken up by antigen presenting cells (APCs) and the TAAs are processed and presented to immune cells by both major histocompatibility complex (MHC) I and II molecules. This leads to an increase in antigen-specific CD8-positive T-cells and gamma/delta T-cells within the tumor microenvironment (TME) and an inhibition of immunosuppressive tumor-infiltrating T-regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs). This may lead to tumor cell death in cells expressing TAAs that are shared across multiple tumor types. The KRAS G12D mutation is thought to drive tumorigenesis and progression in some cancers.

attenuated measles virus encoding SCD transgene TMV-018

A recombinant, attenuated oncolytic measles virus (MV) encoding the prodrug converting enzyme super cytosine deaminase (SCD), that can potentially be used as an antineoplastic adjuvant and with potential antineoplastic activity. Upon intra-tumoral injection, TMV-018 preferentially enters and transfects tumor cells, and expresses SCD, an enzyme that catalyzes the intracellular conversion of the prodrug flucytosine (5-fluorocytosine; 5-FC) into the antineoplastic agent 5-fluorouracil (5-FU). After administration of 5-FC, the tumor can be eradicated upon activation of 5-FU by SCD. In addition, the oncolytic MV may infect and lyse tumor cells. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells. This may further eradicate tumor cells.

attenuated S. typhimurium carrying IL-15/IL-15Ra and engineered STING-encoding DNA plasmid ACTM-838

A genetically modified attenuated Salmonella typhimurium strain carrying a DNA plasmid that encodes payloads consisting of IL-15plex, a complex of the immunostimulating cytokine interleukin (IL-15) and its receptor alpha unit (IL-15Ra), and an engineered, constitutively active stimulator of interferon genes (STING; transmembrane protein 173; TMEM173), with potential immunostimulatory and antineoplastic activities. Upon administration, attenuated S. typhimurium carrying IL-15/IL-15Ra and eSTING-encoding DNA plasmid ACTM-838 accumulates and replicates in the adenosine-rich tumor microenvironment (TME), and is internalized by the phagocytic antigen presenting cells (APCs). This activates innate immunity. Also, ACTM-838 expresses IL-15/IL-15Ra and eSTING, thereby delivering these payload directly into the TME. eSTING activates the STING pathway, which leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. IL-15 stimulates the proliferation of natural killer (NK) cells, CTLs and memory T cells, which further induces an anti-tumor immune response. IL-15Ra complexed with IL-15 increases IL-15 signaling and IL-15 half-life upon expression.

atuveciclib

An inhibitor of positive transcription elongation factor b (P-TEFb), which is composed of cyclin-dependent kinase 9 (CDK9) and cyclin-T (CycT), with potential antineoplastic activity. Upon administration, atuveciclib binds to and inhibits the activity of P-TEFb, thereby preventing the phosphorylation of its downstream target, the carboxyl terminal domain (CTD) of RNA polymerase II (RNA Pol II), and inhibiting the activation of transcriptional elongation by RNA Pol II. This prevents the transcription of tumor promoting genes, induces tumor cell apoptosis, and inhibits tumor cell proliferation. P-TEFb plays an important role in the regulation of gene transcription; over-activation in cancer cells leads to both the transcription of key tumor-promoting genes and cancer cell proliferation.

Aucatzyl

(Other name for: obecabtagene autoleucel)

audencel

A therapeutic interleukin-12 (IL-12)-expressing dendritic cell (DC)-based vaccine composed of autologous monocyte-derived DCs loaded with autologous tumor cell lysate and exposed to the microbial cell wall component lipopolysaccharide (LPS), with potential immunomodulating and antineoplastic activities. The monocyte-derived immature DCs are loaded with autologous tumor cell lysates and are subsequently exposed to LPS and interferon-gamma (IFN-gamma). Upon administration of audencel, the mature DCs migrate into the lymph nodes, express the immune stimulatory cytokine interleukin-12 (IL-12) and activate the immune system by promoting the activation of natural killer (NK) cells and induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. Exposure to LPS and IFN-gamma allows the maturation of DCs and optimizes the presentation of tumor-associated antigens (TAAs) by DCs to T lymphocytes.

Augmentin

(Other name for: amoxicillin-clavulanate potassium)

Augtyro

(Other name for: repotrectinib)

aumolertinib

An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, aumolertinib binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, inhibits the tyrosine kinase activity of EGFR T790M, prevents EGFR T790M-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

Aurimmune

(Other name for: colloidal gold-bound tumor necrosis factor)

Aurixim

(Other name for: rituximab conjugate CON-4619)

Aurolate

(Other name for: gold sodium thiomalate)

Aurora A kinase inhibitor JAB-2485

An orally bioavailable small molecule inhibitor of the serine/threonine protein kinase Aurora A, with potential antimitotic and antineoplastic activities. Upon oral administration, Aurora A kinase inhibitor JAB-2485 binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, inhibition of cell division and the induction of apoptosis in cells overexpressing Aurora A kinase. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis; it plays an essential role in the regulation of spindle assembly. Aurora kinase A is overexpressed in a wide variety of cancers.

Aurora A kinase inhibitor LY3295668

An orally bioavailable inhibitor of the serine/threonine protein kinase aurora A, with potential antimitotic and antineoplastic activities. Upon administration, aurora A kinase inhibitor LY3295668 targets, binds to and inhibits the activity of aurora A kinase. This may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, inhibition of cell division and the induction of apoptosis in cells overexpressing aurora A kinase. Aurora A kinase, overexpressed in a wide variety of cancers, plays an essential role in the regulation of spindle assembly and mitosis.

Aurora A kinase inhibitor MK5108

An orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A, with potential antimitotic and antineoplastic activity. Aurora A kinase inhibitor MK5108 binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and eventually inhibition of cell division, proliferation and an induction of apoptosis in cells overexpressing Aurora A kinase. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aurora kinases are overexpressed in a wide variety of cancers.

aurora A kinase inhibitor VIC-1911

An orally bioavailable inhibitor of the serine/threonine protein kinase aurora A, with potential antimitotic and antineoplastic activities. Upon intravenous administration, aurora A kinase inhibitor VIC-1911 binds to and inhibits aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, inhibition of cell division and the induction of apoptosis in cells overexpressing aurora A kinase. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis; it plays an essential role in the regulation of spindle assembly. Aurora kinase A is overexpressed in a wide variety of cancers.

Aurora A kinase/tyrosine kinase inhibitor ENMD-2076

An orally bioavailable synthetic small molecule with potential antiangiogenic and antineoplastic activities. Aurora A kinase/tyrosine kinase inhibitor ENMD-2076 selectively binds to and inhibits non-specified tyrosine kinases and Aurora kinases (AKs). The inhibition of AKs may result in the inhibition of cell division and proliferation and may induce apoptosis in tumor cells that overexpress AKs; antiangiogenic activity is related to the inhibition of angiogenic tyrosine kinases. AKs are serine-threonine kinases that play an essential role in mitotic checkpoint control during mitosis and are important regulators of cell division and proliferation.

Aurora B Serine/Threonine Kinase Inhibitor TAK-901

A small-molecule inhibitor of the serine-threonine kinase Aurora B with potential antineoplastic activity. Aurora B kinase inhibitor TAK-901 binds to and inhibits the activity of Aurora B, which may result in a decrease in the proliferation of tumor cells that overexpress Aurora B. Aurora B is a positive regulator of mitosis that functions in the attachment of the mitotic spindle to the centromere; the segregation of sister chromatids to each daughter cell; and the separation of daughter cells during cytokinesis. This serine/threonine kinase may be amplified and overexpressed by a variety of cancer cell types.

Aurora B/C kinase inhibitor GSK1070916A

An ATP-competitive inhibitor of the serine/threonine kinases Aurora B and C with potential antineoplastic activity. Aurora B/C kinase inhibitor GSK1070916A binds to and inhibits the activity of Aurora kinases B and C, which may result in inhibition of cellular division and a decrease in the proliferation of tumor cells that overexpress the Aurora kinases B and C. Aurora kinases play essential roles in mitotic checkpoint control during mitosis, and are overexpressed by a wide variety of cancer cell types.

Aurora kinase inhibitor AMG 900

A small-molecule inhibitor of Aurora kinases A, B and C with potential antineoplastic activity. Aurora kinase inhibitor AMG 900 selectively binds to and inhibits the activities of Aurora kinases A, B and C, which may result in inhibition of cellular division and proliferation in tumor cells that overexpress these kinases. Aurora kinases are serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis and are overexpressed by a wide variety of cancer cell types.

Aurora kinase inhibitor BI 811283

A small molecule inhibitor of the serine/threonine protein kinase Aurora kinase with potential antineoplastic activity. Aurora kinase inhibitor BI 811283 binds to and inhibits Aurora kinases, resulting in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation.

Aurora kinase inhibitor MLN8054

An orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A kinase with potential antineoplastic activity. Auora kinase inhibitor MLN8054 binds to and inhibits Aurora kinase A, resulting in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation. Aurora A localizes in mitosis to the spindle poles and to spindle microtubules and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers, including colon and breast cancers.

aurora kinase inhibitor PF-03814735

An aurora kinase inhibitor with potential antineoplastic activity. PF-03814735 binds to and inhibits aurora kinases, serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis. Inhibition of aurora kinases may result in an inhibition of cellular division and proliferation in tumor cells that overexpress aurora kinases.

aurora kinase inhibitor SNS-314

A synthetic small molecule Aurora kinase (AK) inhibitor with potential antineoplastic activity. Aurora kinase inhibitor SNS-314 selectively binds to and inhibits AKs A and B, which may result in the inhibition of cellular division and proliferation in tumor cells that overexpress AKs. AKs are serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis.

Aurora kinase inhibitor TTP607

A small-molecule pan-Aurora kinase inhibitor with potential antineoplastic activity. Aurora kinase inhibitor TTP607 selectively binds to and inhibits Aurora kinases A, B and C, which may result in the disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cellular division and proliferation in Aurora kinase-overexpressing tumor cells. Aurora kinases A, B and C, are serine/threonine kinases that play essential roles in mitotic checkpoint control and are overexpressed by a wide variety of tumor cell types.

Aurora kinase/FLT3 inhibitor EP0042

An orally bioavailable inhibitor of both the serine/threonine protein kinase Aurora kinase and FMS-related tyrosine kinase 3 (FLT3; STK1; CD135; FLK2), with potential antineoplastic activity. Upon oral administration, Aurora kinase/FLT3 inhibitor EP0042 specifically binds to and inhibits Aurora kinase and FLT3, which interferes with the activation of Aurora kinase- and FLT3-mediated signal transduction pathways. This may result in the disruption of the assembly of the mitotic spindle apparatus, the disruption of chromosome segregation and the inhibition of cell proliferation in tumor cells that overexpress Aurora kinase and/or FLT3. Aurora kinase plays essential roles in mitotic checkpoint control during mitosis. Aurora kinase and FLT3 are overexpressed in a variety of cancers and play key roles in tumor cell proliferation.

Aurora kinase/VEGFR2 inhibitor CYC116

An orally bioavailable small molecule multi-kinase inhibitor with antineoplastic activity. Aurora kinase/VEGFR 2 inhibitor CYC116 inhibits Aurora kinases A and B and vascular endothelial growth factor receptor 2 (VEGFR2), resulting in disruption of the cell cycle, rapid cell death, and the inhibition of angiogenesis. Aurora kinases are serine/threonine protein kinases that are only expressed in actively dividing cells and are critical in division or mitosis. VEGFR2 is a receptor tyrosine kinase that appears to account for most of the mitogenic and chemotactic effects of vascular endothelial growth factor (VEGF) on adult endothelial cells.

AuroraB/VEGFr/FGFR inhibitor AL8326

An orally bioavailable inhibitor of the receptor kinases Aurora B, fibroblast growth factor receptor (FGFR), and vascular endothelial growth factor receptor (VEGFR), with potential antimitotic, antiangiogenic and antineoplastic activities. Upon oral administration, Aurora B/VEGFR/FGFR inhibitor AL8326 specifically binds to and inhibits the activity of Aurora B, FGFR and VEGFR. Inhibition of Aurora B causes disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, inhibition of cell division and the induction of apoptosis in cells overexpressing Aurora B. Inhibition of FGFR and VEGFR prevents the activation of their downstream signaling pathways and the proliferation of tumor cells overexpressing these kinases. FGFR and VEGFR are upregulated in a variety of cancer cell types and play key roles in tumor cell proliferation, angiogenesis, and metastasis. Aurora B is a positive regulator of mitosis that plays a key role in the attachment of the mitotic spindle to the centromere; the segregation of sister chromatids to each daughter cell; and the separation of daughter cells during cytokinesis. This serine/threonine kinase may be amplified and overexpressed by a variety of cancer cell types.

autogene cevumeran

An mRNA-based individualized, therapeutic cancer vaccine targeting an unspecified amount of tumor-associated antigens (TAAs) that are specifically expressed in the patient's cancer, with potential immunostimulatory and antineoplastic activities. Upon administration, autogene cevumeran is taken up and translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL)- and memory T-cell-dependent immune responses against cancer cells expressing the TAA(s).

autologous 19-28z/IL-18 CAR T lymphocytes

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) fused to the extracellular, transmembrane and intracellular signaling domains of the T-cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (19-28z), and expressing the human pro-inflammatory cytokine interleukin 18 (IL-18), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, autologous 19-28z/IL-18 CAR T lymphocytes target, bind to, and induce selective toxicity in CD19-expressing tumor cells. IL-18 promotes T-cell persistence and potentiates the immune response against tumor cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of costimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous 1928T2z CAR T cells WZTL-002

A preparation of autologous, third-generation T lymphocytes that have been transduced with a self-inactivating lentiviral vector to express a chimeric antigen receptor (CAR) containing a single-chain variable fragment (scFv) from the monoclonal antibody FMC63, which is directed against the CD19 antigen, and linked to the co-stimulatory intracellular signaling domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta; CD28z), and the Toll/interleukin-1 receptor (TIR) domain from Toll-like receptor 2 (TLR2) as an additional co-stimulatory domain, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous 1928T2z CAR T cells WZTL-002 specifically recognize and bind to CD19-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B cells. In addition to CD28 and CD3zeta, the TLR2-TIR domain provides co-stimulatory activity and may enhance the cytotoxic effect and anti-tumor activity of the CAR T-cells. The TIR domain from TLR2 mediates the intracellular signaling of TLR2; TLR2 stimulation enhances T-cell activation, proliferation and cytokine production.

autologous 4-1BB selected tumor infiltrating lymphocytes

A preparation of autologous tumor infiltrating lymphocytes (TILs) expressing the co-stimulatory signaling domain 4-1BB (CD137), with potential antineoplastic activity. TILs are isolated from a patient's tumor and those expressing 4-1BB are selected for expansion in vitro. Upon re-infusion into the patient, the 4-1BB-expressing TILs re-infiltrate the tumor to initiate tumor cell lysis. 4-1BB, a member of the tumor necrosis factor (TNF) receptor superfamily, enhances TIL survival and antitumor cytolytic activity.

autologous ACTR-CD16-CD28-expressing T lymphocytes ACTR707

A preparation of autologous T lymphocytes that have been genetically modified, using proprietary Antibody-Coupled T-cell Receptor (ACTR) technology, to express a chimeric protein containing, at least, the extracellular Fc receptor domain of CD16, normally found on certain immune cells, such as natural killer (NK) cells, coupled to the co-stimulatory signaling domain of CD28, with potential immunostimulating and antineoplastic activities. Upon reintroduction into the patient with co-administration of a cancer-specific antibody, the co-administered antibody targets and binds to the tumor-associated antigen (TAA) expressed on the tumor cell. In turn, the autologous ACTR-CD16-CD28-expressing T lymphocytes ACTR707 bind to the antibody, become activated and induce the destruction of the tumor cells by a) releasing cytotoxins that directly kill cancer cells; b) releasing cytokines that trigger an immune response and recruit other immune-mediated killer cells to kill the tumor cells; c) targeting and killing adjacent tumor cells that are not bound to the antibody; d) inducing T-cell proliferation and thereby further enhancing the T-cell mediated tumor cell attack. Compared to other T-cell products, ACTR-based products do not target a specific TAA and can potentially be used in a variety of tumors because targeting is based on the specificity of the co-administered antibody.

autologous Ad-CD154-transduced CLL B cells

An autologous tumor cell vaccine containing chronic lymphocytic leukemia (CLL) B cells transduced with an adenoviral vector carrying chimeric CD154 (ad-CD154) with potential antineoplastic activity. Administration of autologous ad-CD154 transduced CLL B cells may result in increases in the numbers of leukemia-specific CD4+ T cells and high serum-levels of IL-12 and IFN-gamma. Due to ligation of CD154 to CD40 on CLL cells, this agent may induce CLL cells to express the proapoptotic molecule Bid and death receptors CD95 (Fas) and DR5, rendering CLL B cells first resistant and then sensitive to Fas-mediated apoptosis. In addition, autologous ad-CD154 transduced CLL B cells may induce MHC class I-dependent cytotoxic T lymphocyte (CTL) responses against autologous leukemia cells. CD154 is a type II membrane glycoprotein and ligand for CD40; both molecules are important in cognate co-stimulatory cell-cell interactions.

autologous AFP-specific T cell receptor T cells C-TCR055

A preparation of human autologous T lymphocytes transduced with a lentiviral vector encoding for a T-cell receptor (TCR) recognizing the human leukocyte antigen (HLA)-A*02:01 restricted human alpha-fetoprotein (AFP) 158-166 peptide (FMNKFIYEI), with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the AFP specific TCR transduced T cells recognize and bind to AFP antigen-positive cells, which results in lysis and killing of AFP-positive cancer cells. AFP is overexpressed in a variety of cancers while its expression is restricted in normal tissues.

autologous ALPG/ALPP-targeted anti-MSLN CAR-Fas/PTPN2 shRNA-miR-expressing T lymphocytes AB-1015

A preparation of autologous T lymphocytes that have been modified to encode a genetic circuit consisting of a priming receptor that induces the expression of a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) mesothelin (MSLN) upon binding to the TAAs alkaline phosphatase (ALP) isozymes ALP germ cell type (ALPG; GCAP) or ALP placental type (ALPP; placental ALP; PLAP), and a dual microRNA-adapted short hairpin RNA (shRNA-miR) targeting Fas (FAS; CD95; APO-1; tumor necrosis factor receptor superfamily member 6; TNFRSF6) and tyrosine-protein phosphatase non-receptor type 2 (PTPN2), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous ALPG/P-targeted anti-MSLN CAR-Fas/PTPN2 shRNA-miR-expressing T lymphocytes AB-1015 target and bind to ALPG/P-expressing tumor cells and induce the expression of anti-MSLN CAR, thereby killing ALPG/P- and MSLN-expressing tumor cells. The downregulation of the expression of Fas by the shRNA-miR prevents Fas-mediated apoptosis of the AB-1015 T cells in the tumor microenvironment (TME). The downregulation of the expression of PTPN2 enhances AB-1015 T-cell expansion and anti-tumor T-cell immune responses. ALPG and ALPP, overexpressed in a variety of cancer cell types, play important roles in tumor cell proliferation and tumor growth. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous alpha-PNE switchable CAR T cells CLBR001

A preparation of autologous T lymphocytes that has been genetically engineered to express a switchable, alpha-peptide neo-epitope (PNE) chimeric antigen receptor (CAR) with a binding domain that can recognize a 14 aa peptide epitope, or PNE, of an antigen-specific adapter molecule, with potential immunomodulating and antineoplastic activities. Upon administration, autologous alpha-PNE switchable CAR T (sCART) cells CLBR001 remain inactivated. Upon administration of an antigen-specific adapter molecule, the binding domain of CLBR001 binds to the PNE of the adapter molecule, and CLBR001 is activated. This induces selective toxicity in and causes lysis of tumor cells expressing the specific antigen.

autologous alpha-PNE switchable CAR T cells CLBR001 and CD19-specific adapter molecule SWI019

A combination of CLBR001, a preparation of autologous T lymphocytes that has been genetically engineered to express a switchable, alpha-peptide neo-epitope (PNE) chimeric antigen receptor (CAR) with a binding domain that can recognize a 14 aa peptide epitope, or PNE, of an antigen-specific adapter molecule, and SWI019, a preparation of adapter molecules consisting of an antibody fragment (Fab) targeting CD19 linked to a PNE recognizable by CLBR001, with potential immunomodulating and antineoplastic activities. Upon administration of autologous alpha-PNE switchable CAR T cells CLBR001 and CD19-specific adapter molecule SWI019, the Fab moiety of SWI019 targets and binds to tumor cells expressing CD19, and the PNE of SWI019 binds to the binding domain of CLBR001, thereby activating CLBR001. This induces selective toxicity in and causes lysis of CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

autologous AML/dendritic cell fusion vaccine

A therapeutic cell-based cancer vaccine consisting of autologous dendritic cells (DCs) fused with autologous acute myeloid leukemia (AML) cells, with potential immunostimulatory and antineoplastic activities. The autologous AML/DC fusion vaccine is generated in vitro by mixing DCs and irradiated AML cells harvested from individual patients, in the presence of polyethylene glycol (PEG), to produce hybrid DC-leukemia fusion cells. Upon re-administration, the autologous AML/DC fusion vaccine may elicit a cytotoxic T-lymphocyte (CTL)-mediated antitumor immune response against a broad array of AML-associated antigens, which may lead to AML cell lysis.

autologous anti-ALK CAR T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the human receptor tyrosine kinase (RTK) anaplastic lymphoma kinase (ALK), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-ALK CAR T-cell recognize and induce selective toxicity against ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types.

autologous anti-ALPP CAR retroviral vector-transduced T cells

A preparation of autologous T lymphocytes that have been transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) targeting alkaline phosphatase, placental type (ALPP; placental alkaline phosphatase; PLAP), with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous anti-ALPP CAR retroviral vector-transduced T cells target and bind to ALPP-expressing tumor cells, thereby inducing selective toxicity in ALPP-expressing tumor cells. ALPP, mainly expressed in placenta and testis, is overexpressed on certain tumor cell types, such as on a proportion of colorectal cancers while not expressed in any other normal tissues. It plays a key role in tumor cell proliferation.

autologous anti-B7-H3 CAR retroviral vector-transduced T cells

A preparation of autologous T lymphocytes that have been transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous anti-B7-H3 CAR retroviral vector-transduced T cells target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

autologous anti-B7-H3 CAR T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous anti-B7-H3 CAR T cells target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

autologous anti-B7-H3 CAR T cells CAR.B7-H3T

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous anti-B7-H3 CAR T cells CAR.B7-H3T target and bind to B7-H3-expressing tumor cells, thereby inducing selective toxicity in B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.

autologous anti-B7-H3 CAR-iC9-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and the suicide gene inducible caspase 9 (iCasp9 or iC9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-B7-H3 CAR-iC9-expressing T lymphocytes specifically target and bind to B7-H3-expressing tumor cells, resulting in tumor cell lysis. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered CAR T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9 and results in apoptosis of the administered CAR T cells.

autologous anti-B7-H3/CD19 CAR T cells SCRI-CARB7H3(s)x19

A preparation of autologous CD4+ and CD8+ T lymphocytes lentivirally transduced to express a chimeric antigen receptor (CAR) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and the tumor-associated antigen (TAA) CD19, and containing, as of yet undisclosed co-stimulatory signaling domains, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon administration, anti-B7-H3/CD19 CAR T cells target and bind to both B7-H3 on T cells and CD19 on tumor cells. This crosslinks T cells and tumor cells, and induces selective toxicity in B7-H3/CD19-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It promotes the activation of T cells. CD19, a transmembrane phosphoglycoprotein expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous anti-BCMA CAR T cells MCARH125

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential antineoplastic activity. Upon administration, the autologous anti-BCMA CAR T cells MCARH125 recognize and induce selective toxicity against BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA CAR T cells PHE885

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential antineoplastic activity. Upon administration, the autologous anti-BCMA CAR T-cells PHE885 recognize and induce selective toxicity against BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA CAR T cells spCART-269

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17; CD269), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA CAR T cells spCART-269 recognize and induce selective toxicity against BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA CAR T cells UF-KURE-BCMA

A preparation of autologous CD4+ and CD8+ T lymphocytes that have been transduced with a lentiviral vector (LV) encoding for a chimeric antigen receptor (CAR) specific for human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA CAR T cells UF-KURE-BCMA specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

Autologous Anti-BCMA CAR T-cells IM21

A preparation of autologous T-lymphocytes that have been transduced with a lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and containing, as of yet undisclosed costimulatory signaling domains, with potential antineoplastic activity. Upon administration, the autologous anti-BCMA CAR T-cells IM21 recognize and induce selective toxicity against BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA CAR-transduced T cells KITE-585

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) derived from a human monoclonal antibody specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused, via an as of yet unknown linker, to the co-stimulatory domain of CD28, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA CAR transduced T cells KITE-585 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. The CD28 co-stimulatory domain optimizes T-cell expansion and function.

autologous anti-BCMA CD8+ CAR T cells Descartes-11

A preparation of autologous CD8-positive T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA CD8+ CAR T cells Descartes-11 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T lymphocytes

A preparation of an approximately equal ratio of autologous CD4- and CD8-positive T lymphocytes that have been ex vivo transduced with a genetically-engineered self-inactivating (SIN) lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137), the CD3-zeta (CD3z) T-cell signaling domain, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA-CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T lymphocytes specifically recognize and induce selective toxicity against BCMA-expressing tumor cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt facilitates both in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing CD4+/CD8+ T lymphocytes JCARH125

A preparation of autologous CD4- and CD8-positive T lymphocytes that have been ex vivo transduced with a genetically-engineered lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137) and the CD3-zeta (CD3z) T-cell signaling domain, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing CD4+/CD8+ T lymphocytes JCARH125 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing memory T lymphocytes bb21217

A preparation of autologous memory T lymphocytes transduced, ex vivo, with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-B-cell maturation antigen (BCMA) single chain variable fragment (scFv) fused to the signaling domain of 4-1BB (CD137) and a CD3-zeta T-cell activation domain, with potential immunostimulating and antineoplastic activities. Upon intravenous administration back into the patient, the autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing memory T lymphocytes bb21217 are directed to, and induce selective toxicity in, BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma survival. BCMA is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing T cells C-CAR088

A preparation of autologous T lymphocytes that have been transduced with a vector expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the epitome cluster E3 in the extracellular domain (ECD) of the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) that is fused to the co-stimulatory domain of 4-1BB (CD137) and the T-cell receptor signaling domain of CD3zeta (CD3z), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing T cells C-CAR088 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in the survival of B lymphocytes and plasma cells. BCMA is found on the surfaces of B cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing T cells CT053

A preparation of autologous T lymphocytes that have been transduced with a vector expressing a chimeric antigen receptor (CAR) containing a humanized single chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) that is fused to the co-stimulatory domain of 4-1BB (CD137) and the T-cell receptor signaling domain of CD3zeta (CD3z), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing T cells CT053 specifically recognize and induce selective toxicity against BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in the survival of B lymphocytes and plasma cells. BCMA is found on the surfaces of B cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-4-1BB-expressing T cells NXC-201

A preparation of autologous T lymphocytes that have been transduced with a retroviral vector encoding for a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-BCMA-CAR-4-1BB-expressing T cells NXC-201 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA, found on the surfaces of plasma cells and overexpressed on malignant plasma cells, plays a key role in plasma cell survival.

autologous anti-BCMA-CAR-expressing CD4+/CD8+ T lymphocytes FCARH143

A preparation of ex vivo expanded autologous CD8+ and CD4+ T cells that have been genetically modified to express a chimeric antigen receptor (CAR) specific for human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA-CAR-expressing CD4+/CD8+ T lymphocytes FCARH143 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-expressing stem memory T cells P-BCMA-101

A preparation consisting of autologous T cells that are enriched to be primarily stem memory T cells (Tscm) and are transfected by electroporation with a proprietary transposon-based DNA plasmid vector (PiggyBac) containing an undisclosed selection gene and encoding both an unidentified human-derived safety switch and a chimeric antigen receptor (CAR) based on a proprietary non-immunoglobulin scaffold molecule Centyrin (CARTyrin), which specifically recognizes human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA-CAR-expressing Tscm P-BCMA-101 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. Use of CARTyrin may elicit less immunotoxicity than agents based on antibody-derived single chain variable fragments (scFv), and this agent may exhibit increased persistence and decreased exhaustion for the administered T cells. If significant side effects occur, the safety switch mechanism can induce the rapid attenuation or elimination of P-BCMA-101. BCMA, a tumor-specific antigen and a member of the tumor necrosis factor receptor superfamily (TNFRSF) that binds to both a proliferation-inducing ligand (APRIL; TNFSF13) and B-cell activating factor (BAFF; TNFSF13B), plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-mRNA-transfected CD8+ T lymphocytes

A preparation of autologous CD8-positive T lymphocytes that have been genetically modified via transient mRNA transfection to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA-CAR-mRNA transfected CD8+ T lymphocytes specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous anti-BCMA-CAR-TCRz/4-1BB-expressing T lymphocytes CART-BCMA

A preparation of autologous T lymphocytes that have been ex vivo transduced with a genetically-engineered lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) containing an extracellular human single chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to an intracellular tandem signaling domain comprised of the co-stimulatory domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3z), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-BCMA-CAR-4-1BB-CD3zeta-expressing T lymphocytes specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous anti-BCMA/CS1 bispecific CAR-T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) targeting both the tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; TNFRSF17) and human CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-BCMA/CS1 bispecific CAR-T cells target and bind to tumor cells expressing BCMA and/or CS1 and induce selective cytotoxicity in those cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells. Targeting the two different TAAs highly expressed on malignant plasma cells may improve coverage and protect against antigen escape and resistance as tumor cells would need to lose both antigens.

autologous anti-CD123 CAR TCR/4-1BB-expressing T lymphocytes

Autologous, genetically engineered T lymphocytes that have been electroporated with a messenger RNA (mRNA) encoding a chimeric antigen receptor (CAR) consisting of an anti-human interleukin-3 receptor alpha chain (IL3RA; CD123) single chain variable fragment (scFv) coupled to the co-stimulatory signaling domains of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCR) CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, the mRNA-electroporated autologous anti-CD123 CAR TCR/4-1BB expressing T lymphocytes attach to cancer cells expressing CD123. This induces selective toxicity in and causes lysis of CD123-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances T cell activation and signaling after recognition of CD123. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.

autologous anti-CD123 CAR-T cells

A preparation of autologous T cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD123 (interleukin-3 receptor alpha chain or IL3RA), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD123 CAR-T cells target and bind to CD123 expressed on the surface of tumor cells. This induces selective toxicity in CD123-expressing tumor cells. CD123, the alpha subunit of the IL-3 receptor, regulates the proliferation, survival and differentiation of hematopoietic cells. It is overexpressed on a variety of cancers, including myeloid leukemia, and the increased expression of CD123 on leukemic stem cells (LSCs) is associated with poor prognosis.

autologous anti-CD147 CAR T cells

A preparation of autologous activated T cells that have been engineered to express chimeric antigen receptors (CARs) specific for the tumor-associated antigen (TAA) CD147 (Basigin; EMMPRIN; extracellular matrix metalloproteinase inducer; OX47; 5A11), with potential antineoplastic activity. Upon administration back into the patient, the anti-CD147 CAR T-cells target and induce selective cytotoxicity in CD147-expressing tumor cells. CD147, a cell-surface glycoprotein of the immunoglobulin G (IgG) superfamily, is overexpressed in certain human tumors and plays an important role in tumor cell proliferation, migration, progression, and metastasis.

autologous anti-CD19 AbTCR-expressing T lymphocytes EB103

A preparation of autologous T lymphocytes transduced with a lentiviral vector encoding an antibody-T-cell-receptor (AbTCR) composed of a CD19-binding domain derived from an antibody fragment antigen binding (Fab) region and an effector domain derived from human gamma/delta TCR, and a co-stimulatory molecule composed of a CD19-binding domain derived from a single-chain variable fragment (scFv) and a co-stimulatory domain derived from a human co-stimulatory receptor, with potential immunostimulating and antineoplastic activities. Upon administration of the autologous anti-CD19 AbTCR-expressing T lymphocytes EB103, both the AbTCR moiety and the co-stimulatory molecule recognize and bind to CD-19-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD19, a B-cell-specific cell surface antigen, is overexpressed in B-cell lineage malignancies.

autologous anti-CD19 CAR T cells 19(T2)28z1xx

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, and linked to the co-stimulatory intracellular signaling domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta; CD28z), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19 CAR-T cells 19(T2)28z1xx specifically recognize and bind to CD19-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B cells. CD28 and CD3zeta provide co-stimulatory activity and may enhance the cytotoxic effect and anti-tumor activity of the CAR-T cells. The 19(T2)28z1xx CAR-T cells include a 1928zeta mutant, 1xx, which contains one instead of all three immunoreceptor tyrosine-based activation motifs (iTAMs). This may help prevent counterproductive T-cell differentiation and exhaustion.

autologous anti-CD19 CAR T cells GC019F

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR T cells GC019F target and bind to CD19-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, the release of cytotoxic molecules and the induction of tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. The processing platform used, FasTCAR, shortens the manufacturing time to produce the CAR T cells.

autologous anti-CD19 CAR T cells GLPG5101

A preparation of autologous stem-like early memory T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunomodulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR T cells GLPG5101 specifically recognize and kill tumor cells expressing CD19. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR TCR-zeta/4-1BB-transduced T lymphocytes BinD19

Autologous T lymphocytes that have been transduced with a lentiviral vector to express a T-cell receptor (TCR) consisting of a single chain variable fragment (scFv) of anti-CD19 coupled to the co-stimulatory molecule 4-1BB (CD137) and to the cytoplasmic portion of the zeta chain of the human T-cell receptor (CD3zeta), with potential immunostimulating and antineoplastic activities. Upon transfusion, the autologous anti-CD19 CAR TCR-zeta/4-1BB-transduced T lymphocytes BinD19 target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, the release of cytotoxic molecules and tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous anti-CD19 CAR TCR-zeta/4-1BB-transduced T lymphocytes huCART19

Autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of a humanized single chain variable fragment (scFv) of anti-CD19 coupled to the cytoplasmic portion of the zeta chain of the human T-cell receptor (CD3zeta) and the co-stimulatory molecule 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon re-introduction into the patient, the autologous anti-CD19 CAR TCR-zeta/4-1BB-transduced T lymphocytes huCART19 target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, resulting in tumor cell lysis. CD19 (cluster of differentiation 19) is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of the co-stimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous anti-CD19 CAR vector-transduced T cells pCAR-19B

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation (CD) 19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR vector-transduced T cells pCAR-19B specifically recognize and kill CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-4-1BB-CD3zeta-expressing T cells CNCT19

A preparation of autologous T lymphocytes that are engineered to express a chimeric antigen receptor (CAR) composed of an anti-cluster of differentiation 19 (CD19) single chain variable fragment (scFv) linked to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CD19 CAR-4-1BB-CD3zeta-expressing T cells CNCT19 target, bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-CD28 T cells ET019002

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19, coupled to the costimulatory domain of CD28, with potential immunostimulating and antineoplastic activities. Upon transfusion, the autologous anti-CD19 CAR-CD28 T cells ET019002 target, bind to, and induce selective toxicity in CD19-expressing B cells. The CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-CD3zeta-4-1BB-expressing T cells

A preparation of autologous T lymphocytes that are engineered to express a chimeric antigen receptor (CAR) composed of an anti-cluster of differentiation 19 (CD19) single chain variable fragment (scFv) linked to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential immunomodulating and antineoplastic activities. Upon administration of the autologous anti-CD19 CAR-CD3zeta-4-1BB-expressing T cells, these cells target, bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-CD3zeta-4-1BB-expressing T cells PZ01

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19, coupled to the costimulatory domains of 4-1BB (CD137) and the zeta chain of the human T-cell receptor (CD3zeta), with potential immunostimulating and antineoplastic activities. Upon transfusion, the autologous anti-CD19 CAR-CD3zeta-4-1BB-expressing T cells PZ01 target, bind to, and induce selective toxicity in CD19-expressing B cells. The CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-CD8alpha-CD28-CD3zeta T cells KYV 101

A preparation of autologous CD4- and CD8-positive T cells that are transduced with a lentiviral vector encoding for a chimeric antigen receptor (CAR) consisting of a human single chain variable fragment (scFv) of anti-CD19 and fused to the hinge and transmembrane domains of CD8alpha co-receptor, the cytoplasmic costimulatory domain of human CD28, and the T-cell antigen receptor complex zeta chain (CD3-zeta), with potential immunostimulating activity. Upon transfusion, autologous anti-CD19 CAR-CD8alpha-CD28-CD3zeta T cells KYV 101 recognize and induce selective toxicity and lysis in CD19-expressing B-cells. CD19, a B-cell-specific cell surface antigen, is overexpressed in B-cell lineage malignancies and in certain B-cell-driven autoimmune diseases.

autologous anti-CD19 CAR-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) that targets the human tumor associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-expressing T lymphocytes bind to and induce selective toxicity against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-expressing T lymphocytes CLIC-1901

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) that targets the human tumor associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-expressing T lymphocytes CLIC-1901 bind to and induce selective toxicity against CD19-expressing tumor cells. The CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-expressing T lymphocytes IC19/1563

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) that targets the human tumor associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-expressing T lymphocytes IC19/1563 bind to and induce selective toxicity against CD19-expressing tumor cells. The CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-expressing T lymphocytes UF-KURE19

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) that targets the human tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-expressing T lymphocytes UF-KURE19 bind to and induce selective toxicity against CD19-expressing tumor cells. The CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-IL-18-expressing T lymphocytes

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), and expressing the pro-inflammatory cytokine interleukin 18 (IL-18), with potential antineoplastic activity. Upon intravenous administration, autologous anti-CD19 CAR-IL-18-expressing T lymphocytes target, bind to, and induce selective toxicity in CD19-expressing tumor cells. IL-18 promotes T-cell persistence and potentiates the immune response against tumor cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of costimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous anti-CD19 CAR-T cells CABA-201

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-lymphocyte antigen CD19, coupled to a costimulatory domain of 4-1BB (CD137), with potential immunomodulatory activity. Upon administration, autologous anti-CD19 CAR-T cells CABA-201 target and bind to CD19-expressing B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing B cells. CD19, a B-cell-specific cell surface antigen that plays an important role in B-cell activation, is overexpressed in some autoimmune diseases.

autologous anti-CD19 CAR-T cells IM19

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-T cells IM19 target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 CAR-T cells TBI-1501

Autologous T lymphocytes that have been transduced, via a proprietary technology involving a recombinant human fibronectin fragment to enhance transduction efficiency, with a retroviral vector to express a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19 coupled to co-stimulatory molecules, with potential immunostimulating and antineoplastic activities. Upon transfusion, anti-CD19-CAR-expressing autologous T lymphocytes TBI-1501 target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, the release of cytotoxic molecules and the induction of tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domains increase proliferation and activation of T cells.

autologous anti-CD19 chimeric antigen receptor T cells C-CAR011

A proprietary preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a second-generation chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed, costimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR T cells C-CAR011 target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 chimeric antigen receptor T cells SJCAR19

A proprietary preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed, costimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR T cells SJCAR19 target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous anti-CD19 DASH CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a gamma-retrovirus vector expressing a second-generation chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 DASH CAR-T cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.

autologous anti-CD19 T-cell receptor fusion construct T cells TC-110

A preparation of autologous T lymphocytes that have been genetically engineered to express a single-domain antibody that recognizes human CD19, fused to the CD3-epsilon T-cell receptor (TCR) subunit which, upon expression is incorporated into the endogenous TCR complex, with potential antineoplastic activity. Upon administration, the autologous anti-CD19 TCR fusion construct (TRuC) T cells TC-110 specifically target and bind to CD19-expressing tumor cells. This leads to T-cell activation and T-cell mediated lysis of CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. Compared to chimeric antigen receptor (CAR) T cells, TRuCs may be associated with less pro-inflammatory cytokine secretion and fewer adverse effects without compromising therapeutic efficacy.

autologous anti-CD19 T-cell receptor T cells ET190L1

Autologous human peripheral blood T ymphocytes transduced with a lentivirus encoding a proprietary expression construct composed of a T-cell receptor (TCR)-like human antibody, which is synthesized by a proprietary phage display platform, targeting peptides derived from the tumor-associated antigen (TAA) CD19 that are presented in the context of major histocompatibility complex (MHC) molecules, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and re-introduction into the patient, the autologous anti-CD19 TCR T cells ET190L1 target and bind to tumor cells expressing CD19 peptide/MHC complexes. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of CD19-positive tumor cells. CD19, cluster of differentiation antigen 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. ET190L1 is able to match the anticancer activity of chimeric antigen receptor (CAR) T cells; however, ET190L1 is less likely to stimulate cytokine release syndrome (CRS) and does not cause CAR T-cell-triggered neurotoxicity.

autologous anti-CD19 TAC-T cells TAC01-CD19

A preparation of autologous T lymphocytes genetically engineered with a T cell Antigen Coupler (TAC), comprising of a domain that targets the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) and another domain that binds to the endogenous T-cell receptor (TCR), anchored in the membrane via the CD4 co-receptor domain, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 TAC-T cells TAC01-CD19 targets and binds to CD19-expressing tumor cells and activates TCR-mediated signaling pathways, leading to T-cell-mediated killing of CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.

autologous anti-CD19/anti-CD20-CAR-CD28-4-1BB-CD3zeta-EGFRt+-expressing Tn/mem cells

A preparation of genetically modified autologous naive/memory T cells (Tn/mem), that have been transduced with a self-inactivating (SIN) lentiviral vector to express a bispecific chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19, derived from the anti-CD19 monoclonal antibody FMC63, in tandem with an anti-CD20 scFv, derived from the anti-CD20 monoclonal antibody Leu16, and fused to the hinge domain of human immunoglobulin (Ig) G4, the transmembrane domain of human CD28, and the cytoplasmic signaling domains of 4-1BB (CD137) and the T-cell antigen receptor complex zeta chain (CD3-zeta) (BBz), and linked via the T2A sequence to a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon transfusion, autologous anti-CD19/anti-CD20-CAR-CD28-4-1BB-CD3zeta-EGFR+-expressing Tn/mem cells recognize and induce selective toxicity in CD19/CD20-expressing tumor cells, resulting in tumor cell lysis. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous anti-CD19/anti-CD79b CAR-expressing bispecific T cells

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) targeting the two tumor-associated antigens (TAAs) CD19 and B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19/anti-CD79b CAR-expressing bispecific T cells are directed to and induce selective toxicity in CD19- and CD79b-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD79b, a B cell surface antigen and critical receptor for successful B cell development, is part of the B cell receptor (BCR) signaling complex. It is widely expressed in certain subtypes of B cell lymphomas. CD19 and CD79b are expressed at high levels on tumor cells but not at significant levels on normal tissues. Targeting two antigens may protect against antigen escape and may enhance CAR-T cell efficacy.

Autologous Anti-CD19/CD20 Bispecific Nanobody-based CAR-T cells

A preparation of autologous T-lymphocytes engineered to express a chimeric antigen receptor (CAR) that is nanobody-based and specific for the two tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19) and CD20, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19/CD20 bispecific nanobody-based CAR-T cells target and bind to CD19- and CD20-expressing tumor B-cells. This induces selective toxicity in tumor B-cells expressing these TAAs. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD19 and CD20 may prevent tumor cell antigen escape and relapse.

autologous anti-CD19/CD20 CAR T cells KITE-363

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the two tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19) and CD20, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19/CD20 CAR T cells KITE-363 target and bind to CD19- and CD20-expressing tumor B cells. This induces selective toxicity in tumor B cells expressing these TAAs. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD19 and CD20 may prevent tumor cell antigen escape and relapse.

autologous anti-CD19/CD20/CD22 CAR T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19), CD20 and CD22, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19/CD20/CD22 CAR T-cells target and bind to CD19, CD20 and CD22 expressed on the surface of certain tumor cells. This induces selective toxicity in tumor cells expressing these TAAs. CD19, CD20 and CD22 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies.

autologous anti-CD19/CD22 CAR-T cells AUTO3

A preparation of autologous T lymphocytes that have been transduced with a bicistronic retroviral vector encoding both an anti-CD19 chimeric antigen receptor (CAR) fused to OX40 co-stimulatory domain and an anti-CD22 CAR linked to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), optimized with a novel pentameric spacer derived from the collagen oligomeric matrix protein (COMP), with potential antineoplastic activity. Upon administration, the autologous anti-CD19/CD22 CAR T cells AUTO3 bind to and induce selectivity in tumor cells expressing CD19 and CD22. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. By simultaneously targeting two B-cell antigens, this preparation may minimize relapse due to single antigen loss in patients with B-cell malignancies.

autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ central memory T lymphocytes JCAR014

A defined preparation of CD4+ and CD8+ central memory (CM) autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv) fused to the signaling domains of CD28, 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+CM T lymphocytes JCAR014 are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The 4-1BB costimulatory signaling domain enhances both proliferation of T cells and antitumor activity.

autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing T lymphocytes

A preparation of genetically modified CD8+ central memory (Tcm) and CD4+ autologous T-lymphocytes (1:1) transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv) derived from the murine IgG1 monoclonal antibody (mAb) FMC63, fused to the signaling domain of 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing T lymphocytes are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T-cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity response. The 4-1BB costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity.

autologous anti-CD19CAR-4-1BB/CD3zeta-HER2tG-expressing CD4+/CD8+ T lymphocytes SCRI-huCAR19v2

A preparation of autologous CD4- and CD8-positive Tlymphocytes that have been transduced with a lentiviral vector (LV) expressing a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) CD19 that is fused to the intracellular cytoplasmic domain of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (CD3zeta), and linked to a truncated form of the hu man epidermal growth factor receptor 2 (HER2tG), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19CAR-4-1BB/CD3zeta-HER2tG-expressing CD4+/CD8+ T lymphocytes SCRI-huCAR19v2 specifically target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and causes tumor cell lysis. CD19 is a B-cell-specific cell surface antigen that is overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domain increases human T-cell function, expansion, and survival. Devoid of both ligand binding domains and tyrosine kinase activity, the co-expressed HER2tG both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a trastuzumab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous anti-CD19CAR-CD28tm/4-1BB/CD3zeta-HER2tG-expressing CD4+/CD8+ T lymphocytes SCRI-huCAR19v1

A preparation of autologous CD4- and CD8-positive T lymphocytes that have been transduced with a third-generation self-inactivating (SIN) lentiviral vector (LV) expressing a human-derived immunoglobulin G4 (IgG4) hinge-optimized chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) specific for CD19 that is fused to a human CD28 transmembrane domain (CD28tm), the intracellular cytoplasmic domain of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (CD3zeta), and linked to a truncated form of the human epidermal growth factor receptor 2 (HER2tG), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous CD4+/CD8+ T lymphocytes SCRI-huCAR19v1 specifically target and bind to CD19-expressing neoplastic B-cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and causes tumor cell lysis. CD19 is a B-cell-specific cell surface antigen that is overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domains of CD28 and 4-1BB increases human T-cell function, expansion, and survival. Devoid of both ligand binding domains and tyrosine kinase activity, the co-expressed HER2tG both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a trastuzumab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous anti-CD19CAR-CD3zeta-4-1BB-IL-15-PD1-expressing tri-functional T lymphocytes

A preparation of autologous T lymphocytes engineered to express a tri-functional chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), and an extracellular domain consisting of interleukin 15 (IL-15) and programmed cell death 1 (PD1; PDCD1; CD279; programmed death-1), linked to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential antineoplastic activity. Upon intravenous administration, autologous anti-CD19CAR-CD3zeta-4-1BB-IL-15-PD1-expressing tri-functional T lymphocytes target, bind to, and induce selective toxicity in CD19-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. The PD1 moiety binds to programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) on tumor cells, reversing T-cell inactivation caused by endogenous PD1/PD-L1 signaling and enhancing the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous anti-CD19CAR-HER2t/CD22CAR-EGFRt-expressing T cells

A preparation of autologous human T lymphocytes engineered to express dual chimeric antigen receptors (CARs) consisting of both anti-CD19 and anti-CD22 binding domains, fused to an as of yet undisclosed co-stimulatory domain, and linked to truncated forms of the human epidermal growth factor receptor 2 (HER2t) and the human epidermal growth factor receptor (EGFRt), respectively with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD19CAR-HER2t/CD22CAR-EGFRt-expressing T cells bind to CD19 and CD22 on the surface of, and induce selective toxicity against, tumor cells expressing CD19 and CD22. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt and HER2t facilitate both in vivo detection of the administered, transduced T cells and can promote elimination of those cells through an antibody-dependent cellular cytotoxicity (ADCC) response. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells.

autologous anti-CD1a CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the T-cell surface glycoprotein CD1a, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD1a CAR T cells bind to and induce selective toxicity in CD1a-expressing tumor cells. CD1a, an antigen-presenting glycoprotein, is exclusively expressed in cortical T-cell acute lymphoblastic leukemia (T-ALL) and otherwise only normally expressed in developing cortical thymocytes and Langerhans cells.

autologous anti-CD1a CAR T cells OC-1

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the T-cell surface glycoprotein CD1a, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD1a CAR T cells OC-1 bind to and induce selective toxicity in CD1a-expressing tumor cells. CD1a, an antigen-presenting glycoprotein, is exclusively expressed in cortical T-cell acute lymphoblastic leukemia (T-ALL) and otherwise only normally expressed in developing cortical thymocytes and Langerhans cells.

autologous anti-CD20 CAR transduced CD4/CD8 enriched T cells MB-CART20.1

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), and CD4/CD8 enriched, with potential immunostimulating and antineoplastic activities. Upon administration, MB-CART20.1 specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies and certain melanoma cell subpopulations.

autologous anti-CD20 CAR-CD28-4-1BB-CD3zeta T lymphocytes MB-106

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) cluster of differentiation 20 (CD20) and coupled to the co-stimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3zeta), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD20CAR-CD28-4-1BB-CD3zeta T lymphocytes MB-106 specifically recognize and kill CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated B-cell specific surface phosphoprotein that plays a role in the differentiation of B cells into plasma cells, is overexpressed in B-cell lineage malignancies and certain melanoma cell subpopulations.

autologous anti-CD22 CAR-4-1BB-TCRz-transduced T lymphocytes CART22-65s

Autologous human T lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric antigen receptor (CAR) consisting of an anti-CD22 human single chain variable fragment (scFv) and linked to the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Upon reintroduction into the patient, the autologous anti-CD22 CAR-4-1BB-TCRz -transduced T lymphocytes CART22-65s express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces, resulting in lysis of CD22-expressing tumor cells. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells.

autologous anti-CD22 CAR-expressing T cells SCRI-CAR22v2

A preparation of autologous human T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD22, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD22 CAR-expressing T cells SCRI-CAR22v2 express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces leading to lysis of CD22-expressing B cells. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells.

autologous anti-CD22 CAR-T cells CLIC-2201

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD22, with potential antineoplastic activity. Upon administration, autologous anti-CD22 CAR-T cells CLIC-2201 recognize and kill CD22-expressing tumor cells. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells.

autologous anti-CD3/anti-EGFR bispecific antibody armed peripheral blood mononuclear cells

A preparation of autologous peripheral blood mononuclear cells (PBMCs) in which T lymphocytes are coated with a bispecific antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor (EGFR; HER1; ErbB1) and the T-cell surface antigen CD3 and activated ex vivo, with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, the autologous anti-CD3/anti-EGFR bispecific antibody armed PBMCs target, bind to and selectively cross-link CD3-expressing T cells and EGFR-expressing tumor cells. This results in the activation of cytotoxic T lymphocytes (CTLs) and selective cytotoxicity towards the EGFR-expressing tumor cells. EGFR, a receptor tyrosine kinase, is overexpressed on the surfaces of various tumor cell types.

autologous anti-CD3/anti-SLAMF7 bispecific antibody-armed activated T lymphocytes

A preparation of autologous activated T lymphocytes that have been coated with a bispecific antibody comprised of an anti-CD3 monoclonal antibody heteroconjugated to an anti-signaling lymphocytic activation molecule family member 7 (SLAMF7; CD319; CRACC; CS-1) monoclonal antibody, with potential immunomodulating and antineoplastic activities. Upon administration, autologous anti-CD3/anti-SLAMF7 bispecific antibody-armed activated T lymphocytes target and bind to both CD3 expressed on T cells and SLAMF7 expressed on tumor cells, thereby cross-linking CD3-expressing T cells and SLAMF7-expressing tumor cells. This results in the activation of cytotoxic T lymphocytes (CTLs) and selective cytotoxicity towards SLAMF7-expressing tumor cells. In addition, cytokine and chemokine secretion by the T cells further activates the immune system, which leads to the recruitment and activation of CTLs, and additional CTL-mediated tumor-specific cell lysis. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells.

autologous anti-CD30 CAR T cells HSP-CAR30

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the CD30 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD30 CAR T cells HSP-CAR30 specifically recognize and bind to CD30-expressing tumor cells, resulting in tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies.

autologous anti-CD38 A2 CAR2-expressing T cells

A preparation of genetically modified autologous T cells expressing a chimeric antigen receptor recognizing the tumor-associated antigen (TAA) cluster of differentiation 38 (CD38), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD38 A2 CAR2-expressing T cells are directed to and induce selective toxicity in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.

autologous anti-CD38 A2 CAR2-expressing T cells

A preparation of genetically modified autologous T cells expressing a chimeric antigen receptor recognizing the tumor-associated antigen (TAA) cluster of differentiation 38 (CD38), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD38 A2 CAR2-expressing T cells are directed to and induce selective toxicity in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.

autologous anti-CD4 CAR T cells LB1901

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD4, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD4 CAR T cells LB1901 target and bind to CD4-expressing tumor cells, thereby inducing selective toxicity in CD4-expressing tumor cells. CD4 antigen is expressed in CD4-positive T-cell lymphomas.

autologous anti-CD5 CAR monocytes MT-101

A preparation of autologous monocytes genetically modified with mRNA technology to express a chimeric antigen receptor (CAR) specific for CD5, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CD5 CAR monocytes MT-101 specifically recognize and bind to CD5-expressing tumor cells, and expose the immune system to the CD5 glycoprotein. This may elicit a cytotoxic T-lymphocyte (CTL) response against CD5-expressing tumor cells. CD5 is a T-cell surface glycoprotein expressed on the surface of normal T cells and overexpressed on various B- and T-cell malignancies.

autologous anti-CD5 CAR T lymphocytes MB-105

A preparation of genetically modified autologous T cells expressing a chimeric antigen receptor (CAR) directed against cluster of differentiation 5 (CD5), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CD5 CAR T lymphocytes MB-105 target and bind to CD5-expressing tumor cells, thereby inducing selective cytotoxicity in CD5-expressing tumor cells. CD5 is a T-cell surface glycoprotein expressed on the surface of normal T cells and overexpressed on various B- and T-cell malignancies.

autologous anti-CD7 CAR T cells PA3-17

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous anti-CD7 CAR T cells PA3-17 specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

autologous anti-CD7 CAR T cells SENL101

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the tumor-associated antigen (TAA) CD7, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous anti-CD7 CAR T cells SENL101 specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

autologous anti-CD7 CAR/28zeta CRISPR-edited T lymphocytes

A preparation of autologous T lymphocytes (ATL) that have been gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-caspase 9 (Casp9) to remove the CD7 antigen and genetically engineered to express a chimeric antigen receptor (CAR) composed of a single-chain variable fragment (scFv) directed against the CD7 antigen and linked to the co-stimulatory domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD7 CAR/28zeta CRISPR-edited T lymphocytes specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas. Removal of the endogenous CD7 antigen from the T-cell surface increases expansion and viability of the CAR-T cells and increases T-cell cytotoxic activity.

autologous anti-CD7-CAR-CD28zeta T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) directed against the CD7 antigen and linked to the co-stimulatory domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD7-CAR-CD28zeta T cells specifically recognize and bind to CD7-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD7 is a transmembrane glycoprotein expressed by T cells and natural killer (NK) cells and their precursors. It is expressed in the majority of lymphoblastic T-cell leukemias and lymphomas and in a subset of peripheral T-cell lymphomas.

autologous anti-CD79a/anti-CD20 CAR T cells bbT369

A preparation of genetically modified autologous T lymphocytes that are transduced with a single lentiviral vector (LVV) to express chimeric antigen receptors (CARs) specific for the two tumor-associated antigens (TAAs) cluster of differentiation 20 (CD20) and the B-cell antigen receptor complex-associated protein alpha chain (CD79a), and transfected with an mRNA encoding the Casitas B-lineage lymphoma proto-oncogene-b (CBLB)-targeting megaTAL enzyme to edit the CBLB gene, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CD20/CD79a CAR T cells bbT369 target and bind to CD20- and CD79a-expressing tumor B cells. This induces selective toxicity in tumor B cells expressing these TAAs. Both CD20 and CD79a are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD20 and CD79a may prevent tumor cell antigen escape and relapse, and may increase anti-tumor activity. The removal of CBLB, an E3 ubiquitin ligase and a negative regulator of T-cell function, will increase T-cell expansion and activation.

autologous anti-CD79b CAR T cells JV-213

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell antigen receptor complex-associated protein beta chain (CD79b; B-cell-specific glycoprotein B29), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD79b CAR-T cells JV-213 target and bind to CD79b-expressing tumor cells, thereby inducing selective toxicity in CD79b-expressing tumor cells. CD79b, a critical receptor for successful B-cell development and part of the B-cell receptor (BCR) signaling complex, is widely expressed in certain subtypes of B-cell lymphomas.

autologous anti-CD83 CAR T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) targeting CD83, with potential antineoplastic activity. Upon administration, autologous anti-CD83 CAR T cells recognize and kill CD83-expressing tumor cells. CD83 is expressed on acute myeloid leukemia (AML) blasts.

autologous anti-CDH17 CAR-T cells CHM-2101

A preparation of autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) cadherin-17 (CDH17), with potential immunomodulatory and antineoplastic activities. After isolation, transduction, and expansion in culture, the autologous anti-CDH17 CAR-T cells CHM-2101 are reintroduced into the patient and are directed to tumor cells expressing CDH17, which may result in a selective toxicity against, and lysis of CDH17-expressing tumor cells. CDH17, a cell surface adhesion protein, is overexpressed in a variety of cancer cell types.

autologous anti-CEA CAR/HLA-A*02-gated inhibitory receptor/B2M shRNA-expressing T lymphocytes A2B530

A preparation of autologous T lymphocytes from a human leukocyte antigen (HLA)-A*02-positive donor that have been transduced with a lentiviral vector expressing an activating chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) carcinoembryonic antigen-related cell adhesion molecule 5 (CEA or CEACAM5), a leukocyte immunoglobulin-like receptor 1 (LIR-1)-based inhibitory receptor specific for HLA-A*02, and a short hairpin RNA (shRNA) targeting beta-2 microglobulin (B2M), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CEA CAR/HLA-A*02-gated inhibitory receptor/B2M shRNA-expressing T lymphocytes A2B530 target and bind to CEA-expressing tumor cells, thereby killing CEA-expressing tumor cells. The inhibitory receptor specific for HLA-A*02 acts as a safety switch that blocks the killing of HLA-A*02-positive CEA-expressing normal cells. HLA-A*02 is expressed on normal cells but not on tumor cells due to loss of heterozygosity (LOH). The B2M shRNA disrupts the expression of the B2M component of the HLA class I molecule. CEA, a member of the CEA family of proteins, plays a key role in cell migration, cell invasion and cell adhesion, and is overexpressed by a variety of cancer types.

autologous anti-Claudin18.2 CAR T cells LB1908

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CLDN18.2 CAR T cells LB1908 specifically recognize and induce selective toxicity in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

autologous anti-Claudin18.2-transduced T lymphocytes CT041

A preparation of autologous T lymphocytes ex vivo transduced with a lentiviral vector encoding for a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CLDN18.2CAR-transduced T lymphocytes specifically recognize and induce selective toxicity in CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

autologous anti-CLDN18.2 TAC T cells TAC01-CLDN18.2

A preparation of autologous T lymphocytes that have been genetically engineered to express a T-cell Antigen Coupler (TAC), comprised of a domain that targets the tumor-associated antigen (TAA) claudin 18.2 (CLDN18.2; A2 isoform of claudin-18) and another domain that binds to the endogenous T-cell receptor (TCR), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CLDN18.2 TAC T cells TAC01-CLDN18.2 target and bind to CLDN18.2-expressing tumor cells and activate TCR-mediated signaling pathways, leading to T-cell-mediated killing of CLDN18.2-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells. Its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

autologous anti-CLDN6 CAR-NK cells

A preparation of autologous natural killer (NK) cells engineered to express a chimeric antigen receptor (CAR) specific for the cell surface protein claudin 6 (CLDN6), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-CLDN6 CAR-NK cells target and bind to CLDN6 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing CLDN6. CLDN6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.

autologous anti-CLL-1-CAR T lymphocytes BG1805

A preparation of autologous T lymphocytes expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) C-type-lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CLL-1-CAR T lymphocytes BG1805 specifically target and bind to CLL-1-expressing tumor cells. This induces selective toxicity in CLL-1-expressing tumor cells. CLL-1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse in myeloid malignancies.

autologous anti-CLL-1-CAR T lymphocytes KITE-222

A preparation of autologous T lymphocytes expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) C-type-lectin-like molecule-1 (CLL-1; CLL1; C-type lectin domain family 12 member A; CLEC12A), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-CLL-1-CAR T lymphocytes KITE-222 specifically target and bind to CLL-1-expressing tumor cells. This induces selective toxicity in tumor cells that express the CLL-1 antigen. CLL-1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

autologous anti-CS1 hinge-optimized CAR-4-1BB-EGFRt-expressing memory-enriched T cells

A preparation of autologous central memory-enriched T cells (Tcm) that have been transduced with a self-inactivating (SIN) lentiviral vector expressing a hinge-optimized chimeric antigen receptor (CAR) comprised of a CS1 (CD2 subset 1; SLAM family member 7; SLAMF7; CD319; CRACC)-specific single chain variable fragment (scFV), fused to the costimulatory signaling domain of 4-1BB (CD137), and a truncated human epidermal growth factor receptor (huEGFRt), with potential antineoplastic activity. Upon intravenous infusion, anti-CS1-CAR-4-1BB-CD3z-EGFRt-expressing Tcm-enriched T lymphocytes target and induce selective toxicity in CS-1-expressing tumor cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed huEGFRt facilitates both in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. CS1, a cell surface glycoprotein of the signaling lymphocyte activation molecule (SLAM) receptor family, is highly expressed on certain malignant plasma cells.

autologous anti-CSPG4 CAR-iC9-expressing T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for chondroitin sulfate proteoglycan 4 (CSPG4) and the suicide gene inducible caspase 9 (iCasp9 or iC9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CSPG4 CAR-iC9-expressing T lymphocytes specifically target and bind to CSPG4-expressing tumor cells, resulting in tumor cell lysis. CSPG4 is overexpressed on a variety of tumor cell types. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered CAR T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9 and results in apoptosis of the administered CAR T cells.

autologous anti-DLL-3 CAR-T cells LB2102

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) delta-like protein 3 (DLL3), with potential immunomodulating and antineoplastic activities. Upon administration, autologous anti-DLL3 CAR-T cells LB2102 recognize and induce selective toxicity in DLL3-expressing tumor cells. DLL3, a Notch pathway protein, is overexpressed on a variety of cancer cell types. It plays a key role in embryonic development and in tumor initiation and proliferation.

autologous anti-EBV CAR T cells BRG01

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) targeting an Epstein-Barr virus (EBV) protein, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous anti-EBV CAR T cells BRG01 targets a specific EBV protein expressed on EBV-positive cancer cells and promotes killing of these cancer cells. EBV infection is associated with various cancers and the expression of certain EBV specific proteins plays a key role in tumor cell proliferation and survival.

autologous anti-EGFR CAR-transduced CXCR 5-modified T lymphocytes

A preparation of autologous, C-X-C chemokine receptor type 5 (CXCR 5)-modified T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the epidermal growth factor receptor (EGFR), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-EGFR CAR-transduced CXCR 5-modified T lymphocytes target and bind to EGFR-expressing tumor cells, thereby inducing selective toxicity in EGFR-expressing tumor cells. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance. CXCR5, and its ligand C-X-C motif chemokine 13 (CXCL13), are associated with a variety of tumors. CXCR5-CXCL13 interactions may be involved in the regulation of lymphocyte infiltration within the tumor microenvironment (TME).

autologous anti-EGFR/anti-IL13Ralpha2 CAR T cells

A preparation of autologous T lymphocytes engineered to co-express two chimeric antigen receptors (CARs) specific for epidermal growth factor receptor (EGFR) epitope 806 and interleukin-13 receptor alpha 2 (IL13Ra2), with potential immunostimulating and antineoplastic activities. After isolation, transduction, expansion and reintroduction into the patient, the autologous anti-EGFR/anti-IL13Ra2 CAR T cells are directed to, bind to, and induce selective toxicity in EGFR deletion mutation variant III (EGFRvIII)-expressing and IL13Ra2-expressing tumor cells. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy. IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell types including glioblastoma multiforme (GBM); it is associated with increased invasiveness of tumor cells. The binding of IL13Ra2 to EGFRvIII upregulates the tyrosine kinase activity of EGFRvIII and promotes tumor cell proliferation.

autologous anti-EGFRvIII 4SCAR-IgT cells

A preparation of autologous T cells that are genetically modified to express immunoglobulins (Igs) that target the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and programmed death-ligand 1 (PD-L1; CD274) and are transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of a single chain variable fragment (scFv) targeting anti-epidermal growth factor receptor variant III (EGFRvIII) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (TCR), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-EGFRvIII 4SCAR-IgT cells are directed to and induce selective toxicity in EGFRvIII-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. EGFRvIII, a tumor-associated antigen (TAA) encoded by an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types and is not expressed by normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity. The anti-PD-1 and anti-PD-L1 antibodies produced by the T cells (IgT) bind to PD-1, expressed on T cells, and its ligand PD-L1 expressed on cancer cells, respectively. This inhibits PD-1/PD-L1-mediated signaling, prevents T-cell inhibition and exhaustion, enhances T-cell activation within the tumor microenvironment (TME), and results in an enhanced T-cell-mediated immune response against and toxicity in the EGFRvIII-expressing tumor cells.

autologous anti-EGFRvIII synNotch receptor-induced anti-EphA2/IL-13Ralpha2 CAR-T cells

A preparation of autologous T lymphocytes engineered to express a synthetic Notch (synNotch) receptor targeting epidermal growth factor receptor variant III (EGFRvIII) that induces the expression of a chimeric antigen receptor (CAR) specific for Ephrin receptor A2 (EphA2) and interleukin-13 receptor alpha 2 (IL13Ra2) upon antigen binding, with potential immunostimulating and antineoplastic activities. After isolation, transduction, expansion and reintroduction into the patient, autologous anti-EGFRvIII synNotch receptor-induced anti-EphA2/IL-13Ralpha2 CAR-T cells target and bind to EGFRvIII-expressing tumor cells, which induces the expression of CAR specific for EphA2 and IL13Ra2. This induces selective toxicity in EphA2-expressing and IL13Ra2-expressing tumor cells locally. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy. IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell types; it is associated with increased invasiveness of tumor cells. EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types. EphA2 expression is associated with poor prognosis.

autologous anti-FcRL5 CAR-T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) targeting Fc receptor-like protein 5 (FcRL5; Fc receptor-homolog 5; FcRH5), with potential antineoplastic activity. Upon administration, autologous anti-FcRL5 CAR-T cells recognize and kill FcRL5-expressing tumor cells. FcRL5, an immune receptor translocation-associated protein/Fc receptor homolog (IRTA/FcRH) family member and a B-cell lineage marker, is overexpressed in multiple myeloma.

autologous anti-FGFR4 CAR T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting human fibroblast growth factor receptor 4 (FGFR4), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-FGFR4 CAR T cells recognize and induce selective toxicity in FGFR4-expressing tumor cells. FGFR4, a receptor tyrosine kinase, is involved in angiogenesis and in the proliferation, differentiation, and survival of tumor cells.

autologous anti-FLT3 CAR T cells AMG 553

A preparation of autologous T lymphocytes genetically engineered with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-FLT3 CAR T cells AMG 553 target and bind to tumor cells expressing FLT3, which results in the cytotoxic T-lymphocyte (CTL)-mediated cell killing of FLT3-expressing tumor cells. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias (AMLs).

autologous anti-FLT3 CAR T cells TAA05

A preparation of autologous T lymphocytes genetically engineered with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-FLT3 CAR T cells TAA05 target and bind to tumor cells expressing FLT3, which results in the cytotoxic T-lymphocyte (CTL)-mediated cell killing of FLT3-expressing tumor cells. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias (AMLs).

autologous anti-FLT3 CAR-T cells HG-CT-1

A preparation of autologous T lymphocytes genetically modified with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-FLT3 CAR-T cells HG-CT-1 target and bind to tumor cells expressing FLT3, which results in the cytotoxic T-lymphocyte (CTL)-mediated cell killing of FLT3-expressing tumor cells. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias (AMLs).

autologous anti-FSHR CER-4-1BB/CD3zeta-expressing T lymphocytes

A preparation of autologous human T lymphocytes genetically modified to express a chimeric endocrine receptor (CER) targeting the human follicle stimulating hormone receptor (FSHR) and coupled to the signaling domains of 4-1BB (CD137) and CD3 zeta, with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous anti-FSHR CER-4-1BB/CD3zeta-expressing T lymphocytes target and bind to the FSHR on FSHR-expressing tumor cell surfaces, thereby killing FSHR-expressing tumor cells. FSHR is not normally expressed in healthy non-ovarian tissue, but is present on several types of ovarian, fallopian tube, or primary peritoneal cancers.

autologous anti-GD2-CAR-BBz-iCasp9 retroviral vector-transduced T lymphocytes

A preparation of genetically modified autologous T lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) derived from the monoclonal antibody 14g2a that is specific for the disialoganglioside GD2 and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), and fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunomodulating and antineoplastic activities. Upon intravenous administration of the autologous anti-GD2-CAR-BBz-iCasp9 retroviral vector-transduced T lymphocytes, these cells target the GD2 antigen on tumor cells, thereby providing selective toxicity towards GD2-expressing tumor cells. The tumor-associated antigen (TAA) GD2 is overexpressed on the surface of neuroblastoma cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered; this binds to the drug binding FKBP12-F36V domain and activates caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent.

autologous anti-GD2/anti-PSMA 4SCAR-expressing bispecific T cells

A preparation of autologous T lymphocytes that are genetically engineered to express a fourth-generation chimeric antigen receptor (4SCAR) targeting the two tumor-associated antigens (TAAs) disialoganglioside (GD2) and prostate-specific membrane antigen (PSMA), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-GD2/anti-PSMA 4SCAR-expressing bispecific T cells are directed to and induce selective toxicity in GD2- and PSMA-expressing tumor cells. GD2 is overexpressed on the surface of neuroblastoma (NB) cells and by other neuroectoderm-derived neoplasms, while it is minimally expressed on normal cells. PSMA, a type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors, including brain tumor, NB and some lymphoma tumor tissues.

autologous anti-GD2CAR-CD28-CD3zeta-IL-15-expressing natural killer T cells

A preparation of autologous natural killer T lymphocytes (NKTs) that have been transduced with a retroviral vector to express both an extracellular domain consisting of interleukin 15 (IL-15) and a chimeric antigen receptor (CAR) specific for the human tumor associated antigen (TAA) GD2, linked to the CD28 and CD3zeta (TCRzeta; CD247) costimulatory signaling domains, with potential antineoplastic activity. Upon intravenous administration, autologous anti-GD2CAR-CD28-CD3zeta-IL-15-expressing NKTs target, bind to, and induce selective toxicity in GD2-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. Incorporation of the costimulatory signaling domains increases T-cell function, expansion, and survival. The CD28 costimulatory molecule signaling domain enhances activation and signaling after recognition of GD2. Additionally, inclusion of the CD28 signaling domain may increase proliferation of T cells and antitumor activity compared to the inclusion of the CD3zeta chain alone. GD2, a disialoganglioside and tumor-associated antigen (TAA), is overexpressed in a variety of tumor cell types.

autologous anti-GFRa4 CAR-TCR-zeta-4-1BB-expressing T cells

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of an anti-glial-derived neurotrophic factor (GDNF) family receptor alpha 4 (GFRa4) single chain variable fragment (scFv), coupled to the zeta chain of the human T-cell receptor (TCR/CD3zeta) and the co-stimulatory molecule 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon re-introduction into the patient, the autologous anti-GFRa4 CAR-TCR-zeta-4-1BB-expressing T cells target and bind to GFRa4-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against GFRa4-expressing tumor cells, resulting in tumor cell lysis. GFRa4 is highly expressed in metastatic medullary thyroid cancer (MTC) and also normally expressed in parafollicular cells within the thyroid and thymus.

autologous anti-glypican-3 CAR-IL-15-iC9-expressing T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3) and express interleukin-15 (IL-15) and the suicide gene, inducible caspase 9 (iCasp9 or iC9), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3-CAR-IL-15-iC9-expressing T lymphocytes specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation. IL-15 is a pro-survival cytokine that potentiates, in addition to promoting T-cell proliferation and persistence, the immune response against tumor cells. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered CAR T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9 and results in apoptosis of the administered CAR T cells.

autologous anti-gp100:154-162 T-cell receptor gene-engineered peripheral blood lymphocytes

Human autologous peripheral blood lymphocytes (PBLs) transduced with a glycoprotein 100 (gp100) epitope-determined T cell receptor (TCR) gene, with potential antineoplastic activity. PBLs are isolated from a melanoma patient and pulsed with a viral vector encoding the TCR specific for amino acid residues 154-162 of gp100 (KTWGQYWQV). After expansion ex vivo, the transduced autologous PBLs, expressing this specific TCR, are reintroduced into the patient and bind to melanoma cells expressing the gp100 protein, which may result in specific cytotoxic T-lymphocyte (CTL) killing of gp100-expressing melanoma cells. gp100 is a melanocyte lineage-specific antigen overexpressed in melanomas.

autologous anti-gp100:154-162 TCR tumor infiltrating lymphocytes

A preparation of human tumor infiltrating lymphocytes (TILs) isolated from a melanoma patient and engineered to encode a T-cell receptor (TCR) specific for the amino acid 154 through 162 of the melanoma antigen glycoprotein 100 (gp100), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, the autologous anti-gp100:154-162 TCR TILs may recognize and halt the growth of gp100-expressing melanoma cells.

autologous anti-gp100CAR-CD3zeta-4-1BB-IL-15-PD1-expressing tri-functional T lymphocytes

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector encoding a tri-functional chimeric antigen receptor (TriCAR) comprised of an extracellular domain consisting of an antigen binding domain specific to glycoprotein 100 (gp100) peptides 209-217 complexed with human leucocyte antigen A2 (HLA-A2), interleukin 15 (IL-15) and programmed cell death 1 (PD1; PDCD1; CD279; programmed death-1), which are linked by a transmembrane domain to the intracellular signaling domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential antineoplastic activity. Upon administration, the autologous anti-gp100CAR-CD3zeta-4-1BB-IL-15-PD1-expressing tri-functional T lymphocytes selectively bind to gp100 peptides presented by HLA-A2. Upon binding to the gp100-HLA complex, the T-cells release cytokines and induce selective toxicity in gp100-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. The PD1 moiety binds to programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) on tumor cells, reversing T-cell inactivation caused by endogenous PD1/PD-L1 signaling and enhancing the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells.

autologous anti-GPC2-CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-2 (GPC2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-GPC2-CAR T cells specifically target and bind to GPC2-expressing tumor cells, resulting in tumor cell lysis. GPC2, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells.

autologous anti-GPC3 CAR T cells BOXR1030

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3) and glutamic-oxaloacetic transaminase 2 (GOT2) transgene, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-GPC3 CAR T cells BOXR1030 specifically targets and binds to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation. The inclusion of GOT2, a mitochondrial enzyme that plays an important role in cellular metabolism, may improve T-cell metabolic function and anti-tumor activity.

autologous anti-GPC3 CAR T lymphocytes JWAT204

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-GPC3 CAR T lymphocytes JWAT204 specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation.

autologous anti-GPC3-CAR T lymphocytes Ori-C101

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3) and a signal activation domain element, Ori, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-GPC3-CAR T lymphocytes Ori-C101 specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan (HSPG) and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells. GPC3 plays an important role in cellular proliferation and differentiation. Ori is able to enhance the expansion of memory T cells, abrogate the immunosuppressive tumor microenvironment (TME), and may enhance the anti-tumor activity and durability of CAR T cells Ori-C101.

autologous anti-GPRC5D CAR-T cells OriCAR-017

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human G-protein coupled receptor family C group 5 member D (GPRC5D), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-GPRC5D CAR-T cells OriCAR-017 specifically recognize and induce selective toxicity in GPRC5D-expressing tumor cells. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation. OriCAR-017 contains a signal activation domain element that may improve CAR-T cells expansion and durability.

autologous anti-GPRC5D-CAR-4-1BB-expressing T cells MCARH109

A preparation of autologous T lymphocytes that have been transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) human G-protein coupled receptor family C group 5 member D (GPRC5D) and the co-stimulatory domain 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-GPRC5D-CAR-4-1BB-expressing T cells MCARH109 specifically recognize and induce selective toxicity in GPRC5D-expressing tumor cells. GPRC5D is overexpressed in certain malignancies, such as multiple myeloma, while minimally expressed in normal, healthy cells. It plays a key role in tumor cell proliferation.

autologous anti-H3.3K27M TCR-expressing T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for the histone H3.3 containing the amino acid substitution mutation lysine (Lys) 27-to-methionine (H3.3K27M), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-H3.3K27M TCR-expressing T cells specifically target and bind to H3.3K27M-expressing tumor cells. This leads to T-cell activation and T-cell mediated lysis of H3.3K27M-expressing tumor cells. The H3.3K27M mutation alters the methylation and acetylation profile of the histone H3 variant H3.3 at Lys 27. Modification of H3.3 at Lys 27 regulates gene expression, and the H3.3K27M mutation occurs in a variety of cancer cell types.

autologous anti-HER2 CAR macrophages CT-0508

A preparation of autologous macrophages transduced with the adenoviral vector Ad5f35 to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous anti-HER2 CAR Macrophages (CAR-M) CT-0508 specifically recognize and bind to HER2-expressing tumor cells, resulting in the phagocytosis of HER2-expressing tumor cells. CAR-M CT-0508 maintain the pro-inflammatory, anti-tumor M1 phenotype within the human tumor microenvironment (TME). In addition, CAR-M CT-0508 may activate an anti-tumor T-lymphocyte immune response resulting in T-cell-mediated killing of tumor cells. HER2, a receptor tyrosine kinase that is mutated or overexpressed in many tumor cell types, plays an important role in tumor cell proliferation and tumor vascularization.

autologous anti-HER2 CAR monocytes CT-0525

A preparation of autologous monocytes genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (HER2; ErbB2; HER-2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-HER2 CAR monocytes CT-0525 specifically recognize and bind to HER2-expressing tumor cells, and expose the immune system to the HER2 antigen. This may elicit a cytotoxic T-lymphocyte (CTL) response against HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation.

autologous anti-HER2 CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human epidermal growth factor 2 (HER2; ErbB2; HER-2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-HER2 CAR T cells target and bind to HER2-expressing tumor cells, thereby inducing selective toxicity in HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation.

autologous anti-HER2 CAR T cells CCT303-406

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human epidermal growth factor 2 (HER2; ErbB2; HER-2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-HER2 CAR T cells CCT303-406 target and bind to HER2-expressing tumor cells, thereby inducing selective toxicity in HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation.

autologous anti-HER2 CAR-CD28 T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) human epidermal growth factor 2 (HER2; ErbB2; HER-2) and coupled to the costimulatory domain of CD28, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-HER2 CAR-CD28 T cells target and bind to HER2-expressing tumor cells, thereby inducing selective toxicity in HER2-expressing tumor cells. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation.

autologous anti-HER2 TAC T cells TAC01-HER2

A preparation of autologous T lymphocytes that are genetically engineered with a T-cell Antigen Coupler (TAC), comprising of a domain that targets the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (HER2) and another domain that binds to the endogenous T-cell receptor (TCR), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-HER2 TAC T cells TAC01-HER2 targets and binds to HER2-expressing tumor cells and activates TCR-mediated signaling pathways, leading to T-cell-mediated killing of HER2-expressing tumor cells. HER-2, a tyrosine kinase receptor for epidermal growth factor (EGF) (also known as neu and ErbB2), is overexpressed by a variety of cancers.

autologous anti-HER2-CAR-4-1BB-CD3zeta-CD19t+-expressing Tcm-enriched T lymphocytes

A preparation of genetically modified autologous central memory (Tcm) enriched T cells transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-human epidermal growth factor 2 (HER2) single chain variable fragment (scFv) derived from trastuzumab, with a 4-1BB (CD137) costimulatory domain that is linked to the signaling domain of the T-cell antigen receptor complex zeta chain (CD3-zeta) (BBz), and truncated CD19 (CD19t), with potential immunostimulatory and antineoplastic activities. Upon intravenous infusion, Anti-HER2-CAR-4-1BB-CD19t+-expressing Tcm-enriched T lymphocytes are directed against HER2-expressing cells, thereby inducing selective toxicity in HER2-expressing tumor cells. HER2, a receptor tyrosine kinase, is mutated or overexpressed in many tumor cell types, plays a significant role in tumor cell proliferation and tumor vascularization. The BBz costimulatory signaling domain enhances proliferation of T cells and antitumor activity, while CD19t, a marker for transduction, is utilized to calculate CAR-T-cell dosing and for CAR-expressing cell tracking. Tcm cells have the capacity for long-lived persistence and retain their ability to proliferate upon antigen re-encounter. The immunoglobulin G4 (IgG4) extracellular spacer contains a double mutation, (L235E;N297Q) (EQ) within the CH2 region to reduce Fc receptor recognition.

autologous anti-HLA-A*02/AFP TCRm-expressing T cells ET140202

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a T-cell receptor mimetic (TCRm) antibody synthesized by a proprietary phage display platform, targeting the immunogenetic human tumor-associated antigen (TAA) alpha-fetoprotein (AFP) complexed with human leukocyte antigen (HLA)-A*02 (HLA-A*02/AFP), with potential antineoplastic and immunomodulatory activities. Upon administration, the autologous anti-HLA-A*02/AFP TCRm-expressing T cells ET140202 specifically recognize and selectively bind to AFP peptides presented by HLA-A*02. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of AFP-expressing tumor cells. AFP, an intracellularly expressed fetal glycoprotein rarely expressed in adult tissues, is overexpressed in certain tumors of endodermal origin and plays a key role in tumor cell proliferation and survival. AFP is processed into peptides and presented by class I major histocompatibility complexes (MHCs) on the surface of tumor cells.

autologous anti-HLA-A*0201/AFP CAR-T cells ET1402L1

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) derived from a human monoclonal antibody specific for an immunogenic human tumor-associated antigen (TAA) alpha-fetoprotein (AFP) epitope, AFP158-166, complexed with human leukocyte antigen (HLA)-A*02:01 (HLA-A*0201/AFP), fused to the co-stimulatory domains of CD28 and CD3zeta, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-HLA-A*0201/AFP CAR-T cells ET1402L1 specifically recognize and selectively bind to the AFP158-166 peptide presented by HLA-A*0201. Upon binding to the AFP-MHC complex, the T cells release cytokines and induce selective toxicity in HLA-A*0201/AFP-positive tumor cells. AFP, an intracellularly expressed fetal glycoprotein rarely expressed in adult tissues, is overexpressed in certain tumors of endodermal origin and plays a key role in tumor cell proliferation and survival. AFP is processed into peptides and presented by class I major histocompatibility complexes (MHCs) on the surface of tumor cells.

autologous anti-HLA-G CAR-T cells IVS-3001

A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) and immune checkpoint protein human leukocyte antigen G (HLA-G), with potential immune checkpoint inhibiting, immunomodulating and antineoplastic activities. Upon administration, autologous anti-HLA-G CAR-T cells IVS-3001 specifically recognize and kill HLA-G-expressing tumor cells. This reverts HLA-G-mediated immune suppression in the tumor microenvironment (TME), thereby restoring anti-tumor immune responses. HLA-G, an immune checkpoint normally expressed at the maternal-fetal interface, is expressed across multiple tumor types and plays a key role in cancer immune evasion. It inhibits immune responses by binding to its inhibitory receptors on a variety of immune cells, such as natural killer cells (NKs), T- and B-lymphocytes, and dendritic cells (DCs).

autologous anti-HPV-16 E6 T-cell receptor gene-engineered peripheral blood lymphocytes

Human autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding a T-cell receptor (TCR) that is specifically directed against the viral oncoprotein human papillomavirus type 16 (HPV-16) E6, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-HPV-16 E6 TCR gene-engineered PBLs bind to HPV-16 E6-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of HPV-16 E6-positive cancer cells. HPV-16 E6, a cell surface glycoprotein, is overexpressed by a variety of HPV-associated cancers and is absent from healthy human tissues.

autologous anti-ICAM-1-CAR-CD28-4-1BB-CD3zeta-expressing T cells AIC100

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) containing the Inserted (I) domain variant of lymphocyte function-associated antigen-1 (LFA-1) which targets intercellular adhesion molecule-1 (ICAM-1 or CD54), and the co-stimulatory signaling domains of CD28, 4-1BB (CD137) and CD3zeta, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-ICAM-1-CAR-CD28-4-1BB-CD3zeta-expressing T cells AIC100 recognize and kill ICAM-1-expressing tumor cells. ICAM-1, normally expressed on leukocytes and endothelial cells, may be overexpressed in a variety of cancers. CAR-T cells AIC100 are also engineered to express somatostatin receptor subtype 2 (SSTR2), allowing the imaging of the CAR-T cells in patients.

autologous anti-IL-1RAP CAR T cells CCTx-001

A preparation of autologous CD4+ and CD8+ T lymphocytes that have been transduced to express a chimeric antigen receptor (CAR) consisting of an anti-interleukin-1 receptor accessory protein (IL-1RAP; IL-1 receptor 3; IL-1R3) single chain variable fragment (scFv) coupled to the hinge domain of human immunoglobulin G1 (IgG1), the co-stimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3zeta), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-IL-1RAP CAR T cells CCTx-001 specifically recognize and kill IL-1RAP-expressing tumor cells. IL-1RAP, a transmembrane glycoprotein, is highly expressed on leukemic cells but not on healthy hematopoietic stem and progenitor cells (HSPCs); its expression has been correlated with poor prognosis.

autologous anti-ILT3 CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the immune inhibitory receptor leukocyte immunoglobulin-like receptor B member 4 (LILRB4; ILT3; ILT-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, autologous anti-ILT3 CAR-T cells target and bind to ILT3-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against ILT3-expressing tumor cells. ILT3, a tumor associated antigen (TAA) and an immune inhibitory receptor expressed on immune suppressive myeloid cells, is highly expressed on certain hematologic cancer cells, such as monocytic acute myeloid leukemia (AML) cells. It functions as an immune checkpoint that negatively regulates T-cell activation as its extracellular domain inhibits T-cell activity. It plays an important role in tumor infiltration, T-cell suppression and immune tolerance.

autologous anti-kappa light chain CAR-CD28-expressing T lymphocytes

A preparation of autologous T lymphocytes (ATL) that have been genetically modified to express a chimeric antigen receptor (CAR) directed against the kappa light chain of immunoglobulin (Ig) and linked to the costimulatory domain of CD28, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-kappa light chain CAR-CD28-expressing T lymphocytes target and bind to the kappa light chain of Ig expressed on tumor cells, resulting in T-cell-mediated tumor cell lysis. In some B-cell malignancies, the expression of the Ig light chain kappa may be increased compared to the expression of Ig light chain lambda.

autologous anti-KK-LC-1 TCR-expressing T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) Kita-Kyushu lung cancer antigen-1 (KK-LC-1), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-KK-LC-1 TCR-expressing T cells specifically target and bind to KK-LC-1-expressing tumor cells. This leads to T-cell activation and T-cell mediated lysis of KK-LC-1-expressing tumor cells. KK-LC-1, a cancer germline (CG) antigen, is expressed in a variety of epithelial cancers and has restricted expression in normal tissues.

autologous anti-L1CAM-CAR-EGFRt-expressing T cells

A preparation of autologous human T lymphocytes expressing a chimeric antigen receptor (CAR) specific for the L1 cell adhesion molecule (L1CAM; L1-CAM; CD171) antigen and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon re-infusion into the patient, the autologous anti-L1CAM-CAR-EGFRt-expressing T cells are directed to and induce selective toxicity in L1CAM-expressing tumor cells. L1CAM, a neuronal cell adhesion molecule and member of the L1 protein family, plays a key role in the development of the nervous system; it is overexpressed in various tumor cell types and is associated with increased chemoresistance, tumor progression, migration and metastasis. Devoid of both ligand-binding domains and tyrosine kinase activity, EGFRt facilitates both the detection of the administered T cells in vivo and the elimination of the modified T cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response.

Autologous Anti-LGR5 CAR-T Cells CNA3103

A preparation of autologous T-lymphocytes transduced to express a chimeric antigen receptor (CAR) targeting the cancer stem cell (CSC) marker leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-LGR5 CAR-T cells CNA3103 selectively target, binds to and lyse LGR5-expressing tumor cells. LGR5, a member of the Wnt signaling pathway, is overexpressed on certain cancer cells; it plays a key role in CSC proliferation and survival, tumor initiation, growth, and metastasis. Its expression is linked to poor survival and poor patient response to therapy. CNA3103 contains the antigen-biding domain of the humanized monoclonal LGR5 antibody BNC101.

autologous anti-LILRB4 CAR-T cells

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a T-cell-receptor (TCR) complex-based chimeric antigen receptor (CAR) specific for two different epitopes of the immune inhibitory receptor leukocyte immunoglobulin-like receptor B member 4 (LILRB4; ILT3; ILT-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, autologous anti-LILRB4 CAR-T cells target and bind to two different epitopes of LILRB4 expressed on tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against LILRB4-expressing tumor cells. LILRB4, a tumor associated antigen (TAA) and an immune inhibitory receptor expressed on immune suppressive myeloid cells, is highly expressed on certain hematologic cancer cells, such as monocytic acute myeloid leukemia (AML) cells. It functions as an immune checkpoint that negatively regulates T-cell activation as its extracellular domain inhibits T-cell activity. It plays an important role in tumor infiltration, T-cell suppression and immune tolerance.

autologous anti-MAGE-A1 TCR-engineered T cells TSC-204-A0201

A preparation of autologous T lymphocytes that are engineered to express a T-cell receptor (TCR) specific for melanoma-associated antigen A1 (MAGE-A1) presented on human leukocyte antigen (HLA)-A*02:01, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MAGE-A1 TCR-engineered T cells TSC-204-A0201 specifically recognize and bind to MAGE-A1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing MAGE-A1. MAGE-A1 is a tumor-associated antigen (TAA) overexpressed by a variety of cancer cell types.

autologous anti-MAGE-A1 TCR-engineered T cells TSC-204-C0702

A preparation of autologous T lymphocytes that are engineered to express a T-cell receptor (TCR) specific for melanoma-associated antigen A1 (MAGE-A1) presented on human leukocyte antigen (HLA)-C*07:02, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MAGE-A1 TCR-engineered T cells TSC-204-C0702 specifically recognize and bind to MAGE-A1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing MAGE-A1. MAGE-A1 is a tumor-associated antigen (TAA) overexpressed by a variety of cancer cell types.

autologous anti-MART-1 F5 T-cell receptor gene-engineered peripheral blood lymphocytes

Human autologous peripheral blood lymphocytes (PBLs) transduced with a melanoma antigen MART-1 epitope-determined T cell receptor (TCR) gene, with potential antineoplastic activity. PBLs are isolated from a melanoma patient and pulsed with a viral vector that encodes the TCR specific for an epitope of MART-1 (F5 TCR). After expansion ex vivo, the transduced autologous PBLs, expressing this specific TCR, are reintroduced into the patient, and bind to melanoma cells expressing the MART-1 antigen, which may result in specific cytotoxic T-lymphocyte (CTL) killing of MART-1-expressing melanoma cells. MART-1 (melanoma antigen recognized by T cells 1), also known as Melan-A, is a melanocyte lineage-specific transmembrane protein.

autologous anti-MART-1 F5 TCR tumor infiltrating lymphocytes

A preparation of human tumor infiltrating lymphocytes (TILs) isolated from a melanoma patient and engineered to encode a T-cell receptor (TCR) specific for an epitope of MART-1 (F5 TCR), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MART-1 F5 TCR TILs may recognize and halt the growth of MART-1-expressing melanoma cells.

autologous anti-mesothelin CAR-CD3zeta-4-1-BB-expressing T cells

A preparation of autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-mesothelin M5 single chain variable fragment (scFv) fused to the costimulatory domains of 4-1BB (CD137) and the zeta chain of the TCR/CD3 complex (TCRzeta; CD247; CD3zeta), with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture and reintroduction into the patient, the autologous anti-mesothelin CAR-CD3zeta-4-1BB-expressing T cells specifically target and induce selective toxicity in mesothelin-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous anti-mesothelin CAR-IL-7-CCL19-expressing T lymphocytes TAK-103

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN) and simultaneously produce interleukin-7 (IL-7) and C-C motif chemokine 19 (CCL19), with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion and reintroduction into the patient, the autologous anti-MSLN CAR-T cells TAK-103 specifically target and kill MSLN-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. IL-7 promotes the proliferation and survival of T cells. CCL19 enhances the migration of T cells and dendritic cells (DCs).

autologous anti-mesothelin CAR-T cells UCLM802

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MSLN CAR-T cells UCLM802 specifically target and kill MSLN-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous anti-mesothelin KIR-CAR-transduced T cells SynKIR-110

A preparation of autologous T lymphocytes that have been genetically modified to express a killer cell immunoglobulin-like receptor (KIR)-based chimeric antigen receptor (CAR) consisting of an anti-mesothelin (MSLN) single chain variable fragment (scFv) fused to the transmembrane and cytoplasmic domains of the stimulatory KIR 2DS2 (KIR2DS2), and the immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor protein and costimulatory chain DAP12, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MSLN KIR-CAR-transduced T cells SynKIR-110 specifically target and kill MSLN-expressing tumor cells. Mesothelin, a tumor-associated antigen (TAA) and cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. KIR is normally expressed by natural killer (NK) cells, and KIR-based CAR may decrease T-cell exhaustion and enhance T-cell persistence.

autologous anti-mesothelin M28z1XXPD1DNR CAR-expressing T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN) linked to the signaling domains for the co-stimulatory molecules CD28 and CD3 zeta, as well as a PD-1 dominant negative receptor (DNR), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MSLN M28z1XXPD1DNR CAR-expressing T-cells specifically target and kill MSLN-expressing tumor cells. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. PD-1 DNR lacks the PD-1 transmembrane and intracellular signaling domains and acts as a decoy receptor, thereby blocking PD-1-mediated signaling. This may decrease T-cell exhaustion and may enhance T-cell activity against MSLN-expressing tumor cells.

autologous anti-mesothelin T-cell receptor fusion construct/PD-1:CD28 switch receptor-expressing T cells TC-510

A preparation of autologous T lymphocytes that have been genetically engineered to express a single-domain antibody that recognizes human tumor-associated antigen (TAA) mesothelin (MSLN), fused to the N-terminus of the CD3-epsilon T-cell receptor (TCR) subunit which, upon expression is incorporated into the endogenous TCR complex, and a PD-1:CD28 switch receptor composed of the extracellular ligand binding domain of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1) fused to the transmembrane and cytoplasmic co-stimulatory signaling domains of CD28, with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, autologous anti-MSLN TCR fusion construct/PD-1:CD28 switch receptor-expressing T cells TC-510 specifically target and bind to MSLN-expressing tumor cells. This leads to T-cell activation and T-cell mediated lysis of MSLN-expressing tumor cells. The switch receptor expressed by the engineered T cells TC-510 targets and binds to the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2), expressed on tumor cells. The nature of the PD-1/CD28 switch receptor fusion protein prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T-lymphocytes. This induces enhanced toxicity against tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous anti-mesothelin TCR-expressing T cells FH-TCR TMSLN

A preparation of autologous T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) human mesothelin (TMSLN), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-mesothelin TCR-expressing T cells FH-TCR TMSLN specifically target and bind to mesothelin-expressing tumor cells. This leads to T-cell activation and T-cell mediated lysis of mesothelin-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous anti-mesothelin TNhYP218 CAR T cells

A preparation of autologous T lymphocytes containing primarily naive and stem cell-like memory (scm) T cells that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the membrane-proximal region of the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. Upon administration, autologous anti-MSLN TNhYP218 CAR T cells specifically target the membrane-proximal region of MSLN and kill MSLN-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types. Targeting the membrane-proximal region of MSLN may increase the killing of tumor cells and improve T-cell persistence. Naive and scm T cells may exhibit increased persistence and decreased exhaustion.

autologous anti-MG7-CAR T lymphocytes

A preparation of autologous, engineered T lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.

autologous anti-MSLN CAR/HLA-A*02-gated inhibitory receptor/B2M shRNA-expressing T lymphocytes A2B694

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector expressing an activating chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) mesothelin (MSLN), a leukocyte immunoglobulin-like receptor 1 (LIR-1)-based inhibitory receptor specific for human leukocyte antigen (HLA)-A*02 (HLA-A*02), and a short hairpin RNA (shRNA) targeting beta-2 microglobulin (B2M; beta2M), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous anti-MSLN CAR/HLA-A*02-gated inhibitory receptor/B2M shRNA-expressing T lymphocytes A2B694 target and bind to MSLN-expressing tumor cells, thereby killing MSLN-expressing tumor cells that have loss of heterozygosity (LOH) for HLA-A*02 protein. The inhibitory receptor specific for HLA-A*02 acts as a self-regulated safety switch that blocks the killing of HLA-A*02-positive MSLN-expressing normal, healthy cells. HLA-A*02 is expressed on normal cells but not on tumor cells due to LOH. The B2M shRNA disrupts the expression of the B2M component of the HLA class I molecule. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous anti-MUC1*-CAR-4-1BB-CD3zeta-expressing T lymphocytes

A preparation of autologous T lymphocytes transduced with a lentiviral vector encoding a human CD8 alpha leader sequence, a humanized MNC2-single chain variable fragment (scFv) targeting the extracellular domain of the cleaved form of mucin-1 (MUC-1), known as MUC1*, portions of human CD8 hinge and transmembrane domains, and human 4-1BB and human CD3-zeta costimulatory domains, with potential antineoplastic and immunostimulating activities. Upon re-introduction into the patient, the autologous anti-MUC1*-CAR-4-1BB-CD3zeta-expressing T lymphocytes specifically recognize and induce selective toxicity in MUC1*-expressing tumor cells. MUC1* is a post-translationally modified form of MUC1, a single pass type I transmembrane protein that is normally expressed in the glandular or luminal epithelial cells of the esophagus, stomach, duodenum, pancreas, uterus, prostate, and lungs, and may be aberrantly expressed in certain tumor types. MUC1* is a growth factor that is activated by ligand-induced dimerization of its extracellular domain, which may stimulate mitogen-activated protein kinase (MAP kinase, MAPK) signaling and promote tumor cell growth. MUC1* is frequently expressed in certain cancer types, with increased expression noted in higher grade lesions and tumor cells resistant to certain chemotherapies.

autologous anti-Muc1/CD33/CD38/CD56/CD123 gene-engineered CAR-T cells

A preparation of genetically modified autologous T cells transduced with lentiviral vectors expressing chimeric antigen receptors (CARs) specific for the tumor-associated antigens (TAAs) mucin 1 (Muc1; MUC1), cluster of differentiation 33 (CD33), CD38, CD56 and CD123 (interleukin-3 receptor alpha chain or IL3RA), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-Muc1/CD33/CD38/CD56/CD123 gene-engineered CAR-T cells are directed to and induce selective toxicity in Muc1/CD33/CD38/CD56/CD123-expressing tumor cells. Muc1/CD33/CD38/CD56/CD123 are present on certain tumor cell types and are minimally expressed on normal, healthy cells. Expression of these TAAs are correlated with poor prognosis. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules included in the CARs, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous anti-MUC16 CAR-mbIL15-safety switch T cells PRGN-3005

A preparation of autologous T lymphocytes that have been genetically modified to co-express three transgenes using the Sleeping Beauty (SB) transposon system and include a chimeric antigen receptor (CAR) targeting the unshed portion of the tumor-associated antigen (TAA) human mucin 16 (MUC16, cancer antigen 125; CA125; FLJ14303), a membrane-bound IL-15 (mbIL15) and a safety/kill switch, with potential immunostimulating and antineoplastic activities. Upon introduction of the autologous anti-MUC16 CAR-mbIL15-safety switch T cells PRGN-3005 into the patient, the T cells target and bind to MUC16-expressing tumor cells, thereby inducing selective toxicity in MUC16-expressing tumor cells. MUC16, a member of the mucin family of glycoproteins, is overexpressed on a variety of cancer cell types. IL-15 is a pro-survival cytokine that is required for the maintenance of long-lived CD8+ memory T cells and use of mbIL15 preserves T stem-cell memory (TSCM) through sustained IL-15 signaling, improves T-cell persistence and potentiates the immune response against tumor cells. The safety switch can promote selective elimination of the CAR-T cells. The SB system permits integration of the CAR, the IL-15 fusion variant and safety switch transgenes into T cells without the need for viral vectors and accelerates the manufacturing process.

autologous anti-NKG2D/anti-CLDN18.2 bispecific CAR T cells KD-496

A preparation of autologous T lymphocytes that have been genetically modified to express a tandem chimeric antigen receptor (CAR) targeting the tumor-associated antigens (TAAs) natural-killer group 2, member D ligands (NKG2DLs) and Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-NKG2DL/anti-CLDN18.2 bispecific CAR-T cells KD-496 specifically and simultaneously recognize and induce selective toxicity in tumor cells expressing NKG2DLs and CLDN18.2. Ligands for NKG2D, such as MHC class I chain-related protein A (MICA), MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on infected cells and most cancer cell types, but are not expressed on most normal, healthy cells. CLDN18.2, a tight junction protein, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa.

autologous anti-NKG2DLs CAR-T cells LEU011

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting natural-killer group 2, member D ligands (NKG2DLs), with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-NKG2DLs CAR-T cells LEU011 specifically recognize and induce selective toxicity in tumor cells expressing NKG2DLs. Ligands for NKG2D, such as MHC class I chain-related protein A (MICA), MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on various cancer cell types, but are not expressed on most normal, healthy cells.

autologous anti-NY-ESO-1 mTCR retroviral vector-transduced PBLs

Human autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding both alpha and beta chains of a murine T-cell receptor (mTCR) specific for the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-NY-ESO-1 mTCR retroviral vector transduced PBLs bind to NY-ESO-1 expressed on tumor cells. This may result in cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types.

autologous anti-NY-ESO-1 TCR/CD8alpha-expressing T cells GSK3901961

A preparation of human autologous T lymphocytes that are genetically modified to express a T-cell receptor (TCR) specific for the human cancer-testis antigen NY-ESO-1 and the CD8alpha co-receptor, with potential immunostimulating and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-NY-ESO-1 TCR/CD8alpha-expressing T cells GSK3901961 recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. Co-expression of CD8alpha may broaden the immune response against tumors and increase antitumor activity by converting CD4+ helper T cells into CD8+ cytotoxic T cells.

autologous anti-NY-ESO-1 TCR/dnTGF-BRII-expressing T cells GSK3845097

A preparation of human autologous T lymphocytes that are genetically modified to express a T-cell receptor (TCR) specific for the human cancer-testis antigen NY-ESO-1 and a dominant negative (dn) form of transforming growth factor-beta (TGF-beta; TGFb) receptor (dnTGF-BRII), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous anti-NY-ESO-1 TCR/dnTGF-BRII-expressing T cells GSK3845097 recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. The inclusion of dnTGF-BRII blocks the signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the GSK3845097 T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression.

autologous anti-PD-1 antibody-activated tumor-infiltrating lymphocytes

A preparation of autologous tumor infiltrating lymphocytes (TILs) activated by an anti-programmed cell death protein 1 (PD1) antibody, with potential immunomodulating activity. The autologous TILs are isolated from an autologous tumor sample and ex-vivo activated in the presence of anti-PD-1 antibody. Upon infusion of the autologous anti-PD1 antibody-activated TILs back into the patient, the cells specifically target and kill the patient's tumor cells.

autologous anti-PD-L1-armored anti-CD22 CAR T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) CD22 and carrying a single-chain variable fragment (scFv) of a monoclonal antibody targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunomodulatory and antineoplastic activities. Upon infusion, the autologous anti-PD-L1-armored anti-CD22 CAR T cells target and bind to CD22-expressing tumor cells, thereby inducing selective toxicity in CD22-expressing tumor cells. The scFv moiety binds to PD-L1, blocking the binding of PD-L1 to its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), thereby preventing PD-1 activation on T lymphocytes. This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types and plays a key role in the downregulation of the immune system and tumor evasion from host immunity. PD-1, found on activated T cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. CD22, a cell surface glycoprotein, is expressed on mature B cells and on most malignant B cells.

autologous anti-PRAME TCR/CD8alphabeta-expressing T cells IMA203CD8

A preparation of autologous T lymphocytes that are genetically modified with a lentiviral vector encoding a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) preferentially expressed antigen in melanoma (PRAME) and a CD8alphabeta (CD8ab) co-receptor, with potential immunostimulating and antineoplastic activities. Upon administration back into the patient, the autologous anti-PRAME TCR/CD8ab-expressing T cells IMA203CD8 specifically recognize and bind to PRAME expressed on cancer cells, which induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against the PRAME-expressing cancer cells. PRAME is overexpressed by a variety of cancer cell types. Co-expression of the CD8ab heterodimer may enhance anti-tumor immune response by engaging CD4+ T cells.

autologous anti-PSCA-CAR-4-1BB/TCRzeta-CD19t-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been immunomagnetically depleted of CD14+ myeloid cells and CD25+ regulatory T cells (Tregs), activated with anti-CD3 and anti-CD28 beads, and transduced with a self-inactivating (SIN) lentiviral vector (LV) encoding a chimeric antigen receptor (CAR) containing a prostate stem cell antigen (PSCA)-specific, humanized and affinity matured A11 single chain variable fragment (scFv), a human immunoglobulin G4 (IgG4) Fc spacer lacking the CH2 domain, a human CD4 transmembrane domain, a costimulatory human 4-1BB (CD137) cytoplasmic signaling domain linked to the zeta chain of the human T-cell receptor (TCR)/CD3 complex (CD3zeta), and a truncated human CD19 sequence (CD19t), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion, the autologous anti-PSCA-CAR-4-1BB/TCRzeta-CD19t-expressing T lymphocytes recognize and induce selective toxicity in PSCA-expressing tumor cells. PSCA, a glycosyl-phosphatidylinositol (GPI)-linked cell surface antigen, is uniquely and highly expressed in certain cancers including bladder, pancreatic, and prostate cancers. Co-expression of CD19t provides an inert, non-immunogenic surface marker that allows for measurement of genetically modified cells and tracking of T cells following adoptive transfer. The costimulatory signaling domains improve T-cell function, selectivity, expansion and survival.

autologous anti-PSMA CAR T cells P-PSMA-101

A preparation of autologous T cells that are enriched to be primarily stem memory T cells (Tscm) and are transfected by electroporation with a proprietary transposon-based DNA plasmid vector (PiggyBac), encoding both a chimeric antigen receptor (CAR) based on a proprietary non-immunoglobulin scaffold molecule Centyrin (CARTyrin), which specifically recognizes the tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA), and a human-derived safety switch that can be activated by rimiducid, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-PSMA CAR T cells P-PSMA-101 specifically recognize and induce selective toxicity in PSMA-expressing tumor cells. Use of CARTyrin may elicit less immunotoxicity than CAR T cells based on antibody-derived single chain variable fragments (scFv), and may allow for increased persistence and decreased exhaustion for the administered T cells. If significant side effects occur, the safety switch mechanism can be activated by the administration of rimiducid, which results in the rapid attenuation or elimination of P-PSMA-101. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.

autologous anti-PSMA CAR/CD2/dnTGF-BRII/PD-1:CD28 switch receptor-expressing T cells TmPSMA-02

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) consisting of an anti-prostate specific membrane antigen (PSMA) single chain variable fragment (scFv) and the co-stimulatory domain CD2, a dominant negative (dn) form of transforming growth factor-beta (TGF-beta; TGFb) receptor (dnTGF-BRII), and a PD-1:CD28 switch receptor composed of the extracellular ligand binding domain of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1) fused to the transmembrane and cytoplasmic co-stimulatory signaling domains of CD28, with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, autologous anti-PSMA CAR/CD2/dnTGF-BRII/PD-1:CD28 switch receptor-expressing T cells TmPSMA-02 are directed to and induce selective toxicity in PSMA-expressing tumor cells. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors. The inclusion of dnTGF-BRII blocks the signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the TmPSMA-02 T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression. The PD-1:CD28 switch receptor expressed by the TmPSMA-02 T cells targets and binds to the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2), expressed on tumor cells. The nature of the PD-1/CD28 switch receptor fusion protein prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T lymphocytes. This induces enhanced toxicity against tumor cells.

autologous anti-PSMA gene-modified T lymphocytes

Autologous prostate specific membrane antigen (PSMA) gene-modified T lymphocytes with potential antineoplastic activity. Human autologous T lymphocytes are isolated and transduced ex vivo with a retrovirus encoding a chimeric immune receptor (CIR) consisting of an antibody fragment against PSMA fused with signaling domains of the T cell. Upon reintroduction into the patient, autologous anti-PSMA gene-modified T cells bind to PSMA-expressing prostate cancer cells, which may result in specific cytotoxic T-lymphocyte (CTL) tumor cell killing.

autologous anti-ROR1 CAR T cells LYL797

A preparation of genetically and epigenetically reprogrammed autologous T lymphocytes transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) targeting the receptor tyrosine kinase-like orphan receptor 1 (ROR1), with potential immunomodulatory and antineoplastic activities. After isolation, transduction, and expansion in culture, the autologous anti-ROR1 CAR T cells LYL797 are reintroduced into the patient and are directed to tumor cells expressing ROR1, which may result in a selective toxicity against, and lysis of ROR1-expressing tumor cells. ROR1 is expressed during embryogenesis and upregulated in certain tumor types. High levels of ROR1 expression often correlate with poor prognosis. Due to the genetically and epigenetically modifications, LYL797 may overcome T-cell exhaustion and inability to self-renew. The T cells are genetically modified to overexpress the protein c-Jun and thereby resist exhaustion and restore their anti-tumor activity. Also, the T cells are reprogrammed to give them durable stemness and effector function.

autologous anti-ROR1 CAR-mbIL15-safety switch/intrinsic PD-1 blockade T cells PRGN-3007

A preparation of autologous T lymphocytes engineered to express, using a single non-viral multicistronic transposon plasmid, a chimeric antigen receptor (CAR) targeting the receptor tyrosine kinase-like orphan receptor 1 (ROR1), membrane-bound IL-15 (mbIL15), a kill switch and an intrinsic programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) checkpoint blockade, with potential immunomodulatory and antineoplastic activities. After isolation, non-viral gene transfer, and expansion in culture, the autologous anti-ROR1 CAR-mbIL15-safety switch/intrinsic PD-1 blockade T cells PRGN-3007 are reintroduced into the patient and are directed to tumor cells expressing ROR1, which may result in a selective toxicity against, and lysis of ROR1-expressing tumor cells. ROR1 is expressed during embryogenesis and upregulated in certain tumor types with minimal expression in healthy adult tissues. High levels of ROR1 expression often correlate with poor prognosis. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against ROR1-expressing tumor cells. mbIL15 enhances T-cell expansion and persistence through sustained IL-15 signaling. The kill switch allows for improved safety as it can promote selective elimination of the CAR-T cells upon treatment with the kill switch activator antibody.

autologous anti-ROR1 CAR-T cells BMS-986403

A preparation of autologous T lymphocytes genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) receptor tyrosine kinase-like orphan receptor 1 (ROR1), with potential immunomodulatory and antineoplastic activities. After isolation, transduction, expansion and reintroduction into the patient, the autologous anti-ROR1 CAR-T cells BMS-986403 are directed to, bind to, and induce selective toxicity in tumor cells expressing ROR1. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in various hematological and solid malignancies. It plays key roles in tumor cell proliferation and survival.

autologous anti-ROR1 CAR-T cells ONCT-808

A preparation of autologous T lymphocytes transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) targeting the receptor tyrosine kinase-like orphan receptor 1 (ROR1; neurotrophic tyrosine kinase receptor-related 1; NTRKR1), with potential immunomodulatory and antineoplastic activities. After isolation, transduction, and expansion in culture, the autologous anti-ROR1 CAR-T cells ONCT-808 are reintroduced into the patient and are directed to tumor cells expressing ROR1, which may result in a selective toxicity against, and lysis of ROR1-expressing tumor cells. ROR1 is expressed during embryogenesis and upregulated in certain tumor types. High levels of ROR1 expression often correlate with poor prognosis.

autologous anti-siglec-6 CAR-T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting sialic acid-binding immunoglobulin (Ig)-like lectin 6 (Siglec-6) and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous anti-Siglec-6 CAR-T cells target and bind to Siglec-6-expressing tumor cells, thereby inducing selective toxicity in Siglec-6-expressing tumor cells. Siglec-6 is overexpressed in certain malignancies, including acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), and not expressed in normal hematopoietic stem and progenitor cells (HSPCs).

autologous anti-SLAMF7 CAR-expressing T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) recognizing human SLAM family member 7 (SLAMF7; CD319 CRACC; CS-1) with potential antineoplastic activity. Upon intravenous administration, the autologous anti-SLAMF7 CAR-expressing T cells target and induce selective toxicity in SLAMF7-expressing tumor cells. SLAMF7 is a member of the signaling lymphocytic activation molecule (SLAM) family of transmembrane receptors that modulate the function of immune cells through immunoreceptor tyrosine-based switch motifs (ITSMs) and intracellular adaptor proteins. SLAMF7 is highly expressed on certain malignant plasma cells and is minimally expressed on healthy immune cells.

autologous anti-TIM-3/anti-CD123 CAR T cells

A preparation of autologous T cells engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD123 (interleukin-3 receptor alpha chain; IL3RA) and the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-TIM-3/anti-CD123 CAR T cells target and bind to both CD123 and TIM-3 that are both expressed on the surface of leukemic stem cells (LSCs) in acute myeloid leukemia (AML). This induces selective toxicity in CD123- and TIM-3-expressing LSCs. CD123, the alpha subunit of the IL-3 receptor, regulates the proliferation, survival and differentiation of hematopoietic cells. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression. TIM-3 has a higher specificity for LSC than CD123, whose expression is not limited to cancer cells. TIM-3 is not expressed on normal hematopoietic stem progenitor cells (HSCP), granulocytes, and macrophages. Targeting both TIM-3 and CD123 may reduce the on-target off-tumor effect and improve efficacy.

autologous anti-TM4SF1 CAR-T cells

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) transmembrane 4 L six family member 1 (TM4SF1) and containing a safety/kill switch composed of a truncated form of the human epidermal growth factor receptor (ErbB1t; EGFRt HER1t), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous anti-TM4SF1 CAR-T cells specifically recognize and bind to TM4SF1-expressing tumor cells, resulting in tumor cell lysis. TM4SF1 plays a key role in the regulation of cell development, activation, growth and motility, and is overexpressed by a variety of tumor cells.

autologous AXL-targeted CAR-T cells CCT301-38

A preparation of genetically modified autologous T lymphocytes transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) targeting the receptor tyrosine kinase (RTK) AXL, with potential immunomodulatory and antineoplastic activities. After isolation, transduction, and expansion in culture, the CCT301-38 cells are reintroduced into the patient and are activated within the tumor microenvironment (TME) using proprietary Conditionally Active Biologic (CAB) technology. Upon activation, CAB antibodies bind to a proprietary T-cell signaling domain, promoting T-cell recognition and killing of AXL-expressing tumor cells. AXL is a RTK and oncogene that is overexpressed in many cancer types and is involved in the stimulation of tumor cell proliferation.

autologous B-cell/monocyte-presenting HER2/neu antigen vaccine BVAC-B

An autologous vaccine composed of the antigen presenting cells (APCs) B lymphocytes and monocytes presenting the tumor-associated antigen (TAA) human epidermal growth factor receptor type 2 (HER2/neu; HER-2; EGFR2; ErbB2). Upon administration of the autologous B-cell- and monocyte-presenting HER2/neu antigen vaccine BVAC-B, the APCs may stimulate the immune system to mount a HER2/neu-specific cytotoxic T-lymphocyte (CTL) immune response as well as a natural killer (NK) cell, and antibody-mediated immune response against HER-2/neu-positive tumor cells, which may result in tumor cell death and decreased tumor growth. HER-2, a tyrosine kinase receptor for epidermal growth factor (EGF), is overexpressed by a variety of tumors.

autologous B7-H3/EGFR806/HER2/IL13-zetakine CAR-expressing CD4+/CD8+ T cells SC-CAR4BRAIN

A preparation of autologous CD4+ and CD8+ T lymphocytes transduced with a lentiviral vector to express four chimeric antigen receptors (CARs) targeting the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), epidermal growth factor receptor (EGFR) mAb806 epitope, human epidermal growth factor 2 (HER2; ErbB2; HER-2), and interleukin-13 receptor alpha 2 (IL13Ra2), with potential immunostimulating and antineoplastic activities. Upon administration, autologous B7-H3/EGFR806/HER2/IL13-zetakine CAR-expressing CD4+/CD8+ T cells SC-CAR4BRAIN target and bind to tumor cells that express B7-H3, EGFR mAb806 epitope, HER2 and IL13Ra2, thereby inducing selective toxicity in these cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance. EGFR806 CAR specifically targets abnormal conformational states of EGFR, including EGFR deletion mutation variant III (EGFRvIII), and activating mutations, with lower affinity for wild-type EGFR. HER2 is overexpressed in a variety of cancer cell types and is associated with increased tumor cell proliferation. IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell types including glioblastoma multiforme (GBM); it is associated with increased invasiveness of tumor cells.

autologous BAFF-expressing CAR T cells LMY-920

A preparation of autologous cluster of differentiation 4 (CD4) -and CD8 positive T lymphocytes that are genetically engineered, using the non-viral transposon system, to express a chimeric antigen receptor (CAR) expressing the B-cell activating factor (BAFF) ligand and targeting BAFF receptor family members, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous BAFF-expressing CAR T cells LMY-920 are directed to, specifically bind to, and induce selective toxicity in tumor cells expressing any of the three BAFF receptor family members, including BAFF receptor (BAFF-R), B-cell maturation antigen (BCMA), and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI). Almost all B-cell cancers are reported to express at least one of these three receptors which play a key role in the regulation of peripheral B-cell survival.

autologous BAFFR-targeting CAR T cells

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) B-cell activating factor receptor (BAFFR; tumor necrosis factor receptor superfamily member 13C; TNFRSF13C; BLyS receptor 3; BR3), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous BAFFR-targeting CAR T cells are directed to and induce selective toxicity in BAFFR-expressing tumor cells. BAFFR, a protein belonging to the TNF receptor superfamily, is expressed on the surface of certain types of cancer cells, including B-cell acute lymphoblastic leukemia. It plays a key role in the regulation of peripheral B-cell survival.

autologous base edited CD34+ HSPCs BEAM-101

A population of autologous cluster of differentiation 34 (CD34)-positive human hematopoietic stem and progenitor cells (HSPCs) ex-vivo base-edited with fusions of a deaminase and clustered regularly interspaced short palindromic repeats (CRISPR)-Cas ribonucleoprotein, with potential usage for transplantation in patients with sickle cell disease (SCD). CD34-positive HSPCs are isolated from human blood upon apheresis and are genetically modified and base-edited ex vivo to disrupt the HBG1/HBG2 gene promoter motif bound by the transcriptional repressor B-cell lymphoma/leukemia 11A (BCL11A) gene. This increases the expression of fetal hemoglobin (HbF) and inhibits hemoglobin S (HbS) polymerization in erythrocytes that differentiate from BEAM-101. Upon infusion back into the patient following myeloablative, conditioning chemotherapy, BEAM-101 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. The increased production of high levels of HbF in red blood cells (RBCs) compensates for the defective or reduced adult hemoglobin (Hb) in patients with SCD. HbF is a form of the oxygen carrying Hb that is naturally present at birth and is then replaced by the adult form of hemoglobin.

autologous BCL11A-disrupted human hematopoietic stem and progenitor cells HIX763

A population of autologous human hematopoietic stem and progenitor cells (HSPCs) that are genetically modified to disrupt the activity of B-cell lymphoma/leukemia 11A (BCL11A), with potential usage for transplantation in patients with sickle cell disease (SCD). Upon infusion into the patient, the autologous BCL11A-disrupted HSPCs HIX763 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. As BCL11A is a suppressor of fetal hemoglobin (HbF; hemoglobin F) expression, disruption of the expression of BCL11A stimulates the expression of HbF in erythrocytes that differentiate from HIX763. HbF may compensate for reduced or absent expression of adult hemoglobin (Hb) in patients with SCD. HbF is a form of the oxygen carrying Hb that is naturally present at birth and is then replaced by the adult form of hemoglobin.

autologous BCMA-4-1BBz-targeted CAR T cells

A preparation of autologous T lymphocytes that have been ex vivo transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) containing a single chain variable fragment (scFv) specific for the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137), and the CD3-zeta (CD3z) T-cell signaling domain (4-1BBz), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous BCMA-4-1BBz-targeted CAR-T cells specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells; it is overexpressed on malignant plasma cells, and plays a key role in plasma cell survival.

autologous BCMA-targeted CAR T cells LCAR-B4822M

A preparation of autologous peripheral blood T lymphocytes (PBTLs) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous BCMA-targeted CAR T cells LCAR-B4822M specifically recognize and kill BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous BCMA-targeted CAR-T cells CC-98633

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, autologous BCMA-targeted CAR-T cells CC-98633 specifically recognize and kill BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous BCMA/TACI-targeted CAR T cells AUTO2

A preparation of autologous T lymphocytes that are genetically engineered to contain a dual-targeted chimeric antigen receptor (CAR), which includes the natural protein a proliferation-inducing ligand (APRIL; TNFSF13), that targets the tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; TNFRSF17) and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI; TNFRSF13B), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous BCMA/TACI-targeted CAR T cells AUTO2 bind to BCMA and TACI expressed on tumor cells and induce selective cytotoxicity in those cells. In addition, AUTO2 carries the universal RQR8 safety "off" switch, which allows selective removal of the T cells through both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) following administration of rituximab if unacceptable side-effects occur.

autologous BCMA/TACI-targeted trimeric APRIL-based CAR T cells

A preparation of autologous T lymphocytes that are genetically engineered to contain a dual-targeted chimeric antigen receptor (CAR), which includes a trimeric form of the natural protein a proliferation-inducing ligand (APRIL; TNFSF13), that targets the tumor-associated antigens (TAAs) B-cell maturation antigen (BCMA; TNFRSF17) and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI; TNFRSF13B), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous BCMA/TACI-targeted trimeric APRIL-based CAR T cells bind to BCMA and TACI expressed on tumor cells and induce selective cytotoxicity in those cells. BCMA and TACI, receptors for both APRIL and B-cell activating factor (BAFF), are members of the tumor necrosis factor receptor superfamily (TNFRSF). They are both found on the surfaces of plasma cells, overexpressed on malignant plasma cells and play key roles in plasma cell proliferation and survival. The incorporation of the trimeric, natural conformation of APRIL into the CAR enhances the binding to BCMA and TACI compared with the monomeric form of APRIL.

autologous bispecific BCMA/CD19-targeted CAR T cells GC012F

A preparation of autologous T lymphocytes engineered to express two separate chimeric antigen receptors (CARs) targeting the tumor-associated antigens (TAAs) BCMA and CD19 and fused to as of yet not fully elucidated co-stimulatory domains, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous bispecific BCMA/CD19-targeted CAR T cells GC012F specifically and simultaneously target and bind to tumor cells expressing BCMA and/or CD19. This induces selective toxicity in tumor cells that express BCMA and/or CD19. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in the survival of B lymphocytes and plasma cells. BCMA is found on the surfaces of B cells and is overexpressed on malignant plasma cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. The processing platform used, FasT CAR T, shortens the manufacturing time to produce the CAR T cells within 24 hours.

autologous bispecific CD19/CD22-targeted CAR-T cells GC022F

A preparation of autologous human T lymphocytes engineered to express chimeric T-cell receptors (chimeric antigen receptors or CARs) targeting the tumor-associated antigens (TAAs) CD19 and CD22 and fused to as of yet not fully elucidated co-stimulatory domains, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous bispecific CD19/CD22-targeted CAR-T cells GC022 bind to CD19 and CD22 on the surface of, and induce selective toxicity against, tumor cells expressing CD19 and CD22. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are overexpressed on malignant B cells.

autologous bladder cell carcinoma RNAs/CD40L RNA electroporated autologous matured dendritic cells

A cell-based preparation in which autologous, mature dendritic cells (DCs) are electroporated with in vitro transcribed (IVT) RNAs encoding for a synthetic form of T-cell protein CD40 ligand (CD40L) and IVT RNA encoding for autologous tumor-associated antigens (TAAs) derived from patient-specific bladder cell carcinoma (BCC) cells, with potential immunostimulatory and antineoplastic activities. Upon electroporation into autologous DCs, the RNA is translated and processed. BCC-specific antigenic peptides are subsequently presented via major histocompatibility complex (MHC) Class I molecules on the DCs surface. When AGS-003-BLD is reintroduced to the patient, the MHC-presented peptides interact with and activate CD8-positive T cells, which elicits a highly specific cytotoxic T-cell (CTL) response against tumor cells expressing the patient-specific BCC TAAs. The signal cascade initiated by expression of the co-stimulatory molecule CD40L results in the secretion of the inflammatory cytokine IL-12, which further stimulates CTLs.

autologous blinatumomab-expanded T cells

A preparation of autologous, peripheral blood-derived polyclonal activated T cells that have been expanded and activated ex-vivo using blinatumomab and recombinant human IL2 (rhIL-2) and depleted of contaminating CD19+ tumor cells, with potential immunomodulating activity. Upon administration, these blinatumomab-expanded T cells (BET), composed of functional polyclonal CD4+ and CD8+ T cells and mostly effector and central memory cells, may induce immunological recovery. BET cell expansion leads to the lysis and elimination of contaminating CD19+ tumor cells. The elimination of contaminating tumor cells is important in the treatment of non-Hodgkin CD20 + indolent lymphoma (iNHL) and chronic lymphatic leukemia (CLL).

autologous bone marrow-derived CD34/CXCR4-positive stem cells AMR-001

A cell-based product containing autologous bone marrow derived CD34 positive and C-X-C chemokine receptor type 4 (CXCR4) positive stem cells with potential antiapoptotic and proangiogenic activities. Upon intracoronary infusion after a myocardial infarction (MI), autologous bone marrow-derived CD34/CXCR4-positive stem cells may preserve cardiac muscle cells and prevent apoptosis; thus improving myocardial perfusion. CD34/CXCR4-positive stem cells are naturally mobilized upon cell injury through signaling by hypoxia inducing factor (HIF), which is secreted in response to hypoxia. In turn, HIF induces the synthesis of stromal-derived factor 1 (SDF-1) and vascular endothelial growth factor (VEGF) which mobilize CD34/CXCR4 positive stem cells; CXCR4 is the receptor for stromal-derived factor 1 (SDF-1).

autologous c-Met/PD-L1-specific CAR T cells

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for human hepatocyte growth factor receptor (HGFR or c-Met) and the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential antineoplastic activities. Upon infusion, the autologous c-Met/PD-L1-specific CAR T cells bind to and induce selective toxicity in c-Met- and PD-L1-expressing tumor cells. cMET, a receptor tyrosine kinase that is overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis. PD-L1 is also overexpressed by many human cancer cell types and plays a key role in the downregulation of the immune system and tumor evasion from host immunity.

autologous CAR T cells KITE-197

A preparation of autologous T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) with an as of yet undisclosed target, with potential immunomodulating and antineoplastic activities. Upon administration, autologous CAR T cells KITE-197 specifically recognize and kill tumor cells expressing the as of yet undisclosed antigen target. This results in a cytotoxic T-lymphocyte (CTL) response against these tumor cells, thereby causing tumor cell lysis.

autologous CAR T cells RD14-01

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) that targets an as of yet unidentified tumor-associated antigen (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration of autologous CAR T cells RD14-01, the T cells target, bind to and induce selective cytotoxicity in tumor cells expressing the TAA.

autologous CAR T cells U87

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential immunostimulating and antineoplastic activities. Upon administration, autologous CAR T cells U87 specifically targets and binds to tumor cells that express the undisclosed TAA, resulting in tumor cell lysis.

autologous CAR-CD28-expressing T lymphocytes

A preparation of autologous T lymphocytes expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) C-type-lectin-like molecule-1 (CLL1; C-type lectin domain family 12 member A; CLEC12A) linked to the CD28 co-stimulatory signaling domain, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous CLL1-CAR-CD28-expressing T lymphocytes specifically target and bind to CLL1-expressing tumor cells. This induces selective toxicity in tumor cells that express the CLL1 antigen. CLL1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

autologous CAR-engineered regulatory T cells SBT777101

A preparation of autologous T-regulatory cells (Tregs) that have been genetically modified to express a chimeric antigen receptor (CAR) targeting citrullinated proteins, with potential immunmodulating activity. Upon administration, the autologous CAR-engineered regulatory T cells SBT777101 target and bind to citrullinated proteins and may decrease inflammation and promote immunologic homeostasis. Citrullinated proteins are found in inflamed disease-associated tissues in many autoimmune and inflammatory diseases.

autologous CAR-mbIL15-safety switch T cells PRGN-3006

A preparation of autologous T lymphocytes that have been genetically modified to co-express three transgenes using the Sleeping Beauty (SB) transposon system, including a chimeric antigen receptor (CAR) targeting an undisclosed tumor-associated antigen (TAA), a membrane-bound IL-15 (mbIL15) and a safety/kill switch, with potential immunostimulating and antineoplastic activities. Upon introduction of the autologous PRGN-3006 T cells into the patient, these T cells target, bind to and induce selective toxicity in cells expressing this particular TAA. IL-15 is a pro-survival cytokine that is required for the maintenance of long-lived CD8+ memory T cells. Use of mbIL15 preserves T stem cell memory (TSCM) through sustained IL-15 signaling, improves T-cell persistence and potentiates the immune response against tumor cells. The safety switch can promote selective elimination of the CAR-T cells. The SB system permits integration of the CAR, the IL-15 fusion variant and safety switch transgenes into T cells without the need for viral vectors and accelerates the manufacturing process.

autologous CAR-T cells B4T2-001

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential immunostimulating and antineoplastic activities. Upon administration, autologous CAR-T cells B4T2-001 target and bind to the TAA-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against the tumor cells, the release of cytotoxic molecules and the induction of tumor cell lysis.

autologous CCR4-CD30CAR-CD28-CD3zeta-expressing T lymphocytes

A preparation of autologous T lymphocytes (ATL) that have been transduced with the retroviral vector SFG, a Moloney murine leukemia (Mo-MuLV) virus-based vector, encoding human C-C chemokine receptor 4 (CCR4), linked via an internal ribosome entry site (IRES), to a chimeric antigen receptor (CAR) composed of a single chain single-chain variable fragment (scFv) directed against the CD30 antigen (CAR.CD30) and linked, via the spacer human IgG1 immunoglobulin heavy constant region (hinge-CH2CH3 region), to the co-stimulatory domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta), with potential immunostimulating and antineoplastic activities. Upon administration of the autologous CCR4-CD30CAR-CD28-CD3zeta-expressing T lymphocytes, the expressed CCR4 on the T cells allows for enhanced migration of the cells to chemokine-secreting tumor cells. The expressed CAR.CD30 moiety specifically recognizes and binds to CD30-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies. CCR4, a G-coupled-protein receptor for C-C chemokines normally expressed on regulatory T cells (Tregs) but not on cytotoxic T lymphocytes (CTLs), is involved in chemokine-mediated cellular migration. The co-expression of CCR4 on these CTLs may enhance their anti-tumor activity compared to T lymphocytes expressing the same CAR-CD30 receptor but without CCR4 expression.

autologous CD123-4SCAR-expressing T cells 4SCAR123

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-CD123 (interleukin-3 receptor alpha chain or IL3RA) single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (TCR), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous CD123-4SCAR-expressing T cells 4SCAR123 are directed to and induce selective toxicity in CD123-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes

A preparation of genetically modified autologous T-cells transduced with a replication-incompetent, self-inactivating lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR), containing a CD28 co-stimulatory signaling domain fused to CD3 zeta, the single-chain variable fragment of CD123 (interleukin-3 receptor alpha chain or IL3RA) antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes are directed to and induce selective toxicity in CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates detection of the administered T-cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity response. The costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents recognition of the CAR by Fc receptors (FcRs).

autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes MB-102

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD123 (interleukin-3 receptor alpha chain or IL3RA) and linked to the CD28 co-stimulatory signaling domain fused to CD3 zeta, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T lymphocytes MB-102 are directed to and induce selective toxicity in CD123-expressing tumor cells. CD123, a subunit of the heterodimeric interleukin-3-receptor (IL-3R), is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates detection of the administered T cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response.

autologous CD133-positive BTSC mRNA-pulsed autologous dendritic cell vaccine

A cancer vaccine consisting of autologous dendritic cells (DCs) loaded with CD133-positive autologous brain tumor stem cells (BTSCs) –derived mRNA with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, autologous CD133-positive BTSC mRNA-pulsed autologous dendritic cell vaccine may elicit a cytotoxic T-lymphocyte (CTL) response against the CD133-positive BTSCs from which the autologous tumor mRNA is derived. CD133, a tumor-associated antigen (TAA) and neural stem cell marker, has been found on a specific subset of glioblastoma multiforme (GBM) stem cells; its presence has been correlated with resistance to conventional chemotherapy and radiotherapy.

autologous CD138-specific CAR T cells

A preparation of autologous T lymphocytes that have been engineered to express a chimeric antigen receptor (CAR) specific for syndecan-1 (CD138), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous CD138 CAR-expressing T cells target and induce selective toxicity in syndecan-1-expressing tumor cells. Syndecan-1, a type 1 transmembrane proteoglycan and tumor-associated antigen (TAA), is overexpressed in a variety of cancer cells and plays a key role in the regulation of cell growth, differentiation, and adhesion.

autologous CD171-specific CAR-CD28 zeta-4-1-BB-EGFRt-expressing T lymphocytes

A preparation of genetically modified autologous human T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the L1 cell adhesion molecule (L1-CAM/CD171) antigen, and the co-stimulatory signaling domains CD28, 4-1BB (CD137) and CD3 zeta, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon re-infusion into the patient, the autologous L1-CAM-specific CAR-CD28 zeta-4-1-BB-EGFRt-expressing T-lymphocytes are directed to and induce selective toxicity in L1-CAM-expressing tumor cells. L1-CAM, a neuronal cell adhesion molecule and member of the L1 protein family, plays a key role in the development of the nervous system; it is overexpressed in various tumor cell types and is associated with increased chemoresistance, tumor progression, migration and metastasis. Devoid of both ligand-binding domains and tyrosine kinase activity, EGFRt facilitates both the detection of the administered T-cells in vivo and the elimination of the modified T-cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The co-stimulatory signaling domains enhance both proliferation of T-cells and antitumor activity.

autologous CD19 CAR+ EGFRt + CD4+ and CD8+ T cells

A preparation of a defined ratio of CD4+ and CD8+ autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv), derived from the CD19-specific murine immunoglobulin (Ig) G1 monoclonal antibody FMC63, fused to the signaling domain of CD28, the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous CD19 CAR+ EGFRt + CD4+ and CD8+ T cells are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous CD19 CAR-expressing CD4+/CD8+ T cells MB-CART19.1

A preparation of CD4+ and CD8+ autologous T lymphocytes transduced with the lentiviral vector pLTG1563 expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous CD19 CAR-expressing CD4+/CD8+ T cells MB-CART19.1 are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous CD19 CAR-expressing T cells YTB323

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous CD19 CAR-expressing T cells YTB323 are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous CD19-28z chimeric antigen receptor-expressing T lymphocytes

Genetically modified autologous T-lymphocytes transduced with a replication-incompetent retroviral vector expressing a chimeric T-cell antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment), fused to the extracellular, transmembrane and intracellular signaling domains of the T cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (CAR19-28z), with potential antineoplastic activities. Upon intravenous administration, autologous CD19-28z CAR-expressing T-lymphocytes are directed to CD19-expressing tumor cells, which induces selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. The inclusion of the CD28 signaling domain may increase proliferation of T-cells and antitumor activity compared to the inclusion of the CD3-zeta chain alone.

autologous CD19-CD8-CD28-CAR-mbIL15-HER1t T cells

A preparation of autologous T lymphocytes, that have been electroporated ex vivo with sleeping beauty (SB)-derived DNA plasmids encoding a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) that is linked to the co-stimulatory molecules T-cell surface glycoproteins CD8 and CD28 and co-expressed with a chimeric membrane-bound fusion protein comprised of interleukin-15 (IL-15) fused to IL-15 receptor (mbIL15) and a safety/kill switch composed of a truncated form of the human epidermal growth factor receptor (ErbB1t; EGFR)(HER1t), with potential immunostimulating and antineoplastic activities. Upon reintroduction of the autologous CD19-CD8-CD28-CAR-mbIL15-HER1t T cells into the patient, the T cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in all B-cell lineage malignancies. HER1t can promote selective elimination of the CAR T cells through cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). IL-15 is a pro-survival cytokine that is required for the maintenance of long-lived CD8+ memory T cells and the use of mbIL15 preserves T stem-cell memory (TSCM) through sustained IL-15 signaling, improves T-cell persistence and potentiates the immune response against tumor cells. The SB system permits electroporation of the CAR, the IL-15 fusion variant and safety switch transgenes into T cells without the need for viral vectors and accelerates the manufacturing process.

autologous CD19-CD8-CD28-CD3zeta-CAR-mbIL15-HER1t T cells

A preparation of autologous, genetically modified T lymphocytes, that have been electroporated ex vivo with sleeping beauty (SB)-derived DNA plasmids, expressing a second-generation chimeric antigen receptor (CAR) composed of a mouse single-chain variable fragment (scFv) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) that is linked to the co-stimulatory molecules T-cell surface glycoproteins CD8 and CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta) and co-expressed with a chimeric membrane-bound fusion protein comprised of interleukin-15 (IL-15) fused to IL-15 receptor (mbIL15) and a safety/kill switch composed of a truncated form of the human epidermal growth factor receptor (ErbB1t; EGFR) (HER1t), with potential immunostimulating and antineoplastic activities. Upon reintroduction of the autologous CD19-CD8-CD28-CD3zeta-CAR-mbIL15-HER1t T cells into the patient, the T cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. HER1t can promote selective elimination of the CAR-T cells through cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). IL-15 is a pro-survival cytokine that is required for the maintenance of long-lived CD8+ memory T-cells and use of mbIL15 preserves T stem-cell memory (TSCM) through sustained IL-15 signaling, improves T-cell persistence and potentiates the immune response against tumor cells. The SB system permits electroporation of the CAR, the IL-15 fusion variant and safety switch transgenes into T cells without the need for viral vectors and accelerates the manufacturing process.

autologous CD19-targeted CAR T cells CC 97540

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous CD19-targeted CAR T cells CC-97540 specifically target and bind to CD19-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors.

autologous CD19-targeted CAR-T cells GC007F

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19 coupled to as of yet not fully elucidated co-stimulatory molecules, with potential immunostimulating and antineoplastic activities. Upon transfusion, autologous CD19-targeted CAR-T cells GC007F target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, the release of cytotoxic molecules and the induction of tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. The processing platform used, FasT (F) CAR-T, shortens the manufacturing time to produce the CAR-T cells within 24 hours.

autologous CD19/CD22 chimeric antigen receptor T cells CT120

A preparation of autologous human T lymphocytes engineered to express a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of one or more binding domains targeting the tumor-associated antigens (TAAs) CD19 and CD22 and fused to one or more co-stimulatory TCR-signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous CD19/CD22 CAR T cells CT120 bind to CD19 and CD22 on the surface of, and induce selective toxicity against, tumor cells expressing CD19 and CD22. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are overexpressed on malignant B cells.

autologous CD19/PD-1 bispecific CAR-T cells

A preparation of autologous T lymphocytes that are transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) and a programmed cell death protein 1 (PD1)/CD28 chimera, with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, the autologous CD19/PD-1 bispecific CAR-T cells target and bind to CD19 and the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2), expressed on tumor cells. The binding to CD19 leads to a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and cell lysis of these cells. The binding of the PD1/CD28 chimera to PD-L1 prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T lymphocytes. This enhances T-lymphocyte proliferation and anti-tumor activity. CD19 antigen is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. PD-1 protein, found on activated T-cells, negatively regulates T-cell activity. It plays a key role in immune evasion and prevents tumor cell lysis. The construct of the PD1/CD28 chimera converts PD-L1 into a co-stimulation ligand of primary human CD8+ cytotoxic T lymphocytes (CTLs). CD28 is a costimulatory molecule expressed by T cells that enhances T-lymphocyte proliferation and activity.

autologous CD19CAR-CD28-CD137/CD27/CD3zeta-iCasp9-expressing T lymphocytes

Autologous T lymphocytes that have been transduced with a fourth generation-lentiviral vector to express the 4SCAR19 gene composed of a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) of anti-CD19 coupled to the co-stimulatory molecules CD28, 4-1BB (CD137), and CD27, and to the cytoplasmic portion of the zeta chain of the human T-cell receptor (CD3zeta), and containing the apoptosis-inducible suicide gene human caspase 9 (iCASP9 or iC9), that is linked to a drug binding domain, with potential immunostimulating and antineoplastic activities. The iCASP9 construct consists of the entire coding sequence for the human FK506-drug binding protein (FKBP12) with an F36V mutation (FKBP12-F36V) that is linked to the gene encoding iC9, which is a modified form of the CASP9 gene where the sequences encoding the endogenous caspase activation and recruitment domains have been deleted. Upon transfusion, anti-CD19-CAR-CD28/CD137/CD27/CD3zeta-iCasp9-expressing autologous T lymphocytes target and bind to CD19-expressing neoplastic B cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells, and causes tumor cell lysis. If the administered T cells cause unacceptable side effects, the chemical homodimerizer AP1903, which binds to the FKBP12-F36V drug-binding domain, can be administered; this induces caspase 9 expression, and results in apoptosis of the administered 4SCAR19 T cells. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. Incorporation of the costimulatory signaling domains increases human T-cell function, expansion, and survival.

autologous CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T cells

A preparation of genetically modified autologous central memory (Tcm) enriched T cells transduced with a replication incompetent lentiviral vector expressing a chimeric antigen receptor (CAR), containing a CD28 signaling domain fused to both CD3 zeta, which targets the CD19 antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T cells are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. The costimulatory signaling domain enhances proliferation of T cells and antitumor activity.

autologous CD20-4SCAR-expressing T cells 4SCAR20

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-CD20 single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (TCR), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD20-4SCAR-expressing T cells 4SCAR20 are directed to and induce selective toxicity in CD20-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous CD22-4SCAR-expressing T cells 4SCAR22

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-CD22 single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (TCR), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD22-4SCAR-expressing T cells 4SCAR22 are directed to and induce selective toxicity in CD22-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B cells. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous CD30CAR-CD28-CD3zeta-expressing T lymphocytes

A preparation of autologous T lymphocytes (ATL) that have been transduced with the retroviral vector SFG, a Moloney murine leukemia (Mo-MuLV) virus-based vector, encoding a chimeric antigen receptor (CAR) composed of a single chain single-chain variable fragment (scFv) directed against the CD30 antigen (CAR.CD30) and linked, via the spacer human IgG1 immunoglobulin heavy constant region (hinge-CH2CH3 region), to the co-stimulatory domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) (CD28zeta), with potential immunostimulating and antineoplastic activities. Upon administration, the autologous CD30CAR-CD28-CD3zeta-expressing T lymphocytes specifically recognize and bind to CD30-expressing tumor cells, resulting in specific T-cell-mediated tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies.

autologous CD34+ enriched alpha-L-iduronidase-expressing hematopoietic stem cells OTL-203

A gene therapy agent composed of a preparation of autologous CD34-enriched hematopoietic stem cells (HSCs) transduced with a lentiviral vector expressing the endogenous human gene alpha-L-iduronidase (IDUA), that may potentially be used in the treatment of mucopolysaccharidosis type I (MPS I; Hurler syndrome). Upon administration, autologous CD34+ enriched IDUA-expressing HSCs OTL-203 express IDUA, which is an enzyme required for the lysosomal degradation of glycosaminoglycans (GAGs). IDUA hydrolyzes the non-reducing terminal alpha-L-iduronic acid residues in GAGs, including dermatan sulfate and heparan sulfate. IDUA deficiency causes accumulations of heparan sulfate and dermatan sulfate in various organs of the body which leads to progressive damage. Mutations in the IDUA gene are responsible for the deficiency of IDUA.

autologous CD34+-enriched HSPCs transduced with lentiviral vector carrying FANCA gene RP-L102

A preparation of autologous CD34+-enriched hematopoietic stem and progenitor cells (HSPCs) from mobilized peripheral blood of patients with Fanconi anemia subtype A (FA-A) that are transduced ex vivo with a lentiviral vector carrying the FANCA gene, with potential to restore FANCA expression and function. Upon re-infusion of autologous CD34+-enriched HSPCs transduced with lentiviral vector carrying FANCA gene RP-L102 back into the patient, these cells express functional FANCA gene. Mutations in the FANCA gene, common in patients with FA, prevent normal DNA repair which may lead to chromosomal breakage, increased sensitivity to oxidative and environmental stress, and bone marrow failure.

autologous CD34+-enriched HSPCs transduced with LV vector carrying TCIRG1 gene RP-L401

A preparation of autologous CD34+-enriched hematopoietic stem and progenitor cells (HSPCs) from mobilized peripheral blood of patients with infantile malignant osteopetrosis (IMO) that are transduced ex vivo with a lentiviral (LV) vector carrying the T-cell immune regulator 1 (TCIRG1) gene, with potential to restore TCIRG1 expression and function. Upon re-infusion of autologous CD34+-enriched HSPCs transduced with LV vector carrying TCIRG1 gene RP-L401 back into the patient, these cells express functional TCIRG1 gene. Mutations in the TCIRG1 gene, found in some patients with IMO, lead to functional impairment of the proton pump of the osteoclast.

autologous CD34+-enriched HSPCs transduced with VSV-G encoding IFN-a2

A preparation of autologous CD34+-enriched hematopoietic stem and progenitor cells (HSPCs) that are genetically modified with a vesicular stomatitis virus-G (VSV-G) pseudo-typed lentiviral vector encoding for the human cytokine interferon-alpha 2 (IFN-a2) gene, with potential immunostimulating and antineoplastic activities. The expression of IFN-a2 is tightly controlled by the human angiopoietin receptor Tie2 enhancer/promoter sequence, found in the tumor-infiltrating macrophages Tie2 expressing monocytes (TEMs), and is under microRNA-126 (miR-126)-mediated control. This enables suppression of IFN-a2 expression in HSPCs while IFN-a2 is selectively expressed in TEMs. Upon administration of the autologous CD34+-enriched HSPCs transduced with VSV-G encoding IFN-a2, the HSPCs travel to the bone marrow and differentiate into various cells including monocytes and macrophages. These cells travel to the tumor microenvironment (TME), and the TEMs, capable of expressing IFN-a2, specifically release IFN-a2 in the TME. IFN-2a binds to specific IFN cell-surface receptors, and activates IFN-mediated signal transduction, resulting in the transcription and translation of genes containing an interferon-specific response element whose protein products mediate anticancer and anti-angiogenic effects. This results in the induction of both G2 cell cycle arrest and apoptosis in tumor cells. In addition, IFN-a2 triggers an indirect anti-tumor immune response involving the activation of natural killer (NK) cells and dendritic cells (DCs), and the induction of immune effector cell cytotoxicity, thereby further killing tumor cells. TEMs, a subset of tumor-infiltrating macrophages characterized by expression of the tyrosine protein kinase angiopoietin receptor Tie2, are upregulated in the TME while infrequently found in normal organs. TEMs promote tumor angiogenesis.

autologous CD34-positive BCL11A-disrupted hematopoietic progenitor cells BIVV003

A population of autologous cluster of differentiation 34 (CD34)-positive hematopoietic progenitor cells (HPCs) that are transfected ex vivo with zinc finger nuclease (ZFN) messenger ribonucleic acid (mRNA) targeting the B-cell lymphoma/leukemia 11A (BCL11A) locus, with potential usage for transplantation in patients with sickle cell disease (SCD). CD34-positive HPCs are isolated from human blood upon apheresis and are genetically modified in vitro using ZFN technology to specifically cleave and disrupt the erythroid enhancer of the BCL11A gene. This suppresses the production of sickle hemoglobin. Upon infusion into the patient following conditioning chemotherapy, the autologous CD34-positive BCL11A-disrupted HPCs BIVV003 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. As BCL11A is a suppressor of fetal hemoglobin (HbF) expression, disruption of the BCL11A enhancer decreases the expression of BCL11A and stimulates the expression of HbF in erythrocytes that differentiate from BIVV003. HbF may compensate for reduced or absent expression of adult hemoglobin in patients with SCD.

autologous CD34-positive BCL11A-disrupted hematopoietic progenitor cells ST-400

A population of autologous CD34-positive, B-cell lymphoma/leukemia 11A (BCL11A)-disrupted hematopoietic progenitor cells (HPCs) that may be used for bone marrow autotransplantation. CD34-positive HPCs are isolated from human blood upon apheresis and are genetically modified in vitro using a proprietary zinc finger nuclease (ZFN) technology to specifically disrupt the transcriptional enhancer sequence for the BCL11A gene. Upon infusion into the patient following conditioning chemotherapy, the autologous CD34-positive BCL11A-disrupted HPCs ST-400 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. BCL11A is a suppressor of fetal hemoglobin (HbF) expression. Therefore, disruption of the BCL11A enhancer decreases the expression of BCL11A and stimulates the expression of HbF in erythrocytes that differentiate from ST-400. HbF may compensate for reduced or absent expression of adult hemoglobin in patients, including those with transfusion-dependent beta-thalassemia.

autologous CD34-positive hematopoietic progenitor cells

A population of autologous CD34-positive hematopoietic progenitor cells (HPCs) that can be used for autotransplantation. CD34+ HPCs are isolated from human blood stem cells upon apheresis. Upon transplantation with the CD34+ HPCs, these cells can differentiate into a variety of cell types including fibroblasts, osteoblasts, chondrocytes, myocytes, adipocytes, and endothelial cells.

autologous CD34-positive peripheral blood stem cells

A population of autologous cluster of differentiation 34 (CD34)-positive peripheral blood stem cells (PBSCs) that can be used for autologous hematopoietic stem cell transplantation (AHSCT). Upon mobilization and collection of the autologous CD34+ PBSCs by leukapheresis, the CD34+ PBSCs are re-infused into the patient. Upon transplantation, these cells can differentiate into a variety of cell types including the formation of new hematopoietic and immune cells.

autologous CD38-4SCAR-expressing T cells 4SCAR38

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-CD38 single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (TCR), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD38-4SCAR-expressing T cells 4SCAR38 are directed to and induce selective toxicity in CD38-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous CD4+/CD8+ 4-1BB-CD3zeta-EGFR806-CAR-EGFRt/4-1BB-CD3zeta- CD19-CAR-HER2tG-expressing CARs T cells

A preparation of CD4+ and CD8+ autologous T lymphocytes transduced with a lentiviral vector that co-expresses two different second generation chimeric antigen receptors (CARs), one composed of a short chain variable fragment (scFv) binding domain derived from depatuxizumab, a human anti-epidermal growth factor receptor (EGFR) monoclonal antibody (MAb806; ABT-806), coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta) and the signaling domain of 4-1BB (CD137), and linked to a truncated form of the human epidermal growth factor receptor (EGFRt), and one composed of a short chain variable fragment (scFv) binding domain derived from an anti-CD19 monoclonal antibody, coupled to CD3-zeta) and 4-1BB, and linked to a truncated form of the human epidermal growth factor receptor 2 (HER2tG), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous CD4+/CD8+ 4-1BB-CD3zeta-EGFR806-CAR-EGFRt/4-1BB-CD3zeta- CD19-CAR-HER2tG-expressing CARs T cells are directed to, bind to, and induce selective toxicity in EGFR deletion mutation variant III (EGFRvIII)-expressing tumor cells. The binding of these T cells to CD19 expressed on B cells enhances their expansion and prolongs their persistence in vivo, thereby increasing the efficacy of these CAR T cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt and HER2tG facilitate in vivo detection of the administered, transduced T cells and can promote elimination of these cells through an antibody-dependent cellular cytotoxicity (ADCC) response. HER2tG allows for enhanced binding by trastuzumab. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy. Depatuxizumab specifically targets abnormal conformational states of EGFR, including EGFRvIII, and activating mutations, with lower affinity for wild-type EGFR. CD19, a transmembrane phosphoglycoprotein is expressed on the surface of cells in the B-lineage.

autologous CD4+/CD8+ EGFR806 specific 4-1BB-CD3zeta-EGFRt-expressing CAR T cells

A preparation of CD4+ and CD8+ autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) composed of a short chain variable fragment (scFv) binding domain derived from depatuxizumab, a human anti-epidermal growth factor receptor (EGFR) monoclonal antibody (MAb806; ABT-806), coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta) and the signaling domain of 4-1BB (CD137), and linked to a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Depatuxizumab specifically targets abnormal conformational states of EGFR, including the EGFR deletion mutation variant III (EGFRvIII), and activating mutations, with very low affinity for wild-type EGFR. Upon intravenous administration, the autologous CD4+/CD8+ EGFR806 specific 4-1BB-CD3zeta-EGFRt-expressing CAR T cells are directed to and induce selective toxicity in EGFRvIII-expressing tumor cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of these cells through an anti-EGFR antibody-dependent cellular cytotoxicity (ADCC) response. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy.

autologous CD4- and CD8-positive truncated CD19-expressing antigen presenting T cells

A preparation of ex vivo expanded, autologous CD4 and CD8 positive antigen presenting T cells (T-APCs), genetically modified with a transgene encoding a truncated form of human cluster of differentiation 19 (CD19t), with potential immunostimulating activity. Upon infusion, autologous CD19t-expressing T-APCs may stimulate the proliferation and activation of preadministered therapeutic CD19-targeted chimeric antigen receptor T cells (CAR-T). This may both improve the persistence of the therapeutic CAR-T cells and prevent relapse in patients with CD19 positive leukemia or lymphoma. CD19 is a B-cell specific cell surface antigen that is expressed in all B-cell lineage malignancies.

autologous CD40L-expressing B-CLL vaccine

A cancer vaccine consisting of autologous, B-chronic lymphocytic leukemia (B-CLL) cells harvested from a patient and transduced with an adenoviral vector encoding the gene for the human CD40 ligand (CD40L; TRAP; CD154), with potential immunostimulating and antineoplastic activities. Upon reintroduction into the patient, the autologous CD40L-expressing B-CLL vaccine expresses the co-stimulatory molecule CD40L, which binds to its cognate receptor, CD40, on antigen presenting cells (APC). This induces apoptosis, stimulates maturation and proliferation of APCs, and facilitates a cytotoxic T-lymphocyte (CTL) response against tumor cells. CD40L is a type II membrane protein that binds to CD40, which is a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor superfamily.

autologous CD5-specific CAR-28 zeta CAR T cells

Autologous T lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD5 single chain variable fragment (scFv) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, the autologous CD5-specific CAR-28 zeta CAR T cells are directed to and induce selective toxicity in CD5-expressing tumor cells. The tumor-associated antigen (TAA) CD5 is a T-cell surface glycoprotein expressed on the surface of normal T cells, and is overexpressed on various B- and T-cell malignancies; its expression is associated with poor prognosis.

autologous CD5KO anti-CD5 CAR 4-1BB-expressing T lymphocytes and autologous CD5KO T lymphocytes

A dual-population preparation of autologous T lymphocytes in which the tumor-associated antigen (TAA) CD5 is knocked out (CD5KO) and is genetically modified to express a chimeric antigen receptor (CAR) specific for CD5 and coupled to the co-stimulatory molecule 4-1BB (CD137), and autologous CD5KO normal untransduced T lymphocytes, with potential immunomodulating and antineoplastic activities. Upon administration of autologous CD5KO anti-CD5 CAR 4-1BB-expressing T lymphocytes and autologous CD5KO T lymphocytes, the autologous CD5KO anti-CD5 CAR 4-1BB-expressing T lymphocytes specifically recognize and kill CD5-expressing tumor cells. CD5 is a T-cell surface glycoprotein expressed on the surface of normal T cells and overexpressed on various B- and T-cell malignancies. CD5 KO in the CART5 cells prevents CART fratricide and enhances CAR-T cell function. The CD5KO normal T cells allow for T-cell reconstitution and may mitigate T-cell toxicity.

autologous CD8+ melanoma-specific T cells

Autologous CD8 T lymphocytes against melanoma-associated antigens, with potential immunomodulating and antineoplastic activities. Following leukapheresis and the ex vivo expansion of cytotoxic T-lymphocytes, the autologous CD8+ melanoma-specific T cells are re-introduced into the melanoma patient. These cytotoxic T-cells recognize and kill the patient's own melanoma cells.

autologous CD8+ SLC45A2-specific T lymphocytes

A preparation of autologous CD8+ T lymphocytes targeting SLC45A2, a melanoma-associated antigen, with potential immunomodulating and antineoplastic activities. Following peripheral blood mononuclear cell (PBMC) collection and ex vivo expansion of SLC45A2-specific cytotoxic T lymphocytes (CTLs), the autologous CD8+ SLC45A2-specific CTLs are re-infused into the patient, where they target and lyse SLC45A2-expressing tumor cells. While SLC45A2 is expressed by approximately 80% of cutaneous melanomas, its expression is limited in mature normal melanocytes, allowing high tumor selectivity and reduced potential for autoimmune toxicity.

autologous CD8-positive PBL sensitized to Drosophila cell-presented melanoma peptides

A preparation of autologous CD8+ (cytotoxic) human peripheral blood lymphocytes (PBLs) sensitized to Drosophila cell-presented melanoma peptides, with potential immunostimulating and antineoplastic activities. Autologous CD8+ T lymphocytes, isolated from a melanoma patient, are exposed in vitro to melanoma peptide-pulsed HLA-A2-expressing Drosophila cells, expanded, and reintroduced into the patient; these tumor-reactive T cells may stimulate a host immune response against tumor cells expressing the melanoma antigens, resulting in tumor cell lysis. Drosophila cells, which do not express any native MHC molecules, have been shown to potently stimulate tumor-reactivity in vitro from human peripheral blood lymphocytes (PBL) when stably transfected with human MHC molecules and appropriate adhesion and costimulatory molecules.

autologous CEA-specific cytotoxic T-lymphocytes

Autologous cytotoxic T-lymphocytes (CTLs) specifically reactive to the tumor-associated antigen (TAA) human carcinoembryonic antigen (CEA), with potential antineoplastic activity. Dendritic cells (DCs) isolated from the patient’s blood are infected with recombinant adeno-associated virus (AAV) expressing the CEA gene. Exposure of T-lymphocytes to DCs creates CEA-specific CTLs which are expanded. Upon reintroduction of these CTLs into the patient, these cells recognize and kill CEA-expressing tumor cells. CEA, a tumor-associated antigen and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion, and cell adhesion and is overexpressed by a variety of cancer types.

autologous cervical cancer-specific engineered immune effector cells

A preparation of autologous immune effector cells genetically modified to target a not yet disclosed cervical cancer-specific tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the autologous cervical cancer-specific engineered immune effector (CC-EIE) cells bind to and induce selective toxicity in tumor cells expressing the TAA.

autologous CISH-inactivated TILs

A preparation of autologous tumor-infiltrating lymphocytes (TILs) where the cytokine-inducible SH2-containing protein gene (CISH) has been inactivated using the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR associated protein 9 (Cas9) editing system, containing guide RNA (gRNA) coupled to a recombinant form of the DNA endonuclease Cas9, with potential immunomodulating and antineoplastic activities. Using the CRISPR/Cas9 system, the autologous TILs are transfected, ex vivo, with a plasmid encoding for a gRNA that site-specifically targets and binds to the human CISH gene. Cas9 cleaves these specific DNA sites, which causes double strand breaks, disrupts the gene encoding CISH and prevents transcription. Upon intravenous administration, the autologous CISH-inactivated TILs are able to induce a T-cell-mediated immune response against tumor cells. CISH, a member of the suppressor of cytokine signaling family (SOCS; cytokine-induced STAT inhibitor; STAT-induced STAT inhibitor; SSI), is induced by T-cell receptor (TCR) stimulation. CISH plays a key role in the negative regulation of both T-cell signaling and CTL-mediated tumor cell eradication. The knockout of the CISH gene enhances the expansion and anti-tumor activities of effector T cells.

autologous CLL1-CD33 compound CAR T cells

Autologous T lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two CARs, one specific for the CD33 antigen and one specific for the C-type-lectin-like molecule-1 (CLL1; C-type lectin domain family 12 member A; CLEC12A), with potential immunomodulating and antineoplastic activities. Upon administration, the lentiviral vector-transduced autologous T lymphocytes, expressing both the anti-CD33 CAR and the anti-CLL1 CAR on their surfaces, specifically and simultaneously target and bind to CD33- and CLL1-expressing tumor cells, with their anti-CD33 CAR and their anti-CLL1 CAR, respectively. This induces selective toxicity in tumor cells that express the CD33 antigen and the CLL1 antigen. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells. CLL1, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed in leukemic stem cells (LSCs) and plays an important role in disease progression and relapse for myeloid malignancies.

autologous clonal neoantigen T cells ATL001

A preparation of personalized tumor-derived T-lymphocytes composed of tumor infiltrating lymphocytes (TILs) that are reactive to clonal cancer neoantigens, with potential immunostimulating and antineoplastic activities. The TILs are removed from the suppressive tumor microenvironment (TME) and re-activated. Upon reintroduction into the patient, the clonal neoantigen T (cNeT) cells recognize and bind to tumor cells expressing the targeted neoantigen, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient's tumor cells.

autologous CLTX-targeted CAR T lymphocytes CHM 1101

A preparation of autologous T lymphocytes genetically modified to express a chimeric antigen receptor (CAR) comprised of a CD28 co-stimulatory signaling domain fused to the zeta chain of the TCR/CD3 complex (CD3zeta) and coupled to chlorotoxin (CLTX), a 36-amino acid peptide derived from the venom of the deathstalker scorpion, with potential immunomodulating and antineoplastic activities. Upon administration of autologous CLTX-targeted CAR T lymphocytes CHM 1101, the CAR-T cells are re-directed to specific brain tumor cells through its tumor-targeting domain CLTX. CLTX targets and binds to the membrane-bound endopeptidase matrix metalloproteinase-2 (MMP-2), thereby inducing selective toxicity in MMP-2-expressing tumor cells. MMP-2 is specifically upregulated in gliomas and related cancers, but is not normally expressed in the brain.

autologous CMV pp65/total tumor mRNA-loaded lipid particle vaccine

An mRNA-based, personalized cancer vaccine consisting of total tumor RNA (TTRNA) derived and amplified from autologous tumor cells, which includes the mRNA encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83), formulated in lipid particles (LPs), with potential immunostimulatory and antineoplastic activities. Upon administration of the autologous CMV pp65/total tumor mRNA-loaded LP vaccine, the mRNA is taken up, translated and presented by antigen presenting cells (APCs), mainly dendritic cells (DCs). This leads to an induction of cytotoxic T-lymphocyte immune responses that specifically target and destroy the patient's cancer cells that express these tumor antigens. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.

autologous CMV-pp65-flLAMP mRNA-loaded dendritic cell vaccine

A cancer cell vaccine consisting of autologous dendritic cells (DCs) loaded with mRNA encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83) as a fusion protein with the full-length lysosome-associated membrane protein (flLAMP), with potential immunostimulatory and antineoplastic activities. Upon vaccination, the autologous CMV-pp65-flLAMP mRNA loaded DC vaccine exposes the immune system to the CMV pp65 peptide, which may elicit a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells. The incorporation of flLAMP may route CMV pp-65 antigens into the lysosomal compartment, resulting in enhanced MHC class II antigen presentation, thereby promoting CD4-positive T-cell responses. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.

autologous CMV-pp65-LAMP mRNA-loaded monocyte vaccine MT-201-GBM

A cancer cell vaccine consisting of autologous monocytes loaded with mRNA encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83) as a fusion protein with the lysosome-associated membrane protein (LAMP), with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous CMV-pp65-LAMP mRNA loaded monocyte vaccine MT-201-GBM exposes the immune system to the CMV pp65 peptide, which may elicit a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells. The incorporation of LAMP may route CMV pp-65 antigens into the lysosomal compartment, resulting in enhanced MHC class II antigen presentation, thereby promoting CD4-positive T-cell responses. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.

autologous CMV-pp65-shLAMP-1 mRNA loaded dendritic cell vaccine

A cancer cell vaccine consisting of autologous dendritic cells pulsed with mRNA encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83) as a fusion construct with a short peptide chimeric antigen from lysosome-associated membrane protein 1 (shLAMP-1), with potential antineoplastic and immunostimulatory activities. Upon vaccination, the autologous CMV-pp65-shLAMP-1 vaccine exposes the immune system to the CMV pp65 peptide, which may elicit a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells. The incorporation of shLAMP-1 may route CMV pp-65 antigens into the lysosomal compartment, resulting in enhanced MHC class II antigen presentation, thereby promoting CD4-positive T-cell responses. The CMV pp65 protein is the primary component of the enveloped sub-viral particle of CMV and is expressed in certain tumor types.

autologous colon cancer cell vaccine

A personalized, proprietary cancer vaccine composed of sterile, irradiated, non-dividing, live colon cancer cells obtained from an individual after tumor resection, with potential immunoactivating and antineoplastic activities. Upon intradermal administration, the autologous colon cancer cell vaccine activates the immune system and elicits a cytotoxic T-lymphocytic (CTL) response against the residual colon cancer cells, which results in tumor cell death. This may prevent cancer recurrence. According to the vaccination schedule, the first two out of the four doses are co-administered with the immunoadjuvant bacillus Calmette-Guerin (BCG), which is an attenuated strain of Mycobacterium bovis that non-specifically enhances the immune response.

autologous colorectal tumor antigen-pulsed dendritic cell vaccine

A dendritic cell (DC)-based cancer vaccine composed of autologous DCs pulsed with tumor cell lysates from a colorectal cancer patient containing tumor-associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous colorectal tumor antigen-pulsed DC vaccine exposes the immune system to colorectal tumor cell antigens, which may result in cytotoxic T-lymphocyte (CTL)-mediated immune responses against the colorectal cancer cells. This leads to cancer cell lysis. The tumor cell lysate contains a range of antigens that are essential for the neoplastic growth and survival of the cancer cells.

autologous CRISPR-Cas9 engineered regnase-1/SOCS1 dual-edited tumor infiltrating lymphocytes KSQ-004EX

A preparation of autologous tumor infiltrating lymphocytes (TILs) gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to inactivate both the endogenous genes suppressor of cytokine signaling 1 (SOCS1) and Regnase-1, with potential immunomodulating and antineoplastic activities. Upon infusion of the autologous CRISPR-Cas9 engineered Regnase-1/SOCS1 dual-edited TILs KSQ-004EX back into the patient, the cells specifically recognize, target and kill the patient's tumor cells. Inactivation of endogenous SOCS1 and Regnase-1 in the TILs increases responsiveness to cytokine signals, increases persistence and memory formation of TILs, and enhances anti-tumor responses.

autologous CRISPR-Cas9 engineered tumor infiltrating lymphocytes KSQ-001EX

A preparation of autologous tumor infiltrating lymphocytes (TILs) gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to inactivate the endogenous gene suppressor of cytokine signaling 1 (SOCS1), with potential immunomodulating and antineoplastic activities. Upon infusion of the autologous CRISPR-Cas9 engineered TILs KSQ-001EX back into the patient, the cells specifically recognize, target and kill the patient's tumor cells. SOCS1 serves as a negative regulator of cytokine signaling in T cells and negatively influences the survival, differentiation, and function of T cells. Inactivation of endogenous SOCS1 in TILs increases responsiveness to cytokine signals, and enhances anti-tumor potency, persistence and memory formation of TILs.

autologous CRISPR-Cas9-modified/BCL11A enhancer-disrupted CD34-positive human hematopoietic stem and progenitor cells CTX001

A population of autologous cluster of differentiation 34 (CD34)-positive human hematopoietic stem and progenitor cells (hHSPCs) that are ex-vivo gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Caspase 9 (Cas9) nuclease complex at the erythroid lineage-specific enhancer of the B-cell lymphoma/leukemia 11A (BCL11A) gene, with potential usage for transplantation in patients with sickle cell disease (SCD) and beta-thalassemia. CD34-positive HSPCs are isolated from human blood upon apheresis and are genetically modified in vitro using CRISPR/Cas9 technology to specifically disrupt the erythroid enhancer of the BCL11A gene. As BCL11A is a suppressor of fetal hemoglobin (HbF; hemoglobin F) expression, disruption of the BCL11A enhancer decreases the expression of BCL11A and stimulates the expression of HbF in erythrocytes that differentiate from CTX001. Upon infusion back into the patient following myeloablative, conditioning chemotherapy, autologous CRISPR-Cas9 modified/BCL11A enhancer-disrupted CD34+ hHSPCs CTX001 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. The increased production of high levels of HbF in red blood cells (RBCs) compensates for the defective or reduced adult hemoglobin (Hb) in patients with SCD and beta-thalassemia. HbF is a form of the oxygen carrying Hb that is naturally present at birth and is then replaced by the adult form of hemoglobin.

autologous CRISPR-Cas9-modified/BCL11A gene-disrupted human hematopoietic stem and progenitor cells OTQ923

A population of autologous cluster of differentiation 34 (CD34)-positive human hematopoietic stem and progenitor cells (hHSPCs) that are ex-vivo gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex at the erythroid lineage-specific enhancer of the B-cell lymphoma/leukemia 11A (BCL11A) gene, with potential usage for transplantation in patients with sickle cell disease (SCD) and beta-thalassemia. CD34-positive HSPCs are isolated from human blood upon apheresis and are genetically modified in vitro using CRISPR/Cas9 technology to specifically disrupt the erythroid enhancer of the BCL11A gene. As BCL11A is a suppressor of fetal hemoglobin (HbF; hemoglobin F) expression, disruption of the BCL11A enhancer decreases the expression of BCL11A and stimulates the expression of HbF in erythrocytes that differentiate from CTX001. Upon infusion back into the patient following myeloablative, conditioning chemotherapy, autologous CRISPR-Cas9 modified/BCL11A enhancer-disrupted CD34+ hHSPCs CTX001 can populate the bone marrow and differentiate into a variety of blood cell types including lymphoid cells, myeloid cells and erythroblasts. The increased production of high levels of HbF in red blood cells (RBCs) compensates for the defective or reduced adult hemoglobin (Hb) in patients with SCD and beta-thalassemia. HbF is a form of the oxygen carrying Hb that is naturally present at birth and is then replaced by the adult form of hemoglobin.

Autologous CRISPR-edited Anti-CD19 CAR T Cells XYF19

A preparation of autologous T-lymphocytes transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, and electroporated with clustered regularly interspaced short palindromic repeats (CRISPR) guide RNA to disrupt expression of endogenous hematopoietic progenitor kinase 1 (HPK1), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the autologous CRISPR-edited anti-CD19 CAR T-cells XYF19 recognize and bind to CD19-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. Disrupting the expression of HPK1 may enhance immune response and autoimmunity. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. HPK1 is a Ste20-like serine/threonine kinase that suppresses immune responses and autoimmunity.

autologous CRISPR-edited tumor infiltrating lymphocytes GT316

A preparation of autologous tumor-infiltrating lymphocytes (TILs) derived from each patient's resected tumor and edited with the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated protein 9 (Cas9) system to eliminate the expression of as of yet not elucidated immunoregulatory targets, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, autologous CRISPR-edited TILs GT316 specifically recognize and kill the patient's tumor cells. The knockout of the immunoregulatory targets may enhance the proliferation and cytokine release of the TILs.

autologous CT-RCC-1 HERV-E-TCR-transduced-HLA-A11-restricted CD8+/CD34t+ T cells

A preparation of autologous T lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) sequence specific for CT-RCC-1, a tumor-associated antigen (TAA) and HLA-A11-restricted peptide encoded by human endogenous retrovirus (HERV) type E as well as a truncated CD34 chain (CD34t), with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous CT-RCC-1 HERV-E-TCR-transduced-HLA-A11-restricted CD8+/CD34t+ T cells bind to and induce selective toxicity in tumor cells expressing both the HLA-A11 allele and the CT-RCC-1 HERV-E antigen. The CD34t protein allows the transduced cells to be identified with an anti-CD34 antibody, and facilitates monitoring of the genetically modified T cells following adoptive transfer. CT-RCC-1 HERV-E is a TAA found in a high percentage of clear cell renal cell carcinoma (ccRCC) cells.

autologous CT7/MAGE-A3/WT1 mRNA-electroporated Langerhans-type dendritic cells

An autologous tumor cell vaccine containing CD34+ hematopoietic progenitor cell (HPC)-derived Langerhans-type dendritic cells (LCs) electroporated with mRNA encoding the full-length cancer-testis antigens, CT7 and melanoma-associated antigen 3 (MAGE-A3), and the self-differentiation tumor antigen, Wilms tumor 1 (WT1) with potential immunomodulating and antineoplastic activity. The autologous CT7/MAGE-A3/WT1 mRNA-electroporated Langerhans-type dendritic cells are prepared by drawing a blood sample containing the CD34+ HPCs from a cancer patient. The CD34+ HPCs are treated with a combination of cytokines which specifically support LC development, and the LC population is enriched and expanded ex vivo. The cultured LCs are allowed to mature for one day and then electroporated separately with CT7, MAGE-A3 or WT1 mRNA before final maturation. Upon intradermal administration into the patient, the mature LCs may activate cell-mediated immunity and induce both cytotoxic CD8+ T cells and CD4+ helper T cells against cancer cells expressing CT7, MAGE-A3 and WT1 tumor antigens. This may result in the immune-mediated inhibition of tumor cell proliferation, leading to tumor cell death. CT7 and MAGE-A3 are tumor-specific proteins overexpressed in a number of cancers but not in healthy tissues other than testis and placenta. WT1 is a transcription factor important in development and cancer pathogenesis, which is overexpressed in a variety of cancers, including multiple myeloma, leukemia, ovarian cancer, malignant mesothelioma, neural tumors and renal carcinoma.

autologous cultured acute myeloid leukemia-specific cytotoxic T lymphocytes

A preparation of cytotoxic, autologous acute myelogenous leukemia (AML)-reactive T lymphocytes (CTL), with potential immunomodulating and antineoplastic activities. The autologous cultured AML-specific CTLs are prepared using a specific AML-CTL culture method. Autologous peripheral blood lymphocytes are taken from an AML patient and the autologous AML blasts are treated with granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4), both of which promote ex vivo differentiation of AML blasts into dendritic cells (DCs). In the same culture, T cells are treated and activated by low-dose interleukin 2 (IL-2), and expanded using anti-CD3. This results in cultured AML-reactive CTLs which are administered back into the patient after autologous hematopoietic stem cell transplant (AHSCT). The autologous cultured AML-specific CTLs may eradicate residual AML cells.

autologous CXCR2-modified CD70 CAR T cells

A preparation composed of ex-vivo expanded CXC chemokine receptor 2 (CXCR2) modified patient-derived activated CD70 (CD27 ligand; tumor necrosis factor superfamily member 7; TNFSF7) chimeric antigen receptor (CAR) (8R-70CAR) T cells, with potential immunostimulating and antineoplastic activities. Upon admi nistration of the autologous CXCR2-modified CD70 CAR Tcells, the anti-CD70-CARs on the T cell surfaces target and bind to the CD70 antigen on tumor cell surfaces. This induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against CD70-expressing tumor cells. CD70, a cytokine belonging to the tumor necrosis factor superfamily (TNFSF) and the ligand for the costimulatory receptor CD27, is expressed on the surfaces of various types of cancer cells; its overexpression may play an important role in the evasion of immune surveillance. CXCR2, a transmembrane protein also known as interleukin (IL)-8 receptor B (IL-8RB), plays a key role in inflammation and cancer progression. Certain CXCR2 ligands, such as CXCL1 and CXCL8 (IL-8), are expressed by tumor cells. CXCR2-modified CARs enhance intratumoral T-cell trafficking toward tumor cells and promotes persistence of T cells. This may enhance the T-cell-mediated immune response against the CD70-expressing tumor cells.

autologous cytokine-induced killer cells

A proprietary formulation of autologous cytokine-induced killer (CIK) T lymphocytes, with immunopotentiating and antineoplastic activities. These CIK cells are generated by ex vivo incubation of autologous peripheral blood lymphocytes with an undisclosed mixture of compounds to stimulate killer T-cell differentiation; this is followed by expansion of the cells. Upon reintroduction into the patient, the autologous CIK cells are able to target and kill tumor cells.

autologous cytokine-induced killer cells/vaccinia virus DD-CDSR CRX100

A preparation of autologous cytokine-induced killer (CIK) cells that have been generated ex vivo from killer cells treated with cytokines and infected with the oncolytic vaccinia virus DD-CDSR (vvDD-CDSR; double-deleted vaccinia virus plus CD/SMR), with potential immunomodulatory and antineoplastic activities. CIK cells are CD3- and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T lymphocytes. Upon infusion of autologous CIK cells/vvDD-CDSR CRX100, the CIK cells protect the oncolytic virus vvDD-CDSR from immune attack and enhance the delivery of the oncolytic virus to tumor cells. The oncolytic virus vvDD-CDSR preferentially targets and infects tumor cells causing oncolysis. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells.

autologous cytomegalovirus-specific cytotoxic T lymphocytes

A population of autologous cytotoxic lymphocytes (CTLs) specifically reactive to the herpes virus cytomegalovirus (CMV) with potential immunomodulating and antiviral activities. Upon administration with the autologous CMV-specific CTLs, these CTLs lyse CMV-infected cells, thereby preventing or decreasing the occurrence of CMV viral disease, or reducing the amount of antiviral drug therapy needed to eradicate CMV.

autologous cytoplasmic activated PD-1 CAR-Tcells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19), carrying cytoplasmic activated programmed cell death 1 (PD1; PDCD1; CD279; programmed death-1), with potential antineoplastic activity. Upon intravenous administration, autologous cytoplasmic activated PD-1 CAR-T cells target, bind to, and induce selective toxicity in CD19-expressing tumor cells. The cytoplasmic activated PD1, a negative immunoregulatory human cell surface receptor, normally binds to programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) on tumor cells, causing T-cell inactivation. By preventing PD1/PD-L1 signaling, T-cell exhaustion is abrogated, and T-cell activation is enhanced leading to an increased cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors.

autologous cytotoxic T lymphocytes exposed to dendritic cells loaded with 6B11 anti-idiotype minibody

A preparation of autologous cytotoxic T lymphocytes (CTLs) that are exposed, ex vivo, to autologous dendritic cells (DCs) loaded with the anti-idiotype minibody 6B11, which mimics the epithelial ovarian tumor-associated antigen (TAA), OC166-9, with potential immunostimulatory and antineoplastic activities. Upon administration, the CTLs exposed to DCs loaded with 6B11 anti-idiotype minibody target and kill autologous ovarian cells expressing the TAA.

autologous cytotoxic T lymphocytes induced with MUC1 gene-transfected dendritic cells

A preparation of autologous cytotoxic T-lymphocytes (CTL), specifically reactive to the tumor-associated antigen (TAA) mucin-1 (MUC1), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are collected from the patient with MUC1-positive tumors and are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding MUC1 to generate MUC1-specific CTLs, which are subsequently expanded in vitro. Upon re-infusion of autologous CTLs induced with MUC1 gene-transfected DCs to the patient, the CTLs target and lyse the MUC1-expressing tumor cells. This inhibits tumor cell proliferation. MUC1 is expressed by a variety of tumor cell types.

autologous cytotoxic T lymphocytes induced with MUC1 peptide-transfected dendritic cells

A preparation of autologous cytotoxic T-lymphocytes (CTL), specifically reactive to the tumor-associated antigen (TAA) mucin-1 (MUC1), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are collected from the patient with MUC1-positive tumors and are exposed ex vivo to dendritic cells (DCs) that are pulsed with a MUC1 peptide to generate MUC1-specific CTLs, which are subsequently expanded in vitro. Upon re-infusion of autologous CTLs induced with MUC1 peptide-pulsed DCs to the patient, the CTLs target and lyse the MUC1-expressing tumor cells. This inhibits tumor cell proliferation. MUC1 is expressed by a variety of tumor cell types.

autologous deep IL-15 primed T cells TRQ15-01

A preparation of genetically modified, multi-antigen-directed autologous T lymphocytes, that have particles, consisting of multiple chemically crosslinked human cytokine interleukin-15 (IL-15)/IL-15 receptor alpha (IL-15Ra)/Fc heterodimers, attached to their surface, with potential immunostimulating and antineoplastic activities. TRQ15-01 is made from monocyte-derived dendritic cells (moDCs) that are pulsed with peptides from multiple tumor-associated antigens (TAAs) to expand cytotoxic T lymphocytes (CTLs) that are subsequently loaded with IL-15 particles. Upon administration of the autologous deep IL-15 primed T cells, the IL-15/IL-15Ra fusion proteins are slowly released in vivo from the T cells in a controlled manner and induce autocrine cytokine stimulation of the administered T cells, thereby increasing T-cell division of the administered T cells. The expanded T cells target, bind to and kill tumor cells. This increases tumor cell growth inhibition by T cells. IL-15 is a pro-survival, inflammatory cytokine and causes sustained T-cell expansion and enhanced anti-tumor activity. Compared to systemically delivered IL-15, IL-15 attached to the T cells greatly increases target CD8 T-cell concentrations in the tumor, without significant systemic effects.

autologous dendritic cell vaccine ACT2001

A cell-based cancer vaccine composed of autologous, immature dendritic cells (DCs), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, immature DCs are isolated and re-administered intra-tumorally. The immature DCs internalize and process the tumor-associated antigens (TAAs), migrate to the lymphatic system, and then expose the immune system to the TAAs. This induces a specific cytotoxic T-lymphocyte (CTL) response against the cancer cells leading to tumor cell lysis.

autologous dendritic cell-adenovirus CCL21 vaccine

A cancer vaccine comprised of autologous dendritic cells (DCs) that have been transduced ex vivo with an adenoviral vector containing the CCL21 gene with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration, autologous dendritic cell-adenovirus CCL21 vaccine expresses the chemokine CCL21, which may induce an antitumoral cytotoxic immune response in the tumor microenvironment. CCL21 [chemokine (C-C motif) ligand 21] has been shown to attract antigen presenting cells (APCs), like leukocytes and DCs, and natural killer (NK) cells and their T-cell effectors to induce a cytotoxic immune response.

autologous dendritic cell-adenovirus p53 vaccine

An autologous vaccine composed of dendritic cells (DC) that have been transduced with a p53 tumor suppressor gene-modified virus. When the autologous dendritic cell-adenovirus p53 vaccine is administered, the host cytotoxic T lymphocytes (CTL) are directed against p53-positive tumor cells, which may result in tumor cell death and decreased tumor growth.

autologous dendritic cell-allogeneic melanoma tumor cell lysate vaccine

A cell-based vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from heat-treated allogeneic melanoma tumor cells. Upon administration, this vaccine may stimulate anti-tumoral cytotoxic T-cell and antibody responses to melanoma cells bearing shared melanoma antigens such as MelanA/MART-1, gp100, MAGE3, resulting in tumor cell lysis.

autologous dendritic cell-autologous tumor mRNA-human CD40L vaccine

A cancer vaccine consisting of autologous dendritic cells transfected with autologous tumor mRNA and the human CD40 ligand (CD40L) gene with immunostimulatory and antitumor activities. Vaccination with autologous dendritic cell-autologous tumor mRNA-human CD40L vaccine may elicit a cytotoxic T cell response against tumor cells from which the autologous tumor mRNA was derived. When expressed by dendritic cells, tumor antigens and the co-stimulatory molecule CD40L, which binds to CD40 receptors on antigen presenting cells (APC), facilitate both humoral and cellular immune responses against tumor cells.

autologous dendritic cell-tumor fusion vaccine

A therapeutic cancer vaccine consisting of autologous dendritic cells (DCs) fused with autologous tumor cells with potential immunostimulatory and antineoplastic activities. Autologous dendritic cell-tumor fusion vaccine is generated in vitro by mixing DCs and irradiated tumor cells harvested from individual patients and treating them with polyethylene glycol (PEG) to produce DC-tumor cell fusion hybrid cells. Upon administration, autologous dendritic cell-tumor fusion vaccine may elicit antitumor humoral and cellular immune responses.

autologous dendritic cell/myeloma fusion vaccine

A therapeutic cancer vaccine consisting of autologous dendritic cells (DCs) fused with patient-derived plasma cell (multiple) myeloma cells with potential immunostimulatory and antineoplastic activities. Upon administration, autologous DC/multiple myeloma fusions stimulate both helper and cytotoxic T-lymphocyte (CTL) responses through the presentation of internalized and newly synthesized tumor associated antigens (TAAs). This may promote cellular and humoral antitumor immune responses in patients with plasma cell myeloma.

autologous dendritic cells pulsed with MART-1 (26-35) peptide

A cell-based vaccine consisting of autologous HLA-A2*0201-restricted dendritic cells (DC), which were derived from patient-harvested adherent peripheral blood monocytes cultured in vitro with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), that were pulsed with a peptide fragment comprised of amino acid residues 26 through 35 of melanoma antigen recognized by T cells 1 (MART-1 (26-35)), with potential immunostimulatory and antineoplastic activities. Upon intradermal vaccination, autologous DC pulsed with MART-1 (26-35) peptide may stimulate the host immune system to mount a cytotoxic T-lymphocyte immune response against tumor cells expressing MART-1. MART-1, a protein involved in melanosome biogenesis, is overexpressed by melanoma cells. The MART-1 (26-35) peptide is highly immunogenic for the HLA-A2*0201 haplotype.

autologous dendritic cells transduced with wild-type p53 adenovirus vaccine

A cancer vaccine consisting of autologous dendritic cells (DCs) transduced with a recombinant replication-defective adenoviral (Ad) vector encoding the full-length wild-type (wt) cancer tumor antigen p53 protein (TP53; p53), with potential immunomodulating activity. Intradermal vaccination with the autologous DCs transduced with wt p53 Ad vaccine may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells overexpressing wt and mutant forms of p53, resulting in tumor cell lysis. p53, a tumor suppressor gene, is overexpressed and/or mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.

autologous desmoglein-3 chimeric autoantibody receptor T cells DSG3-CAART

A preparation of autologous T lymphocytes that have been engineered to express a chimeric autoantibody receptor (CAAR) containing the autoantigen desmoglein-3 (desmoglein 3; DSG3) that is fused to the co-stimulatory domain of 4-1BB (CD137) and the T-cell receptor signaling domain of CD3zeta (CD3z), with potential immunomodulatory activity. Upon administration, the autologous DSG3 chimeric autoantibody receptor T cells (CAART) DSG3-CAART specifically recognize and induce selective toxicity in aberrant B cells expressing DSG3 autoantibodies. This inhibits the production of DSG3 autoantibodies. DSG3 is a protein expressed in desmosomes that plays an important role in cell adhesion. DSG3 autoantibodies are produced and expressed by aberrant B cells in the autoimmune disease mucosal-dominant pemphigus vulgaris.

autologous dinitrophenyl-modified ovarian cancer vaccine

A cancer vaccine consisting of autologous ovarian cancer cell peptide antigens conjugated to the hapten 2,4-dinitrophenol (DNP) with potential immunostimulating and antineoplastic activities. Administration of autologous dinitrophenyl-modified ovarian cancer vaccine may induce a cytotoxic T-lymphocyte (CTL) response against ovarian cancer cells. DNP conjugation may enhance the immunogenicity of weakly immunogenic antigens.

autologous dnTGF-BRII-armored anti-GPC3 CAR T cells AZD5851

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3) and the dominant negative (dn) form of transforming growth factor-beta (TGF-beta; TGFb) receptor 2 (dnTGF-BRII; dnTGFbR2), with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, autologous dnTGF-BRII-armored anti-GPC3 CAR T cells AZD5851 are directed to and induce selective toxicity in GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation. The inclusion of dnTGF-BRII blocks the signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the AZD5851 T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression.

autologous dnTGF-BRII-armored anti-STEAP2 CAR T cells AZD0754

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the metalloreductase six-transmembrane epithelial antigen of prostate-2 (STEAP2; STAMP1) and the dominant negative (dn) form of transforming growth factor-beta (TGF-beta; TGFb) receptor 2 (dnTGF-BRII; dnTGFbR2), with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, autologous dnTGF-BRII-armored anti-STEAP2 CAR T cells AZD0754 are directed to and induce selective toxicity in STEAP2-expressing tumor cells. STEAP2 is a cell surface antigen overexpressed in prostate cancer with limited expression in normal tissue. The inclusion of dnTGF-BRII blocks the signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the AZD0754 CAR T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression.

autologous E6 T cell receptor genetically-modified T cells

A preparation of human autologous peripheral blood lymphocytes (PBLs) that have been genetically engineered to express a T-cell receptor (TCR) that specifically targets the viral oncoprotein human papillomavirus type 16 (HPV-16) E6, with potential antineoplastic activity. Upon administration, the HPV E6 TCR genetically-modified T cells target and bind to HPV-16 E6-expressing tumor cells, which leads to specific cytotoxic T-lymphocyte (CTL)-mediated killing of HPV-16 E6-positive tumor cells. HPV-16 E6, a cell surface glycoprotein, plays a key role in the tumorigenesis of various HPV-associated tumors and is absent from healthy human tissues.

autologous EBV-CTL CD19CAR zeta

Autologous Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocytes (CTL) that have been genetically modified to express a T-cell chimeric antigen receptor (CAR) targeting the CD19 antigen, with potential immunotherapeutic activity. The CAR consists of a single chain Fv of anti-CD19 IgG1 coupled with an intracellular signaling region of the zeta-chain of the TCR/CD3 complex (CD3 zeta). Autologous EBV-CTL CD19CAR zeta directs the T-lymphocytes to CD19-expressing tumor cells, stimulating a selective toxicity to tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous EBV-transformed B lymphoblastoid-tumor fusion cell vaccine

A cell-based vaccine composed of autologous tumor cells fused with Epstein-Barr virus-transformed B-lymphoblastoid cells. Upon administration, this vaccine may stimulate a cytotoxic T cell response against tumor cells, resulting in tumor cell lysis.

autologous EGFR-specific CAR-T cells expressing anti-PD-1/CTLA-4 antibodies

A preparation of autologous T lymphocytes that have been activated and genetically modified to express immune checkpoint antibodies against the negative immunoregulatory receptors human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR), with potential immunomodulating and antineoplastic activities. After isolation, activation, transduction, expansion in culture and reintroduction into the patient, the T cells in the autologous EGFR specific CAR-T cells expressing anti-PD-1/CTLA4 antibodies specifically target and kill EGFR-expressing tumor cells. The anti-PD-1 antibody secreted from the CAR-T cells binds to PD-1 expressed on T cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion. The anti-CTLA4 expressed by the CAR-T cells targets and binds to CTLA4 expressed on T-cells, and inhibits the CTLA4-mediated downregulation of T-cell activation. Both antibodies enhance T-cell activation, improve immunosuppression in the tumor microenvironment (TME) and improve the T-cell mediated immune response against and toxicity in EGFR-expressing tumor cells. Both PD-1 and CTLA-4 negatively regulate T-cell activation and proliferation, and play a key role in immunosuppression within the TME. EGFR, a receptor tyrosine kinase that is overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation.

autologous EGFRt/19-28z/4-1BBL CAR T lymphocytes

Genetically modified autologous T lymphocytes transduced with a replication incompetent retroviral vector expressing both tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) and a chimeric T-cell antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment), fused to the extracellular, transmembrane and intracellular signaling domains of the T-cell co-stimulatory receptor CD28, the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (19-28z), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous EGFRt/19-28z/4-1BBL CAR T lymphocytes are directed to CD19-expressing tumor cells, which induces selective toxicity in CD19-expressing tumor cells. These cells also express 4-1BBL, a secreted protein and member of the TNFSF of growth factors, that induces proliferation of T cells and may help reverse immunosuppression in the tumor environment. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. The inclusion of the CD28 signaling domain may increase proliferation of T cells and antitumor activity compared to the inclusion of the CD3-zeta chain alone. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response.

autologous EGFRt/BCMA-41BBz-targeted CAR T cells

A preparation of autologous T lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) fused to the co-stimulatory domain of 4-1BB (CD137) and the CD3-zeta (CD3z) T-cell signaling domain, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous EGFRt/BCMA-41BBz-targeted CAR T cells are directed to, and induce selective toxicity in, BCMA-expressing tumor cells. Devoid of both ligand-binding domains and tyrosine kinase activity, the expressed EGFRt facilitates in vivo detection of the administered, transduced T cells and, if the administered T cells cause unacceptable side effects, can promote elimination of those cells through a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The 4-1BB costimulatory signaling domain enhances both proliferation of T cells and antitumor activity. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and is overexpressed on malignant plasma cells.

autologous engineered TCR-T cells KSH01

A preparation of autologous T lymphocytes genetically modified to express a T-cell receptor (TCR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with a TCR specific for the TAA, and expanded ex-vivo. Upon reintroduction into the patient, the autologous engineered TCR-T cells KSH01 target and bind to tumor cells expressing the TAA, which may induce cell death in and halt the growth of cancer cells expressing the undisclosed TAA.

autologous engineered TCR-T cells KSX01

A preparation of autologous T lymphocytes genetically modified to express a T-cell receptor (TCR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with a TCR specific for the TAA, and expanded ex-vivo. Upon reintroduction into the patient, the autologous engineered TCR-T cells KSX01 target and bind to tumor cells expressing the TAA, which may induce cell death in and halt the growth of cancer cells expressing the undisclosed TAA.

autologous enhanced NY-ESO-1 TCR engineered T cells GSK4427296

A preparation of human autologous engineered T lymphocytes that express an affinity-enhanced T-cell receptor (TCR) specific for the cancer-testis antigen 1 (NY-ESO-1; New York esophageal antigen-1), with potential immunostimulating and antineoplastic activities. Upon administration, autologous enhanced NY-ESO-1 TCR engineered T cells GSK4427296 recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA) and member of the cancer-testis antigen (CTA) family, is found in normal testis and on the surface of various tumor cell types, and is not, or is minimally, expressed in normal, healthy cells. The TCR T cells are manufactured and expanded using specific epigenetic reprogramming (Epi-R) technology with continuous NY-ESO-1 antigen exposure and stimulation to alter the phenotypic T-cell profile. This allows for the creation of more CD8-positive stem-like T cells, thereby increasing stemness properties which could potentially improve T-cell function, and increase T-cell proliferation, functional persistence, metabolic fitness, self-renewal, and enhance durable anti-tumor responses.

autologous Epstein-Barr virus-specific cytotoxic T lymphocytes

A preparation of lymphocytes harvested from a patient with an Epstein-Barr virus (EBV)-positive tumor. Ex vivo, the lymphocytes are activated against EBV-specific antigens and then returned to the patient, where they mount a specific immune response against EBV-positive tumor cells.

autologous Epstein-Barr virus-transformed B-lymphoblastoid cell vaccine

A cell-based vaccine composed of autologous lymphoblastoid B cells activated against Epstein-Barr virus (EBV) in vitro with potential immunoprotective activity. Upon prophylactic administration, this vaccine may stimulate specific cytotoxic T-lymphocyte (CTL) and antibody responses against EBV-transformed B cells, thereby preventing an EBV-induced post-transplantation lymphoproliferative disorder.

autologous expanded mesenchymal stem cells OTI-010

Multipotent self-renewing adherent non-hematopoietic stromal cells harvested from a patient's bone marrow and grown in vitro. When injected back into the patient, autologous expanded mesenchymal stem cells OTI-010 may differentiate into various mesenchyme-derived cell types and, in some instances, may augment bone marrow engraftment after whole-body irradiation.

autologous follicular lymphoma-derived idiotype vaccine

A patient-specific cancer vaccine directed against the soluble protein idiotype of an individual follicular lymphoma with potential antineoplastic activity. A patient-specific follicular lymphoma-derived anti-idiotype vaccine may be composed of a patient-specific, synthetic idiotype-related peptide (such as one corresponding to a hypervariable region of an IgG heavy chain) conjugated to the immunostimulant carrier protein keyhole limpet hemocyanin (KLH). Upon administration, this vaccine may induce an idiotype-specific cytotoxic T-lymphocyte (CTL) response against follicular lymphoma cells expressing the idiotype, resulting in tumor cell lysis.

autologous FRa-4SCAR-expressing T cells 4SCAR-FRa

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-folate receptor alpha (FRa; folate receptor 1; FOLR1) single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (CD3zeta; CD3z), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous FRa-4SCAR-expressing T cells 4SCAR-FRa are directed to and induce selective toxicity in FRa-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. FRa is overexpressed in various tumor cell types, and is associated with increased leukemic cell proliferation and aggressiveness. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous gamma delta T-cell receptor-expressing T cells TEG002

A preparation of autologous T lymphocytes genetically engineered to express a defined gamma delta T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon administration of the autologous gamma delta TCR-expressing T cells TEG002, these cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.

autologous gamma-globinG16D/sh RNA734 gene-transduced CD34-positive cells CSL200

A preparation of autologous, CD34-positive hematopoietic stem cells (HSCs) transduced ex vivo with a lentiviral vector encoding for an engineered form of human gamma-globin (hemoglobin-gamma) gene, gamma-globin G16D, and a short-hairpin (sh) RNA734, with potential to restore gamma-globin expression and function. Autologous CD34-positive stem cells are isolated from the patient's own bone marrow and the cells are transduced with the lentiviral vector. Upon re-infusion of the CD34-positive cells back into the patient, these cells express gamma-globinG16D, thereby replacing defective beta globin chains with gamma globin chains allowing the body to make fetal hemoglobin (HbF) and thus healthy red blood cells with a greater oxygen-carrying capacity. Gamma-globin comprises is the gamma-chain of HbF; reactivation of HbF in disorders where beta-globin is defective in adult hemoglobin (HbA), such as sickle cell disease and beta thalassemia, may ameliorate these conditions. The G16D form of gamma-globin has increased anti-sickling activity compared to the wild type protein. The shRNA734 is used for positive gene selection.

autologous gamma-retroviral MSGV1 139 scFv EGFRvIII CAR gene-modified T cells

A preparation of autologous T lymphocytes transduced with the gamma retroviral vector MSGV1 expressing a chimeric T-cell antigen receptor (CAR) consisting of a single-chain variable fragment (scFv) from a specific antibody clone (mAb139) that targets a mutant form of epidermal growth factor receptor (EGFR) known as variant III (EGFRvIII; EGFR-vIII), with potential antineoplastic activity. Upon intratumoral administration, the gamma-retroviral MSGV1 139 scFv EGFRvIII CAR gene-modified T cells specifically target and bind to tumor cells expressing EGFRvIII, leading to selective cytotoxicity in EGFRvIII-expressing tumor cells. EGFRvIII, a tumor-associated antigen (TAA) encoded by an in-frame deletion of exons 2-7 in the EGFR gene, is specifically overexpressed by a subset of tumor cells and is not expressed in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.

autologous GCC-targeting CAR T Cells GCC19CART

A preparation of autologous T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) targeting the enterocyte differentiation antigen guanylyl cyclase C (GUCY2C) that are activated with CAR T cells specific for the CD19 antigen, and coupled to as of yet not fully elucidated signaling domains, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous GCC-targeting CAR T cells GCC19CART are directed to, specifically bind to, activate, proliferate and release cytokines that promote killing of GCC-expressing tumor cells. GCC is overexpressed in various tumor cell types. The activation of the GCC-targeting T cells by activated CD19 CAR that secrete cytokines, enhances CAR T-cell activation and proliferation, and may increase the T-cell-mediated killing of GCC-expressing tumor cells.

autologous GCC-targeting CAR T cells LCAR-G08

A preparation of autologous T lymphocytes that are genetically engineered, using a lentiviral vector, to express a chimeric antigen receptor (CAR) targeting the enterocyte differentiation antigen guanylyl cyclase C (GUCY2C), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous GCC-targeting CAR T cells LCAR-G08 are directed to, specifically bind to, activate, proliferate and release cytokines that promote killing of GCC-expressing tumor cells. GCC is overexpressed in various tumor cell types.

autologous gene-modified gamma delta T cells

A preparation of genetically modified autologous gamma delta T lymphocytes transduced with a lentiviral vector to encode a DNA repair enzyme, with potential immunomodulating and antineoplastic activities. Upon administration, the autologous gene-modified gamma delta T cells secrete interferon-gamma (IFN-g) and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The transduction of gamma delta T cells may confer resistance to alkylating chemotherapeutic agents including temozolomide and allow the use of gamma delta T cells as an adjunct to these agents.

autologous gene-modified PD-1-positive T lymphocytes Sc610

A preparation of autologous programmed cell death protein 1 (PD-1; PDCD1; CD279)-positive T lymphocytes transduced with a lentiviral vector encoding for an as of yet undisclosed receptor, with potential immunostimulatory and antineoplastic activities. Upon administration, autologous gene-modified PD-1-positive T lymphocytes Sc610 bind to tumor cells expressing the antigen for the as of yet undisclosed receptor, which may result in specific cytotoxic T-lymphocyte (CTL)-mediated tumor cell killing.

autologous gene-modified PD-1-positive T lymphocytes ScTIL210

A preparation of autologous programmed cell death protein 1 (PD-1; PDCD1; CD279)-positive T lymphocytes transduced with a lentiviral vector encoding for an as of yet undisclosed receptor, with potential immunomodulating activity. Upon administration, autologous gene-modified PD-1-positive T lymphocytes ScTIL210 may recognize and kill the patient's tumor cells through as of yet not elucidated receptor binding.

autologous genetically-modified MAGE-A4 C1032 CD8alpha T cells

Autologous human T lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human melanoma antigen A4 (MAGE-A4) and the CD8alpha co-receptor, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous genetically-modified MAGE-A4 C1032 CD8alpha T cells bind to tumor cells expressing MAGE-A4. This may result in both inhibition of growth and increased cell death of MAGE-A4-expressing tumor cells. The tumor-associated antigen MAGE-A4, a member of the MAGE-A family of cancer testis antigens, is overexpressed by a variety of cancer cell types. Co-expression of CD8alpha may broaden the immune response against tumors and increase antitumor activity by converting CD4+ helper T cells into CD8+ cytotoxic T cells.

autologous glioma cell lysate

A cell lysate derived from glioma cells with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous glioma cell lysate exposes the immune system to an undefined amount of glioma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the glioma TAA-expressing cells, resulting in glioma cell lysis.

autologous GM-CSF-secreting breast cancer vaccine

An autologous tumor cell vaccine containing irradiated breast cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Autologous breast cancer cells are transduced ex vivo with an adenovirus vector encoding the GM-CSF gene and irradiated and then reintroduced into the patient. Upon repeated subcutaneous administration of the vaccine, autologous GM-CSF-secreting breast cancer cells secrete GM-CSF, which may stimulate a tumor-specific cytotoxic T-lymphocyte (CTL) response.

autologous GM-CSF-secreting lethally irradiated colorectal cancer cell vaccine

A lethally irradiated, autologous colorectal cancer vaccine consisting of patient-specific colorectal cancer cells genetically modified to secrete the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon vaccination, the autologous GM-CSF-secreting lethally irradiated colorectal cancer cell vaccine releases GM-CSF. In turn, GM-CSF may increase the body's immune response against tumor cells by promoting the maturation and activation of dendritic cells (DCs), and enhancing tumor-specific antigen presentation to both B- and T-cells, which leads to better recognition of tumors by the immune system. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.

autologous GM-CSF-secreting lethally irradiated leukemia cell vaccine

An autologous cancer vaccine composed of lethally irradiated leukemia cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injection, the autologous GM-CSF-secreting lethally irradiated leukemia cell vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the immune system to attack tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B and T lymphocytes. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.

autologous GM-CSF-secreting lethally irradiated lung cancer vaccine

An autologous lung cancer vaccine consisting of patient-specific lung cancer cells genetically modified to secrete granulocyte-macrophage colony stimulating factor (GM-CSF), an immunostimulatory cytokine. GM-CSF modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production and may reverse treatment-induced neutropenias. This agent also promotes antigen presentation, up-regulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function and may augment host antitumoral immunity. For safety, cells are irradiated prior to vaccination.

autologous GM-CSF-secreting lethally irradiated pancreatic cancer vaccine

An irradiated, autologous pancreatic cancer vaccine consisting of patient-specific pancreatic cancer cells genetically modified to secrete the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon vaccination, GVAX pancreatic cancer vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the body's immune system against tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B and T cells. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.

autologous GPC3/NY-ESO-1/AFP-specific CD8-positive T lymphocytes

A preparation of autologous CD8-positive T lymphocytes that are exposed, ex vivo, to multiple specific hepatocellular carcinoma (HCC) antigens, including glypican (GPC)-3, New York esophageal squamous cell carcinoma-1 (NY-ESO-1) and alpha-fetoprotein (AFP), with potential immunostimulating and antineoplastic activities. Upon infusion of the GPC3/NY-ESO-1/AFP-specific CD8-positive T lymphocytes, the T cells specifically target and lyse cells expressing the targeted HCC neoantigens.

autologous HBV-specific TCR-expressing T lymphocytes SCG101

A preparation of human autologous T lymphocytes transduced with a retroviral vector encoding for a T-cell receptor (TCR) specific for HLA-A*02-restricted human hepatitis B virus (HBV) surface antigen (HBsAg) peptide, with potential antineoplastic activity. Upon administration, the autologous HBV-specific TCR-expressing T lymphocytes SCG101 recognize and bind to HBV antigen-positive cells, which induces cytotoxic T-lymphocyte (CTL)-mediated elimination of HBV antigen-positive cells, including those in HBV-related hepatocellular carcinoma (HCC).

autologous HBV-specific TCR-redirected T lymphocytes

A preparation of human autologous T-lymphocytes transduced with a viral vector encoding for a T cell receptor (TCR) specific for a human hepatitis B virus (HBV) surface antigen (HBsAg), with potential antineoplastic activity. Following administration, the autologous HBV antigen specific TCR-redirected autologous T lymphocytes recognize and bind to the HBV antigen-positive cells, which induces cytotoxic T-lymphocyte (CTL)-mediated elimination of HBV antigen-positive cancer cells. HBV antigens are found on HBV-positive cells and HPV-induced hepatocellular carcinoma (HCC).

autologous heat-shock protein 70 peptide vaccine AG-858

A recombinant cancer vaccine made with tumor-derived heat shock protein 70 (HSP70) peptide complexes. HSP70 associates with antigenic peptides, transporting them into antigen presenting cells (APC) for processing. Tumor-derived HSP70-peptide complexes used in vaccine preparations have been shown to prime tumor immunity and tumor-specific T cells in animal models.

autologous HER2-CAR-modified adenovirus-specific cytotoxic T lymphocytes

A population of autologous cytotoxic T lymphocytes (CTLs) specifically reactive to human adenovirus (Ad) that have been transduced with a retroviral vector expressing a second-generation human epidermal growth factor receptor type 2 (HER2; EGFR2; ErbB2)-specific chimeric antigen receptor (CAR) comprised of an exodomain based on a anti-CD22 single chain variable fragment (scFv) from the anti-HER2 monoclonal antibody FRP5 that is linked to the costimulatory domains of CD28 and the zeta chain of the TCR/CD3 complex (CD3zeta), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous HER2-CAR-modified Ad-specific CTLs are directed to and induce selective toxicity in HER2-expressing tumor cells. Additionally, these cells may help reconstitute Ad-specific CTL responses in immunocompromised individuals and others at risk of developing Ad-infection. HER2, a receptor tyrosine kinase (RTK) overexpressed by a variety of tumor cell types, belongs to the EGFR superfamily and plays a key role in tumor cell proliferation.

autologous HER2-specific/EGFRt-expressing CD4/CD8-positive CAR T cells

A preparation of CD4+ and CD8+ autologous T lymphocytes transduced with a lentiviral vector expressing a human epidermal growth factor receptor type 2 (HER2; EGFR2; ErbB2)-specific chimeric antigen receptor (CAR) coupled to a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, the autologous HER2-specific/EGFRt-expressing CD4/CD8-positive CAR T cells are directed to and induce selective toxicity in HER2-expressing tumor cells. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of these cells through an anti-EGFR antibody-induced antibody-dependent cellular cytotoxicity (ADCC) response. HER2, a receptor tyrosine kinase (RTK) overexpressed by a variety of tumor cell types, belongs to the EGFR superfamily and plays a key role in tumor cell proliferation.

autologous HER2-targeted dual-switch CAR T cells BPX-603

A preparation of autologous T lymphocytes that express a chimeric antigen receptor (CAR) for the human epidermal growth factor receptor 2 (EGFR2; HER2; HER-2) and a dual-switch composed of chemical inducer of dimerization (CID)-inducible co-activation domain MyD88/CD40 (inducible MC; iMC), in which both the MyD88 and CD40 lack their extracellular domains, and an inducible caspase 9 (iCasp9) safety switch (CaspaCIDe), consisting of the CID-binding domain coupled to the signaling domain of caspase-9, with potential immunomodulating and antineoplastic activities. Upon administration of autologous HER2-targeted dual-switch CAR T cells BPX-603, the T cells target and bind to HER2-expressing cancer cells. Upon subsequent administration of the CID agent rimiducid (AP1903), this agent targets and binds to the drug binding domain of iMC and activates iMC, which leads to the activation of both CD40- and MyD88-mediated signal transduction pathways. This allows for enhanced T-cell proliferation, persistence and resistance to T-cell exhaustion and upregulation of immunomodulatory cytokines within the tumor microenvironment (TME). This increases the anti-tumor activity of the administered T cells, compared to T cells without the iMC activation-switch. As these T cells are engineered to only be fully activated by binding to both the HER2 antigen and rimiducid, T-cell proliferation, activity and toxicity can be controlled by adjusting the dose of rimiducid, thereby preventing uncontrolled T-cell activation which increases the safety of the administered T cells. The binding of rimiducid to the CID binding domain of iCasp9 results in the cross-linking and dimerization of iCasp9, which causes its activation. This results in the induction of caspase-mediated apoptosis of the transduced cells and allows for the removal of inappropriately activated cells, thereby preventing toxicity of the administered cells. HER2, a tumor-associated antigen (TAA), plays a key role in tumor cell proliferation and tumor vascularization.

autologous HIV Gag-specific CD4+ T cells AGT103-T

A preparation of autologous, human immunodeficiency virus (HIV) Gag-specific, cluster of differentiation 4 (CD4)-positive T lymphocytes, with potential antiviral activity. Autologous HIV Gag-specific CD4+ T cells AGT103-T are prepared via ex vivo stimulation of autologous peripheral blood mononuclear cells (PBMCs) with Gag peptides, and the Gag-specific CD4+ T cells are transduced with the recombinant lentiviral vector AGT103 encoding inhibitory RNA targeting the HIV coreceptor C-C chemokine receptor type 5 (CCR5) and HIV sequences within the Vif/Tat coding regions. Upon administration, autologous HIV Gag-specific CD4+ T cells AGT103-T may prevent infection by CCR5- or CXCR4-tropic strains of HIV, reduce the depletion of CD4+ T cells upon HIV exposure and prevent latently-infected cells from releasing new HIV particles.

autologous HLA-A*11:01 KRASG12V-specific TCR-expressing CD8- and CD4-positive T lymphocytes AFNT-211

A preparation of autologous HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-positive CD8- and CD4-positive T lymphocytes that have been transduced with a lentiviral vector expressing a HLA-A*11:01-restricted T-cell receptor (TCR) that recognizes the glycine to valine point mutation at position 12 (G12V) variant of Kirsten rat sarcoma (K-RAS; KRAS), and enhanced with the wildtype CD8alpha/beta (CD8a/b) coreceptor, and a FAS-41BB switch receptor, and subsequently expanded ex vivo, with potential immunomodulating and antineoplastic activities. When reintroduced into the patient, the autologous HLA-A*11:01 KRASG12V-specific TCR-expressing CD8- and CD4-positive T lymphocytes AFNT-211 specifically recognize and bind to KRASG12V expressed on tumor cells, which results in both cytokine secretion and cell lysis in tumor cells overexpressing KRASG12V. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. The KRASG12V mutation is overexpressed in a variety of cancer cell types. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis. CD8a/b coreceptor and a FAS-41BB switch receptor improve T-cell persistence. The introduction of the CD8a/b coreceptor enables a coordinated CD4+/CD8+ T-cell response and enables CD4+ T-cell recognition of KRASG12V and enhances cytotoxicity. FAS-41BB converts the FAS ligand (FASL) tumor microenvironment (TME) death signal into a costimulatory signal through 41BB activation, thereby enhancing the durability of the anti-tumor immune response against FASL-expressing tumor cells.

autologous HNSCC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine

A vaccine consisting of lethally irradiated human fetal lung fibroblasts (Medical Research Council 5 or MRC-5) transfected with autologous tumor DNA derived from a head and neck squamous cell carcinoma (HNSCC), with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous HNSCC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine expresses HNSCC tumor-associated antigens (TAAs), which may activate the immune system to induce a cytotoxic T-lymphocyte (CTL) response against HNSCC cells. The MRC-5 cell line, established in 1966, is a human diploid lung fibroblast cell line derived from the human lung tissue of a 14-week-old male fetus.

autologous HPV-16/18 E6/E7-specific TGF-beta-resistant T lymphocytes

A preparation of autologous transforming growth factor-beta (TGF-beta)-resistant cytotoxic T-lymphocytes (CTL) reactive to human papilloma virus (HPV) types 16 and 18 E6/E7 antigens, with potential antineoplastic activity. Autologous T-lymphocytes from a HPV-positive cancer patient are exposed to and stimulated with dendritic cells (DCs) loaded with the HPV-16/18 proteins E6 and E7. In turn, the HPV-16/18 E6/E7-specific T-lymphocytes are transduced with a retroviral vector expressing a dominant-negative mutant of type II transforming growth factor (TGF)-beta receptor, which blocks signaling mediated by all three TGF-beta isoforms. Following re-administration to patients with HPV-positive tumors, the HPV-16/18 E6/E7-specific TGF-beta-resistant T-lymphocytes target HPV16/18 E6/E7-positive cells, which may result in a specific cytotoxic T-lymphocyte (CTL) response, followed by cell lysis and the inhibition of tumor cell proliferation. Tumors expressing TGF-beta inhibit T-lymphocyte activation and expansion.

autologous HPV-E6/E7-targeting T cells

A preparation of autologous T lymphocytes that are specifically reactive towards the human papillomavirus (HPV) viral oncoproteins E6 and E7, with potential immunomodulating and antineoplastic activities. Following leukapheresis and ex vivo priming and expansion, the autologous HPV E6/E7-targeting T cells are re-introduced into the patient, where they target and kill tumor cells expressing these HPV tumor-associated antigens (TAAs). HPV E6 and E7 are overexpressed on certain tumor cell types and play key roles in tumor cell proliferation.

autologous HPV-specific cytotoxic T lymphocytes

A population of autologous cytotoxic T lymphocytes (CTLs) that are specifically reactive to human papillomavirus (HPV), with potential antiviral and antineoplastic activities. Upon infusion of the autologous HPV-specific CTLs, these CTLs induce selective toxicity in HPV-positive cancer cells and other HPV-infected cells. HPV is associated with various cancer cell types.

autologous HPV16 E7-specific HLA-A*02:01-restricted TCR gene engineered lymphocytes KITE-439

A preparation of autologous T lymphocytes that have been genetically modified to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*02:01-restricted human papillomavirus type 16 isoform E7 protein (HPV16 E7) with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous HPV16 E7-specific HLA-A*02:01-restricted T lymphocytes KITE-439 target and bind HPV16 E7-expressing tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing the HPV16 E7 antigen. HPV16 E7, a cell surface glycoprotein and tumor-associated antigen (TAA), is overexpressed in various HPV-mediated cancers.

autologous HPV16/HPV18/Survivin-specific CD8+ T cells NEXI-003

A preparation of autologous CD3+ CD4- CD8+ T cells targeting multiple human papilloma virus (HPV) tumor-associated antigens, including HPV types 16 and 18 antigens and survivin, with potential immunomodulating and antineoplastic activities. Following leukapheresis and ex vivo priming and expansion, the autologous HPV16/HPV18/survivin-specific CD8+ T cells NEXI-003 are re-introduced into the patient, where they target and kill tumor cells expressing these HPV tumor-associated antigens.

autologous human anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T lymphocytes

A preparation of a defined ratio of CD4+ and bulk CD8+ autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing a human anti-CD19 single chain variable fragment (scFv) fused to the signaling domain of 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous human anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T lymphocytes are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response. The 4-1BB costimulatory signaling domain enhances both proliferation of T cells and antitumor activity.

autologous iC9-deltaNGFR-CD19CAR-CD3zeta-4-1BB-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been transduced with a retroviral vector to express a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) fused to a human immunoglobulin G1 (IgG1) hinge and a CD8alpha transmembrane domain, linked to the co-stimulatory molecule 4-1BB (CD137) and the cytoplasmic portion of the zeta chain of the human T-cell receptor (CD3zeta), containing the apoptosis-inducible suicide gene human caspase 9 (iCASP9 or iC9), linked to a drug binding domain, and a truncated low-affinity nerve growth factor receptor (deltaNGFR), with potential immunostimulating and antineoplastic activities. The iC9 construct consists of the sequence of the human FK506-binding protein (FKBP12) with an F36V mutation, connected through a Ser-Gly-Gly-Gly-Ser linker to the gene-encoding human caspase 9, which is deleted of its endogenous caspase activation and recruitment domain. Upon transfusion, the iCasp9-deltaNGFR-CD19CAR-CD3zeta-4-1BB-expressing autologous T lymphocytes target and bind to CD19-expressing neoplastic B cells. Prior to administration, deltaNGFR is used to select the CAR19-transduced T cells for further enrichment by flow cytometry using an anti-NGFR antibody.

autologous iC9-GD2-CAR-expressing VZV-specific T lymphocytes

Genetically modified, autologous varicella zoster virus (VZV)-specific T-lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the disialoganglioside GD2, which contains the signaling domains for the co-stimulatory molecules CD28 and CD134 (OX-40), and the suicide gene, inducible caspase 9 (iCasp9 or iC9), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, iC9-GD2-CD28-OX40-expressing T lymphocytes target the GD2 antigen on tumor cells for selective toxicity against GD2-expressing tumor cells. iCasp9 consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the FKBP12-F36V drug binding domain, activates caspase 9, and results in apoptosis of the administered T-cells. Expression of the iCasp9 gene in T cells for adoptive transfer increases safety and broadens the scope for their clinical applications. The tumor-associated antigen GD2 is overexpressed on the surface of almost all tumors of neuroectodermal origin. OX40 and CD28, both T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation. An additional VZV vaccine can be administered to increase T-cell activity.

autologous iC9-GD2CAR-CD28-CD3zeta-IL-15-expressing T lymphocytes

A preparation of autologous T lymphocytes that have been transduced with the retroviral vector SFG, a Moloney murine leukemia (Mo-MuLV) virus-based vector, expressing both an extracellular domain consisting of interleukin 15 (IL-15) and a GD2-specific chimeric antigen receptor (CAR) derived from the monoclonal antibody 14G2a, linked to the CD28 and CD3zeta (TCRzeta; CD247) costimulatory signaling domains and containing the suicide gene, inducible caspase 9 (iCasp9 or iC9), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous iC9-GD2CAR-CD28-CD3zeta-IL-15-expressing T lymphocytes recognize, bind to and induce selective cytotoxicity in GD2-expressing tumor cells. IL-15 is a pro-survival cytokine that promotes T-cell persistence and potentiates the immune response against tumor cells. Incorporation of the costimulatory signaling domains increases T-cell function, expansion, and survival. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered CAR-T cells lead to unacceptable side effects, the chemical homodimerizer AP1903, which binds to the FKBP12-F36V drug-binding domain, activates caspase 9 and results in apoptosis of the administered CAR-T cells, can be administered. GD2, a disialoganglioside and tumor-associated antigen (TAA), is overexpressed on the surface of neuroblastoma cells and other neuroectoderm-derived neoplasms and is minimally expressed on normal, healthy cells.

autologous iCASP9-CD19-expressing T lymphocytes

A preparation of autologous T lymphocytes that are transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19 and the inducible suicide gene human caspase 9 (iCASP9 or iC9), that is linked to a drug binding domain, with potential immunomodulating and antineoplastic activities. The iCASP9 construct consists of the entire coding sequence for the human FK506-drug binding protein (FKBP12) with an F36V mutation (FKBP12-F36V) that is linked to the gene encoding iC9, which is a modified form of the CASP9 gene where the sequences encoding the endogenous caspase activation and recruitment domains have been deleted. Upon intravenous administration, autologous iCASP9-CD19-expressing T lymphocytes (iC9-CAR19 T-cells) target and bind to CD19-expressing tumor cells, thereby selectively lysing these tumor cells. If the administered T cells cause unacceptable side effects, the chemical homodimerizer AP1903, which binds to the FKBP12-F36V drug-binding domain, can be administered; this induces caspase 9 expression, and results in apoptosis of the administered iC9-CAR19 T cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.

autologous iCasp9-deltaNGFR-CD19CAR-expressing T cells

A preparation of autologous T lymphocytes that are transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the CD19 antigen, the suicide gene, inducible human caspase 9 (iCasp9 or iC9), and a truncated low-affinity nerve growth factor receptor (deltaNGFR), with potential immunomodulating and antineoplastic activities. The iCasp9 construct consists of the entire coding sequence for the human FK506-drug binding protein (FKBP12) with an F36V mutation (FKBP12-F36V) that is linked to the gene encoding human caspase 9, which is deleted of its endogenous caspase activation and recruitment domains. Upon intravenous administration, autologous iCasp9-deltaNGFR-CD19CAR-expressing T cells are selectively toxic to CD19-expressing tumor cells. If the administered T-cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the FKBP12-F36V drug binding domain, activates caspase 9, and results in apoptosis of the administered CAR19 T cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Prior to administration, deltaNGFR, is used to select the CAR19-transduced T cells for further enrichment by flow cytometry using an anti-NGFR antibody.

autologous IL-12/multi-targeted primed T cells RPTR 168

A preparation of genetically modified, multi-antigen-targeted autologous T lymphocytes, tethered with the human immunostimulatory cytokine interleukin-12 (IL-12), with potential immunostimulating and antineoplastic activities. RPTR 168 is prepared from monocyte-derived dendritic cells (moDCs) that are pulsed with five tumor-associated antigens (TAAs) to expand cytotoxic T lymphocytes (CTLs) that are subsequently loaded with IL-12. Upon administration, the autologous IL-12/multi-targeted primed T cells RPTR 168 specifically target tumor cells expressing the five TAAs, which lead to a specific cytotoxic T-lymphocyte (CTL)-mediated killing of these tumor cells. In addition, IL-12 expression activates the immune system by promoting the secretion of interferon-gamma (IFN-g), activating natural killer cells (NKs), and inducing CTL responses, which may further increase tumor cell death and decrease tumor cell proliferation.

autologous IL-15-expanded HER2-specific CD4+ T cells

A preparation of autologous, interleukin-15 (IL-15)-expanded, human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2)-specific, cluster of differentiation 4 (CD4)-positive T lymphocytes, with potential immunostimulating and antineoplastic activities. Autologous HER2-specific CD4+ T cells are expanded ex vivo with IL-15. Upon reintroduction into the patient, the autologous IL-15-expanded HER2-specific CD4+ T-cells recognize and stimulate a T-cell-mediated immune response against HER2-expressing tumor cells. HER2, a receptor tyrosine kinase (RTK) mutated or overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. IL-15 is a cytokine that enhances T-cell expansion.

autologous IL-15/IL-21-armored anti-glypican-3 CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3), interleukin-15 (IL-15) and interleukin-21 (IL-21), with potential immunostimulating and antineoplastic activities. Upon administration, autologous IL-15/IL-21-armored anti-GPC3 CAR T cells specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation. The cytokines IL-15 and IL-21 promote T-cell survival, expansion and persistence, which may potentiate the immune response against tumor cells.

autologous IL-2-expressing B-CLL vaccine

A cancer vaccine consisting of autologous, B-chronic lymphocytic leukemia (B-CLL) cells harvested from a patient and transduced ex vivo with an adenoviral vector encoding the gene for the human cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon reintroduction into the patient, the autologous IL-2-expressing B-CLL vaccine expresses IL-2, stimulates natural killer (NK) cells, and may enhance the cytotoxic T-lymphocyte (CTL) immune response against the patient's B-CLL cells.

autologous IL-21-modulated CD8+ MART1-specific T cells

A preparation of interleukin 21 (IL-21) stimulated, CD8+ T-lymphocytes sensitized to MART-1 (melanoma antigen recognized by T-cells) antigen with potential immunostimulating and antineoplastic activities. CD8+ T-lymphocytes are exposed ex vivo to autologous dendritic cells (DCs) pulsed with MART-1 antigen peptide and grown in the presence of IL-21. These tumor-reactive T-cells may stimulate a host immune response against tumor cells expressing the MART-1 antigen, resulting in tumor cell lysis. MART-1 is expressed by certain types of melanoma cells. IL-21, a cytokine involved in the regulation of cellular immune responses, may play a key role during priming of antigen-specific CD8+ T cells and may enhance proliferation of the CTLs.

autologous IL-7-expanded HER2-specific CD4+ T cells

A preparation of autologous, interleukin-7 (IL-7)-expanded, human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2)-specific, cluster of differentiation 4 (CD4)-positive T lymphocytes, with potential immunostimulating and antineoplastic activities. Autologous HER2-specific CD4+ T cells are expanded ex vivo with IL-7. Upon reintroduction into the patient, the autologous IL-7-expanded HER2-specific CD4+ T cells recognize and stimulate a T-cell-mediated immune response against HER2-expressing tumor cells. HER2, a receptor tyrosine kinase (RTK) mutated or overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. IL-7 is a cytokine that promotes the proliferation and survival of T cells.

autologous IL-7-expressing TILs ADP-TILIL7

A preparation of autologous tumor infiltrating lymphocytes (TILs) engineered to express the cytokine interleukin-7 (IL-7), with potential immunomodulating and antineoplastic activities. The TILs are isolated from an autologous tumor sample and transduced with a lentiviral vector to express IL-7. Upon infusion of the autologous IL-7-expressing TILs ADP-TILIL7 back into the patient, the TILs specifically recognize, target and kill the patient's tumor cells. IL-7 is a cytokine that promotes the proliferation and survival of T cells and may enhance the activity and durability of the TILs.

autologous IL-7/CCL19-expressing anti-GM2 CAR T cells NIB-101

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) ganglioside GM2 (GM2) and producing the immune regulators interleukin-7 (IL-7) and C-C motif chemokine 19 (CCL19) using PRIME (proliferation-inducing and migration-enhancing) technology, with potential immunostimulating and antineoplastic activities. Upon administration, autologous IL-7/CCL19-expressing anti-GM2 CAR T cells NIB-101 target and bind to GM2-expressing tumor cells, thereby inducing selective toxicity in GM2-expressing tumor cells. In addition, as IL-7 promotes the proliferation and survival of T-cells and CCL19 enhances the migration of host T cells and dendritic cells (DCs), the production of IL-7 and CCL19 by NIB-101 allows for enhanced trafficking and accumulation of the PRIME CAR T cells and other endogenous immune cells, including T cells and DCs in tumor tissues. This further activates the host immune system to induce anti-tumor immune responses to various cancer antigens and against tumor cells lacking the CAR target antigen. GM2, a type of glycosphingolipid, is overexpressed on the surface of many cancer cells, such as multiple myeloma (MM) cells and neuroblastoma cells.

autologous IL-7Ra-expressing Tris-CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified and lentivirally transduced to express a dual-target chimeric antigen receptor (CAR) and a truncated form of the cytokine receptor interleukin-7 (IL-7) receptor alpha (IL-7Ra), with potential immunostimulating and antineoplastic activities. Upon administration, autologous IL-7Ra-expressing Tris-CAR T cells target and bind to tumor cells expressing the targets, thereby inducing selective toxicity in these tumor cells. In addition, as IL-7/IL-7Ra-mediated signaling promotes the proliferation and survival of T cells, these tumor re-directed T cells may show enhanced expansion, survival and cytotoxicity.

autologous immunoglobulin idiotype-KLH conjugate vaccine

A cancer vaccine composed of tumor-specific idiotype determinants derived from an individual's tumor cells which are conjugated to keyhole limpet hemocyanin, an immunostimulant carrier protein. When injected into the individual from whom the tumor cells were isolated, this vaccine may stimulate an antitumoral cytotoxic T-lymphocytic immune response.

autologous interferon-producing killer dendritic cells

A preparation of autologous dendritic cells (DC) with a molecular expression profile similar to both natural killer (NK) cells and DCs, with potential antineoplastic activity. Autologous interferon-producing killer dendritic cells (IKDCs) are characterized by double-negative expression of CD3 and CD19; these cells also express low levels of CD11 and are positive for B220. They are distinguished from plasmacytoid DCs (pDCs) by the absence of lymphocyte antigen 6C (Ly6C, Gr-1) expression. IKDCs produce interferon gamma (IFN-gamma) and interleukin (IL) -12, and are able to kill typical NK target cells using NK receptors while retaining DC-like antigen-presenting activity. Upon administration of the autologous IKDCs, these cells secrete high levels of IFN-gamma and, when in contact with tumor cells, mediate TNF-related apoptosis-inducing ligand (TRAIL)-dependent direct lysis of tumor cells. The resulting apoptotic tumor antigens may be presented by the IKDCs, thus activating the immune system to exert a cytotoxic T-lymphocyte (CTL) response to further eliminate tumor cells.

autologous interleukin-15-armored anti-glypican-3 CAR-iC9-expressing T lymphocytes

A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3) and express interleukin-15 (IL-15) and the suicide gene, inducible caspase 9 (iCasp9 or iC9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous IL-15-armored anti-GPC3 CAR-iC9-expressing T lymphocytes specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed on normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation. IL-15 is a pro-survival cytokine that potentiates, in addition to promoting T-cell proliferation and persistence, the immune response against tumor cells. The iCasp9 safety switch consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered CAR T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the FKBP12-F36V drug-binding domain, activates caspase 9 and results in apoptosis of the administered CAR T cells.

autologous KRAS G12D mutant-specific HLA-C*08:02-/KRAS G12D mutant-specific HLA-A*11:01-/KRAS G12V mutant-specific HLA-C*01:02-/TP53 R175H mutant-specific HLA-A*02:01-restricted TCR genes engineered T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-C*08:02-restricted oncogenic K-RAS (KRAS) substitution mutation G12D, a TCR specific for the HLA-A*11:01-restricted KRAS G12D, a TCR specific for the HLA-C*01:02-restricted KRAS G12V, and a TCR specific for the HLA-A*02:01-restricted oncogenic TP53 (p53) substitution mutation R175H, with potential antineoplastic activity. Upon isolation of peripheral blood lymphocytes (PBLs), transduction, expansion ex vivo and re-introduction into the patient, the autologous KRAS G12D mutant-specific HLA-C*08:02-/KRAS G12D mutant-specific HLA-A*11:01-/KRAS G12V mutant-specific HLA-C*01:02-/TP53 R175H mutant-specific HLA-A*02:01-restricted TCR genes engineered T-lymphocytes target and bind to tumor cells expressing the mutants KRAS G12D, KRAS G12V and/or TP53 R175H, resulting in cytotoxic T-lymphocyte (CTL)-mediated killing of KRAS G12D, KRAS G12V and/or TP53 R175H-expressing tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis. p53, a tumor suppressor gene, is mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.

autologous KRAS G12D-specific HLA-C*08:02-restricted TCR gene engineered T lymphocytes NT-112

A preparation of autologous T lymphocytes that have been genetically modified to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-C*08:02-restricted oncogenic K-RAS (KRAS) substitution mutation G12D, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous KRAS G12D-specific HLA-C*08:02-restricted TCR gene engineered T lymphocytes NT-112 target and bind to KRAS G12D-expressing tumor cells, resulting in cytotoxic T-lymphocyte (CTL)-mediated killing of KRAS-G12D-expressing tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.

autologous LMP1-/LMP2- specific cytotoxic T-lymphocytes

A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, with potential antineoplastic activity. Autologous dendritic cells and EBV-infected lymphoblastoid cell lines (LCL) from patients with EBV-positive nasopharyngeal carcinoma (NPC) are transduced with an LMP1/LMP2-expressing adenoviral vector, are irradiated, and then are used to stimulate and expand autologous CTL to produce autologous LMP1-/LMP2-specific CTL ex vivo. Administration of autologous LMP1-/LMP2- specific cytotoxic T-lymphocytes may result in a specific CTL response against tumor cells expressing LMP1 and LMP2, resulting in cell lysis and inhibition of tumor cell proliferation in vivo. Among a limited set of viral antigens expressed by NPC cells, LMP1 and LMP2 are weak immunogens which, nevertheless, are capable of inducing a T-lymphocyte response.

autologous LMP1/LMP2/EBNA1-specific HLA-A02:01/24:02/11:01-restricted TCR-expressing T lymphocytes YT-E001

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector encoding a T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A02:01/24:02/11:01-restricted Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, and EBV nuclear antigen 1 (EBNA1), with potential antineoplastic activity. Upon administration, the autologous LMP1/LMP2/EBNA1-specific, HLA-A02:01/24:02/11:01-restricted TCR-expressing T lymphocytes YT-E001 recognize and bind to HLA-presented EBV peptides, which may promote cell death and inhibit the growth of tumor cells expressing LMP1, LMP2 or EBNA1. LMP1, LMP2, and EBNA1 are expressed in various, EBV-associated malignancies, including nasopharyngeal cancer and EBV-positive Hodgkin lymphoma.

autologous lymphoid effector cells specific against tumor cells

A preparation of cytotoxic, autologous lymphoid effector cells specifically targeted towards tumor cells, with potential immunomodulating and antineoplastic activities. The autologous lymphoid effector cells are prepared by drawing a blood sample containing the required precursors for CD4+ helper T-cells, CD8+ cytotoxic T-cells, and natural killer (NK) cells from a cancer patient. The precursor cells are activated, selected and expanded to generate mature autologous lymphoid effector cells with the potential for enhanced tumor recognition. Upon readministration into the patient, the autologous lymphoid effector cells may induce both humoral and cellular immune responses against tumor cells. This may result in the immune-mediated inhibition of tumor cell proliferation, leading to tumor cell death.

autologous lymphoma cell lysate-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous lymphoma cells with potential immunostimulatory and antineoplastic activities. Upon intranodal administration, autologous lymphoma cell lysate-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against lymphoma cells, which may result in lymphoma cell lysis.

autologous lymphoma cell/allogeneic dendritic cell electrofusion hybrid vaccine

A cell-based cancer vaccine consisting of hybrid cells created by electrofusing allogeneic dendritic cells (DCs) and autologous lymphoma cells with potential immunostimulating and antitumor activities. Upon administration, autologous lymphoma cell/allogeneic dendritic cell electrofusion hybrid vaccine may stimulate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against specific autologous lymphoma-associated antigens, resulting in lymphoma cell apoptosis.

autologous lymphoma cell/autologous dendritic cell electrofusion hybrid vaccine

A cell-based cancer vaccine consisting of hybrid cells created by electrofusing autologous dendritic cells (DCs) and autologous lymphoma cells with potential immunostimulating and antitumor activities. Upon administration, autologous lymphoma cell/autologous dendritic cell electrofusion hybrid vaccine may stimulate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against specific autologous lymphoma-associated antigens, resulting in lymphoma cell apoptosis.

autologous lymphoma immunoglobulin-derived scFV-chemokine DNA vaccine

A plasmid DNA vaccine encoding an autologous lymphoma-derived idiotype-targeting immunoglobulin (Ig)-derived single chain variable fragment (scFv) fused to the chemokine macrophage inflammatory protein 3 alpha (MIP3a), with potential immunostimulating and antineoplastic activities. Upon intramuscular vaccination, the autologous lymphoma immunoglobulin-derived scFv-chemokine DNA vaccine is taken up by antigen-presenting cells (APCs) and stimulates the immune system to exert a cytotoxic T-lymphocyte (CTL) response against the idiotype expressed on the surface of B lymphoma cells. MIP3a, also called chemokine (C-C motif) ligand 20 (CCL20), is a chemotactic cytokine able to enhance the immune response through binding to chemokine receptors expressed on APCs.

autologous MAGE-A10-specific HLA-A2-restricted TCR c796 gene-engineered lymphocytes

Human autologous T lymphocytes transduced with a retroviral vector encoding a high-affinity T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A2-restricted, human melanoma-associated antigen A10 (MAGE-A10), clone 796 (c796), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-MAGE-A10(c796)-HLA-A2 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A2-positive patient. Upon reintroduction, the autologous MAGE-A10-specific, HLA-A2-restricted TCR c796 gene-engineered lymphocytes bind to tumor cells expressing the MAGE-A10 antigen, which may induce cell death in and halt the growth of MAGE-A10-expressing cancer cells. The tumor-associated antigen MAGE-A10, a member of the MAGE-A family of cancer/testis tumor-associated antigens (CT-TAAs), is overexpressed by a variety of cancer cell types.

autologous MAGE-A3-specific HLA-A*01-restricted T cell receptor gene engineered lymphocytes

Human autologous T lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*01-restricted, human melanoma-associated antigen A3 (MAGE-A3), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-MAGE-A3-HLA-A*01 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A*01-positive patient. Then, the autologous MAGE-A3-specific, HLA-A*01-restricted TCR gene engineered lymphocytes bind to tumor cells expressing the MAGE-A3 antigen, which may increase cell death and halt the growth of MAGE-A3-expressing cancer cells. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types.

autologous MAGE-A3-specific, HLA-A*01-restricted T cell receptor gene engineered lymphocytes

Human autologous T-lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*01-restricted, human melanoma-associated antigen A3 (MAGE-A3), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-MAGE-A3-HLA-A*01 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A*01-positive patient. Then, the autologous MAGE-A3-specific, HLA-A*01-restricted TCR gene engineered lymphocytes bind to tumor cells expressing the MAGE-A3 antigen, which may increase cell death and halt the growth of MAGE-A3-expressing cancer cells. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types.

autologous MAGE-A3/A6-specific TCR gene-engineered lymphocytes KITE-718

Human autologous T lymphocytes genetically modified to express a T-cell receptor (TCR) that specifically targets human melanoma-associated antigen A3 (MAGE-A3) and MAGE-A6 (MAGEA3/A6; MAGE-A3/A6), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with a gene expressing a TCR specific for the MAGE-A3/A6 antigens, expanded ex vivo, and reintroduced into the patient. Then, the autologous MAGE-A3/A6-specific TCR gene engineered lymphocytes KITE-718 target and bind to tumor cells expressing the MAGE-A3 and/or MAGE-A6 antigens. This halts the growth of and kills MAGE-A3/A6-expressing cancer cells. The tumor-associated antigens MAGE-A3 and MAGE-A6 are overexpressed on a variety of tumor cell types.

autologous MAGE-C2-specific HLA-A2-restricted TCR T lymphocytes

A preparation of autologous T lymphocytes genetically modified to express a T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A2-restricted, melanoma-associated antigen C2 (MAGE-C2; MC2), ALK epitope, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-MAGE-C2-HLA-A2 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A2-positive patient. Upon reintroduction, the autologous MAGE-C2-specific HLA-A2-restricted TCR T lymphocytes bind to tumor cells expressing the MAGE-C2 antigen, which may induce cell death in and halt the growth of MAGE-C2-expressing cancer cells. MAGE-C2, a cancer/testis tumor-associated antigen (CT-TAA), is overexpressed by a variety of cancer cell types.

autologous mbIL-12-expressing tumor infiltrating lymphocytes GT202

A preparation of autologous tumor infiltrating lymphocytes (TILs) engineered to express membrane-bound interleukin-12 (mbIL-12), with potential immunomodulating and antineoplastic activities. The TILs are isolated from an autologous tumor sample and engineered to express mbIL-12. Upon infusion of the autologous mbIL-12-expressing TILs GT202 back into the patient, the cells specifically recognize, target and kill the patient's tumor cells. IL-12 expression activates the immune system by promoting the secretion of interferon-gamma (IFNg), activating natural killer cells (NKs), and inducing cytotoxic T-lymphocyte (CTL) responses, further killing tumor cells.

autologous MCPyV-specific HLA-A02-restricted TCR-transduced CD4+ and CD8+ T cells FH-MCVA2TCR

A preparation of autologous CD4+ and CD62L-expressing CD8+ T cells transduced with a third generation lentiviral vector (LV) to express the high affinity T-cell receptor (TCR) A2 -MCC1, specific for the human leucocyte antigen (HLA)-A02-restricted Merkel cell polyomavirus (MCPyV; MCV) viral oncoprotein, with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, the autologous MCPyV-specific HLA-A02-restricted TCR-transduced CD8+ and CD4+ T cells FH-MCVA2TCR selectively bind to the KLLEIAPNC epitope (KLL epitope) within the MCPyV viral oncoprotein. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing the MCPyV viral oncoprotein. Additionally, tumor-specific HLA-A02-restricted CD4+ cells promote class I-restricted CD8+ proliferation, survival and effector functions by producing interleukin (IL)-2 and facilitating the activation of dendritic cells (DCs). MCPyV viral oncoprotein is highly expressed in Merkel cell carcinoma (MCC) caused by MCPyV.

autologous mDC3 vaccine

An antineoplastic vaccine composed of autologous mature dendritic cells (mDCs) pulsed with mutated peptides, with potential immunostimulating and antineoplastic activities. Upon administration, the autologous mDC3 vaccine may elicit a cytotoxic T-cell (CTL) response against cancer cells.

autologous mDC3/8-KRAS vaccine

An antineoplastic vaccine composed of autologous mature dendritic cells (mDCs) pulsed with mutant KRAS peptides specific to a patient's tumor mutation and human leukocyte antigen (HLA) type, with potential immunostimulating and antineoplastic activities. Upon administration, this vaccine, which is administered as an mDC3 primer, followed by an mDC8 booster, may elicit a cytotoxic T-cell (CTL) response against cancer cells expressing certain KRAS mutations. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.

autologous melanoma lysate-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous melanoma cells containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against melanoma cells, which may result in melanoma cell lysis.

autologous melanoma lysate/KLH-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous melanoma cells containing tumor associated antigens (TAAs) and conjugated to the immunostimulant Keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate/KLH-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against melanoma cells, which may result in melanoma cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses and can be used to evaluate vaccine efficacy.

autologous melanoma lysate/NY-ESO-1-pulsed autologous dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with both a lysate from autologous melanoma cells containing tumor associated antigens (TAAs) and a synthetic peptide derived from the tumor associated antigen human cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate/NY-ESO-1-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody-mediated immune responses against melanoma cells, which may result in melanoma cell lysis. NY-ESO-1 is expressed in normal testes and on the surfaces of various tumor cells, and plays a key role in tumor cell proliferation and survival.

autologous memory cytokine-enriched natural killer cells

A population of cryopreserved, autologous CD56-positive memory cytokine-enriched natural killer (NK) cells (m-ceNKs), armed with NK cell-activating surface receptors, with potential immunomodulating and antitumor activities. Autologous NK cells are pre-activated ex vivo with a cytokine cocktail, which induces the differentiation of the NK cells into immune-memory m-ceNKs, which possess a unique phenotype. The pretreated NKs exhibit enhanced cytotoxicity and increased interferon-gamma (IFN-g) production. Upon administration, the autologous m-ceNKs may recognize and kill tumor cells.

autologous mesenchymal stem cells apceth_101

Human autologous mesenchymal stem cells (MSCs) harvested from the bone marrow of a patient and genetically modified with a self-inactivating retroviral vector expressing the suicide gene herpes simplex virus thymidine kinase (HSV-TK), that can be used to activate synthetic acyclic guanosine analogues when co-administered. Upon intravenous administration of autologous mesenchymal stem cells apceth_101, the cells are actively recruited to the tumor stroma, differentiate into more mature mesenchymal cells, and become part of the tumor microenvironment. When a synthetic acyclic guanosine analogue, such as ganciclovir, is co-administered, the HSV-TK within the HSV-TK-transduced MSCs will monophosphorylate this prodrug. Subsequently the monophosphate form is further converted to the diphosphate form and then to its active triphosphate form by cellular kinases. The active form of ganciclovir kills the HSV-TK-transduced MSCs and leads to a bystander effect, which eliminates neighboring cancer cells. Therefore, synthetic acyclic guanosine analogues are activated only at the tumor site, which increases their local efficacy and reduces systemic toxicity.

autologous mesenchymal stem cells-poly lactic-co-glycolic acid

A preparation of autologous bone marrow derived mesenchymal stem cells (MSC) that are seeded on biodegradable poly lactic-co-glycolic acid (PLGA)-containing polymer scaffolds, that can potentially be used for bone marrow engraftment. When administered into the bone lesion of the patient, the autologous MSC-PLGA can be used for bone marrow engraftment.

autologous mesothelin-specific CAR-T cells

Genetically modified, autologous T lymphocytes transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin, with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the autologous mesothelin-specific CAR-T cells specifically target and kill mesothelin-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous mesothelin-specific CAR-T cells expressing anti-PD-1/CTLA-4 antibodies

A preparation of autologous, engineered T lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.

autologous mesothelin-specific human mRNA CAR-transfected PBMCs MCY-M11

Autologous peripheral blood mononuclear cells (PBMCs) transfected with anti-mesothelin chimeric antigen receptor (CAR) mRNA, with potential antineoplastic activity. Upon intraperitoneal (IP) administration, the autologous mesothelin-specific human mRNA CAR-transfected PBMCs MCY-M11 recognize, bind to, phagocytose and directly kill cancer cells expressing mesothelin. In addition, MCY-M11 stimulates the immune system to induce a cytotoxic T-lymphocyte response against the mesothelin-expressing cancer cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in many epithelial-derived cancers.

autologous MG-7-pulsed dendritic cell vaccine

A dendritic cell (DC)-based cancer vaccine composed of autologous DCs pulsed with the human gastric carcinoma-associated antigen MG7, with potential immunostimulatory and antineoplastic activities. Upon administration at the inguinal lymph nodes, autologous MG7-pulsed DC vaccine may stimulate the immune system to mount an anti-tumoral cytotoxic T-lymphocyte (CTL) response against MG7-expressing tumor cells, which may result in tumor cell lysis. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types.

autologous MGMTP140K lentiviral vector-transduced HSCs

A preparation of autologous CD34+ hematopoietic stem cells (HSCs) transduced with a lentiviral-based proviral vector encoding for MGMTP140K, a mutant version of the human DNA repair protein O6-alkylguanine-DNA methyltransferase (MGMT), with potential protective activity against myelosuppression. MGMTP140K is resistant to the MGMT inhibitor O6-benzylguanine (O6BG; BG). Upon administration of the autologous MGMTP140K lentiviral vector-transduced HSCs back into the patient, the HSCs expressing the BG-resistant mutant MGMT protein could, when used in combination with BG, protect the hematopoietic system against the hematopoietic toxicity of BG by enabling normal methyltransferase activity. This protects hematopoiesis and allows for temozolomide (TMZ) and BG chemotherapy without myelosuppression. MGMT repairs TMZ-induced DNA methylation. The MGMT inhibitor BG depletes MGMT and thereby maximizes TMZ-mediated anti-tumor response. The depletion of MGMT in hematopoietic cells leads to unacceptable bone marrow toxicity.

autologous monocyte-derived lysate-pulsed dendritic cells PV-001-DC

A cell-based cancer vaccine composed of autologous, monocyte-derived dendritic cells (mDCs) pulsed with tumor cell lysate containing tumor associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon administration,the autologous tumor cell lysate-pulsed mDCs vaccine PV-001-DC may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the patient's tumor cell-specific TAAs, which may result in tumor cell lysis.

autologous mRNA-encoding NSCLC neoantigens dendritic cell vaccine

A dendritic cell (DC)–based cancer vaccine in which the autologous, in vitro activated DCs are loaded with messenger RNA (mRNA) encoding neoantigens from the patient’s non-small cell lung cancer (NSCLC), with potential immunomodulating and antineoplastic activities. Upon administration of autologous mRNA–encoding NSCLC neoantigens DC vaccine, the mRNA gets expressed into neoantigens in cells and the neoantgens activate the immune system to induce robust neoantigen-specific T-cell responses against the NSCLCs expressing these neoantigens. The neoantigens are predicted from the patient-individual tumor's mutanome.

autologous mRNA-modified anti-cMET CAR-T cells

A preparation of autologous, genetically-engineered T lymphocytes that have been electroporated with an mRNA encoding a chimeric antigen receptor (CAR) consisting of an anti-human hepatocyte growth factor receptor (HGFR or cMET) single chain variable fragment (scFv), with potential antineoplastic activities. Upon administration, autologous mRNA-modified anti-cMET CAR-T cells direct T cells to cMET-expressing tumor cells, which induces selective toxicity against cMET-expressing tumor cells and causes tumor cell lysis. cMET, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.

autologous mRNA-transfected anti-BCMA-CAR T lymphocytes SYS6020

A preparation consisting of autologous T lymphocytes that have been transfected with lipid nanoparticle (LNP)-mRNA encoding for a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and containing as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, autologous mRNA-transfected anti-BCMA-CAR T lymphocytes SYS6020 specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.

autologous MUC1-activated T cells

A preparation of autologous T lymphocytes that have been activated against the tumor associated antigen (TAA) mucin-1 (MUC1), with potential immunomodulating and antineoplastic activities. Upon re-introduction into the patient, autologous MUC1-activated T cells specifically recognize and induce selective toxicity in MUC1-expressing tumor cells. MUC1, a glycoprotein overexpressed on the surface of a variety of cancer cells, plays a key role in tumor cell survival and proliferation.

autologous MUC1-mannan fusion protein pulsed dendritic cell vaccine

A cancer vaccine containing autologous dendritic cells pulsed with a fusion product of an epitope of human tumor-associated epithelial mucin 1 (MUC1) antigen and the vaccine adjuvant mannan (oxidized mannose), with potential antineoplastic activity. When the modified dendritic cells are returned to the patient, they may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the MUC1 antigen, resulting in tumor cell lysis. Addition of manna in this vaccine, enhances immune recognition. MUC1 antigen, a high-molecular-weight transmembrane glycoprotein, is overexpressed on many tumor cells.

autologous multi-lineage potential cells

A preparation of autologous multi-lineage potential cells (AMPC) which were induced to de-differentiate from somatic leukocytes from peripheral blood, with potential immunomodulating and antineoplastic activities. Upon introduction into the patient, the AMPC may help replace the abnormal cells in the body to create healthy bone marrow in the treatment of acute myeloid leukemia (AML).

autologous multiple antigen-specific T cells MASE-T

A preparation of autologous T cells targeting multiple antigens expressed by melanoma cells, with potential immunomodulating and antineoplastic activities. Peripheral blood T cells from the patient are collected, processed with artificial antigen-presenting scaffolds, and enriched and expanded ex-vivo to generate multiple antigen-specific endogenously-derived T cells (MASE-T) targeting multiple antigens expressed by melanoma cells. Upon administration, the autologous multiple antigen-specific T cells MASE-T are re-introduced into the patient, where they target and kill melanoma cells expressing these specific antigens.

autologous muscle-derived cells for gastrointestinal repair

A preparation of autologous human muscle-derived stem cells (MDSCs), that can potentially be used for engraftment purposes for gastrointestinal (GI) repair (GIR). Upon administration, autologous muscle-derived cells (AMDC) for GI repair (AMDC-GIR) differentiate and self-renew. This allows for certain damaged GI tissues to be repaired.

autologous MuSK-CD3z/4-1BB-expressing chimeric autoantibody receptor T cells MuSK-CAART

A preparation of autologous T lymphocytes that have been engineered to express a chimeric autoantibody receptor (CAAR) containing the autoantigen muscle, skeletal receptor tyrosine-protein kinase (MuSK; muscle-specific kinase) that is fused to the co-stimulatory domain of 4-1BB (CD137) and the T-cell receptor signaling domain of CD3zeta (CD3z), with potential immunomodulatory activity. Upon administration, the autologous MuSK-CD3z/4-1BB-expressing CAAR T cells MuSK-CAART specifically recognize and induce selective toxicity in aberrant B cells expressing MuSK autoantibodies. This inhibits the production of MuSK autoantibodies. MuSK is a transmembrane protein expressed on skeletal muscle cell membrane that plays an important role in the formation and maintenance of the neuromuscular junction. MuSK autoantibodies are produced and expressed by aberrant B cells in MuSK-associated myasthenia gravis.

autologous native ESR1-pulsed DC1 vaccine alternating with autologous mutated ESR1-pulsed DC1 vaccine

A dendritic cell (DC)-based cancer vaccine composed of autologous, type-1 polarized dendritic cells (DC1s) pulsed with either native or mutated estrogen receptor alpha (ERa; estrogen receptor 1; ESR1), with potential immunomodulatory and antineoplastic activities. Autologous DCs were treated to produce DC1s and pulsed with either native or mutated ESR1. Alternating weekly between autologous native ESR1-pulsed and mutated ESR1-pulsed DC1 vaccine, upon administration, the autologous native and/or mutated ESR1-pulsed DC1 vaccine may stimulate a potent cytotoxic T-lymphocyte (CTL) response against ESR1-positive tumor cells, which may result in tumor cell death and decreased tumor growth. ESR1 is overexpressed and/or mutated in certain cancers.

autologous natural killer cell-like CTLs

A preparation of cytotoxic T lymphocytes (CTLs) that express natural killer (NK)-like features (nCTLs), with potential immunomodulating and antineoplastic activities. The nCTLs are derived from autologous lymphocytes that have been in vitro exposed to autologous alpha-type-1 polarized dendritic cells that are pulsed with specific autologous tumor-associated antigens (TAAs); the nCTLs are subsequently expanded in the presence of the cytokine human interleukin-2 (IL-2). The generated nCTLs are potent CTLs that produce high amounts of granzyme B and perforin, and interferon-gamma (IFNg) with high killer activity and tumor-homing potential. Upon infusion of the autologous nCTLs, these cells specifically recognize the TAAs on the tumor cells, then bind to and directly lyse tumor cells.

autologous natural killer cells SNK01

A preparation of autologous, ex-vivo expanded and activated natural killer (NK) cells, with potential cytolytic and antineoplastic activities. Upon infusion back into the patient, the autologous NK cells SNK01 may lyse cancer cells. These cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response.

autologous nectin-4/FAP-targeted CAR-T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) nectin-4 and cell surface protein fibroblast activation protein (FAP), and additionally an inducible expression cassette encoding transgenic interleukin (IL) 7 (IL-7) or 12 (IL-12), with potential immunostimulating and antineoplastic activities. Upon intratumoral administration, the autologous nectin-4/FAP-targeted CAR-T cells target and bind to nectin-4-expressing tumor cells and FAP-expressing cancer associated fibroblasts (CAFs). This results in a cytotoxic T-lymphocyte (CTL) response against nectin-4-expressing tumor cells and FAP-expressing CAFs, leading to cell lysis of these cells. Upon the binding to nectin-4 and FAP and the activation of the CAR-T cells, cytokine IL-7 or IL-12 is also released. This further augments the immune responses against the tumor cells, which may include the attack of nectin-4-negative tumor cells by tumor necrosis factor alpha (TNFa). Nectin-4, a TAA belonging to the nectin family, is overexpressed in a variety of cancers, including breast, bladder, lung and pancreatic cancer. FAP, a cell surface glycoprotein, is overexpressed on CAFs but minimally expressed on normal, healthy cells.

autologous neoantigen-specific T lymphocytes GEN-011

A preparation of autologous, personalized, immunogenic and tumor neoantigen-specific T lymphocytes, with potential immunostimulating and antineoplastic activities. Tumor-specific neoantigen targets of autologous CD4+ and/or CD8+ T cells are identified and T cells that target immunogenic and stimulatory neoantigens are expanded ex vivo. Upon administration, the autologous neoantigen-specific T lymphocytes GEN-011 recognize and bind to tumor cells expressing the targeted neoantigens, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient's tumor cells.

autologous neuroblastoma lysate/KLH-pulsed dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a cell lysate from an autologous neuroblastoma containing tumor-associated antigens (TAAs) and the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous neuroblastoma lysate/KLH-pulsed DC vaccine may stimulate the immune system to mount an anti-tumoral cytotoxic T-lymphocyte (CTL) response against neuroblastoma cells, which may result in tumor cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses.

autologous NKG2D CAR T cells KD-025

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) encoding human natural-killer group 2, member D receptor protein (NKG2D or KLRK1) coupled to the co-immunostimulatory signaling domain 4-1BB, normally expressed on T cells, and linked to the intracellular CD3 zeta domain (CD3z), which is needed for TCR signaling, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous NKG2D CAR T cells KD-025 specifically recognize and bind to tumor cells expressing NKG2D ligands (NKG2DLs), resulting in cytokine secretion and lysis of NKG2D ligand-expressing tumor cells. NKG2DLs, such as MICA, MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on a variety of cancer cell types, but are not expressed on most normal, healthy cells.

autologous NKG2D CAR-CD3zeta-DAP10-expressing T lymphocytes CYAD-01

A preparation of autologous peripheral blood T lymphocytes (PBTLs) that have been genetically modified and transduced with a retroviral vector to express a chimeric antigen receptor (CAR) encoding full-length human natural-killer group 2, member D receptor protein (NKG2D or KLRK1) fused to the CD3zeta cytoplasmic signaling domain and containing the naturally-expressed adaptor molecule DNAX-activating protein of 10 kDa (DAP10), with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous NKG2D CAR-CD3zeta-DAP10-expressing T lymphocytes CYAD-01 specifically recognize and bind to tumor cells expressing NKG2D ligands. This induces secretion of pro-inflammatory cytokines and results in the lysis of NKG2D ligand-expressing tumor cells. In addition, CYAD-01 targets, binds to and kills NKG2D ligand expressing tumor-associated endothelial cells in the neovasculature and immunosuppressive cells, such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) that express NKG2D ligands. It also activates macrophages within the TME. Ligands for NKG2D, such as MHC class I chain-related protein A (MICA), MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on infected cells and most cancer cell types, but are not expressed on most normal, healthy cells. NKG2D, a dimeric, type II transmembrane protein expressed on human natural killer (NK) and certain T cells, in association with the natural adaptive protein DAP10, promotes the elimination of NKG2D ligand-expressing cells. The CD3zeta signaling domain and DAP10 provide co-stimulatory signaling upon ligand binding, enhance the secretion of pro-inflammatory cytokines in response to binding to NKG2D ligand-expressing tumor cells and enhances T-cell cytotoxicity. DAP10 also associates with and stabilizes NKG2D, which facilitates expression of the NKG2D-CAR-CD3zeta construct at the cell surface.

autologous NKG2D CAR-expressing T lymphocytes ASP2802

A preparation of autologous T lymphocytes that are genetically modified to express a chimeric antigen receptor (CAR) for a modified and inactivated form of the type II transmembrane protein human natural-killer group 2, member D receptor protein (NKG2D; KLRK1), that can be used for potential immunostimulating and antineoplastic activities upon activation in vivo. Upon infusion back into the patient, autologous NKG2D CAR-expressing T lymphocytes ASP2802 are inert. Upon subsequent administration of MA-20 (ASP101G; MicAbody), a bispecific adaptor molecule composed of an anti-CD20 antibody linked to a UL16-binding protein (ULBP) 2 ligand, the anti-CD20 antibody moiety of MA-20 targets and binds to CD20-expressing tumor cells and the ULBP2 ligand targets and binds to the NKG2D CAR moiety of the convertible CAR T-cells ASP2802, thereby activating the inactivated CAR T cells, which induce selective toxicity in and lysis of CD20-expressing tumor cells. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies.

autologous NKG2D CAR-T cells CYAD-02

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a retroviral vector to co-express a chimeric antigen receptor (CAR) encoding human natural-killer group 2, member D receptor protein (NKG2D or KLRK1) with a short hairpin RNA (shRNA) targeting MHC class I chain-related protein A (MICA) and MICB, with potential immunostimulating and antineoplastic activities. Upon infusion back into the patient, autologous NKG2D CAR-T cells CYAD-02 specifically recognize and bind to tumor cells expressing NKG2D ligands, resulting in the lysis of NKG2D ligand-expressing tumor cells. In addition, CYAD-02 targets, binds to and kills NKG2D ligand expressing tumor-associated endothelial cells in the neovasculature and immunosuppressive cells, such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) that express NKG2D ligands. It also activates macrophages within the TME. Ligands for NKG2D, such as MICA, MICB, and members of the UL16-binding proteins (ULBP)/retinoic acid early transcript 1 (RAET1) family, are overexpressed on infected cells and most cancer cell types, but are not expressed on most normal, healthy cells. NKG2D, a dimeric, type II transmembrane protein expressed on human natural killer (NK) and certain T cells, in association with the natural adaptive protein DAP10, promotes the elimination of NKG2D ligand-expressing cells. The shRNA downregulates the expression of MICA and MICB on the CAR-T cells, which increases in-vitro cell expansion. This may enhance their persistence and increase anti-tumor activity.

autologous NSCLC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine

A vaccine consisting of irradiated human fetal lung fibroblasts (Medical Research Council 5 or MRC-5) transfected with autologous non-small cell lung cancer (NSCLC)-derived DNA with potential immunostimulatory and antineoplastic activities. Upon administration, autologous NSCLC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine expresses NSCLC tumor-associated antigens (TAAs) in addition to MHC class I-determinants and the co-stimulatory molecule B7.1, which may induce a cytotoxic T-lymphocyte (CTL) response against NSCLC cells. The MRC-5 cell line is a human diploid lung fibroblast cell line extablished in 1966.

autologous NSCLC peptide-specific dendritic cell vaccine

A personalized cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with immunogenic peptides derived from autologous non-small cell lung cancer (NSCLC) cells, with potential immunostimulating and antineoplastic activities. During leukapheresis, mature DCs are loaded with autologous NSCLC-derived peptides. Upon re-administration of the NSCLC peptide-specific DC vaccine, the immune system is exposed to NSCLC-associated antigens. This results in the induction of a specific cytotoxic T-lymphocyte (CTL) response against NSCLC cells and tumor cell lysis.

autologous NY-ESO-1 TCR-targeted T lymphocytes

A preparation of human autologous T lymphocytes that are transduced with a gene encoding a T-cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential immunostimulating and antineoplastic activities. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the anti-NY-ESO-1 TCR-transduced autologous T cells recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types, and is not, or is minimally, expressed in normal, healthy cells.

autologous NY-ESO-1-melanoma-specific CD8+ T lymphocytes

A preparation of autologous CD8+ (cytotoxic) T lymphocytes sensitized to cancer-testis antigen NY-ESO-1 antigen with potential immunostimulating and antineoplastic activities. Autologous CD8+ T lymphocytes, isolated from a melanoma patient, are exposed to an NY-ESO-1 peptide ex vivo, expanded, and reintroduced into the patient; these tumor-reactive T-cells may stimulate a host immune response against tumor cells expressing the NY-ESO-1 antigen, resulting in tumor cell lysis. NY-ESO-1, an antigen found in normal testis, may be upregulated in various cancers, including bladder, breast, hepatocellular, melanoma, and prostate cancers.

autologous NY-ESO-1-redirected CRISPR-edited T cells

A preparation of human autologous T lymphocytes that are transduced with a lentiviral vector (LV) encoding a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) cancer-testis antigen NY-ESO-1 and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR and programmed cell death 1 (PD-1) expression, with potential immunostimulating and antineoplastic activities. The CRISPR guide RNA (gRNA) specifically targets and binds to complementary sites on TCRalpha, TCRbeta and PD-1. In turn, Cas9 cleaves these specific DNA sites, thereby disrupting transcription. Upon isolation, transduction, electroporation with TCRalpha, TCRbeta and PD-1 gRNAs which are complexed to Cas9 RNA to disrupt expression of endogenous TCRalpha, TCRbeta and PD-1, expansion ex vivo, and reintroduction into the patient, the anti-NY-ESO-1 TCR LV-transduced CRISPR-edited autologous T cells recognize and bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of NY-ESO-1-positive tumor cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types, and is not, or is minimally, expressed in normal, healthy cells. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed cell death ligand 1 (PD-L1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the NY-ESO-1-expressing tumor cells. Removal of endogenous TCR reduces TCR competition for expression, increases the persistence and function of the expressed transgenic TCR, enhances resistance to T-cell exhaustion and increases T-cell activity.

autologous NY-ESO-1-specific CD8-positive T lymphocytes

A preparation of autologous CD8+ T lymphocytes specifically reactive to the cancer-testis antigen NY-ESO-1, with potential immunostimulating and antineoplastic activities. Autologous NY-ESO-1-specific CD8+ T lymphocytes were generated from T cells isolated from a particular cancer patient, which were made specifically reactive to the NY-ESO-1 antigen, expanded ex vivo, and reintroduced into the patient. These tumor-reactive T cells may stimulate a host immune response against tumor cells expressing the NY-ESO-1 antigen, resulting in tumor cell lysis. NY-ESO-1, an antigen found in normal testis, may be upregulated in various cancers.

autologous NY-ESO-1/LAGE-1a-specific HLA-A*02:01-restricted TCR-expressing T lymphocytes MDG1015

A preparation of autologous T lymphocytes that have been genetically engineered to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*02:01-restricted cancer-testis antigens (CTAs) NY-ESO-1 and L antigen family member 1 isoform A (LAGE-1A; LAGE-A1; CT6.2a), and a programmed cell death protein 1 (PD-1; PDCD1; CD279)-4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) costimulatory switch protein (CSP), with potential immunomodulating and antineoplastic activities. Upon reintroduction into the patient, autologous NY-ESO-1/LAGE-1a-specific HLA-A*02:01-restricted TCR-expressing T lymphocytes MDG1015 specifically targets and binds to NY-ESO-1 and/or LAGE-1A expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing NY-ESO-1 and/or LAGE-1A. In addition, upon binding of the TCR-T cells MDG1015 to NY-ESO-1 and/or LAGE-1A expressed on tumor cells, the PD-1-4-1BB CSP is activated. This abrogates PD-1-mediated signaling in T cells and PD-1-mediated T-cell inhibition, and activates 4-1BB signaling locally in the tumor microenvironment (TME), which enhances the activity and persistence of the TCR-T cells MDG1015. NY-ESO-1 and LAGE-1A, members of the CTA family, are overexpressed on the surface of various tumor cell types; they share a specific HLA-A*02:01 epitope, 157-165, which is expressed on certain tumor cell types while its expression is not found on normal, healthy cells.

autologous OFA-iLRP RNA-transfected dendritic cell vaccine

A cancer vaccine consisting of autologous, mature monocyte-derived dendritic cells (DCs) transfected with oncofetal antigen immature laminin receptor protein (OFA-iLRP) RNA, with potential antineoplastic activity. Upon administration, DCs in the OFA-iLRP RNA-transfected autologous dendritic cell vaccine express, process, and present OFA-iLRP to the host immune system, which may mount a potent cytotoxic T-cell (CTL) response against OFA-iLRP-expressing tumor cells. As a highly conserved protein, OFA-iLRP is preferentially expressed in fetal tissues and in many types of cancer, including hematopoietic malignancies, but is not detectable in normal differentiated adult cells.

autologous orthogonal IL-2Rbeta-expressing anti-CD19 CAR T cells SYNCAR-001

A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 fused to the extracellular, transmembrane and intracellular signaling domains of the T-cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) and expressing a mutated orthogonal (ortho) interleukin (IL)-2beta receptor (hoRbeta; hoRb), with potential immunostimulating and antineoplastic activities. Upon administration, autologous hoRb-expressing anti-CD19 CAR T-cells SYNCAR-001 target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Stimulation of hoRb specifically by orthogonal (ortho) IL-2 STK-009 allows for IL-2 signaling specifically in SYNCAR-001 and leads to increased proliferation, persistence and anti-tumor activity of SYNCAR-001. This may lead to dose reduction of SYNCAR-001. hoRb does not respond to the native IL-2 ligand. As STK-009 does not cause IL-2-mediated signaling in other immune cells, systemic toxicity is limited.

autologous ovarian cancer immunogene-modified T lymphocytes

A preparation of autologous immunogene modified T lymphocytes (IgT) that have been genetically engineered to be specifically reactive to ovarian cancer (OC) cells, with potential antineoplastic and immunostimulating activities. Upon administration of the autologous OC-IgT cells, the T cells recognize and induce specific toxicity in the OC cells.

autologous ovarian cancer-specific antigens-pulsed dendritic cells Cellgram-DC

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with ovarian cancer-specific antigen(s), with potential immunostimulatory and antineoplastic activities. Upon subcutaneous administration of the autologous ovarian cancer-specific antigens-pulsed DCs Cellgram-DC near the lymph nodes, the DCs stimulate a specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the ovarian cancer cells expressing the antigens, resulting in tumor cell lysis.

autologous ovarian cancer-specific cytotoxic T lymphocytes

A preparation of autologous cytotoxic T lymphocytes (CTLs) genetically modified to target a not yet disclosed ovarian cancer-specific tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the autologous ovarian cancer-specific cytotoxic T lymphocytes (OC-CTLs) bind to and induce selective toxicity in tumor cells expressing the TAA.

Autologous Ovarian Tumor Cell Lysate-Pulsed Dendritic Cell Vaccine

A cell-based cancer vaccine composed of autologous, irradiated dendritic cells (DCs) pulsed with ovarian tumor cell lysate containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous ovarian tumor cell lysate-pulsed dendritic cell vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against ovarian tumor cells expressing the patients ovarian tumor cell-specific TAAs, which may result in ovarian tumor cell lysis.

autologous oxidized ovarian tumor cell lysate vaccine

An autologous cancer vaccine composed of oxidized ovarian tumor cell lysate, with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous oxidized ovarian tumor cell lysate vaccine exposes the immune system to an undefined amount of tumor-associated antigens (TAAs), which may result in the induction of both anti-tumor cytotoxic T-lymphocytes (CTLs) and antibody-dependent responses against TAA-expressing cells, leading to tumor cell lysis. Compared to non-oxidized tumor cell lysate vaccines, oxidized tumor cell lysate vaccines induce necrotic cell death, increase the immunogenicity of the TAAs and may enhance the anti-tumor immune response.

autologous pancreatic adenocarcinoma lysate- and mRNA-loaded dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) loaded with pancreatic adenocarcinoma lysate and mRNA containing and encoding tumor associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon administration by perinodal injection using ultrasound guidance, the autologous pancreatic adenocarcinoma lysate and mRNA-loaded DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the patient's tumor cell-specific TAAs, which may result in tumor cell lysis.

autologous PBLs retrovirally-transduced with TCRs targeting neoantigens

Autologous human peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding T-cell receptors (TCRs) specific for a patient's individual and unique mutated antigens, with potential immunostimulating and antineoplastic activities. Tumor cells are analyzed to identify and isolate specific mutated tumor-associated antigens (TAAs) that are expressed by the patient's tumor cells; then T-cell receptor coding sequences are engineered to target the patient's TAAs and inserted into retroviral vectors. After transduction, expansion in culture, and reintroduction into the patient, neoantigen-specific TCRs retroviral vector-transduced autologous PBLs recognize and bind to tumor cells expressing the patient's neoantigens, which results in a specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient's tumor cells.

autologous PBMC-derived engineered leukocyte immunostimulatory cells-activated effector cells

A preparation of cytotoxic, autologous effector cells specifically targeted towards tumor cells and comprised primarily of natural killer (NK) cells, CD56+ NK T cells (NKTs), CD8+ T-cells and gamma delta T cells stored in cryogenic media, with potential immunomodulating and antineoplastic activities. The autologous effector cells are prepared by collecting peripheral blood mononuclear cells (PBMCs) from cancer patients, which are stimulated with the induction reagent engineered leukocyte immunostimulatory (ENLIST) cells to activate and differentiate the PBMCs; the activated cells are expanded with cytokines, and the tumor killing effector cells, including NK cells, CD8+ T cells, TCRgd T cells, NKT cells and some CD4+ T cells, are cryopreserved. Upon intravenous re-administration into the patient, the autologous PBMC-derived ENLIST cells-activated effector cells recognize and induce an immune-mediated killing of tumor cells. ENLIST cells are engineered SK-MEL2 melanoma cell lines (APX-DC and APX-L) that express immunomodulatory proteins that are engineered for membrane expression and contain endogenous tumor-associated antigens (TAAs).

autologous PBMCs in GM-CSF

Autologous peripheral blood mononuclear cells (PBMCs) that are suspended in a solution containing the immunostimulant granulocyte-macrophage colony stimulating factor (GM-CSF).

autologous PBTL CD19CAR-28 zeta

A preparation of autologous peripheral blood T lymphocytes (PBTL) that have been genetically modified to express the chimeric antigen receptor (CAR) anti-CD19/CD3 zeta chain fusion protein coupled to the intracellular signal domain of CD28 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, autologous PBTL CD19CAR-28 zeta may stimulate host cytotoxic T lymphocyte (CTL) and antibody responses against CD19-expressing tumor cells, resulting in tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the T-cell receptor (TCR)/CD3 complex and regulates the assembly of complete TCR complexes and their expression on the cell surface. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.

autologous PD-1 antibody-expressing mesothelin-specific CAR-T cells

Genetically modified, autologous T lymphocytes that express an antibody that targets the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin, with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the autologous PD-1 antibody expressing mesothelin specific CAR-T cells specifically target and kill mesothelin-expressing tumor cells. The anti-PD-1 expressed on the CAR-T cells binds to PD-1 expressed on T cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion, enhances T-cell activation, and results in enhanced toxicity in mesothelin-expressing tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation and overexpression within the tumor microenvironment and inhibits T-cell function. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous PD-1 nanobody-expressing anti-MSLN CAR T cells

A preparation of autologous T lymphocytes that have been genetically modified to express a nanobody that targets the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) mesothelin (MSLN), with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the autologous PD-1 nanobody-expressing anti-MSLN CAR T cells specifically target and kill MSLN-expressing tumor cells. The anti-PD-1 expressed on the CAR T cells binds to PD-1 expressed on T cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on tumor cells. This prevents PD-1-mediated signaling and T-cell exhaustion, enhances T-cell activation, and results in enhanced toxicity in MSLN-expressing tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation and overexpression within the tumor microenvironment (TME) and inhibits T-cell function. MSLN, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.

autologous PD-1-knockout tumor-infiltrating lymphocytes IOV-4001

A preparation of autologous tumor-infiltrating lymphocytes (TILs) where the programmed cell death protein 1 (PD-1; PDCD1; CD279; programmed death-1) gene has been disrupted using transcription activator-like effector nuclease (TALEN), with potential immunomodulating and antineoplastic activities. The autologous TILs are isolated from an autologous tumor sample, expanded ex-vivo and genetically modified to inactivate PD-1. Upon administration, the autologous PD-1-knockout TILs IOV-4001 induce a T-cell-mediated immune response against tumor cells. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in cytotoxic T-lymphocyte (CTL) suppression, T-cell exhaustion and CTL apoptosis. PD-1 knockout may abrogate T-cell exhaustion and increase T-cell activity and cytotoxicity.

autologous PD-1-targeted chimeric switch receptor-modified T lymphocytes

Autologous human T lymphocytes that are genetically engineered to express a chimeric switch receptor (CSR) composed of the extracellular ligand binding domain of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1) fused to the transmembrane and cytoplasmic co-stimulatory signaling domains of CD28 (PD1CD28; PD-1:CD28 switch receptor), with potential immunomodulating and antineoplastic activities. Upon reintroduction of autologous PD-1-targeted CSR-modified T-lymphocytes into the patient, the switch receptor expressed by the engineered T cells targets and binds to the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2) expressed, on tumor cells. The nature of the PD-1/CD28 switch receptor fusion protein prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T lymphocytes. This induces enhanced toxicity against PD-L1-expressing tumor cells. PD-1 protein, found on activated T cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. Exchanging the transmembrane and intracellular domain of PD-1 with that of CD28 converts PD-L1 into a co-stimulation ligand of primary human CD8+ cytotoxic T lymphocytes (CTLs). CD28, is a molecule expressed by T cells that stimulates increased T-lymphocyte proliferation and activity.

autologous PD-L1/CD80/CD86-targeted CAR-T cells

A preparation of autologous human T lymphocytes engineered to express a chimeric antigen receptor (CAR) composed of a modified from of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1), in which the intracellular signal domain of PD-1 is transformed to allow for stimulatory signaling but with an intact extracellular ligand binding domain that specifically binds the tumor-associated antigen (TAA) programmed cell death-1 ligand 1 (PD-L1), and a modified form of the T-cell inhibitory receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with a transformed intracellular signal domain to allow for stimulatory signaling, which specifically binds the B7 proteins CD80 (B7-1) and CD86 (B7-2), with potential immunostimulating and antineoplastic activities. Usually, ligand binding to PD-1 and CTLA-4 inhibits T-cell activity; however, these modified forms of PD-1 and CTLA-4 promote T-cell stimulatory signaling. Upon administration, the autologous PD-L1/CD80/CD86-targeted CAR-T cells target and bind to PD-L1 expressed on certain tumor cells and to CD80/CD86 expressed on antigen-presenting cells (APCs). This stimulates T-cell activation, T-cell proliferation and enhanced cytokine production, which induces selective toxicity in tumor cells expressing PD-L1. PD-1, found on activated T cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PD-L1 is often overexpressed on tumor cell types and plays a key role in immune evasion. The co-stimulatory molecules CD80 and CD86 play a key role in T-lymphocyte activation upon binding to CD28 upon antigen recognition; however, binding of CD80 and CD86 to wild-type CTLA-4 inhibits T-cell activity and results in T-cell exhaustion.

autologous PD1-inhibiting anti-CD19 4-1BB CAR T cells

A preparation of autologous T lymphocytes that are transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) cluster of differentiation 19 (CD19) linked to the intracellular signaling domain of 4-1BB (CD137) that also encodes a cell-intrinsic programmed cell death 1 (PD1; PDCD1; CD279; programmed death-1) short/small hairpin RNA (shRNA)-expressing cassette, with potential immunomodulating and antineoplastic activities. Upon administration of the autologous PD1-inhibiting anti-CD19 4-1BB CAR T cells, these cells target, bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The shRNA silences expression of PD1, abrogates T-cell exhaustion, increases CAR T-cell activity and enhances tumor cytotoxicity. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in CTL suppression, T-cell exhaustion and CTL apoptosis.

autologous PD1-knockout CD19-specific CAR T cells

A preparation of autologous CD4+ and CD8+ T lymphocytes gene-edited to integrate a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and to eliminate the programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1) gene, with potential immunomodulating and antineoplastic activities. Upon administration, autologous PD1-knockout CD19-specific CAR T cells specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in CTL suppression, T-cell exhaustion and CTL apoptosis. PD-1 knockout may abrogate T-cell exhaustion and increase T-cell activity and cytotoxicity.

autologous PD1-knockout CD19-specific CAR T cells BRL-201

A preparation of autologous T lymphocytes that are non-virally gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to integrate a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 in the locus of the programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1) gene, with potential immunomodulating and antineoplastic activities. Upon administration, autologous PD1-knockout CD19-specific CAR T cells BRL-201 specifically target and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in cytotoxic T-lymphocyte (CTL) suppression, T-cell exhaustion and CTL apoptosis. PD-1 knockout may abrogate T-cell exhaustion and increase T-cell activity and cytotoxicity.

autologous peripheral blood lymphocytes cotransduced with retroviral vectors encoding inducible IL-12 and anti-NY-ESO-1 TCR

Human autologous peripheral blood lymphocytes (PBLs) transduced with two retroviral vectors, one encoding a T-cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1 and a second that encodes an inducible single chain form of interleukin-12 (IL-12) driven by a nuclear factor of activated T cells (NFAT)-responsive promoter, with potential immunomodulating and antineoplastic activities. Following isolation of lymphocytes, retroviral vector transduction, and expansion of the cells ex vivo, the inducible IL-12/anti-NY-ESO-1 TCR-expressing autologous PBLs are re-administered into the patient by intravenous injection. As the transduced PBLs traverse the patient's circulation, they can bind to NY-ESO-1-overexpressing tumor cells. This binding activates the TCR signaling pathway in the transduced PBLs, which promotes NFAT-dependent gene transcription and induces expression of the cotransduced IL-12. IL-12 expression activates the immune system by promoting the secretion of interferon-gamma, activating natural killer cells (NKs), and inducing cytotoxic T-cell responses, which may result in both decreased cell proliferation and increased cell death for the NY-ESO-1-overexpressing tumor cells. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. NFAT, a family of transcription factors involved in immune responses, is activated by calcium signaling, which can occur downstream of TCR activation. Use of a retroviral vector to express an inducible IL-12 may remove the requirement for concomitant administration of interleukin-2 (IL-2) as is the case for conventional cell transfer immunotherapies.

autologous peripheral blood lymphocytes from ibrutinib-treated chronic lymphocytic leukemia patients IOV-2001

A preparation of autologous peripheral blood lymphocytes (PBLs) harvested from chronic lymphocytic leukemia (CLL) patients previously treated with the Brutons’ tyrosine kinase (BTK) inhibitor ibrutinib with potential immunostimulating and antineoplastic activities. Upon intravenous administration, IOV-2001 generates an enhanced cytotoxic T-cell response against autologous leukemic B-cells in patients who have relapsed during treatment with ibrutinib. IOV-2001 is mostly comprised of T-cells of which the majority are of the effector memory phenotype which augments the specificity of the immune response.

autologous pluripotent ALDHbr stem cells ALD-451

A specific population of autologous, pluripotent bone marrow derived cells that express high levels of the cytosolic enzyme aldehyde dehydrogenase (ALDH) with potential protective and neuro-cognition improving activity. Expression of high levels of ALDH is an indicator of the biological activity in heterogenous early stage stem cells. Upon intravenous administration, these ALDH bright cells may protect normal cells and may repair damaged cells. These cells may also protect brain cells from damage and may improve neurocognition.

autologous polyclonal tumor infiltrating lymphocytes LYL845

A preparation of autologous, epigenetically reprogrammed, polyclonal tumor infiltrating lymphocytes (TILs), with potential immunomodulating and antineoplastic activities. The autologous TILs LYL845 are prepared and expanded ex vivo by co-culturing autologous tumor cells with specific Epi-R cell culture media containing optimized cytokine composition and cell activation which creates TILs enriched with CD8-positive T cells with diverse tumor-reactive clones and an enhanced proportion of stem-like T cells. Upon administration, the autologous TILs LYL845 may target and kill tumor cells and secrete pro-inflammatory cytokines. LYL845 shows increased durability of expanded TILs, enhanced polyclonality and increased tumor-reactive cytolytic T cells compared to TILs derived from the standard process.

autologous PRAME-targeting TCR-engineered T cells IMA203

A preparation of autologous T lymphocytes that are genetically modified with a lentiviral vector encoding a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) preferentially expressed antigen in melanoma (PRAME), with potential antineoplastic activity. Upon intravenous administration back into the patient, the autologous PRAME-targeting TCR-engineered T cells IMA203 specifically recognize and bind to PRAME expressed on cancer cells, which induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against the PRAME-expressing cancer cells. PRAME is overexpressed by a variety of cancer cell types.

autologous PRAME-targeting TCR-modified T cells MDG1011

Human autologous T lymphocytes transduced with a retroviral vector encoding a human leukocyte antigen (HLA)-A*02:01-restricted T-cell receptor (TCR) specific for the human tumor-associated antigen (TAA) preferentially expressed antigen in melanoma (PRAME) coupled to the CD3 signaling complex, with potential antineoplastic activity. Upon reintroduction into the patient, the autologous PRAME-targeting TCR-modified T cells MDG1011 target and bind to tumor cells expressing PRAME. This may induce cell death in and halt the growth of PRAME-expressing tumor cells. The TAA PRAME is overexpressed by a variety of cancer cell types.

autologous prostate cancer antigen-expressing dendritic cell vaccine BPX-101

A genetically-modified autologous dendritic cell-based vaccine expressing a drug-inducible costimulatory CD40 receptor (iCD40) with potential immunomodulating and antineoplastic activities. Autologous dendritic cells (DCs) are genetically modified to express the iCD40 receptor and are pulsed with the tumor antigen prostate-specific membrane antigen (PSMA). Upon intradermal administration, these DCs accumulate in local draining lymph nodes. Twenty-four hours after vaccination, the dimerizer agent AP1903 is administered; AP1903 binds to and activates iCD40 receptors presented on DC surfaces, thus activating the DCs and stimulating a cytotoxic T-lymphocyte (CTL) response against host tumor cells that express PSMA. This delayed activation strategy optimizes DC accumulation in local draining lymph nodes prior to DC activation. iCD40 contains a membrane-localized cytoplasmic CD40 domain fused to a drug-binding domain.

autologous prostate cancer-specific antigens-pulsed dendritic cells Cellgram-DC-PC

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with prostate cancer (PC)-specific antigen(s), with potential immunostimulatory and antineoplastic activities. Upon administration of the autologous PC-specific antigens-pulsed DCs injected subcutaneously near the inguinal lymph nodes, the DCs stimulate a specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the PC cells expressing the antigens, resulting in tumor cell lysis.

autologous prostate stem cell antigen-specific CAR T cells BPX-601

A preparation of autologous T lymphocytes expressing a chimeric antigen receptor (CAR) consisting of an anti-human prostate stem cell antigen (PSCA) scFv (single chain variable fragment) coupled to the zeta chain of the T-cell receptor (TCRzeta) and a drug-induced co-stimulatory molecule, composed of an inducible, chimeric MyD88/CD40 (inducible MC; iMC) co-stimulatory domain, in which both the MyD88 and CD40 lack their extracellular domains, with potential antineoplastic activity. Upon administration of BPX-601, the T cells target and bind to PSCA-expressing cancer cells. Upon subsequent administration of the chemical inducer of dimerization (CID) agent rimiducid, this agent targets and binds to the drug binding domain, which leads to iMC expression, activation of both CD40- and MyD88-mediated signal transduction pathways, and an induction of selective cytotoxicity in, and eradication of PSCA-expressing cancer cells. iMC activation by rimiducid increases T-cell survival and anti-tumor activity of the administered T cells, compared to T cells without the drug iMC activation-switch. As these T cells are engineered to only be fully activated by binding to both antigen and rimiducid, T-cell proliferation, activity and toxicity can be controlled by adjusting the dose of rimiducid, thereby preventing uncontrolled T-cell activation which increases the safety of the administered T cells. PSCA is a glycosylphosphatidylinositol (GPI)-anchored cell surface antigen overexpressed in many cancer cell types.

autologous PSMA-4SCAR-expressing T cells 4SCAR-PSMA

A preparation of genetically modified autologous T cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a fourth generation chimeric antigen receptor (4SCAR) consisting of an anti-prostate-specific membrane antigen (PSMA) single chain variable fragment (scFv) that is coupled to the costimulatory signaling domains CD28, CD137, CD27 and the zeta chain of the T-cell receptor (CD3zeta; CD3z), and is fused with the suicide gene inducible caspase 9 (iCasp9), with potential immunostimulating and antineoplastic activities. Upon administration, autologous PSMA-4SCAR-expressing T-cells 4SCAR-PSMA are directed to and induce selective toxicity in PSMA-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered. AP1903 binds to the drug binding FKBP12-F36V domain and induces activation of caspase 9, which results in the apoptosis of the administered T cells and enhances safety of this agent. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells. CD28, CD137 and CD27, T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation and enhance both proliferation of T cells and antitumor activity.

autologous PSMA-inducible anti-CA9 CAR T cells AB-2100

A preparation of autologous T lymphocytes that have been modified to encode a genetic circuit consisting of a priming receptor that induces the expression of a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) carbonic anhydrase IX (CAIX; carbonic anhydrase 9; CA9; G250) upon binding to the TAA prostate-specific membrane antigen (PSMA), and a microRNA-adapted short hairpin RNA (shRNA-miR) module targeting Fas (FAS; CD95; APO-1; tumor necrosis factor receptor superfamily member 6; TNFRSF6) and human transforming growth factor beta (TGF-beta) receptor II (TGFbRII; TGFBR2), with potential immunomodulating and antineoplastic activities. Upon administration, autologous PSMA-inducible anti-CA9 CAR T cells AB-2100 target and bind to PSMA expressed on tumor cells and in tumor-associated neovasculature, and induce the expression of anti-CA9 CAR, thereby killing PSMA- and CA9-expressing tumor cells. The downregulation of the expression of Fas by the shRNA-miR prevents Fas-mediated apoptosis of the AB-2100 T-cells in the tumor microenvironment (TME). The downregulation of the expression of TGFbRII abrogates TGF-beta-mediated immunosuppression in the TME. PSMA is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as in a variety of other tumors, including renal cell carcinomas. CA9 is a member of the carbonic anhydrase family that is found in a majority of renal cell carcinomas while absent in most normal tissues. AB-2100 T cells have also been engineered to include a constitutive synthetic pathway activator that increases signal transducer and activator of transcription 3 (STAT3) signaling, thereby promoting T-cell cytotoxicity and expansion.

autologous PSMA-specific TGFβ-resistant CAR T cells

Autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-prostate specific membrane antigen (PSMA) single chain variable fragment (scFv) and expressing a dominant negative (DN) form of transforming growth factor-beta (TGF-beta; TGFb) receptor, with potential immunomodulating and antineoplastic activities. Upon transfusion, the autologous PSMA-specific TGFb-resistant CAR T cells are directed to and induce selective toxicity in PSMA-expressing tumor cells. The tumor-associated antigen (TAA) PSMA is overexpressed by prostate cancers; its expression is associated with poor prognosis and metastasis. The inclusion of the DN TGFb receptor blocks signaling of the immunosuppressive cytokine TGFb in the tumor microenvironment (TME) and makes the CAR T cells resistant to TGFb. TGFb negatively regulates T-cell proliferation and activation and plays a key role in tumor immune suppression.

autologous rapamycin-resistant Th1/Tc1 cells RAPA-201

A preparation of autologous rapamycin-resistant Th1/Tc1 cells, with potential immunomodulating activity. Upon administration, autologous rapamycin-resistant Th1/Tc1 cells RAPA-201 may recognize and kill tumor cells. Ex-vivo induction of rapamycin-resistance may increase the persistence of T-cells after adoptive transfer.

Autologous Renal Cell Carcinoma Tumor Lysate-Pulsed Dendritic Cell Vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with renal cell carcinoma (RCC) tumor cell lysate containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous renal cell carcinoma tumor lysate-dendritic cell vaccine may stimulate anti-tumoral cytotoxic T-lymphocyte (CTL) and antibody responses against RCC tumor cells expressing RCC TAAs, resulting in RCC tumor cell lysis.

autologous retroviral vector MSGV1-transduced anti-PSCA-8T28Z CAR gamma delta T cells

A preparation of autologous gamma delta T lymphocytes transduced with the gamma retroviral vector MSGV1 expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) prostate stem cell antigen (PSCA), and expressing a hinge/transmembrane domain derived from CD8alpha (CD8a) and a single co-stimulatory domain derived from CD28 (8t28z), with potential immunomodulating and antineoplastic activities. Upon administration, the autologous retroviral vector MSGV1-transduced anti-PSCA-8T28Z CAR gamma delta T cells specifically target, bind to and kill tumor cells expressing PSCA. PSCA is a glycosyl-phosphatidylinositol (GPI)-linked cell surface antigen found in various cancers.

autologous ROR2-targeted CAR-T cells CCT301-59

A preparation of genetically modified autologous T lymphocytes transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) targeting the receptor tyrosine kinase-like orphan receptor 2 (ROR2), with potential immunomodulatory and antineoplastic activities. After isolation, transduction, and expansion in culture, CCT301-59 cells are reintroduced into the patient and are activated within the tumor microenvironment (TME) using proprietary Conditionally Active Biologic (CAB) technology. Upon activation, CAB antibodies bind to a proprietary T-cell signaling domain, promoting T-cell recognition and killing of ROR2-expressing tumor cells. ROR2 is involved in Wnt signal transduction and is involved in tumorigenesis and progression. ROR2 expression is upregulated in certain tumor types and high levels of ROR2 expression often correlates with poor prognosis.

autologous sarcoma cell lysate

A cell lysate derived from sarcoma cells with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous sarcoma cell lysate exposes the immune system to an undefined amount of sarcoma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the sarcoma TAA-expressing cells, resulting in sarcoma cell lysis.

autologous sarcoma lysate-pulsed dendritic cell vaccine

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from sarcoma cells with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous sarcoma lysate-pulsed dendritic cell vaccine exposes the immune system to an undefined amount of sarcoma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the sarcoma TAA-expressing cells, resulting in sarcoma cell lysis.

autologous SIRPa-depleted activated macrophages SI-101

A preparation of autologous macrophages that are ex vivo activated and depleted of signal-regulatory protein alpha (SIRP-alpha; SIRPa; CD172a), with potential immunostimulatory and antineoplastic activities. Upon reintroduction into the patient, autologous SIRPa-depleted activated macrophages SI-101 elicits an anti-tumor immune response via the phagocytosis of tumor cells. In addition, the autologous SIRPa-depleted activated macrophages SI-101 promotes a pro-inflammatory tumor microenvironment (TME) and activates a cancer neoantigen-specific cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. The depletion of SIRPa, an inhibitory protein expressed on macrophages and dendritic cells (DCs), prevents SIRPa/CD47-mediated inhibition of macrophage activity.

autologous spermatogonial stem cells

A preparation of autologous spermatogonial stem cells (SSCs), that can potentially be used for intratesticular transplantation purposes. Upon injection into the testis, the autologous SCCs may recolonize and induce spermatogenesis, leading to mature spermatozoa, and thereby restoring fertility.

autologous T-lymphocytes-expressing NY-ESO-1-C259-specific enhanced T-cell receptors

Human autologous lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the cancer/testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous T-lymphocytes expressing NY-ESO-1-C259-specific enhanced T cell receptors bind to NY-ESO-1-overexpressing tumor cells. This may result in the specific cytotoxic T-lymphocyte (CTL) killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types; the TCR is specific for SLLMWITQC, an NY-ESO-1-derived peptide, in a complex with human leukocyte antigen (HLA) A2 peptide.

autologous TAAs-loaded autologous dendritic cells AV-GBM-1

A preparation of autologous dendritic cells (DCs) loaded with immunogenic tumor-associated antigens (TAAs) derived from cultured autologous glioblastoma multiforme (GBM) tumor cells, with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous TAA-loaded DCs AV-GBM-1 expose the immune system to the GBM neoantigens, which results in a cytotoxic T-lymphocyte (CTL)-mediated immune response against the autologous GBM cells leading to GBM cell lysis.

autologous TBX-4000-treated peripheral blood mononuclear cells TBX-3400

An autologous cell preparation in which the autologous peripheral blood mononuclear cells (PBMCs) are treated ex vivo with TBX-4000, a recombinant TAT-MYC fusion protein, with potential antineoplastic and immunomodulating activities. Upon reintroduction of the TBX-3400 cells into the patient, the generated T cells may activate the immune system and exert a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. The TBX-4000 recombinant fusion protein consists of the N-terminal 9 amino acid segment of the HIV TAT protein transduction domain (PTD) fused to the MYC protein. TBX-4000 TAT-MYC rapidly localizes to the nucleus and transiently provides signals to drive proliferation and survival of T cells.

autologous TCR-engineered T cells IMA201

A preparation of autologous T lymphocytes that are genetically modified with a lentiviral vector encoding a T-cell receptor (TCR) specific for an as of yet not identified tumor-associated antigen (TAA), with potential antineoplastic activity. Upon intravenous administration back into the patient, the autologous TCR-engineered T cells IMA201 specifically recognize and bind to the TAA on cancer cells, which induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against the TAA-positive cancer cells.

autologous TCR-engineered T cells IMA202

A preparation of autologous T lymphocytes that are genetically modified with a lentiviral vector encoding a T-cell receptor (TCR) targeting patient-specific tumor associated antigens (TAAs), with potential antineoplastic activity. Upon intravenous administration back into the patient, the autologous TCR-engineered T cells IMA202 specifically recognize and bind to the TAA on cancer cells, which induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against the TAA-positive cancer cells.

autologous TCRm-expressing T cells ET140203

A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector to express a T-cell receptor mimetic (TCRm) construct targeting as of yet undisclosed tumor associated antigen(s) (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration, the autologous TCRm-expressing T cells ET140203 specifically recognize and selectively bind to the as of yet undisclosed TAA(s). This results in cytotoxic T-lymphocyte (CTL)-mediated killing of tumor cells expressing the TAA(s).

autologous tetravalent dendritic cell vaccine MIDRIX4-LUNG

A therapeutic cancer vaccine composed of autologous, dendritic cells (DCs) that have been loaded with a proprietary selection of four antigens that covers more than ninety percent of all non-small cell lung cancer (NSCLC) patients, with potential immunostimulatory and antineoplastic activities. Upon administration, autologous tetravalent dendritic cell vaccine MIDRIX4-LUNG may induce and stimulate both T-helper and antigen-specific cytotoxic T-lymphocyte (CTL) responses, leading to tumor cell lysis in patients with NSCLC.

autologous TGFbeta-resistant HER2/EBV-specific cytotoxic T lymphocytes

A preparation of transforming growth factor-beta (TGF-beta)-resistant Epstein-Barr virus (EBV)-specific cytotoxic T lymphocytes (CTLs) directed to EBV through their native receptor and HER2 through a retrovirally transduced HER2 chimeric antigen receptor (CAR) with potential antineoplastic activity. Autologous EBV-specific CTLs are produced by exposing autologous CTLs to "stimulator" autologous EBV-transformed lymphoblastoid cell lines (EBV-LCLs). Subsequently, autologous EBV-specific CTLs are transduced with retroviral vectors expressing the mutant type II TGF-beta dominant-negative receptor (DNR), which blocks signaling by all three TGF-beta isoforms, and the HER2 CAR. After transduction, transgenic EBV-CTLs are expanded on EBV-LCLs. Upon administration, autologous HER2 chimeric receptor/TGFbeta dominant negative receptor-expressing EBV-specific cytotoxic T lymphocytes may bind to HER2-expressing tumors cells, which may result in CTL-mediated cell lysis and inhibition of tumor cell proliferation. Tumor-expressed TGF-beta inhibits T lymphocyte activation and expansion.

autologous TGFbRII-knockout anti-interleukin-13 receptor alpha 2 CAR T cells

A preparation of autologous T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for interleukin-13 receptor alpha 2 (IL13Ra2), and to knock out the expression of transforming growth factor-beta receptor II (TGFbRII), with potential immunostimulating and antineoplastic activities. Upon administration, autologous TGFbRII-KO anti-IL13Ra2 CAR T cells target and bind to IL13Ra2 expressed on the surface of tumor cells. This induces selective toxicity in tumor cells expressing IL13Ra2. IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell types including glioblastoma multiforme (GBM); it is associated with increased invasiveness of tumor cells. By knocking out the expression of TGFbRII, the immunosuppressive cytokine TGF-beta is unable to bind to the T-cells and prevent the activation of the T-cells. TGF-beta contributes to the immunosuppressive nature of the tumor microenvironment (TME), and plays a key role in promoting tumor initiation, metastasis, and suppressing anti-tumor immunity.

autologous TIM-4 chimeric engulfment receptor T cells CER-1236

A preparation of autologous T cells genetically engineered to express a chimeric engulfment receptor (CER) that contains the phosphatidylserine (PS) receptor T-cell immunoglobulin and mucin domain-containing protein 4 (TIM-4) extracellular signaling domain linked to the transmembrane domain of the co-stimulatory signaling protein CD28 and the zeta chain of the TCR/CD3 complex (CD3-zeta) fused to the Toll/interleukin-1 receptor (TIR) domain from Toll-like receptor 2 (TLR-2; TLR2; Toll/Interleukin 1 Receptor-Like 4) (TLR2-TIR) as an additional innate signaling domain to enhance antigen-presenting cell (APC)-function, with potential phagocytic, immunomodulating and antineoplastic activities. Upon administration, autologous TIM-4 CER T cells CER-1236 target and bind to the phospholipid and TIM-4 ligand (TIM-4-L) phosphatidylserine expressed on tumor cells. This binding induces cytolytic and phagocyte-like engulfment activity of the CER T cells, thereby killing TIM-4-L expressing tumor cells. Activation of the T-cell signaling domains activate and enhance the cytotoxic T-lymphocyte response against the tumor cells, thereby further killing tumor cells. In addition, the tumor-associated antigens (TAAs) that are leaked from the tumor cells are taken up by CER-1236 and are processed and presented to the immune system through an APC-like presentation, thereby inducing secondary immune responses and activating bystander T cells. Aberrant TIM-4-L expression is observed on malignant cells of multiple lineages, but its expression is minimal on normal, healthy cells.

autologous Tn-MUC1-specific CAR T lymphocytes

A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) Tn glycoform of mucin-1 (Tn-MUC1; TnMUC1), with potential antineoplastic and immunostimulating activities. Upon re-introduction into the patient, the autologous Tn-MUC1-specific CAR T lymphocytes specifically recognize and induce selective toxicity in TnMUC1-expressing tumor cells. TnMUC1 is overexpressed in certain tumor types.

autologous TNS9.3.55-transduced CD34-positive cells

A preparation of autologous, CD34-positive hematopoietic progenitor cells (HPCs) ex vivo transduced with TNS9.3.55, a lentiviral vector encoding the human beta-globin (hemoglobin-beta, HBB) gene, with potential to restore beta-globin expression and function. Autologous CD34-positive stem cells are isolated from the patient's own bone marrow, the deficient HBB gene is removed, and the cells are transduced with the lentiviral vector. Upon re-infusion of the TNS9.3.55-transduced CD34-positive cells back into the patient, these cells express beta-globin, thereby allowing the body to make normal hemoglobin and thus normal, healthy red blood cells. Beta-globin, the beta-chain of the most common form of hemoglobin, is encoded by the HBB gene; mutations in this gene prevent normal beta-globin production.

autologous tolerogenic proinsulin peptide-loaded dendritic cells PIpepTolDC

A vaccine composed of autologous tolerogenic dendritic cells (DCs) loaded with the beta cell protein proinsulin peptide (PIpep), C19-A3, with potential immunosuppressive and immune-regulating activities. Upon intradermal administration, the autologous tolerogenic PIpep-loaded DCs may induce proinsulin-specific regulatory T cells (Tregs). This may suppress the autoimmune destruction of the insulin-producing beta cells, thereby protecting the beta cells.

autologous total tumor mRNA and CMV-pp65-flLAMP mRNA- loaded liposome vaccine

An mRNA-based, personalized cancer vaccine consisting of total tumor RNA (TTRNA) derived and amplified from autologous tumor cells and mRNA encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83) as a fusion protein with the full-length lysosome-associated membrane protein (flLAMP), formulated in DOTAP lipid particles, with potential immunostimulatory and antineoplastic activities. Upon administration of the autologous total tumor mRNA and CMV-pp65-flLAMP mRNA loaded liposome vaccine, the mRNA is taken up, translated and presented by antigen presenting cells (APCs). This leads to an induction of both cytotoxic T-lymphocyte and memory T-cell dependent immune responses that specifically target and destroy the patient's cancer cells that express these tumor antigens. The incorporation of flLAMP may route CMV pp-65 antigens into the lysosomal compartment, resulting in enhanced MHC class II antigen presentation, thereby promoting CD4-positive T-cell responses. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.

autologous total tumor mRNA loaded liposome vaccine

An mRNA-based, personalized cancer vaccine consisting of total tumor RNA (TTRNA) derived from autologous tumor cells, formulated in DOTAP lipid nanoparticles, with potential immunostimulatory and antineoplastic activities. Upon administration of the autologous total tumor mRNA loaded liposome vaccine, the mRNA is taken up, translated and presented by antigen presenting cells (APCs). The expressed epitopes are then presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL)- and memory T-cell-dependent immune responses that specifically target and destroy the patient's cancer cells that express these tumor antigens.

autologous TP53 R175H mutant-specific HLA-A*02:01-restricted TCR gene engineered T lymphocytes NT-175

A preparation of autologous T lymphocytes that have been genetically modified to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*02:01-restricted TP53 (p53) R175H mutant, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous TP53 R175H mutant-specific HLA-A*02:01-restricted TCR gene engineered T lymphocytes NT-175 target and bind to tumor cells expressing the TP53 R175H mutant. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing the TP53 R175H mutant. p53, a tumor suppressor gene, is mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.

autologous TROP2-CAR-transduced PD-1-positive T cells T60c

A preparation of autologous programmed cell death protein 1 (PD-1; PDCD1; CD279)-positive T lymphocytes transduced with a lentivirus expressing a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) trophoblast cell surface protein 2 (trophoblast antigen 2; tumor-associated calcium signal transducer 2; TROP2; TROP-2; TACSTD2; GA733-1; M1S1), with potential immunostimulating and antineoplastic activities. Upon administration, autologous TROP2-CAR-transduced PD-1-positive T cells T60c target, bind to and induce selective cytotoxicity in TROP2-expressing tumor cells. TROP2 is a transmembrane protein overexpressed in various tumors. Its expression is associated with enhanced tumor aggressiveness, metastasis, drug resistance and increased tumor cell survival.

autologous tumor cell proteoliposome chronic lymphocytic leukemia vaccine

An autologous chronic lymphocytic leukemia cancer vaccine consisting of patient-specific membrane proteins directly extracted from patient autologous tumor cells and incorporated into liposomes along with Interleukin 2 (IL-2) to produce membrane-patched proteoliposomes, with potential immunostimulating and antineoplastic activities. After subcutaneous injection of the autologous tumor cell proteoliposomes chronic lymphocytic leukemia vaccine, liposomes deliver the encapsulated tumor antigens into the cytosol of antigen presenting cells (APCs). Subsequently, the APCs process the antigens and present antigen-derived peptides to the immune system. This may enhance recognition of tumors by the immune system, and activate both cytotoxic CD8+ T cells and CD4+ helper T cells against tumor cells. IL-2 is incorporated into the vaccine to leverage its ability to expand activated T cells.

autologous tumor cell vaccine

A therapeutic agent produced by isolating tumor cells from an individual and processing these tumor cells into a vaccine formulation in vitro; the vaccine is then administered to the individual from whom the tumor cells were isolated. Typically combined with an adjuvant immunostimulant, an autologous cell vaccine may elicit a cytotoxic T-lymphocytic immune response to cell surface-expressed tumor-associated antigens (TAAs), resulting in tumor cell death.

autologous tumor cells/bacillus Calmette-Guérin/formalin-based vaccine

A therapeutic personalized breast cancer vaccine composed of autologous tumor cells and bacillus Calmette-Guerin (BCG) in a liquid vehicle containing formalin, with potential immunomodulating and antineoplastic activities. Upon vaccination, the autologous tumor cells/BCG/formalin-based vaccine, which contains an individual’s unique set of tumor-associated antigens (TAAs), may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against the breast cancer cells, resulting in decreased tumor growth. The BCG component serves as an adjuvant, a nonspecific stimulator of the immune response.

autologous tumor infiltrating lymphocytes BST02

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from the patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs BST02 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes C-TIL052A

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs C-TIL052A specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes GT101

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs GT101 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes GT201

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs GT201 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes HV-101

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, autologous TILs HV-101 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes ITIL-168

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's digested and cryopreserved tumor, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs ITIL-168 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes LM103

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs LM103 specifically recognize and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes LN-145

A proprietary preparation of autologous tumor infiltrating lymphocytes (TILs), with potential immunomodulating activity. The autologous TILs are isolated from an autologous tumor sample and expanded ex vivo in the presence of interleukin-2 (IL-2). Upon infusion of the autologous TILs LN-145 back into the patient, the cells specifically recognize, target and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes LN-145-S1

A proprietary preparation of autologous tumor infiltrating lymphocytes (TILs), with potential immunomodulating and antineoplastic activities. The autologous TILs are isolated from an autologous tumor sample and expanded ex vivo in the presence of interleukin-2 (IL-2). Upon infusion of the autologous TILs LN-145-S1 back into the patient, the cells specifically recognize, target and kill the patient's tumor cells.

autologous tumor infiltrating lymphocytes TBio-4101

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs TBio-4101 specifically recognize and kill the patient's tumor cells.

autologous tumor killer cells

A preparation of autologous tumor killer cells (TKCs) which consists of the innate immune cells natural killer (NK) cells and gamma delta T (gdT) cells, which are T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs), with potential cytolytic and antineoplastic activities. NK cells and gdT cells are isolated from the patients' peripheral blood mononuclear cells (PBMCs) and co-cultured ex vivo in a certain proportion with TKC technology. Upon administration, autologous TKCs may lyse cancer cells, and further stimulate an anti-tumor immune response.

autologous tumor membrane vesicles vaccine

An autologous personalized tumor vaccine composed of tumor membrane vesicles (TMV) derived from the patient's own tumor cells, with potential immunostimulating and antineoplastic activities. Upon administration of the autologous TMV vaccine, the antigenic proteins in the vaccine are presented to the immune system and activate antigen-presenting cells (APCs). This may stimulate the immune system to mount cytotoxic T-lymphocyte (CTL) and helper T-lymphocyte responses against the patient's tumor cells that express these same antigens, thereby killing the tumor cells. TCMVs contain tumor proteins and surface antigens that can stimulate an immune response.

autologous tumor-associated antigen-specific cytotoxic T lymphocytes

A preparation of autologous cytotoxic T lymphocytes (CTLs) specifically reactive to the tumor associated antigens (TAAs) human Wilms tumor protein (WT1), preferentially expressed antigen of melanoma (PRAME, melanoma antigen preferentially expressed in tumors; Opa-interacting protein 4), and survivin (baculoviral IAP repeat-containing protein 5), with potential antineoplastic activities. Upon collection, expansion, and stimulation with antigen presenting cells pulsed with an overlapping peptide library spanning the TAAs, the multi-antigen associated CTLs are re-introduced into the patient and may induce a CTL-mediated response against tumor cells expressing WT1, PRAME, or survivin, potentially leading to tumor cell lysis and inhibition of tumor cell proliferation. WT1, PRAME, and survivin, are expressed on certain tumor cell types and play key role in tumor cell proliferation and survival.

autologous tumor-associated peptide antigen-pulsed dendritic cell vaccine

A dendritic cell (DC)-based cancer vaccine composed of autologous DCs pulsed with specific tumor-associated peptide antigens (TAPA), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous TAPA-pulsed DC vaccine exposes the immune system to the specific TAPAs, which may result in cytotoxic T-lymphocyte (CTL)-mediated immune responses against the TAPA-expressing cancer cells. This leads to cancer cell lysis. This vaccine is specific towards peptides derived from the following proteins: sperm autoantigenic protein 17 (SP17), ropporin, A-kinase anchor protein 4 (AKAP4), pituitary tumor-transforming 1 (PTTG1) and SPANX family member B (SPANX-B).

autologous tumor-draining lymph node-derived lymphocytes

A preparation of autologous lymphocytes that are isolated from each patient's tumor-draining lymph nodes and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous tumor-draining LNLs specifically recognize and kill the patient's tumor cells.

autologous tumor-infiltrating lymphocytes C-TIL051

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs C-TIL051 specifically recognize and kill the patient's tumor cells.

autologous tumor-infiltrating lymphocytes GC101

A preparation of autologous tumor-infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs GC101 specifically recognize and kill the patient's tumor cells.

autologous tumor-infiltrating lymphocytes GT307

A preparation of autologous tumor-infiltrating lymphocytes (TILs) derived from each patient's resected tumor and edited with the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated protein 9 (Cas9) system to eliminate the expression of as of yet not elucidated immunoregulatory targets, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, autologous TILs GT307 specifically recognize and kill the patient's tumor cells. The knockout of the immunoregulatory targets may enhance the proliferation and cytokine release of the TILs.

autologous tumor-infiltrating lymphocytes HS-IT101

A preparation of autologous tumor infiltrating lymphocytes (TILs) derived from each patient's resected tumor and expanded ex vivo, with potential immunomodulating and antineoplastic activities. Upon administration back into the patient, the autologous TILs HS-IT101 specifically recognize and kill the patient's tumor cells.

autologous tumor-infiltrating lymphocytes MDA-TIL

A preparation of autologous tumor-infiltrating lymphocytes (TILs) with potential antineoplastic activity. TILs are isolated from a patient’s tumor tissue, then cultured and expanded in vitro in the presence of interleukin-2 (IL-2) and an agonistic anti-4-1BB (CD137) antibody. Upon infusion of the autologous expanded TILs back into the patient, the cells specifically recognize, target, and kill the patient’s tumor cells.

autologous tumor-infiltrating lymphocytes-central memory T cells

An agent that targets the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA) and redirects T-cells to PSMA-expressing tumor cells, with potential antineoplastic activity. Although the mechanism of action has not been elucidated, upon administration, PSMA-targeting T-cell redirecting agent JNJ-80038114 targets PSMA found on PSMA-expressing tumor cells, and redirects T cells to the PSMA-expressing tumor cells. This may result in T-cell-mediated cell death of PSMA-expressing tumor cells. PSMA, a type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.

autologous tumor-specific antigen-loaded dendritic cells

A cell-based cancer vaccine composed of autologous dendritic cells (DCs) loaded with tumor-specific antigen(s) (TSAs), with potential immunostimulatory and antineoplastic activities. Upon administration of the autologous TSA-loaded DCs, the DCs stimulate a specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the tumor cells expressing the TSA(s), resulting in tumor cell lysis.

autologous UCD19 CAR T cells

A preparation of autologous peripheral blood lymphocytes (PBLs) that have been transduced with a lentiviral vector to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon transfusion, the autologous UCD19 CAR-T cells recognize and bind to CD19-expressing tumor cells, thereby selectively lysing CD19-expressing tumor cells. CD19, a B-cell-specific cell surface antigen is overexpressed in B-cell lineage malignancies.

autologous universal CAR-expressing T lymphocytes UniCAR02-T

A preparation of autologous T lymphocytes that has been genetically engineered to express a fully humanized, universal, second generation chimeric antigen receptor (CAR) with a CD28/CD3zeta co-stimulatory domain, and a binding domain that can recognize a peptide motive of an antigen-specific targeting module (TM), with potential immunomodulating and antineoplastic activities. Upon administration, autologous universal CAR-expressing T lymphocytes UniCAR02-T remain inactivated. Upon administration of an antigen-specific TM, the binding domain of UniCAR02-T binds to the nuclear antigen motif of the TM, and UniCAR02-T is activated when the antigen-binding moiety of the TM binds to the specific antigen expressed on tumor cells. This induces selective toxicity in and causes lysis of tumor cells expressing the specific antigen.

autologous UV-oHSV2-activated peripheral blood mononuclear cells

A preparation of autologous peripheral blood mononuclear cells (PBMCs) activated ex vivo by ultraviolet-inactivated oncolytic herpes simplex virus type 2 (UV-oHSV2), with potential immunomodulating and antineoplastic activities. Upon reintroduction of the autologous UV-oHSV2-activated PBMCs into the patient, the activated immune cells kill tumor cells. Ex vivo UV-oHSV2 treatment induces natural killer (NK) cell proliferation and the secretion of interferon-gamma (IFNg). This leads to immune-mediated tumor cell death and the inhibition of tumor cell proliferation.

autologous vaccine-enhanced ex vivo activated cancer neoantigens-specific T cells TVI-Brain-1

A preparation of autologous T lymphocytes collected from the patient after the administration of a personalized cancer vaccine composed of an attenuated form of patient-specific cancer cells and an immunological adjuvant, via leukapheresis, and activated ex vivo, with potential immunostimulating and antineoplastic activities. Cancer neoantigens-specific T cells are collected after the administration of the personalized cancer vaccine and expanded ex vivo. Upon administration, the autologous vaccine-enhanced ex vivo activated cancer neoantigens-specific T cells TVI-Brain-1 recognize and bind to tumor cells expressing the cancer neoantigens, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient's tumor cells.

autologous WT1-directed CRISPR/Cas9-engineered TCR-T cells NTLA-5001

A preparation of human autologous T lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous T-cell receptor (TCR) and modified to express a TCR specific for the tumor-associated antigen (TAA) Wilms tumor 1 (WT1) epitope, WT1 37-45, and human leukocyte antigen (HLA)-A*02:01, with potential immunostimulating and antineoplastic activities. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous WT1-directed CRISPR/Cas9-engineered TCR-T cells NTLA-5001 recognize and bind to WT1-expressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of WT1-expressing tumor cells. WT1 protein, a zinc finger DNA-binding transcriptional regulator, is overexpressed in various leukemias and solid tumors, while expression in normal, healthy tissues is very limited; its expression is correlated with aggressiveness and poor prognosis. The removal of endogenous TCR reduces TCR competition for expression, increases the persistence and function of the expressed transgenic TCR, enhances resistance to T-cell exhaustion and increases T-cell activity.

autologous WT1-TCRc4 gene-transduced CD8-positive Tcm/Tn lymphocytes

Autologous, human CD8 T lymphocytes, comprised of both central memory T cells (Tcm) and naïve T cells (Tn), that are transduced, ex vivo, with a self-inactivating (SIN) lentiviral vector encoding a high-affinity T-cell receptor (TCRc4) specific for the human tumor antigen Wilms tumor 1 (WT1) epitope 126-134 (RMFPNAPYL), with potential antineoplastic activity. Upon isolation of peripheral blood lymphocytes (PBLs), transduction, expansion ex vivo, priming of the Tn subset, but not the Tcm subset, with interleukin-21 (IL-21), and reintroduction of equal amounts of Tcm and Tn cells into the patient, WT1-TCRc4 gene-transduced CD8-positive Tcm/Tn lymphocytes redirect T lymphocytes to WT1-expressing tumor cells and specifically bind to and lyse those cells. This inhibits proliferation of WT1-expressing tumor cells. WT1 protein, a zinc finger DNA-binding transcriptional regulator, is overexpressed in most leukemias and various solid tumors, while expression in normal, healthy tissues is very limited; its expression is correlated with aggressiveness and poor prognosis.

avadomide

A novel, small molecule cereblon-modulating agent with potential antineoplastic, antiangiogenic and immunomodulatory activities. Upon oral administration, avadomide binds to and modulates cereblon to promote recruitment of the hematopoietic transcription factors Aiolos and Ikaros to the Cullin-4 RING E3 ubiquitin ligase complex. This binding results in the ubiquitination and rapid proteasomal degradation of Aiolos and Ikaros and the derepression of interferon (IFN)-stimulated genes, including DDX58 and IRF7, leading to apoptosis of certain tumor cells. Additionally, Aiolos degredation leads to derepression of the IL2 gene, thereby enhancing interleukin-2 production, costimulation of T lymphocytes and IL-2-induced T-cell proliferation. Avadomide may also promote the activation of natural killer (NK) cells, potentially enhancing tumor cell killing. Aiolos and Ikaros are transcriptional repressors known to play an important role in normal B and T cell function.

avadomide hydrochloride

The hydrochloride salt form of avadomide, a novel, small molecule, cereblon-modulating agent with potential antineoplastic, antiangiogenic and immunomodulatory activities. Upon oral administration, avadomide binds to and modulates cereblon to promote recruitment of the hematopoietic transcription factors Aiolos and Ikaros to the Cullin-4 RING E3 ubiquitin ligase complex. This binding results in the ubiquitination and rapid proteasomal degradation of Aiolos and Ikaros and the derepression of interferon (IFN)-stimulated genes, including DDX58 and IRF7, leading to apoptosis of certain tumor cells. Additionally, Aiolos degredation leads to derepression of the IL2 gene, thereby enhancing interleukin-2 production, costimulation of T-lymphocytes and IL-2-induced T-cell proliferation. Avadomide may also promote the activation of natural killer (NK) cells, potentially enhancing tumor cell killing. Aiolos and Ikaros are transcriptional repressors known to play an important role in normal B- and T-cell function.

Avage

(Other name for: tazarotene)

avanafil

An orally available phosphodiesterase type 5 (PDE5) inhibitor with vasodilatory activity. Avanafil selectively inhibits PDE5, thus inhibiting the degradation of cyclic guanosine monophosphate (cGMP) found in the smooth muscle of the corpus cavernosa of the penis. The inhibition of cGMP degradation results in prolonged muscle relaxation, vasodilation, and blood engorgement of the corpus cavernosa, thereby prolonging penile erection.

Avandia

(Other name for: rosiglitazone maleate)

avapritinib

An orally bioavailable inhibitor of specific mutated forms of platelet-derived growth factor receptor alpha (PDGFR alpha; PDGFRa) and mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, avapritinib specifically binds to and inhibits specific mutant forms of PDGFRa and c-Kit, including the PDGFRa D842V mutant and various KIT exon 17 mutants. This results in the inhibition of PDGFRa- and c-Kit-mediated signal transduction pathways and the inhibition of proliferation in tumor cells that express these PDGFRa and c-Kit mutants. PDGFRa and c-Kit, protein tyrosine kinases and tumor-associated antigens (TAAs), are mutated in various tumor cell types; they play key roles in the regulation of cellular proliferation.

avasopasem manganese

A mimetic of the enzyme superoxide dismutase (SOD) that may potentially be used to reduce oral mucositis and esophagitis associated with radiation therapy and chemoradiotherapy. Upon administration, avasopasem manganese may mimic native SODs and catalyze the formation of molecular oxygen and hydrogen peroxide from the burst of superoxide anion present in the irradiated tissues upon radiation and/or induced by chemotherapy. This may decrease the damage of radiation and/or chemotherapy to normal tissues.

Avastin

(Other name for: bevacizumab)

avatrombopag maleate

The maleate salt form of avatrombopag, an orally available platelet thrombopoietin receptor (TPOR; MPL) agonist, with potential megakaryopoiesis stimulating activity. Upon administration, avatrombopag binds to and stimulates TPOR, which may lead to the proliferation and differentiation of megakaryocytes from bone marrow progenitor cells. This increases the production of platelets and may prevent chemotherapy-induced thrombocytopenia (CIT). TPOR is a cytokine receptor and member of the hematopoietin receptor superfamily.

avdoralimab

A human monoclonal antibody targeting the C5a receptor (C5aR), with potential immunomodulating activity. Upon administration, avdoralimab specifically targets, binds to and blocks C5aR expressed on subsets of myeloid-derived suppressor cells (MDSCs) and neutrophils. This prevents the binding of its ligand C5a to C5aR and prevents the C5aR-mediated activation and accumulation of these cells in the tumor microenvironment (TME), and abrogates the secretion of inflammatory and angiogenic factors by these cells. This results in the activation of T- and natural killer (NK) cells, the induction of anti-tumor immune responses and inhibits tumor cell proliferation. C5a, a factor in the complement cascade, is often overexpressed in tumors, where it attracts and activates MDSCs and neutrophils in the TME.

Aveeno cream

(Other name for: colloidal oatmeal cream)

Avelox

(Other name for: moxifloxacin hydrochloride)

Avelumab

A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.

Avemar

(Other name for: fermented wheat germ extract)

Avena sativa

The whole plant of the vascular plant Avena sativa (cultivated common oat). The whole extract of Avena sativa can be used for various purposes.

avexitide

A truncated form of the glucagon-like peptide 1 receptor (GLP-1R) agonist exendin-4 peptide, with GLP-1 receptor (GLP-1R) antagonistic and GLP-1R-mediated signaling inhibiting activities. Upon administration, avexitide competitively binds to and inhibits the activity of GLP-1R, thereby inhibiting GLP-1/GLP-1R-mediated signaling. This antagonizes the glucagonostatic and the insulinotropic effects of GLP-1. By abrogating GLP-1-mediated simulation of insulin release and reduction of glucagon secretion after food intake, exendin 9-39 may be used to help study the potential effects of overproduction of GLP-1 on food intake, weight loss and glucose levels. GLP-1R, located on pancreatic beta cells, is overexpressed on certain tumor cell types. GLP-1 is a gastrointestinal (GI) and insulinotropic hormone that is released after a meal and plays a key role in the regulation of blood glucose levels.

Aviane

(Other name for: ethinyl estradiol/levonorgestrel)

Avinza

(Other name for: morphine sulfate)

aviptadil

A synthetic form of vasoactive intestinal polypeptide (VIP), with potential anti-cytokine, anti-inflammatory, and immune-regulatory activities. Upon administration, aviptadil mimics endogenous VIP. In the lungs, aviptadil may prevent N-Methyl-D-aspartic acid (NMDA)-induced caspase-3 activation, inhibits the production of certain pro-inflammatory mediators, such as interleukin-6 (IL-6) and tumor-necrosis factor-alpha (TNFa), and may protect the lungs against a cytokine storm and inflammation. As cytokines cause the air sacs of the lungs to fill with water, making the sacs impermeable to oxygen, aviptadil may protect against pulmonary edema, and restores the barrier function at the endothelial/alveolar interface. This may improve blood oxygenation, respiratory distress, and prevent lung injury. VIP is a naturally synthesized peptide hormone that is highly concentrated in the lungs.

aviscumine

A recombinant protein that inactivates the ribosome with potential antineoplastic and immunomodulating activities. Aviscumine binds to the cell surface sialyltransferase CD75 and is internalized; intracellularly, aviscumine cleaves an adenine-specific N-glycosidic bond on the 28S ribosomal subunit, which may result in tumor cell apoptosis. This agent has also been shown to activate natural killer (NK) cells, induce cytokine receptor expression, and stimulate the release of cytokines. CD75 is expressed on mature B cells and subsets of T cells and erythrocytes.

Avita

(Other name for: tretinoin)

Avlosulfon

(Other name for: dapsone)

Avmacol

(Other name for: broccoli sprout/broccoli seed extract supplement)

AVN944

An orally available, synthetic small molecule with potential antineoplastic activity. AVN944 inhibits inosine monosphosphate dehydrogenase (IMPDH), an enzyme involved in the de novo synthesis of guanosine triphosphate (GTP), a purine molecule required for DNA and RNA synthesis. Inhibition of IMPDH deprives cancer cells of GTP, resulting in disruption of DNA and RNA synthesis, inhibition of cell proliferation, and the induction of apoptosis. AVN944 appears to have a selective effect on cancer cells in that deprivation of GTP in normal cells results in a temporary slowing of cell growth only. IMPDH is overexpressed in some cancer cells, particularly in hematological malignancies.

Avodart

(Other name for: dutasteride)

avotaciclib

An orally bioavailable, cyclin dependent kinase 1 (CDK1) inhibitor, with potential antineoplastic activity. Upon administration, avotaciclib targets, binds to and inhibits the activity of CDK1. This may inhibit cancer stem cell (CSC) division, cause cell cycle arrest, and induce apoptosis. This may inhibit tumor cell proliferation. CDK1, an ATP-dependent serine/threonine kinase, plays a key role in regulating cell division, cell cycle progression and proliferation. It is frequently overexpressed in tumor cells.

avutometinib

An orally bioavailable inhibitor of the serine/threonine protein kinases Raf and mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK), with potential antineoplastic activity. Upon oral administration, avutometinib specifically targets, binds to and inhibits the kinase activities of Raf and MEK, resulting in the inhibition of Raf/MEK-mediated signal transduction pathways. This results in the inhibition of Raf/MEK-dependent tumor cell proliferation and survival. The RAS/RAF/MEK/extracellular signal-regulated kinase (ERK) signaling pathway is often dysregulated in human cancers and plays a key role in tumor cell proliferation, differentiation and survival.

Avycaz

(Other name for: ceftazidime/avibactam sodium)

axalimogene filolisbac

A cancer vaccine containing a live-attenuated strain of the bacterium Listeria monocytogenes (Lm) encoding human papillomavirus (HPV) type 16 E7 fused to a non-hemolytic listeriolysin O protein with potential immunostimulatory and antineoplastic activities. Upon vaccination with axalimogene filolisbac, Listeria expresses the HPV 16 E7 antigen and activates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing HPV 16 E7. This may result in tumor cell lysis. In addition, the Listeria vector itself may induce a potent immune response. HPV 16 E7, a cell surface glycoprotein and tumor associated antigen, is overexpressed in the majority of cervical cancer cells.

axatilimab

A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against colony-stimulating factor 1 receptor (CSF-1R; CSF1R; macrophage-CSFR; M-CSFR; CD115; c-fms), with potential antineoplastic activity and anti-inflammatory, immunomodulating and anti-fibrotic activities. Upon intravenous administration, axatilimab binds to the ligand binding domain of CSF-1R expressed on monocytes and macrophages, thereby preventing binding and consequent activation by its natural ligands, interleukin-34 (IL-34) and colony-stimulating factor 1 (CSF-1). Inhibition of CSF-1R activation and CSF1R-mediated signaling may reduce the levels of these circulating pro-inflammatory and pro-fibrotic monocytes and monocyte-derived macrophages. This prevents the secretion of a variety of pro-inflammatory cytokines by monocytes and macrophages, reduces inflammation, and inhibits the tumor necrosis factor-beta (TGF-b) secretion by profibrotic (M2) macrophages. This inhibits the TGF-b-mediated development of fibrosis and may treat chronic graft-versus-host disease (cGVHD). In addition, by blocking CSF-1R activation and CSF-1R-mediated signaling in tumor-associated macrophages (TAMs), axatilimab may abrogate the TAMs-mediated immunosuppression in the tumor microenvironment (TME) and may enhance T-cell infiltration and antitumor T-cell immune responses. This may inhibit the proliferation of tumor cells. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival. CSF-1R is a tyrosine protein kinase that plays an essential role in the regulation, proliferation, survival and differentiation of tissue macrophages as well as TAMs.

axicabtagene ciloleucel

A preparation of autologous peripheral blood T lymphocytes (PBTL) that have been transduced with a gammaretoviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion and re-introduction of axicabtagene ciloleucel into the patient, these cells bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen that is expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it regulates both the assembly and cell surface expression of TCR complexes. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.

axitinib

An orally bioavailable tyrosine kinase inhibitor. Axitinib inhibits the proangiogenic cytokines vascular endothelial growth factor (VEGF) and platelet-derived growth factor receptor (PDGF), thereby exerting an anti-angiogenic effect.

AXL inhibitor AB801

An orally bioavailable inhibitor of the receptor tyrosine kinase AXL (UFO), with potential immunostimulating and antineoplastic activities. Upon oral administration, AXL inhibitor AB801 targets, reversibly binds to, and prevents the activation of AXL. This blocks AXL-mediated signal transduction pathways, and inhibits both AXL-mediated tumor cell growth, proliferation and migration and AXL-mediated immunosuppression. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion, and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis.

AXL inhibitor DS-1205c

An orally available and selective inhibitor of the receptor tyrosine kinase AXL (UFO), with potential antineoplastic activity. Upon administration, DS-1205c targets, binds to and prevents the activation of AXL. This blocks AXL-mediated signal transduction pathways and inhibits tumor cell proliferation and migration. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types. It plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.

AXL inhibitor FC084CSA

An orally bioavailable inhibitor of the receptor tyrosine kinase AXL (UFO), with potential immunostimulating and antineoplastic activities. Upon oral administration, AXL inhibitor FC084CSA specifically targets, binds to, and prevents the activation of AXL. This blocks AXL-mediated signal transduction pathways, and inhibits both AXL-mediated tumor cell growth, proliferation and migration and AXL-mediated immunosuppression. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T-cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion, and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis.

AXL inhibitor NTQ2494

An orally bioavailable and selective inhibitor of the receptor tyrosine kinase AXL (UFO), with potential antineoplastic activity. Upon oral administration, AXL inhibitor NTQ2494 targets, binds to and prevents the activation of AXL. This blocks AXL-mediated signal transduction pathways, and inhibits AXL-mediated tumor cell growth, proliferation and migration, and AXL-mediated immunosuppression and immune evasion. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and a variety of immune cells. It plays a key role in tumor cell proliferation, survival, invasion and metastasis, and its expression is associated with drug resistance and poor prognosis.

AXL inhibitor SLC-391

An orally bioavailable and selective inhibitor of the receptor tyrosine kinase AXL (UFO), with potential immunostimulating and antineoplastic activities. Upon oral administration, SLC-391 targets, binds to and prevents the activation of AXL. This blocks AXL-mediated signal transduction pathways, and inhibits both AXL-mediated tumor cell growth, proliferation and migration and AXL-mediated immunosuppression. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and also expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis.

AXL receptor tyrosine kinase/cMET inhibitor BPI-9016M

An orally available inhibitor of the AXL receptor tyrosine kinase (AXL; UFO) and the receptor tyrosine kinase c-Met/hepatocyte growth factor receptor (HGFR) with antineoplastic activity. Upon administration, AXL receptor tyrosine kinase/cMET inhibitor BPI-9016M, binds to both AXL and cMet, thereby disrupting both AXL- and c-Met-mediated signaling pathways. Altogether, this agent inhibits growth in AXL and cMet-overexpressing tumor cells. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases, and cMet, both overexpressed by many tumor cell types, play key roles in tumor cell proliferation, survival, invasion and metastasis.

AXL/ FLT3/VEGFR2 inhibitor KC1036

An orally bioavailable inhibitor of three receptor tyrosine kinases: AXL (UFO), FMS-like tyrosine kinase-3 (Flt3; CD135; fetal liver kinase-2; Flk2), and the vascular endothelial growth factor receptor type 2 (VEGFR2), with potential anti-angiogenesis and antineoplastic activities. Upon oral administration, KC1036 targets, binds to and prevents the activation of AXL, FLT3 and VEGFR2. This blocks AXL, FLT3 and VEGFR2-mediated signal transduction pathways, and inhibits both AXL-, FLT3- and VEGFR2-mediated proliferation of tumor cells and the VEGFR2-mediated proliferation, survival and migration of endothelial cells. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and also expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias. VEGFR2 is frequently overexpressed by a variety of tumor types and tumor‐associated endothelial cells.

AXL/FLT3 inhibitor TT-00973

An orally bioavailable inhibitor of the receptor tyrosine kinases AXL (UFO) and FMS-like tyrosine kinase-3 (FLT3; CD135; fetal liver kinase-2; Flk2), with potential antineoplastic activity. Upon oral administration, AXL/FLT3 inhibitor TT-00973 binds to and inhibits AXL and FLT3, including the FLT3-ITD-F691L gatekeeper mutation. Inhibition of these kinases leads to the disruption of downstream signaling pathways and the inhibition of cell growth of tumors in which these kinases are overexpressed or mutated. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and also expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.

AXL/FLT3/NTRK inhibitor HH30134

An orally bioavailable inhibitor of multiple kinases, including the receptor tyrosine kinases AXL (UFO) and FMS-like tyrosine kinase-3 (FLT3; CD135; fetal liver kinase-2; Flk2), and the neurotrophic tyrosine receptor kinases (NTRKs), with potential antineoplastic activity. Upon oral administration, AXL/FLT3/NTRK inhibitor HH30134 binds to and inhibits wild-type, point mutants and fusion proteins of AXL, FLT3 and NTRK. Inhibition of these kinases leads to the disruption of downstream signaling pathways and the inhibition of cell growth of tumors in which these kinases are overexpressed, rearranged or mutated. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases, is overexpressed by many tumor cell types and also expressed in a variety of immune cells including macrophages, natural killer (NK) cells, and regulatory T cells (Tregs). It plays a key role in tumor cell proliferation, survival, invasion and metastasis, and is a mediator of immunosuppression. Its expression is associated with drug resistance and poor prognosis. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.

Axl/Mer inhibitor INCB081776

An orally available and selective inhibitor of the receptor tyrosine kinases (RTKs) Axl (UFO) and Mer, with potential antineoplastic activity. Upon administration, INCB081776 targets and binds to both Axl and Mer, and prevents their activity. This blocks Axl- and Mer-mediated signal transduction pathways, and inhibits proliferation and migration of Axl- and Mer-overexpressing tumor cells. Axl and Mer, both members of the TAM (Tyro3, Axl and Mer) family of RTKs, are overexpressed by many tumor cell types. They play key roles in tumor cell proliferation, survival, invasion, angiogenesis and metastasis, and their expression is associated with enhanced immunosuppression, drug resistance and poor prognosis.

Axl/Mer inhibitor PF-07265807

An inhibitor of the receptor tyrosine kinases (RTKs) Axl (UFO) and Mer, with potential antineoplastic activity. Upon administration, Axl/Mer inhibitor PF-07265807 specifically targets and binds to both Axl and Mer, and prevents their activity. This blocks Axl- and Mer-mediated signal transduction pathways, and inhibits proliferation and migration of Axl- and Mer-overexpressing tumor cells. Axl and Mer, both members of the TAM (Tyro3, Axl and Mer) family of RTKs, are overexpressed by many tumor cell types. They play key roles in tumor cell proliferation, survival, invasion, angiogenesis and metastasis, and their expression is associated with drug resistance and poor prognosis.

Axl/Mer/CSF1R inhibitor Q702

An orally bioavailable inhibitor of the receptor tyrosine kinases (RTKs) Axl (UFO), Mer, and colony stimulating factor-1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), with potential immunomodulatory, chemo-sensitizing and antineoplastic activities. Upon oral administration, Axl/Mer/CSF1R inhibitor Q702 targets, binds to and blocks the activity of Axl, Mer and CSF1R, thereby blocking Axl-, Mer- and CSF1R-mediated signaling pathways. This inhibits proliferation of Axl- and Mer-expressing tumor cells. In addition, blocking Axl- and Mer-mediated signaling may re-activate the innate immune system against cancer cells. Blocking CSF1R-mediated signaling inhibits the activities of tumor-associated macrophages (TAMs), regulatory T cells (Tregs) and recruitment of myeloid-derived suppressor cells (MDSCs). Altogether, this abrogates immune suppression in the tumor microenvironment (TME), enhances antitumor T-cell immune responses and inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor that plays major roles in tumor cell proliferation, metastasis, and cancer-associated immune suppression. Axl and Mer, both members of the TAM (Tyro3, Axl and Mer) family of RTKs, are overexpressed by many tumor cell types. They play key roles in tumor cell proliferation, survival, invasion, angiogenesis and metastasis, and the inactivation of innate immunity in cancer. Their expression is associated with drug resistance and poor prognosis.

Axumin

(Other name for: fluciclovine F18)

Aygestin

(Other name for: norethindrone acetate)

Ayvakit

(Other name for: avapritinib)

azacitidine

A pyrimidine nucleoside analogue of cytidine with antineoplastic activity. Azacitidine is incorporated into DNA, where it reversibly inhibits DNA methyltransferase, thereby blocking DNA methylation. Hypomethylation of DNA by azacitidine may activate tumor suppressor genes silenced by hypermethylation, resulting in an antitumor effect. This agent is also incorporated into RNA, thereby disrupting normal RNA function and impairing tRNA cytosine-5-methyltransferase activity.

Azactam

(Other name for: aztreonam)

azapicyl

A hydrazine compound that has been investigated for antineoplastic activity.

azaribine

The triacetate salt of azauridine, a synthetic triazine nucleoside derivative possessing antineoplastic and anti-psoriatic activity. After metabolism to 6-azauridine-5-prime monophosphate, 6-Azauridine inhibits de novo pyrimidine biosynthesis and its 5-prime triphosphate metabolite gets incorporated into RNA, thereby preventing RNA synthesis.

azaserine

A naturally occurring serine derivative diazo compound with antineoplastic properties, Azaserine functions as a purine antagonist and glutamine analogue (glutamine amidotransferase inhibitor) that competitively inhibits pathways in which glutamine is metabolized. An antibiotic and antitumor agent, Azaserine is used in clinical studies as a potential antineoplastic agent.

AzaSite

(Other name for: azithromycin)

azathioprine sodium

The sodium salt form of azathioprine, a pro-drug of purine analogue with immunosuppressive activity. Azathioprine is converted in vivo to its active metabolite 6-mercaptopurine (6-MP), which substitutes for the normal nucleoside and mistakenly gets incorporated into DNA sequences. This leads to inhibition of DNA, RNA, and protein synthesis. As a result, cell proliferation may be inhibited, particularly in lymphocytes and leukocytes.

Azedra

(Other name for: cold contaminant-free Iobenguane I-131)

Azedra

(Other name for: Iobenguane I-131)

azeliragon

An orally bioavailable inhibitor of the receptor for advanced glycation end-products (RAGE), with potential antineoplastic activity. Upon oral administration, azeliragon targets and binds to RAGE, thereby preventing binding of RAGE ligands to RAGE, and prevents RAGE-mediated signaling, This may inhibit proliferation and induce apoptosis of tumor cells in which the RAGE pathway is overactivated. RAGE, a receptor belonging to the immunoglobulin superfamily, plays a key role in inflammation and is overexpressed in a variety of cancers. It plays a key role in tumor cell proliferation, survival and metastasis.

azenosertib

An inhibitor of the tyrosine kinase Wee1 (Wee1-like protein kinase; Wee1A kinase; WEE1hu) with potential antineoplastic sensitizing activity. Although the exact mechanism of action by which this agent inhibits Wee1 has yet to be disclosed, upon administration of ZN-c3, this agent targets and inhibits Wee1. Inhibition of Wee1 promotes both premature mitosis and a prolonged mitotic arrest leading to cell death in susceptible tumor cells, such as p53-deficient or mutated human cancers that lack the G1 checkpoint, upon treatment with DNA-damaging chemotherapeutic agents. Unlike normal cells, most p53-deficient or mutated human cancers lack the G1 checkpoint as p53 is the key regulator of the G1 checkpoint and these cells rely on the G2 checkpoint for DNA repair to damaged cells. Annulment of the G2 checkpoint may therefore make p53-deficient tumor cells more vulnerable to antineoplastic agents and enhance their cytotoxic effect. Overexpression of Wee1 occurs in several cancer types and high expression of Wee1 is associated with poor outcomes. Wee1 phosphorylates Cdc2 in the Cdc2/cyclin B (CDK1/cyclin B) complex which blocks progression from G2 into mitosis; it negatively regulates the G2 checkpoint by disallowing entry into mitosis in response to DNA damage.

azercabtagene zapreleucel

A preparation of allogeneic, off-the-shelf, T-lymphocytes that have been genetically modified using a proprietary synthetic nuclease-based system to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 (cluster of differentiation 19) with potential immunostimulating and antineoplastic activities. Upon administration, azercabtagene zapreleucel specifically recognize and kill CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B-cells.

azimexon

Azimexon (2-cyanaziridinyl-2-carbamoyl-aziridinyl-1-propane) is a derivative of 2-cyanaziridine. Immunostimulant which shows therapeutic effects in tumor models and experimental infections in vitro, enhancing T lymphocyte transformation and phagocytosis. The mode of action of azimexon is unknown. It has been suggested that azimexon may alkylate DNA. In cancer patients it increases leukocytosis, blood active T rosettes, T4/T8 ratio, and is used as an adjuvant to chemotherapy in the treatment of melanoma and myeloma.

Aziridinylbenzoquinone RH1

A water-soluble, synthetic aziridinylbenzoquinone with potential antineoplastic activity. Bioactivation of aziridinylbenzoquinone RH1 occurs through the two-electron reduction of the quinone to the hydroquinone by the two-electron quinone reductase DT-diaphorase (DTD). The resultant hydroquinone selectively alkylates and cross-links DNA at the 5'-GNC-3' sequence, inihibiting DNA replication, inducing apoptosis, and inhibiting tumor cell proliferation. DTD is over-expressed in many tumors relative to normal tissue, including lung, colon, breast and liver tumors.

azithromycin

An azalide, derived from erythromycin, and a member of a subclass of macrolide antibiotics with bacteriocidal and bacteriostatic activities. Azithromycin reversibly binds to the 50S ribosomal subunit of the 70S ribosome of sensitive microorganisms, thereby inhibiting the translocation step of protein synthesis, wherein a newly synthesized peptidyl tRNA molecule moves from the acceptor site on the ribosome to the peptidyl (donor) site, and consequently inhibiting RNA-dependent protein synthesis leading to cell growth inhibition and cell death.

azithromycin monohydrate

The monohydrate form of azithromycin, an orally bioavailable azalide derived from erythromycin, and a member of a subclass of macrolide antibiotics, with anti-bacterial activity. Upon oral administration, azithromycin reversibly binds to the 23S rRNA of the 50S ribosomal subunit of the bacterial ribosome of susceptible microorganisms, thereby inhibiting the translocation step of protein synthesis by preventing the assembly of the 50S ribosomal subunit. This inhibits bacterial protein synthesis, inhibits cell growth and causes cell death.

Azixa

(Other name for: verubulin hydrochloride)

Azlin

(Other name for: azlocillin)

azlocillin

A semisynthetic, extended spectrum acylampicillin with antibacterial activity. Azlocillin binds to penicillin-binding proteins (PBPs) located inside the bacterial cell wall, thereby inhibiting the cross-linking of peptidoglycans, which are critical components of the bacterial cell wall. This prevents proper bacterial cell wall synthesis, thereby results in the weakening of the bacterial cell wall and eventually leading to cell lysis.

AZP

An aziridinyl-substituted cyclophosphazene and a putrescence derivative that may cause DNA cross-linkage.

aztreonam

A monocyclic beta-lactam antibiotic originally isolated from Chromobacterium violaceum with bactericidal activity. Aztreonam preferentially binds to and inactivates penicillin-binding protein-3 (PBP-3), which is involved in bacterial cell wall synthesis, thereby inhibiting bacterial cell wall integrity and leading to cell lysis and death. This agent differs from other beta-lactam antibiotics because it is resistant to beta-lactamase hydrolysis, and it is usually used to treat infections caused by gram-negative aerobic microorganisms.

Azulfidine

(Other name for: sulfasalazine)

azurin-derived cell-penetrating peptide p28

A water-soluble, amphipathic, 28 amino acid (amino acids 50-77), 2.9 kD fragment peptide (p28) derived from the protein azurin with potential antineoplastic and antiangiogenic activities. Although the mechanism has yet to be fully elucidated, the preferential cellular uptake of azurin-derived cell-penetrating peptide p28 by tumor cells and endothelial cells is likely via caveolae-mediated endocytosis; the C-terminal 18 amino acid residues (50-67) appear to responsible for this preferential uptake. After cell entry, the first 12 amino acid residues interact with tumor suppressor p53 and form a p28:p53 complex, which may result in a reduction of proteasomal degradation of p53, increased p53 levels, and p53-mediated cell cycle inhibition and apoptosis. Azurin is a cupredoxin secreted by the bacterium Pseudomonas aeruginosa. Cell penetrating peptides (CPPs) are cationic and/or amphipathic peptides, typically less than 30 amino acids in length, that can penetrate cell membranes easily and may transport molecular cargo.