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NCI Drug Dictionary

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466 results found for: E

E-101 solution
An oxidant-generating coupled-enzyme system-based, topical solution comprised of two enzymes, Aspergillus niger-derived glucose oxidase (GO) and porcine myeloperoxidase (p-MPO), as well as glucose, sodium chloride and stabilizing amino acids, with potential broad-spectrum microbicidal activity. Following direct administration of E-101 solution into the surgical incisional wound via microspray, the enzyme GO converts oxygen into hydrogen peroxide (H2O2). In turn, p-MPO catalyzes the reaction of H2O2 with hypochlorous acid (HOCl), which is formed through oxidation of the chloride ion, to generate singlet oxygen (O2*). As p-MPO binds to microorganisms, O2* is able to exert direct oxidative damage to microorganisms, resulting in potent antimicrobial activity. E-101 may act as an anti-bactericidal agent against a variety of microorganisms, including multidrug-resistant strains. This may prevent infection at the surgical site.
E-Mycin
(Other name for: erythromycin)
E-Z Prep
(Other name for: povidone-iodine solution)
E-Z Scrub
(Other name for: povidone-iodine solution)
E. coli CD-expressing genetically modified neural stem cells
Genetically-modified neural stem cells (NSCs) transfected with the Escherichia coli (E. coli) suicidal gene cytosine deaminase (CD), with potential antineoplastic adjuvant activity. Upon intracerebral injection, E. coli CD-expressing genetically modified NSCs express the E. coli cytosine deaminase, an enzyme that catalyzes the intracellular conversion of the nontoxic prodrug 5-fluorocytosine (5-FC) into the cytotoxic 5-fluorouracil (5-FU). Co-administration of this agent with 5-FC and upon local activation of 5-FU in the brain tumor, 5-FU disrupts DNA synthesis in tumor cells thereby impeding cellular proliferation with minimal systemic exposure and toxicity.
E2F1 pathway activator ARQ 171
A second-generation E2F1 pathway activator with potential antineoplastic activity. ARQ 171 induces the expression of E2F transcription factor 1, thereby activating the E2F1-mediated checkpoint process. E2F1, down-regulated in cancer cells, regulates expression of genes involved in the cell cycle progression from G1 into S phase. The G1/S checkpoint process selectively induces cell cycle arrest in cancer cells with irreparable DNA damages and triggers subsequent apoptosis, while allowing cell division to proceed in cells without or with minor reparable DNA damage. As a result, this agent exerts anti-tumor activity through checkpoint activation independent of p53 mediated tumor suppression.
East Indian sandalwood oil cream
A cream containing an essential oil derived from the East Indian sandalwood tree (Santalum album), containing alpha- and beta-santalols, with potential anti-inflammatory, anti-proliferative, anti-bacterial, anti-viral and immunomodulating activities. Upon topical application of the East Indian sandalwood oil (EISO) cream to an affected area of skin, the active ingredients in the cream may suppress various enzymes, such as cyclooxygenase (COX) and cyclic adenosine monophosphate (cAMP) phosphodiesterases (PDEs), prevent the production of pro-inflammatory cytokines and chemokines and directly cause apoptosis in susceptible cell types, including certain cancer cells and virally-infected cells.
East Indian sandalwood oil mouth rinse
A mouth rinse containing 0.25% East Indian sandalwood oil, which is derived from the heartwood of Santalum album, a tree native to southern Asia, with potential anti-inflammatory, anti-infective and anti-mucositis activities. East Indian sandalwood oil (EISO) is primarily comprised of the sesquiterpene alcohols alpha- and beta-santalol. Although the exact mechanisms of action through which EISO exerts its effects have yet to be fully elucidated, upon rinsing the oral cavity with the EISO mouth rinse, the active ingredients in the oil may inhibit the production of pro-inflammatory cytokines and chemokines, most likely through the inhibition of the activity of key inflammatory enzymes, including the cyclooxygenases. This prevents inflammation of the mucosal membranes and may prevent or decrease chemotherapy- and/or radiation-induced oral mucositis.
EBNA-1 inhibitor VK-2019
An orally available, small molecule inhibitor of Epstein-Barr nuclear antigen 1 (EBNA-1) with potential antineoplastic activity. Upon administration, EBNA-1 inhibitor VK-2019 binds to EBNA-1 and inhibits EBNA-1 DNA binding activity. This disrupts the replication, maintenance and segregation of the Epstein-Barr virus (EBV) genome, which may lead to tumor cell death in EBV-associated malignancies. EBNA1, a sequence-specific DNA binding protein, plays an important role in EBV episomal genome maintenance and gene transactivation.
EBP inhibitor DSP-0390
An orally bioavailable inhibitor of emopamil-binding protein (EBP), with potential antineoplastic activity. Upon oral administration, EBP inhibitor DSP-0390 targets, binds to and inhibits the activity of EBP. This inhibits EBP-mediated de novo cholesterol synthesis. As cholesterol is essential for tumor cell proliferation and survival, this inhibits tumor cell proliferation. The inhibition of EBP also results in the accumulation of its substrates zymostenol and zymosterol, and autophagy in tumor cells. EBP, a non-glycosylated type I integral membrane protein of endoplasmic reticulum, plays an important role in cholesterol biosynthesis, autophagy and oligodendrocyte formation, and is overexpressed in certain tumors.
ebselen-containing oral capsule SPI-1005
An oral capsule containing a proprietary formulation of the organoselenium compound ebselen, with potential anti-oxidant, anti-inflammatory and cytoprotective activity. Upon oral administration of SPI-1005, this agent mimics the activity of glutathione peroxidase (GPx) and can utilize glutathione to reduce other unstable molecules, thus preventing the formation of reactive oxygen species (ROS) and reducing oxidative stress on the cell. In the cochlea, this agent may prevent drug-induced injury to the auditory hair cells thereby preventing hearing loss. GPx is the main antioxidant enzyme in the cochlea and protects the inner ear from loud sounds and biochemical damage. In addition, ebselen is able to inhibit the activity of many enzymes involved in inflammation.
EBV LMP-2A-specific autologous CD8+ T cells
A preparation of autologous cytotoxic T lymphocytes (CTLs) that are specifically reactive to Epstein-Barr virus (EBV) latent membrane protein-2A (LMP-2A) and expressing the co-stimulatory domain 4-1BB (CD137), with potential antineoplastic activity. Upon administration of the EBV/LMP-2A-specific autologous CD8+ T cells to patients with EBV-positive tumors, these cells bind to and cause cell death in EBV-infected cells. This inhibits proliferation of EBV LMP-2A-expressing tumor cells. EBV LMP-2A is expressed in various malignancies and plays a key role in tumor cell proliferation and survival. 4-1BB, an inducible costimulatory member of the tumor-necrosis factor receptor (TNFR) family, is expressed on activated T cells. It activates additional CD8+ T cells, prevents activation-induced cell death of CD8+ T cells, and selectively induces T-helper 1 (Th1)-type cytokines such as interferon (IFN)-gamma and tumor-necrosis factor-alpha (TNF-alpha).
echinomycin
A polypeptide quinoxaline antineoplastic antibiotic isolated from the bacterium Streptomyces echinatus. Echinomycin intercalates into DNA at two locations simultaneously in a sequence-specific fashion, thereby inhibiting DNA replication and RNA synthesis.
Ecotrin
(Other name for: aspirin)
ecromeximab
A low-fucose, human-mouse chimeric IgG1 monoclonal antibody directed against the ganglioside GD3, a surface antigen expressed on many malignant melanoma cells, with potential antineoplastic activity. Ecromeximab binds to GD3-positive cells, thereby initiating antibody-dependent cytotoxicity against GD3-positive cells. This agent is prepared by fusing murine immunoglobulin (Ig) light and heavy variable regions derived from the murine IgG3 antibody KM-641 to a human constant (Fc) region. The low fucose content of the oligosaccharide side chains of this antibody may enhance binding of the antibody Fc region to lymphocyte Fc receptors.
ECT-001 expanded cord blood
A preparation of umbilical cord blood (UCB) co-cultured and expanded in an optimized culture system with a small molecule agonist of hematopoietic stem cell (HSC) renewal, with potential use in hematopoietic cell transplantation (HCT). Upon administration, the ECT-001 expanded cord blood cells increase and restore the number of hematopoietic stem and progenitor cells (HSPCs) that can differentiate into a variety of cell types and promote blood cell recovery. Compared to untreated UBCs, ECT-001 expanded UCB cells may exhibit enhanced stem cell proliferation and engraftment.
ECT204 transgene-transduced autologous T cells ECT204
A preparation of autologous human T lymphocytes transduced with a lentiviral vector expressing the ECT204 transgene that encodes an antibody-based antigen-binding domain targeting the tumor-associated antigen (TAA) glypican-3 (GPC3) and an effector-binding domain, with potential immunomodulating and antineoplastic activities. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and re-introduction into the patient, the ECT204 transgene-transduced autologous T cells ECT204 target and bind to tumor cells expressing GPC3. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of GPC3-positive 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.Compared to conventional CAR T cells, ECT204 may be less likely to stimulate cytokine release syndrome (CRS) and other cytokine-mediated toxicities.
ectoine mouthwash
A mouthwash consisting of the natural bacteria-derived tetrahydropyrimidine and extremolyte ectoine, with potential hydrating and anti-inflammatory activities. Upon administration as a mouthwash, ectoine may stabilize the membranes, rehydrate the mucosal lining of the oral cavity and help prevent oral infections. Ectoine may also reduce inflammation of the mucosal lining of the oral cavity through its various actions on the inflammatory cytokines such as interleukins (IL) 6 (IL-6) and 8 (IL-8), the ceramide signaling pathway, and the mitogen-activated protein kinase (MAPK) signaling pathway.
eculizumab
A humanized monoclonal antibody directed against terminal complement protein C5. Eculizumab binds to terminal complement protein C5, thereby blocking C5 cleavage into pro-inflammatory components and blocking the complement-mediated destruction of paroxysmal nocturnal hemoglobinuria (PNH) red blood cells.
edatrexate
A polyglutamatable folate antagonist analogue of methotrexate with antineoplastic activity. Edatrexate inhibits dihydrofolate reductase, thereby increasing cellular levels of polyglutamates, inhibiting thymidylate synthase and glycinamide ribonucleotide formyl transferase, impairing synthesis of purine nucleotides and amino acids, and resulting in tumor cell death. Edatrexate may overcome tumor resistance to methotrexate, which loses its activity after it is polyglutamated.
EDB-FN-targeting gadolinium-based contrast agent MT218
A contrast agent composed of a peptide of seven amino acids targeting the extradomain B (EDB) of fibronectin (FN) conjugated to the contrast agent gadolinium, with potential contrast-enhancing activity upon magnetic resonance (MR) imaging. Upon administration of EDB-FN-targeting gadolinium-based contrast agent MT218, the EDB-FN-targeting peptide moiety targets and binds to EDB-FN overexpressed on various tumor cells. Upon MRI, gadolinium produces a large magnetic moment and thus a large local magnetic field. This enhances the relaxation rate of nearby protons and increases the signal intensity of tissue images. This allows visualization and specific localization of EDB-FN-expressing tumor cells. EDB of fibronectin, an oncogenic extracellular matrix protein, is expressed in many aggressive solid human tumors, whereas it is not detectable in normal vessels and tissues.
Edecrin
(Other name for: ethacrynic acid)
edotecarin
A synthetic indolocarbazole with antineoplastic activity. Edotecarin inhibits the enzyme topoisomerase I through stabilization of the DNA-enzyme complex and enhanced single-strand DNA cleavage, resulting in inhibition of DNA replication and decreased tumor cell proliferation.
edoxaban
An orally active inhibitor of coagulation factor Xa (activated factor X) with anticoagulant activity. Edoxaban is administered as edoxaban tosylate. This agent has an elimination half-life of 9-11 hours and undergoes renal excretion.
edoxaban tosylate
The tosylate salt form of edoxaban, an orally active inhibitor of coagulation factor Xa (activated factor X) with anticoagulant activity. Edoxaban is administered as edoxaban tosylate. This agent has an elimination half-life of 9-11 hours and undergoes renal excretion.
Edralbrutinib
An orally available irreversible inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) with potential antineoplastic activity. Upon administration, edralbrutinib covalently binds to and irreversibly inhibits BTK activity, thereby preventing the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This may inhibit 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 or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B-lymphocytes.
edrecolomab
A murine monoclonal IgG2a antibody to tumor-associated epithelial cell adhesion molecule (EpCAM, or 17-1A) antigen. Edrecolomab attaches to EpCAM, a human cell surface glycoprotein that is found on normal epithelial cells and some tumor cells, such as those of colon and breast carcinomas. Upon binding, this agent recruits the body's immune effector cells, which may exhibit antitumor cytotoxicity.
EED inhibitor APG-5918
An orally bioavailable, small molecule, allosteric inhibitor of the polycomb repressive complex 2 (PRC2) component embryonic ectoderm development (EED) protein, with potential antineoplastic activity. Upon oral administration, EED inhibitor APG-5918 targets and binds to EED. This inhibits the binding of EED with trimethylated histone H3 on lysine 27 (H3K27me3), prevents the interaction of EED with the histone methyltransferase (HMT) and the catalytic subunit of the PRC2 enhancer zeste homolog 2 (EZH2), and prevents H3K27 methylation. The decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in EZH2-mutated and PRC2-dependent cancer cells. EZH2 is overexpressed or mutated in a variety of cancer cells. EED is essential for the histone methyltransferase activity of PRC2.
EED inhibitor BR1733
An orally bioavailable inhibitor of the polycomb repressive complex 2 (PRC2) component embryonic ectoderm development (EED) protein, with potential antineoplastic activity. Upon oral administration, EED inhibitor BR1733 targets and binds to EED. This inhibits the binding of EED with trimethylated histone H3 on lysine 27 (H3K27me3), prevents the interaction of EED with the histone methyltransferase (HMT) and the catalytic subunit of the PRC2 enhancer zeste homolog 2 (EZH2), and prevents H3K27 methylation. The decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in EZH2-mutated and PRC2-dependent cancer cells. EZH2 is overexpressed or mutated in a variety of cancer cells. EED is essential for the histone methyltransferase activity of PRC2.
EED inhibitor MAK683
An inhibitor of embryonic ectoderm development protein (EED) and allosteric inhibitor of polycomb repressive complex 2 (PRC2), with potential antineoplastic activity. Upon administration, MAK683 selectively binds to the domain of EED that interacts with trimethylated lysine 27 on histone 3 (H3K27me3), which leads to a conformational change in the EED H3K27me3-binding pocket and prevents the interaction of EED with the histone methyltransferase enhancer zeste homolog 2 (EZH2). Disruption of the EED-EZH2 protein-protein interaction (PPI) results in a loss of H3K27me3-stimulated PRC2 activity and prevents H3K27 trimethylation. This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in EZH2-mutated and PRC2-dependent cancer cells. PRC2, a histone H3 lysine 27 methyltransferase and multi-protein complex comprised of EZH2, EED and suppressor of zeste 12 (SUZ12), plays a key role in gene regulation, especially during embryonic development. EZH2, the catalytic subunit of PRC2, is overexpressed or mutated in a variety of cancer cells. EED is essential for the histone methyltransferase activity of PRC2 because EED directly binds to H3K27me3.
EF5
A fluorinated derivative of the 2-nitroimidazole etanidazole. EF5 is effective in accessing oxygen levels in tumor tissue through its adduct formation to intracellular macromolecules in the absence of oxygen. Reduction of this agent is carried out by a diverse group of enzymes in the cytoplasm, microsomes and mitochondria. Tissue hypoxia detection via EF5 has been reported in several cancers, including squamous cell carcinoma of the cervix and the head and neck, and in sarcoma.
efalizumab
A humanized IgG1 monoclonal antibody directed against CD11a, the alpha subunit of human leukocyte-function-associated antigen type 1 (LFA-1), with immunosuppressant activity. Efalizumab binds to CD11a, which is expressed on all leukocytes, resulting in a reduction in the cell surface expression of CD11a. In addition, this agent inhibits the binding of LFA-1 to intercellular adhesion molecule-1 (ICAM-1), resulting in the inhibition of leukocyte adherence and the suppression of cell-mediated immunity. LFA-1 binding to ICAM-1 is involved in the activation of T lymphocytes, adhesion of T lymphocytes to endothelial cells, and migration of T lymphocytes to sites of inflammation.
efanesoctocog alfa
A recombinant fusion protein comprising a single chain B-domain deleted (BDD) analog of human antihemophilic factor (coagulation factor VIII; FVIII) covalently fused to the Fc domain of human immunoglobulin G1 (IgG1), the FVIII-binding D'D3 domain of human von Willebrand factor (VWF), and two XTEN polypeptides, that can be used to treat and control bleeding episodes in hemophilia A (congenital factor VIII deficiency). Upon administration, efanesoctocog alfa temporarily replaces the missing coagulation factor VIII, which binds factor IXa. Factor X is then converted to factor Xa. This facilitates the clotting cascade by converting prothrombin to thrombin, and leads to the conversion of fibrinogen to fibrin, and thus clot formation. This normalizes the activated partial thromboplastin time (aPTT) that is needed for effective hemostasis. Patients with hemophilia A lack factor VIII, a protein needed for normal clotting of the blood. B-domain has no known biological function. The FVIII-binding D'D3 domain of human VWF component of the fusion protein prevents FVIII interaction with endogenous VWF. The Fc region of human IgG1 binds to the neonatal Fc receptor (FcRn). The two XTEN polypeptides alter the hydrodynamic radius of the fusion protein. Altogether, they extend the half-life of the fusion protein.
efaproxiral
A synthetic small molecule with radiosensitizing activity. Efaproxiral increases oxygen levels in hypoxic tumor tissues by binding non-covalently to the hemoglobin tetramer and decreasing hemoglobin-oxygen binding affinity. Increasing tumor oxygenation reduces tumor radioresistance.
efatutazone dihydrochloride
The dihydrochloride salt of efatutazone, an orally bioavailable agonist of peroxisome proliferator-activated receptor gamma (PPAR-gamma) with potential antineoplastic activity. Efatutazone binds to and activates PPAR-gamma, a nuclear hormone receptor and a ligand-activated transcription factor controling gene expression involved in macromolecule metabolism and cell differentiation, specifically adipocyte differentiation. Mediated through activation of PPAR-gamma, this agent is capable of inducing cell differentiation and apoptosis, thereby leading to a reduction in cellular proliferation.
efavirenz
A synthetic non-nucleoside reverse transcriptase (RT) inhibitor with antiviral activity. Efavirenz binds directly to the human immunodeficiency virus type 1 (HIV-1) RT, an RNA-dependent DNA polymerase, blocking its function in viral DNA replication. In combination with other antiretroviral drugs, this agent has been shown to significantly reduce HIV viral load, retarding or preventing damage to the immune system and reducing the risk of developing AIDS. Efavirenz induces activity of the cytochrome P450 system, accelerating its own metabolism.
efavirenz/emtricitabine/tenofovir disoproxil fumarate
A fixed combination of efavirenz, a non-nucleoside reverse transcriptase (RT) inhibitor (NNRTI); emtricitabine, a nucleoside RT inhibitor (NRTI) analog of cytidine; and tenofovir disoproxil fumarate, an NRTI analog of adenosine monophosphate, that is used to treat human immunodeficiency virus (HIV) infection. Upon oral administration, efavirenz, emtricitabine, and tenofovir disoproxil fumarate inhibit the activity of HIV RT by competing with natural deoxyribonucleosides for incorporation into the growing viral DNA chain resulting in early chain termination. This interferes with the generation of DNA copies of viral RNA, which is necessary for the synthesis of new virions.
efbemalenograstim alfa
A recombinant dimeric fusion peptide of the human granulocyte colony-stimulating factor (G-CSF; filgrastim), with immunomodulating and hematopoietic activities. Efbemalenograstim alfa binds to the cell surface G-CSF receptors (G-CSFRs) inducing receptor dimerization and activation of signaling cascades such as the Jak-STAT and mitogen-activated protein kinase pathways. This stimulates neutrophil progenitor proliferation and differentiation. Compared to other preparations of monomer recombinant G-CSF, dimeric filgrastim may allow for stronger activation of G-CSFRs and a faster myeloid precursor response thus enhancing neutrophil recovery upon myelosuppressive therapy.
Effexor
(Other name for: venlafaxine)
Effexor XR
(Other name for: venlafaxine hydrochloride extended release)
efgartigimod alfa
A human immunoglobulin G1 (IgG1)-derived Fc fragment that targets the neonatal Fc receptor (FcRn), with potential FcRn blocking activity. Upon administration, efgartigimod alfa targets, binds to and blocks FcRn, thereby preventing FcRn from recycling IgG back into the systemic circulation. This causes a reduction in IgG blood levels, including the abnormal acetylcholine receptor (AChR) antibodies that are present in myasthenia gravis. FcRn binds to IgGs and prevents their lysosomal degradation, thereby extending IgG half-life and increases the availability of pathogenic IgG antibodies that are present in certain severe autoimmune diseases.
efgivanermin alfa
A homogenous hexameric agonist fusion protein composed of the extracellular domain (ECD) of the T-cell costimulatory receptor human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor superfamily, member 18; TNFRSF18; GITR) ligand (GITRL) and an immunoglobulin (Ig) G1 Fc domain, with potential immunomodulating and antineoplastic activities. Upon administration, efgivanermin alfa binds to and activates GITR found on multiple types of T cells, thereby inducing both the activation and proliferation of tumor antigen-specific T-effector cells. This abrogates the suppression of T-effector cells which is induced by inappropriately activated T-regulatory cells (Tregs), suppresses Tregs and decreases Treg tumor infiltration, and activates the immune system to help eradicate tumor cells. GITR, a member of the TNF receptor superfamily, is expressed on the surface of multiple types of immune cells, including Tregs, effector T cells, B cells, dendritic cells (DCs) and natural killer (NK) cells.
efineptakin alfa
A long-acting immunoglobulin (Ig) fusion protein composed of a recombinant form of the endogenous human protein interleukin-7 (rhIL-7) and fused to a hybrid Fc (hyFc) region of a human antibody, with hematopoietic and immunopotentiating activities. Upon administration of efineptakin alfa, IL-7 stimulates the proliferation, differentiation, trafficking and survival of a variety of T-cell subsets, including naive, central memory (CM), effector memory (EM), terminally differentiated effector memory (TEMRA) and natural killer (NK) T cells, and enhances T-cell-mediated anti-tumor immune responses. Compared to rhIL-7 alone, fusion to the hyFc region enhances the half-life of IL-7. The hyFc region is composed of the hinge and N-terminal portion of heavy chain constant (CH) region 2 (hinge-CH2) of human IgD, which is fused to the C-terminal region of CH2 and the entire CH3 region of human IgG4.
efizonerimod
An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Upon administration, efizonerimod selectively binds to and activates the OX40 receptor, by mimicking the action of 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 (TNF) receptor family, is expressed on T lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells.
eflapegrastim
A long-acting, recombinant analog of the endogenous human granulocyte colony-stimulating factor (G-CSF) with hematopoietic activity. Similar to G-CSF, eflapegrastim binds to and activates specific cell surface receptors and stimulates neutrophil progenitor proliferation and differentiation, as well as selected neutrophil functions. Therefore, this agent may decrease the duration and incidence of chemotherapy-induced neutropenia. Eflapegrastim extends the half-life of G-CSF, allowing for administration once every 3 weeks.
eflornithine
A difluoromethylated ornithine compound with antineoplastic activity. Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells. This agent has been shown to induce apoptosis in leiomyoma cells.
eflornithine hydrochloride
The hydrochloride form of eflornithine, a difluoromethylated ornithine compound with antineoplastic activity. Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells.
eflornithine hydrochloride ointment
An ointment formulation of the hydrochloride salt of an ornithine decarboxylase (ODC) inhibitor with hair-growth inhibitory and potential chemopreventive activities. When administered topically, eflornithine irreversibly inhibits skin ODC activity, thereby inhibiting the synthesis of polyamines; inhibition of polyamine synthesis may result in diminished hair growth and epidermal cell turnover.
efmarodocokin alfa
A recombinant fusion protein consisting of human cytokine interleukin (IL) 22 (IL-22) fused to the Fc portion of human immunoglobulin (Ig) G4, with potential cell protective and immunomodulatory activities. Upon administration of efmarodocokin alfa, IL-22 binds to its cognate receptor IL-22R, which is highly expressed in parenchymal tissues and epithelial cells at mucosal surfaces. This leads to the activation of IL-22/IL-22R-mediated signal transduction pathways, and results in the activation of signal transducer and activator of transcription 3 (STAT3). STAT3 activation may have a protective and regenerative effect and may protect against the development of various inflammatory and immunological diseases. IL-22, a member of the IL-10 family of cytokines, is produced by various immune cells and upregulated during inflammation. It plays a key role in controlling immune responses and bacterial infection, and in the enhancement of intestinal barrier function, gut immunity, and tissue repair.
efocipegtrutide
A long-acting glucagon/gastric inhibitory peptide (GIP)/glucagon-like peptide-1 (GLP-1) triple receptor agonist conjugated with constant region of human immunoglobulin via a non-peptidyl flexible linker, with potential antihyperglycemic, anti-inflammatory and anti-fibrotic activities. Upon administration, efocipegtrutide binds to and activates multiple incretin receptors, including glucagon receptor (GCGR), GIP receptor (GIPR) and GLP-1 receptor (GLP-1R), which may decrease liver fat accumulation, inflammation and fibrogenesis, and normalize blood glucose levels.
EFS-ADA lentiviral vector-transduced CD34-positive autologous lymphocytes
A preparation of autologous, CD34-positive stem/progenitor cells transduced with a lentrivral vector encoding the human adenosine deaminase (ADA) gene under the control of the human elongation factor alpha short promoter (EFS), with potential to restore ADA expression and function. Autologous hematopoietic CD34+ cells are isolated from the patient’s own bone marrow, peripheral blood or cord blood, and transduced with the EFS-ADA lentiviral vector ex vivo. Upon re-infusion of the EFS-ADA vector-transduced lymphocytes back into the patient, these cells may both restore ADA activity and prevent severe combined immunodeficiency (SCID) due to ADA deficiency. ADA, an enzyme that catalyzes the deamination of adenosine to inosine, plays a key role in the development and functioning of the immune system.
eftilagimod alpha
A T-cell immunostimulatory factor, derived from the soluble form of the lymphocyte-activation gene 3 (LAG-3) protein, with potential antineoplastic activity. Upon administration, alone or in combination with tumor antigens, eftilagimod alpha binds with high affinity to MHC class II molecules expressed by dendritic cells (DC), potentially resulting in DC maturation, DC migration to lymph nodes, enhanced DC cross-presentation of antigens to T cells, and antitumor cytotoxic T cell responses.
eftozanermin alfa
A fusion protein composed of a tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor agonist consisting of six receptor binding domains (RBDs) of TRAIL fused to the Fc-domain of a human immunoglobulin G1 (IgG1) antibody, with potential pro-apoptotic and antineoplastic activities. Upon administration of eftozanermin alfa, this fusion protein binds to TRAIL-receptors, pro-apoptotic death receptors (DRs) TRAIL-R1 (death receptor 4; DR4) and TRAIL-R2 (death receptor 5; DR5), expressed on tumor cells, thereby inducing tumor cell apoptosis. ABBV-621 is designed to maximize receptor clustering for optimal efficacy. TRAIL, a member of the TNF superfamily of cytokines, plays a key role in the induction of apoptosis through TRAIL-mediated death receptor pathways.
Efudex
(Other name for: topical fluorouracil)
Eg5 kinesin-related motor protein inhibitor 4SC-205
A small-molecule inhibitor of the human kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor 4SC-205 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein essential for the regulation of spindle dynamics, including assembly and maintenance, during mitosis.
Eg5 kinesin-related motor protein inhibitor ARQ 621
A small-molecule inhibitor of the kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor ARQ 621 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein involved in the regulation of spindle dynamics, including assembly and maintenance, during mitosis.
egaptivon pegol
An optimized, second-generation, PEGylated aptamer with antithrombotic property. Egaptivon pegol blocks the binding of von Willebrand factor (vWF), via the A1 domain, and ultra-large vWF multimers to platelets, as well as interferes with the binding of platelet receptor glycoprotein Ib, thus reducing platelet adhesion, aggregation and thrombus growth in arterial beds. Unlike other antiplatelet agents, this aptamer can be readily reversed by binding to a complementary sequence of oligonucleotides, and may therefore offer potential therapeutic benefit in surgery.
EGb761
A standardized ginkgo biloba extract with antioxidant and neuroprotective activities. EGb761 has been shown to inhibit the proliferation of certain tumor cells in vitro.
EGF vaccine EGF-PTI
A cancer vaccine containing epidermal growth factor (EGF), with immunomodulating and antineoplastic activities. Upon administration of the EGF vaccine EGF-PTI, EGF induces an immune response against EGFR, which results in the formation of anti-EGF-specific neutralizing antibodies. This causes binding of the anti-EGF antibodies to endogenous EGF, reduces levels of circulating EGF and prevents the binding of EGF to its receptor EGFR. This prevents EGF/EGFR pathway activation and may result in an inhibition of proliferation in EGFR-overexpressing tumor cells. EGF/EGFR-mediated signaling is overactivated in certain cancer types and drives tumor cell proliferation and progression.
EGFR antagonist Hemay022
An orally available, irreversible inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, Hemay022 covalently binds to and inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR antisense DNA
A synthetic sequence of DNA constructed in the antisense orientation to a sequence of DNA in epidermal growth factor receptor (EGFR), a member of the erbB gene family. EGFR antisense DNA suppresses the expression of EGFR by tumor cells, thereby inhibiting tumor cell proliferation and decreasing tumor growth. This agent also appears to reduce the invasiveness of certain breast cancer cells. Members of the erbB gene family are overexpressed in many cancers and play roles in carcinogenesis and the regulation of cell proliferation.
EGFR antisense DNA BB-401
A recombinant, plasmid DNA expression vector encoding a 39 nucleotide (nt) short hairpin RNA (shRNA) specific for the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon intratumoral administration, the EGFR antisense DNA BB-401 is taken up by tumor cells and shRNA is transcribed. The shRNA is converted into small interfering RNA (siRNA) via the RNA interference (RNAi) pathway. The siRNA targets and binds to EGFR RNA expressed by tumor cells. This blocks EGFR mRNA translation and prevents EGFR protein expression.
EGFR CAR-CD3zeta-4-1BB-expressing autologous T-lymphocytes
Autologous human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) chimeric T cell receptor (chimeric antigen receptor or CAR) gene coupled to the signaling domains from both CD3 zeta and CD137 (4-1BB), with potential immunostimulatory and antineoplastic activities. Upon administration, the chimeric EGFR antigen receptor-modified autologous T lymphocytes bind to the EGFR antigen on tumor cell surfaces; subsequently, EGFR-expressing tumor cells may be lysed. Following binding to EGFR, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. EGFR, a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, plays key roles in tumor cell proliferation and tumor angiogenesis.
EGFR exon 20 inhibitor
Any agent that inhibits the activity of the tyrosine kinase epidermal growth factor receptor (EGFR) exon 20.
EGFR exon 20 insertion inhibitor BLU-451
An orally bioavailable, central nervous system (CNS) penetrating, mutant-selective covalent inhibitor of epidermal growth factor receptor (EGFR) exon 20 insertion (Ex20ins) activating mutations, with potential antineoplastic activity. Upon oral administration, EGFR Ex20ins inhibitor BLU-451 selectively targets, irreversibly binds to and inhibits the activity of EGFR Ex20ins and some other oncogenic point mutations. This prevents EGFR Ex20ins-mediated signaling. This may induce cell death and inhibit tumor growth in EGFR Ex20ins-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumors, plays a key role in tumor cell proliferation and tumor vascularization. BLU-451 is able to penetrate the blood-brain-barrier (BBB) and may therefore exert its activity against EGFR Ex20ins-driven CNS primary tumors and CNS metastases. BLU-451 does not inhibit the activity of wild-type (WT) EGFR. EGFR Ex20ins are oncogenic driver mutations that constitutively upregulate kinase activity.
EGFR inhibitor ASP8273
An orally available, irreversible, third-generation, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, ASP8273 covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. ASP8273 preferentially inhibits mutated forms of EGFR including T790M, a secondarily acquired resistance mutation, and may have therapeutic benefits in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.
EGFR inhibitor AZD3759
An orally available inhibitor of the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, AZD3759 binds to and inhibits the activity of EGFR as well as certain mutant forms of EGFR. This prevents EGFR-mediated signaling, and may lead to both induction of cell death and inhibition of tumor growth in EGFR-overexpressing cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR inhibitor EGF816
An orally available, irreversible, third-generation, mutant-selective epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGF816 covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. EGF816 preferentially inhibits mutated forms of EGFR including T790M, a secondarily acquired resistance mutation, and may have therapeutic benefits in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.
EGFR inhibitor ERAS-801
An orally bioavailable, central nervous system (CNS) penetrating inhibitor of epidermal growth factor receptor (EGFR; ErbB1; HER1) amplifications driven by both oncogenic EGFR variants and wildtype EGFR, with potential antineoplastic activity. Upon oral administration, EGFR inhibitor ERAS-801 selectively targets, binds to and inhibits the activity of EGFR. This prevents EGFR-mediated signaling. This may induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated and overexpressed in many tumors, plays a key role in tumor cell proliferation and tumor vascularization. ERAS-801 is able to penetrate the blood-brain-barrier (BBB) and may therefore exert its activity against EGFR-driven CNS primary tumors and CNS metastases.
EGFR inhibitor JIN-A02
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, mutant-selective EGFR inhibitor JIN-A02 targets, binds to, and inhibits the activity of certain EGFR mutations, specifically double and triple mutations containing C797S mutations, including the double mutations Ex19Del/C797S and L858R/C797S, and the Ex19Del/T790M/C797S triple mutation. This prevents EGFR-mediated signaling in cancer cells harboring these mutations. This may result in the inhibition of proliferation in EGFR-expressing tumors cells. EGFR, a receptor tyrosine kinase that plays a major role in tumor cell proliferation, is often overexpressed or mutated in cancer cells.
EGFR inhibitor NRC-2694
An orally bioavailable, small-molecule inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, EGFR inhibitor NRC-2694 binds to and inhibits EGFR, which prevents EGFR-mediated signaling and leads to cell death in 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.
EGFR inhibitor NRC-2694 dihydrochloride
The dihydrochloride salt form of NRC-2694, an orally bioavailable, small-molecule inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, EGFR inhibitor NRC-2694 binds to and inhibits EGFR, which prevents EGFR-mediated signaling and leads to cell death in 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.
EGFR inhibitor NRC-2694 hydrochloride
The monohydrochloride salt form of NRC-2694, an orally bioavailable, small-molecule inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, EGFR inhibitor NRC-2694 binds to and inhibits EGFR, which prevents EGFR-mediated signaling and leads to cell death in 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.
EGFR inhibitor TY-9591
An orally available inhibitor of epidermal growth factor receptor (EGFR), including activating mutations, with potential antineoplastic activity. Upon administration, the EGFR inhibitor TY-9591 binds to and inhibits EGFR activating mutations, including the resistance mutation T790M, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-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.
EGFR inhibitor WJ13404
An orally bioavailable, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR inhibitor WJ13404 targets, binds to, and inhibits the activity of EGFR, including wild-type EGFR and multiple EGFR resistance mutations, such as triple mutations Del19/T790M/C797S and L858R/T790M/C797S. This prevents EGFR-mediated signaling, which induces cell death and inhibits tumor growth in EGFR-overexpressing 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.
EGFR inhibitor XZP-5809 tartrate
The tartrate salt form of XZP-5809, an orally bioavailable third-generation inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, and the L858R and del 19 mutations, with potential antineoplastic activity. Upon oral administration, EGFR inhibitor XZP-5809 specifically and irreversibly binds to and inhibits selective EGFR mutations, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. This agent shows higher activity against EGFR mutants compared with wild-type EGFR (WT EGFR). EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR mutant-selective inhibitor BBT-176
A fourth-generation, orally bioavailable, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor BBT-176 targets, binds to, and inhibits the activity of EGFR with C797S triple mutations including Del19/T790M/C797S and L858R/T790M/C797S, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. BBT-176 inhibits EGFR with C797S mutations, which prevents covalent bond formation with third-generation EGFR inhibitors leading to drug resistance. BBT-176 may have enhanced anti-tumor effects in tumors with C797S-mediated resistance when compared to other EGFR tyrosine kinase inhibitors.
EGFR mutant-selective inhibitor BLU-701
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor BLU-701 targets, reversibly binds to and inhibits the activity of the activating/ sensitizing mutations EGFR exon 19 deletion (ex19del) and L858R, and the C797S resistance EGFR mutations, including the resistance double mutants ex19del/C797S and L858R/C797S. This prevents EGFR mutant-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR mutant-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumors, plays a key role in tumor cell proliferation and tumor vascularization. BLU-701 is able to penetrate the blood-brain-barrier (BBB) and could exert its activity against CNS metastases in EGFR-driven tumors. BLU-701 does not inhibit the activity of wild-type (WT) EGFR.
EGFR mutant-selective inhibitor BLU-945
A fourth-generation, orally bioavailable, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor BLU-945 targets, binds to and inhibits the activity of EGFR with C797S triple mutations including ex19del/T790M/C797S and L858R/T790M/C797S, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. BLU-945 inhibits mutated forms of EGFR with C797S mutation, which prevents covalent bond formation with third-generation EGFR inhibitors leading to drug resistance. BLU-945 may have enhanced anti-tumor effects in tumors with C797S-mediated resistance when compared to other EGFR tyrosine kinase inhibitors.
EGFR mutant-selective inhibitor BPI-361175
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor BPI-361175 targets, binds to and inhibits the activity of EGFR with C797S and other related mutations, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. BPI-361175 inhibits mutated forms of EGFR with C797S and other related mutations that are resistant to third-generation EGFR inhibitors.
EGFR mutant-selective inhibitor FWD1509 MsOH
The methanesulfonic acid salt form of FWD1509, an orally bioavailable, irreversible, small molecule, mutant-selective inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor FWD1509 MsOH targets, binds to, and inhibits the activity of EGFR with exon20 insertion mutations, as well as L858R, exon19del and T790M mutations, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. FWD1509 MsOH is able to cross the blood-brain barrier (BBB).
EGFR mutant-selective inhibitor HS-10375
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor HS-10375 targets, binds to and inhibits the activity of EGFR with C797S mutations, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. HS-10375 inhibits EGFR with C797S mutations, which prevents covalent bond formation with third-generation EGFR inhibitors leading to drug resistance.
EGFR mutant-selective inhibitor NX-019
An orally bioavailable, central nervous system (CNS)-penetrating, mutant-selective epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor NX-019 targets, binds to, and inhibits the activity of EGFR mutations, including exon 19 deletions, L858R, T790M, exon 20 insertions, and certain other mutations, thereby preventing EGFR-mediated signaling, which induces cell death and inhibits tumor growth in EGFR mutant-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. NX-019 is selective for mutant EGFR over wild-type EGFR.
EGFR mutant-selective inhibitor QLH11811
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor QLH11811 targets, binds to and inhibits the activity of EGFR with selective mutations, including ex19del, L858R, T790M and C797S, thereby preventing EGFR mutant-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR mutant-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR mutant-selective inhibitor TQB3804
A fourth-generation, orally bioavailable, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor TQB3804 binds to and inhibits the activity of mutant forms of EGFR, including the C797S EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. TQB3804 inhibits mutated forms of EGFR including C797S, which prevents covalent bond formation with third-generation EGFR inhibitor osimertinib leading to drug resistance. TQB3804 may have enhanced anti-tumor effects in tumors with C797S-mediated resistance when compared to other EGFR tyrosine kinase inhibitors.
EGFR mutant-selective inhibitor TRX-221
An orally bioavailable, mutant-selective, fourth-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGFR mutant-selective inhibitor TRX-221 targets, binds to and inhibits the activity of EGFR with selective mutations, including Del19/T790M/C797S, L858R/T790M/C797S, Del19/C797S, L858R/C797S, Del19/T790M, L858R/T790M, Del19, and L858R, thereby preventing EGFR mutant-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR mutant-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. TRX-221 is able to cross the blood-brain barrier (BBB). By sparing wild-type (WT) EGFR, TRX-221 may avoid EGFR-related toxicities.
EGFR mutant-selective inhibitor WZ4002
An inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, EGFR mutant-selective inhibitor WZ4002 specifically targets, binds to and inhibits EGFR T790M, which prevents EGFR T790M mutant-mediated signaling and leads to cell death in EGFR T790M mutant-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.
EGFR mutant-specific inhibitor BPI-7711
An orally available third-generation and selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutations T790M and L858R, as well as exon 19 deletion, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor BPI-7711 specifically and covalently binds to and inhibits selective EGFR mutations, with particularly high selectivity against the T790M mutation, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to some other EGFR inhibitors, BPI-7711 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (wt EGFR), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which also inhibit wt EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR mutant-specific inhibitor CK-101
An orally available third-generation and selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, and the L858R and exon 19 deletion (del 19) mutations, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor CK-101 specifically and covalently binds to and inhibits specific EGFR mutations, with particularly high selectivity against the T790M mutation; this prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to some other EGFR inhibitors, CK-101 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which also inhibit WT EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR mutant-specific inhibitor DZD6008
An orally available, blood-brain-barrier (BBB) penetrant, mutant-specific inhibitor of the receptor tyrosine kinase epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, EGFR inhibitor DZD6008 targets, binds to and inhibits certain EGFR mutations. This prevents EGFR-mediated signaling and may result in the inhibition of tumor growth in susceptible tumor cells. EGFR plays a major role in tumor cell proliferation and is often mutated in cancer cells.
EGFR mutant-specific inhibitor ZN-e4
An orally available selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, with potential antineoplastic activity. Upon administration, the EGFR mutant-specific inhibitor ZN-e4 specifically binds to and inhibits selective EGFR mutations, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to other EGFR inhibitors, ZN-e4 may offer therapeutic benefits in tumors with T790M-mediated drug resistance and may limit toxicities associated with non-selective EGFR inhibitors. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR T790M antagonist BPI-15086
An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. EGFR T790M antagonist BPI-15086 specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-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.
EGFR T790M inhibitor PF-06747775
An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. EGFR T790M inhibitor PF-06747775 specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. Compared to some other EGFR inhibitors, PF-06747775 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which can inhibit WT EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
EGFR tri-specific natural killer cell engager DF9001
A tri-specific natural killer (NK) cell engager targeting epidermal growth factor receptor (EGFR), with potential immunostimulating and antineoplastic activities. Upon administration, EGFR tri-specific NK cell engager DF9001 targets and binds to EGFR on tumor cells and simultaneously binds to NK cells, thereby bringing EGFR-expressing tumor cells and NK cells together. This stimulates the NK cells and results in the selective NK cell-mediated killing of EGFR-expressing tumor cells. In addition, the NK cells activate T- and B-cells, and enhance a cytotoxic T-lymphocyte (CTL)-mediated immune response against EGFR-expressing tumor cells. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival.
EGFR-targeted IL-2/IL-10 dual cytokine fusion protein DK210 (EGFR)
A dual cytokine fusion protein comprised of high-affinity interleukin-10 (IL-10), fused to a single chain variable fragment (scFv) scaffolding system that is linked to wild-type interleukin-2 (IL-2) in the hinge region of the scFv, in which six complementarity determining regions (CDRs) of the scFv are replaced by CDRs from an anti-epidermal growth factor receptor (EGFR) monoclonal antibody, with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, EGFR-targeted IL-2/IL-10 dual cytokine fusion protein DK210 (EGFR) targets and binds to EGFR expressed on tumor cells. This allows the IL-2 moiety to specifically bind to IL-2 receptor (IL-2R) and activate IL-2R-mediated signaling in CD8+ T cells in the tumor microenvironment (TME). This enhances cytotoxic T-lymphocyte (CTL)-mediated cytotoxic immune responses against tumor cells. IL-10 stimulates the differentiation and expansion of tumor specific cytotoxic CD8+ T cells, thereby further enhancing the CTL-mediated cytotoxic immune responses against tumor cells. IL-10 may also reduce the toxicities of IL-2 by suppressing the secretion of pro-inflammatory cytokines associated with IL-2 toxicities. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.
EGFR-targeting agent
Any agent that targets the human epidermal growth factor receptor (EGFR).
EGFR/CD3-targeting T-cell engaging molecule TAK-186
A T-cell engaging bispecific antibody and Conditional Bispecific Redirected Activation (COBRA) protein targeting both the tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR; HER1; ErbB1) and the T-cell surface antigen CD3, and containing a protease cleavable linker and a human serum albumin (HSA) binding part, with potential immunostimulating and antineoplastic activities. Upon administration, EGFR/CD3-targeting T-cell engaging molecule TAK-186 is cleaved by proteases in the tumor microenvironment (TME). Upon cleavage, TAK-186 dimerizes to form the active molecule and binds to both CD3 on cytotoxic T lymphocytes (CTLs) and EGFR on EGFR-expressing tumor cells. This activates and redirects CTLs to EGFR-expressing tumor cells, leading to CTL-mediated killing of EGFR-expressing tumor cells. EGFR, upregulated and/or mutated in a variety of tumor cell types, plays a key role in tumor cell proliferation. The albumin-binding domain targets and binds to serum albumin, thereby extending the serum half-life of the inactivated TAK-186. Upon cleavage of the HSA-binding component, the activated TAK-186 dimer will be eliminated after cancer cell killing; this improves the safety profile of this agent by reducing its ability to cause damage to healthy cells.
EGFR/EGFRvIII inhibitor CM93
An orally bioavailable, blood-brain-barrier (BBB) penetrable, third-generation, covalent inhibitor of epidermal growth factor receptor (EGFR) and various EGFR mutations, including the EGFR variant III (EGFRvIII) mutant form, with potential antineoplastic activity. Upon oral administration, EGFR/EGFRvIII inhibitor CM93 specifically targets, irreversibly binds to and inhibits EGFR and specific EGFR mutations, which prevents EGFR/EGFR mutant-mediated signaling and leads to cell death in EGFR/EGFR mutant-expressing tumor cells. EGFR, a receptor tyrosine kinase (RTK) that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and survival.
EGFR/EGFRvIII inhibitor WSD0922-FU
A blood-brain-barrier (BBB) penetrable selective inhibitor of epidermal growth factor receptor (EGFR) and various EGFR mutations, including but not limited to the EGFR variant III (EGFRvIII) mutant form, with potential antineoplastic activity. Upon administration of EGFR/EGFRvIII inhibitor WSD0922-FU, this agent is able to penetrate the BBB and specifically targets, binds to and inhibits EGFR and specific EGFR mutations, which prevents EGFR/EGFR mutant-mediated signaling and leads to cell death in EGFR/EGFR mutant-expressing tumor cells. Compared to other EGFR inhibitors that are not able to penetrate the BBB, WSD0922-FU may have therapeutic benefits in brain tumors, such as glioblastoma (GBM) and metastatic CNS tumors. EGFR, a receptor tyrosine kinase (RTK) that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and survival.
EGFR/FLT3/Abl inhibitor SKLB1028
An orally available inhibitor of epidermal growth factor receptor (EGFR), FMS-related tyrosine kinase 3 (FLT3, STK1, CD135 or FLK2), and the non-receptor tyrosine kinase ABL (Abl), with potential antineoplastic activity. Upon administration, the EGFR/FLT3/Abl inhibitor SKLB1028 specifically binds to and inhibits EGFR, FLT3 and Abl, which interferes with the activation of EGFR-, FLT3- and Abl-mediated signal transduction pathways and reduces cell proliferation in cancer cells that overexpress EGFR, FLT3 and/or Abl. EGFR, EGFR and Abl are all overexpressed in a variety of cancers and play key roles in tumor cell proliferation.
EGFR/HER2 inhibitor AV-412
A second-generation, orally bioavailable dual kinase inhibitor with potential antineoplastic activity. EGFR/HER2 inhibitor AV-412 binds to and inhibits the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2), which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to first-generation kinase inhibitors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization.
EGFR/HER2 inhibitor TAS2940
An orally bioavailable, small molecule inhibitor of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 inhibitor TAS2940 targets, binds to and inhibits EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization.
EGFR/HER2 kinase inhibitor TAK-285
An orally bioavailable, small molecule and dual kinase inhibitor of human epidermal growth factor receptors 1 (EGFR/ErbB1) and 2 (HER2/ErbB2), with potential antineoplastic activity. EGFR/HER2 kinase inhibitor TAK-285 binds to and inhibits EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to trastuzumab. EGFR and HER2, receptor tyrosine kinases overexpressed in a variety of tumor cell types, play major roles in tumor cell proliferation and tumor vascularization. In addition, TAK-285 appears to pass the blood brain barrier (BBB) and does not appear to be a substrate for efflux pumps.
EGFR/HER2 mutant-selective inhibitor BH-30643
An orally bioavailable, mutant-selective, reversible macrocyclic inhibitor of human epidermal growth factor receptor (EGFR) and epidermal growth factor receptor 2 (HER2), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 mutant-selective inhibitor BH-30643 targets, reversibly binds to, and inhibits the activity of EGFR with selective mutations, including, but not limited to, classical mutations, exon 20 insertion (Ex20ins) activating mutations as well as various resistance mutations, such as ex19del/T790M, ex19del/C797S, ex19del/T790M/C797S, L858R/T790M, L858R/C797S, and L858R/T790M/C797S. In addition, BH-30643 reversibly binds to and inhibits HER2 mutations, including ex20ins mutations. This prevents EGFR- and HER2-mediated signaling and may result in the inhibition of tumor growth in certain mutant EGFR/HER2-expressing tumors. EGFR and HER2, receptor tyrosine kinases mutated or overexpressed in many tumor cell types, play major roles in tumor cell proliferation and tumor vascularization. By largely sparing wild-type (WT) EGFR, BH-30643 may decrease the risk of EGFR-related toxicities. Since BH-30643 concurrently targets activating mutations in EGFR and HER2, it reduces the chances of resistance.
EGFR/HER2 mutant-selective inhibitor HS-10376
An orally bioavailable, mutant-selective, dual kinase inhibitor of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 mutant-selective inhibitor HS-10376 targets, binds to, and inhibits the activity of EGFR and HER2 with exon20 insertion mutations, thereby preventing EGFR- and HER2-mediated signaling. This may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization.
EGFR/HER2 mutant-selective inhibitor STX-721
An orally bioavailable, mutant-selective, small molecule inhibitor of human epidermal growth factor receptor (EGFR) and epidermal growth factor receptor 2 (HER2), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 mutant-selective inhibitor STX-721 targets, binds to, and inhibits the activity of EGFR and HER2 with exon20 insertion mutations, thereby preventing EGFR- and HER2-mediated signaling. This may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. EGFR and HER2, receptor tyrosine kinases mutated or overexpressed in many tumor cell types, play major roles in tumor cell proliferation and tumor vascularization.
EGFR/TGFb fusion monoclonal antibody BCA101
A bifunctional monoclonal antibody targeting both the receptor tyrosine kinase epidermal growth factor receptor (EGFR) and the pro-inflammatory cytokine human transforming growth factor beta (TGF-beta; TGFb), with potential antineoplastic activity. Upon administration of EGFR/TGFb fusion monoclonal antibody BCA101, the anti-EGFR moiety targets, binds to and prevents activation of EGFR-mediated signaling. This leads to an inhibition of EGFR-dependent downstream pathways and EGFR-dependent tumor cell proliferation and metastasis. The anti-TGFb moiety targets and binds to TGFb, thereby preventing the activation of TGFb-mediated signaling pathways. This may inhibit the proliferation of tumor cells in which TGFb is overactivated. EGFR and TGFb, mutated and/or overexpressed on the surfaces of various tumor cell types, play key roles in tumor cell proliferation and progression.
EGFR/VEGFR/RET inhibitor HA121-28
An orally available inhibitor of the epidermal growth factor receptor (EGFR), the proto-oncogene receptor tyrosine kinase rearranged during transfection (RET) and vascular endothelial growth factor receptor (VEGFR), with potential anti-angiogenic and antineoplastic activities. Upon oral administration of HA121-28, this agent targets, binds to and inhibits the activity of EGFR, RET and VEGFR. This prevents EGFR-, RET- and VEGFR-mediated signaling, and may lead to the induction of apoptosis and inhibition of tumor growth in EGFR-, RET- and VEGFR-overexpressing cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. Dysregulation of RET activity plays a key role in the development and progression of a variety of cancers. Expression of VEGFR is upregulated in a variety of tumor cell types; it plays a key role in the migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death.
EGFRBi-armed autologous activated T cells
Autologous activated T cells, loaded with a bispecific antibody produced by heteroconjugation of anti-CD3 and anti-epidermal growth factor receptor (EGFR) monoclonal antibodies, with potential antineoplastic activity. Binding of EGFRBi-armed autologous activated T cells to EGFR-positive tumor cells may result in increased T cell-mediated cytotoxicity towards tumor cells expressing EGFR. Arming activated T cells with this bispecific antibody may significantly increase T cell secretion of anti-tumor associated cytokines such as IL2, RANTES, IFN-gamma, and TNF-alpha.
EGFRt/19-28z/IL-12 CAR T lymphocytes
A preparation of 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), a truncated form of the human epidermal growth factor receptor (EGFRt), and the human pro-inflammatory cytokine interleukin-12 (IL-12), with potential immunostimulating and antineoplastic activities. Upon administration, EGFRt/19-28z/IL-12 CAR T lymphocytes are directed to and induce selective toxicity in CD19-expressing tumor cells. In addition, the administered T cells secrete IL-12 which induces the secretion of interferon-gamma (IFN-g), promotes the activation of natural killer cells (NKs), and induces cytotoxic T-lymphocyte (CTL) responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. 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 the T-cells and their antitumor activity compared with the inclusion of the CD3-zeta chain alone. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt facilitates both the in vivo detection of the administered T cells and the elimination of the administered T cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response.
eggplant peel extract cream
A cream containing an extract from the skin of the vegetable Solanum melongena (eggplant; S. melongena; aubergine; brinjal) containing high levels of bioactive components, such as anthocyanins, with potential anti-oxidant, keratolytic, and antineoplastic activities. Upon topical administration of the eggplant peel extract cream, the active ingredients in the eggplant extract may exert antioxidant, anti-proliferative and protective effects on skin cells.
eicosapentaenoic acid
An essential, polyunsaturated, 20-carbon omega-3 fatty acid with anti-inflammatory and potential antineoplastic and chemopreventive activities. Eicosapentaenoic acid (EPA) may activate caspase 3, resulting in apoptosis in susceptible tumor cell populations. In addition, this agent may inhibit cyclooxygenase-2 (COX-2), resulting in inhibition of prostaglandin synthesis and prostaglandin-mediated inflammatory processes.
eicosapentaenoic acid monoacylglyceride
An eicosapentaenoic acid derivative with potential antineoplastic activities. Upon oral administration, eicosapentaenoic acid monoacylglyceride (MAG-EPA) may inhibit epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR) and serine/threonine protein kinase AKT (protein kinase B)-mediated signaling pathways and reduce vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1-alpha (HIF1-alpha) expression levels in tumor cells. This may promote apoptosis and inhibit tumor cell growth in cells expressing EGFR, AKT, and VEGFR. MAG-EPA may also inhibit androgen-stimulated tumor cell growth and repress androgenic induction of prostate-specific antigen (PSA) expression. PSA, a tumor associated antigen (TAA), is expressed by prostate epithelial cells and is overexpressed in prostate cancer. The AKT signaling pathway is often dysregulated in cancer and is associated with tumor cell proliferation, survival and migration. EGFR and VGFR are receptor tyrosine kinases that are mutated or upregulated in many tumor cell types and play a key role in tumor cell proliferation and tumor vascularization.
eicosapentaenoic acid-enriched nutritional supplement
A nutritional supplement enriched with eicosapentaenoic acid (EPA), which is an essential, polyunsaturated, 20-carbon omega-3 fatty acid found in fish oil, with potential anti-inflammatory and anti-cachectic activities. Upon oral intake of the EPA-enriched nutritional supplement, EPA is incorporated in cell membrane phospholipids and replaces arachidonic acid. This affects the production of pro-inflammatory mediators, such as tumor necrosis factor-alpha (TNF-a), interleukin-1 (IL-1) and IL-6, through the inhibition of nuclear factor kappa B (NF-kB) activity. This inhibits inflammation and may abrogate the cachexia-mediated decrease of lean body mass (LBM), which may lead to increased body weight. Pro-inflammatory mediators, such as TNF-a, interferon-gamma, and certain interleukins, such as IL-6 and IL-1b, play a key role in cachexia.
eIF4E antisense oligonucleotide ISIS 183750
A second-generation antisense oligonucleotide targeting the eukaryotic translation initiation factor 4E (eIF4E) with potential antitumor activity. Antisense oligonucleotide ISIS EIF4ERx suppresses the expression of eIF4E in fast dividing tumor cells. Blocking the expression of eIF4E results in inhibition of the synthesis of tumor angiogenic factors, thereby leading to the inhibition of cellular proliferation and apoptosis in tumor cells. eIF4E is overexpressed in a variety of cancers, is involved in the mRNA-ribosome binding step of eukaryotic protein synthesis and is the rate-limiting component of the eukaryotic translation apparatus.
eiletoclax
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, eiletoclax targets and binds to the P2 pocket of Bcl-2, thereby inhibiting 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.
elacestrant hydrochloride
The hydrochloride salt form of elacestrant, an orally available, selective estrogen receptor degrader (SERD), with antineoplastic activity. Upon oral administration, elacestrant acts as a SERD, which binds to the estrogen receptor (ER) and induces a conformational change that results in the proteosomal degradation of the receptor. This prevents ER-mediated signaling and inhibits proliferation of ER-expressing cancer cells.
elacytarabine
The lipophilic 5'-elaidic acid ester of the deoxycytidine analog cytosine arabinoside (cytarabine; Ara-C) with potential antineoplastic activity. As a prodrug, CP-4055 is converted intracellularly into cytarabine triphosphate by deoxycytidine kinase and subsequently competes with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis. Compared to cytarabine, CP-4055 shows increased cellular uptake and retention, resulting in increased activation by deoxycytidine kinase to cytarabine triphosphate, decreased deamination and deactivation by deoxycytidine deaminase, and increased inhibition of DNA synthesis. This agent also inhibits RNA synthesis, an effect not seen with cytarabine.
elagolix
An orally bioavailable, second-generation, non-peptide based, small molecule compound and selective gonadotropin-releasing hormone (GnRH; LHRH) receptor antagonist, with potential hormone production inhibitory activity. Upon oral administration, elagolix competes with GnRH for receptor binding and inhibits GnRH receptor signaling in the anterior pituitary gland. This inhibits the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. In women, inhibition of FSH and LH prevents the production of estrogen by the ovaries. Inhibition of GnRH signaling may treat or prevent symptoms of sex hormone-dependent disease states.
Elahere
(Other name for: mirvetuximab soravtansine)
Elapegademase
A recombinant form of the enzyme adenosine deaminase (rADA), based on the bovine amino acid sequence and covalently conjugated, with a succinimidyl carbamate linker, to monomethoxypolyethylene glycol (mPEG) (SC-PEG rADA), that can be used as an enzyme replacement agent for the treatment of adenosine deaminase severe combined immune deficiency (ADA-SCID). Upon intramuscular administration, elapegademase, as an exogenous source of ADA, replaces the deficient ADA enzyme and acts in the same manner as the endogenous enzyme. ADA is involved in purine metabolism and mainly catalyzes the irreversible hydrolytic deamination of adenosine or deoxyadenosine to inosine or deoxyinosine, respectively, as well as several naturally occurring methylated adenosine compounds. Elapegademase decreases toxic levels of adenosine and deoxyadenosine nucleotides, increases lymphocyte levels and helps maintain the proper functioning of immune cells. Elevated adenosine levels, as seen in ADA deficiency, induce apoptosis and inhibit the differentiation of thymocytes, resulting in T-lymphopenia. Low levels of deoxyadenosine and adenosine play key roles in the regulation of lymphocyte levels and the proper functioning of immune cells.
elasomeran
A vaccine consisting of a lipid nanoparticle (LNP) encapsulating a messenger RNA (mRNA) encoding the full-length, prefusion stabilized spike (S) protein of SARS-CoV-2, with potential immunizing activity against SARS-CoV-2. Upon administration of elasomeran, the lipid nanoparticle binds to the plasma membrane of cells and releases the mRNA into the cells. The mRNA is then translated by ribosomes to produce the SARS-CoV-2 S protein. This may activate both humoral and cellular immune responses which may result in protection against SARS-CoV-2 infection.
Elavil
(Other name for: amitriptyline hydrochloride)
elbasvir/grazoprevir
A fixed dose combination of elbasvir, an inhibitor of the hepatitis C virus (HCV) non-structural protein 5A (NS5A), and grazoprevir, a second-generation inhibitor of the HCV NS3/4A serine protease, with activity against certain HCV genotypes. Upon oral administration of elbasvir/grazoprevir, elbasvir inhibits the activity of the NS5A protein, leading to disruption of the viral RNA replication complex, blockage of HCV RNA production, and inhibition of viral replication. Grazoprevir inhibits the NS3/4A serine protease enzyme, thereby disrupting the cleavage of the virally encoded polyprotein into mature proteins and preventing the formation of the viral replication complex. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family; HCV infection is associated with the development of certain cancers.
Eldecort
(Other name for: therapeutic hydrocortisone)
Eldepryl
(Other name for: selegiline hydrochloride)
Eldisine
(Other name for: vindesine sulfate)
Eldopar
(Other name for: levodopa)
electrokinetically modified water
Orally available, nanobubble-based, electrokinetically modified water (EMW) composed of reverse osmosis water where the minerals calcium chloride, magnesium chloride, and potassium bicarbonate have been added and with an increased oxygen concentration compared to normal water. Upon consumption, the EMW may have a beneficial effect on fatigue. This water may protect muscle cells against damage and may improve skeletal muscle function. The water is pretreated with strong, controlled turbulence to create charge-stabilized nanostructures.
electrolyte-free parenteral nutrition emulsion
An electrolyte-free emulsion for infusion consisting of a three chamber bag system containing glucose, amino acids and lipids that can be used to provide parenteral nutritional supplementation. The lipid emulsion portion contains soybean oil, medium-chain triglycerides, olive oil and fish oil; the amino acid solution contains alanine, arginine, glycine, histidine, leucine, isoleucine, lysine, methionine, phenylalanine, proline, serine, taurine, threonine, tryptophan, tyrosine, and valine. The electrolyte-free parenteral nutrition emulsion contains no electrolytes, trace elements and vitamins. The three separate bags containing glucose, amino acids and lipids are mixed together before infusion.
elenestinib
An orally bioavailable protein tyrosine kinase inhibitor of the mutated form of the tumor-associated antigen (TAA) mast/stem cell factor receptor c-Kit (SCFR), D816V, with potential antineoplastic activity. Upon oral administration, elenestinib binds to and inhibits the specific c-Kit mutant D816V. This may result in an inhibition of cell proliferation in mast cells that overexpress this c-Kit mutation. D816V, a mutation in which the amino acid asparagine aspartic acid at position 816 in the mast/stem cell growth factor receptor Kit protein is replaced by valine, may drive mastocytosis and other mast cell disorders.
elesclomol
A small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.
elesclomol sodium
The water soluble sodium salt of a small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.
Elidel
(Other name for: pimecrolimus cream)
Eligard
(Other name for: leuprolide acetate)
eliglustat
A ceramide analog and an orally bioavailable inhibitor of glucosylceramide synthase (GCS; ceramide glucosyltransferase), that may be used to decrease the production of glycosphingolipids (GSLs) including glucosylceramide, also known as glucocerebroside. Upon oral administration, eliglustat inhibits GCS, which catalyzes the initial step in the synthesis of glucosylceramide and other GSLs. This decreases the production of glucosylceramide and other GSLs, which have important roles in various diseases and cellular processes, including immune processes and functions. Eliglustat may be used in substrate reduction therapy in diseases in which the enzyme glucocerebrosidase (GCase), responsible for the breakdown of glucocerebroside, is deficient.
elimusertib
An orally available ataxia telangiectasia and Rad3-related (ATR)-specific kinase inhibitor, with potential antineoplastic activity. Upon oral administration, elimusertib selectively binds to and inhibits the activity of ATR, which prevents ATR-mediated signaling. This inhibits DNA damage checkpoint activation, disrupts DNA damage repair and induces apoptosis in ATR-overexpressing tumor cells. 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 cell survival.
elinzanetant
An orally bioavailable neurokinin/tachykinin 1 receptor (NK1-receptor; NK1R; NK-1R) and NK3 receptor (NK-3R; NK3R) antagonist, that may be used to treat vasomotor symptoms in menopausal woman. Upon oral administration, elinzanetant targets, competitively binds to and blocks the activity of the NK1R and NK3R in the central nervous system (CNS), thereby inhibiting the binding of the endogenous ligands and neuropeptides substance P (SP; neurokinin-1; NK1) and neurokinin B (NKB). This inhibits NK1R/NK3R-mediated signal transduction and may prevent certain menopausal synpmtoms such as hot flashes. Neurokinin-mediated signaling may increase during hormone deficiency and may cause hot flashes.
Eliquis
(Other name for: apixaban)
elironrasib
An orally bioavailable, covalent inhibitor of the active, guanosine triphosphate (GTP)-bound form of the oncogenic KRAS substitution mutation G12C, KRAS G12C(ON), with potential antineoplastic activity. Upon oral administration, elironrasib forms a tri-complex with the intracellular chaperone protein and immunophilin cyclophilin A (CypA) and KRAS G12C(ON). This tri-complex inhibits KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. 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.
elisidepsin
A marine-derived, synthetic cyclic depsipeptide with potential antineoplastic activity. Elisidepsin is a derivative of a natural marine compound that belongs to a family of dehydro aminobutyric acid-containing peptides (kahalalides) isolated from the herbivorous marine mollusk Elysia rufescens. Although the primary mechanism of action has yet to be elucidated, this agent exhibits anti-proliferative activity in a wide variety of cancer cell types, including breast, colon, pancreas, lung, and prostate; it appears to induce oncolytic rather than apoptotic cell death.
elisrasib
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, elisrasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible 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.
Elitek
(Other name for: rasburicase)
Elixophyllin
(Other name for: theophylline)
Elizaria
(Other name for: eculizumab)
ellagic acid/Annona muricata supplement
A nutritional supplement containing the phytochemical polyphenol, ellagic acid, and an extract of Annona muricata, with potential chemopreventive activity. Although the exact mechanism of action for ellagic acid has yet to be fully elucidated, this agent acts as an anti-oxidant and reduces oxidative stress. This agent also appears to protect the body against certain carcinogens, either through preventing DNA binding or by increasing the rate of their metabolism and deactivation. Certain extracts of Annona muricata, a member of the custard apple plants and belonging to the Annonaceae family, may have antiviral activity, potential targets include human papilloma virus (HPV), and may be cytotoxic against various types of cancer cells.
Ellence
(Other name for: epirubicin hydrochloride)
elliptinium acetate
Acetate salt of elliptinium, a derivative of the alkaloid ellipticine isolated from species of the plant family Apocynaceae, including Bleekeria vitensis, a plant with anti-cancer properties. As a topoisomerase II inhibitor and intercalating agent, elliptinium stabilizes the cleavable complex of topoisomerase II and induces DNA breakages, thereby inhibiting DNA replication and RNA and protein synthesis.
Elmiron
(Other name for: pentosan polysulfate sodium)
Elocon
(Other name for: mometasone furoate)
Elopram
(Other name for: citalopram hydrobromide)
elotuzumab
A humanized monoclonal antibody directed against the human CS1 (CD2 subset 1, CRACC, SLAMF7) antigen with potential antineoplastic activity. Elotuzumab binds to the CS1 antigen, which may trigger antibody-dependent cellular cytotoxicity (ADCC) in cells expressing CS1. CS1 is a cell surface glycoprotein belonging to the CD2 subset of the immunoglobulin superfamily (IgSF) and is highly expressed by multiple myeloma cells, but minimally expressed by normal cells.
Eloxatin
(Other name for: oxaliplatin)
elraglusib
A maleimide-based, small molecule inhibitor of glycogen synthase kinase-3 (GSK-3; serine/threonine-protein kinase GSK3) with potential antineoplastic activity. Upon intravenous administration, elraglusib binds to and competitively inhibits GSK-3, which may lead to downregulation of nuclear factor kappa B (NF-kappaB) and decreased expression of NF-kappaB target genes including cyclin D1, B-cell lymphoma 2 (Bcl-2), anti-apoptotic protein XIAP, and B-cell lymphoma extra-large (Bcl-XL). This may inhibit NF-kappaB-mediated survival and chemoresistance in certain tumor types. GSK-3, a constitutively active serine/threonine kinase that plays a role in numerous pathways involved in protein synthesis, cellular proliferation, differentiation, and metabolism, is aberrantly overexpressed in certain tumor types and may promote tumor cell survival and resistance to chemotherapy and radiotherapy.
elranatamab-bcmm
A bispecific monoclonal antibody against human CD3, a T-cell surface antigen, and human B-cell maturation antigen (BCMA; TNFRSF17), a tumor-associated antigen (TAA) expressed on plasma cells, with potential antineoplastic activity. Upon administration, elranatamab-bcmm binds to both CD3 on T cells and BCMA expressed on malignant plasma cells. This results in the cross-linking of T cells and tumor cells, and induces a potent cytotoxic T-lymphocyte (CTL) response against BCMA-expressing plasma 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.
Elrexfio
(Other name for: elranatamab-bcmm)
elsamitrucin
A heterocyclic antineoplastic antibiotic isolated from the bacterium Actinomycete strain J907-21. Elsamitrucin intercalates into DNA at guanine-cytosine (G-C)-rich sequences and inhibits topoisomerase I and II, resulting in single-strand breaks and inhibition of DNA replication.
elsiglutide
A synthetic glucagon-like peptide-2 (GLP-2) analogue with potential antidiarrheal and intestinotrophic activities. Upon subcutaneous administration, elsiglutide, a 39 amino acid polypeptide, binds to GLP-2 receptors and thereby promotes proliferation of epithelial cells. Regeneration of endothelial cells damaged during chemotherapy may prevent or decrease chemotherapy-induced diarrhea. In addition, elsiglutide may prevent chemotherapy-induced intestinal injury. GLP-2, a peptide hormone primarily produced in the small intestines in response to food, plays a key role in intestinal epithelial growth, metabolism and regeneration of epithelial cells.
Elspar
(Other name for: asparaginase)
eltanexor
An orally bioavailable inhibitor of exportin-1 (XPO1; chromosome region maintenance 1 protein homolog; CRM1), with potential antineoplastic activity. Upon administration, eltanexor binds to the XPO1 cargo binding site, which prevents the XPO1-mediated nuclear export of cargo proteins such as tumor suppressor proteins (TSPs), including p53, p73, BRCA1/2, pRB, FOXO, and other growth regulatory proteins and leads to their selective accumulation in the nuclei of tumor cells. As a selective inhibitor of nuclear export (SINE), KPT-8602 restores the nuclear localization and function of tumor suppressing proteins which leads to the induction of apoptosis in tumor cells. XPO1, the major export factor that transports proteins from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types while minimally expressed in normal, healthy cells. The export of tumor suppressor proteins into the cytoplasm prevents them from initiating apoptosis and leads to uncontrolled tumor cell proliferation.
eltrapuldencel-T
A therapeutic melanoma vaccine consisting of autologous dendritic cells (DCs) pulsed with antigens from lethally irradiated autologous tumor cells derived from a patient-specific, continuously proliferating and melanoma-initiating cell line and suspended in a solution containing the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulatory and antineoplastic activities. Upon subcutaneous administration, eltrapuldencel-T may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against the patient's repertoire of melanoma-associated antigens, particularly tumor stem cell antigens, found in the irradiated autologous cancer cells. As an immunostimulant, GM-CSF enhances the activation of dendritic cells (DCs) and promotes antigen presentation to both B and T lymphocytes.
eltrombopag olamine
The orally active ethanolamine salt of eltrombopag, a small-molecule, nonpeptide thrombopoietin receptor agonist with megakaryopoiesis-stimulating activity. Eltrombopag binds to and stimulates the transmembrane domain of the platelet thrombopoietin receptor (TPO-R or CD110), a member of the hematopoietin receptor superfamily. Activation of TPO-R leads to the proliferation and differentiation of cells in the megakaryocytic lineage and an increase in platelet production.
Elucirem
(Other name for: gadopiclenol)
eluvixtamab
A proprietary recombinant bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) CD33 fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of eluvixtamab, this bispecific antibody binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD33 antigen found on CD33-expressing tumor cells. 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 cells and overexpressed on neoplastic cells in patients with acute myeloid leukemia.
Elzonris
(Other name for: tagraxofusp-erzs)
elzovantinib
An orally bioavailable, multi-targeted kinase inhibitor with potential antineoplastic activity. Upon oral administration, elzovantinib binds to and inhibits three tyrosine kinases that are often overexpressed in a variety of cancer cell types, including MET (c-Met; hepatocyte growth factor receptor; HGFR) , Src, and colony stimulating factor 1 receptor (CSF1R; CSF-1R; C-FMS; CD115; macrophage colony-stimulating factor receptor; M-CSFR) thereby disrupting their respective signaling pathways. MET, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and in tumor angiogenesis. Src, a non-receptor tyrosine kinase upregulated in many tumor cell types, plays an important role in tumor cell proliferation, motility, invasiveness and survival. CSF1R is a cell-surface receptor for colony stimulating factor 1 (CSF1); this receptor tyrosine kinase is overexpressed by tumor-associated macrophages (TAMs) in the tumor microenvironment (TME), and plays a major role in both immune suppression and the induction of tumor cell proliferation.
emactuzumab
A humanized monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115), also known as macrophage colony-stimulating factor receptor (M-CSFR), with potential antineoplastic and immunomodulating activities. Upon administration, emactuzumab binds to CSF1R expressed on macrophages and inhibits the binding of colony-stimulating factor-1 (CSF-1) to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells, which blocks the production of inflammatory mediators by macrophages and reduces inflammation. By blocking both the activity of CSF1R-dependent tumor-associated macrophages (TAMs) and the recruitment of TAMs to the tumor microenvironment, emactuzumab enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival.
emapalumab-lzsg
A human monoclonal antibody against the cytokine interferon-gamma (IFN-gamma; IFNg), with potential immunomodulating activity. Upon administration, emapalumab binds to and neutralizes IFNg. This inhibits IFNg-mediated signaling pathways and suppresses the activation of the immune system. IFNg, a cell-signaling protein, plays a key role in the regulation and activation of the immune system; its upregulation is associated with certain auto-immune and auto-inflammatory diseases in which the immune system is abnormally activated.
emavusertib
An orally bioavailable, reversible inhibitor of interleukin-1 receptor-associated kinase 4 (IRAK4), with potential antineoplastic, immunomodulating and anti-inflammatory activities. Upon oral administration, emavusertib targets, binds to, and blocks the kinase activity of IRAK4. This inhibits IRAK4-mediated signaling, prevents the activation of IRAK4-mediated nuclear factor-kappa B (NF-kB) signaling and decreases the expression of inflammatory cytokines and certain pro-survival factors. This inhibits proliferation of IRAK4-overactivated tumor cells, which are found in cells harboring MYD88 activating mutations or those with overactivated toll-like receptor (TLR) pathways. In addition, CA-4948 may inhibit inflammation and immune-mediated cell destruction in inflammatory and auto-immune diseases where TLR or interleukin 1 receptor (IL-1R) signaling is overactivated and MYD88 is dysregulated. IRAK4, a serine/threonine-protein kinase that plays a key role in both the TLR and IL-1R signaling pathways, is activated though the adaptor protein MYD88 and links the TLR and IL-1R signaling pathway to the NF-kB pathway.
Embospheres
(Other name for: tris-acryl gelatin microspheres)
Emcyt
(Other name for: estramustine phosphate sodium)
Emend
(Other name for: aprepitant)
emepepimut-S
A liposome-encapsulated peptide vaccine consisting of a synthetic peptide derived from the mucin 1 (MUC-1) antigen with potential antineoplastic activity. Upon vaccination, emepepimut-S may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against MUC-1-expressing tumor cells, resulting in growth inhibition. MUC-1 antigen is a high-molecular-weight transmembrane glycoprotein that is overexpressed on the cell surfaces of many epithelial tumor cells as well as on the cell surfaces of some B-cell lymphoma cells and multiple myeloma cells.
emerfetamab
A bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) CD33 fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, emerfetamab binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD33 antigen found on CD33-expressing tumor cells. 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 cells and overexpressed on a variety of cancer cell types, including acute myeloid leukemia (AML). It plays a key role in tumor initiation, proliferation and progression.
Emergent-EZ
(Other name for: hydrocortisone sodium succinate)
emfizatamab
An anti-CD19/anti-CD3/anti-PD-L1/anti-4-1BB tetra-specific antibody, with potential immunostimulatory and antineoplastic activities. Upon administration, emfizatamab targets and binds to the tumor-associated antigen (TAA) CD19 overexpressed on the surface of B-cells, the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) expressed on tumor cells, the T-cell surface antigen CD3 and the costimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) expressed on a variety of leukocyte subsets including activated T lymphocytes. This may crosslink CD19-expressing tumor B cells and cytotoxic T lymphocytes (CTLs) and result in a potent CTL-mediated cell lysis of CD19-expressing B lymphocytes. In addition, 4-1BB binding results in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, GNC-038 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. CD19, a B-cell specific membrane antigen, is expressed during normal B-cell development and on B-cell malignancies.
Emflaza
(Other name for: deflazacort)
emicizumab
A humanized, immunoglobulin G4 (IgG4), bispecific monoclonal antibody against both the activated coagulation factor IX (FIXa) and factor X (FX) that can be used for the treatment of hemophilia A (HA). Upon administration, emicizumab targets and binds to both the FIXa and to FX, thereby bridging FIXa and FX, activating FX, and allowing for the activation and continuation of the coagulation cascade. FX is normally activated by coagulation factor VIII (FVIII); FVIII is missing in HA patients.
empagliflozin
An orally available competitive inhibitor of sodium-glucose co-transporter 2 (SGLT2; SLC5A2) with antihyperglycemic activity. Upon oral administration, empagliflozin selectively and potently inhibits SGLT2 in the kidneys, thereby suppressing the reabsorption of glucose in the proximal tubule. Inhibition of SGLT2 increases urinary glucose excretion by the kidneys, resulting in a reduction of plasma glucose levels in an insulin-independent manner. Inhibition of SGLT2 in the kidneys also suppresses the renal reabsorption of 1,5-anhydroglucitol (1,5AG). This lowers serum 1,5AG and neutrophil 1,5-anhydroglucitol-6-phosphate (1,5AG6P) levels, which may improve neutropenia and neutrophil dysfunction in patients with glycogen storage disease type Ib (GSD Ib). SGLT2, a transport protein exclusively expressed in the proximal renal tubules, mediates approximately 90% of renal glucose reabsorption from tubular fluid.
Empaveli
(Other name for: pegcetacoplan)
empegfilgrastim
A long-acting form and covalent conjugate of recombinant human granulocyte colony-stimulating factor (G-CSF) filgrastim with 30 kDa polyethylene glycol (PEG), with potential hematopoietic activity. Upon administration, empegfilgrastim acts similarly to endogenous G-CSF and binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. Therefore, this agent may prevent the incidence and shorten the duration of chemotherapy-induced neutropenia. Conjugation of the cytokine with a PEG molecule significantly increases this agent's therapeutic half-life compared to filgrastim.
Empirin
(Other name for: aspirin)
Empliciti
(Other name for: elotuzumab)
Emsam
(Other name for: selegiline hydrochloride)
emtricitabine
A synthetic fluoro derivative of thiacytidine with potent antiviral activity. Emtricitabine is phosphorylated to form emtricitabine 5'-triphosphate within the cell. This metabolite inhibits the activity of human immunodeficiency virus (HIV) reverse transcriptase both by competing with the natural substrate deoxycytidine 5'-triphosphate and by incorporation into viral DNA causing a termination of DNA chain elongation (due to the lack of the essential 3'-OH group).
Emtriva
(Other name for: emtricitabine)
emvododstat
An orally bioavailable, small molecule inhibitor of vascular endothelial growth factor (VEGF) synthesis with potential antiangiogenesis and antineoplastic activities. Emvododstat targets post-transcriptionally by selectively binding the 5'- and 3'-untranslated regions (UTR) of VEGF messenger RNA (mRNA), thereby preventing translation of VEGF. This inhibits VEGF protein production and decreases its levels in the tumor and bloodstream. In turn, this may result in the inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and eventually the induction of tumor cell death. VEGFs are upregulated in a variety of tumor cell types and play key roles during angiogenesis. In addition, emvododstat may enhance the antitumor activity of other chemotherapeutic agents.
emzadirib
An orally bioavailable inhibitor of the DNA damage repair protein RAD51, with potential antineoplastic and sensitizing activities. Upon oral administration, emzadirib targets, binds to and inhibits the activity of RAD51. This prevents RAD51-mediated DNA damage repair in susceptible tumor cells and induces tumor cell apoptosis. RAD51, the central protein involved in homologous repair (HR) of DNA double-strand breaks (DSBs), is overexpressed in many tumor cell types.
Enacard
(Other name for: enalapril maleate)
enadenotucirev
A complex, replication-selective, chimeric adenovirus type 11p (Ad11p)/Ad3 oncolytic virus vaccine, with potential antineoplastic and immunomodulating activities. Enadenotucirev has the Ad11p backbone with a large deletion in the E3-region and a small E4-domain (E4orf4) deleted, in addition to a partial E2B substitution by the Ad3 E2B genes. Upon intravenous administration of enadenotucirev, the adenovirus selectively reaches the tumor cells due to the leaky tumor vasculature and replicates in cancer cells; however, it is unable to replicate in normal, healthy cells. This induces a selective adenovirus-mediated cytotoxicity in cancer cells, which leads to cancer lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent cells, which both induces further tumor cell oncolysis and may activate, through the release of tumor-associated antigens (TAAs) and inflammatory mediators from the lysed tumor cells, the immune system to mount an anti-tumor immune response. This further kills tumor cells. This may also stimulate long-term anti-tumor immunity. Although the cancer-selectivity of enadenotucirev is not entirely understood, the virus does not efficiently infect normal cells.
enadenotucirev-expressing anti-CD40 agonistic monoclonal antibody NG-350
An oncolytic adenoviral vector, enadenotucirev (EnAd), that expresses a full-length agonistic anti-CD40 monoclonal antibody, with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of NG-350A, enadenotucirev specifically infects and replicates in tumor cells and not in normal, noncancerous tissue, and selectively expresses the agonistic anti-CD40 antibody. The locally expressed anti-CD40 antibody targets and binds to CD40 on a variety of immune cells, including B cells, T cells and dendritic cells (DCs) in the tumor microenvironment (TME). This induces CD40-dependent signaling pathways, which activates these immune cells and induces a cytotoxic T-lymphocyte (CTL)-mediated antitumor immune response and leads to tumor cell death. 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.
enadenotucirev-expressing FAP/CD3 bispecific FAP-TAc NG-641
An oncolytic adenoviral vector, a transgene-modified variant of enadenotucirev (EnAd), that expresses a bi-specific T-cell activator molecule FAP-TAc together with immune enhancer molecules C-X-C motif chemokine 9 (CXCL9), C-X-C motif chemokine 10 (CXCL10) and interferon alpha (IFNalpha), with potential immunomodulating and antineoplastic activities. Upon administration of NG-641, EnAd specifically infects and replicates in tumor cells and not in normal, noncancerous tissue, and selectively expresses FAP-TAc. The locally expressed FAP-TAc targets and binds to both fibroblast activating protein (FAP) on cancer associated fibroblasts (CAFs) and CD3 on T cells. This leads to T-cell activation and T-cell mediated killing of CAFs in tumor stroma. NG-641 also encodes the transgenes CXCL9, CXCL10 and IFNalpha. The production of CXCL9, CXCL10 and IFNalpha leads to the recruitment and further activation of T cells, enhancing the overall immune response and cancer cell killing. FAP, a cell surface glycoprotein, is overexpressed on tumor-associated fibroblasts but minimally expressed on normal, healthy cells.
enalapril maleate
The maleate salt form of enalapril, a dicarbocyl-containing peptide and angiotensin-converting enzyme (ACE) inhibitor with antihypertensive activity. As a prodrug, enalapril is converted by de-esterification into its active form enalaprilat. Enalaprilat competitively binds to and inhibits ACE, thereby blocking the conversion of angiotensin I to angiotensin II. This prevents the potent vasoconstrictive actions of angiotensin II and results in vasodilation. Enalapril also decreases angiotensin II-induced aldosterone secretion by the adrenal cortex, which leads to an increase in sodium excretion and subsequently increases water outflow.
enasidenib mesylate
The mesylate salt form of enasidenib, an orally available inhibitor of specific mutant forms of the mitochondrial enzyme isocitrate dehydrogenase type 2 (IDH2), with potential antineoplastic activity. Upon administration, enasidenib specifically inhibits various mutant forms of IDH2, including the IDH2 variants R140Q, R172S, and R172K, which inhibits the formation of 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH2-expressing tumor cells. IDH2, an enzyme in the citric acid cycle, is mutated in a variety of cancers; it initiates and drives cancer growth by blocking differentiation and the production of the oncometabolite 2HG.
enavatuzumab
A humanized monoclonal antibody directed against the tumor necrosis factor-like weak inducer of apoptosis receptor (TWEAKR) with potential antineoplastic, immunomodulating and antiangiogenic activities. Enavatuzumab binds to TWEAKR and inhibits TWEAK ligand binding and activation of NF-kappaB-mediated cytokine release, which may result in tumor cell apoptosis. TWEAKR is a cell-surface receptor with homology to tumor necrosis factor receptors. Upon binding with its ligand, TWEAKR has been shown to stimulate cytokine release and cell proliferation, migration, and survival; it may also promote apoptosis under some conditions. This receptor may be overexpressed in a variety of tumors including those of the pancreas, colon, lung, kidney, and breast.
Enbrel
(Other name for: etanercept)
encapsulated rapamycin
An orally bioavailable nanoparticle-based formulation composed of sub-micron particles of the macrolide antibiotic rapamycin incorporated into a pH-sensitive poly(methyl methacrylate) polymer, with potential immunomodulating and antineoplastic activities. Upon oral administration of the encapsulated rapamycin, the nanoparticle specifically delivers rapamycin at the tumor site. Rapamycin binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate a complex that binds to and inhibits the activation of the serine/threonine kinase mammalian target of rapamycin (mTOR), a key regulatory kinase. This may suppress mTORC1 activity. In addition, inhibition of mTOR may modulate central memory CD8 T cells, CD3+/CD56+ natural killer (NK) cells and CD8 T-cell responses. This may kill tumor cells. Compared to the administration of rapamycin alone, this formulation improves oral bioavailability of rapamycin with more consistent rapamycin levels, thereby allowing for administration of lower rapamycin dosage, which improves and minimizes rapamycin's toxicity. Upregulated in some tumors, mTOR is a serine/threonine kinase involved in regulating cellular proliferation, motility, and survival that is located downstream of the PI3K/Akt signaling pathway.
enclomiphene citrate
The orally bioavailable citrate salt of enclomiphene, the trans-isomer of the nonsteroidal triphenylethylene compound clomiphene, with tissue-selective estrogenic and antiestrogenic activities. As a selective estrogen receptor modulator (SERM), enclomiphene binds to hypothalamic estrogen receptors, blocking the negative feedback of endogenous estrogens and stimulating the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus; released GnRH subsequently stimulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, resulting in ovulation. In addition, this agent may bind to estrogen receptors on breast cancer cells, resulting in the inhibition of estrogen-stimulated proliferation in susceptible cell populations.
encochleated amphotericin B
A proprietary, orally bioavailable, nanoparticle-based encochleated formulation composed of amphotericin B, a polyene antifungal antibiotic produced by Streptomyces nodosus, encochleated within lipid-based crystals, which are composed of multi-layered, rolled-up sheets of soy-derived phosphatidylserine (PS) bilayers and calcium, with broad-spectrum antifungal activity. Upon oral administration, the cochleate crystal structure protects amphotericin B from degradation within the gastrointestinal (GI) tract. The lipid structure facilitates uptake into the bloodstream where the nanoparticles are taken up by macrophages and fungal cells though phagocytosis. Amphotericin B is released from the cochleate due to the calcium differential between the inside of the cell, which has low calcium levels, and the outside of the cell, which has high calcium levels. This delivers amphotericin B directly to the fungal-infected site and to its target cells. In turn, 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 causes fungal cell death and prevents fungal infections. Compared to amphotericin B alone, which can only be administered intravenously (IV), this formulation permits oral administration and reduces treatment-limiting side effects that are seen with IV amphotericin B, particularly nephro- and hepato-toxicity.
encorafenib
An orally available Raf kinase inhibitor with potential antineoplastic activity. Encorafenib specifically inhibits Raf kinase, a serine/threonine enzyme in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway. By inhibiting the activation of the RAF/MEK/ERK signaling pathway, the administration of encorafenib may result in a decrease in proliferation of tumor cells. The Raf mutation BRAF V600E is frequently upregulated 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.
Endari
(Other name for: glutamine)
Endep
(Other name for: amitriptyline hydrochloride)
EndoClot
(Other name for: absorbable modified polymer hemostatic powder)
Endometrin
(Other name for: progesterone vaginal insert)
endoxifen hydrochloride
The hydrochloride salt and the z (cis-) stereoisomer of endoxifen with potential antineoplastic activity. Endoxifen, the active metabolite of tamoxifen, competitively inhibits the binding of estradiol to estrogen receptors, thereby preventing the receptor from binding to the estrogen-response element on DNA and thus reducing DNA synthesis. Unlike tamoxifen, however, which relies on CYP2D6 activity for its conversion to the active metabolite endoxifen, the direct administration of endoxifen bypasses the CYP2D6 route. As CYP2D6 activity can vary widely among individuals due to genetic CYP2D6 polymorphisms, endoxifen is therefore theoretically more potent and more uniform in its bioavailability across patient populations.
enfortumab vedotin-ejfv
An antibody drug conjugate (ADC) containing a human monoclonal antibody AGS-22 targeting the cell adhesion molecule nectin-4 and conjugated to the cytotoxic agent monomethyl auristatin E (MMAE), via a proprietary enzyme-cleavable linker (AGS-22CE), with potential antineoplastic activity. The monoclonal antibody moiety of enfortumab vedotin-ejfv electively 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.
Engerix-B
(Other name for: hepatitis B vaccine (recombinant))
engineered human umbilical vein endothelial cells AB-205
A population of ex vivo expanded, genetically engineered CD31 (platelet endothelial cell adhesion molecule; PECAM-1)-positive human umbilical vein endothelial cells (HUVECs) derived from human umbilical vein tissue, that can be used to enhance the hematopoietic stem and progenitor cells (HSPCs) transplantation potential and improve blood cell recovery. Following autologous stem cell transplantation (ASCT) and upon the administration of the engineered HUVEC AB-205, the endothelial cells secrete angiocrine growth factors and interact with the HSPCs, thereby forming endothelial cell network structures and improving engraftment potential. AB-205 also interacts with injured or damaged vascular niche cells, thereby promoting blood cell recovery and improving tissue regeneration. This enhances recovery from toxicities related to chemo/radiation regimens.
engineered IL-12 prodrug WTX-330
An engineered, prodrug form of the human cytokine interleukin-12 (IL-12), composed of wild-type IL-12 linked to a high affinity blockade element via a tumor protease-sensitive linker, and a half-life extension domain, with potential immunomodulatory and antineoplastic activities. Upon administration of engineered IL-12 prodrug WTX-330, IL-12 is bound to the blockade element and pharmacologically inactive. Upon proteolytic cleavage in the tumor microenvironment (TME), active IL-12 is released. IL-12 activates the immune system by promoting the secretion of interferon-gamma (IFN-g) and activating CD8+ T-cells, CD4+ T cells and natural killer cells (NKs). The activation and expansion of these immune cells mediate cytolytic immune responses against tumor cells, thereby killing tumor cells and inhibiting tumor cell proliferation. The selective activation in the TME enhances the IL-12-mediated cytolytic responses against tumor cells while sparing the unwanted effects of systemic, peripheral immune activation. The inclusion of the half-life extension domain prolongs the agent's exposure in the tumor.
engineered IL-12 variant/aluminum hydroxide complex ANK-101
An anchored drug complex-based formulation consisting of an engineered variant of the cytokine interleukin-12 (IL-12) linked to an inert scaffolding composed of aluminum hydroxide, with potential immunomodulatory and antineoplastic activities. Upon intratumoral administration of engineered IL-12 variant/aluminum hydroxide complex ANK-101, IL-12 activates the immune system by promoting the secretion of interferon-gamma (IFN-g) and activating CD8+ T cells, CD4+ T cells and natural killer cells (NKs) in the tumor microenvironment (TME). The activation and expansion of these immune cells mediate cytolytic immune responses against tumor cells, thereby killing tumor cells and inhibiting tumor cell proliferation. The linking of IL-12 to aluminum hydroxide reduces the clearance of IL-12 from the tumor, prevents systemic accumulation of IL-12 and allows local and sustained accumulation of IL-12, thereby prolonging the half-life and reducing systemic toxicities.
engineered IL-2 prodrug WTX-124
An engineered, prodrug form of the human endogenous cytokine interleukin-2 (IL-2), composed of IL-2 linked to an inactivation domain via a tumor protease-sensitive linker, and a half-life extension domain, with potential immunoregulatory and antineoplastic activities. Upon administration of engineered IL-2 prodrug WTX-124, IL-2 is bound to the inactivation domain and pharmacologically inactive. Upon proteolytic cleavage in the tumor microenvironment (TME), active IL-2 is released. IL-2 binds to the high-affinity IL-2 receptors expressed on CD8+ T cells and natural killer (NK) cells, thereby activating IL2R-mediated signaling. The activation and expansion of CD8+ T cells and NK cells mediate cytolytic immune responses against tumor cells, which kills tumor cells and inhibits tumor cell proliferation. The selective activation in the TME enhances the IL-2-mediated cytolytic responses against tumor cells while sparing the unwanted effects of systemic, peripheral immune activation. The inclusion of the half-life extension domain prolongs the agent's exposure in the tumor.
engineered interferon alpha-2b prodrug JZP898
An engineered, prodrug form of the human cytokine interferon alpha-2b (IFN-alpha-2b), composed of IFN-alpha-2b linked to a high affinity blockade element via a tumor protease-sensitive linker, and a half-life extension domain, with potential immunomodulatory and antineoplastic activities. Upon administration of engineered IFN-alpha-2b prodrug JZP898, IFN-alpha-2b is bound to the blockade element and pharmacologically inactive. Upon proteolytic cleavage in the tumor microenvironment (TME), active IFN-alpha-2b is released. IFN-alpha-2b binds to specific IFN cell-surface receptors. This activates IFN-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-stimulated response elements (ISREs); the protein products mediate immunomodulating and antiproliferative effects. The selective activation in the TME enhances the IFN-alpha-2b-mediated immune responses against tumor cells while sparing the unwanted effects of systemic, peripheral immune activation. The inclusion of the half-life extension domain prolongs the agent's exposure in the tumor.
engineered interferon ORB-011
An attenuated, cis-targeted interferon (IFN), with potential immunostimulating and antineoplastic activities. Upon administration, engineered IFN ORB-011 specifically targets, binds to and activates type 1 conventional dendritic cell (cDC1). As these are specific immune cells that specialize in presenting tumor antigens to, and activating, tumor cytotoxic CD8 T cells, ORB-011 may be able to stimulate a specific cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response. ORB-011 is engineered in such a way as to minimize off-target IFN-based binding and thereby avoiding systemic toxicity.
engineered PBLs
A preparation of autologous peripheral blood lymphocytes (PBLs) that have been genetically modified to express T-cell receptors (TCRs) specific for K-RAS (KRAS) mutations, with potential immunomodulating and antineoplastic activities. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous KRAS mutant-specific TCRs gene engineered PBLs target and bind to KRAS mutants-expressing tumor cells, resulting in a cytotoxic T-lymphocyte (CTL)-mediated killing of KRAS mutants-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.
engineered red blood cells coexpressing 4-1BBL and IL-15TP RTX-240
A preparation of allogeneic, off-the-shelf (OTS) red blood cells (RBCs) engineered to express both the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) and a fusion protein composed of the trans-presented cytokine interleukin (IL)-15/IL-15-receptor alpha (IL-15Ra) (IL-15TP) with potential modulating and antineoplastic activities. CD34+ hematopoietic precursor cells (HPC) are collected by apheresis from a healthy O negative donor, purified, and engineered with a lentiviral vector to express 4-1BBL and IL-15TP. The cells are then further expanded and differentiated until the nucleus is ejected, resulting in a mature reticulocyte. Upon administration of the engineered red blood cells co-expressing 4-1BBL and IL-15TP RTX-240, the RBCs express both 4-1BBL and IL-15TP on their cell surfaces. 4-1BBL and IL-15TP bind to and subsequently induce the proliferation and activation of natural killer (NK) cells and T cells. This enhances the secretion of cytokine interferon-gamma (IFN-g) and results in the induction of an anti-tumor immune response.
engineered red blood cells expressing 4-1BBL/IL-12 RTX-224
An off-the-shelf (OTS) preparation of allogeneic red blood cells (RBCs) genetically engineered with a lentiviral vector to express on the cell surface the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) and the immunostimulatory cytokine interleukin-12 (IL-12), with potential immunomodulating and antineoplastic activities. Upon administration of the engineered RBCs expressing 4-1BBL/IL-12 RTX-224, 4-1BBL and IL-12 expressed on these cells bind to 4-1BB and IL-12 receptors. This induces the proliferation and activation of CD4- and CD8-positive T cells and natural killer (NK) cells, which induces the production of inflammatory cytokines and chemokines, and leads to the activation of antigen-presenting cells (APCs) and enhanced antigen presentation. Altogether, this activates both the adaptive and innate immune system and leads to the induction of anti-tumor immune responses, thereby killing the 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. IL-12 promotes the activation of NK cells.
engineered red blood cells expressing HPV16 E7/4-1BBL/IL-12 RTX-321
A preparation of allogeneic red blood cells (RBCs) engineered to act as artificial antigen presenting cells (aAPCs) and express on the cell surface the human papillomavirus (HPV) type 16 E7 protein on the major histocompatibility complex (MHC) I, the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) and the immunostimulatory cytokine interleukin-12 (IL-12), with potential immunomodulating and antineoplastic activities. Upon administration of the engineered RBCs expressing HPV16 E7/4-1BBL/IL-12 RTX-321, these cells activate the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing HPV16 E7. In addition, 4-1BBL and IL-12 expressed on these cells bind to 4-1BB and IL-12 receptors and subsequently induce the proliferation and activation of natural killer (NK) cells and T cells. This enhances the secretion of cytokine interferon-gamma (IFN-g) and further induces an anti-tumor immune response. HPV16 E7 plays an important role in the development of certain types of cancer. 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. IL-12 promotes the activation of NK cells, which induces both the secretion of IFN-g and a CTL response against the tumor cells.
engineered toxin body targeting CD38 TAK-169
An engineered toxin body (ETB) containing a single chain variable fragment (scFv) from an antibody targeting the cell surface glycoprotein ADP-ribosyl cyclase 1 (CD38) that is fused to a cytotoxic payload composed of the enzymatically active, de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA), with potential antineoplastic activity. Upon administration, the anti-CD38 scFv moiety of TAK-169 specifically targets and binds to CD38-expressing tumor cells. Upon internalization, the SLTA moiety is released and acts as an N-glycosidase, which binds to and removes an adenine nucleobase from the 28S RNA component of the 60S ribosomal subunit.of ribosomes This prevents ribosome activity, This inhibits protein synthesis and leads to apoptosis 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.
engineered toxin body targeting CTLA-4 MT-8421
An engineered toxin body (ETB) composed of biparatopic heavy chain variable domains (VHHs) targeting the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), fused to the enzymatically active, de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of ETB targeting CTLA-4 MT-8421, the antibody fragments specifically target and bind to two non-overlapping epitopes on CTLA-4-expressing T regulatory cells (Tregs) in the tumor microenvironment (TME). Upon internalization, the SLTA 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 leads to apoptosis in CTLA-4-expressing Tregs in the TME. The depletion of the immune suppressive Tregs in the TME may enhance a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), is overexpressed by Tregs in the TME and plays a key role in the downregulation of the immune system.
engineered toxin body targeting PD-L1 MT-6402
An engineered toxin body (ETB) composed of a single chain variable fragment (scFv) targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), fused to the enzymatically active de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA) and a class I antigen derived from the human cytomegalovirus (CMV) phosphoprotein pp65, with potential immunomodulatory and antineoplastic activities. Upon administration, the scFv moiety of ETB targeting PD-L1 MT-6402 specifically targets and binds to PD-L1-expressing tumor and immune cells in the tumor microenvironment (TME). Upon internalization, the SLTA 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 leads to apoptosis in PD-L1-expressing tumor and immune cells in the TME. In addition, MT-6402 delivers the foreign class I antigen derived from CMV pp65 peptide. This may result in a CMV-specific immune response against PD-L1-expressing tumor and immune cells in the TME. 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.
engineered toxin body-targeting HER2 MT-5111
An engineered toxin body (ETB) composed of a single chain variable fragment (scFv) from an antibody targeting the human epidermal growth factor receptor 2 (HER2; HER-2), fused to the enzymatically active de-immunized, ribosome-inactivating cytotoxic payload Shiga-like toxin-A subunit (SLTA), with potential antineoplastic activity. Upon administration, the scFv moiety of MT-5111 specifically targets and binds to a distinct epitope on HER2-expressing cells. Upon internalization, the SLTA 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 leads to apoptosis in HER2-expressing tumor cells. HER2, a tumor-associated antigen (TAA), is overexpressed in a variety of tumor cell types.
Enhanzyn
(Other name for: Detox-B adjuvant)
Enhertu
(Other name for: fam-trastuzumab deruxtecan-nxki)
eniluracil
An orally-active fluoropyrimidine analogue. Eniluracil inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil (5-FU) in the liver. Co-administration of ethynyluracil permits the oral administration of 5-FU.
eniluracil/5-FU combination tablet
A combination tablet of ethynyluracil and fluorouracil. Fluorouracil is an antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Ethynyluracil is an orally-active fluoropyrimidine analog that inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil in the liver. This may lead to an increase in the bioavailability and, effectiveness of fluorouracil.
enlonstobart
A recombinant 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, enlonstobart 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.
enoblituzumab
An Fc-domain optimized, humanized monoclonal antibody directed against cancer stem cells (CSCs), with potential immunomodulating and antineoplastic activities. After binding of enoblituzumab to an as of yet not elucidated target expressed on CSCs and differentiated tumor cells, this agent may induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against CSCs. CSCs are tumor initiating cells that are able to self-renew and are responsible for tumor cell growth and resistance.
enobosarm
A non-steroidal agent with anabolic activity. Enobosarm is designed to work like testosterone, thus promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength. Mimicking testosterone's action, this agent may increase lean body mass, thereby ameliorating muscle wasting in the hypermetabolic state of cancer cachexia.
enoxaparin sodium
The sodium salt of enoxaparin, a low molecular weight, synthetic heparin. As an anticoagulant/antithrombotic agent, enoxaprin's mechanism of action is similar to that of heparin, although it exhibits a higher ratio of anti-Factor Xa to anti-Factor IIa activity. This agent also has anti-inflammatory properties, inhibiting monocyte adhesion to tumor necrosis factor alpha- or lipopolysaccharide-activated endothelial cells. Compared to unfractionated heparins, the use of enoxaparin is associated with lower incidences of osteoporosis and heparin-induced thrombocytopenia.
enozertinib
An orally bioavailable, central nervous system (CNS) penetrating, mutant-selective covalent inhibitor of epidermal growth factor receptor (EGFR; ErbB1) and human epidermal growth factor receptor 2 (HER2; EGFR2; ErbB2) alterations, including exon 20 insertion (Ex20ins) mutations, with potential antineoplastic activity. Upon oral administration, enozertinib selectively targets, irreversibly binds to and inhibits the activity of EGFR or HER2 insertions or mutations. This prevents EGFR/HER2-mediated signaling. This may induce cell death and inhibit tumor growth in EGFR/HER2-overexpressing tumor cells. Enozertinib is able to penetrate the blood-brain-barrier (BBB) and may therefore exert its activity against EGFR Ex20ins-driven CNS primary tumors and CNS metastases. The ErbB receptor tyrosine kinase family is involved in key cellular functions, including cell growth and survival. EGFR and HER2 alterations constitutively upregulate kinase activity.
ENPP1 inhibitor RBS2418
A selective small molecule inhibitor of ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), with potential immunomodulating and antineoplastic activities. Upon administration, ENPP1 inhibitor RBS2418 targets and binds to ENPP1, thereby inhibiting the activity of ENPP1. This inhibits ENPP1-mediated 2'-3'-cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) and adenosine triphosphate (ATP) hydrolysis and stabilizes extracellular endogenous cGAMP and ATP. This leads to the extracellular accumulation of cGAMP and ATP, and inhibits the production of immunosuppressive adenosine in the tumor microenvironment (TME). This allows for induction of anticancer immune responses. ENPP1, overexpressed in a number of tumor types, mediates nucleotide recycling by breaking down ATP to AMP, which is then converted to adenosine. It suppresses anti-tumor immune responses and increases metastasis.
ENPP1 inhibitor SR-8541A
An orally bioavailable selective small molecule inhibitor of ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), with potential immunomodulating and antineoplastic activities. Upon oral administration, ENPP1 inhibitor SR-8541A selectivelly targets and binds to ENPP1, thereby inhibiting the activity of ENPP1. This inhibits ENPP1-mediated 2'-3'-cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) and adenosine triphosphate (ATP) hydrolysis and stabilizes extracellular endogenous cGAMP and ATP. This leads to the extracellular accumulation of cGAMP and ATP, and inhibits the production and accumulation of immunosuppressive adenosine in the tumor microenvironment (TME). This allows for the activation of stimulator of interferon genes (STING), and the induction of anticancer immune responses. ENPP1, overexpressed in a number of tumor types, mediates nucleotide recycling by breaking down ATP to AMP, which is then converted to adenosine. It suppresses anti-tumor immune responses and increases metastasis.
Enpresse
(Other name for: ethinyl estradiol/levonorgestrel)
enristomig
A recombinant, humanized, 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, enristomig 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, enristomig acts as a conditional 4-1BB agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, Ienristomig 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.
Ensacove
(Other name for: ensartinib hydrochloride)
ensartinib hydrochloride
The hydrochloride salt form of ensartinib, an orally available small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, ensartinib binds to and inhibits ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-expressing tumor cells. In addition, ensartinib inhibits various other kinases, including the receptor tyrosine kinase c-Met (hepatocyte growth factor receptor; HGFR; MET) and the receptor tyrosine kinase C-ros oncogene 1 (ROS1). 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.
ensituximab
A chimeric monoclonal antibody against human colorectal and pancreatic carcinoma-associated antigens (CPAAs) with potential immunomodulating and anti-tumor activities. Ensituximab binds to CPAAs, which may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response and an antibody-dependent cellular cytotoxicity (ADCC) response against CPAA-expressing tumor cells. CPAAs, cell surface proteins, are upregulated on colon and pancreatic tumor cells. Ensituximab contains the variable region of the heavy and light chain of murine NPC-1 and linked in-frame to constant regions of a human IgG1 isotype.
Ensure
(Other name for: nutritional supplement drink)
entacapone
A nitrocatechol compound with anti-parkinsonian property. Entacapone is a selective and reversible inhibitor of catechol-O-methyltransferase (COMT), which catalyzes the transfer of the methyl group of S-adenosyl-L-methionine to the phenolic group of substrates that contain a catechol structure including dihydroxyphenylalanine (DOPA), catecholamines (dopamine, norepinephrine, and epinephrine) and their hydroxylated metabolites. When administered in conjunction with dopaminergic agents such as L-DOPA, entacapone prevents the metabolism and inactivation of adjunct drugs, thereby increasing the bioavailability of these compounds by facilitating their passage across the blood-brain barrier.
entecavir
A synthetic analog of 2-deoxyguanosine with antiviral activity against hepatitis B virus (HBV). Entecavir is activated in vivo to a 5-triphosphate metabolite. In turn, the triphosphate form competes with the natural substrate deoxyguanosine triphosphate (dGTP) for incorporation into viral DNA. The incorporation of the activated triphosphate metabolite of entecavir inhibits the reverse transcriptase (RT) viral RNA-dependent HBV DNA polymerase and, so, the replication of viral DNA and transcription.
Enterade
(Other name for: amino acid/electrolyte mixture-based dietary supplement)
EnteraGam
(Other name for: serum-derived bovine immunoglobulin protein isolate)
Entereg
(Other name for: alvimopan)
enteric-coated TRPM8 agonist D-3263 hydrochloride
An enteric-coated orally bioavailable formulation of the hydrochloride salt of a small-molecule agonist for transient receptor potential melastatin member 8 (TRPM8 or Trp-p8) with potential antineoplastic activity. The active ingredient in enteric-coated TRPM8 agonist D-3263 hydrochloride binds to and activates TRPM8, which may result in an increase in calcium and sodium entry; the disruption of calcium and sodium homeostasis; and the induction of cell death in TRPM8-expressing tumor cells. This agent may decrease dihydrotestosterone (DHT) levels, which may contribute to its inhibitory effects on prostate cancer and BPH. TRPM8 is a transmembrane calcium channel protein that is normally expressed in prostate cells and appears to be overexpressed in benign prostatic hyperplasia (BPH) and in prostate cancer.
enteric-coated zoledronic acid tablet MER-101
An oral tablet formulation containing zoledronic acid combined with a proprietary absorption enhancer for improved zoledronic acid gastrointestinal absorption with anti-bone-resorption activity. The third-generation bisphosphonate zoledronic acid binds to hydroxyapatite crystals in the bone matrix, slowing their dissolution and inhibiting the formation and aggregation of these crystals. This agent also inhibits farnesyl pyrophosphate synthase, an enzyme involved in terpenoid biosynthesis. Inhibition of this enzyme prevents the biosynthesis of isoprenoid lipids, donor substrates of farnesylation and geranylgeranylation during the post-translational modification of small GTPase signalling proteins, which are important in the process of osteoclast turnover. The proprietary absorption enhancer is a GRAS (generally-recognized-as-safe) food additive.
Entericin
(Other name for: aspirin)
Enterococcus gallinarum strain MRx0518
A live strain of the flagellin-producing Gram-positive bacterium Enterococcus (E.) gallinarum that is isolated from a healthy human gut , with potential immunomodulating and antineoplastic activities. Upon oral administration, MRx0518 modulates the intestinal microbiota and targets both intestinal epithelial cells (IECs), and various immune cells, such as macrophages and dendritic cells (DCs) and is able to induce the production of both pro- and anti-inflammatory mediators, such as interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-a), IL-1beta, IL-6, IL-23, in these cells and activates the innate immune system. The flagellin produced by MRx0518 interacts with and activates toll-like receptor 5 (TLR5), thereby activating the adaptive immune system and modulating the tumor microenvironment (TME). This activates the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells.
entinostat
A synthetic benzamide derivative with potential antineoplastic activity. Entinostat binds to and inhibits histone deacetylase, an enzyme that regulates chromatin structure and gene transcription. This agent appears to exert dose-dependent effects in human leukemia cells including cyclin-dependent kinase inhibitor 1A (p21/CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations; a marked induction of reactive oxygen species (ROS); mitochondrial damage; caspase activation; and, at higher concentrations, apoptosis. In normal cells, cyclin-dependent kinase inhibitor 1A expression has been associated with cell-cycle exit and differentiation.
entolimod
A polypeptide derived from the Salmonella filament protein flagellin with potential radioprotective and anticancer activities. As a toll-like receptor 5 (TLR5) agonist, entolimod binds to and activates TLR5 thereby stimulating tumor necrosis factor production and activating nuclear factor kappa B (NF-kB). This induces NF-kB-mediated signaling pathways and inhibits the induction of apoptosis. This may prevent apoptosis in normal, healthy cells during radiotherapy of cancerous cells and may allow for increased doses of ionizing radiation. In addition, entolimod may inhibit radiation-independent proliferation in TLR5-expressing tumor cells.
entospletinib
An orally available inhibitor of spleen tyrosine kinase (Syk), with potential antineoplastic activity. Upon oral administration of entospletinib, this agent may inhibit the activity of Syk, which inhibits B-cell receptor (BCR) signaling and leads to an inhibition of tumor cell activation, migration, adhesion and proliferation. Syk, a non-receptor cytoplasmic, BCR-associated tyrosine kinase, is expressed in hematopoietic tissues and is often overexpressed in hematopoeitic malignancies.
entrectinib
An orally bioavailable inhibitor of the tyrosine kinases tropomyosin receptor kinases (Trk) A, B and C, C-ros oncogene 1 (ROS1) and anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon administration, entrectinib binds to and inhibits TrkA, TrkB, TrkC, ROS1 and ALK. Inhibition of these kinases may result in a disruption of TrkA-, TrkB-, TrkC-, ROS1-, and ALK-mediated signaling. This leads to an induction of apoptosis and an inhibition of tumor cell proliferation in tumor cells that express these kinases. TrkA, TrkB, TrkC, ROS1 and ALK are overexpressed in a variety of cancer cell types.
Entresto
(Other name for: sacubitril)
Entyvio
(Other name for: vedolizumab)
envafolimab
An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab 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.
enzalutamide
An orally bioavailable, organic, non-steroidal small molecule targeting the androgen receptor (AR) with potential antineoplastic activity. Through a mechanism that is reported to be different from other approved AR antagonists, enzalutamide inhibits the activity of prostate cancer cell ARs, which may result in a reduction in prostate cancer cell proliferation and, correspondingly, a reduction in the serum prostate specific antigen (PSA) level. AR over-expression in prostate cancer represents a key mechanism associated with prostate cancer hormone resistance.
Enzaprost E
(Other name for: dinoprostone)
enzastaurin hydrochloride
The hydrochloride salt of enzastaurin, a synthetic macrocyclic bisindolemaleimide with potential antineoplastic activity. Binding to the ATP-binding site, enzastaurin selectively inhibits protein kinase C beta, an enzyme involved in the induction of vascular endothelial growth factor (VEGF)-stimulated neo-angiogenesis. This agent may decrease tumor blood supply and so tumor burden.
enzymatically hydrolyzed whey protein-based nutritional supplement
An orally available, gluten-free, enzymatically hydrolyzed cysteine-rich whey-protein based nutritional supplement containing essential vitamins, minerals, and trace elements, as well as fat and carbohydrates. Upon oral intake of the nutritional supplement, the whey protein may improve gastric functioning and gastrointestinal health, thereby reducing vomiting and diarrhea. The whey-based hydrolyzed protein helps to alleviate the digestive burden for the pancreas and may be beneficial for patients with a pancreas-associated disease, such as pancreatitis or pancreatic cancer. Due to the high levels of cysteine in the whey protein, this supplement increases levels of the antioxidant glutathione (GSH). The polyunsaturated fatty acids in this supplement are incorporated in cell membranes and affect the production of pro-inflammatory mediators, eliciting an anti-inflammatory effect. Medium chain triglycerides (MCT) in this supplement enhance fat absorption and may aid in the prevention of fat malabsorption. Altogether, this supplement may prevent both malnutrition and weight loss.
enzyme-inducing antiepileptic drug
Any antiepileptic drug (AED) that induces a variety of enzymes, including a broad range of cytochrome P450 (CYP) family of enzymes and uridine 5'-diphospho-glucuronyltransferase (UGT) isoenzymes. This stimulates the metabolism and reduce serum concentrations of other administered agents and endogenous substrates, and alters biological pathways.
Eoquin
(Other name for: apaziquone)
Eovist
(Other name for: Gadoxetate Disodium)
EP2/EP4 antagonist TPST-1495
An orally bioavailable, dual antagonist of the human prostaglandin E2 receptor subtypes 2 (EP2) and 4 (EP4), with potential immunomodulating and antineoplastic activities. Upon oral administration, the EP2/EP4 antagonist TPST-1495 selectively targets and binds to EP2 and EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP2 and EP4. This prevents the activation of EP2 and EP4, and inhibits PGE2-EP2/EP4-mediated signaling. This inhibits PGE2-driven immune suppression by preventing the PGE2-mediated inhibition of anti-tumor immune effector cells in the tumor microenvironment (TME), such as natural killer (NK) cells, T-lymphocytes, dendritic cells (DCs) and M1 macrophages, and blocking the PGE2-mediated increase in suppressive immune cells, such as myeloid derived suppressor cells (MDSCs), M2 macrophages, and regulatory T cells (Tregs). This inhibits the proliferation of tumor cells in which the PGE2-EP2/4 signaling pathway is over-activated. EP2 and EP4, G protein-coupled receptors (GPCRs) that are overexpressed in certain types of cancers, promote tumor cell proliferation, invasion, survival, and metastasis.
EP4 antagonist CR6086
A small molecule, orally bioavailable antagonist of the prostaglandin E2 receptor subtype 4 (PTGER4; EP4), with potential immunomodulating and antineoplastic activities. Upon oral administration, EP4 antagonist CR6086 selectively targets and binds to EP4, thereby inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4 and preventing the activation of EP4. This inhibits PGE2-EP4-mediated signaling and inhibits the proliferation of tumor cells in which the PGE2-EP4 signaling pathway is overactivated. In addition, EP4 inhibition prevents the activity of tumor-associated myeloid cells (TAMCs) in the tumor microenvironment (TME) by inhibiting interleukin-23 (IL-23) production and the IL-23-mediated expansion of T-helper 17 (Th17) cells. EP4, a prostanoid receptor, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.
EP4 antagonist DT-9081
An orally bioavailable small molecule antagonist of the prostaglandin E2 receptor EP4 subtype (PTGER4; EP4), with potential immunomodulating and antineoplastic activities. Upon oral administration, EP4 antagonist DT-9081 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling. This inhibits PGE2-driven immune suppression by preventing the PGE2-mediated inhibition of anti-tumor immune effector cells in the tumor microenvironment (TME), such as natural killer (NK) cells, T lymphocytes, dendritic cells (DCs) and M1 macrophages, and blocking the PGE2-mediated increase in suppressive immune cells, such as myeloid derived suppressor cells (MDSCs), M2 macrophages, and regulatory T cells (Tregs). This inhibits the proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. EP4, a G protein-coupled receptor (GPCR) overexpressed in certain types of cancers, promotes tumor cell proliferation and invasion.
EP4 antagonist INV-1120
A small molecule and antagonist of the prostaglandin E2 receptor subtype 4 (PTGER4; EP4), with potential immunomodulating and antineoplastic activities. Upon administration, the EP4 antagonist INV-1120 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling, thereby inhibiting proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. In addition, EP4 inhibition prevents the activity of tumor-associated myeloid cells (TAMCs) in the tumor microenvironment (TME) by inhibiting interleukin-23 (IL-23) production and the IL-23-mediated expansion of Th17 cells. EP4, a prostanoid receptor, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.
EP4 antagonist ONO-4578
An orally bioavailable antagonist of the prostaglandin E2 receptor subtype 4 (PTGER4; EP4), with potential analgesic, immunomodulating and antineoplastic activities. Upon administration, the EP4 antagonist ONO-4578 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling, thereby inhibiting proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. In addition, EP4 inhibition prevents the activity of tumor-associated myeloid cells (TAMCs) in the tumor microenvironment (TME) by inhibiting interleukin-23 (IL-23) production and the IL-23-mediated expansion of Th17 cells. EP4, a prostanoid receptor, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.
EP4 receptor antagonist YY001
An orally bioavailable small molecule antagonist of the prostaglandin E2 receptor EP4 subtype (PTGER4; EP4), with potential immunomodulating and antineoplastic activities. Upon oral administration, EP4 receptor antagonist YY001 selectively targets and binds to EP4, inhibiting the binding of the immunosuppressive prostaglandin E2 (PGE2) to EP4. This prevents the activation of EP4 and inhibits PGE2-EP4-mediated signaling. This inhibits PGE2-driven immune suppression by preventing the PGE2-mediated inhibition of anti-tumor immune effector cells in the tumor microenvironment (TME), such as natural killer (NK) cells, T lymphocytes, dendritic cells (DCs) and M1 macrophages, and blocking the PGE2-mediated increase in suppressive immune cells, such as myeloid derived suppressor cells (MDSCs), M2 macrophages, and regulatory T cells (Tregs). This activates an anti-tumor immune response and inhibits the proliferation of tumor cells in which the PGE2-EP4 signaling pathway is over-activated. EP4, a G protein-coupled receptor (GPCR) overexpressed in certain types of cancers, promotes tumor cell proliferation and invasion.
epacadostat
An orally available hydroxyamidine and inhibitor of indoleamine 2,3-dioxygenase (IDO1), with potential immunomodulating and antineoplastic activities. epacadostat targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, epacadostat increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), NK cells, and T-lymphocytes, as well as interferon (IFN) production, and a reduction in tumor-associated regulatory T cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may inhibit the growth of IDO1-expressing tumor cells. IDO1 is overexpressed by a variety of tumor cell types and DCs.
EpCAM-specific CAR-expressing autologous T lymphocytes
A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the antigen epithelial cell adhesion molecule (EpCAM), with potential immunostimulating and antineoplastic activities. Upon administration, the EpCAM-specific CAR-expressing autologous T lymphocytes specifically recognize and bind to EpCAM-expressing tumor cells, resulting in tumor cell lysis. EpCAM, a cell surface protein, is expressed by a variety of tumor cells.
epcoritamab-bysp
A bispecific monoclonal antibody, with potential immunomodulating and antineoplastic activities. Epcoritamab-bysp contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CD20, a tumor-associated antigen (TAA) that is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, epcoritamab-bysp 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.
EphA2-targeting DOPC-encapsulated siRNA
A liposomal formulation consisting of short-interfering RNAs (siRNAs) directed against ephrin type-A receptor 2 (EphA2) and encapsulated into 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) neutral liposomes, with potential antineoplastic activity. Upon internalization, EphA2-targeting DOPC-encapsulated siRNA can hybridize to EphA2 DNA and mRNA, thereby interfering with both the transcription and translation of EphA2, and thus inhibiting tumor cell growth. 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 and plays an important role in tumor growth.
EpiCept NP-1
(Other name for: ketamine/amitriptyline NP-H cream)
EpiCeram
(Other name for: ceramide/CLA/cholesterol controlled-release skin barrier emulsion)
epidermal growth factor ointment
A topical ointment containing a recombinant form of human epidermal growth factor (EGF) with potential protective activity against EGF receptor (EGFR/HER1) inhibitor-induced cutaneous toxicities. Upon topical application of the EGF ointment, EGF locally activates EGFR, thereby abrogating EGFR inhibition in the skin caused by systemic EGFR inhibiting agents. This may help inhibit the skin rash induced by EGFR antagonists. EGFR, a tyrosine kinase, plays a key role in maintaining epidermal integrity.
epidiferphane
An orally bioavailable, proprietary botanical-based formulation and nutritional supplement consisting of three botanical extracts, including broccoli powder and curcumin, that may be used to reduce taxane-induced side effects and toxicities. Upon oral administration, epidiferphane may be able to decrease inflammation and pain by reducing cytokine levels. It may also reduce taxane-mediated toxicities such as anemia, neutropenia, peripheral neuropathy, and protect the endogenous neural stem cell population against destruction thereby preventing memory problems associated with the loss of neural stem cells.
Epidiolex
(Other name for: cannabidiol)
epigallocatechin gallate
A phenolic antioxidant found in a number of plants such as green and black tea. It inhibits cellular oxidation and prevents free radical damage to cells. It is under study as a potential cancer chemopreventive agent.
epigallocatechin gallate/vitamin D/vitamin B6/D-chiro-inositol supplement
A dietary supplement composed of the four ingredients epigallocatechin gallate (EGCG), vitamin D, vitamin B6, and D-chiro-inositol, that may potentially be used to treat uterine fibroids (UFs). Upon oral administration of the EGCG/vitamin D/vitamin B6/D-chiro-inositol supplement, the active ingredients EGCG and vitamin D may work synergistically to reduce proliferation, increase apoptosis, and remodel the extracellular matrix (ECM) in the UF. This reduces its volume and improves menstrual bleeding and anemia. D-chiro-inositol may increase insulin sensitivity, improve glucose tolerance, and affect reproductive hormones and functions. Vitamin B6 is essential to red blood cells (RBCs), and helps improve anemia and maintain normal blood glucose levels.
Epilex
(Other name for: divalproex sodium)
Epipen
(Other name for: therapeutic epinephrine)
epirubicin hydrochloride
The hydrochloride salt of the 4'-epi-isomer of the anthracycline antineoplastic antibiotic doxorubicin. Epirubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation.
epitinib succinate
The succinate salt form of epitinib, an orally available epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon administration, epitinib inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may lead to induction of cell death and inhibition of tumor growth in EGFR-overexpressing tumor cells. EGFR is a receptor tyrosine kinase (RTK) that is overexpressed in certain tumor types and plays a key role in tumor cell proliferation and vascularization.
epitiostanol
An androgenic anabolic steroid having potent anti-estrogenic effect, which inhibits the progression of estrogen-stimulated cancers such as breast cancer. (NCI)
Epitol
(Other name for: carbamazepine)
Epival
(Other name for: divalproex sodium)
Epivir
(Other name for: lamivudine)
Epkinly
(Other name for: epcoritamab-bysp)
eplerenone
A selective aldosterone receptor antagonist. Eplerenone binds to the mineralocorticoid receptor and blocks the binding of aldosterone, thereby decreasing sodium resorption and subsequently increasing water outflow. This leads to a decrease in blood pressure. Eplerenone is used in the treatment of hypertension and congestive heart failure.
eplontersen
An antisense oligonucleotide (ASO) targeting transthyretin (TTR) that is conjugated to three N-acetyl galactosamine (GalNAc) residues, which can be used in the treatment of polyneuropathy of hereditary TTR-mediated amyloidosis (hATTR amyloidosis). Upon subcutaneous administration, eplontersen targets and binds to messenger RNA (mRNA) for both variant and wild-type forms of TTR inside liver cells, thereby inhibiting translation of both mutant and wild-type TTR. Inhibition of TTR protein synthesis lowers TTR blood levels and decreases the amount of and/or prevents TTR amyloid deposits, which accumulate in and cause damage to various body organs and tissues. ATTR is caused by mutations in the TTR gene, which lead to TTR protein misfolding. Misfolded wild-type and mutant forms of TTR protein accumulate in tissues as amyloid deposits in most ATTR patients. The GalNAc residues enable delivery of the ASO to hepatocytes.
EPOCH regimen
A chemotherapy regimen consisting of etoposide, prednisone, vincristine (Oncovin), cyclophosphamide and doxorubicin hydrochloride (hydroxydaunorubicin hydrochloride), which may be used in combination with rituximab (R-EPOCH) for the treatment of various aggressive B-cell and T-cell non-Hodgkin lymphomas.
EPOCH-O regimen
An immune-chemotherapy regimen consisting of etoposide, prednisone, vincristine (Oncovin), cyclophosphamide, doxorubicin (hydroxydaunorubicin) and ofatumumab, which may be used for the treatment of various aggressive non-Hodgkin lymphomas.
epoetin alfa
A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine human erythropoietin (EPO). Produced primarily by cells of the peritubular capillary endothelium of the kidney in response to hypoxia, circulating EPO binds to EPO receptors on the surface of committed erythroid progenitors in the bone marrow resulting in their replication and maturation into functional erythrocytes.
epoetin beta
A recombinant therapeutic agent that is chemically identical to or similar to the endogenous cytokine human erythropoietin (EPO). Produced primarily by cells of the peritubular capillary endothelium of the kidney in response to hypoxia, circulating EPO binds to EPO receptors on the surface of committed erythroid progenitors in the bone marrow resulting in their replication and maturation into functional erythrocytes.
epoetin zeta
A recombinant form of the endogenous human cytokine erythropoietin (EPO) with erythropoiesis-stimulating activity. Similar to EPO, epoetin zeta binds to and activates erythropoietin receptors on the surface of committed erythroid progenitors in the bone marrow resulting in their proliferation and differentiation into functional erythrocytes. This may enhance red blood cell counts and hemoglobin levels. Epoetin zeta differs from other epoetins in its glycosylation profile. EPO is a glycosylated polypeptide primarily produced by renal peritubular cells and its synthesis is regulated by a serum oxygenation feedback mechanism.
Epogen
(Other name for: epoetin alfa)
epothilone D
A natural polyketide compound isolated from the myxobacterium Sorangium cellulosum. Also known as desoxyepothilone B, epothilone D binds to tubulin and inhibits the disassembly of microtubules, resulting in the inhibition of mitosis, cellular proliferation, and cell motility.
epothilone KOS-1584
A second-generation epothilone with potential antineoplastic activity. Epothilone KOS-1584 binds to tubulin and induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to first-generation epothilones, this agent exhibits greater safety and efficacy with an enhanced pharmaceutical profile, including enhanced water solubility and tumor penetration, and reduced CNS exposure. In addition, epothilone KOS-1584 is a poor substrate for the P-glycoprotein (P-gp) drug efflux pump.
epratuzumab
A recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells. After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC).
epratuzumab-cys-tesirine
An antibody-drug conjugate (ADC) composed of a cysteine-engineered version of epratuzumab (hLL2), a humanized anti-CD22 monoclonal antibody derived from the murine immunoglobulin (Ig) G2a monoclonal antibody LL2 (EPB-2), site-specifically conjugated to the cross-linking cytotoxic agent tesirine (SG3249), a cathepsin B-cleavable valine-alanine pyrrolobenzodiazepine dimer (PBD), with potential antineoplastic activity. Upon administration of epratuzumab-cys-tesirine, the epratuzumab moiety targets and binds to the B-cell-specific CD22 receptor and is rapidly internalized. Upon cleavage, the imine groups of tesirine target and bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD22-overexpressing tumor cells. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B cells.
eprenetapopt
A methylated derivative and structural analog of PRIMA-1 (p53 re-activation and induction of massive apoptosis), with potential antineoplastic activity. Upon administration, eprenetapopt covalently modifies the core domain of mutated forms of cellular tumor antigen p53 (p53) through the alkylation of thiol groups. These modifications restore both the wild-type conformation and function to mutant p53, which reconstitutes endogenous p53 activity, leading to cell cycle arrest and apoptosis in tumor cells. This agent may work synergistically with other antineoplastic agents. p53, a tumor suppressor and transcription factor normally activated upon DNA damage, is frequently mutated and overexpressed in cancer cells; it plays a key role in both DNA repair and the induction of apoptosis.
eprodisate disodium
The orally available disodium salt form of eprodisate, a negatively charged sulfonated inhibitor of fibrillogenesis, that can be used in the treatment of amyloid A (AA) amyloidosis. Upon administration, eprodisate competitively binds to the glycosaminoglycan binding sites on serum amyloid A (SAA), which inhibits the formation of the glycosaminoglycan-amyloid fibril aggregate. This prevents the formation of amyloid deposits in certain organs, especially the kidneys, in AA amyloidosis.
EPS8 peptide-specific dendritic cells
A preparation of dendritic cells (DCs) pulsed with peptides derived from epidermal growth factor receptor (EGFR) pathway substrate 8 (EPS8), with potential immunostimulating and antineoplastic activities. Upon administration of the EPS8 peptide-specific DCs, the immune system is exposed to the EPS8 antigens. This results in the induction of a specific cytotoxic T-lymphocyte (CTL) response against EPS8-expressing tumor cells and tumor cell lysis. EPS8, a tumor-associated antigen (TAA), is overexpressed in a variety of tumor cell types but rarely in normal tissues. As a substrate for the EGFR kinase, it plays a key role in tumor progression through the EGFR-dependent pathway. Its expression is correlated with a poor prognosis.
Epstein-Barr virus gp350-ferritin nanoparticle vaccine with saponin-based adjuvant
A ferritin-based, nanoparticle vaccine consisting of the Epstein-Barr Virus (EBV) envelop glycoprotein gp350 and a saponin-based adjuvant, with potential immunizing activity against EBV. Upon intramuscular administration of EBV gp350-ferritin nanoparticle vaccine with saponin-based adjuvant, the EBV gp350 may activate both humoral and cellular immune responses which may result in protection against EBV infection. EBV, a ubiquitous human herpes virus, is associated with infectious mononucleosis and various malignancies, including nasopharyngeal carcinoma, Hodgkin disease, non-Hodgkin lymphoma, and other lymphomas.
equecabtagene autoleucel
A preparation of autologous T lymphocytes that have been transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) with a fully human single chain variable fragment (scFv) targeting 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. Upon administration, equecabtagene autoleucel 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.
ER alpha-targeting chimeric protein degrader AC682
An orally bioavailable, selective estrogen receptor (ER) alpha-targeted chimeric protein degrader, with potential antineoplastic activity. Upon oral administration, ER alpha-targeting chimeric protein degrader AC682 targets ER alpha wild-type and mutants and induces the degradation of ER alpha proteins. This decreases ER alpha protein levels, decreases the expression of ER alpha-target genes and halts ER-mediated signaling. This results in an inhibition of proliferation in ER alpha-overexpressing tumor cells. ER alpha is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation. AC682 is able to cross the blood-brain barrier (BBB).
ERa36 Modulator Icaritin
A metabolite of icariin, a principal flavonoid glycoside in Herba Epimedii (a traditional Chinese medicine herb used in treating osteoporosis) with potential antineoplastic activity. ERa36 modulator icaritin selectively binds to a novel variant of estrogen receptor alpha, a36, and mediates a membrane-initiated "nongenomic" signaling pathway, which is linked to activate signaling pathways like the MAPK/ERK and the PI3K/Akt pathways. This agent induces cell cycle arrest at G1, or G2/M arrest depending upon the dose. Consistently with G1 arrest, icaritin increases protein expressions of pRb, p27(Kip1) and p16(Ink4a), while decreasing phosphorylated pRb, Cyclin D1 and CDK4. 40% of ER-negative breast cancer tumors express high levels of ERa36, and this subset of patients is less likely to benefit from tamoxifen treatment compared with those with ERa66-positive/ERa36-negative tumors.
eragidomide
A modulator of cereblon (CRBN), which is part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and pro-apoptotic activities. Upon administration, eragidomide specifically binds to CRBN, thereby affecting the activity of the ubiquitin E3 ligase complex. This leads to the ubiquitination of certain substrate proteins and induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T lymphocytes. In addition, this downregulates the expression of other proteins, including interferon regulatory factor 4 (IRF4) and c-myc, which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
eramkafusp alfa
A humanized monoclonal antibody directed against the human B-cell-specific cell surface antigen CD20 and fused to the recombinant cytokine, interferon-alpha (IFN-a), with potential antineoplastic and immunomodulating activities. Upon administration of eramkafusp alfa, the antibody moiety specifically targets and binds to CD20. In turn, the IFN-a moiety binds to the IFN receptor, and activates IFN-mediated signal transduction, which induces the transcription and translation of genes whose protein products mediate anticancer effects. This results in the induction of both G2 cell cycle arrest and apoptosis in CD20-expressing tumor cells. In addition, IGN002 causes the induction of complement-dependent cytotoxicity (CDC) and 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.
erastin analogue PRLX 93936
A structural analogue of erastin with potential antineoplastic activity. Erastin analogue PRLX 93936 appears to inhibit mitochondrial outer membrane protein VDACs (voltage-dependent anion channels) 2 and 3, resulting in an oxidative, non-apoptotic cell death. Erastin analogue PRLX 93936 exhibits greater lethality in cell lines harboring mutations in the GTPase protein oncogenes HRAS and KRAS or the serine-threonine protein kinase oncogene BRAF than in non-tumorigenic cell lines. VDACs 2 and 3 are up-regulated in a wide variety of tumor cell lines.
Eraxis
(Other name for: anidulafungin)
erb-38 immunotoxin
A bivalent fusion protein consisting of disulfide-stabilized Fv fragments of an anti-HER2 (erbB2) monoclonal antibody (e23) and a truncated version of the M(r) 38 fragment of Pseudomonas exotoxin that lacks the toxin's cell binding domain. ERB-38 immunotoxin binds specifically to cells that overexpress HER2, the antigenic target of the monoclonal antibody; the exotoxin portion of the immunotoxin then lyses the cells bound by the antibody portion.
Erbitux
(Other name for: cetuximab)
erdafitinib
An orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. Upon oral administration, erdafitinib binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways and thus the inhibition of tumor cell proliferation and tumor cell death in FGFR-overexpressing tumor cells. FGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival.
erdafitinib-releasing intravesical system TAR-210
A controlled-release intravesical system consisting of a pretzel-shaped tube releasing erdafitinib, a pan fibroblast growth factor receptor (FGFR) inhibitor, with potential antineoplastic activity. Upon placement of the erdafitinib-releasing intravesical system TAR-210 into the bladder, erdafitinib is gradually and continuously released from the system over an extended period of time before being removed from the bladder. Upon release, erdafitinib targets, binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways and thus the inhibition of tumor cell proliferation and tumor cell death in FGFR-overexpressing tumor cells. FGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival.
erenumab
A human immunoglobulin G2 (IgG2) monoclonal antibody targeting calcitonin gene-related peptide receptor (CGRPR), that can be used in the preventive treatment of migraine. Upon subcutaneous administration, erenumab specifically targets, binds to and blocks the activity of CGRPR. This may relief CGRPR-triggered migraine.
erfonrilimab
A bispecific monoclonal antibody directed against both the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, erfonrilimab targets and binds to both PD-L1 expressed on tumor cells and CTLA-4 expressed on T cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), and inhibits the PD-1 and CTLA-4-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-L1, which is overexpressed in many human cancer cell types, and CTLA-4, an inhibitory T-cell receptor, play a role in the downregulation of the immune system and tumor evasion from host immunity.
Ergamisol
(Other name for: levamisole hydrochloride)
ergocalciferol
Vitamin D2, a fat-soluble vitamin important for many biochemical processes including the absorption and metabolism of calcium and phosphorus. In vivo, ergocalciferol is formed after sun (ultraviolet) irradiation of plant-derived ergosterol, another form of vitamin D. Ergocalciferol is the form of vitamin D usually found in vitamin supplements.
Eribulin Mesylate
The mesylate salt of a synthetic analogue of halichondrin B, a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression.
eritoran
A synthetic analogue of the lipid A portion of the endotoxin lipopolysaccharide (LPS) with potential immunomodulating activity. Eritoran binds to a receptor complex composed of toll-like receptor 4 (TLR4), CD14 and MD2 (MD-2, LY96) that is present on most cells of the immune system, inhibiting the activation of the receptor complex by LPS, which may result in the inhibition of pro-inflammatory cytokine secretion and a potentially fatal systemic inflammatory response syndrome (SIRS). LPS is found in the outer membrane of Gram-negative bacteria and binds to the TLR4/CD14/MD2 receptor complex of immune cells, including macrophages, resulting in the release of pro-inflammatory cytokines.
eritoran tetrasodium
The tetrasodium salt of a synthetic analogue of the lipid A portion of the endotoxin lipopolysaccharide (LPS) with potential immunomodulating activity. Eritoran binds to the Toll-like receptor (TLR)/CD14/MD2 receptor complex present on most cells of the immune system, inhibiting the activation of the receptor complex by LPS, which may result in the inhibition of pro-inflammatory cytokine secretion and a potentially fatal systemic inflammatory response syndrome (SIRS). LPS is found in the outer membrane of Gram-negative bacteria and binds to the TLR/CD14/MD2 receptor complex of immune cells, especially macrophages, resulting in the release of pro-inflammatory cytokines.
Erivedge
(Other name for: vismodegib)
ERK 1/2 inhibitor ASTX029
An orally bioavailable inhibitor of the extracellular signal-regulated kinases (ERK) 1 and 2, with potential antineoplastic activity. Upon administration, ASTX029 specifically binds to and inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK inhibitor CC-90003
An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, CC-90003 inhibits ERK activity, and prevents the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.
ERK inhibitor LTT462
An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, LTT462 binds to and inhibits ERK, thereby preventing the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is upregulated in numerous tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.
ERK inhibitor MK-8353
An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, MK-8353 inhibits both ERK phosphorylation and activation of ERK-mediated signal transduction pathways; thereby, preventing ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a role in tumor cell proliferation, differentiation and survival.
ERK1/2 inhibitor ATG-017
An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor ATG-017 specifically targets, binds to and inhibits the activity of the serine/threonine-protein kinases ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor ERAS-007
An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERAS-007 specifically binds to and inhibits the serine/threonine-protein kinase activities of both ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor GH55
An orally bioavailable and selective inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor GH55 specifically targets, binds to and inhibits the serine/threonine-protein kinase activities of both ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor HH2710
An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor HH2710 specifically targets, binds to and inhibits the activity of the serine/threonine-protein kinases ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor IPN01194
An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor IPN01194 specifically targets, binds to and inhibits the serine/threonine-protein kinase activities of both ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor JSI-1187
An orally bioavailable inhibitor of the extracellular signal-regulated kinases 1 (ERK1) and 2 (ERK2), with potential antineoplastic activity. Upon oral administration, ERK1/2 inhibitor JSI-1187 specifically targets, binds to and inhibits the activity of the serine/threonine-protein kinases ERK1 and ERK2, thereby preventing the phosphorylation of ERK1/2 substrates and the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent proliferation and survival of tumor cells. The MAPK/ERK pathway, also known as the RAS/RAF/MEK/ERK pathway, is hyperactivated in a variety of tumor cell types due to mutations in upstream targets. It plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor KO-947
An inhibitor of the extracellular signal-regulated kinases (ERK) 1 and 2, with potential antineoplastic activity. Upon intravenous administration, KO-947 specifically binds to and inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in the proliferation, differentiation and survival of tumor cells.
ERK1/2 inhibitor LY3214996
An orally available inhibitor of extracellular signal-regulated kinase (ERK) 1 and 2, with potential antineoplastic activity. Upon oral administration, LY3214996 inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.
Erleada
(Other name for: apalutamide)
erlotinib hydrochloride
The hydrochloride salt of a quinazoline derivative with antineoplastic properties. Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic domain of epidermal growth factor receptor (EGFR) tyrosine kinase, thereby reversibly inhibiting EGFR phosphorylation and blocking the signal transduction events and tumorigenic effects associated with EGFR activation.
ertapenem sodium
The sodium salt of ertapenem, a 1-beta-methyl carbapenem and a broad-spectrum beta-lactam antibiotic with bactericidal activity. Ertapenem binds to penicillin binding proteins (PBPs) located on the bacterial cell wall, in particular PBPs 2 and 3, thereby inhibiting the final transpeptidation step in the synthesis of peptidoglycan, an essential component of the bacterial cell wall. Inhibition of peptidoglycan synthesis results in weakening and lysis of the cell wall and cell death. In vitro, this agent has shown activity against Gram-positive and Gram-negative aerobic and anaerobic bacteria. Erapenem is resistant to hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases and extended-spectrum beta-lactamases.
ertumaxomab
A murine monoclonal antibody with two antigen-recognition sites: one for CD3, an antigen expressed on mature T cells, and one for HER-2-neu, a tumor-associated antigen that promotes tumor growth. Ertumaxomab attaches to CD3-expressing T cells and HER-2-neu-expressing tumor cells, selectively cross-linking tumor and immunologic cells which results in the recruitment of cytotoxic T cells to the T cell/tumor cell aggregate.
Erwinaze
(Other name for: asparaginase Erwinia chrysanthemi-rywn)
Ery-Tab
(Other name for: erythromycin)
eryaspase
A suspension of erythrocytes encapsulating L-asparaginase with potential antineoplastic activity. Upon administration of eryaspase, L-asparagine is hydrolyzed to L-aspartic acid and ammonia in plasma, thereby depleting tumor cells of asparagine. Due to low asparagine synthetase activity in tumor cells, de novo synthesis of asparagine is suppressed within tumor cells. Shortage of asparagine prevents synthesis of important proteins necessary for tumor cell growth. Encapsulation of asparaginase in erythrocytes decreases the immunogenicity of exogenous protein, enhances its circulation time and may limit toxicity.
ERYC
(Other name for: erythromycin)
erythromycin
A broad-spectrum, topical macrolide antibiotic with antibacterial activity. Erythromycin diffuses through the bacterial cell membrane and reversibly binds to the 50S subunit of the bacterial ribosome. This prevents bacterial protein synthesis. Erythromycin may be bacteriostatic or bactericidal in action, depending on the concentration of the drug at the site of infection and the susceptibility of the organism involved.
erythromycin topical cream
A topical cream formulation containing the broad-spectrum macrolide antibiotic erythromycin with anti-bacterial activity. Erythromycin interacts with the 50S subunit of the bacterial 70S ribosomal RNA complex resulting in the inhibition of protein synthesis and bacterial cell death.
erzotabart
A hexamerization-enhanced human immunoglobulin G1 (IgG1) monoclonal antibody that targets the cell surface glycoprotein CD-38 and carries the E430G mutation, with potential immunomodulating and antineoplastic activities. Upon administration, erzotabart targets and binds to CD38 on CD38-positive tumor cells, thereby forming antibody hexamers through increased intermolecular Fc-Fc interactions upon antigen binding. This may trigger direct cell killing, antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cell mediated phagocytosis (ADCP) and antibody-mediated complement dependent cytotoxicity (CDC) in CD38-expressing tumor cells. In addition, binding to CD38 by GEN3014 induces downmodulation of CD38, inhibits CD38 cyclase activity, and may abrogate immune suppression in the tumor microenvironment (TME). CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies.
escitalopram
The active S-stereoisomer of the selective serotonin reuptake inhibitor (SSRI) citalopram with antidepressant, anti-obsessive-compulsive and antibulimic properties. Escitalopram inhibits the reuptake of the neurotransmitter serotonin (5-HT) at the serotonin reuptake pump of the neuronal membrane of the presynaptic cell, thereby increasing levels of 5-HT within the synaptic cleft and enhancing the actions of serotonin on 5HT1A autoreceptors. Unlike other SSRIs, escitalopram appears to not only bind to a primary high-affinity site on the serotonin transporter protein but also to a secondary lower-affinity allosteric site that is considered to stabilize and prolong drug binding.
escitalopram oxalate
The oxalate salt of escitalopram, a pure S-enantiomer of the racemic bicyclic phthalane derivative citalopram, with antidepressant activity. As a selective serotonin reuptake inhibitor (SSRI), escitalopram blocks the reuptake of serotonin by neurons in the central nervous system (CNS), thereby potentiating CNS serotonergic activity.
Eskalith
(Other name for: lithium carbonate)
esketamine
A cyclohexanone derivative and S-enantiomer of racemic ketamine, with analgesic, anesthetic and antidepressant activities. Although the mechanism of action is not fully understood, upon administration, esketamine targets, non-competitively binds to, and blocks N-methyl D-aspartate (NMDA) receptors. This reduces pain perception, induces sedation, and produce dissociative anesthesia.
esmolol
The hydrochloride salt form of esmolol, a short, rapid-acting, selective beta-adrenergic receptor blocker, devoid of intrinsic sympathomimetic activity, and with anti-arrhythmic, antihypertensive and potential analgesic activities. Upon intravenous administration, esmolol binds to and blocks the beta-1 receptor in the myocardium thereby preventing the action of epinephrine and norepinephrine. This leads to a reduction in the force and rate of cardiac contractions and thereby preventing tachycardia, arrythmias and/or hypertension. At higher doses, esmolol also blocks beta-2 receptors located in bronchial and vascular smooth muscle, thereby leading to smooth muscle relaxation. In addition, esmolol exerts a peripheral analgesic effect and intraoperative use of this agent may decrease the amount of opioid administration postoperatively. As the ester moiety in esmolol is rapidly hydrolyzed byplasma esterases, this agent has a very short half-life.
esomeprazole magnesium
The magnesium salt of esomeprazole, the S-isomer of omeprazole, with gastric proton pump inhibitor activity. In the acidic compartment of parietal cells, esomeprazole is protonated and converted into the active achiral sulphenamide; the active sulphenamide forms one or more covalent disulfide bonds with the proton pump hydrogen-potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting its activity and the parietal cell secretion of H+ ions into the gastric lumen, the final step in gastric acid production. H+/K+ ATPase is an integral membrane protein of the gastric parietal cell.
esomeprazole topical cream
A topical cream formulation containing the proton pump inhibitor (PPI) esomeprazole, with potential antioxidant, anti-inflammatory and antifibrotic activities. Upon topical administration, esomeprazole inhibits the enzyme dimethylarginine dimethylaminohydrolase (DDAH), which increases the levels of the nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA). In addition, esomeprazole increases the expression of the antioxidant enzyme heme oxygenase-1 (HO-1). Together, these actions reduce oxidative stress which may protect cells from reactive oxygen species (ROS), cellular damage, inflammation and fibrosis.
esorubicin
A synthetic derivative of the anthracycline antineoplastic antibiotic doxorubicin with potential antineoplastic activity. Esorubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent exhibits less cardiotoxicity than the parent antibiotic doxorubicin, but may cause more severe myelosupression compared to other compounds within the anthracycline class.
ESR1 peptides/GM-CSF/Montanide ISA vaccine
A vaccine comprised of estrogen receptor alpha (ERa; estrogen receptor 1; ESR1) mutant peptides, combined with the immunoadjuvants granulocyte-macrophage colony-stimulating factor (GM-CSF) and montanide ISA, with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, the ESR1 mutant peptides in the ESR1 peptides/GM-CSF/montanide ISA vaccine may activate the immune system to induce an immune response against tumor cells expressing these ESR1 mutations. Constitutively activating mutations in ESR1 sometimes emerge with the treatment of estrogen receptor (ER)-positive breast cancer with endocrine therapy, leading to resistance to endocrine therapy. GM-CSF and montanide ISA potentiate the anti-tumor immune response.
Essiac
An herbal formula containing burdock root (Arctium lappa), Turkey rhubarb root (Rheum palmatum), sheep sorrel (Rumex acetosella), and slippery elm bark (Ulmus fulva) with potential immunostimulating, anti-inflammatory and anti-tumor activities. The exact chemical profile, their respective concentrations and the mechanism of action of Essiac are largely unknown due to the proprietary nature of the formula and product inconsistency. Several chemical classes in Essiac are consistently represented and may attribute to its therapeutic effect, including anthraquinone derivatives such as rhein and emodin, high molecular polysaccharides, and lignans such as arctigenin. However, all these chemicals are unlikely to occur in high concentrations in Essiac, and its potential therapeutic effect may be attributed to a potential synergistic effect of these various compounds.
Estinyl
(Other name for: ethinyl estradiol)
Estrace
(Other name for: therapeutic estradiol)
estradiol vaginal ring
A flexible elastomer ring containing 17 beta-estradiol used for estrogen replacement. Upon vaginal insertion, estradiol vaginal ring releases a consistent low-dose of estrogen which binds to and activates nuclear receptors in estrogen-responsive tissues. By increasing the amount of estradiol locally, symptoms of vaginal dryness or decreased sexual interest may improve. 17 beta-estradiol is the major naturally occurring estrogen produced in the ovaries of premenopausal women.
estradiol valerate
The parenterally-administered synthetic valerate ester of estradiol, a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females. As the primary, most potent estrogen hormone produced by the ovaries, estradiol binds to and activates specific nuclear receptors. This agent exhibits mild anabolic and metabolic properties, and increases blood coagulability.
estradiol/norethindrone acetate tablet
An orally bioavailable tablet formulation containing the semisynthetic estrogen estradiol in combination with the acetate form of the synthetic progestin norethindrone, with estrogenic and progesteronic activities. Estradiol binds to and activates intracellular estrogen receptors found in the reproductive tract and other estrogen-responsive tissues. The activated complex enters the nucleus, binds to the estrogen response elements on DNA, and activates the transcription of genes involved in the maintenance of the female reproductive system and secondary sexual characteristics, the proliferation of the endometrium, and bone metabolism. Norethindrone binds to the intracellular progesterone receptors in the reproductive system and the activated ligand/receptor complex interacts with specific DNA response elements, resulting in an alteration in protein synthesis; inhibition of luteinizing hormone (LH) and follicle stimulating hormone (FSH) release; inhibition of ovulation; an increase in cervical mucus production; and induction of the secretory phase of the endometrial cycle. Administration of estradiol/norethindrone acetate may abrogate vasomotor symptoms associated with menopause and prevent bone loss associated with the postmenopause. Because chronic estrogen stimulation unopposed by progesterone may increase the risk of endometrial carcinoma, administration of a combination estrogen-progestin in postmenopause may reduce the risk for women who require estrogen replacement therapy.
estramustine phosphate sodium
The orally available disodium salt, monohydrate, of estramustine phosphate, a synthetic molecule that combines estradiol and nornitrogen mustard through a carbamate link. Estramustine and its major metabolite estramustine bind to microtubule-associated proteins (MAPs) and tubulin, thereby inhibiting microtubule dynamics and leading to anaphase arrest in a dose-dependent fashion. This agent also exhibits anti-androgenic effects.
Estratest
(Other name for: methyltestosterone)
ESTRING
(Other name for: estradiol vaginal ring)
estriol
A synthetic form of the endogenous human estriol, a weak oestrogen and natural metabolite of estradiol, that can be used for hormone replacement. Upon administration, estriol maintains adequate levels of estrogen, binds to estrogen receptors, and relieves symptoms caused by estrogen deficiency.
estriol vaginal gel
A vaginal gel formulation containing a very low concentration of the estrogen estriol, that can be used for hormone replacement. Upon topical application to the vagina, estriol maintains adequate levels of estrogen in the vagina, and decreases vaginal atrophy and its associated symptoms, such as vaginal dryness and itching.
Estrobene
(Other name for: diethylstilbestrol)
EstroGel
(Other name for: transdermal estrogen)
estrogen receptor agonist GTx-758
An orally available, nonsteroidal selective estrogen receptor (ER) alpha agonist with potential antineoplastic activity. Upon administration of GTx-758, this agent suppresses the secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the pituitary gland through feedback inhibition. In males, the inhibition of LH secretion prevents the synthesis of androgens, including testosterone, by the testes. This may result in suppressed total serum testosterone to the levels observed in castration.
estrogen receptor degrader AC699
An orally bioavailable estrogen receptor (ER)-targeted chimeric protein degrader composed of ligands of ER and cereblon (CRBN) E3 ubiquitin ligase, with potential antineoplastic activity. Upon oral administration of ER degrader AC699, the ER-targeting moiety targets and binds to ER, and the CRBN-binding moiety recruits CRBN, a component of the CRL4-CRBN E3 ubiquitin ligase complex. This catalyzes ubiquitination and proteasome-mediated degradation of ER, prevents ER-mediated signaling, and inhibits both the growth and survival of ER-expressing cancer cells. ER is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation.
Estrosyn
(Other name for: diethylstilbestrol)
esuberaprost sodium
The sodium salt form of esuberaprost, the 314-d isomer of beraprost, with potential anti-inflammatory activity. Upon administration, esuberaprost activates the prostaglandin E2 receptor EP4 subtype (PTGER4; EP4), and inhibits the nuclear factor-kappa B (NF-kB) pro-inflammatory pathway. This may attenuate cytokine production and decrease inflammation.
eszopiclone
A nonbenzodiazepine cyclopyrrolone and active dextrorotatory stereoisomer of zopiclone with hypnotic and sedative activities and without significant anxiolytic activity. Although the exact mechanism of action remains to be fully elucidated, eszopiclone binds to and activates the omega-1 subtype of the alpha subunit of the gamma-aminobutyric acid-benzodiazepine GABA receptor complex (GABA-A), a chloride ionophore complex in the central nervous system (CNS). This leads to the opening of chloride channels, causing hyperpolarization and inhibition of neuronal firing, which may result in a hypnotic effect and the induction of sleep.
etalocib
A second-generation selective leukotriene B4 receptor (LTB4R) antagonist with potential antineoplastic activity. Although the exact underlying mechanism through which LY293111 exerts its effects has not been fully elucidated, this agent selectively binds to and blocks LTB4Rs, thereby inhibiting the downstream signalling pathway. LY29311 has been shown to induce apoptosis and inhibits cellular proliferation in LTB4R expressing cells, such as pancreatic cancer cells.
etanercept
A recombinant soluble dimeric fusion protein consisting of the extracellular ligand-binding region of recombinant human tumor necrosis factor (rhTNF) receptor attached to the constant (Fc) region of human immunoglobulin G (FcIgG). The receptor moiety of etanercept binds to circulating TNF (2 molecules of TNF per receptor) and inhibits its attachment to endogenous TNF cell surface receptors, thereby rendering TNF inactive and inhibiting TNF-mediated mechanisms of inflammation.
etanidazole
A 2-nitroimidazole with radiosensitizing properties. Etanidazole depletes glutathione and inhibits glutathione transferase, thereby enhancing the cytotoxicity of ionizing radiation. This agent may also be useful as an imaging agent for identifying hypoxic, drug-resistant regions of primary tumors or metastases.
etaracizumab
A humanized monoclonal IgG1 antibody directed against the vitronectin receptor alpha v beta 3 integrin. Etaracizumab blocks the binding of ligands, such as vitronectin, to alpha v beta 3 integrin, resulting in inhibition of angiogenesis and metastasis. Alpha v beta 3 integrin is a cell adhesion and signaling receptor that is expressed on the surface of tumor vessel endothelial cells, some tumor cells, and a number of other cell types.
etavopivat
An orally available, small-molecule allosteric activator of the selective red blood cell (RBC) isoform of pyruvate kinase (PK-R), with potential to improve symptoms in sickly cell disease (SCD) patients. Upon oral administration, etavopivat allosterically binds to and activates PK-R, thereby enhancing the glycolytic pathway activity in RBCs. This improves adenosine triphosphate (ATP) levels and reduces 2,3-diphosphoglycerate (2,3-DPG) levels in RBCs. This results in increased oxygen affinity, improved RBC deformability, decreased sickle RBC hemolysis, increased hemoglobin (Hb) levels and improved RBC membrane function. Mutations in PK-R cause deficiency in PK-R which prevents adequate RBC glycolysis, leading to a buildup of the upstream glycolytic intermediate 2,3-DPG and deficiency in the PK-R product ATP.
etelcalcetide
A calcimimetic and calcium-sensing receptor (CaSR) agonist composed of a synthetic peptide comprised of seven D-amino acids that can be used to treat secondary hyperparathyroidism (sHPT) in hemodialysis patients with chronic kidney disease (CKD). Upon intravenous administration, etelcalcetide mimics calcium and allosterically binds to and activates the CaSR expressed by the parathyroid gland. This suppresses the synthesis and secretion of parathyroid hormone (PTH), thereby reducing PTH levels and lowering serum calcium and phosphorus levels. Elevated PTH is often observed in patients with CKD and is associated with dysregulated calcium-phosphate homeostasis.
ethacrynic acid
An aryloxy-acetic acid derivative belonging to the class of loop diuretics. Ethacrynic acid interferes with the chloride binding site of the Na+, K+, Cl- cotransporter system in the thick ascending loop of Henle, thereby inhibiting the reabsorption of sodium, potassium, and chloride ions. This leads to an increase in the excretion of sodium, potassium, chloride, calcium, and water.
ethambutol
An antibiotic with bacteriostatic, antimicrobial and antitubercular properties. Ethambutol interferes with the biosynthesis of arabinogalactan, a major polysaccharide of the mycobacterial cell wall. It inhibits the polymerization of cell wall arabinan of arabinogalactan and lipoarabinomannan by blocking arabinosyl transferases and induces the accumulation of D-arabinofuranosyl-P-decaprenol, an intermediate in arabinan biosynthesis. This results in halting bacterial growth.
ethanol-containing nasal solution
An intranasal solution containing ethanol with antimicrobial activity. Upon intranasal application, ethanol-containing nasal solution may prevent colonization of the nasal cavity. The antimicrobial effect of ethanol is due, in part, to its denaturing of microbial proteins.
ethaselen
An orally bioavailable organoselenium inhibitor of thioredoxin reductase 1 (TrxR1), with potential antineoplastic activity. Upon oral administration, ethaselen specifically binds to the selenocysteine-cysteine redox pair in the C-terminal active site of TrxR1 and inhibits its activity, which may result in growth inhibition and the induction of apoptosis in TrxR1-overexpressing tumor cells. TrxR1, upregulated in many cancer cell types, plays a key role in various redox-dependent cellular pathways, regulates transcription factor activity, inhibits apoptosis, and promotes cell growth and survival.
Ethinoral
(Other name for: ethinyl estradiol)
ethinyl estradiol
A semisynthetic estrogen. Ethinyl estradiol binds to the estrogen receptor complex and enters the nucleus, activating DNA transcription of genes involved in estrogenic cellular responses. This agent also inhibits 5-alpha reductase in epididymal tissue, which lowers testosterone levels and may delay progression of prostatic cancer. In addition to its antineoplastic effects, ethinyl estradiol protects against osteoporosis. In animal models, short-term therapy with this agent has been shown to provide long-term protection against breast cancer, mimicking the antitumor effects of pregnancy.
ethinyl estradiol/levonorgestrel
A combination of two steroid sex hormones, an estrogen and a progestin, used for contraceptive purposes. Estradiol, the endogenous counterpart of ethinyl estradiol (EE), is the principal, most potent estrogen hormone produced by the ovaries and is vital to the maintenance of fertility and secondary sexual characteristics in females. Levonorgestrel is a synthetic progestogen. This drug combination prevents or delays ovulation and causes a variety of hormonal changes. Ethinyl estradiol inhibits the release of follicle stimulating hormone (FSH), thus suppressing the development of ovarian follicle; levonorgestrel inhibits the release of luteinizing hormone (LH), thus preventing ovulation. This combination of agents alters the endometrium in such a way as to discourage implantation.
ethinyl estradiol/norethindrone
An oral contraceptive formulation containing the semisynthetic estrogen, ethinyl estradiol, combined with the synthetic progestin, norethindrone, with estrogenic and progestogenic activities, respectively. Ethinyl estradiol binds to and activates intracellular estrogen receptors found in the reproductive tract and other estrogen-responsive tissues. The activated complex enters the nucleus, binds to the estrogen response elements on DNA, activates the transcription of genes involved in the maintenance of the female reproductive system, inhibits the release of follicle stimulating hormone (FSH) from the anterior pituitary, and suppresses the development of the ovarian follicle. Norethindrone binds to intracellular progesterone receptors in progesterone-responsive tissues, such as the pituitary and those found in the reproductive system, and the activated ligand/receptor complex interacts with specific progesterone response elements on DNA, which results in the alteration in protein synthesis, the inhibition of ovulation, an increase in cervical mucus production, the induction of the secretory phase of the endometrial cycle, and the inhibition of luteinizing hormone (LH) release. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system and alters the structure of the endometrium to discourage implantation.
ethiodized oil
A synthetic iodine addition product of the ethyl ester of the fatty acids of poppyseed oil. Ethiodized oil contains 37% organically bound iodine and is used as a diagnostic radiopaque medium or, labeled with I-131, as an antineoplastic agent. Selectively retained in tumor vessels for long periods, ethiodized oil is used for imaging organs such as liver, lung, stomach, and thyroid. Labeled with I-131 or other beta emitters (Y-90 or P-32), ethiodol can deliver a high internal radiation dose to certain tumors with minimal effect on healthy tissues.
ethosuximide
A succinimide with anticonvulsant activity. The exact mechanism of action is not entirely understood, but most likely ethosuximide exerts its effects by partial antagonism of T-type calcium channels of the thalamic neurons. This leads to a decrease in burst firing of thalamocortical neurons, which stabilizes the nerve activity in the brain and prevents seizures.
ethyl alcohol mouthwash
A mouthwash containing ethyl alcohol, with topical antibacterial activity. Upon rinsing the oral cavity with the ethyl alcohol mouthwash, ethyl alcohol denatures bacterial proteins, and dissolves and disrupts the bacterial lipid membrane, thereby killing the bacteria. This reduces oral colonization with harmful bacteria and may prevent oral mucositis.
ethyl icosapentate
A highly purified omega-3 fatty acid that can decrease serum triglyceride levels. Ethyl icosapentate reduces serum triglycerides without an increase in LDL cholesterol, but increases the cholesterol and triglyceride content in skeletal muscle.
ethylene-vinyl alcohol copolymer-based embolic agent
A non-adhesive, non-absorbable, permanent liquid embolic agent comprised of ethylene vinyl alcohol (EVOH) copolymer dissolved in dimethyl sulfoxide (DMSO), and of micronized tantalum powder that can be used to occlude blood vessels. Upon administration of the EVOH-based embolic agent, contact with fluids, such as blood, induces the solidification of EVOH into a sponge-like material. This causes occlusion of blood vessels and prevents blood flow to the treated area.
Ethyol
(Other name for: Amifostine)
Etidronate-Cytarabine Conjugate MBC-11
A synthetic conjugate composed of the bisphosphonate etidronate linked to the cytostatic agent and antimetabolite cytarabine, with potential antineoplastic and antiresorptive activities. Upon intravenous administration of the etidronate-cytarabine conjugate MBC-11, the etidronate moiety targets bone and the two moieties are released upon hydrolysis. Etidronate binds to hydroxyapatite crystals in bone tissues and prevents its resorption. This prevents bone destruction and induces bone cell mineralization. In addition, the bone-targeting nature of this agent allows for the accumulation of cytarabine in bone tissue, where it is able to exert its antitumor effect locally by competing with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis, while reducing systemic exposure. This leads to a destruction of bone-associated tumor cells, an inhibition of tumor cell proliferation and bone metastasis, and prevents tumor-mediated bone destruction.
etigilimab
A monoclonal antibody targeting the human 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, etigilimab binds to TIGIT expressed on various immune cells, including T cells, and prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; 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-positive T cells, and leads to CD226 dimerization and CD226-mediated signaling. This activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family 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.
Etilamide
(Other name for: buserelin)
etirinotecan pegol
An extended-release (ER) formulation composed of irinotecan, which is a semisynthetic derivative of camptothecin and a topoisomerase I-inhibitor prodrug, that is conjugated, via a proprietary biodegradable ester-based linker, to polyethylene glycol (PEG), with antineoplastic activity. Upon administration of etirinotecan pegol (EP), the agent penetrates into the leaky tumor vasculature and accumulates in the tumor. The linker slowly hydrolyzes and releases irinotecan, which leads to sustained exposure of the tumor to irinotecan. In turn, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN38) by a carboxylesterase. SN38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA; this results in DNA breaks that inhibit DNA replication and trigger apoptosis. Pegylation provides improved systemic exposure, increases drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic effects while lowering the toxicity profile.
etodolac
A pyranocarboxylic acid and non-steroidal anti-inflammatory drug (NSAID) with antipyretic and analgesic activities. Etodolac inhibits the activity of cyclooxygenase I and II, thereby preventing the formation of prostaglandin which is involved in the induction of pain, fever, and inflammation. It also inhibits platelet aggregation by blocking platelet cyclooxygenase and the subsequent formation of thromboxane A2.
Etopophos
(Other name for: etoposide phosphate)
etoposide
A semisynthetic derivative of podophyllotoxin, a substance extracted from the mandrake root Podophyllum peltatum. Possessing potent antineoplastic properties, etoposide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
etoposide phosphate
A phosphate salt of a semisynthetic derivative of podophyllotoxin. Etoposide binds to the enzyme topoisomerase II, inducing double-strand DNA breaks, inhibiting DNA repair, and resulting in decreased DNA synthesis and tumor cell proliferation. Cells in the S and G2 phases of the cell cycle are most sensitive to this agent.
etoposide toniribate
A prodrug of etoposide, a semisynthetic derivative of podophyllotoxin extracted from the mandrake root Podophyllum peltatum, with potential antineoplastic activity. Upon intravenous administration of etoposide toniribate, etoposide is released after enzymatic cleavage of CAP7.1 by specific carboxylesterases (CE) 1 and 2, which are upregulated in certain tumor cell types. Etoposide acts primarily in the G2 and S phases of the cell cycle. This drug binds to and inhibits topoisomerase II, an enzyme elevated in tumor cells. This results in the accumulation of double-strand DNA breaks, the inhibition of DNA replication and transcription and the induction of apoptotic cell death. The tumor-specific activation of etoposide increases its efficacy while lowering its systemic toxicity.
etoricoxib
A synthetic, nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, analgesic ,and potential antineoplastic properties. Etoricoxib specifically binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in inhibition of the conversion of arachidonic acid into prostaglandins. Inhibition of COX-2 may induce apoptosis and inhibit tumor cell proliferation and angiogenesis.
Etrenol
(Other name for: hycanthone)
Etretin
(Other name for: acitretin)
etrumadenant
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 administration, etrumadenant 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 AB928 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.
Ets-family transcription factor inhibitor TK216
A proprietary biologic that inhibits the transcriptional-promoting activity of E26 transformation-specific (Ets, E-twenty-six) family transcription factors, with potential antineoplastic activity. Although the exact mechanism(s) of action through which this agent exerts its effect has yet to be fully elucidated, upon administration, Ets-family transcription factor inhibitor TK216 inhibits transcriptional activation mediated by Ets family proteins, including the oncogenic Ewing sarcoma breakpoint region 1/Friend leukemia virus integration 1 (EWSR1/FLI1; EWS/FLI1) fusion protein. This agent may both inhibit the malignant downstream effects mediated by genomic rearrangements that result in the overexpression of Ets family transcription factors and decrease tumor cell growth and proliferation. A chromosomal translocation t(11;22)(q24;q12) fuses the EWSR1 gene and the FLI1 gene and encodes the EWSR1/FLI1 fusion protein, which is an oncoprotein expressed by peripheral primitive neuroectodermal (pPNET) tumors.
Eucerin
(Other name for: therapeutic lotion)
Eucrisa
(Other name for: crisaborole ointment)
eurestobart
A humanized immunoglobulin G1 (IgG1) 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, eurestobart 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.
Evaux spring water-based cream
A cream containing Evaux thermal spring water, with potential moisturizing and skin protecting activities. Upon application to the skin, Evaux spring water-based cream forms a protective barrier, which prevents water loss, provides moisture to the skin, protects the skin from damage, and soothes irritated skin. The Evaux thermal spring water contains the trace elements lithium and manganese which may help heal the skin.
Evaux spring water-based topical spray
A skin spray composed of Evaux thermal spring water, the emulsifier polysorbate 20, the preservatives phenoxyethanol and chlorphenesin, zinc gluconate, and the moisturizer caprylyl glycol with prophylactic and calming activity. Evaux thermal spring water is rich in mineral elements particularly of lithium, strontium and manganese. When sprayed directly onto the skin or scalp, this topical spray may have a calming, moisturizing, healing and nurturing effect. This agent may prevent or decrease skin rashes associated with the administration of EGFR inhibitors or with radiochemotherapy-induced skin reactions.
Evaux thermal spring water-based solution
A topical solution containing Evaux thermal spring water, with potential moisturizing and skin protecting activities. Upon application to the nails and surrounding skin, Evaux spring water-based solution forms a film on the nails that serves as a protective barrier. This prevents water loss from, provides moisture to, and strengthens the nails, and protects them from damage. The solution also relieves pain caused by cracked, peeled, thinning or soft nails. Evaux thermal spring water contains the elements lithium, manganese and strontium which may help heal the nails and prevent onycholysis. It also contains chlorphenesin and piroctone olamine, both of which have antifungal activity. Some chemotherapy and/or radiation therapy can induce damage to the nails.
Evenity
(Other name for: romosozumab)
everolimus
A derivative of the natural macrocyclic lactone sirolimus with immunosuppressant and anti-angiogenic properties. In cells, everolimus binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate an immunosuppressive complex that binds to and inhibits the activation of the mammalian Target of Rapamycin (mTOR), a key regulatory kinase. Inhibition of mTOR activation results in the inhibition of T lymphocyte activation and proliferation associated with antigen and cytokine (IL-2, IL-4, and IL-15) stimulation and the inhibition of antibody production.
everolimus tablets for oral suspension
Tablets for oral suspension containing everolimus, a derivative of the natural macrocyclic lactone sirolimus, with immunosuppressive and antineoplastic activities. After suspension of the everolimus tablets in water and oral administration, this agent inhibits the activation of the serine/threonine kinase mammalian target of rapamycin (mTOR) by binding to mTOR's cytosolic receptor immunophilin FK Binding Protein-12 (FKBP-12). Inhibition of the mTOR complex may result in the inhibition of the phosphatidylinositol 3 kinase/Akt/mTOR pathway and an inhibition in the expression of vascular endothelial cell growth factor (VEGF) and hypoxia-inducible factor. Ultimately, this may result in decreased tumor cell proliferation and tumor angiogenesis. This pediatric formulation can dissolve easily in a small volume of water making it easier to swallow and is available in smaller dose increments thereby allowing for greater dosing flexibility.
everolimus/exemestane regimen
A regimen consisting of everolimus and exemestane that is used as a treatment for breast cancer.
Everone
(Other name for: testosterone enanthate)
evexomostat
A synthetic copolymer-drug conjugate of a fumagillin-derived methionine aminopeptidase 2 (MetAP2) inhibitor conjugated to the bio-compatible polymer poly(N-(hydroxypropyl)methacrylamide) (HPMA), with potential antineoplastic activity. Upon administration of SDX-7320, the active moiety SDX7539 is released inside the tumor cells. SDX7539 binds to and inhibits MetAP2, which prevents MetAP2-mediated signal transduction pathways and results in tumor cell death. MetAP2, a member of the dimetallohydrolase family upregulated in certain tumor cell types, plays a key role in angiogenesis, proliferation and survival. Polymer conjugation reduces systemic drug exposure and increases this agent's efficacy as compared to non-polymer conjugates.
Evista
(Other name for: raloxifene hydrochloride)
eVLP CMV gB-pp65 plus GM-CSF VBI-1901
A cancer vaccine composed of enveloped virus-like particles (eVLPs) containing the human cytomegalovirus (CMV) antigens glycoprotein B (gB) and phosphoprotein 65 (pp65; UL83) that are combined with the immunoadjuvant granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulatory and antineoplastic activities. Upon intradermal administration of VBI-1901, the eVLPs are taken up by and activate immune cells, such as dendritic cells (DCs), thereby stimulating the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against CMV gB and pp65-expressing tumor cells. This may lyse and inhibit the proliferation of CMV-infected cancer cells. eVLPs, derived from viral structural proteins, stimulate the immune system and promote CTL responses. CMV gB and pp65 are expressed in certain tumor cell types, such as glioblastoma multiforme (GBM). GM-CSF stimulates the immune system and potentiates the antitumor immune response.
evocalcet
An orally available calcium receptor (CaR) modulator, with potential calcimimetic activity. Upon administration, evocalcet allosterically binds to and inhibits the activity of CaR, thereby suppressing the production of serum parathyroid hormone (PTH) and prevents the PTH-mediated efflux of calcium from bone and normalizes calcium levels.
evofosfamide
A hypoxia-activated prodrug of the cytotoxin bromo-isophosphoramide mustard (Br-IPM) conjugated with 2-nitroimidazole, with potential antineoplastic activity. When exposed to hypoxic conditions, such as those found in hypoxic tumors, the 2-nitroimidazole moiety of evofosfamide is reduced. This releases the DNA-alkylating Br-IPM moiety, which introduces intra- and inter-strand DNA crosslinks in nearby cells; the crosslinks inhibit both DNA replication and cell division, and may lead to apoptosis of cells in the tumor. The inactive form of the prodrug is stable under normoxic conditions, which may limit systemic toxicity.
Evomela
(Other name for: melphalan hydrochloride)
EvoNail
(Other name for: Evaux thermal spring water-based solution)
Evorpacept
A variant of signal regulatory protein alpha (SIRPa) that antagonizes the human cell surface antigen CD47, with potential phagocytosis-inducing, immunostimulating and antineoplastic activities. Upon administration, evorpacept binds to CD47 expressed on tumor cells and prevents the interaction of CD47 with its ligand 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 the pro-phagocytic signal 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 cytotoxic T-lymphocyte (CTL) 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.
Evoskin cream
(Other name for: Evaux spring water-based cream)
Evoxac
(Other name for: cevimeline hydrochloride)
Evusheld
(Other name for: cilgavimab/tixagevimab)
ex vivo-activated autologous lymph node lymphocytes
Autologous human lymph node T-lymphocytes, with potential immunostimulatory and antineoplastic activity. Upon collection of immune cells from the tumor-draining lymph node, the human lymph node lymphocytes are activated with anti-CD3/anti-CD28 microbeads, cultured with recombinant, human interleukin-2 (IL-2), expanded and isolated ex vivo. Upon reintroduction into the patient, the ex vivo-activated autologous lymph node lymphocytes recognize and lyse the tumor cells.
ex vivo-expanded allogeneic gamma 9 delta 2 T cells
A preparation of a subset of ex vivo-expanded, allogeneic T lymphocytes that express gamma 9 delta 2 T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration of the ex vivo-expanded allogeneic gamma 9 delta 2 T cells, 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. Gamma 9 delta 2 T cells, a subset of gamma delta T cells, may have a stronger association with antitumor immune responses compared with other gamma delta T-cell subtypes.
ex vivo-expanded autologous T cells IMA101
A preparation of autologous cytotoxic T lymphocytes, specifically recognizing certain tumor-associated antigens (TAAs), with potential antineoplastic activity. The endogenous T cells are isolated, expanded ex vivo, and reintroduced back into the patient. Upon administration, the ex vivo-expanded autologous T cells IMA101 target and kill tumor cells. The T cells are analyzed beforehand for their ability to specifically recognize certain TAAs, based on a proprietary antigen warehouse.
ex vivo-expanded HER2-specific T cells
T cells specific for the human epidermal growth factor receptor 2 (HER2) with potential immunopotentiating activity. T cells directed against HER2, overexpressed on many tumor cells, are collected from HER2-expressing tumor tissue, expanded ex vivo and, then re-introduced in the patient. Re-introduction of ex vivo-expanded HER2-specific T cells may enhance the cytotoxic T cell response against tumor cells overexpressing HER2, resulting in inhibition of tumor growth.
exatecan mesylate
A semisynthetic, water-soluble derivative of camptothecin with antineoplastic activity. Exatecan mesylate inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA and inhibiting religation of DNA breaks, thereby inhibiting DNA replication and triggering apoptotic cell death. This agent does not require enzymatic activation and exhibits greater potency than camptothecin and other camptothecin analogues.
Exelon
(Other name for: rivastigmine tartrate)
exemestane
A synthetic androgen analogue. Exemestane 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.
exenatide
A 39 amino acid peptide and synthetic version of exendin-4, a hormone found in the saliva of the venomous lizard Gila monster, with insulin secretagogue and antihyperglycemic activity. Exenatide is administered subcutaneously and mimics human glucagon-like peptide-1 (GLP-1). Compared to GLP-1, exenatide has a longer half-life of 2.4 hours.
Exherin
(Other name for: ADH-1)
exicorilant
An orally available, selective glucocorticoid receptor (GR) antagonist, with potential antineoplastic activity. Upon oral administration, exicorilant competitively and selectively binds to GRs, inhibiting the activation of GR-mediated proliferative and anti-apoptotic gene expression pathways. The GR, a member of the nuclear receptor superfamily of ligand-dependent transcription factors, is overexpressed in certain tumor types and may be associated with tumor cell proliferation and treatment resistance. Inhibition of GR activity may potentially slow tumor cell growth and disease progression in certain cancers.
exisulind
An inactive metabolite of the nonsteroidal, anti-inflammatory agent sulindac. After oral administration, sulindac undergoes extensive biotransformation including irreversible oxidation to sulindac sulfone. Approximately, one half of an administered dose of sulindac is eliminated through the urine, mostly as the conjugated sulfone metabolite.
Exjade
(Other name for: deferasirox)
Exkivity
(Other name for: mobocertinib succinate)
exlinkibart
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, exlinkibart targets and binds to CD137, thereby activating CD137 expressed on avariety 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.
exoIL-12
(Other name for: IL-12-expressing exosome CDK-003)
exoIL-12
(Other name for: IL-12-expressing exosome CDK-003)
expanded cord blood stem cells mixed with engineered human endothelial cells AB-110
A population of ex vivo expanded, CD34-positive-enriched hematopoietic progenitor cells (HPCs), which are derived from allogeneic human umbilical cord blood (UCB), and are co-cultured and expanded with a proprietary preparation of human endothelial cells (ECs), which are genetically modified with an adenovirus (Ad) vector that includes the Ad E4 region that encodes the ORF1 (E4ORF1) gene, that can be used for transplantation. Upon transplantation of the expanded cord blood stem cells mixed with engineered human ECs AB-110, the UCB-derived cells can differentiate into a variety of cell types and promote blood cell recovery. Compared to bone marrow transplants, these HPCs demonstrate a decreased risk of causing graft-versus-host disease (GvHD), increase survival and enhance the potential for transplant and engraftment in any given patient as there is no need for a matched donor. Compared to HPCs alone, inclusion of the ECs increases blood stem cell count, enhances engraftment potential and increases the chances for blood cell recovery, thereby further increasing the potential for a successful cord blood transplantation. Insertion of the Ad E4ORF1 gene enhances survival and replication of the ECs ex vivo, preserves the ECs' vascular functions and improves the ability of the ECs to secrete angiocrines, which promotes stem cell proliferation and increases engraftment.
expanded/activated gamma/delta T lymphocytes
A preparation of gamma delta T lymphocytes derived from donor T cells that have been expanded and activated ex-vivo and further depleted of alpha and beta T-cell receptors (TCRs), with potential immunomodulating and antineoplastic activities. Upon administration, these expanded/activated gamma delta (EAGD) 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.
Exparel
(Other name for: bupivacaine hydrochloride liposome injectable suspension)
extended release bupivacaine hydrochloride resorbable matrix formulation
An extended release (ER) injectable formulation composed of the hydrochloride salt form of bupivacaine, an amide-type, long-acting local anesthetic, in a resorbable sucrose acetate isobutyrate-based matrix, with analgesic activity. Following administration in or around a specific site, ER bupivacaine is released from the matrix over an extended period of time. Upon release, bupivacaine reversibly binds to specific voltage-gated sodium ion channels in the neuronal membrane, resulting in a decrease in the voltage-dependent membrane permeability to sodium ions, membrane destabilization, and depolarization inhibition thus disrupting nerve impulse conduction. This eventually leads to a reversible loss of sensation. This formulation may provide pain relief up to 72 hours.
extended release metformin hydrochloride
An extended-release (ER) tablet composed of the hydrochloride salt form of the biguanide metformin, with antihyperglycemic and potential prostate-cancer protective and antineoplastic activities. Upon oral administration, metformin targets and inhibits complex I (NADPH:ubiquinone oxidoreductase) of the mitochondrial respiratory chain and increases the cellular adenosine monophosphate (AMP) to adenosine triphosphate (ATP) ratio leading to activation of AMP-activated protein kinase (AMPK). This modulates AMPK-mediated transcription of target genes, which prevents hepatic gluconeogenesis, decreases intestinal absorption of glucose, enhances insulin sensitivity and fatty acid oxidation, and increases glucose uptake and utilization in target tissues. This lowers blood glucose levels. Metformin may exert antineoplastic effects through AMPK-mediated or AMPK-independent inhibition of mammalian target of rapamycin (mTOR), which is up-regulated in many cancer tissues. It also reduces cyclin D1. This inhibits cancer cell proliferation. Furthermore, this agent also inhibits tumor cell migration and invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression which is mediated through the suppression of transcription activator protein-1 (AP-1) activation. Also, metformin reduces hyperinsulinemia which may contribute to an anti-tumor effect. Metformin may increase the prostate-specific antigen (PSA) doubling time and may lower serum PSA levels.
extended-release flucytosine
An extended release (ER) oral tablet that contains flucytosine (5-FC), a fluorinated cytosine analog, with antifungal activity and potential anti-cancer activity. Following oral administration of ER 5-FC, the 5-FC is deaminated to its active metabolite 5-fluorouracil (5-FU). 5-FU replaces uracil during RNA synthesis, which consequently inhibits downstream protein synthesis. In addition, 5-FU is metabolized further to 5-fluorodeoxyuridylic acid monophosphate, which inhibits thymidylate synthetase. Inhibition of this enzyme interrupts nucleotide synthesis, DNA replication and cell proliferation. Negative regulation of protein synthesis, DNA replication and cell proliferation can lead to cell death. Following ingestion of ER 5-FC, intravenous injection of a retroviral vector encoding cytosine deaminase (TC 511) at a tumor site may result in higher local concentrations of 5-FU and its metabolites, and increased tumor cell death than other 5-FU treatment regimens.
extended-release galantamine hydrobromide
An extended-release (ER) formulation of the hydrobromide salt form of galantamine, a tertiary alkaloid obtained synthetically or naturally from the bulbs and flowers of Narcissus and several other genera of the Amaryllidaceae family, with anticholinesterase and neurocognitive-enhancing activities. Upon administration, galantamine competitively and reversibly inhibits acetylcholinesterase, thereby increasing the concentration and enhancing the action of acetylcholine (Ach). In addition, galantamine is a ligand for nicotinic acetylcholine receptors, which may increase the presynaptic release of Ach and activate postsynaptic receptors. This agent may improve neurocognitive function in mild and moderate Alzheimer's disease and may, through its Ach stimulating effect on nicotinic receptors, help quit smoking and reduce abstinence-induced cognitive symptoms that promote smoking relapse.
extended-release granisetron polymer formulation
An extended-release (ER), polymer-based injectable formulation containing the indazole derivative granisetron, a selective serotonin (5-hydroxytryptamine; 5-HT) receptor type 3 (5-HT3) antagonist, with anti-emetic activity. Upon subcutaneous administration, granisetron is released from the polymer in a sustained manner, which is based upon the controlled hydrolysis of the polymers, and selectively binds to and inhibits the activity of the 5-HT3 receptors located peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone (CTZ) of the area postrema. By preventing stimulation of 5-HT3 receptors, granisetron is able to suppress chemotherapy-induced nausea and vomiting (CINV). Compared to the injection of granisetron alone, injection of the polymer-based formulation allows for therapeutic levels of granisetron over an extended period of time.
extended-release MetAP2 inhibitor APL-1501
An extended-release (ER) formulation of APL-1501, an orally available inhibitor of methionine aminopeptidase II type (MetAP2), with potential antiangiogenic and antineoplastic activities. Upon administration, ER MetAP2 inhibitor APL-1501 is released from the formulation over an extended period of time and targets, binds to and reversibly inhibits MetAP2, thereby preventing MetAP2-mediated signal transduction pathways. This may suppress endothelial cell growth and inhibit tumor angiogenesis, resulting in tumor cell death. MetAP2, a member of the dimetallohydrolase family, is upregulated in certain tumor cell types and plays a key role in angiogenesis, proliferation and survival. Compared to APL-1202, APL-1501 has improved pharmacokinetic (PK) characteristics. The ER formulation allows for controlled drug release, enhanced drug plasma exposure time and reduced medication intake frequency.
extended-release microsphere capsule-based oxycodone
A wax microsphere capsule formulation of oxycodone, a semi-synthetic, morphine-like opioid alkaloid, with analgesic activity. Upon administration, oxycodone exerts its analgesic activity by binding to the mu-receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opioids. Due to the unique formulation, extended-release microsphere capsule-based oxycodone may provide an identical pharmacokinetic profile regardless of whether the capsule is intact when ingested or if ingested via enteral feeding tube, leading to a predictable level of analgesia in patients that must be transitioned from oral to enteral administration.
extended-release onapristone
An extended-release (ER) formulation of onapristone, an orally bioavailable progesterone receptor (PR) antagonist, with antineoplastic activity. Onapristone binds to the PR and inhibits both PR activation and the associated expression of PR-responsive genes. This may inhibit PR-mediated proliferative effects in cancer cells overexpressing PR. PR is expressed on certain cancer cell types and plays a key role in proliferation and survival.
Extren
(Other name for: aspirin)
Eylea
(Other name for: ziv-aflibercept)
ezabenlimab
A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, ezabenlimab selectively binds to and blocks the activation of PD-1, an immunoglobulin (Ig) superfamily transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T cells and T-cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.
ezatiostat hydrochloride
The hydrochloride salt of a liposomal small-molecule glutathione analog inhibitor of glutathione S-transferase (GST) P1-1 with hematopoiesis-stimulating activity. After intracellular de-esterification, the active form of ezatiostat binds to and inhibits GST P1-1, thereby restoring Jun kinase and MAPK pathway activities and promoting MAPK-mediated cellular proliferation and differentiation pathways. This agent promotes the proliferation and maturation of hematopoietic precursor cells, granulocytes, monocytes, erythrocytes and platelets.
ezetimibe
An azetidinone derivative and a cholesterol absorption inhibitor with lipid-lowering activity. Ezetimibe appears to interact physically with cholesterol transporters at the brush border of the small intestine and inhibits the intestinal absorption of cholesterol and related phytosterols. As a result, ezetimibe causes a decrease in the level of blood cholesterol or an increase in the clearance of cholesterol from the bloodstream. Overall, the following effects observed are a reduction of hepatic cholesterol stores and a reduction of total cholesterol, LDL cholesterol, and other triglycerides in the blood.
ezetimibe/simvastatin
An orally bioavailable combination agent containing the cholesterol absorption inhibitor ezetimibe and the hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin, with lipid-lowering activity. Upon oral administration, ezetimibe binds to the sterol transporter Niemann-Pick C1-Like 1 (NPC1L1) at the brush border of the small intestine and inhibits the intestinal absorption of biliary and dietary cholesterol and related phytosterols. This decreases blood cholesterol levels, decreases the delivery of intestinal cholesterol to the liver, reduces hepatic cholesterol stores and enhances the clearance of cholesterol from the bloodstream. Upon administration of simvastatin and subsequent hydrolyzation to its active beta-hydroxyacid form, this statin competitively inhibits HMG-CoA reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, which is an essential step in cholesterol synthesis. Ezetimibe and simvastatin together reduce blood levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), very-low-density lipoproteins (VLDL), and apolipoprotein B (Apo B), and increase the plasma concentration of high-density lipoprotein cholesterol (HDL-C). Higher cholesterol blood levels appear to be associated with an increased risk in the proliferation of certain cancer cells, such as prostate cancer cells.
EZH1/2 inhibitor HH2853
An orally bioavailable inhibitor of the histone lysine methyltransferases enhancer of zeste homolog 1 (EZH1) and 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH1/2 inhibitor HH2853 inhibits the activity of both wild-type and mutated forms of EZH1 and EZH2. Inhibition of EZH1/2 specifically prevents the methylation of lysine 27 on histone H3 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways, enhances transcription of certain target genes, and results in decreased proliferation of EZH1/2-expressing cancer cells. EZH1/2, histone lysine methyltransferase (HMT) class enzymes and catalytic subunits of the polycomb repressive complex 2 (PRC2), are overexpressed or mutated in a variety of cancer cells and play key roles in tumor cell proliferation, progression, stem cell self-renewal and migration.
EZH2 inhibitor CPI-1205
An orally available selective inhibitor of the histone lysine methyltransferase EZH2, with potential antineoplastic activity. Upon oral administration, CPI-1205 selectively inhibits the activity of both wild-type and mutated forms of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, a histone lysine methyltransferase (HMT) class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.
EZH2 inhibitor PF-06821497
An orally available selective inhibitor of the histone lysine methyltransferase (HMT) enhancer of zeste homolog 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH2 inhibitor PF-06821497 selectively targets, binds to and inhibits the activity of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, an HMT class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.
EZH2 inhibitor SHR2554
An orally available selective inhibitor of the histone lysine methyltransferase (HMT) enhancer of zeste homolog 2 (EZH2), with potential antineoplastic activity. Upon oral administration, EZH2 inhibitor SHR2554 selectively targets, binds to and inhibits the activity of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, an HMT class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.
ezurpimtrostat
An orally bioavailable, quinolone-derived, small molecule inhibitor of palmitoyl-protein thioesterase 1 (PPT1), with potential antineoplastic activity. Upon oral administration, ezurpimtrostat targets and inhibits the activity of PPT1 and induces lysosomal disruption, which results in the inhibition of autophagy and the induction of apoptosis via caspase activation. This may inhibit tumor cell proliferation and tumor growth. PPT1, a lysosomal thioesterase that plays an important role in lysosomal function and autophagy, is overexpressed in certain cancers.