NCI Drug Dictionary

280 results found for: O

O6-benzylguanine: A guanine analogue with antineoplastic activity. O(6)-benzylguanine binds the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT), transferring the benzyl moiety to the active-site cysteine and resulting in inhibition of AGT-mediated DNA repair. Co-administration of this agent potentiates the effects of other chemotherapeutic agents that damage DNA.
oat biscuit: A biscuit containing oats.
obatoclax mesylate: The mesylate salt of obatoclax, a synthetic small-molecule inhibitor of the bcl-2 family of proteins with potential pro-apoptotic and antineoplastic activities. Obatoclax binds to members of the Bcl-2 protein family, preventing the binding of these anti-apoptotic proteins to the pro-apoptotic proteins Bax and Bak and so promoting the activation of the apoptotic pathway in Bcl-2-overexpressing cells. The Bcl-2 family of proteins (bcl-2, bcl-xl, bcl-w, and Mcl-1) are overexpressed in a wide variety of cancers, including those of the lymphatic system, breast, lung, prostate, and colon.
obecabtagene autoleucel: A preparation of autologous T lymphocytes that have been genetically modified and transduced with a lentiviral vector expressing a second-generation chimeric antigen receptor (CAR), CAT-41BBz CAR, targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, obecabtagene autoleucel target and bind to CD19-expressing tumor cells. This results in a cytotoxic T-lymphocyte (CTL) response against CD19-expressing tumor cells and tumor cell lysis. CD19, cluster of differentiation 19, is a B-cell-specific cell surface antigen overexpressed in B-cell lineage tumors. The CAT-41BBz CAR has a faster off-rate compared with FMC63-41BBz CAR. This may minimize cytokine release and reduce toxicities, and enhance persistence of the CAR T cells.
obefazimod: An orally available, small molecule binder of the cap binding complex (CBC) 80/20, with potential antiviral and anti-inflammatory activities. Upon oral administration, obefazimod binds to the CBC, a complex at the 5'-end of the pre-mRNA transcript that promotes the initial interaction with transcription and processing machinery. This leads to a conformational change in the CBC and enhanced splicing of viral RNA variants and upregulation of the anti-inflammatory microRNA, miR-124, via splicing of a long noncoding RNA at the miR-124-1 locus. In human immunodeficiency virus type 1 (HIV-1)-infected cells, obefazimod interacts with the CBC of HIV-1 mRNA and inhibits viral replication by preventing Rev-mediated export of unspliced HIV-1 transcripts to the cytoplasm. Rev facilitates the nuclear export of unspliced or incompletely spliced viral pre-mRNAs, an essential step in HIV-1 replication. In inflammatory conditions, miR-124 reduces the production of various inflammatory mediators, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and C-C motif chemokine 2 (CCL2; MCP-1.). miR-124 plays a critical role in innate and adaptive immune responses and is a critical mediator of cholinergic anti-inflammatory action.
obeticholic acid: An orally bioavailable semi-synthetic bile acid derivative and an agonist of the nuclear bile acid receptor farnesoid X receptor (FXR) that may be used to lower hepatic exposure to bile acids. Upon oral administration, obeticholic acid targets and binds to FXR expressed in the liver and intestine, activating FXR-mediated bile acid, inflammatory, fibrotic, and metabolic pathways. This suppresses the production of bile acid in the hepatocytes and increases bile acid transport out of the hepatocytes, thereby reducing hepatic exposure to bile acids. FXR plays an important role in bile acid homeostasis and is involved in hepatic and intestinal inflammation and liver fibrosis.
obexelimab: A humanized immunoglobulin G1 (IgG1) noncytolytic monoclonal antibody directed against the B-cell-specific cell surface antigen CD-19, Fc-engineered for increased affinity to Fc gamma receptor IIB (FcgRIIB; CD32B), with potential immunomodulatory activity. Upon administration, obexelimab simultaneously targets and binds to both CD19 and FcgRIIB expressed on the surface of B cells, and inhibits B-cell receptor (BCR) signaling and the activity of B cells without depleting the B-cells. This may alleviate manifestations of autoimmune diseases including systemic lupus erythematosus (SLE). CD19 and FcgRIIB, both expressed on the surface of B-cells, play important roles in BCR signaling, and B-cell activity and survival.
obinutuzumab: A glycoengineered, humanized IgG1 monoclonal antibody with potential antineoplastic activity. Obinutuzumab, a third generation type II anti-CD20 antibody, selectivity binds to the extracellular domain of the human CD20 antigen on malignant human B cells. The Fc region carbohydrates of the antibody, enriched in bisected non-fucosylated glycosylation variants, contribute to its higher binding affinity for human FcgammaRIII receptors compared to non-glycoengineered antibodies, resulting in enhanced antibody-dependent cellular cytotoxicity (ADCC) and caspase-independent apoptosis. In addition, modification of elbow hinge sequences within the antibody variable framework regions may account for the strong apoptosis-inducing activity of R7159 upon binding to CD20 on target cells.
oblimersen sodium: The sodium salt of a phosphorothioate antisense oligonucleotide targeted to the initiation codon region of mRNA for the anti-apoptotic gene Bcl-2. Oblimersen inhibits Bcl-2 mRNA translation, which may result in decreased expression of the Bcl-2 protein and tumor cell apoptosis. This agent may enhance the efficacy of standard cytotoxic chemotherapy. The anti-apoptotic bcl-2 protein is an integral outer mitochondrial membrane protein (OMMP) that is overexpressed in some cancer cell types and is linked to tumor drug resistance.
Ocaliva: (Other name for: obeticholic acid)
ocaratuzumab: An Fc-engineered monoclonal antibody directed against human CD20 with potential antineoplastic activity. Ocaratuzumab specifically binds to CD20 antigen (B1), preventing mitogen-induced B-cell proliferation; inhibiting B-cell differentiation; and promoting antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis of B cells expressing CD20. The Fc portion of this monoclonal antibody has been engineered to possess a higher binding affinity for variant Fc receptors on T helper cells, resulting in an augmentation of the anti-tumor immune response. Because of Fc engineering, this agent may be significantly more potent than rituximab in inducing B cell-directed ADCC. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development.
Ocifisertib Fumarate: An orally available fumarate salt form of CFI-400945, a polo-like kinase 4 (PLK4) inhibitor with potential antineoplastic activity. Upon oral administration, polo-like kinase 4 inhibitor CFI-400945 selectively inhibits PLK4, which results in the disruption of mitosis and the induction of apoptosis. PLK4 inhibition also prevents cell division and inhibits proliferation of PLK4-overexpressing tumor cells. PLK4, a member of the polo family of serine/threonine kinases overexpressed in a variety of cancer cell types, plays a crucial role in the regulation of centriole duplication during the cell cycle.
ociperlimab: A humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, ociperlimab targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.
ocrelizumab: A Fc-modified, humanized monoclonal antibody directed against the B-cell CD20 cell surface antigen, with immunosuppressive activity. Ocrelizumab binds to CD20 on the surfaces of B-cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B-cells overexpressing CD20. The CD20 antigen, a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel, is found on over 90% of B-cells, B-cell lymphomas, and other lymphoid tumor cells of B-cell origin; it plays an important role in B-cell functioning.
Octagam: (Other name for: human immunoglobulin G)
Octreoscan: (Other name for: indium In 111 pentetreotide)
OctreoTher: (Other name for: yttrium Y 90-edotreotide)
octreotide acetate: The acetate salt of a synthetic long-acting cyclic octapeptide with pharmacologic properties mimicking those of the natural hormone somatostatin. Octreotide is a more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Similar to somatostatin, this agent also suppresses the luteinizing hormone response to gonadotropin-releasing hormone, decreases splanchnic blood flow, and inhibits the release of serotonin, gastrin, vasoactive intestinal peptide (VIP), secretin, motilin, pancreatic polypeptide, and thyroid stimulating hormone.
octreotide depot formulation CAM2029: A long-acting depot formulation of the synthetic octapeptide and somatostatin analog octreotide, with potential growth hormone (GH) secretion-inhibiting and antineoplastic activities. Upon subcutaneous administration of octreotide depot formulation CAM2029, octreotide binds to and activates somatostatin receptors (SSTRs), including subtypes 2 and 5, which leads to an inhibition in the secretion of human growth hormone (hGH) in the pituitary gland and results in decreased production of insulin-like growth factor (IGF-1). This may inhibit IGF-1-mediated cell signaling pathways, and lead to apoptosis. Octreotide may also block key survival pathways such as the phosphatidylinositol 3-kinase (PI3K) and the mitogen-activated protein kinase (MAPK) signaling pathways. In addition, octreotide may inhibit tumor angiogenesis. Altogether, this may result in tumor cell death and inhibition of tumor cell proliferation and angiogenesis. SSTRs are overexpressed by some neuroendocrine and non-neuroendocrine tumor cells, and GH is over-produced in the pituitary gland in acromegaly.
octreotide pamoate: A synthetic long-acting octapeptide analogue of endogenous somatostatin. Octreotide pamoate binds to somatostatin receptors expressed by some neuroendocrine and non-neuroendocrine tumor cells, thereby initiating somatostatin receptor-mediated apoptosis. Other possible antineoplastic activities of this agent include suppression of tumor angiogenesis and tumor growth-promoting insulin-like growth factor 1 (IGF-1).
octreotide sustained-release formulation Debio 4126: A sustained-release (SR) formulation of the synthetic octapeptide and somatostatin analog octreotide, with potential growth hormone (GH) secretion-inhibiting and antineoplastic activities. Upon intramuscular administration of octreotide SR formulation Debio 4126, octreotide binds to and activates somatostatin receptors (SSTRs), including subtypes 2 and 5, which leads to an inhibition in the secretion of human growth hormone (hGH) in the pituitary gland and results in decreased production of insulin-like growth factor (IGF-1). This may inhibit IGF-1-mediated cell signaling pathways, and lead to apoptosis. Octreotide may also block key survival pathways such as the phosphatidylinositol 3-kinase (PI3K) and the mitogen-activated protein kinase (MAPK) signaling pathways. In addition, octreotide may inhibit tumor angiogenesis. Altogether, this may result in tumor cell death and inhibition of tumor cell proliferation and angiogenesis. SSTRs are overexpressed by some neuroendocrine and non-neuroendocrine tumor cells, and GH is over-produced in the pituitary gland in acromegaly.
odanacatib: An inhibitor of cathepsin K with potential anti-osteoporotic activity. Odanacatib selectively binds to and inhibits the activity of cathepsin K, which may result in a reduction in bone resorption, improvement of bone mineral density, and a reversal in osteoporotic changes. Cathepsin K, a tissue-specific cysteine protease that catalyzes degradation of bone matrix proteins such as collagen I/II, elastin, and osteonectin plays an important role in osteoclast function and bone resorption.
odetiglucan: An injectable formulation of the polysaccharide beta-1,3/1,6 glucan derived from the cell wall of a strain from the yeast Saccharomyces cerevisiae and pathogen-associated molecular pattern (PAMP) molecule, with potential immunomodulating and antineoplastic activities. Upon administration, odetiglucan binds to innate immune effector cells through complement receptor 3 (CR3) and Fc gamma receptor IIA (FcgammaIIA; CD32A), thereby activating innate immune cells and enabling direct killing of tumor cells. In addition, odetiglucan repolarizes the immunosuppressive tumor microenvironment (TME), shifts the suppressive M2-state macrophages to a more M1 pro-inflammatory state, activates the maturation of antigen presenting cells (APCs), enables CD4 and CD8 T-cell expansion, and increases production of certain anti-tumor cytokines, such as interferon gamma (IFNg). Altogether, this induces and enhances anti-tumor immune responses.
Odomzo: (Other name for: sonidegib)
odronextamab: A bispecific, human monoclonal antibody with potential antineoplastic activity. Anti-CD20/CD3 monoclonal antibody REGN1979 contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CD20, a tumor-associated antigen that is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, odronextamab binds to both T cells and CD20-expressing tumor B cells, which cross-links the T cells to tumor cells, and may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B cells.
OEPA regimen: A regimen consisting of vincristine, etoposide, prednisone and doxorubicin for the treatment of male patients with childhood Hodgkin lymphoma.
Oestrogenine: (Other name for: diethylstilbestrol)
Oestromenin: (Other name for: diethylstilbestrol)
Oestromon: (Other name for: diethylstilbestrol)
ofatumumab: A fully human, high-affinity IgG1 monoclonal antibody directed against the B cell CD20 cell surface antigen with potential antineoplastic activity. Ofatumumab binds specifically to CD20 on the surfaces of B cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B cells overexpressing CD20. The CD20 antigen, found on over 90% of B cells, B cell lymphomas, and other B cells of lymphoid tumors of B cell origin, is a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel; it is exclusively expressed on B cells during most stages of B cell development.
OFF regimen: A chemotherapy regimen that includes leucovorin, 5-fluorouracil and oxaliplatin, which may be used in the treatment of pancreatic cancer.
ofloxacin: A fluoroquinolone antibacterial antibiotic. Ofloxacin binds to and inhibits bacterial topoisomerase II (DNA gyrase) and topoisomerase IV, enzymes involved in DNA replication and repair, resulting in cell death in sensitive bacterial species.
ofranergene obadenovec: A non-replicating adenovirus 5 (Ad-5, El-deleted) encoding a human Fas-chimera (Fas-c) transgene under the control of a modified murine pre-proendothelin-1 (PPE-1) promoter, with potential anti-angiogenic activity. Upon the administration of ofranergene obadenovec, the modified murine PPE-1 promoter is specifically activated in PPE-1-expressing angiogenic endothelial cells residing in the tumor microvasculature. Subsequently, the Fas-c pro-apoptotic transgene, containing the human tumor necrosis factor (TNF) receptor 1 (TNFR-1/p55) and the signaling domain of Fas, is expressed in angiogenic endothelial cells. Fas-mediated apoptosis is activated via binding of the TNFR-1 receptor with TNF-alpha, which is more abundant in the tumor microenvironment (TME), enhancing specificity and limiting systemic toxicities.
Ogivri: (Other name for: trastuzumab)
oglufanide disodium: The disodium salt of a synthetic form of a naturally-occurring dipeptide consisting of L-glutamic acid and L-tryptophan with potential antiangiogenic and potential immunomodulating activities. Oglufanide inhibits vascular endothelial growth factor (VEGF), which may inhibit angiogenesis. This agent has also been reported to stimulate the immune response to hepatitic C virus and intracellular bacterial infections.
Ogsiveo: (Other name for: nirogacestat hydrobromide)
ointment OQL011: An ointment that can potentially be used to treat vascular endothelial growth factor receptor (VEGFR) inhibitor (VEGFRi)-associated hand-foot skin reaction (HFSR).
Ojemda: (Other name for: tovorafenib)
Ojjaara: (Other name for: momelotinib dihydrochloride monohydrate)
olanzapine: A synthetic derivative of thienobenzodiazepine with antipsychotic, antinausea, and antiemetic activities. As a selective monoaminergic antagonist, olanzapine binds with high affinity binding to the following receptors: serotoninergic, dopaminergic, muscarinic M1-5, histamine H1, and alpha-1-adrenergic receptors; it binds weakly to gamma-aminobutyric acid type A, benzodiazepine, and beta-adrenergic receptors. The antinausea and antiemetic effects of this agent appear to be due to the blockade of 5-HT2 and 5-HT3 receptors for serotonin. Although its exact mechanism of action in schizophrenia is unknown, it has been proposed that olanzapine's antipsychotic activity is mediated through antagonism to dopamine D2 receptors with rapid ligand-receptor dissociation kinetics that help to minimize extrapyramidal symptoms (EPS). Olanzapine may also stimulate appetite.
olaparib: A small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.
olaptesed pegol: A 45-mer L-stereoisomer RNA oligonucleotide linked to a 40 kDa polyethyleneglycol that targets the small chemokine stromal cell-derived factor 1 (SDF-1 or CXCL12) with potential antineoplastic and hematopoietic stem cell-mobilization activities. SDF-1 targeted agent NOX-A12 specifically binds to SDF-1 thereby preventing the binding of SDF-1 to its receptors CXCR4 and CXCR7 blocking the subsequent receptor activation. This may prevent angiogenesis, tumor cell proliferation, invasion and metastasis and could sensitize tumor cells to chemotherapy. In addition, inhibition of SDF-1/CXCR4 interaction may induce mobilization of hematopoietic cells from the bone marrow into blood. The unique mirror-image configuration of this agent renders it resistant to hydrolysis and does not hybridize with native nucleic acids. Furthermore, this agent does not induce the innate immune response and has shown a favorable immunogenicity profile.
olaratumab: A fully human IgG1 monoclonal antibody directed against the platelet-derived growth factor receptor alpha (PDGFR alpha) with potential antineoplastic activity. Olaratumab selectively binds to PDGFR alpha, blocking the binding of its ligand, PDGF; signal transduction downstream of PDGFR through the MAPK and PI3K pathways is inhibited, which may result in inhibition of angiogenesis and tumor cell proliferation. Overexpressed by various cancer cell types, PDGFR is a transmembrane protein tyrosine kinase receptor, consisting of isoforms A and B, that is important in regulating cellular growth and differentiation and angiogenesis.
oleandrin: A lipid soluble cardiac glycoside with potential antineoplastic activity. Upon administration, oleandrin specifically binds to and inhibits the alpha3 subunit of the Na/K-ATPase pump in human cancer cells. This may inhibit the phosphorylation of Akt, upregulate MAPK, inhibit NF-kb activation and inhibit FGF-2 export and may downregulate mTOR thereby inhibiting p70S6K and S6 protein expression. All of this may lead to an induction of apoptosis. As cancer cells with relatively higher expression of the alpha3 subunit and with limited expression of the alpha1 subunit are more sensitive to oleandrin, one may predict the tumor response to treatment with lipid-soluble cardiac glycosides such as oleandrin based on the tumors Na/K-ATPase pump protein subunit expression. Overexpression of the alpha3 subunit in tumor cells correlates with tumor proliferation.
oleclumab: A monoclonal antibody against the ectoenzyme CD73 (cluster of differentiation 73), also known as 5'-nucleotidase (5'-NT; ecto-5'-nucleotidase) with potential antineoplastic activity. Upon administration, oleclumab targets and binds to CD73, leading to clustering of and internalization of CD73. This prevents CD73-mediated conversion of adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine. This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells. This also activates macrophages, and reduces both myeloid-derived suppressor cells (MDSCs) and regulatory T-lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against cancer cells, tumor cell growth decreases. In addition, clustering and internalization of CD73 decreases the migration of cancer cells and prevents metastasis. CD73, a plasma membrane protein upregulated on a number of cancer cell types, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.
oleogel-S10: A topical gel formulation containing 10% birch tree bark (Betulae cortex) extract in 90% sunflower oil, with potential wound healing accelerating activities in various skin conditions, including epidermolysis bullosa (EB), partial thickness wounds and dermatitis. The birch bark extract is rich in the birch triterpene betulin and also contains lupeol, betulinic acid, erythrodiol and oleanolic acid. Upon topical administration of oleogel-S10 to the affected areas, the birch bark extract, containing mostly betulin, stimulates keratinocytes migration and differentiation into epithelial skin cells, thereby accelerating wound closure, skin restoration and wound healing. It also regulates the inflammatory response involved in wound healing, which further accelerates wound repair. This may decrease the wound healing process time and may reduce radiation dermatitis upon external beam radiation therapy.
oligo-fucoidan: A sulfated polysaccharide low-molecular-weight fucoidan, with potential antioxidant, anti-inflammatory, antiproliferative, anti-angiogenic and pro-apoptotic activities. Upon administration of oligo-fucoidan, this agent seems to exert numerous effects through various mechanisms of action, some of which remain to be fully elucidated. Oligo-fucoidan induces cell cycle arrest, activates caspases, induces apoptosis, and inhibits tumor cell proliferation in susceptible tumor cells. It also increases the expression of tumor suppressors, such as p53, while decreasing levels of certain tumor promoters. Oligo-fucoidan also promotes the degradation of transforming growth factor-beta (TGFb) receptor and the inhibition of epithelial-mesenchymal transition (EMT). It prevents tumor progression, alters tumor microenvironment (TME) and decreases the tumor-promoting M2 macrophages in the TME. Oligo-fucoidan has anti-inflammatory effects that suppress the expression of nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and monocyte chemoattractant protein-1 (MCP-1/CCL2), and decrease the production of certain pro-inflammatory cytokines, such as interleukin-1beta (IL-1b) and tumor necrosis factor (TNF)-alpha (TNFa). This agent may also suppress angiogenic activity by inhibiting vascular endothelial growth factor (VEGF) receptor expression and VEGF-induced endothelial cell proliferation. As an antioxidant, this agent protects cells against oxidative stress by scavenging superoxide radicals and induces the expression of the anti-oxidant nuclear factor erythroid-2-related factor 2 and that of its target gene, superoxide dismutase; and prevents reactive oxidative species (ROS) generation in cancer cells and ROS release into the TME. Fucoidan also has immune-modulatory effects and enhances the proliferation of natural killer (NKs) cells and cytotoxic T cells (CTLs).
oligofructose-enriched inulin: A mixture of non-digestible carbohydrates, containing the fermentable plant fructans oligosaccharide and inulin, with potential prebiotic activity. Resisting hydrolysis by intestinal digestive enzymes, inulin and oligofructose serve as growth media and energy substrates for bifidobacteria in the colon; beneficial colonic commensal bacteria such as bifidobacteria may inhibit the colonization of the intestine by pathogenic bacteria and have been inplicated to inhibit colon carcinogenesis. Oligofructose-enriched inulin may be administered in combination with probiotic bifidobacteria. In addition, this agent may promote the absorption of calcium and magnesium from the gastrointestinal tract.
oligomeric procyanidin complex: A preparation containing plant-derived polyphenolic bioflavonoids composed of multimers (dimers, trimers, or higher order polymers) of the flavan-3-ol-based monomers catechin and epicatechin that are extracted from sources rich in these chemicals (such as grape seeds, grape skin and pine bark), with potential anti-oxidant, anti-inflammatory, anti-microbial, anti-cancer and protective activities. Upon oral administration of oligomeric procyanidin complex (OPC), the polyphenols exert anti-oxidant activity by scavenging free radicals, which prevents both the formation of reactive oxygen species (ROS), particularly nitrous oxide (NO), and DNA damage. OPC also inhibits chemical-induced lipid peroxidation. In addition, OPC reduces the production of advanced glycation end-products (AGEs), decreases AGE accumulation in tissues, and inhibits the progression of AGE/receptor for AGE (RAGE)-mediated inflammatory transduction pathways, which inhibits the activation of pro-inflammatory transcriptional regulators, and prevents the secretion of pro-inflammatory cytokines/chemokines. This ultimately prevents inflammatory-driven damage to end organs and may reduce inflammation-induced cancer formation and progression. In addition, OPC inhibits the activity of a variety of enzymes, including xanthine oxidase, collagenase, elastase, hyaluronidase and beta-glucuronidase.
oligonucleotide SPC2996: A synthetic antisense oligonucleotide against Bcl-2 messenger RNA with potential antitumor activity. Oligonucleotide SPC2996 binds to and inactivates Bcl-2 mRNA, thereby inhibiting the expression of Bcl-2 protein, promoting tumor cell apoptosis, and potentially enhancing the efficacy of standard cytotoxic chemotherapy. Linked to tumor drug resistance, the antiapoptotic protein Bcl-2 is upregulated in several types of cancers.
olinvacimab: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, olinvacimab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression.
olive oil: Produced by pressing olives, olive oil has a high content of monounsaturated fats, thought beneficial for health. Major components of the phenolic fraction of olive oil, lignans and pinoresinols are potent antioxidants present in extra virgin (first pressed) oils. Containing vitamins E and F, other antioxidant compounds, foods containing high amounts of lignan precursors may be protective against breast, colon, and prostate cancer, as well as heart diseases. Used mainly in cooking today, olive oil has been used for medicines and in cosmetics.
olive oil extract/curcumin-based capsule: A capsule containing an extract of olive oil, rich in polyphenols and curcumin, the polyphenol derived from the plant Curcuma longa, also known as turmeric, with potential anti-neoplastic, -angiogenic, -inflammatory, -oxidant and chemopreventive activities. The olive oil extract/curcumin-based capsule is rich in phytonutrients, especially polyphenols. Upon oral administration, the polyphenols, and other active ingredients in this supplement may exert anti-inflammatory activity by decreasing the production of inflammation mediators, such as TNF-alpha, interleukin (IL) 1-beta, IL-6, IL-10, interferon gamma, thromboxane B2, and leukotriene B4. They also inhibit a variety of pro-inflammatory enzymes, such as cyclooxygenase 1 (COX-1) and COX-2, block the formation of reactive-oxygen species and neutralize free radicals. In addition, curcumin and some other polyphenols disrupt cell signal transduction pathways involved in carcinogenesis. Specifically, curcumin inhibits cell invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression by suppressing NF-kB and AP-1 activation.
olive oil/soya oil/egg lecithin-based emulsion: An injectable, isotonic, nutritional lipid emulsion composed of approximately 80% refined olive oil and 20% refined soybean oil, used for parenteral nutrition. The olive oil/soya oil/egg lecithin emulsion provides about 15% of saturated fatty acids (SFA), 65% of mono-unsaturated fatty acids (MUFA) and 20% of essential poly-unsaturated fatty acids (EPUFA). Upon parenteral administration, the emulsion supplies calories, for energy, and essential fatty acids that can be incorporated into cell membranes. The fatty acids may decrease the production of certain pro-inflammatory cytokines, including interleukin 1 (IL-1), IL-6 and tumor necrosis factor (TNF). In addition to olive oil and soya oil, this lipid emulsion contains egg lecithin and provides phosphorus and choline, which are needed to maintain cell membrane integrity.
olmutinib: An orally available small molecule, mutant-selective inhibitor of epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Olmutinib binds to and inhibits mutant forms of EGFR, thereby leading to cell death of EGFR-expressing tumor cells. 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 the EGFR wild type form.
olomorasib: An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, olomorasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
olorofim: A systemic antifungal agent that can potentially be used in the treatment of systemic fungal infections.
olutasidenib: An orally available inhibitor of isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble) with a mutation at arginine (R) 132, IDH1(R132), with potential antineoplastic activity. Upon administration, olutasidenib specifically inhibits IDH1(R132), thereby inhibiting the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH(R132). IDH1(R132) mutations are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.
Olux-E: (Other name for: clobetasol propionate)
olverembatinib: An orally bioavailable inhibitor of a variety of kinases, including the Bcr-Abl tyrosine kinase, the mast/stem cell growth factor receptor Kit (c-Kit), the serine/threonine protein kinase Akt (protein kinase B), and the extracellular signal-regulated kinase (ERK) with antineoplastic activity. Upon administration,olverembatinib targets, binds to and inhibits the kinase activities of Bcr-Abl, AKT, c-Kit and ERK. This inhibits their mediated signaling pathways and inhibits proliferation of tumor cells in which these kinases are overexpressed and/or mutated. Bcr-Abl, c-Kit, AKT and ERK play key roles in the proliferation, differentiation and survival of tumor cells.
Olysio: (Other name for: simeprevir)
OMA1 activator BTM-3566: An orally bioavailable activator of the mitochondrial protease OMA1, with potential antineoplastic activity. Upon oral administration, OMA1 activator BTM-3566 activates OMA1. This leads to OMA1-dependent cleavage of DAP3-binding cell death enhancer 1 (DELE1) and mitochondrial dynamin-like GTPase OPA1, mitochondrial fragmentation, and activation of the eIF2alpha-kinase heme-regulated inhibitor (HRI), and induces cyclic AMP-dependent transcription factor ATF-4-mediated integrated stress response (ISR) and hyperactivates mitochondrial ISR, which result in apoptosis. OMA1 plays a key role in the activation of the ISR pathway in response to hypoxia, amino acid deprivation, and accumulation of misfolded proteins. While ISR promotes the adaptation of tumor cells to hypoxic stress, prolonged activation of ISR induces apoptosis.
omacetaxine: A protein translation inhibitor and cytotoxic plant alkaloid homoharringtonine isolated from the evergreen tree Cephalotaxus, with potential antineoplastic activity. Although the exact mechanism of action has not been fully elucidated, upon administration, omacetaxine targets and binds to the 80S ribosome in eukaryotic cells and inhibits protein synthesis by interfering with chain elongation. This reduces levels of certain oncoproteins and anti-apoptotic proteins.
omacetaxine mepesuccinate: A semisynthetic formulation of the cytotoxic plant alkaloid homoharringtonine isolated from the evergreen tree Cephalotaxus with potential antineoplastic activity. Omacetaxine binds to the 80S ribosome in eukaryotic cells and inhibits protein synthesis by interfering with chain elongation. This agent also induces differentiation and apoptosis in some cancer cell types.
omalizumab: A humanized monoclonal antibody directed against the C-epsilon 3 domain of immunoglobulin E. Olizumab binds to this IgE domain, thereby preventing IgE from binding to its high-affinity mast-cell receptor.
omaveloxolone: A member of the synthetic oleanane triterpenoid class of compounds and an activator of nuclear factor erythroid 2 [NF-E2]-related factor 2 (Nrf2, Nfe2l2), with potential chemopreventive activity. Upon administration, omaveloxolone activates the cytoprotective transcription factor Nrf2. In turn, Nrf2 translocates to the nucleus, dimerizes with a small Maf protein (sMaf), and binds to the antioxidant response element (ARE). This induces the expression of a number of cytoprotective genes, including NAD(P)H quinone oxidoreductase 1 (NQO1), sulfiredoxin 1 (Srxn1), heme oxygenase-1 (HO1, HMOX1), superoxide dismutase 1 (SOD1), gamma-glutamylcysteine synthetase (gamma-GCS), thioredoxin reductase-1 (TXNRD1), glutathione S-transferase (GST), glutamate-cysteine ligase catalytic subunit (Gclc) and glutamate-cysteine ligase regulatory subunit (Gclm), and increases the synthesis of the antioxidant glutathione (GSH). Nrf2, a leucine zipper transcription factor, plays a key role in the maintenance of redox balance and cytoprotection against oxidative stress.
ombitasvir/paritaprevir/ritonavir: An orally bioavailable combination agent containing ombitasvir, an inhibitor of the hepatitis C virus (HCV) non-structural protein 5A (NS5A) replication complex, paritaprevir, a synthetic acylsulfonamide inhibitor of the HCV protease complex comprised of non-structural protein 3 and 4A (NS3/NS4A), and the cytochrome P450 (CYP) 3A4 inhibitor ritonavir, with potential activity against HCV. Upon oral administration of ombitasvir/paritaprevir/ritonavir, ombitasvir, enters the cell and binds to and blocks the activity of the NS5A protein. This results in the disruption of the viral RNA replication complex, blockage of HCV RNA production, and inhibition of viral replication. After intracellular uptake, paritaprevir reversibly binds to the active center and binding site of the HCV NS3/NS4A protease and prevents NS3/NS4A protease-mediated polyprotein maturation. This disrupts both the processing of viral proteins and the formation of the viral replication complex, which inhibits viral replication in HCV genotype 1-infected host cells. Although ritonavir is not active against HCV, it strongly inhibits the activity of CYP3A4, thereby blocking the degradation of paritaprevir, which is a CYP3A4 substrate. This leads to an increased concentration and half-life of paritaprevir as compared to the administration of paritaprevir without ritonavir. NS5A, a zinc-binding and proline-rich hydrophilic phosphoprotein, plays a crucial role in HCV RNA replication. NS3, a serine protease essential for the proteolytic cleavage of multiple sites within the HCV polyprotein, plays a key role during HCV ribonucleic acid (RNA) replication. NS4A is an activating factor for NS3. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family, and infection is associated with the development of hepatocellular carcinoma (HCC).
ombrabulin: A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), with potential vascular-disrupting and antineoplastic activities. Ombrabulin binds to the colchicine binding site of endothelial cell tubulin, inhibiting tubulin polymerization and inducing mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis.
omega-3 fatty acid: Any fatty acid that contains an unsaturated bond originating from the 3rd carbon from the methyl end. Omega-3 fatty acids do not occur naturally with chain lengths shorter than 16 carbon units.
omega-3-acid ethyl esters: An ethyl ester form of omega-3 fatty acid derived from fish oil, with activity in decreasing serum triglyceride levels. Although its mechanism of action isn't known, omega-3-acid ethyl esters may work by decreasing the amount of triglycerides and other fats made in the liver.
omeprazole: A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.
omidubicel: A population of cryopreserved, ex vivo expanded and nicotinamide (NAM)-treated, CD34-positive hematopoietic progenitor cells (HPCs) derived from allogeneic, CD34+ cells isolated from human umbilical cord blood (UCB) that can be used during transplantation. CD34+ HPCs were isolated from human UCB mononuclear cells, and expanded ex vivo. Upon transplantation with omidubicel, these cells can differentiate into a variety of cell types including fibroblasts, osteoblasts, chondrocytes, myocytes, adipocytes, and endothelial cells. Compared to bone marrow transplants, these HPCs have decreased risk of causing graft-versus host disease (GvHD), increased survival, and enhanced transplant and engraftment potential for any given patient as there is no need for a matched donor. Compared to untreated HPCs, treating the cells ex vivo with NAM increases the number of HPCs from UCB, enhances migration, bone marrow (BM) homing, engraftment and increases neutrophil and platelet recovery.
omiganan pentahydrochloride: A pentahydrochloride salt of omiganan, a synthetic cationic antimicrobial peptide with wide-spectrum activity against both gram-positive and gram-negative bacteria and fungi. Omiganan pentahydrochloride, an analog of indolicidin, acts by disrupting bacterial cytoplasmic membranes and has been tested in a topical gel for the prevention of catheter-related bloodstream infections.
Omisirge: (Other name for: omidubicel)
Omnipaque: (Other name for: iohexol)
OmniScan: (Other name for: gadodiamide)
Onalta: (Other name for: yttrium Y 90-edotreotide)
onapristone: An orally bioavailable progesterone receptor (PR) antagonist, with potential antineoplastic activity. Upon oral administration, 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. In addition, onapristone may downregulate cancer stem cell mobilization and block immune evasion. PR is expressed on certain cancer cell types and plays a key role in tumor cell proliferation and survival.
onartuzumab: A humanized monovalent monoclonal antibody directed against the hepatocyte growth factor receptor (c-Met) with potential antineoplastic activity. Onartuzumab binds to the extracellular domain of c-Met, preventing the binding of its ligand, hepatocyte growth factor (HGF); the activation of the c-Met signaling pathway is thus inhibited, which may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase, is overexpressed on the cell surfaces of a variety of cancer cell types and may play a key role in their proliferation, invasion and survival.
onatasertib: An orally available inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. Onatasertib inhibits the activity of mTOR, which may result in the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/AKT/mTOR signaling pathway, which is frequently dysregulated in human cancers.
Oncaspar: (Other name for: pegaspargase)
Oncobax-AK: (Other name for: Akkermansia muciniphila probiotic)
OncoGel: (Other name for: PGLA/PEG copolymer-based paclitaxel)
OncoLAR: (Other name for: octreotide pamoate)
oncolytic adenoviris GM103: An oncolytic adenovirus, with potential antineoplastic and immunomodulating activities. Upon intratumoral administration of oncolytic adenovirus GM103, the oncolytic virus specifically infects and replicates in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune response, thereby inducing a cytotoxic T-lymphocyte (CTL)-mediated immune response and killing nearby non-infected tumor cells.
oncolytic adenovirus Ad5-DNX-2401: An adenovirus serotype 5 strain, selectively replication competent in cells defective in the Rb/p16 tumor suppressor pathway, with potential oncolytic activity. Oncolytic adenovirus Ad5-Delta 24RGD contains an integrin binding RGD-4C motif, allowing Coxsackie adenovirus receptor-independent infection of tumor cells, which are often deficient for Coxsackie and adenovirus receptors (CARs). Selectively replication competent in cells that are defective in retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (p16), active replication of oncolytic adenovirus Ad5-Delta 24RGD in tumor cells may induce oncolysis or cell lysis. As integral components of the late G1 restriction point, the Rb gene product and p16 are negative regulators of the cell cycle; ovarian cancer cells and non-small cell lung cancer cells may be defective in the Rb/p16 pathway.
oncolytic adenovirus AdAPT-001: A replication competent human attenuated adenoviral vector, TAV-255, modified to express a human transforming growth factor beta (TGF-b) trap fusion protein that neutralizes TGF-b, with potential oncolytic, immunomodulating and antineoplastic activities. Upon administration, oncolytic adenovirus AdAPT-001 selectively binds to and replicates in tumor cells and induces tumor cell lysis. In addition, tumor cell lysis releases a variety of tumor-associated antigens (TAAs) which may potentially result in the activation of a systemic immune response against the TAAs-expresssing tumor cells. AdAPT-001 has been attenuated to prevent replication in healthy cells.
oncolytic adenovirus CAdVEC: A genetically modified oncolytic viral strain of human adenovirus (Ad) with potential immunostimulating and antineoplastic activities. Upon intratumoral administration, the oncolytic adenovirus CAdVEC selectively infects and replicates in tumor cells, leading to tumor cell lysis. Additionally, CAdVEC has been genetically modified to express currently undisclosed immunomodulatory molecules that may enhance the anti-tumor effects of endogenous T lymphocytes as well as adoptively transferred chimeric antigen receptor (CAR) T cells.
oncolytic adenovirus expressing interferon beta/CD40 ligand MEM-288: A conditionally replicative, oncolytic adenovirus that has been genetically engineered to encode the transgenes for the human cytokine interferon beta (IFN-beta) and MEM40, a recombinant, chimeric form of CD40 ligand (CD40L), with potential immunostimulating and antineoplastic activities. Upon intratumoral administration, the oncolytic adenovirus expressing IFN-beta/CD40L MEM-288 selectively infects and replicates in tumor cells, leading to tumor cell lysis. In addition, the IFN-beta expressed by the oncolytic adenovirus activates T lymphocytes, dendritic cells (DCs) and natural killer (NK) cells, and induces an anti-tumor immune response against the tumor cells. The CD40L expressed by the oncolytic adenovirus specifically binds to and activates CD40, a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor family and is expressed on various immune cells, such as B lymphocytes, monocytes, and DCs. Activation of CD40 induces proliferation and activation of B lymphocytes, shifts the induction of immunosuppressive macrophages towards immunostimulatory macrophages, activates monocyte-derived DCs (moDCs) and leads to the secretion of inflammatory cytokines. This activates the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells.
oncolytic adenovirus expressing interferon YSCH-01: An oncolytic adenovirus that has been genetically engineered to express interferon (IFN), with potential immunostimulating and antineoplastic activities. Upon intratumoral administration, the oncolytic adenovirus expressing IFN YSCH-01 selectively infects and replicates in tumor cells, leading to tumor cell lysis. In addition, tumor cell lysis releases a variety of tumor-associated antigens (TAAs), which may potentially result in the activation of a systemic immune response against the TAAs-expressing tumor cells. The IFN expressed by the oncolytic adenovirus also activates T-lymphocytes, dendritic cells (DCs) and natural killer (NK) cells and induces an anti-tumor immune response against the tumor cells.
oncolytic adenovirus ICOVIR5-infected allogeneic mesenchymal stem cells: A preparation of bone marrow-derived allogeneic mesenchymal stem cells (MSCs) infected with the oncolytic, replication-competent adenovirus ICOVIR5, with potential antineoplastic activity. Upon infusion of the oncolytic adenovirus ICOVIR5-infected allogeneic MSCs, these cells target the adenovirus to tumors. The oncolytic virus then selectively transfects and replicates in the tumor cells causing a direct cytotoxic effect and lysis of the tumor cells. In addition, the viral infection and the subsequent release of tumor-associated antigens (TAAs) upon lysis may stimulate an immune response against the tumor cells. This may lead to an inhibition of cancer cell proliferation. ICOVIR-5, a virus derived from wild-type human adenovirus serotype 5 (Had5), has been modified to selectively replicate in tumor cells that have a deregulated retinoblastoma/E2F pathway.
oncolytic adenovirus ICOVIR5-infected autologous mesenchymal stem cells: Bone marrow-derived autologous mesenchymal stem cells (MSCs) infected with the oncolytic, replication-competent adenovirus ICOVIR5, with potential antineoplastic activity. Upon infusion of the oncolytic adenovirus ICOVIR5-infected autologous MSCs, these cells target the adenovirus to tumors. The oncolytic virus then selectively transfects and replicates in the tumor cells causing a direct cytotoxic effect and lysis of the tumor cells. In addition, the viral infection may stimulate an immune response against the virally-infected tumor cells. This may lead to an inhibition of cancer cell proliferation. ICOVIR-5, a virus derived from wild-type human adenovirus serotype 5 (Had5), has been modified to selectively replicate in tumor cells that have a deregulated retinoblastoma/E2F pathway.
oncolytic adenovirus ICVB-1042: A genetically-engineered, replication competent, optimized E2 transcription factor (E2F)-dependent oncolytic adenovirus (Ad) composed of an Ad serotype 5 (Ad5) backbone that contains genomic modifications to include an Ad5/Ad34 chimeric fiber and dual modifications in E1A and E4orf6/7, and a modified capsid hexon protein, with potential antineoplastic activity. Upon administration, the oncolytic adenovirus ICVB-1042 selectively targets and binds to CD46 that is overexpressed on many cancer cells. Upon viral entry, ICVB-1042 infects and specifically replicates in tumor cells, which may result in tumor cell lysis. ICVB-1042 replicates only in cells with defects in the p16/Rb/E2F pathway, attributed to a mutation common in many solid tumors, and protects normal, non-proliferative cells from viral-mediated toxicity. The Ad5/Ad34 mutation improves viral entry into target tumor cells, enhancing tropism by enabling and increasing viral entry via CD46. The modifications in E1A and E4orf6/7 increases tumor selectivity. The modified capsid hexon protein allows for IV delivery and mediates cell interaction with CD46. ICVB-1042 includes expression of a fluorescent reporter protein (YPet) to aid in tracking viral replication.
oncolytic adenovirus ORCA-010: A replication competent, oncolytic adenovirus serotype 5 (Ad5) that has been modified with a delta24 (d24) deletion, an incorporation of an RGD-4C motif in the Ad fiber protein, and an insertion of the T1 mutation in E3/19K gene, with potential oncolytic activity. Upon administration, oncolytic adenovirus ORCA-010 binds to specific Ad3 receptors that are highly expressed on certain tumor cells. This results in the replication of oncolytic adenovirus Ad5/3-delta24 in tumor cells and induces tumor cell lysis which may potentially result in the activation of a systemic immune response against tumor-associated antigens (TAAs). The Ad5/3-delta24 has a 24 base pair deletion in constant region 2 of the E1A gene which allows for selective replication in cells that are defective in the retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (CDKN2A or p16INK4a). As most tumor cells are defective in the Rb/p16 pathway, this virus selectively replicates in these cells. The RGD-4C motif is a 9-amino acid peptide that binds to various and enhances viral-cell receptor binding by allowing for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells, which is the natural route of viral binding, as CAR expression is often deficient on cancer cells. As integrins are often overexpressed on tumor cell surfaces, integrin receptor binding enhances tumor cells binding and infection by the Ad. The T1 mutation enhances the Ad5 release from tumor cells and promotes spreading throughout the tumor, thereby enhancing anti-tumor activity. The T1 mutation, a single Adenine insertion at position 445 of the nucleotide sequence of the E3/19K gene of Adenovirus, creates a truncated E3/19K protein that is relocated to the plasma membrane due to the disruption of its ER retention signal. This increases plasma membrane permeability and enhances the release of Ad5.
oncolytic herpes simplex virus-1 expressing anti-CTLA-4 antibody/CD40L/4-1BBL RP3: A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, expressing an antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), CD40 ligand (CD40L; CD154; TRAP; TNFSF5) and the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-1 expressing anti-CTLA-4 Antibody/CD40L/4-1BBL RP3 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Oncolytic virus RP3 expresses a fusogenic protein, GALV-GP R-, for optimal tumor cell infection and killing. In addition, Oncolytic virus RP3 promotes the expression of anti-CTLA-4 antibody, CD40L and 4-1BBL by the tumor cells. Anti-CTLA-4 antibody targets and binds to CTLA-4 expressed on T cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. CD40L specifically binds to and activates CD40, a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor family and is expressed on various immune cells, such as B lymphocytes, monocytes, and dendritic cells (DCs). Activation of CD40 induces proliferation and activation of B lymphocytes, shifts the induction of suppressive macrophages towards immunostimulatory macrophages, activates monocyte-derived DCs (moDCs), and leads to the secretion of inflammatory cytokines, which activates the immune system to induce the proliferation and activation of CTLs against tumor cells. 4-1BBL binds to and subsequently induces 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.
oncolytic herpes simplex virus-1-encoding GM-CSF: An ICP34.5-, ICP47-deleted, oncolytic herpes simplex type-1 virus (HSV-1) isolated from the mouth of an HSV-1-infected patient of Chinese Han ethnicity, and encoding the immunostimulating factor cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential immunostimulating and antineoplastic activities. Upon administration, the recombinant human GM-CSF HSV-1 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells. Interruption of the ICP6 gene, which encodes the large subunit of the viral ribonucleotide reductase, in the viral vector also enhances selective replication in tumor cells.
oncolytic HSV-1 C134: A neurovirulent, oncolytic second-generation, replication-competent, recombinant and genetically-engineered herpes simplex virus type 1 (HSV-1) where the gene for ICP34.5 has been deleted and the gene encoding the human cytomegalovirus (HCMV), protein kinase R (PKR) evasion protein IRS1, with potential oncolytic and immunostimulating activities. Upon intratumoral administration, oncolytic HSV-1 C134 specifically infects and replicates within the rapidly dividing, glioma cells, thereby directly lysing tumor cells. The released virus particles, in turn, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Deletion of the gene encoding for ICP34.5 imparts tumor selectivity by preventing replication in healthy cells. IRS1 expression allows the virus to replicate within tumors but limits viral spread.
oncolytic HSV-1 expressing anti-PD-1 scFv-Fc/TGFbRII decoy/IL-12 STI-1386: A second-generation, genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing a single-chain variable fragment (scFv)-Fc targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), a human transforming growth factor beta receptor 2 (TGFbRII) decoy and the human immunostimulating cytokine interleukin-12 (IL-12), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, oHSV-1 expressing anti-PD-1 scFv-Fc/TGFbRII decoy/IL-12 STI-1386 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing anti-PD-1 scFv-Fc/TGFbRII decoy/IL-12 STI-1386 promotes the secretion of anti-PD-1 scFv-Fc, TGFbRII decoy and IL-12 by the tumor cells. The anti-PD-1 scFv-Fc targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. The TGFbRII decoy targets and binds to TGF-beta and prevents the activation of TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the TGF-beta-mediated immunosuppression in the TME. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response. IL-12 promotes the activation of natural killer (NK) cells, which induces both the secretion of interferon-gamma and a CTL response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation.
oncolytic HSV-1 expressing IL-12 and IL-15/IL-15-receptor alpha VG2025: An oncolytic herpes simplex virus type 1 (oHSV-1) genetically engineered to express the human immunostimulating cytokine interleukin (IL)-12 and a complex of the immunostimulating cytokine IL-15 and its receptor alpha unit (IL-15Ra), with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration, oHSV-1 expressing IL-12 and IL-15/IL-15Ra VG2025 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12 and IL-15/IL-15Ra VG2025 promotes the secretion of IL-12 and IL-15/IL-15Ra complex by the tumor cells locally in the tumor microenvironment (TME). IL-12 promotes the activation of natural killer (NK) cells, which induces both the secretion of interferon-gamma and a CTL response against the tumor cells. IL-15 stimulates the proliferation of NK cells, CTLs and memory T cells, which induces an anti-tumor immune response. IL-15Ra complexed with IL-15 increases IL-15 signaling and IL-15 half-life upon expression. These actions of the cytokines may increase tumor cell killing and decrease tumor cell proliferation.
oncolytic HSV-1 expressing IL-2 and IL-12 KB707: An oncolytic herpes simplex virus type 1 (HSV-1) genetically engineered to express the human immunostimulating cytokines interleukin (IL)-2 and IL-12, with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration, oncolytic HSV-1 expressing IL-2 and IL-12 KB707 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oncolytic HSV-1 expressing IL-2 and IL-12 KB707 promotes the secretion of IL-2 and IL-12 by the tumor cells locally in the tumor microenvironment (TME). This may further stimulate anti-tumor immune responses, increase tumor cell killing and decrease tumor cell proliferation.
oncolytic HSV-1 JNJ-87704916: A recombinant oncolytic herpes simplex virus type 1 (HSV-1), with potential oncolytic and antineoplastic activities. Upon intratumoral administration, oncolytic HSV-1 JNJ-87704916 preferentially infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells.
oncolytic HSV-1 NV1020: A genetically engineered oncolytic virus with potential antineoplastic property. NV1020 is constructed from the herpes simplex virus 1 (HSV-1) by the deletion of a single copy of the gamma (1)34.5 gene and the substitution of the UL23 region of the thymidine kinase (tk) gene with a DNA fragment from HSV-2, thereby resulting in a replication-competent, attenuated virus. This modified virus preferentially transfects rapidly dividing cells, which causes cell lysis in tumor cells. NV1020 has shown reduced virulence against normal tissues and a decreased neurovirulence in comparison with some other modified HSV strains.
oncolytic HSV-1 R130: A recombinant oncolytic herpes simplex virus type 1 (HSV-1), with potential oncolytic and antineoplastic activities. Upon intratumoral or intraperitoneal administration, oncolytic HSV-1 R130 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells.
oncolytic HSV-1 rQNestin34.5v.2: A neuroattenuated, replication-competent, recombinant and genetically-engineered herpes simplex virus type 1 (HSV-1), with potential oncolytic and immunostimulating activities. In rQNestin34.5v.2, the UL39 gene encoding for the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6) and both endogenous copies of the gamma34.5 gene that encodes for the RL1 neurovirulence protein infected cell protein 34.5 (ICP34.5), which is needed for robust viral growth in an infected cell, are deleted, and one copy of the gamma34.5 gene is reinserted under control of a nestin promoter, which is selectively activated in gliomas. Upon intratumoral administration, oncolytic HSV-1 rQNestin34.5v.2 preferentially infects and replicates within the rapidly dividing, glioma cells, thereby directly lysing tumor cells. The released virus particles, in turn, infect and replicate in neighboring tumor cells, thereby further killing tumor cells. rQNestin34.5v.2 also elicits a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. By inactivating UL39, viral ribonucleotide reductase activity is disrupted, resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in non-dividing, healthy cells but not in dividing cells. Glioma-selective expression of ICP34.5 imparts tumor selectivity by preventing replication in healthy cells.
oncolytic HSV-1 rRp450: A gene therapy agent containing an attenuated, replication-competent, genetically engineered mutant form of the Herpes simplex virus 1 (HSV-1) strain KOS with potential antineoplastic activity. Upon infusion into the hepatic artery, oncolytic HSV-1 rRp450 replicates in hepatocellular carcinoma (HCC) cells and exerts direct cytotoxic effects eventually disrupting cancer cell membranes and liberating progeny virions thereby infecting adjacent tumor cells. In addition, rRp450 expresses the cytochrome P450 transgene that activates oxazaphosphorines, such as cyclophosphamide (CPA). Therefore, CPA can become activated in the presence of rRp450 and exert its antineoplastic effect. rRp450 is deleted for the HSV-1 gene UL39, encoding the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6), thereby disrupting the activity of viral ribonucleotide reductase and resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in nondividing cells but not in dividing cells. UL39 is replaced by the rat CYP2B1 gene, encoding a cytochrome P450 enzyme that activates oxazaphosphorines. rRp450 also expresses viral thymidine kinase, which activates the cancer prodrug ganciclovir.
oncolytic HSV-1-expressing IL-12 and anti-PD-1 antibody MVR-C5252: A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an 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 intratumoral administration into the glioma, oHSV-1 expressing IL-12 and anti-PD-1 antibody MVR-C5252 specifically infects and replicates in glioma cells causing viral-mediated glioma cell lysis. The released virus particles, in turn, infect and replicate in neighboring glioma cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected glioma cells. In addition, as MVR-C5252 carries exogenous genes, it is also able to express IL-12 and anti-PD-1 antibody and are released by the infected cells, both of which are able to promote an immune response in the tumor microenvironment (TME). IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against uninfected glioma cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. The anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
oncolytic HSV-1-expressing IL-12 and anti-PD-1 antibody T3011: A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an 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 intratumoral administration, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 promotes the secretion of IL-12 and anti-PD-1 antibody by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
oncolytic HSV-1-expressing IL-12, IL-15/IL-15-receptor alpha and PD-L1-blocking peptide VG161: A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin (IL)-12, the immunostimulating cytokine IL-15 and its receptor alpha unit (IL-15Ra), and a blocking peptide directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. The blocking peptide is a fusion protein composed of the TF peptide, derived from fragments of human programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1) protein, fused to an immunoglobulin G4 (IgG4) Fc (TF-Fc). Upon intratumoral administration, oHSV-1 expressing IL-12, IL-15/IL-15Ra and PD-L1 blocking peptide VG161 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12, IL-15/IL-15Ra and PD-L1 blocking peptide VG161 promotes the secretion of IL-12, IL-15/IL-15Ra and PD-L1 blocking peptide by the tumor cells locally in the TME. IL-12 promotes the activation of natural killer (NK) cells, which induces both the secretion of interferon-gamma and a CTL response against the tumor cells. IL-15 stimulates the proliferation of NK cells, CTLs and memory T cells, which induces an anti-tumor immune response. These actions of the cytokines may increase tumor cell killing and decrease tumor cell proliferation. PD-L1 blocking peptide targets, binds to and inhibits PD-L1, preventing the binding and subsequent activation of its receptor, PD-1. This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the CTL-mediated anti-tumor immune response. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T cells, limits the expansion and survival of CD8+ T cells, suppresses the immune system and results in immune evasion. IL-15Ra complexed with IL-15 increases IL-15 signaling and IL-15 half-life upon expression.
oncolytic HSV-1716: A neuroattenuated, replication-restricted, ICP34.5 deleted (RL1 gene)-mutant herpes simplex virus (HSV) type I, constructed from wild-type strain 17, with potential oncolytic activity. Upon intratumoral injection, oncolytic HSV1716 transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. Because the RL1 gene is deleted , HSV1716 is unable to replicate in non-dividing cells.
oncolytic influenza A virus: An attenuated oncolytic influenza A virus, with hemagglutinin and neuraminidase genes of influenza virus strain A/California/07/2009 codon-pair deoptimized, with potential oncolytic activity. Upon intratumoral administration, oncolytic influenza A virus selectively targets and replicates in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent tumor cells, which both induces further tumor cell oncolysis and may activate the immune system to exert an anti-tumor immune response against the tumor cells.
oncolytic measles virus encoding Helicobacter pylori neutrophil-activating protein: An attenuated oncolytic Edmonston (Ed) strain of measles virus (MV) encoding the N-terminus of the human lambda immunoglobulin light chain containing the Helicobacter pylori neutrophil-activating protein (NAP), with potential immunostimulating and antineoplastic activities. Upon administration, the oncolytic measles virus encoding H. pylori NAP selectively infects and replicates in tumor cells, leading to syncytia formation and tumor cell lysis. The expressed NAP, a toll-like receptor-2 (TLR2) agonist, may stimulate the secretion of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1 and IL-6, leading to local inflammatory reaction in the tumor microenvironment (TME). H. pylori NAP, a bacterial antigen and potent immunomodulator, may enhance the antitumor effect of oncolytic MV.
oncolytic measles virus encoding thyroidal sodium iodide symporter: An attenuated oncolytic Edmonston (Ed) strain of measles virus encoding the human thyroidal sodium iodide symporter (MV-NIS) with potential gene expression and antineoplastic activities. After attachment to and fusion with host tumor cell membranes, MV-NIS may induce tumor cell syncytia and tumor cell lysis. When combined with iodine 123 (I-123), expressed NIS facilitates uptake of I-123 by MV-NIS-infected tumor cells, allowing noninvasive imaging of these cells. MV-NIS may also enhance the oncolytic activity of MV against radiosensitive tumor cells by facilitating the uptake of iodine 131 (I-131) by MV-NIS-infected cells. The cellular receptor for MV is the human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types.
oncolytic Newcastle disease virus: An oncolytic viral agent containing the oncolytic, live-attenuated strain of the paramyxovirus Newcastle disease virus (NDV), with potential antineoplastic activity. Upon administration, NDV specifically infects and replicates in cancer cells. This may result in a direct cytotoxic effect involving the lysis of tumor cells via apoptotic mechanisms and may eventually lead to an inhibition of cancer cell proliferation.
oncolytic Newcastle disease virus MEDI5395: An oncolytic viral agent containing the oncolytic, live-attenuated, replication-competent strain of the avian paramyxovirus Newcastle disease virus (NDV) that has been engineered to include a transgene encoding granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunostimulating activities. Upon administration, MEDI5395 specifically infects and replicates in cancer cells. This may result in a direct cytotoxic effect involving the lysis of tumor cells via apoptotic mechanisms and may eventually lead to an inhibition of cancer cell proliferation through the increased production and secretion of pro-inflammatory cytokines and chemokines which are able to recruit mediators of both the innate and adaptive immune responses. Additionally, the inclusion of the GM-CSF transgene in the viral construct leads to expression of GM-CSF, which may potentiate and strengthen the anti-tumor immune response.
oncolytic RNA virus IVX037: A receptor-targeted oncolytic RNA virus, with potential antineoplastic and immunomodulating activities. Upon intra-tumoral administration, the oncolytic RNA virus IVX037 selectively targets specific receptors overexpressed on cancer cells, thereby allowing for selective replication in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent tumor cells, which both induces further tumor cell oncolysis and may beneficially alter the tumor microenvironment (TME). This may further activate both innate and adaptive immune responses against cancer cells.
oncolytic type 2 herpes simplex virus expressing anti-PD-L1/CD3 bispecific antibody BS-006: A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex virus type 2 (HSV-2), derived from the HG52 strain and encoding a bispecific antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the T-cell surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, oncolytic HSV-2 expressing anti-PD-L1/CD3 bispecific antibody BS-006 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, BS-006 promotes the secretion of anti-PD-L1/CD3 bispecific antibody by the infected tumor cells. The bispecific antibody targets and binds to both the CD3 on T cells and the PD-L1 expressed on tumor cells. This results in the cross-linking of T cells and tumor cells and may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against PD-L1-expressing tumor cells. At the same time, BS-006 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 further 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. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Deletion of ICP47 also leads to an increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and the oncolysis of tumor cells.
oncolytic type 2 Herpes simplex virus expressing granulocyte macrophage colony-stimulating factor OH2: A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex type-2 virus (HSV-2), derived from the HG52 strain, encoding the immunostimulating factor cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-2 expressing GM-CSF OH2 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells. Mutation of the ICP6 gene, which encodes the large subunit of the viral ribonucleotide reductase, in the viral vector also enhances selective replication in tumor cells.
oncolytic vaccinia virus expressing anti-CD19/CD3 bispecific antibody RGV004: A genetically-engineered vaccinia virus (VV) encoding a bispecific antibody specific for the tumor-associated antigen (TAA) CD19 and the T-cell surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic VV expressing anti-CD19/CD3 bispecific antibody RGV004 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific cytotoxic T-lymphocyte (CTL)-mediated immune response, thereby killing nearby non-infected tumor cells. In addition, RGV004 promotes the secretion of the anti-CD19/CD3 bispecific antibody by the infected tumor cells. The bispecific antibody targets and binds to both the CD3 on T cells and the CD19 antigen expressed on tumor cells. This results in the cross-linking of T cells and tumor cells and may induce a CTL-mediated immune response against CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.
oncolytic vaccinia virus expressing anti-CTLA-4 antibody and GM-CSF BT-001: An oncolytic vaccinia virus (VV; VACV) genetically engineered to express 4-E03, an immunoglobulin G1 (IgG1) antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4) and the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential oncolytic, immunostimulating and antineoplastic activities. Upon intra-tumoral administration, the oncolytic VV expressing anti-CTLA-4 antibody and GM-CSF BT-001 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oncolytic virus BT-001 promotes the secretion of anti-CTLA-4 antibody 4-E03 and GM-CSF by the tumor cells. GM-CSF attracts dendritic cells (DCs) and may further stimulate a CTL-mediated immune response against tumor cells. Anti-CTLA-4 antibody 4-E03 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This enhances the CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.
oncolytic vaccinia virus expressing leptin/IL-2 fusion protein ASP1012: An oncolytic vaccinia virus (VV) engineered to express a fusion protein comprised of the metabolic modulator and adipokine leptin and the human cytokine interleukin (IL)-2, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, oncolytic VV expressing leptin/IL-2 fusion protein ASP1012 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific cytotoxic T-lymphocyte (CTL)-mediated immune response, thereby killing nearby non-infected tumor cells. In addition, the leptin/IL-2 fusion protein is expressed by the oncolytic VV in infected cancer cells. Leptin may modulate and improve T-cell metabolic function in the tumor microenvironment (TME), and enhance T-cell-mediated anti-tumor immune responses. IL-2 may further stimulate anti-tumor immune responses, thereby increasing tumor cell killing and decreasing tumor cell proliferation.
oncolytic vaccinia virus OVV-01: An oncolytic vaccinia virus (VV), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of the oncolytic vaccinia virus OVV-01, the virus preferentially targets and infects tumor cells, thereby causing oncolysis. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells. This further kills tumor cells.
oncolytic Vaccinia virus PF-07263689: An engineered oncolytic vaccinia virus (VV), with potential immunomodulating and antineoplastic activities. Upon administration of oncolytic VV PF-07263689, the virus preferentially targets and infects tumor cells, thereby causing oncolysis. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells. This further kills tumor cells.
oncolytic vaccinia virus T601: A modified, replicative oncolytic vaccinia virus (VV), deleted of the genes for tyrosine kinase (TK) and ribonucleotide reductase (RR), and expressing the yeast-originated, bifunctional cytosine deaminase/uracil phosphoribosyltransferase gene (FCU1), with potential immunomodulating and antineoplastic activities. Upon intravenous administration of the oncolytic vaccinia virus T601, the virus preferentially targets and infects tumor cells, causing oncolysis. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells. Upon concomitant administration of the non-cytotoxic prodrug flucytosine (5-fluorocytosine; 5-FC), the FCU1 expressed in the infected cancer cells produce the enzymes cytosine deaminase and uracil phosphoribosyltransferase which catalyze the conversion of 5-FC into the cytotoxic forms 5-fluorouracil (5-FU) and 5-fluoro-uridilyl monophosphate (5-FUMP); 5-FU and 5-FUMP exert a cytotoxic effect in the infected tumor cells. Double gene deletion (TK-RR-) restricts the propagation of T601 to the tumor cells, thereby reducing toxicity to normal cells.
oncolytic vesicular stomatitis virus: A recombinant form of oncolytic vesicular stomatitis virus (VSV), with potential immunomodulating and antineoplastic activities. Upon administration, oncolytic VSV preferentially replicates in tumor cells. This induces VSV-mediated cytolytic activity towards the tumor cells. VSV, a single-stranded RNA virus belonging to the genus Vesiculovirus of the family Rhabdoviridae, is relatively nonpathogenic to healthy humans but is able to rapidly replicate in and induce apoptosis of tumor cells.
oncolytic virus ASP9801: An engineered oncolytic virus with potential antineoplastic and immunomodulating activities. Upon intratumoral injection of ASP-9801, the oncolytic virus selectively targets and replicates in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent tumor cells, which both induces further tumor cell oncolysis and may activate the immune system to exert an anti-tumor immune response against the tumor cells.
oncolytic virus CF33-expressing hNIS/anti-PD-L1 antibody: A genetically modified oncolytic virus (OV) composed of a replication competent orthopoxviral chimera engineered to express the human sodium iodine symporter (hNIS) and a human monoclonal antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential oncolytic, immunostimulating and antineoplastic activities that can be used for radioimaging upon positron emission tomography (PET) and radiotherapeutic applications. Upon subcutaneous (SC) intratumoral (IT) administration of the oncolytic virus CF33-expressing hNIS/anti-PD-L1 antibody, the oncolytic virus specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, the anti-PD-L1 antibody produced by the infected tumor cells targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), a transmembrane protein and negative regulator of the immune system, expressed on activated T cells. This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the CTL-mediated anti-tumor immune response against PD-L1-expressing tumor cells, thereby further killing tumor cells. Upon subsequent administration of certain iodine-containing imaging agents, hNIS expression by the infected tumor cells allows visualization and tracking of viral biodistribution, and analysis and quantification of CF33-infected tumor cells by PET. Also, administration of iodine I 131 results in its uptake by hNIS-expressing tumor cells, which may result in the selective accumulation of a cytotoxic dose of radiation in tumor cells while sparing adjacent normal tissue.
oncolytic virus M1-c6v1: A mutant variant of the recombinant oncolytic alphavirus M1, with potential antineoplastic activity. Upon intravenous administration, oncolytic virus M1-c6v1 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells.
oncolytic virus RT-01: An oncolytic virus with potential antineoplastic and immunomodulating activities. Upon administration of RT-01, the oncolytic virus selectively targets and replicates in cancer cells without being able to infect and replicate in normal, healthy cells. This induces selective oncolytic virus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent tumor cells, which both induces further tumor cell oncolysis and may activate the immune system to exert an anti-tumor immune response against the tumor cells.
oncolytic VSV-GP BI 1821736: An oncolytic virus derived from the vesicular stomatitis virus (VSV), a single-stranded RNA virus, and containing a genetically modified glycoprotein (GP) and a human CD80 (B7.1) Fc fragment, with potential immunomodulating and antineoplastic activities. Upon administration, oncolytic VSV-GP BI 1821736 preferentially replicates in tumor cells, and induces VSV-mediated cytolytic activity towards the tumor cells. Viral infection also stimulates the immune system to recognize these same tumor cells, leading to immune-mediated killing of both infected and non-infected tumor cells, thereby further killing tumor cells. In addition, BI 1821736 secretes CD80, which targets and binds to CD28, and in the presence of antigenic T-cell receptor (TCR) signaling leads to the co-stimulation of T-cell responses including the activation of naive and memory T cells. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells.
Onconase: (Other name for: ranpirnase)
Oncophage: (Other name for: vitespen)
Oncoquest-L vaccine: (Other name for: autologous tumor cell proteoliposome chronic lymphocytic leukemia vaccine)
OncoVax-PR: (Other name for: PSA prostate cancer vaccine)
Oncoxin: (Other name for: green tea extract-based antioxidant supplement)
ondansetron: A carbazole derivative with antiemetic activity. As a selective serotonin receptor antagonist, ondansetron competitively blocks the action of serotonin at 5HT3 receptors, resulting in suppression of chemotherapy- and radiotherapy-induced nausea and vomiting.
ondansetron hydrochloride: The hydrochloride salt of the racemic form of ondansetron, a carbazole derivative and a selective, competitive serotonin 5-hydroxytryptamine type 3 (5-HT3) receptor antagonist with antiemetic activity. Although its mechanism of action has not been fully characterized, ondansetron appears to competitively block the action of serotonin at 5HT3 receptors peripherally in the gastrointestinal tract as well as centrally in the area postrema of the CNS, where the chemoreceptor trigger zone (CTZ) for vomiting is located, resulting in the suppression of chemotherapy- and radiotherapy-induced nausea and vomiting.
onfekafusp alfa: An immunocytokine consisting of human pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) fused to a human single-chain variable fragment (scFv) directed against the extra-domain B (ED-B) of fibronectin (L19), with potential immunopotentiating and antineoplastic activities. Upon adinistration, the L19 moiety of onfekafusp alfa binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. In turn, the TNFalpha moiety may locally induce an immune response against ED-B fibronectin-expressing tumor cells and may specifically decrease the proliferation of ED-B-expressing tumor cells. ED-B is predominantly expressed during angiogenesis and tumor growth.
onilcamotide: A cancer vaccine composed of an immunogenic peptide derived from the Ras homolog family member C (RhoC; Rho-related GTP-binding protein RhoC) that is emulsified in the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, onilcamotide may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) response against tumor cells expressing RhoC, which results in tumor cell lysis. RhoC, a tumor-associated antigen (TAA) that is overexpressed in a variety of tumor cell types, is associated with increased metastatic potential.
Onivyde: (Other name for: irinotecan sucrosofate)
Onrigin: (Other name for: laromustine)
Onsolis: (Other name for: fentanyl buccal soluble film)
Ontruzant: (Other name for: trastuzumab)
Onureg: (Other name for: azacitidine)
onvansertib: An orally bioavailable, adenosine triphosphate (ATP) competitive inhibitor of polo-like kinase 1 (PLK1; PLK-1; STPK13), with potential antineoplastic activity. Upon administration, onvansertib selectively binds to and inhibits PLK1, which disrupts mitosis and induces selective G2/M cell-cycle arrest followed by apoptosis in PLK1-overexpressing tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase that is crucial for the regulation of mitosis, and plays a key role in tumor cell proliferation. PLK1 expression is upregulated in a variety of tumor cell types and high expression is associated with increased aggressiveness and poor prognosis.
onvansertib fumarate: The fumarate form of onvansertib, an orally bioavailable, adenosine triphosphate (ATP) competitive inhibitor of polo-like kinase 1 (PLK1; PLK-1; STPK13), with potential antineoplastic activity. Upon administration, onvansertib selectively binds to and inhibits PLK1, which disrupts mitosis and induces selective G2/M cell-cycle arrest followed by apoptosis in PLK1-overexpressing tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase that is crucial for the regulation of mitosis, and plays a key role in tumor cell proliferation. PLK1 expression is upregulated in a variety of tumor cell types and high expression is associated with increased aggressiveness and poor prognosis.
onvatilimab: A human monoclonal antibody against the protein V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative checkpoint regulatory and antineoplastic activities. Upon administration, onvatilimab targets and binds to VISTA. This inhibits VISTA signaling, abrogates the VISTA-induced suppression of T-lymphocyte-mediated immune responses, enhances cytotoxic T-cell responses against tumor cells and inhibits tumor cell growth. VISTA, mainly expressed on hematopoietic cells, plays a key role in immunosuppression.
onvitrelin ucalontide: A water-soluble, positively charged fusion protein consisting of a luteinizing hormone releasing hormone (LHRH) receptor-targeting ligand conjugated to the membrane-disrupting peptide CLIP 71 with membrane-disrupting and potential antineoplastic activities. The LHRH ligand moiety of onvitrelin ucalontide specifically binds to LHRH receptors, which are upregulated on a variety of human cancer cell types. Subsequently, the positively charged CLIP 71 moiety of this agent interacts with the negatively charged membrane on the cancer cell surface, which may result in cell membrane disruption and cell lysis.
Onyx: (Other name for: ethylene-vinyl alcohol copolymer-based embolic agent)
ONYX-015: An E1B-55kDa-deleted adenovirus that is able to selectively replicate in and lyse TP53-deficient human tumor cells. After tumor cell lysis, released viruses infect neighboring tumor cells, tripping a chain of ONYX-015-mediated tumor cell cytotoxicity.
onzigolide: A chimeric dopamine (DA)-somatostatin (SST) compound, with potential antineoplastic activity. Upon administration, onzigolide binds with high affinity to dopamine D2 receptor (D2R) and somatostatin receptor subtype 2 (SSTR2), and to a lesser extent to somatostatin receptor subtype 5 (SSTR5). This agent appears to exert its effect mainly by binding to D2R to activate the ERK1/2 and p38 MAPK pathways, thus inducing apoptosis and inhibiting cellular proliferation in non-functioning pituitary adenoma (NFPA) and neuroendocrine tumors. By binding to SSTR2, this agent may inhibit the secretion of growth hormone (GH) by the pituitary gland.
Oozfix: (Other name for: carboxymethyl starch topical powder)
opaganib: An orally available, aryladamantane compound and selective inhibitor of sphingosine kinase-2 (SK2) with potential antineoplastic activity. Upon administration, opaganib competitively binds to and inhibits SK2, thereby preventing the phosphorylation of the pro-apoptotic amino alcohol sphingosine to sphingosine 1-phosphate (S1P), the lipid mediator that is pro-survival and critical for immunomodulation. This may eventually lead to the induction of apoptosis and may result in an inhibition of cell proliferation in cancer cells overexpressing SK2. SK2 and its isoenzyme SK1 are overexpressed in numerous cancer cell types.
Opana: (Other name for: oxymorphone hydrochloride)
OPCs/green tea,/spirullina/curcumin/antrodia camphorate/fermented soymilk extract capsule: A capsule containing a fermented soymilk extract and oligomeric proanthocyanidins (OPCs), green tea, spirullina, curcumin and antrodia camphorate powder, with potential antioxidant, immunomodulating, anti-infective and anti-cancer activities. OPCs/green tea/spirullina/curcumin/antrodia camphorate/fermented soymilk extract capsule may boost the immune system and may alleviate fatigue and poor appetite in cancer chemotherapy patients.
Opdivo: (Other name for: nivolumab)
Opdivo Qvantig: (Other name for: nivolumab and hyaluronidase-nvhy)
Opdualag: (Other name for: nivolumab/relatlimab-rmbw)
opebacan: An injectable formulation composed of opebacan, a 21 kDa recombinant fragment of human bactericidal/permeability-increasing protein (BPI), with potential anti-infective activity. Upon intravenous administration, opebacan is able to mimic BPI and binds to and neutralizes lipopolysaccharides (LPS or endotoxins), which are components of the cell wall of gram-negative bacteria that induce a potent innate immune response. This may prevent an endotoxin-mediated inflammatory response and may prevent graft-versus-host-disease (GvHD) after myeloablative allogeneic hematopoietic stem cell transplantation (aHSCT). BPI, a host-defense protein against microbial infection, is naturally produced by neutrophils. Chemotherapy and radiation therapy induce neutropenia and depletion of endogenous BPI. These therapies also cause intestinal damage and release of bacterial endotoxins into the bloodstream, which initiate a systemic inflammatory response, activate donor T-lymphocytes and possibly cause GvHD following aHSCT.
opelconazole: A synthetic triazole antifungal agent, with activity against a variety of pathogenic fungi that can potentially be used against invasive pulmonary aspergillosis. Upon inhalation by nebulizer, opelconazole is delivered in high concentrations to the lungs and resides in the lung tissues for a long period of time with minimal systemic exposure. Opelconazole selectively binds to and inhibits the CYP450-dependent 14-alpha-sterol demethylase in fungi, thereby preventing the production of ergosterol, which is an essential constituent of the fungal cell membrane. This results in fungal cell lysis and inhibits fungal infection in the lungs.
opevesostat: An orally bioavailable, non-steroidal, selective inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc) (CYP11A1), with potential antineoplastic activity. Upon oral administration, opevesostat targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone (Preg), which is the first rate-liming step in steroid hormone biosynthesis.
opioid agonist GIC-1001: A sulfonate-based salt form of a trimebutine derivative, an orally available, peripherally-acting opioid agonist and muscarinic antagonist, with potential visceral analgesic activity. Upon oral administration of GIC-1001, this agent may exert its therapeutic effects through the potential mechanisms of action for the trimebutine and sulfonate moieties: The trimebutine moiety can act as a motility enhancer in the gastrointestinal (GI) tract, as an antispasmodic agent to reduce colonic spasms, as an agonist of colonic mu and kappa opioid receptors, which could provide an analgesic effect, and blocks sodium channels and the release of a variety of GI peptides, which modulates the activity of visceral afferents. The sulfonate moiety releases hydrogen sulfide (H2S), which is involved, through an as of yet not fully elucidated mechanism of action, in the modulation of visceral perception and pain, possibly through the activation of ATP-sensitive potassium (KATP) ion channels and mu opioid receptors. Altogether, administration of this agent may both facilitate the insertion of the colonoscope during a colonoscopy and reduce colonic spasms and pain.
opioid agonist GIC-1002: An orally available, peripherally-acting opioid agonist, with potential visceral analgesic activity. Upon oral administration of GIC-1002, this agent binds to colonic mu and kappa opioid receptors causing analgesic effects.
opioid growth factor: An endogenous pentapeptide with potential antineoplastic and antiangiogenic activities. Opioid growth factor (OGF) binds to and activates the opioid growth factor receptor (OGFr), present on some tumor cells and vascular cells, thereby inhibiting tumor cell proliferation and angiogenesis.
opium tincture: Also known as laudanum and formulated for oral administration, opium tincture is made of air-dried poppy (Papaver somniferum) latex and contains alkaloids such as morphine and codeine. As an antidiarrheal agent, it slows transit of intestinal contents by increasing intestinal smooth muscle tone and inhibiting motility; water is absorbed from fecal contents, decreasing diarrhea.
opnurasib: An inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon administration, opnurasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
Oporia: (Other name for: lasofoxifene)
oportuzumab monatox: A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a truncated form of Pseudomonas exotoxin A with potential antineoplastic activity. Oportuzumab monatox binds to Ep-CAM-positive tumor cells, thereby delivering the Pseudomonas exotoxin A moiety specifically; the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in target cells. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers.
OPPA regimen: A regimen consisting of vincristine, prednisone, procarbazine and doxorubicin (OPPA) used in combination with radiation therapy for the treatment of female patients with childhood Hodgkin lymphoma with low-risk features.
oprelvekin: A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine interleukin 11 (IL-11). Secreted by bone marrow stromal cells and a number of mesenchymal cells, IL-11 binds to and activates its cell-surface receptor, promoting primary and secondary immune responses, modulating antigen-specific antibody reactions, and preventing apoptotic cell death. This agent also stimulates the T-cell-dependent development of IgG-secreting B-cells in spleen cell cultures and may be an important regulator of megakaryocytopoiesis.
oprozomib: An orally bioavailable proteasome inhibitor with potential antineoplastic activity. Oprozomib inhibits the activity of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome; this may result in an accumulation of unwanted or misfolded proteins. Disruption of various cell signaling pathways may follow, eventually leading to the induction of apoptosis and inhibition of tumor growth. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquitinated.
OptiPEA: (Other name for: palmidrol)
OptiPrep: (Other name for: iodixanol)
Optiray: (Other name for: chemokine modulation therapy)
Optison: (Other name for: perflutren protein-type A microspheres)
Ora-Testryl: (Other name for: fluoxymesterone)
Oracit: (Other name for: sodium citrate)
Oradoxel: (Other name for: oral docetaxel)
Oragest: (Other name for: medroxyprogesterone acetate)
oral aminolevulinic acid hydrochloride: A powder for an oral solution comprised of the hydrochloride salt of 5-aminolevulinic acid (ALA) with a potential application for photodynamic therapy. After oral administration, ALA is converted intracellularly into the photosensitizer protoporphyrin IX (PpIX). Upon exposure to light of appropriate wavelength (violet to blue range), excited PpIX emits a characteristic red fluorescence which could facilitate guided resection, and generates excited singlet oxygen molecules that could kill cells when appropriate laser dosage is applied. ALA is preferentially taken up by and accumulates in many types of cancer cells compared to normal, healthy cells. Consequently, cancer cells can be visualized and can be distinguished from normal, healthy cells.
oral azacitidine: An orally bioavailable formulation of azacitidine, a pyrimidine nucleoside analogue of cytidine, with antineoplastic activity. Upon oral administration, azacitidine is taken up by cells and metabolized to 5-azadeoxycitidine triphosphate. The incorporation of 5-azadeoxycitidine triphosphate into DNA reversibly inhibits DNA methyltransferase, and blocks DNA methylation. Hypomethylation of DNA by azacitidine may re-activate tumor suppressor genes previously silenced by hypermethylation, resulting in an antitumor effect. In addition, the incorporation of 5-azacitidine triphosphate into RNA disrupts normal RNA function and impairs tRNA (cytosine-5)-methyltransferase activity, resulting in an inhibition of RNA and protein synthesis.
oral bowel contrast agent NX9: An orally-administered bowel contrast agent that may be used for the imaging of the bowel upon computed tomography (CT). Upon administration, oral bowel contrast agent NX9 may allow for enhanced contrast and visualization of the bowel at CT.
oral cancer vaccine V3-OVA: An orally available cancer vaccine composed of autologous ovarian cancer antigens obtained from hydrolyzed, inactivated blood and tumor tissue of patients with ovarian cancer, with potential immunostimulatory and antineoplastic activities. Upon oral administration of the oral cancer vaccine V3-OVA, the ovarian cancer antigens stimulate the immune system and activate a cytotoxic T-lymphocyte (CTL) immune response against ovarian cancer cells.
oral cancer vaccine V3-P: An orally bioavailable, therapeutic cancer vaccine composed of the carbohydrate antigen sialyl-Lewis A (carbohydrate antigen 19-9; CA19.9; CA19-9) that is derived from pooled blood of pancreatic cancer patients, with potential immunomodulating activity. Upon oral administration of the oral pancreatic cancer vaccine V3-P, the CA19.9 antigens may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated immune response against pancreatic cancer cells expressing the CA19.9 antigen. CA19.9 is overexpressed on a number of different tumor cell types and plays a key role in tumor cell survival and metastasis.
oral docetaxel: An oral proprietary P-glycoprotein (P-gp) pump inhibitor-based formulation containing the taxane docetaxel, a semisynthetic analogue of paclitaxel, and a P-gp pump inhibitor, with potential antineoplastic activity. Upon administration of oral docetaxel, the P-gp pump inhibitor moiety, which is not absorbed, binds to the P-gp pump in the gastrointestinal (GI) tract and prevents the P-gp pump-mediated efflux of docetaxel from cells the docetaxel has been internalized by back into the GI tract. This decreases P-gp-mediated excretion and enhances absorption of docetaxel. Upon absorption, docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizes tubulin and inhibits microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death. The P-gp pump inhibitor enhances the bioavailability of certain poorly bioavailable agents and thereby allows oral administration of those agents. P-gp, an efflux membrane transporter, plays a key role in active drug export, and prevents cellular uptake and accumulation of certain substances.
oral fludarabine phosphate: An oral formulation of the phosphate salt of fludarabine, a synthetic purine nucleoside analogue antimetabolite with antineoplastic activity. Fudarabine is preferentially transported into malignant cells and metabolized by deoxycytidine kinase to its active form, 2-fluoro-ara-ATP; 2-fluoro-ara-ATP competes directly with deoxyadenosine triphosphate (dATP) and inhibits alpha DNA polymerase, RNA reductase, and DNA primase, which may result in inhibition of DNA synthesis and cell death.
oral Hsp90 inhibitor IPI-493: An orally bioavailable formulation of the ansamycin derivative 17-amino-17-demethoxygeldanamycin (17-AG) with potential antineoplastic activity. Oral Hsp90 inhibitor IPI-493 binds to and inhibits Hsp90, which may result the in growth inhibition in sensitive tumor cell populations. Hsp90, a 90 kDa molecular chaperone, may be highly expressed in tumor cells, playing a key role in the conformational maturation, stability and function of other substrate or "client" proteins within the cell; many of these client proteins are involved in signal transduction, cell cycle regulation and apoptosis, and may include kinases, transcription factors and hormone receptors.
oral irinotecan hydrochloride formulation VAL-413: An orally bioavailable flavored formulation composed of the hydrochloride salt form of irinotecan, a semisynthetic derivative of camptothecin, with potential antineoplastic activity. Upon oral administration of oral irinotecan HCl formulation VAL-413, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. In turn, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA, resulting in DNA breaks. This results in an inhibition of DNA replication and an induction of apoptosis in cancer cells. VAL-413 may improve tolerability of oral irinotecan and improve compliance.
oral microencapsulated diindolylmethane: An orally bioavailable microencapsulated formulation of diindolylmethane, an indole phytonutrient found in cruciferous vegetables, with estrogen-modulating, antiandrogenic, and potential antineoplastic activities. As a dimer of indole-3-carbinol, diindolylmethane (DIM) modulates estrogen balance by reducing the levels of 16-hydroxy estrogen metabolites and increasing the formation of beneficial 2-hydroxy estrogen metabolites. DIM also antagonizes androgen receptor activity, which may result in diminished cell proliferation and apoptosis in susceptible tumor cell populations. Pure DIM, which is relatively hydrophobic, is poorly absorbed after oral administration. This oral formulation, which consists of DIM, d-alpha-tocopheryl acid succinate, phosphatidylcholine, and silica microencapsulated in starch, significantly improves the gastrointestinal absorption of DIM.
oral moisturizing jelly: An edible, gel-based formulation containing an artificial saliva substitute, composed of water, electrolytes and buffering agents, with potential anti-xerostomia and protective activities. Upon application of the oral moisturizing jelly (OMJ), the natural electrolyte and pH balance of human saliva is restored, which increases moisture of mucosal tissues of the mouth, tongue and oropharynx. This relieves dryness, enhances lubrication, and increases salivary flow. OMJ makes it easier to chew, swallow and talk, and also prevents xerostomia-induced infections, as well as tooth decay.
oral myoma vaccine V3-myoma: An orally available therapeutic myoma vaccine containing pooled antigens derived from hydrolyzed, inactivated blood and tumor tissue samples from patients with uterine myoma, with potential antineoplastic and immunomodulatory activities. Upon oral administration, V3-myoma may stimulate the immune system to mount a cytotoxic T-lymphocyte-mediated response against cells expressing myoma-associated antigens. This may reduce the myoma growth and improve myoma-related symptoms.
oral picoplatin: An oral preparation of picoplatin, a third generation platinum compound with antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and RNA transcription and the induction of apoptosis. Because of the increase in steric bulk around the platinum center, there is a relative reduction in the inactivation of picoplatin by thiol-containing species such as glutathione and metallothionein in comparison to cisplatin.
oral rehydration solution: An aqueous solution composed of glucose and electrolytes, including sodium, potassium, chloride, magnesium, and phosphorus, with dehydration preventative and rehydration activities. Upon oral administration of the oral rehydration solution (ORS), water, electrolytes and glucose are absorbed from the gastrointestinal (GI) tract into the systemic circulation. This replenishes the body's supply of water, carbohydrates and electrolytes, and prevents both dehydration and renal dysfunction.
oral sodium phenylbutyrate: An orally active derivative of the short-chain fatty acid butyrate with potential antineoplastic activity. 4-Phenylbutyrate inhibits histone deacetylase, resulting in cell cycle gene expression modulation, reduced cell proliferation, increased cell differentiation, and apoptosis. This agent also initiates fragmentation of genomic DNA, resulting in decreased DNA synthesis and the inhibition of tumor cell migration and invasion.
oral therapeutic vaccine V3-X: An orally bioavailable therapeutic vaccine consisting of the tumor-associated antigen (TAA) oligosaccharide antigen sialyl Lewis A (CA19-9; sialylated Lewis A antigen; carbohydrate antigen 19-9; cancer antigen 19-9), with potential immunostimulating and antineoplastic activities. Upon oral administration, oral therapeutic vaccine V3-X induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing CA19-9. CA19-9 is an antigen that is overexpressed in a variety of cancer cell types, and plays a key role in tumor cell survival and metastasis.
oral topotecan hydrochloride: An oral formulation of the hydrochloride salt of topotecan, a semisynthetic derivative of the quinoline alkaloid camptothecin, with potential antineoplastic activity. Topotecan selectively inhibits topoisomerase I activity by stabilizing topoisomerase I-DNA covalent complexes during the S phase of the cell cycle, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery.
Oralet: (Other name for: fentanyl citrate)
Oramorph: (Other name for: morphine sulfate)
Oramorph SR: (Other name for: morphine sulfate)
orantinib: An orally bioavailable receptor tyrosine kinase inhibitor. Orantinib binds to and inhibits the autophosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), thereby inhibiting angiogenesis and cell proliferation. Orantinib also inhibits the phosphorylation of the stem cell factor receptor tyrosine kinase c-kit, often expressed in acute myelogenous leukemia cells.
Orathecin: (Other name for: rubitecan)
oraxol: A combination formulation composed of a capsule containing the taxane compound paclitaxel and a tablet containing the multidrug resistance (MDR) efflux pump P-glycoprotein (P-gp) inhibitor HM30181A, with potential antineoplastic activity. Upon oral administration of oraxol, the HM30181A moiety binds to and inhibits P-gp, which prevents P-gp-mediated efflux of paclitaxel, therefore enhancing its oral bioavailability. In turn, paclitaxel binds to and stabilizes microtubules, preventing their depolymerization, which results in the inhibition of cellular motility, mitosis, and replication. Altogether, this may result in greater intracellular concentration of paclitaxel, and enhanced cytotoxicity against tumor cells, when compared to the administration of paclitaxel alone. P-gp, encoded by the MDR-1 gene, is a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters; it prevents the intestinal uptake and intracellular accumulation of various cytotoxic agents.
Orazol: (Other name for: enteric-coated zoledronic acid tablet MER-101)
Orca-T: (Other name for: partially engineered T-regulatory cell donor graft TRGFT-201)
Orchisterone-M: (Other name for: methyltestosterone)
ordastobart: An agonistic, recombinant, humanized, hexavalent immunoglobulin G (IgG) antibody targeting the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory and antineoplastic activities. Upon administration, ordastobart selectively binds to six OX40 receptors per molecule, thereby clustering and activating OX40. This induces the proliferation of memory and effector T-lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T cells. Utilizing a hexavalent OX40 antibody may improve receptor clustering and downstream signaling over tetravalent or bivalent OX40 antibodies.
ordesekimab: A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human pro-inflammatory cytokine interleukin-15 (IL-15), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, ordesekimab binds to and neutralizes IL-15, thereby preventing IL-15-mediated pro-inflammatory signaling. By inhibiting IL-15-mediated immune responses, ordesekimab decreases natural killer (NK) cell activation and proliferation, reduces T-cell infiltration, increases T-cell apoptosis, and may prevent the growth of IL-15-driven cancer cells. IL-15 plays a key role in inflammation and is associated with a variety of autoimmune and inflammatory disorders as well as with cell proliferation in certain cancer types, such as T-cell lymphomas. IL-15 is required for the proliferation of certain T cells and NK cells.
oregovomab: A murine monoclonal antibody that attaches to the tumor-associated antigen CA125. Vaccination with monoclonal antibody B43.13 may stimulate a host cytotoxic immune response against tumor cells that express CA125.
orelabrutinib: A small molecule inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) with potential antineoplastic activity. Upon administration, orelabrutinib binds to and inhibits the activity of BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways, inhibiting 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.
Orencia: (Other name for: abatacept)
Orestralyn: (Other name for: ethinyl estradiol)
Oreton Methyl: (Other name for: methyltestosterone)
Oreton Methyl: (Other name for: methyltestosterone)
Orgaran: (Other name for: danaparoid sodium)
Orgovyx: (Other name for: relugolix)
Orilissa: (Other name for: elagolix)
orludodstat: An orally available inhibitor of dihydroorotate dehydrogenase (DHODH), with potential antineoplastic activity. Upon administration, orludodstat specifically targets, binds to and prevents the activation of DHODH, thereby preventing the fourth enzymatic step in de novo pyrimidine synthesis. This prevents uridine monophosphate (UMP) formation, DNA synthesis, cell division and cellular proliferation, causes reactive oxygen species (ROS) production, enables differentiation and induces apoptosis in susceptible tumor cells. DHODH, a mitochondrial enzyme, catalyzes the conversion of dihydroorotate (DHO) to orotate in the endogenous synthesis of UMP.
ormaplatin: A platinum(IV) analogue with antineoplastic activity. Ormaplatin alkylates DNA, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity.
Orotecan: (Other name for: oral irinotecan hydrochloride formulation VAL-413)
orphenadrine citrate: The citrate salt form of orphenadrine with a muscle relaxant property. Although the mechanism of action has not been fully elucidated, orphenadrine citrate appears to block cholinergic receptors, thereby interfering with the transmission of nerve impulses from the spinal cord to the muscles. It does not produce myoneural block, nor does it affect crossed extensor reflexes.
Orplatna: (Other name for: satraplatin)
Orserdu: (Other name for: elacestrant hydrochloride)
ortataxel: A semisynthetic, second-generation taxane derivative with potential antineoplastic activity. Ortataxel binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly. This results in the inhibition of cell division and cellular proliferation. As it represents a poor substrate for P-glycoprotein (P-gp), multi-drug resistance protein (MRP-1) and breast cancer resistance protein (BCRP) mediated efflux, ortataxel modulates multi-drug resistance mechanisms and may be useful for treating multi-drug resistant tumors that express Pgp, MRP-1 and BCRP.
orteronel: An orally bioavailable non-steroidal androgen synthesis inhibitor of steroid 17alpha-monooxygenase (17,20 lyase) with potential antiandrogen activity. Orteronel binds to and inhibits the steroid 17alpha-monooxygenase in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1 (P450C17), localized to the endoplasmic reticulum (ER), exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones, such as progestins, mineralocorticoids, glucocorticoids, androgens, and estrogens.
Ortho-Novum: (Other name for: ethinyl estradiol/norethindrone)
Orthoclone OKT3: (Other name for: muromonab-CD3)
Orudis: (Other name for: ketoprofen)
Oruvail: (Other name for: ketoprofen)
osanetant: An orally bioavailable, brain penetrating, non-peptide neurokinin/tachykinin 3 receptor (NK1-receptor; NK3R; NK-3R) antagonist, that may potentially be used to treat vasomotor symptoms (VMS) in menopausal woman and in men on androgen deprivation therapy (ADT) and to suppress the production of certain hormones. Upon oral administration, osanetant targets, competitively binds to and blocks the activity of NK3R in the central nervous system (CNS), thereby inhibiting NK3R-mediated signal transduction and may prevent certain menopausal symptoms such as hot flashes and VMS in men deprived of androgen. Neurokinin-mediated signaling may increase during hormone deficiency and may cause hot flashes. In addition, osanetant may, by inhibiting NK3R, suppress secretion of various hormones, such as testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). By suppressing testosterone production, osanetant may inhibit the proliferation of hormone-sensitive prostate cancer.
OSE 2101: A proprietary cancer DNA vaccine that contains multiple natural and modified epitopes derived from the four tumor associated antigens, CEA, HER2/neu, p53, and MAGE 2/3. OSE 2101 also includes CAP1-6D, a heteroclitic CEA analog, and PADRE, a proprietary universal T-cell epitope that serves to enhance the immunogenicity of the epitopes. This agent has been shown to elicit cytotoxic T-lymphocyte responses against tumor cells expressing these multiple epitopes.
oseltamivir phosphate: The phosphate salt of oseltamivir, a synthetic derivative prodrug of ethyl ester with antiviral activity. By blocking neuraminidases on the surfaces of influenza viruses, oseltamivir interferes with host cell release of complete viral particles.
osemitamab: A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18), with potential immunostimulating and antineoplastic activities. Upon administration, osemitamab specifically targets, binds to and inhibits CLDN18.2 expressed on tumor cells. This may kill CLDN18.2-expressing tumor cells by antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), and inhibit cell proliferation. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is overexpressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. Osemitamab is produced with reduced fucosylation.
OSI-7904L: A liposome-encapsulated formulation of the benzoquinazoline folate analog OSI-7904 with antineoplastic activity. As a thymidylate synthase inhibitor, OSI-7904 noncompetitively binds to thymidylate synthase, resulting in inhibition of thymine nucleotide synthesis and DNA replication. Liposome encapsulation improves the efficacy and increases the half-life of OSI-7904.
osilodrostat: An orally bioavailable inhibitor of both steroid 11beta-hydroxylase (cytochrome P450 (CYP) 11B1) and aldosterone synthase (CYP11B2; steroid 18-hydroxylase), with potential anti-adrenal activity and ability to treat Cushing disease (CD). Upon administration, osilodrostat binds to and inhibits the activity of CYP11B1, the enzyme that catalyzes the final step of cortisol synthesis from the precursor 11-deoxycortisol, and CYP11B2, the enzyme that catalyzes aldosterone synthesis from corticosterone and 11-deoxycorticosterone in the adrenal gland. The inhibition of CYP11B1 prevents the production of excess cortisol, thereby decreasing and normalizing the levels of cortisol. CD is most often caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary tumor.
osimertinib: A third-generation, orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, osimertinib covalently binds to and inhibits the activity of numerous mutant forms of EGFR, including the secondarily-acquired resistance mutation T790M, L858R, and exon 19 deletions, 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. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.
Osmitrol: (Other name for: mannitol)
Ossirene: (Other name for: Ammonium Trichlorotellurate)
Ostarine: (Other name for: enobosarm)
Osteocrete: (Other name for: magnesium-based bone void filler)
osugacestat: A small-molecule gamma secretase (GS) and pan-Notch inhibitor, with potential antineoplastic activity. Upon intravenous administration, osugacestat binds to GS and blocks activation of Notch receptors, which may inhibit the proliferation of tumor cells with an overly-active Notch pathway. The integral membrane protein GS is a multi-subunit protease complex that cleaves single-pass transmembrane proteins, such as Notch receptors, at residues within their transmembrane domains that lead to their activation. Overactivation of the Notch signaling pathway, often triggered by activating mutations, has been correlated with increased cellular proliferation and poor prognosis in certain tumor types.
Otezla: (Other name for: apremilast)
otlertuzumab: A recombinant single-chain polypeptide engineered to exhibit the full binding and activity of an anti-CD37 monoclonal antibody with potential immunostimulatory and antineoplastic activities. Otlertuzumab binds to CD37 on B-cells, which may result in antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis. CD37 is a transmembrane glycoprotein expressed at high-levels on B cells and to a lesser extent on T cells and myeloid cells. This agent may have a longer half-life in vivo than conventional monoclonal antibodies.
OVA BiP peptide: A 19 amino-acid hybrid peptide antigen with immune adjuvant property. OVA-BiP peptide consists of 8 amino acids from ovalbumin joined via a tripeptide linker to a stretch of 8 amino acids, the minimum binding domain of BiP (immunoglobulin heavy chain-binding protein, aka grp78), a member of the heat shock protein (hsp) 70 family. As a chaperon, BiP binds to newly synthesized, unfolded mu immnoglobulin heavy chains prior to its assembly with light chains in the endoplasmic reticulum. In conjunction with a tumor antigen, this hybrid peptide is used to potentiate antigen presentation and consequently prime cytotoxic T lymphocyte responses.
ovapuldencel-T: A cancer vaccine consisting of autologous dendritic cells (DCs) loaded with autologous, lethally irradiated cancer cells and mixed with the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulatory and antineoplastic activities. Upon vaccination, ovapuldencel-T may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against the repertoire of tumor associated antigens (TAAs) found in the irradiated cancer cells. GM-CSF enhances the activation of dendritic cells (DCs) and promotes antigen presentation to both B- and T-lymphocytes.
OvaRex: (Other name for: oregovomab)
ovarian cancer peptide vaccine: A cancer vaccine comprised of synthetic peptides corresponding to naturally-occurring peptides derived from ovarian cancer cell antigens. Ovarian cancer peptide vaccine may elicit a cytotoxic T-cell response against tumor cells expressing the related ovarian cancer cell antigens.
ovarian cancer stem cell/hTERT/Survivin mRNAs-loaded autologous dendritic cell vaccine DC-006: A cancer vaccine containing autologous dendritic cells (DCs) that are transfected with mRNAs extracted from amplified ovarian cancer stem cells, and mRNAs of the universal tumor antigens human telomerase reverse transcriptase (hTERT) and survivin with potential immunostimulatory and antineoplastic activities. Upon administration, ovarian cancer stem cell/hTERT/survivin mRNAs-loaded autologous DC-006 vaccine may elicit a highly specific cytotoxic T-cell (CTL) response against ovarian cancer cells expressing hTERT, survivin, and specific ovarian cancer stem cell antigens. hTERT, the catalytic subunit of human telomerase, and survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types, playing key roles in tumor cell growth and survival. Ovarian cancer stem cells contain a specific range of antigens that are essential for the neoplastic growth and survival of ovarian cancer cells.
ovarian tumor antigen-activated autologous dendritic cell vaccine: A dendritic cell (DC)-based cancer vaccine composed of autologous dendritic cells (DCs) activated with an ovarian tumor cell lysate containing tumor-associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, the ovarian tumor antigen-activated autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against ovarian cancer cells expressing ovarian tumor cell-specific antigens, which may result in ovarian tumor cell lysis.
OVax: (Other name for: autologous dinitrophenyl-modified ovarian cancer vaccine)
Ovcon: (Other name for: ethinyl estradiol/norethindrone)
Overstin: (Other name for: estriol)
Ovrette: (Other name for: norgestrel)
Ovuplant: (Other name for: deslorelin)
OX40L-expressing oncolytic adenovirus DNX-2440: A selectively replication competent oncolytic adenovirus that is engineered to express OX40 ligand (OX40L) with potential oncolytic and immunostimulatory activities. Upon administration, OX40L-expressing oncolytic adenovirus DNX-2440, which contains an integrin binding RGD-4C motif, infects tumor cells in a Coxsackievirus-adenovirus receptor-independent manner and selectively replicates in tumor cells that are defective in retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (p16). Tumor cell selectivity is achieved through a 24-base pair deletion in the E1A gene, which renders the oncolytic adenovirus unable to replicate in normal cells that maintain a functional Rb pathway, but fully replication competent in Rb/p16 defective tumor cells. Active replication of the OX40L-expressing oncolytic adenovirus DNX-2440 within tumor cells may induce oncolysis and release of OX40L. OX40L may then bind to and activate signaling pathways downstream of its cognate receptor, tumor necrosis factor receptor superfamily member 4 (TNFRSF4; OX40), which is expressed on activated T cells. OX40L/OX40 binding promotes increased cytokine production, which can induce proliferation of memory and effector T lymphocytes and promote the killing of nearby tumor cells. OX40L, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) ligand family, provides a co-stimulatory signal for the proliferation and survival of activated T cells. The Rb gene product and p16 are negative regulators of the cell cycle and are defective in certain tumor types.
oxaliplatin: An organoplatinum complex in which the platinum atom is complexed with 1,2-diaminocyclohexane (DACH) and with an oxalate ligand as a 'leaving group.' A 'leaving group' is an atom or a group of atoms that is displaced as a stable species taking with it the bonding electrons. After displacement of the labile oxalate ligand leaving group, active oxaliplatin derivatives, such as monoaquo and diaquo DACH platinum, alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. The DACH side chain appears to inhibit alkylating-agent resistance.
oxaliplatin eluting beads: A formulation of drug-eluting beads (DEB) consisting of polymeric microbeads impregnated with the organoplatinum complex and alkylating agent oxaliplatin, with potential antineoplastic activity. The beads consist of polyvinyl alcohol (PVA) microspheres modified with sulfonic acid groups and loaded with oxaliplatin. During transarterial chemoembolization (TACE) in the hepatic artery, the oxaliplatin eluting beads occlude tumor blood vessels that feed the tumor and induce ischemic necrosis of tumor tissue due to mechanical blockage of the tumor vasculature. The beads release cytotoxic oxaliplatin locally, which may result in oxaliplatin-mediated inhibition of tumor cell proliferation through formation of both inter- and intra-strand platinum-DNA crosslinks, and the inhibition of DNA replication.
oxaliplatin-encapsulated transferrin-conjugated N-glutaryl phosphatidylethanolamine liposome: A nanoparticle formulation containing N-glutaryl phosphatidylethanolamine (NGPE)-liposomes encapsulating oxaliplatin and conjugated to the human transferrin (Tf) ligand, with potential antineoplastic activity. Upon infusion of oxaliplatin-encapsulated transferrin-conjugated NGPE liposomes, the transferrin moiety targets and binds to the Tf receptor, which is overexpressed on a variety of human cancer cells. Upon binding and internalization, oxaliplatin is released and its active derivatives alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, resulting in an inhibition of DNA replication and transcription. By extending the circulation time and specifically targeting transferrin receptors, this formulation may improve the efficacy and safety of oxaliplatin therapy, compared to administration of oxaliplatin alone. NGPE, a reactive phospholipid, is used as a linker to attach the Tf ligand, to the liposome.
Oxandrin: (Other name for: oxandrolone)
oxandrolone: A synthetic, anabolic steroid hormone analog of testosterone. Similar to testosterone, oxandrolone binds to and activates specific nuclear receptors. This agent may be used for testosterone replacement therapy in hypogonadal men, in HIV-wasting syndrome, and in other conditions in order to increase nitrogen retention and fat-free muscle mass.
oxcarbazepine: A dibenzazepine carboxamide derivative with an anticonvulsant property. As a prodrug, oxcarbazepine is converted to its active metabolite, 10-monohydroxy. Although the mechanism of action has not been fully elucidated, electrophysiological studies indicate this agent blocks voltage-gated sodium channels, thereby stabilizing hyper-excited neural membranes, inhibiting repetitive neuronal firing, and decreasing the propagation of synaptic impulses.
Oxecta: (Other name for: oxycodone hydrochloride)
Oxepa: (Other name for: gluten-free DHA/EPA/GLA/antioxidant-rich nutritional liquid)
oxidative phosphorylation inhibitor IACS-010759: An orally bioavailable oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon administration of the OxPhos inhibitor IACS-010759, this agent binds to and inhibits complex I of the electron transport chain (NADH ubiquinone oxidoreductase), thereby selectively depriving tumor cells of nutrients, and energy, and inhibiting nucleotide and amino acid production, which induces autophagy, causes tumor cell death and inhibits cell proliferation. Mitochondrial complex I, which is hyperactivated in cancer cells to meet their increased demands for energy, plays a key role in the promotion of cancer cell proliferation.
oxidized avidin: An oxidized form of the glycoprotein avidin, that can be used as a linking agent for tissue-pretargeted radionuclide therapy. Upon intralesional administration, the aldehyde groups of oxidized avidin strongly bind to the amino groups on tissue proteins, via the formation of Schiff bases. As avidin is able to strongly bind to biotin, intravenous administration of radiolabeled biotin may lead to the selective eradication of the pre-targeted tumor cells.
oxitriptan: An aromatic amino acid with antidepressant activity. In vivo, oxitriptan is converted into 5-hydroxytryptamine (5-HT or serotonin) as well as other neurotransmitters. Oxitriptan may exert its antidepressant activity via conversion to serotonin or directly by binding to serotonin (5-HT) receptors within the central nervous system (CNS). Endogenous 5-hydroxytryptophan (5-HTP) is produced from the essential amino acid L-tryptophan. Exogenous therapeutic 5-HTP is isolated from the seeds of the African plant Griffonia simplicifolia.
OxPhos Inhibitor VLX600: A lipophilic cation-based triazinoindolyl-hydrazone compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon infusion, in normal cells and proliferating tumor cells where glucose is readily available, inhibition of OxPhos by VLX600 induces a hypoxia-inducible factor 1-alpha (HIF-1alpha)-dependent shift to, and an increase in glycolysis. Glycolysis alone does not produce enough energy to support the growth of tumor cells in this environment, and the induction of autophagy occurs. In the metabolically compromised tumor microenvironment, the availability of oxygen and glucose is limited due to poor vascularization and perfusion of tumor micro-areas. Tumor cells growing in this environment are thus unable to compensate for decreased mitochondrial function by increasing glycolysis. This leads to nutrient depletion, decreased energy production, induction of autophagy, tumor cell death and an inhibition of cell proliferation in quiescent tumor cells. Mitochondrial OxPhos, which is hyperactivated in cancer cells, plays a key role in the promotion of cancer cell proliferation.
Oxsoralen: (Other name for: methoxsalen)
Oxsoralen-Ultra: (Other name for: methoxsalen)
oxybutynin chloride: The chloride salt form of oxybutynin, a tertiary amine and anticholinergic agent with antispasmodic activity. Oxybutynin chloride exerts its antimuscarinic effect on bladder smooth muscle by blocking muscarinic receptors in smooth muscle, thereby inhibiting acetylcholine binding. This results in a relaxation of bladder smooth muscle, a reduction of involuntary muscle contractions and delays the initial desire to void.
oxycodone hydrochloride: The hydrochloride salt of oxycodone, a methylether of oxymorphone and semisynthetic opioid agonist with analgesic and antitussive properties. Oxycodone binds to mu-receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opiates. In addition to analgesia and a depressive effect on the cough center in the medulla, this agent may cause euphoria, anxiolysis, miosis, sedation, physical dependence, constipation, and respiratory depression, depending on dosage and variations in individual metabolism.
oxycodone hydrochloride/naloxone hydrochloride prolonged-release tablet: A prolonged-release tablet formulation composed of the hydrochloride salt form of the opioid receptor agonist oxycodone and the hydrochloride salt form of the opioid receptor antagonist naloxone which may produce analgesia while relieving opioid-mediated gastrointestinal (GI) side effects. Upon oral administration, oxycodone binds to opioid receptors, thereby mimicking the effects of endogenous opiates to provide analgesia. As naloxone is very poorly absorbed, this agent binds locally to opiate receptors in the GI tract, thereby preventing oxycodone from binding to these receptors. This relieves the opioid-related side effects on the GI tract, including opioid-induced constipation.
oxycodone/acetaminophen: A combination preparation of the analgesic and antipyretic acetaminophen and the semisynthetic opioid agonist oxycodone with analgesic and antitussive properties. Acetaminophen exerts its analgesic activity by inhibiting prostaglandin synthesis, while oxycodone exerts its analgesic activity by binding to the mu-receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opioids.
OxyContin: (Other name for: oxycodone hydrochloride)
oxygen carrier YQ23: A bovine-derived, stabilized, non-polymeric, cross-linked, tetrameric hemoglobin-based oxygen carrier, with potential oxygen carrying, immunomodulating and antineoplastic activities. Upon administration, oxygen carrier YQ23 may increase the oxygen level in the tumor microenvironment (TME). This may prevent the increase of circulating endothelial progenitor cells (EPCs) and regulatory T cells (Tregs) that results from tissue ischemia and hypoxia. EPCs play important roles in tumor vasculogenesis, tumor growth and metastases. Tregs play an important role in antitumor immune responses.
oxymorphone hydrochloride: The hydrochloride salt form of oxymorphone, a semisynthetic opioid with a potent analgesic property. Oxymorphone hydrochloride binds to and activates opiate receptors, specifically mu-receptors, in the central nervous system (CNS). This results in sedation, analgesia, decreased gastrointestinal motility, and respiratory depression.
oxyquinoline sulfate/sodium lauryl sulfate vaginal gel: A carbomer-based vaginal gel preparation containing oxyquinoline sulfate and sodium lauryl sulfate, that may be used for vaginal lubrication and for the restoration and maintenance of normal vaginal acidity. Upon intravaginal administration, oxyquinoline sulfate/sodium lauryl sulfate vaginal gel may coat the vaginal wall with a lubricating film and moisturize vaginal tissue, and restore and maintain normal vaginal acidity.
ozanimod hydrochloride: The hydrochloride salt form of ozanimod, an orally bioavailable sphingosine-1-phosphate (S1P) receptors 1 (S1PR1, S1P1) and 5 (S1PR5, S1P5) modulator, with potential anti-inflammatory and immunomodulating activities. Upon oral administration, ozanimod selectively targets and binds to S1PR1 on lymphocytes and induces S1PR1 internalization and degradation. This results in the sequestration of lymphocytes in lymph nodes. By preventing egress of lymphocytes, ozanimod reduces both the amount of circulating peripheral lymphocytes and the infiltration of lymphocytes into target tissues. This prevents a lymphocyte-mediated immune response and may reduce inflammation. S1PR1, a G-protein coupled receptor, plays a key role in lymphocyte migration from lymphoid tissues. Modulation of S1PR5 by ozanimod may be neuroprotective.
ozarelix: A highly modified, fourth generation linear decapeptide with gonadotropin-releasing hormone (GnRH or LHRH) antagonizing properties. Ozarelix competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. As a result, this may relieve symptoms associated with hormonally dependent disease states such as hormone-dependent prostate cancer.
Ozempic: (Other name for: semaglutide)
Ozurdex: (Other name for: dexamethasone intravitreal implant)
ozuriftamab vedotin: An antibody-drug conjugate (ADC) composed of ozuriftamab, a conditionally active biologic (CAB) antibody against receptor tyrosine kinase-like orphan receptor 2 (ROR2) conjugated to monomethyl auristatin E, with potential antineoplastic activity. Upon administration of ozuriftamab vedotin, the anti-ROR2 antibody becomes activated through an as of yet not fully elucidated process, only under the unique microphysical conditions that are present in the tumor microenvironment (TME) as a result of the glycolytic metabolism of cancer cells and not in the microenvironment of normal, healthy tissues. Upon binding to ROR2-expressing cancer cells and internalization, the cytotoxic agent kills the cancer cells. ROR2, highly expressed during embryonic development while only minimally expressed on certain normal, healthy cells, is involved in Wnt signal transduction and is overexpressed on certain cancer cells. It plays a key role in cancer cell proliferation, migration and invasion. High levels of ROR2 expression often correlates with poor prognosis. The CAB antibody allows for efficient binding to ROR2-expressing cancer cells only, thereby maximizing efficacy while minimizing toxicity by avoiding activation and thus binding of the antibody to normal, healthy ROR2-expressing cells under normal conditions.