NCI Drug Dictionary

954 results found for: C

c-Met inhibitor ABN401: An orally bioavailable, highly selective inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, ABN401 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met inhibitor AL2846: An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration AL2846 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met Inhibitor AMG 208: A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 208 inhibits the ligand-dependent and ligand-independent activation of c-Met, inhibiting its tyrosine kinase activity, which may result in cell growth inhibition in tumors that overexpress c-Met. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase, plays an important role in epithelial cell proliferation and has been shown to be overexpressed in a variety of cancers.
c-Met Inhibitor AMG 337: An orally bioavailable inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 337 selectively binds to c-Met, thereby disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.
c-Met inhibitor ANS014004: An orally bioavailable, next-generation, type II inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor ANS014004 selectively targets and specifically binds to the inactive state of c-Met (DFG-out) in the ATP pocket and inhibits the activity of the c-Met protein, including various c-Met oncogenic alterations such as MET exon 14 skipping mutation (METdeltaex14) and acquired mutations in codons D1228 and Y1230. This prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in and inhibit proliferation of tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis. Type II c-Met inhibitors may overcome resistance to type I c-Met inhibitors. Post-treatment resistance to type I c-Met inhibitors often occurs through acquired mutations in codons D1228 and Y1230.
c-Met inhibitor CBT-101: An orally bioavailable inhibitor of the proto-oncogene hepatocyte growth factor receptor (c-Met; HGFR), with potential antineoplastic activity. Upon administration, CBT-101 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in c-Met-overexpressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met inhibitor GST-HG161: An orally bioavailable, selective inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor GST-HG161 targets and binds to c-Met protein, thereby disrupting c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met inhibitor HS-10241: An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, HS-10241 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met inhibitor JNJ-38877605: An orally bioavailable, small-molecule receptor tyrosine kinase inhibitor with potential antineoplastic activity. c-Met inhibitor JNJ-38877605 selectively inhibits c-Met, a receptor tyrosine kinase (RTK) involved in cancer cell survival and invasiveness, and tumor angiogenesis. c-Met is also known as hepatocyte growth factor receptor (HGFR).
c-Met inhibitor MK2461: A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor MK2461 preferentially inhibits activated c-Met in an ATP-competitive manner, thereby inhibiting its tyrosine kinase activity, which may inhibit c-Met signaling and result in cell growth inhibition in tumors that overexpress c-Met. c-Met, encoding the hepatocyte growth factor receptor (HGFR) tyrosine kinase, plays an important role in tumor cell proliferation and has been shown to be overexpressed or mutated in a variety of cancers.
c-Met inhibitor SPH3348: An orally bioavailable inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor SPH3348 targets and binds to c-Met protein, thereby disrupting c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
c-Met-targeting tri-specific natural killer cell engager ABBV-303: An engineered immune modulating agent based on tri-specific natural killer (NK) cell engager therapy (TriNKET) that is targeting c-Met (hepatocyte growth factor receptor; HGFR), with potential immunostimulating and antineoplastic activities. Upon administration, c-Met-targeting tri-specific NK cell engager ABBV-303 targets and binds to c-Met on tumor cells and simultaneously binds to NK cells via the receptors CD16 and NKG2D (natural killer group 2D; killer cell lectin-like receptor K1; KLRK1), thereby bringing c-Met-expressing tumor cells and NK cells together. This activates NK cells and results in the selective NK cell-mediated killing of c-Met-expressing tumor cells. In addition, the NK cells activate T and B cells, and enhance a cytotoxic T-lymphocyte (CTL)-mediated immune response against c-Met-expressing tumor cells. C-Met, a receptor tyrosine kinase that is overexpressed or mutated in many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis. Its expression is associated with poor prognosis in many tumor types.
c-Met/FLT3/TRK/CDK8/19 inhibitor TSN084: An orally bioavailable type II protein kinase inhibitor of multiple kinases, including c-Met (hepatocyte growth factor receptor; HGFR), FMS-like tyrosine kinase-3 (FLT3; CD135; fetal liver kinase-2; Flk2), tropomyosin-related-kinase (tyrosine receptor kinase; TRK), and cyclin-dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and immunomodulating activities. Upon oral administration, c-Met/FLT3/TRK/CDK8/19 inhibitor TSN084 targets, binds to and inhibits the activity of various kinases, such as c-Met, FLT3, TRK and CDK8/19, and prevents activation of oncogenic signaling pathways mediated by these kinases, blocks selective transcription of various tumor-promoting genes, and inhibits proliferation of susceptible tumor cells that overexpress these kinases. These kinases are overexpressed or mutated in certain cancer cell types and play key roles in tumor cell proliferation, survival, invasion, treatment resistance and immune evasion.
C-myb antisense oligonucleotide G4460: A 24-base phosphorothiolate antisense oligodeoxynucleotide (ODN) for the proto-oncogene c-myb with potential antineoplastic activity. C-myb antisense oligonucleotide G4460 binds to codon sequences 2 to 9 of c-myb mRNA, inhibiting translation of the transcript. Suppression of c-myb expression with this agent may result in the restoration of normal differentiation pathways, increased antiproliferative effects, and the induction of apoptosis in early progenitor hematopoietic cells and in tumor cells that overexpress c-myb. Tumor-cell overexpression of c-myb blocks differentiation, promotes proliferation, and inhibits apoptosis.
c-Myb mRNA degrader REM-422: An orally bioavailable, small molecule mRNA degrader of the proto-oncogene c-Myb, with potential antineoplastic activity. Upon oral administration, c-Myb mRNA degrader REM-422 promotes the inclusion of poison exon into the c-Myb pre-mRNA transcript, resulting in the degradation of c-Myb mRNA and the reduction of both c-Myb mRNA and c-Myb protein levels. This may decrease proliferation in tumor cells with c-Myb dysregulation or overexpression. c-Myb, an oncogenic transcription factor that plays a key role in the regulation of hematopoietic cell differentiation and proliferation, is dysregulated or overexpressed in a variety of tumor cell types.
c-Myb mRNA degrader RGT-61159: An orally bioavailable, small molecule mRNA modulator of the proto-oncogene c-Myb, with potential antineoplastic activity. Upon oral administration, c-Myb mRNA degrader RGT-61159 targets c-Myb RNA and selectively induces the inclusion of the cryptic "poison" exon into the c-Myb RNA transcript, resulting in the elimination of c-Myb mRNA transcript. This inhibits the production of the c-Myb protein. Suppression of c-Myb expression results in the restoration of normal differentiation pathways, increased antiproliferative effects, and the induction of apoptosis in tumor cells that overexpress c-Myb. c-Myb, an oncogenic transcription factor that plays a key role in the regulation of hematopoietic cell differentiation and proliferation, is dysregulated or overexpressed in a variety of tumor cell types.
c-raf antisense oligonucleotide ISIS 5132: A synthetic, 20-base antisense oligodeoxynucleotide that hybridizes to c-raf kinase messenger RNA. ISIS 5132 has been shown to specifically suppress Raf-1 expression both in vitro and in vivo. Raf-1 serine/threonine kinase functions as a critical effector of Ras-mediated signal transduction; constitutive activation of this pathway directly contributes to malignant transformation.
C-VISA BikDD:liposome: A formulation composed of DOTAP:cholesterol liposome nanoparticles complexed with the plasmid C-VISA BiKDD, with potential antineoplastic activity. C-VISA BikDD: liposome consists of a pancreatic-cancer-specific expression vector VISA (VP16-GAL4-WPRE integrated systemic amplifier) and a pancreatic-cancer-specific promoter CCKAR (cholecystokinin type A receptor) (CCKAR-VISA or C-VISA) which drives expression of the gene BikDD, a mutant form of the potent proapoptotic gene Bik (Bcl-2 interacting killer). Upon administration and transduction into pancreatic tumor cells, expression of BikDD by C-VISA BikDD:liposome may induce pancreatic tumor cell apoptosis and suppress pancreatic tumor cell proliferation. BikDD binds with greater affinity to anti-apoptotic proteins bcl-2, bcl-xl, bcl-w and Mcl-1 and is more potent than wild-type Bik. DOTAP:cholesterol liposome is composed of cationic lipid dioleoyl-trimethylammonium propane (DOTAP) and cholesterol at molar ratio of 1:1.
C/EBP beta antagonist ST101: A peptide antagonist of the transcription factor CCAAT/enhancer-binding protein beta (C/EBP beta), with potential antineoplastic activity. Upon administration, C/EBP beta antagonist ST101 targets and inhibits the activity of C/EBP beta. This prevents the expression of C/EBP beta target genes and proteins, including the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), cyclins and inhibitor of differentiation (ID) family of proteins, which are involved in cell proliferation, differentiation, and cell cycle regulation. This may lead to apoptosis in tumor cells. C/EBP beta is overexpressed in many cancers and plays an important role in the regulation of cell differentiation; its expression is associated with tumor cell survival and proliferation.
C7R-expressing EBVSTs: A preparation of human Epstein-Barr virus (EBV)-specific T lymphocytes (EBVSTs) that have been genetically modified to express the constitutively active interleukin 7 (IL-7) receptor (C7R; IL-7R), with potential immunostimulating and antineoplastic activities. Upon administration, the CR7-expressing EBVSTs specifically recognize and bind EBV-infected tumor cells, resulting in tumor cell lysis. EBV, a ubiquitous human herpes virus, is associated with various malignancies, specifically nasopharyngeal carcinoma and lymphomas, including Hodgkin and non-Hodgkin. C7R triggers IL-7-mediated signaling that promotes T-cell proliferation and survival. The enhanced T-cell survival prolongs EBV-infected tumor cell killing and anti-tumor activity.
cabazitaxel: A semi-synthetic derivative of the natural taxoid 10-deacetylbaccatin III with potential antineoplastic activity. Cabazitaxel binds to and stabilizes tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2/M phase, and the inhibition of tumor cell proliferation. Unlike other taxane compounds, this agent is a poor substrate for the membrane-associated, multidrug resistance (MDR), P-glycoprotein (P-gp) efflux pump and may be useful for treating multidrug-resistant tumors. In addition, cabazitaxel penetrates the blood-brain barrier (BBB).
cabergoline: A synthetic ergoline derivative and a long-acting dopamine receptor agonist with high affinity for the dopamine D2 receptor. Cabergoline exerts an inhibitory effect on prolactin secretion by acting on dopamine receptors present in pituitary lactotrophs. This drug also binds to dopamine D2 receptors in the corpus striatum, thereby mimicking the actions of dopamine on motor control. Cabergoline also possesses antioxidant and neuroprotective properties due to its free radical scavenging activity. Cabergoline is used in the treatment of Parkinson's disease and in the treatment of hyperprolactinemia.
cabiralizumab: A humanized monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R), also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), with potential antineoplastic activity. Upon administration, anti-CSF1R monoclonal antibody FPA008 binds to CSF1R expressed on monocytes, macrophages, and osteoclasts and inhibits the binding of the CSF1R ligands colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34), to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment and activity of CSF1R-dependent tumor-associated macrophages (TAMs), FPA008 enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. Additionally, FPA008 prevents the activation of osteoclasts and blocks bone destruction. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival.
Cablivi: (Other name for: caplacizumab-yhdp)
Cabometyx: (Other name for: cabozantinib S-malate)
cabotegravir: A human immunodeficiency virus type 1 (HIV-1) integrase strand transfer inhibitor (INSTI), that is used for pre-exposure prophylaxis (PrEP) to reduce the risk of sexually acquired HIV-1 infection. Upon gluteal intramuscular administration, cabotegravir binds to the active site of HIV integrase and inhibits the activity of HIV integrase, an HIV-1 coded enzyme that is necessary for viral replication. Inhibition of integrase prevents the integration of HIV-1 DNA into host genomic DNA.
cabozantinib: An orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.
cabozantinib S-malate: The s-malate salt form of cabozantinib, an orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.
cadazolid: An oxazolidinone-type antibiotic, with activity against gram-positive bacteria, including Clostridium difficile. Although the exact mode of action through which cadazolid exerts its effect has yet to be fully elucidated, upon administration, this agent inhibits bacterial protein synthesis and leads to bacterial cell death.
cadonilimab: A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cadonilimab targets and binds to both PD-1 and CTLA4 expressed on tumor-infiltrating T lymphocytes (TILs), and inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD1 and CTLA4 with cadonilimab may enhance T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.
CAF regimen: A regimen consisting of oral cyclophosphamide, doxorubicin and fluorouracil, used as a treatment for recurrent and metastatic breast cancer.
cafelkibart: A monoclonal antibody against C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon administration, cafelkibart targets, binds to and blocks the activity of CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression. High expression is correlated with poor prognosis.
caffeic acid: An orally bioavailable, hydroxycinnamic acid derivative and polyphenol, with potential anti-oxidant, anti-inflammatory, and antineoplastic activities. Upon administration, caffeic acid acts as an antioxidant and prevents oxidative stress, thereby preventing DNA damage induced by free radicals. Caffeic acid targets and inhibits the histone demethylase (HDM) oncoprotein gene amplified in squamous cell carcinoma 1 (GASC1; JMJD2C; KDM4C) and inhibits cancer cell proliferation. GASC1, a member of the KDM4 subgroup of Jumonji (Jmj) domain-containing proteins, demethylates trimethylated lysine 9 and lysine 36 on histone H3 (H3K9 and H3K36), and plays a key role in tumor cell development.
caffeine: A methylxanthine alkaloid found in the seeds, nuts, or leaves of a number of plants native to South America and East Asia that is structurally related to adenosine and acts primarily as an adenosine receptor antagonist with psychotropic and anti-inflammatory activities. Upon ingestion, caffeine binds to adenosine receptors in the central nervous system (CNS), which inhibits adenosine binding. This inhibits the adenosine-mediated downregulation of CNS activity; thus, stimulating the activity of the medullary, vagal, vasomotor, and respiratory centers in the brain. This agent also promotes neurotransmitter release that further stimulates the CNS. The anti-inflammatory effects of caffeine are due the nonselective competitive inhibition of phosphodiesterases (PDEs). Inhibition of PDEs raises the intracellular concentration of cyclic AMP (cAMP), activates protein kinase A, and inhibits leukotriene synthesis, which leads to reduced inflammation and innate immunity.
caffeine-based cream: A topical cream containing the alkaloid caffeine in a lipoderm base, with potential anti-inflammatory, anti-fibrotic, protective and antioxidant activities. Upon topical application of the caffeine-based cream to the affected area(s), the caffeine inhibits phosphodiesterase (PDE) activity, thereby stimulating the degradation of fats during lipolysis. Caffeine also reduces the levels of certain pro-inflammatory cytokines, such as the profibrotic cytokine transforming growth factor beta (TGFb,) and matrix metalloproteinases (MMPs), thereby preventing inflammation and protecting against collagen degradation. In addition, caffeine protects cells from oxidative stress. This may help protect skin, reduce skin-related complications and improve skin appearance.
CAIX inhibitor DTP348: An orally bioavailable, nitroimidazole-based sulfamide, carbonic anhydrase IX (CAIX) inhibitor with potential antineoplastic activity. Upon administration, CAIX inhibitor DTP348 inhibits tumor-associated CAIX, a hypoxia-inducible transmembrane glycoprotein that catalyzes the reversible reaction and rapid interconversion of carbon dioxide and water to carbonic acid, protons, and bicarbonate ions. This prevents the acidification of the tumor's extracellular microenvironment and decreases the intracellular pH. This results in increased cell death in CAIX-expressing, hypoxic tumors. In addition, DTP348, through its nitroimidazole moiety, is able to sensitize hypoxic tumor cells to irradiation. CAIX is overexpressed in various tumors and plays a key role in intra- and extracellular pH regulation, cancer cell progression, survival, migration and invasion.
calaspargase pegol-mknl: An intravenous formulation containing E.coli-derived L-asparaginase II conjugated with succinimidyl carbonate monomethoxypolyethylene glycol (SC-PEG), with potential antineoplastic activity. Upon administration of calaspargase pegol-mknl, L-asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting cells of asparagine; asparagine depletion blocks protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle and ultimately induces tumor cell death. Asparagine is critical to protein synthesis in acute lymphoblastic leukemia (ALL) cells which, unlike normal cells, cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Pegylation decreases enzyme antigenicity and increases its half life. SC is used as a PEG linker to facilitate attachment to asparaginase and enhances the stability of the formulation.
Calcijex: (Other name for: Calcitriol)
calcipotriene: A synthetic vitamin D derivative usually formulated for topical dermatological use, antipsoriatic Calcipotriene (calcipotriol) competes equally with active 1,25-hydroxy-2D3 (the natural form of vitamin D) for 1,25-hydroxy-2D3 receptors in regulating cell proliferation and differentiation. It induces differentiation and suppresses proliferation of keratinocytes, reversing abnormal keratinocyte changes in psoriasis, and leads to normalization of epidermal growth.
Calcitriol: A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers.
calcium aluminosilicate anti-diarrheal: A clay compound consisting of aluminosilicate and calcium ions with potential antidiarrheal activity. Calcium aluminosilicate anti-diarrheal consists of microscopically large flat plates of aluminosilicate separated by calcium ions that may sorb toxic chemotherapeutic drugs and their metabolites and inflammatory proteins such as TNF-alpha, which may help minimize chemotherapy-mediated or radiation therapy-mediated damage to the intestinal epithelium and so therapy-related diarrhea.
calcium carbonate: The carbonic salt of calcium (CaCO3). Calcium carbonate is used therapeutically as a phosphate buffer in hemodialysis, as an antacid in gastric hyperacidity for temporary relief of indigestion and heartburn, and as a calcium supplement for preventing and treating osteoporosis.
calcium chloride: A crystalline, white substance, soluble in water, calcium chloride is the chloride salt of calcium, a bivalent metallic element with many crucial biological roles. Calcium is a major constituent of the skeleton but plays many roles as an intracellular and plasma ion as well. In medicine, calcium chloride is also used as a 10% solution in injection, for calcium replenishment.
calcium citrate: The citrate salt of calcium. An element necessary for normal nerve, muscle, and cardiac function, calcium as the citrate salt helps to maintain calcium balance and prevent bone loss when taken orally. This agent may also be chemopreventive for colon and other cancers.
calcium gluconate: The gluconate salt of calcium. An element or mineral necessary for normal nerve, muscle, and cardiac function, calcium as the gluconate salt helps to maintain calcium balance and prevent bone loss when taken orally. This agent may also be chemopreventive for colon and other cancers.
calcium release-activated channel inhibitor CM4620: A calcium (Ca2+) release-activated channel (CRAC) inhibitor, with potential anti-inflammatory and protective activities. Upon administration, CM4620 targets, binds to and inhibits the calcium release-activated calcium channel protein 1 (Orai1), which forms the pore of CRAC, and is expressed on both parenchymal cells and immune cells. This prevents the transport of extracellular Ca2+ into the cell and inhibits the subsequent activation of Ca2+-mediated signaling and transcription of target genes. This may prevent Ca2+ entry-mediated cell death. It may also inhibit the proliferation of immune cells and prevents the release of various inflammatory cytokines in immune cells, such as interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-a). This may lead to a reduction of inflammatory responses in inflammatory-mediated diseases. CRACs, specialized plasma membrane Ca2+ ion channels composed of the plasma membrane based Orai channels and the endoplasmic reticulum (ER) stromal interaction molecules (STIMs), mediate store operated Ca2+ entry (SOCE) and play a key role in calcium homeostasis. CRACs are overactivated in a variety of cell types, especially certain immune cells during inflammation, including T lymphocytes, neutrophils and macrophages.
calcium release-activated channels inhibitor RP4010: A calcium (Ca2+) release-activated channel (CRAC) inhibitor, with potential antineoplastic activity. Upon administration, RP4010 binds to and inhibits CRACs, thereby preventing the transport of extracellular Ca2+ into the cell and inhibiting the subsequent activation of Ca2+-mediated signaling and transcription of target genes. CRACs, specialized plasma membrane Ca2+ ion channels composed of the plasma membrane based Orai channels and the endoplasmic reticulum (ER) stromal interaction molecules (STIMs), play key roles in calcium homeostasis and are over-activated in a number of cancer cell types. Aberrant activation of CRACs leads to increased cancer cell proliferation.
calcium saccharate: The calcium salt form of glucaric acid, a natural substance found in many fruits and vegetables, with potential anti-cancer property. One of the key processes in which the human body eliminates toxic chemicals as well as hormones (such as estrogen) is by attaching glucuronic acid to them in the liver and then excreting the complex in the bile. When beta-glucuronidase breaks the bond, it prolongs the stay of the hormone or toxic chemical in the body. Elevated beta-glucuronidase activity has been implicated to be associated with an increased risk for hormone-dependent cancers like breast, prostate, and colon cancers. Therefore, supplementing calcium glucarate may suppress the developments of hormone-dependent cancers.
calcium-41 chloride aqueous solution: An orally bioavailable aqueous solution containing the chloride salt of the radioisotope calcium-41 (41Ca) with phosphate-binding and radioisotopic activities. Upon administration of calcium-41 chloride aqueous solution, calcium-41 is preferentially taken up by osteoblasts, which generate mineralized osteoid containing calcium. Calcium-41 accumulation and turnover in bone can be measured with bone scintigraphy and urinary isotope excretion.
calcium-46 chloride aqueous solution: An orally bioavailable aqueous solution containing the chloride salt of the radioisotope calcium-46 (46Ca) with phosphate-binding and radioisotopic activities. Upon administration of calcium-46 chloride aqueous solution, calcium-46 is preferentially taken up by osteoblasts, which generate mineralized osteoid containing calcium. Calcium-46 accumulation and turnover in bone can be measured with bone scintigraphy and urinary isotope excretion testing.
Calculus bovis/Moschus/Olibanum/Myrrha capsule: An orally available traditional Chinese medicine (TCM)-based capsule formulation containing Calculus bovis, the dried gallstones of cattle, Moschus, also referred to as deer musk, the resin Olibanum and the resin Myrrha, with potential antineoplastic and chemopreventive activities. Although the exact mechanisms of action through which the active ingredients in the Calculus bovis/Moschus/Olibanum/Myrrha capsule elicit their effects have yet to be fully elucidated, they may, upon intake, exert their antineoplastic activity through modulation of the immune system, inhibition of tumor cell proliferation and induction of apoptosis.
Caldolor: (Other name for: ibuprofen injection)
caldonirimab: A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, caldonirimab targets and binds to both PD-1 and CTLA4 expressed on tumor-infiltrating T lymphocytes (TILs), and inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity.
Calendula officinalis/Plantago major/Cochlearia armoracia/ Hamamelis virginiana herbal toothpaste: A phytochemical-based toothpaste containing Calendula officinalis, Plantago major, Cochlearia armoracia, Hamamelis virginiana with potential soothing activity. Calendula officinalis/Plantago major/Cochlearia armoracia/ Hamamelis virginiana herbal toothpaste may relieve the discomfort associated with radiation-induced mucositis.
calendula ointment: An ointment containing the flowers of the marigold plan, Calendula officinalis, with potential skin protective and healing activities. Upon topical administration, Calendula ointment may provide a protective skin barrier, and may promote healing of damaged or irritated skin.
calfactant: A sterile suspension composed of an extract of bovine pulmonary surfactant with surfactant activity. Calfactant contains phospholipids, neutral lipids, and hydrophobic surfactant-associated proteins B (SP-B) and C (SP-C). Upon intratracheal administration, this agent, mimicking endogenous pulmonary surfactant, lines the alveoli and smallest bronchioles, keeping alveoli open during expiration by lowering surface tension. Resulting improvements in lung compliance and respiratory gas exchange may lead to improvements in ventilation and oxygenation.
Calomist: (Other name for: cyanocobalamin)
Calquence: (Other name for: acalabrutinib maleate monohydrate)
CALR exon 9 mutant peptide vaccine/Montanide ISA-51: A peptide vaccine consisting of a calreticulin (CALR) mutant peptide, CALRLong36, and montanide ISA 51 with potential antineoplastic activity. Upon vaccination, the CALR exon 9 mutant peptide vaccine may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated response against tumor cells harboring mutations in exon 9 of the calreticulin gene. CALR, an endoplasmic reticulum chaperone protein that normally facilitates protein folding, immune response, and hematopoiesis, is often mutated in patients with chronic myeloproliferative neoplasms. In its mutant form, CALR is secreted into the plasma, where it binds to and activates the thrombopoietin receptor MPL and initiates downstream JAK/STAT signaling. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil (w/o) emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
Calusterone: A 17-alkylated orally active androgenic steroid. Calusterone may alter the metabolism of estradiol and reduce estrogen production.
Camcevi: (Other name for: leuprolide mesylate)
Camidanlumab Tesirine: An immunoconjugate consisting of a human immunoglobulin (Ig) G1 monoclonal antibody directed against the alpha subunit of the interleukin-2 receptor (IL-2R alpha or CD25) and conjugated, via a cleavable linker, to a synthetic, cross-linking agent pyrrolobenzodiazepine (PBD) dimer that targets DNA minor grooves, with potential antineoplastic activity. The monoclonal antibody portion of the anti-CD25 antibody-drug conjugate (ADC) ADCT-301 specifically binds to the cell surface antigen CD25. This causes the internalization of ADCT-301 and the subsequent release of the cytotoxic PBD moiety. The imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD25-overexpressing tumor cells. CD25, a transmembrane receptor and tumor-associated antigen (TAA), is expressed on certain cancer cells.
camizestrant: An orally available selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon administration, camizestrant binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.
camonsertib: An orally available inhibitor of ataxia telangiectasia and Rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, camonsertib selectively targets and inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase checkpoint kinase 1 (CHK1). This prevents ATR-mediated signaling, which results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival. It is activated by DNA damage caused during DNA replication-associated stress.
camoteskimab: A human immunoglobulin G1 (IgG1) monoclonal antibody against the pro-inflammatory cytokine interleukin-18 (IL-18), with potential anti-inflammatory and antineoplastic activities. Upon administration, camoteskimab selectively targets and binds to IL-18, thereby inhibiting IL-18-mediated signaling and inflammation mediated by this pathway. In addition, this may inhibit IL-18-mediated immunosuppression in the multiple myeloma microenvironment. IL-18 is a member of the interleukin-1 (IL-1) cytokine superfamily. Elevated IL-18 level is associated with disease progression and poor prognosis in multiple myeloma.
Campath: (Other name for: alemtuzumab)
camphor/herbal formulation-based topical plaster: A combination topical plaster preparation containing camphor and herbal ingredients including Lamiophlomis rotata extra ct, turmeric, Oxytropis chiliophylla, Myricaria paniculata stem, safflower and Szechuan peppercorn, with potential analgesic activity. Upon administration, camphor, a terpenoid extracted from camphor laurel (Cinnamonum camphora) tree, can be absorbed readily through the skin and produces a cooling feeling. The camphor/herbal formulation-based topical plaster may be used for the temporary relief of aches and pains.
Camptogen: (Other name for: rubitecan)
Camptosar: (Other name for: irinotecan hydrochloride)
camptothecin: An alkaloid isolated from the Chinese tree Camptotheca acuminata, with antineoplastic activity. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, 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. (NCI)
camptothecin analogue TLC388: A synthetic analogue of camptothecin with potential antineoplastic and radio-sensitizing activities. Camptothecin analogue TLC388 selectively stabilizes topoisomerase I-DNA covalent complexes during S-phase, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Topoisomerase I relaxes negative super-coiled DNA during replication and transcription. This agent has been chemically modified to enhance the potency and stability of camptothecin.
camptothecin-20(S)-O-propionate hydrate: The hydrated, crystalline propionate ester (attached in position C-20) prodrug of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, with potential antineoplastic activity. Upon entry into cells, camptothecin-20(S)-O-propionate is hydrolyzed by esterases into the active form camptothecin. Camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, 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, thus inhibiting DNA replication and triggering apoptotic cell death. Camptothecin readily undergoes hydrolysis at physiological pH, changing its conformation from the active, S-configured lactone structure to an inactive carboxylate form. The ester chain in the vicinity of the S-configured lactone moiety, a key determinant for the chemotherapeutic efficacy of the camptothecins, inhibits protein binding, rendering this agent resistant to hydrolysis and prolonging its half-life.
camrelizumab: A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1,) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1210 binds to and blocks the binding of PD-1, expressed on activated T lymphocytes, B cells and natural killer (NK) cells, to its ligands programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen presenting cells (APCs). This prevents the activation of PD-1 and its downstream signaling pathways. This restores immune function through the activation of cytotoxic T lymphocytes (CTLs) and cell-mediated immune responses against tumor cells or pathogens. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.
camsirubicin: A synthetic non-cardiotoxic analogue of the anthracycline antibiotic doxorubicin with potential antineoplastic activity. Camsirubicin intercalates DNA and impedes the activity of topoisomerase II, inducing single and double-stranded breaks in DNA; inhibiting DNA replication and/or repair, transcription, and protein synthesis; and activating tumor cell apoptosis.
canagliflozin: A C-glucoside with a thiophene ring that is an orally available inhibitor of sodium-glucose transporter 2 (SGLT2) with antihyperglycemic activity. Canagliflozin is also able to reduce body weight and has a low risk for hypoglycemia.
canakinumab: A recombinant monoclonal antibody targeting human interleukin-1 beta (IL-1b), with anti-inflammatory and immunomodulating activities. Canakinumab binds IL-1b and prevents the binding of IL-1b to the IL-1 receptor and inhibits IL-1b-mediated signaling. This may suppress inflammatory responses mediated by IL-1b. IL-1b, a proinflammatory cytokine, plays a key role in inflammation.
canarypox-hIL-12 melanoma vaccine: A vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) that encodes the gene for human interleukin-12 (hIL-12). Produced mainly by B-cells, IL-12 is an endogenous cytokine that activates natural killer (NK) cells, promotes cytotoxic T lymphocyte (CTL) responses, induces the release of interferon-gamma (IFN-gamma), and may exhibit antitumor and anti-angiogenic effects. Vaccination with canarypox-hIL-12 melanoma vaccine may stimulate the host immune system to mount an immune response against tumor cells, thereby inhibiting tumor growth and/or metastasis.
cancell: Cancell (Entelev or Cantron), is a liquid that has been produced in various forms, principally by two manufacturers, since the late 1930s. The exact composition of Cancell/Entelev is unknown, but the U.S. Food and Drug Administration (FDA) has listed the components as inositol, nitric acid, sodium sulfite, potassium hydroxide, sulfuric acid, and catechol. NCI studies determined that the mixture lacked substantial antitumor activity. (from CancerNet)
cancer cell metabolism modulator OMT-111: A cancer cell metabolism modulator, with potential antineoplastic activity. Upon administration, OMT-111 inhibits pyruvate dehydrogenase kinase (PDH), resulting in the activation of the citric acid cycle in mitochondria, which leads to the degradation of hypoxia-inducible factor 1-alpha (HIF1A). This may result in decreased expression of HIF1A downstream target genes important to tumor growth and survival, a reduction in tumor cell proliferation, and the induction of tumor cell apoptosis. OMT-111 may stimulate apoptosis in cancer cells by restoring normal mitochondrial-induced apoptotic signaling.
cancer peptide vaccine S-588410: A cancer peptide vaccine containing five human leukocyte antigen (HLA)-A*2402-restricted epitope peptides derived from as of yet not disclosed oncoantigens, with potential immunostimulating and antineoplastic activities. Upon administration of the cancer peptide vaccine S-588410, the peptides may stimulate a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing the antigens. This decreases proliferation of susceptible tumor cells.
Cancidas: (Other name for: caspofungin acetate)
Candesartan Cilexetil: A synthetic, benzimidazole-derived angiotensin II receptor antagonist prodrug with antihypertensive activity. After hydrolysis of candesartan cilexetil to candesartan during gastrointestinal absorption, candesartan selectively competes with angiotensin II for the binding of the angiotensin II receptor subtype 1 (AT1) in vascular smooth muscle, blocking angiotensin II-mediated vasoconstriction and inducing vasodilatation. In addition, antagonism of AT1 in the adrenal gland inhibits angiotensin II-stimulated aldosterone synthesis and secretion by the adrenal cortex; sodium and water excretion increase, followed by a reduction in plasma volume and blood pressure.
Candida albicans antigen injection: An injectable formulation composed of antigens derived from the culture filtrate and cells of two different strains of Candida albicans (C. albicans), with immunomodulatory activity. Upon intralesional administration into the cutaneous human papilloma virus (HPV)-infected warts, the C. albicans antigens stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated immune response against the injected antigens and cause a delayed type hypersensitivity response against other local antigens, including antigens within the wart tissue. This leads to the production of Th1 cytokines, and the activation of natural killer (NK) cell- and CTL- mediated killing of HPV-infected cells. This causes clearing of both local and distant warts, and prevents both HPV infection and wart formation that results from HPV infection.
Candida albicans skin test reagent: A culture filtrate of cells of Candida albicans propagated in a chemically defined medium and used as a recall antigen to evaluate cellular immunity in infection, cancer, and other disease states. (NCI)
Candida antigen extract patch VDMN-21: An dissolvable microarray-based formulation containing an extract of Candida albicans (C. albicans) antigens, with immunomodulatory activity. Upon administration of the C. albicans antigen extract patch VDMN-21 adjacent to the cutaneous human papilloma virus (HPV)-infected wart(s), the C. albicans antigens, upon release from the microarray, stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated immune response against the C. albicans antigens and cause a delayed type hypersensitivity response against other local antigens, including antigens within the wart tissue. This leads to the production of Th1 cytokines, and the activation of natural killer (NK) cell- and CTL- mediated killing of HPV-infected cells. This causes clearing of both local and distant warts, and prevents HPV infection and wart formation that results from HPV infection.
Candin: (Other name for: Candida albicans antigen injection)
canerpaturev: A non-engineered, naturally oncolytic, replication-competent spontaneous herpes simplex virus (HSV) type I mutant variant. Upon intratumoral injection, canerpaturev transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. In addition, this agent may increase host immune responses that may kill non-infected tumor cells.
Canertinib Dihydrochloride: The hydrochloride salt of an orally bio-available quinazoline with potential antineoplastic and radiosensitizing activities. Canertinib binds to the intracellular domains of epidermal growth factor receptor tyrosine kinases (ErbB family), irreversibly inhibiting their signal transduction functions and resulting in tumor cell apoptosis and suppression of tumor cell proliferation. This agent also acts as a radiosensitizing agent and displays synergistic activity with other chemotherapeutic agents.
canfosfamide hydrochloride: The hydrochloride salt of a modified glutathione analogue with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 into an alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor proliferation. S-transferase P1-1 is an enzyme that is overexpressed in many human malignancies.
Cannabics SR: (Other name for: Cannabis extract oil SR capsule)
cannabidiol: A phytocannabinoid derived from Cannabis species, which is devoid of psychoactive activity, with analgesic, anti-inflammatory, antineoplastic and chemopreventive activities. Upon administration, cannabidiol (CBD) exerts its anti-proliferative, anti-angiogenic and pro-apoptotic activity through various mechanisms, which likely do not involve signaling by cannabinoid receptor 1 (CB1), CB2, or vanilloid receptor 1. CBD stimulates endoplasmic reticulum (ER) stress and inhibits AKT/mTOR signaling, thereby activating autophagy and promoting apoptosis. In addition, CBD enhances the generation of reactive oxygen species (ROS), which further enhances apoptosis. This agent also upregulates the expression of intercellular adhesion molecule 1 (ICAM-1) and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) and decreases the expression of inhibitor of DNA binding 1 (ID-1). This inhibits cancer cell invasiveness and metastasis. CBD may also activate the transient receptor potential vanilloid type 2 (TRPV2), which may increase the uptake of various cytotoxic agents in cancer cells. The analgesic effect of CBD is mediated through the binding of this agent to and activation of CB1.
cannabinoid-derived inhalation capsule PPP011: A capsule-based inhalation formulation containing a blend of synthetic cannabinoids, including cannabidiol (CBD) and tetrahydrocannabinol (THC), with potential anti-cachexia and analgesic activities. Upon inhalation of PPP011, the CBDs target and bind to the cannabinoid (CB) receptors. This may increase appetite, food intake and may relief pain. CB receptors, belonging to the G protein-coupled receptor superfamily, are involved in the regulation of appetite, food intake, body weight and nociception.
Cannabinol: A cannabinoid isolated from the plant Cannabis that is a metabolite of tetrahydrocannabinol (THC), with potential immunosuppressive and anti-inflammatory activities. Cannabinol preferentially binds to the cannabinoid G-protein coupled receptor CB2, which is mainly expressed on a variety of immune cells, such as T cells, B cells, macrophages and dendritic cells. Stimulation of CB2 receptors by cannabinol may both trigger apoptosis in these cells and inhibit the production of a variety of cytokines. Cannabinol exerts minimal affinity for CB1 and has a weak effect on the central nervous system.
Cannabis extract oil SR capsule: A sustained-release (SR), oil-based oral capsule composed of a cannabis extract, which contains a variety of cannabinoids but is comprised mainly of tetrahydrocannabinol (THC), with potential anti-cachexic and analgesic activities. Upon oral administration, the cannabinoids bind to the cannabinoid G-protein coupled receptor CB1, which is located in both central and peripheral neurons; CB1 receptor activation inhibits adenyl cyclase, increases various signal transduction pathways, and modulates the activity of various ion channels. This provides an analgesic effect, increases appetite, decreases chemotherapy-induced nausea and vomiting, and improves weight gain. The formulation allows for the immediate release of cannabinoids and quick onset of action, which is followed by a gradual release of cannabinoids. The SR form facilitates longer lasting therapeutic effects and causes fewer psychoactive side effects when compared to non-SR cannabinoid-containing oral formulations.
Cannabis sativa extract: An extract from the flowering top of Cannabis sativa, which contains a variety of cannabinoids such as tetrahydrocannabinol (THC), with potential anti-cachexic, muscle relaxing and analgesic activities. Upon administration, the cannabinoids bind to the cannabinoid G-protein coupled receptor CB1, which is located in both central and peripheral neurons. CB1 receptor activation inhibits adenyl cyclase, increases various signal transduction pathways, and modulates the activity of various ion channels. This provides an analgesic effect, may prevent muscle spasms, and may increase appetite.
Cannabis SR capsules: (Other name for: Cannabis extract oil SR capsule)
Cantrixil: A cyclodextrin-encapsulated, third generation super-benzopyran (SBP) compound with potential antineoplastic activity. Upon intraperitoneal (IP) administration, cantrixil enhances the activation and expression of c-Jun, downregulates phosphorylated extracellular signal-regulated kinase (p-ERK) and induces activation of caspase-3, -7 and -9, thereby inducing tumor cell apoptosis. c-Jun, an activator protein-1 (AP-1) transcription factor component, is involved in a wide range of cellular processes including cell cycle progression, differentiation, cell transformation and apoptosis.
cantuzumab ravtansine: An immunotoxin of a humanized monoclonal antibody C242 (MoAb HuC242) conjugated to a derivative of the cytotoxic agent maytansine, DM4, with potential antitumor activity. Cantuzumab ravtansine is generated from MoAb C242, which is raised against a cell surface superantigen, CA242, found in a variety of human tumor cells. Upon binding and entry, the immunoconjugate releases the maytansinoid agent DM4, which binds to tubulin, thereby affecting microtubule assembly/disassembly dynamics. As a result, this agent prevents cell division and reduces cell growth of cancer cells that express CA242.
capecitabine: A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites. As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells. FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand.
capecitabine rapidly disintegrating tablet: A rapidly disintegrating film-coated tablet composed of the fluoropyrimidine carbamate antimetabolite capecitabine with antineoplastic activity. As a prodrug, capecitabine is converted to 5'-deoxy-5-fluorocytidine (5'-DFCR) by hepatic carboxylesterase and then to 5'-deoxy-5-fluorouridine (5'-DFUR) by cytidine deaminase and is eventually activated by thymidine phosphorylase to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine triphosphate production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. Capecitabine rapidly disintegrating tablet (RDT) contains the water insoluble, disintegrating agent crospovidone which very rapidly disperses and swells in water making this RDT easier to swallow than the traditional capecitabine tablet.
capecitabine/methotrexate/vinorelbine regimen: A regimen composed of capecitabine, methotrexate and vinorelbine that can potentially be used in the treatment of breast cancer.
Capesaris: (Other name for: estrogen receptor agonist GTx-758)
Caphosol: (Other name for: supersaturated calcium phosphate rinse)
capivasertib: A novel pyrrolopyrimidine derivative, and an orally available inhibitor of the serine/threonine protein kinase AKT (protein kinase B) with potential antineoplastic activity. Capivasertib binds to and inhibits all AKT isoforms. Inhibition of AKT prevents the phosphorylation of AKT substrates that mediate cellular processes, such as cell division, apoptosis, and glucose and fatty acid metabolism. A wide range of solid and hematological malignancies show dysregulated PI3K/AKT/mTOR signaling due to mutations in multiple signaling components. By targeting AKT, the key node in the PIK3/AKT signaling network, this agent may be used as monotherapy or combination therapy for a variety of human cancers.
caplacizumab-yhdp: A humanized, bivalent anti-von Willebrand factor (VWF) nanobody, with potential anti-platelet and anti-thrombotic activities. Upon administration, caplacizumab-yhdp specifically binds, with its two identical monovalent moieties, to the A1 domain of the adhesive glycoprotein VWF, thereby inhibiting and neutralizing VWF activity. This prevents the interaction of ultra-large VWF (ULVWF) with the platelet glycoprotein (GP)Ib-IX-V receptor complex, and prevents ULVWF-mediated platelet adhesion, and aggregation, which reduces thrombus formation. VWF is a glycoprotein and plays a key role in blood coagulation. Increased VWF, which is seen in a number of diseases, is associated with an increased risk in thrombosis; in thrombotic thrombocytopenic purpura (TTP), increased levels of ULVWF and thus increased and abnormal platelet aggregation are seen due to impaired breakdown of ULVWF. The nanobody formulation allows for rapid distribution, onset of action and clearance. The nanobody is based on the smallest functional fragments of the immunoglobulin heavy-chain variable domains that occur naturally in the Camelidae family.
capmatinib: An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Capmatinib selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
capmatinib hydrochloride: The hydrochloride salt form of capmatinib, an orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Capmatinib selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
Capoten: (Other name for: captopril)
CAPOX regimen: A regimen consisting of capecitabine and oxaliplatin used as a treatment for advanced stage colorectal cancer. This regimen differs from a similar regimen, XELOX, with regards to the dosing schedule for oxaliplatin.
Caprelsa: (Other name for: vandetanib)
capsaicin: A chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.
capsase-9-PP2A interaction inhibitor PEP-010: A cell penetrating and interfering peptide composed of a cell-penetrating part that delivers the peptide into the cellular cytosol and an interfering part that inhibits the interaction between the proteins intracellular caspase-9 and protein phosphatase 2A (PP2A) proteins, with potential antineoplastic activity. Upon administration, the cell-penetrating part of capsase-9-PP2A interaction inhibitor PEP-010 delivers the peptide into the cellular cytosol and the interfering part of PEP-010 disrupts the interaction between intracellular caspase-9 and PP2A. This leads to the release and the activation of caspase-9, thereby restoring tumor cell apoptosis. Activated caspase-9 is involved in the induction of caspase-dependent apoptosis. PP2A, a serine/threonine phosphatase, plays a key role in the control of cell growth and DNA damage repair.
Captisol-enabled Melphalan IV: (Other name for: melphalan hydrochloride/sulfobutyl ether beta-cyclodextrin complex)
captopril: A sulfhydryl-containing analog of proline with antihypertensive activity and potential antineoplastic activity. Captopril competitively inhibits angiotensin converting enzyme (ACE), thereby decreasing levels of angiotensin II, increasing plasma renin activity, and decreasing aldosterone secretion. This agent may also inhibit tumor angiogenesis by inhibiting endothelial cell matrix metalloproteinases (MMPs) and endothelial cell migration. Captopril may also exhibit antineoplastic activity independent of effects on tumor angiogenesis.
CaPVax: (Other name for: dendritic cell-recombinant prostate-specific membrane antigen vaccine)
CAR NK cells SZ003: A preparation of natural killer cells (NKs) expressing a chimeric antigen receptor (CAR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. Upon administration, the CAR NK cells SZ003 recognize and induce selective cytotoxicity in tumor cells expressing the TAA.
CAR-NK cells SZ011: A preparation of natural killer cells (NKs) expressing a chimeric antigen receptor (CAR) specific for an as of yet undisclosed tumor-associated antigen (TAA), with potential immunomodulating and antineoplastic activities. Upon administration, the CAR-NK cells SZ011 recognize and induce selective cytotoxicity in tumor cells expressing the TAA.
CAR-T cells AMG 119: A preparation of T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) that targets an as of yet unidentified tumor-associated antigen (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration of the CAR T-cells AMG 119, the T cells target, bind to and induce selective cytotoxicity in tumor cells expressing the TAA.
Carac: (Other name for: fluorouracil)
Carac: (Other name for: topical fluorouracil)
caracemide: An agent derived from acetohydroxamic acid with potential antineoplastic activity. Caracemide inhibits ribonuclease reductase, resulting in decreased DNA synthesis and tumor growth; it also inhibits acetylcholinesterase. In vivo, caracemide contributes to the formation of the neurotoxin methyl isocyanate; this effect, along with the agent's acetylcholinesterase activity, may be responsible for the severe central nervous system toxicity observed in clinical trials.
carbamazepine: A tricyclic compound chemically related to tricyclic antidepressants (TCA) with anticonvulsant and analgesic properties. Carbamazepine exerts its anticonvulsant activity by reducing polysynaptic responses and blocking post-tetanic potentiation. Its analgesic activity is not understood; however, carbamazepine is commonly used to treat pain associated with trigeminal neuralgia.
carbendazim: A broad-spectrum benzimidazole antifungal with potential antimitotic and antineoplastic activities. Although the exact mechanism of action is unclear, carbendazim appears to binds to an unspecified site on tubulin and suppresses microtubule assembly dynamic. This results in cell cycle arrest at the G2/M phase and an induction of apoptosis.
carbenicillin: A broad-spectrum, semi-synthetic penicillin antibiotic with bactericidal and beta-lactamase resistant activity. Carbenicillin acylates the penicillin-sensitive transpeptidase C-terminal domain by opening the lactam ring. This inactivation prevents the cross-linkage of peptidoglycan strands, thereby inhibiting the third and last stage of bacterial cell wall synthesis. This leads to incomplete bacterial cell wall synthesis and eventually causes cell lysis.
carbetimer: Carbetimer (carboxyimamidate) is a low molecular weight derivatized copolymer of ethylene and maleic anhydride. It has demonstrated antitumor activity against several animal models. It has calcium chelation activity but seems to inhibit growth of sensitive cells by disrupting nucleoside uptake and metabolism.
carbetocin: A long-acting synthetic agonist analogue of human oxytocin, with antihemorrhagic and uterotonic activities. Upon administration, carbetocin targets, binds to and activates peripheral oxytocin receptors that are present on the smooth musculature of the uterus. This causes uterus contractions and prevents excessive bleeding after childbirth, particularly following Cesarean section, and may be used to decrease blood loss during hysteroscopic myomectomy.
carbidopa: A hydrazine derivative of dopa. Carbidopa is a peripheral dopa decarboxylase inhibitor that is used as an adjunct to levodopa administration to prevent peripheral biosynthesis of levodopa to dopamine, thereby reducing peripheral side effects. Carbidopa does not penetrate the blood brain barrier so that levodopa, after it reaches the brain, can be metabolized to dopamine by dopa decarboxylase where it exerts its effect on dopamine receptors.
carbidopa/levodopa: An orally available combination of carbidopa, an inhibitor of aromatic amino acid decarboxylation, and levodopa, an inert, metabolic precursor to dopamine, with dopaminergic and antiparkinsonian properties. Upon oral administration, levodopa crosses the blood-brain barrier (BBB) and is decarboxylated to dopamine via dopa decarboxylase in the brain, promoting increased activation of dopamine receptors. Carbidopa inhibits dopa decarboxylase in the periphery, thereby preventing decarboxylation of levodopa in extracerebral tissues and increasing the delivery of dopamine to the central nervous system (CNS). As carbidopa does not cross the BBB, it does not interfere with CNS levodopa metabolism.
Carbocaine: (Other name for: mepivacaine hydrochloride)
carbogen: An inhalant consisting of hyperoxic gas (95%-98% oxygen and 2%-5% carbon dioxide) with radiosensitizing properties. Inhaled carbogen reduces diffusion-limited tumor hypoxia, increasing tumor radiosensitivity due to the increased availability of molecular oxygen for cytotoxic radiation-induced oxygen free radical production.
carbohydrate supplement drink: A nutritional supplement drink containing 12.5% carbohydrates, which may enhance recovery following gastrointestinal (GI) surgery. Oral intake of the carbohydrate drink before surgery may prevent insulin resistance and associated hyperglycemia. It may also maintain adequate protein balance and muscle function. Ultimately, giving carbohydrates immediately before surgery may improve overall recovery time and return of GI function. It may also decrease muscle loss.
carbomer/polycarbophil-based vaginal gel: A carbomer and polycarbophil-based vaginal gel preparation that may be used for vaginal lubrication and for the restoration and maintenance of normal vaginal acidity. Upon intravaginal administration of carbomer/polycarbophil-based vaginal gel, polycarbophil may adhere to vaginal epithelial cells and moisturize vaginal tissue, and restore and maintain normal vaginal acidity.
carbon C 11 alpha-methyltryptophan: A radiopharmaceutical containing an analogue of tryptophan, alpha-methyltryptophan (AMT), labeled with carbon 11 (11C), used to measure serotonin synthesis in the human brain using positron emission tomography (PET). Upon administration and once it crosses the blood-brain barrier and into the cytoplasm of serotonergic neurons, carbon C 11 alpha-methyltryptophan acts as a substrate for the enzyme tryptophan hydroxylase and undergoes conversion to carbon C 11 alpha-methyl-5-hydroxytryptophan, also known as C 11 alpha-methyl-serotonin (AMS). C 11 AMS accumulates in serotonergic nerve terminals in proportion to the synthesis rate of serotonin because C 11 AMS cannot be broken down by the enzyme monoamine oxidase, and thus the synthesis rate of serotonin can be imaged using PET. C 11 AMT is not incorporated into proteins, nor are metabolites released into the blood pool, making C 11 AMT an excellent tracer for serotonin synthesis in vivo.
carbon C 11 AZ14193391: A radioconjugate composed of AZ14193391, a central nervous system (CNS) penetrant and selective inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, labeled with the positron-emitting isotope carbon C 11, with potential use in imaging via positron emission tomography (PET). Upon administration, carbon C 11 AZ14193391 specifically targets and binds to PARP1. Upon PET imaging, this radioligand may allow for the assessment of PARP1 expression in tumors and visualization of AZ14193391. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs).
carbon C 11 choline: A radiotracer consisting of choline labeled with the positron-emitting isotope carbon C 11 with potential imaging use. Upon administration, C-11 choline incorporates into tumor cells through an active, carrier-mediated transport mechanism for choline and then is phosphorylated intracellularly by choline kinase, an enzyme frequently upregulated in human tumors, yielding phosphoryl C-11 choline. In turn, phosphoryl C-11 choline is integrated into phospholipids in the cell membrane as part of phosphatidylcholine. As the proliferation of cancer cells is much higher than normal cells, tumor cells exhibit an increased rate of C-11 choline uptake and incorporation, allowing tumor imaging with positron emission tomography (PET).
carbon C 11 erlotinib hydrochloride: The hydrochloride salt form of the quinazoline derivative erlotinib labeled with the positron-emitting isotope carbon C 11, with potential use in imaging. Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic tyrosine kinase domain of the epidermal growth factor receptor (EGFR). Following exposure to this agent, EGFR expression status can be determined and EGFR overexpressing tumor cells can be visualized using positron emission tomography (PET) imaging. This may be useful in determining the tumor cell response to a particular EGFR kinase inhibitor in individual patients. EGFR, a receptor tyrosine kinase, is overexpressed in numerous cancer cell types, and plays a significant role in tumor cell progression.
carbon C 11 glutamine: Upon intravenous administration of 11C-glutamine, glutamine is preferentially taken up by cancer cells. Upon PET, the biodistribution and uptake by cancer cells can be assessed. Tumor cells use the amino acid glutamine for nutritional purposes including energy production and growth; as tumor cells proliferate more rapidly than normal healthy cells, glutamine uptake is higher in certain cancer cells.
carbon C 11 martinostat: A radioconjugate composed of martinostat, a histone deacetylase (HDAC) inhibitor, labeled with the positron-emitting isotope carbon C 11, with potential use in imaging via positron emission tomography (PET)/magnetic resonance imaging (MRI). Upon intravenous administration of carbon C 11 martinostat, the martinostat moiety targets and binds to HDAC on tumor cells. Upon PET/MRI imaging, this radioligand may allow for the assessment of HDAC-expressing tumor cells. HDACs, upregulated in many tumor cell types, are a family of metalloenzymes responsible for the deacetylation of chromatin histone proteins.
carbon C 11 metformin: A radiopharmaceutical tracer containing the anti-diabetic agent metformin, a biguanide and hydrophilic organic cation, and labeled with carbon 11 (11C), used to measure metformin uptake by cancer cells using positron emission tomography (PET). Upon administration of carbon C 11 metformin, the metformin moiety targets and binds to cancer cells; in turn, the compound is taken up by cancer cells. Upon PET, metformin distribution into cancer cells can be visualized, which allows for a prediction of the anti-cancer efficacy of metformin, based on tumor cell uptake. Metformin transport, such as uptake into cancer cells, appears to be correlated with the expression of organic cation transporters (OCT) 1-3, multidrug and toxin extrusion (MATE) 1 and 2, and plasma membrane monoamine transporter (PMAT). OCTs, MATEs and PMAT play a key role in the distribution and excretion of organic cationic compounds.
carbon C 11 methylaminoisobutyrate: A synthetic neutral amino acid analog radiolabeled with carbon C 11 with potential use for metabolic tumor imaging during positron emission tomography (PET). Upon administration, carbon C 11 methylaminoisobutyrate ([(11)C]MeAIB) is taken up by and accumulates in cancer cells through the A-type (alanine-preferring) amino acid transport system. Upon imaging of the radioisotope, the distribution patterns of MeAIB and its uptake by cancer cells can be further elucidated. This may establish its usefulness as a tumor tracer in the diagnosis of certain cancers. Amino acid transport system A is highly upregulated in malignant cells and facilitates the uptake of amino acids needed for tumor cell proliferation.
carbon C 11 N-desmethyl-loperamide: A radiopharmaceutical containing N-desmethyl loperamide (dLop) labeled with carbon 11 (11C), used to measure the activity of efflux transporter P-glycoprotein (P-gp) in positron emission tomography (PET). Upon administration, carbon C 11 N-desmethyl-loperamide acts as a substrate for the efflux transporter P-gp. Upon uptake by P-gp at the blood-brain barrier (BBB) and subsequent PET imaging, this radioligand may allow for prediction of P-gp function and expression in brain tumor patients. As P-gp activity may influence response to therapy, measuring P-gp activity may be beneficial when choosing chemotherapy. P-gp, encoded by the MDR-1 gene and a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters, is overexpressed by some MDR tumors and may contribute to multidrug resistance to chemotherapy.
carbon C 11 PBR-28: A radioconjugate composed of a ligand for the 18 kDa translocator protein (TSPO) conjugated to the radioisotope carbon C 11, that can be used as a diagnostic imaging agent to detect TSPO-expressing cells using positron emission tomography (PET). Upon administration of carbon C 11 PBR-28, the PBR-28 moiety targets and binds to TSPO-expressing cells. Upon PET, carbon C 11 can be detected and TSPO-expressing cells can be visualized. This can facilitate detection of inflammatory sites and cancer cells. TSPO, also called the peripheral benzodiazepine receptor (PBR), is found on the outer mitochondrial membrane and is overexpressed on a variety of cancer cells and during inflammation.
carbon C 11 Pittsburgh compound B: A radioconjugate composed of the beta-amyloid binding agent Pittsburgh compound B (PiB), a derivative of the amyloid-binding dye thioflavin T (ThT), that is conjugated to the radioisotope carbon C11, with potential amyloid imaging activity upon positron emission tomography (PET). Upon administration of carbon C 11 PiB, the PiB moiety targets and binds to beta-amyloid plaques in the brain, which can then be detected and analyzed using PET imaging. Increased production and concentration of amyloid beta protein and the deposition of amyloid plaques in the brain are correlated with the cognitive decline seen in neurodegenerative diseases, such as dementia, Alzheimer's disease (AD) and chemotherapy-induced cognitive impairment (CICI).
carbon C 11 sarcosine: A radiotracer consisting of sarcosine, the N-methyl derivative of the amino acid glycine, labeled with the positron-emitting isotope carbon C 11, that can be used for tumor imaging upon positron emission tomography/computed tomography (PET/CT). Upon administration, C-11 sarcosine is taken up by and accumulates in tumor cells, thereby allowing tumor imaging with PET/CT. Sarcosine, a non-proteinogenic amino acid and oncometabolite, is elevated in certain tumor cell types. Its expression seems to correlate with increased tumor invasiveness.
carbon C 11 sepantronium bromide: A radiotracer composed of the bromide salt form of sepantronium, a small-molecule survivin antagonist and proapoptotic agent, labeled with the radionuclide carbon C 11, with potential positron emission tomography (PET) imaging activity. Upon administration, sepantronium is selectively taken up by tumor cells, binds to the survivin promoter and inhibits the transcription of survivin, which results in decreased survivin expression. Upon PET imaging, the tissue distribution of sepantronium and its tumor uptake can be assessed. Survivin, a member of the inhibitor of apoptosis (IAP) gene family, is overexpressed in a variety of human cancers; its expression in tumors is associated with a more aggressive phenotype, increased cancer cell proliferation, shorter survival times, and a decreased response to chemotherapy.
carbon C 11 YJH08: A radioconjugate composed of YJH08, a synthetic glucocorticoid receptor (GR) agonist, labeled with the positron-emitting isotope carbon C 11, with potential use in imaging via positron emission tomography (PET). Upon intravenous administration of carbon C 11 YJH08, the YJH08 moiety targets and binds to GR on tumor cells. Upon PET imaging, this radioligand may allow for the assessment of GR-expressing tumor cells. This also allows assessment of YJH08's pharmacokinetic profile and affinity of GR-positive tumor cells. The GR, a member of the nuclear receptor superfamily of ligand-dependent transcription factors, is overexpressed in certain tumor types and may be associated with tumor cell proliferation and treatment resistance.
carbon C 11-JNJ-63779586: A radioconjugate composed of JNJ-63779586 labeled with the positron-emitting isotope carbon C 11, with potential use in imaging via positron emission tomography (PET). Upon administration of carbon C 11-JNJ-63779586, the JNJ-63779586 moiety acts as a substrate for the efflux transporter P-glycoprotein (P-gp) and the breast cancer resistance protein (BCRP). Upon PET imaging, this radioligand may allow for the assessment of P-gp and BCRP function and expression in tumors. As P-gp and BCRP activity may influence response to therapy, measuring P-gp and BCRP activity may be beneficial when choosing chemotherapy. P-gp and BCRP, efflux transporters, are overexpressed by certain tumor cells and may contribute to multidrug resistance to chemotherapy.
carbon C 11-osimertinib: A radioconjugate composed of osimertinib, a third-generation, orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, labeled with the positron-emitting isotope carbon C 11, with potential use in imaging via positron emission tomography (PET). Upon intravenous administration of carbon C 11 osimertinib, the osimertinib targets and binds to mutant forms of EGFR on tumor cells. Upon PET imaging, this radioligand may allow for the assessment of EGFR mutant-expressing tumor cells. This also allows assessment of osimetinib’s pharmacokinetic profile and affinity of EGFR mutant-positive cancer cells and may identify patients who may respond well to osimertinib.
carbon C 13 acetate: The non-radioactive, naturally occurring isotope of acetate, carbon C 13 acetate, with potential use for metabolic tumor imaging upon nuclear magnetic resonance (NMR) spectroscopy. Upon infusion, carbon C 13 acetate is taken up by cancer cells and is utilized by metabolic pathways in the tumor cell. Specifically, the tumor cells oxidize acetate, in the form of acetyl coenzyme A (acetyl-CoA), in the citric acid cycle. Upon 13C-NMR, the metabolic phenotype of a tumor can be assessed. Certain alternative metabolic pathways are activated in tumor cells and use substrates other than glucose, such as acetate, for acetyl-CoA production.
carbon C 13 dextromethorphan: A radioconjugate consisting of dextromethorphan, a synthetic, methylated dextrorotatory analogue of levorphanol, conjugated with carbon-13 [(13)C] with radiotracer activity. (13)C-dextromethorphan can be used in a breath-test phenotype assay of CYP2D6 activity, based on the principle that CYP2D6-mediated O-demethylation cleaves a (13)CH3 that enters the body's carbon pool to be eliminated ultimately as (13)CO2 in expired air, which can be measured. The (13)C-dextromethorphan breath test may prove useful in identifying poor CYP2D6 metabolizers of such important clinical drugs as tamoxifen.
carbon C 13 hyperpolarized bicarbonate: A hyperpolarized (HP) bicarbonate labeled with carbon C 13 (13C), with potential usage in the diagnostic nuclear magnetic resonance (NMR) imaging of cancer cells. Upon administration, carbon C 13 hyperpolarized bicarbonate can be used for the in vivo pH mapping of tumors. As tumor microenvironment (TME) are often acidic, the acidic extracellular pH can be detected and visualized upon NMR using 13C HP bicarbonate. Hyperpolarization of 13C-bicarbonate enhances NMR signals. The acidity of the TME is correlated in tumor aggressiveness, metastatic potential, and therapeutic response.
carbon C 13 idasanutlin: A radiopharmaceutical agent composed of an orally available, small-molecule antagonist of MDM2 (mouse double minute 2; Mdm2 p53 binding protein homolog), and labeled with the radioisotope carbon C 13, with potential use for evaluating the distribution patterns, metabolism and excretion of idasanutlin using nuclear magnetic resonance (NMR) spectroscopy. Upon administration, idasanutlin binds to MDM2 blocking the interaction between the MDM2 protein and the transcriptional activation domain of the tumor suppressor protein p53. By preventing the MDM2-p53 interaction, p53 is not enzymatically degraded and the transcriptional activity of p53 is restored. This may lead to p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger nuclear phosphoprotein and negative regulator of the p53 pathway, is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival. Labeling of idasanutlin with the radioactive tracer carbon C 13 permits the evaluation of idasanutlin's distribution patterns, including binding to and uptake by tumors, metabolism and excretion. This may aid in the understanding of the bioactivity of this agent.
carbon C 13 lycopene: Carbon C 13 labeled lycopene used as a tracer for carotenoid metabolism studies in vivo. After oral administration of carbon C 13 lycopene, in combination with C 13 labeled phytoene and phytofluene, the absorption kinetics, distribution patterns, metabolism and targets of these carotenoids can be measured upon imaging of the non-radioactive C 13. Lycopene, a carotenoid pigment found in high concentrations in tomatoes as well as in other fruits and vegetables, serves as an antioxidant in vivo; its intake has been associated with a reduced risk of certain types of cancer and cardiovascular diseases.
carbon C 13 phytoene: A 40-carbon hydrocarbon precursor of carotenoids radiolabeled to carbon C 13 and potentially used for tracer purposes of phytoene in vivo. Upon administration, phytoene is taken up and accumulates in various tissues. Upon imaging of the radioisotope, the distribution patterns and metabolism of phytoene can be further elucidated which may aid in the understanding of the bioactivity of this agent. Phytoene is a colorless precursor of many carotenoids, including the antioxidant lycopene.
carbon C 13 phytofluene: A 40-carbon hydrocarbon precursor of carotenoids radiolabeled to carbon C 13 and potentially used for tracer purposes of phytofluene in vivo. Upon administration, phytofluene is taken up and accumulates in various tissues. Upon imaging of the radioisotope, the distribution patterns and metabolism of phytofluene can be further elucidated which may aid in the understanding of the bioactivity of this agent. Phytofluene is a colorless precursor of many carotenoids, including the antioxidant lycopene.
carbon C 13 sodium octanoate: The sodium salt form of the medium-chain fatty acid octanoate, and labeled with the isotope carbon C13, used in the octanoate breath test (OBT) to assess hepatic mitochondrial function. Upon ingestion of carbon C13 octanoate, this agent is metabolized in the liver via mitochondrial beta-oxidation. Upon determination of the ratio between 13C/12C of CO2 in exhaled breath, liver function can be assessed.
carbon C 13/nitrogen N 15-labeled valine: A radioconjugate composed of the essential amino acid valine radiolabeled to carbon C 13 and nitrogen N 15, that can potentially be used as a tracer for protein metabolism in vivo using mass spectrometry (MS). Upon administration of carbon C 13/nitrogen N 15-labeled valine, the exogenous valine is taken up by cells and incorporated into proteins. Upon imaging, protein biomarkers containing radiolabeled valine are secreted by tumor cells and can be identified by MS. This may aid in cancer diagnosis and prognosis. Compared to normal cells, tumor cells rapidly take up amino acids to use as protein building blocks.
carbon C 14 anlotinib hydrochloride: A radioconjugate composed of the orally bioavailable hydrochloride salt form of anlotinib, a receptor tyrosine kinase (RTK) inhibitor, labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of anlotinib. Upon administration of carbon C 14 anlotinib hydrochloride, anlotinib targets multiple RTKs, including vascular endothelial growth factor receptor type 2 (VEGFR2) and type 3 (VEGFR3). This agent may both inhibit angiogenesis and halt cell growth in tumor cells that overexpress these RTKs. Labeling of anlotinib with the radioactive tracer carbon C 14 permits the evaluation of this agent's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 dacomitinib: A radioconjugate consisting of an orally bioavailable small-molecule inhibitor of the epidermal growth factor receptor (erbB or HER) family of tyrosine kinases radiolabeled with carbon-14 with potential antineoplastic and beta-emitting radioisotope activity. Dacomitinib specifically and irreversibly binds to and inhibits human Her-1, Her-2, and Her-4, resulting in the proliferation inhibition and apoptosis of tumor cells that overexpress these receptors. The HER receptor family of tyrosine kinases, often overexpressed by a variety of tumor cell types, may contribute to tumor cell proliferation, differentiation, migration, and survival. Dacomitinib radiolabeled with carbon C-14 may be used as a radiotracer in pharmacological studies of dacomitinib metabolism.
carbon C 14 eribulin acetate: A radioconjugate containing the acetate salt of eribulin, labeled with the beta particle-emitting radioisotope carbon C 14, with radioisotopic and potential antineoplastic activities. Upon administration, eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression. The radioisotope moiety of this agent acts as a radioactive tracer.
carbon C 14 fluzoparib: An orally bioavailable radioconjugate composed of fluzoparib, an orally bioavailable inhibitor of poly (ADP-ribose) polymerase (PARP) types 1 and 2, radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of fluzoparib. Upon administration of carbon C 14 fluzoparib, fluzoparib targets, binds to and inhibits PARP, which results in the inhibition of tumor cell proliferation and survival. Labeling of fluzoparib with the radioactive tracer carbon C 14 allows for the evaluation of fluzoparib's pharmacokinetic profile, including its absorption, distribution, metabolism and excretion (ADME).
carbon C 14 gilteritinib: A radioconjugate composed of gilteritinib, an inhibitor of the receptor tyrosine kinases (RTKs) FMS-related tyrosine kinase 3 (FLT3, STK1, or FLK2), AXL (UFO or JTK11) and anaplastic lymphoma kinase (ALK or CD246), labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of gilteritinib. Gilteritinib binds to and inhibits both the wild-type and mutated forms of FLT3, AXL and ALK. This may result in an inhibition of FLT3, AXL, and ALK-mediated signal transduction pathways and the reduction of tumor cell proliferation in cancers that overexpress these RTKs. Labeling of gilteritinib with the radioactive tracer carbon C 14 allows for the evaluation of gilteritinib's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 ibcasertib: An orally bioavailable radioconjugate composed of ibcasertib, an orally bioavailable inhibitor of select serine-threonine kinases including aurora kinase B (aurora B), vascular endothelial growth factor receptors (VEGFRs), stem cell factor receptor (c-KIT) and platelet-derived growth factor receptors (PDGFRs), radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of chiauranib. Upon oral administration of carbon C 14 ibcasertib, ibcasertib targets, binds to and inhibits the activity of aurora B, VEGFRs, c-kit and PDGFRs, which may result in a decrease in the proliferation of tumor cells that overexpress these kinases. Labeling of ibcasertib with the radioactive tracer carbon C 14 allows for the evaluation of chiauranib's pharmacokinetic profile, including its absorption, distribution, metabolism and excretion (ADME).
carbon C 14 idasanutlin: A radiopharmaceutical agent composed of an orally available, small-molecule antagonist of MDM2 (mouse double minute 2; Mdm2 p53 binding protein homolog), and labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetics of idasanutlin. Upon oral administration, idasanutlin binds to MDM2 blocking the interaction between the MDM2 protein and the transcriptional activation domain of the tumor suppressor protein p53. By preventing the MDM2-p53 interaction, p53 is not enzymatically degraded and the transcriptional activity of p53 is restored. This may lead to p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger nuclear phosphoprotein and negative regulator of the p53 pathway, is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival. . Labeling of idasanutlin with the radioactive tracer carbon C 14 permits the evaluation of idasanutlin's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 lenvatinib mesylate: A radioconjugate composed of the orally bioavailable mesylate salt form of lenvatinib, a receptor tyrosine kinase (RTK) inhibitor, labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of lenvatinib. Upon administration of carbon C14 lenvatinib mesylate, lenvatinib targets and binds strongly to multiple RTKs, including vascular endothelial growth factor receptor 1 (VEGFR1;FLT1), VEGFR2 (KDR), VEGFR3 (FLT4), fibroblast growth factor receptor 1 (FGFR1), FGFR2, FGFR3, and FGFR4, platelet derived growth factor receptor alpha (PDGFRa), KIT, and RET. This inhibits growth of tumor cells that overexpress these RTKs. Labeling of lenvatinib with the radioactive tracer carbon C 14 permits the evaluation of lenvatinib's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 lerociclib: An orally bioavailable radioconjugate composed of lerociclib, an orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of lerociclib. Upon administration, carbon C 14 lerociclib selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. Labeling of lerociclib with the radioactive tracer carbon C 14 allows for the evaluation of lerociclib's pharmacokinetic profile, including its absorption, distribution, metabolism and excretion (ADME).
carbon C 14 mivavotinib citrate: A radioconjugate composed of the citrate form of mivavotinib, an orally bioavailable selective inhibitor of the non-receptor tyrosine kinase (RTK) spleen tyrosine kinase (Syk), labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of mivavotinin. Upon administration of carbon C 14 mivavotinib citrate, mivavotinib targets, binds to and inhibits Syk. Labeling of mivavotinib with the radioactive tracer carbon C 14 permits the evaluation of this agent's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME). Syk, a B-cell receptor (BCR)-associated non-receptor tyrosine kinase that mediates B-cell activation, chemotaxis, adhesion and proliferation, is expressed in hematopoietic tissues and is often overexpressed in hematopoietic malignancies.
carbon C 14 ombrabulin: A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), labeled with carbon C 14 with potential antineoplastic activity. The ombrabulin moiety of carbon C 14 ombrabulin binds to the colchicine binding site of endothelial cell tubulin, thereby 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. The radioisotope moiety of this agent acts as a radioactive tracer.
carbon C 14 oxaliplatin: A radioconjugate composed of the platinum agent oxaliplatin labeled with the isotope carbon C 14, that can be used to predict the response to oxaliplatin therapy using accelerator mass spectrometry (AMS). Upon intravenous administration of a microdose of carbon C 14 oxaliplatin, the oxaliplatin moiety covalently links to DNA and forms mono- and di-DNA adducts. The platinum-DNA adduct formation can be measured through quantification of C14-labeled drug-DNA adducts by using AMS. By measuring the microdose-induced DNA damage, the response to oxaliplatin-based chemotherapy can be assessed and predicted. Measurements that indicate either low drug-DNA adduct formation or increased DNA repair (C14 removal from DNA) are correlated with increased resistance to platinum-based chemotherapeutics.
carbon C 14 pevonedistat: An orally bioavailable radioconjugate composed of pevonedistat, a small molecule inhibitor of NEDD8-activating enzyme (NAE), radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of pevonedistat. Pevonedistat binds to and inhibits NAE, which results in the inhibition of tumor cell proliferation and survival. Labeling of pevonedistat with the radioactive tracer carbon C 14 allows for the evaluation of pevonedistat's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 roniciclib: An orally bioavailable radioconjugate composed of roniciclib, a cyclin dependent kinase (CDK) inhibitor, radiolabeled with carbon C 14, with potential use for evaluating the pharmacokinetic profile of roniciclib. Roniciclib selectively binds to and inhibits the activity of various CDK subtypes, which leads to cell cycle arrest and an inhibition of tumor cell proliferation. Labeling of roniciclib with the radioactive tracer carbon C 14 allows for the evaluation of roniciclib’s pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME). CDKs, serine/threonine kinases overexpressed in various tumor cell types, play key roles in the regulation of both cell cycle progression and cellular proliferation.
carbon C 14 selumetinib: A radioconjugate containing the orally available selumetinib, an inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) types 1 and 2, labeled with the radioisotope carbon C 14. Upon oral administration, selumetinib selectively inhibits MEK1/2, which prevents the activation of MEK1/2 dependent effector proteins and transcription factors. This leads to an inhibition of cellular proliferation in MEK1/2-overexpressing tumor cells. MEK 1 and 2 are dual-specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in various cancer cells. Selumetinib radiolabeled with carbon C-14 may be used as a radiotracer for pharmacokinetic studies of this agent, including its absorption, distribution, metabolism and excretion (ADME).
carbon C 14 telotristat etiprate: An orally bioavailable, tryptophan hydroxylase (TPH) inhibitor prodrug labeled with carbon C 14, which could be used to evaluate the pharmacokinetic profile of telotristat etiprate. Upon administration, telotristat etiprate is converted to its active moiety, telotristat (LP-778902), which binds to and blocks the activity of TPH. This may result in a reduction in peripheral serotonin (5-HT) production and improvement of serotonin-mediated gastrointestinal adverse side effects, such as severe diarrhea. TPH, the rate-limiting enzyme in serotonin biosynthesis, is overexpressed in carcinoid tumor cells. Telotristat radiolabeled with carbon C 14 facilitates the evaluation of the pharmacokinetic characteristics of this agent, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14 vemurafenib: A radioconjugate composed of vemurafenib, an ATP-competitive, small-molecule inhibitor of BRAF(V600E) kinase, labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of vemurafenib. Vemurafenib selectively binds to the ATP-binding site of BRAF(V600E) kinase and inhibits its activity, which may result in both an inhibition of an over-activated MAPK signaling pathway in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. Labeling of vemurafenib with the radioactive tracer carbon C 14 allows for the evaluation of vemurafenib's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME). The BRAF(V600E) gene mutation in which valine is substituted for glutamic acid at residue 600 (V600E), is found in many cancer cell types and plays a key role in the over-activation of the MAPK signaling pathway.
carbon C 14-AC0010: A radioconjugate composed of AC0010, an orally available, third generation, selective inhibitor of mutant forms of the epidermal growth factor receptor (EGFR), including the second-site resistance mutation T790M, that is labeled with the radioisotope carbon C 14, with potential use in evaluating the pharmacokinetic profile of AC0010. Upon administration, the AC0010 moiety specifically and irreversibly binds to and inhibits the activity of mutant forms of EGFR.Labeling of AC0010 with the radioactive tracer carbon C 14 allows for the evaluation of AC0010's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME).
carbon C 14-labeled ixazomib: A radioconjugate comprised of the orally-available, reversible 20S proteasome inhibitor ixazomib and labeled with the isotope carbon C 14. Upon administration, the ixazomib moiety hydrolyzes and generates its active form, MLN2238, which inhibits the activity of the 20S catalytic core subunit of the proteasome. This blocks the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins. The accumulation of protein may disrupt various cell signaling pathways, induce apoptosis, and inhibit tumor growth. In addition, this agent targets tumor suppressor microRNA-33b (miR-33b). Labeling with the radioactive tracer carbon C 14 allows for evaluation of ixazomib’s absorption, distribution, metabolism and excretion (ADME).
carbon C 14-pamiparib: An orally bioavailable radioconjugate composed of pamiparib, a nuclear enzyme poly(ADP-ribose) polymerase (PARP) inhibitor, radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of pamiparib. Pamiparib targets, binds to and inhibits PARP, which results in the inhibition of tumor cell proliferation and survival. Labeling of pamiparib with the radioactive tracer carbon C 14 allows for the evaluation of pamiparib's pharmacokinetic profile, including its absorption, distribution, metabolism and excretion (ADME).
carbon C11 nicotine: A radiotracer consisting of nicotine radiolabeled with the positron-emitting isotope carbon C11, with potential imaging use upon positron emission tomography/computed tomography (PET/CT). Upon administration via inhalation, carbon C11 nicotine binds to nicotine receptors in the lungs. Upon PET/CT the binding, pulmonary distribution, and clearance of nicotine in the lungs can be assessed.
carbon C11 temozolomide: A radioconjugate composed of temozolomide, a imidazotetrazine analog of dacarbazine, labeled with the radioisotope carbon C11, with potential positron emission tomography (PET) imaging activity. As a cytotoxic alkylating agent, temozolomide is hydrolyzed at physiologic pH to the pharmacologically active compound, 5-(3-methyl-(triazen-1-yl)-imidazole)-4-carboxamide (MTIC). MTIC is further hydrolyzed to 5-aminoimidazole-4-carboxamide (AIC) and a methyldiazonium cation. The cation is able to methylate DNA, particularly at the O6 and N7 positions of guanine residues, resulting in cell cycle arrest, inhibition of DNA replication and the induction of apoptosis. Temozolomide is metabolized to MITC at all sites, crosses the blood-brain-barrier and penetrates well into the central nervous system. Upon PET, the biodistribution, uptake in cancer cells and the efficacy of temozolomide can be assessed.
carbon C14 EGFR inhibitor ASP8273: A radioconjugate composed of ASP8273, an orally available, third-generation, mutant-selective, irreversible epidermal growth factor receptor (EGFR) inhibitor, labeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of ASP8273 during positron emission tomography (PET). Upon administration of carbon C 14 ASP8273, ASP8273 targets, covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M mutant form. Labeling of ASP8273 with the radioactive tracer carbon C 14 permits the evaluation of this agent's pharmacokinetic profile, including its absorption, distribution, metabolism, and excretion (ADME) using PET.
carbon C14-labeled carboplatin: A radioconjugate composed of the platinum compound carboplatin conjugated to the isotope carbon C 14 (14C-carboplatin), which can potentially be used to predict chemoresistance to carboplatin using accelerator mass spectrometry (AMS). Upon administration of a microdose of 14C-carboplatin, the carboplatin moiety covalently binds to DNA and forms carboplatin-DNA monoadducts. Using AMS, the 14C-carboplatin-DNA monoadducts can be detected and measured. The levels of microdose-induced carboplatin-DNA monoadducts can be used to assess the degree of chemoresistance to carboplatin and can predict cancer response to carboplatin-based chemotherapy. The carboplatin microdose is defined as 1/100 of the pharmacologically effective concentration of carboplatin. Low levels of carboplatin monoadduct formation and increased DNA repair, measured by a decrease in the detection of carboplatin-DNA monoadducts over a given time period, are correlated with increased resistance to platinum-based chemotherapeutics.
carbon nanoparticle-based formulation: A nanoparticle-based formulation containing carbon, with both a mean size of 150 nm, and potential use as a stain for lymph node draining. Upon injection of the carbon nanoparticles at the tumor site, these nanoparticles travel to regional lymph nodes and stain the lymph nodes black due to the presence of the carbon. This may allow for a more precise surgical removal of tumor-draining lymph nodes.
carbon-11 acetate: The acetate salt of the radioisotope carbon-11. Although the mechanism is unclear, carbon-11 acetate preferentially accumulates in tumor tissue, serving as a tracer for imaging tumors with positron emission tomography (PET).
carboplatin: A second-generation platinum compound with a broad spectrum of antineoplastic properties. Carboplatin contains a platinum atom complexed with two ammonia groups and a cyclobutane-dicarboxyl residue. This agent is activated intracellularly to form reactive platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, thereby inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These carboplatin-induced DNA and protein effects result in apoptosis and cell growth inhibition. This agent possesses tumoricidal activity similar to that of its parent compound, cisplatin, but is more stable and less toxic.
carboplatin/etoposide/melphalan regimen: A regimen containing carboplatin, etoposide and melphalan used for the treatment of childhood neuroblastoma.
carboplatin/paclitaxel regimen: A regimen consisting of carboplatin and paclitaxel that may be used for the treatment of breast, kidney, cervical, vulvar, endometrial, ovarian, fallopian tube, primary peritoneal, head and neck, including cancer of the nasopharynx, esophageal and esophagogastric junction, and gastric cancers; non-small cell lung cancer (NSCLC); anaplastic carcinoma; anal, small bowel and non-urothelial and urothelial bladder cancer; salivary gland, malignant germ cell and malignant sex cord-stromal tumors; cutaneous and uveal melanoma; squamous cell skin cancer; thymomas and thymic carcinoma; occult primary adenocarcinoma or squamous cell carcinoma. Paclitaxel/carboplatin every 21 days regimen may be used for the treatment of esophageal and esophagogastric junction, and gastric cancers.
carboxyamidotriazole: An orally-active agent with potential antineoplastic activity. Carboxyamidotriazole binds to and inhibits non-voltage-operated Ca2+ channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores and resulting in the disruption of calcium channel-mediated signal transduction and inhibition of vascular endothelial growth factor (VEGF) signaling, endothelial proliferation, and angiogenesis. This agent may also inhibit tumor cell growth, invasion and metastasis.
carboxyamidotriazole orotate: The orotate salt form of carboxyamidotriazole (CAI), an orally bioavailable small molecule with potential antiangiogenic and antiproliferative activities. Carboxyamidotriazole binds to and inhibits non-voltage-operated calcium channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores, resulting in the disruption of calcium channel-mediated signal transduction. CAI inhibits PI3 activity and vascular endothelial growth factor (VEGF) signaling. This may inhibit endothelial proliferation, tumor cell growth, invasion and metastasis.
carboxylesterase-expressing allogeneic neural stem cells: A preparation of allogeneic neural stem cells (NSC), derived from a human fetal cell line, that are adenovirally-transduced to express a modified form of the human enzyme carboxylesterase (CE) hCE1m6, with potential adjuvant activity. Upon intracranial administration, NSCs localize to tumor sites, due to their tumor-trophic nature, and transiently express hCE1m6. Intravenous co-administration of the prodrug irinotecan allows for the selective conversion by hCE1m6 to its active metabolite and topoisomerase I inhibitor, SN-38, in the vicinity of tumor sites. This leads to a local anti-neoplastic effect and causes reduced toxicity and increased therapeutic efficacy of irinotecan. Since NSCs freely cross the blood-brain barrier, these cells can also be intravenously administered to target brain tumor cells. hCE1m6 shows increased activity as compared to unmodified human CE.
carboxymethyl starch topical powder: A topical powder formulation composed of an ionic assembly of carboxymethyl starch and calcium, with potential hemostatic activity. Upon topical administration to a bleeding site, the carboxymethyl starch topical powder absorbs the blood, forms a barrier, and enhances blood coagulation.
carboxyphenyl retinamide: A synthetic phenylretinamide analogue of retinol (vitamin A) with potential antineoplastic and chemopreventive activities. Carboxyphenyl retinamide induces cell differentiation and inhibits tumor cell growth and carcinogenesis. This agent may also induce cell cycle arrest in the G1 phase in some cancer cell types.
carbutamide: A first-generation sulfonylurea with hypoglycemic activity. Carbutamide was one of the first sulfonylurea compounds used but was withdrawn from the market due to toxic effects on bone marrow. This agent has a long half-life.
carcinoembryonic antigen peptide 1: A nine amino acid peptide fragment of carcinoembryonic antigen (CEA), a protein that is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung. Autologous vaccination with activated autologous dendritic cells (DC) or peripheral blood mononuclear cells (PBMC) which have been exposed to CEA peptide 1 in vitro may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing CEA, thereby inhibiting tumor growth.
carcinoembryonic antigen peptide 1-6D: A 9-residue human leukocyte antigen (HLA)-restricted fragment of carcinoembryonic antigen (CEA). Vaccination with carcinoembryonic antigen peptide 1-6D, which has the amino acid sequence YLSGANLNL, may elicit a cytotoxic T lymphocyte (CTL) immune response against tumors expressing CEA.
carcinoembryonic antigen peptide 1-6D virus-like replicon particles vaccine: A cancer vaccine, consisting of alphavirus vector-derived virus-like replicon particles expressing the 9-amino-acid carcinoembryonic antigen peptide (CAP) 1-6D, with potential antineoplastic activity. Vaccination with this agent may elicit a cytotoxic T lymphocyte (CTL) immune response against CEA-expressing tumor cells.
carcinoembryonic antigen RNA-pulsed DC cancer vaccine: A vaccine comprising autologous dendritic cells pulsed with mRNA-encoded Carcinoembryonic Antigen (CEA) that targets tumor cells expressing CEA.
carcinoembryonic antigen-expressing measles virus: An attenuated oncolytic Edmonston (Ed) strain of measles virus (MV) encoding the soluble extracellular N-terminal domain of human carcinoembryonic antigen (CEA) (MV-CEA) with potential antineoplastic activity. The cellular receptor of MV is human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types. Mediated through CD46, both haemagglutinin and fusion glycoproteins of MV are required for the attachment to and fusion of host cell membranes, thereby leading to syncytia and cell lysis. The expressed CEA, a tumor associated antigen, can be detected in serum and used as a sensitive marker to monitor viral gene expression in order to easily optimize individual therapy. Compared to wild-type MV, the Ed strain of MV has a lower affinity for the MV receptor signaling lymphocyte-activation molecule (CD150), mainly expressed in B- and T-lymphocytes, but a higher affinity for CD46.
CARD11-BCL10-MALT1 complex inhibitor XL114: An orally bioavailable inhibitor of the caspase recruitment domain-containing protein 11 (CARD11; CARMA1)-B-cell lymphoma/leukemia 10 (BCL10)-mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) complex, with potential antineoplastic activity. Upon oral administration, CARD11-BCL10-MALT1 complex inhibitor XL114 inhibits the CARD11-BCL10-MALT1 complex and the CARD11-BCL10-MALT1 signaling pathway. This prevents the proliferation of susceptible cancer cells. The CARD11-BCL10-MALT1 signaling pathway promotes B- and T-cell lymphoma survival and proliferation.
Cardiogoxin: (Other name for: digoxin)
Cardiolite: (Other name for: technetium Tc-99m sestamibi)
cardioprotective agent DH001: An orally bioavailable agent, with potential cardiac protective activity. Upon oral administration, cardioprotective agent DH001 may be able to reduce doxorubicin cardiotoxicity and improve cardiac function.
Cardizem: (Other name for: diltiazem hydrochloride)
Cardura: (Other name for: doxazosin mesylate)
carfilzomib: An epoxomicin derivate with potential antineoplastic activity. Carfilzomib irreversibly binds to and inhibits the chymotrypsin-like activity of the 20S catalytic core subunit of the proteasome, a protease complex responsible for degrading a large variety of cellular proteins. Inhibition of proteasome-mediated proteolysis results in an accumulation of polyubiquinated proteins, which may lead to cell cycle arrest, induction of apoptosis, and inhibition of tumor growth.
caricotamide/tretazicar: A combination therapy consisting of the prodrug tretazicar and the enzyme co-substrate caricotamide with potential antineoplastic activity. In the presence of separately and simultaneously administered caricotamide, tretazicar is converted to the short-lived cytotoxic DNA cross-linking agent dinitrobenzamide by NAD(P)H quinine oxidoreductase 2 (NQO2), resulting in the inhibition of DNA replication and the induction of apoptosis. NQO2 has been found to be elevated in certain cancers such as hepatocellular carcinoma (HCC).
carlumab: A human IgG1 kappa monoclonal antibody directed against human CC chemokine ligand 2 (CCL2) with potential antineoplastic activity. Carlumab binds to and inhibits CLL2, which may result in inhibition of angiogenesis and, so, tumor cell proliferation. Endothelium-derived CLL2 (monocyte chemoattractant protein; MCP1) is a member of the beta-chemokine family, can stimulate monocyte/macrophage migration and smooth muscle cell (SMC) proliferation, and plays a role in angiogenesis and tumor cell migration; CCL2 induction of angiogenesis may involve the upregulation of hypoxia-inducible factor 1 alpha (HIF-1 alpha) gene expression which, in turn, induces vascular endothelial growth factor-A (VEGF-A) gene expression.
carmustine: An antineoplastic nitrosourea. Carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. This agent also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
carmustine implant: A synthetic, biodegradable wafer containing the agent carmustine with antineoplastic activity. Used to deliver drug directly into a brain tumor site and typically implanted post-surgically, the wafer is made of a biodegradable poly-anhydride copolymer and contains the nitrosourea carmustine. As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
carmustine in ethanol: A formulation containing carmustine dissolved in ethanol for intra-tumoral administration that allows carmustine to enter both aqueous and lipid compartments of the target tissue. As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
carmustine sustained-release implant wafer: A sustained release (SR) implant wafer containing the lipophilic nitrosourea carmustine (BCNU) with antineoplastic activity. Upon intracranial administration of the implant wafer and subsequent release of BCNU from the wafer, this agent alkylates and cross-links DNA during all phases of the cell cycle, resulting in the disruption of DNA function, cell cycle arrest, and apoptosis. This wafer contains the biodegradable copolymer PLGA (poly(lactide-co-glycolide) as the major drug delivery vehicle which is slowly degraded into water and carbon dioxide thereby continuously releasing BCNU over approximately 3-4 weeks. Compared to systemic administration of BCNU alone, this local SR formulation is able to maintain higher drug concentrations locally over a longer period of time while minimizing exposure to other tissues.
carmustine with propylene glycol formulation VI-0609: An injectable ethanol-free formulation containing carmustine with propylene glycol, with antineoplastic activity. Upon administration, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. The ethanol-free formulation of carmustine may lead to fewer toxicities than the ethanol-based formulation.
Carnitor: (Other name for: levocarnitine)
carnosine: A dipeptide comprised of a beta-alanine and a 3-methyl-L-histidine, which is found in dietary red meat, with potential antioxidant, metal-chelating and anti-glycation activities. Carnosine scavenges both reactive oxygen species (ROS) and unsaturated aldehydes produced by cell membrane lipid peroxidation. Additionally, this dipeptide may reduce the rate of formation of advanced glycation end-products (AGE). Altogether, this may protect cells against oxidative damage. In addition, carnosine is able to chelate toxic metals.
carnosine/hibiscus-based oral mucoadhesive tablet: A plant-based formulation and food supplement composed of carnosine and hibiscus, with potential anti-xerostomia activity. These two ingredients are mixed in specific proportions to allow for the formation of a pH buffering system in the oral cavity which maintains the pH of the oral cavity at the desired value needed for the regular secretion of saliva. Upon administration of the mucoadhesive tablet, the tablet adheres to the internal side of the cheek and both carnosine and hibiscus are gradually released over a period of at least two hours, thereby creating a buffering system that stimulates the salivary glands and increases saliva production. This produces a protective film of moisture that is deposited over the mucous membranes of the mouth and throat and may relieve radiotherapy-induced xerostomia.
carotuximab: A human/murine chimeric monoclonal antibody directed against endoglin (CD105) with potential antiangiogenic and antineoplastic activities. Carotuximab binds to endoglin, which may result in inhibition of tumor angiogenesis and decreased tumor cell proliferation. The glycoprotein endoglin is a transforming growth factor beta-1 (TGF beta-1) accessory receptor that is highly expressed on tumor vessel endothelial cells and appears to be essential for angiogenesis.
carrageenan-containing gel: A water-based, vaginal moisturizing gel containing a mixture of lambda- and kappa- carrageenans, sulfated polysaccharides derived from red seaweed (Chondrus crispus), with potential microbicidal activity against various viruses, including human papillomavirus (HPV), human immunodeficiencyvirus (HIV) and human herpes simplex virus (HSV). Upon vaginal insertion via an applicator, carrageenan specifically binds to the viral capsids, which prevents the binding of virions to heparan sulfate proteoglycan (HSPG) receptors or other, as of yet not fully identified, cellular proteins. In addition, the viral binding of carrageenan may also interfere with conformational changes within the virions after cellular attachment. This inhibits viral infection. Certain HPV types cause cervical cancer; therefore, the prevention of HPV infection by this gel may subsequently prevent the development of cervical cancer.
carrimycin: A 16-membered macrolide antibiotic, with potential antibacterial and immunomodulatory activities. Upon administration, carrimycin targets and binds to bacterial ribosomes, thereby inhibiting protein synthesis. Carrimycin may be active against some Gram-positive bacteria and Mycobacterium tuberculosis. It may also have immunomodulatory activity, presumably through a different mechanism, which has not yet been characterized.
carrot juice: The juice from carrots, with potential antioxidant and protective activities. Carrot juice, depending on the carrot varieties, may contain nutrients that include the provitamin A carotenoids alpha-carotene and beta-carotene, the non-provitamin A carotenoid lycopene, and the flavonoids anthocyanins, luteolin, quercetin and kaempferol. The antioxidants in carrot juice scavenge free radicals, thereby protecting cells from damage.
carrot/Jilin ginseng/licorice root/tangerine peel/soy beverage: A soy-based powdered nutritional supplement drink containing carrot, Jilin ginseng, licorice root and tangerine peel with potential antioxidant, immunomodulating and protective activities. Besides vitamin C, E and other phytochemicals, carrot/Jilin ginseng/licorice root/tangerine peel/soy beverage contains a high amount of soy protein. This beverage may have a beneficial effect on overall nutrition and the immune system.
Cartilade: (Other name for: shark cartilage)
carubicin: An anthracycline antineoplastic antibiotic isolated from the bacterium Actinomadura carminata. Carubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.
carvedilol: A synthetic antihypertensive methoxyphenoxy- 2-propanol derivative with no intrinsic sympathomimetic activity, Carvedilol acts as a nonselective beta-adrenoceptor blocking agent (S(-) enantiomer) and as an alpha 1-adrenoceptor blocker (R(+) and S(-) enantiomers). Its acts more strongly on beta-receptors than on alpha 1-receptors, reduces peripheral vascular resistance by vasodilation, and prevents reflex tachycardia (beta-blockade) so that heart rate is either unchanged or decreased. Carvedilol also reduces renin release through beta-blockade.
carvedilol phosphate: The phosphate salt form of carvedilol, a racemic mixture and adrenergic blocking agent with antihypertensive activity and devoid of intrinsic sympathomimetic activity. The S enantiomer of carvedilol nonselectively binds to and blocks beta-adrenergic receptors, thereby exerting negative inotropic and chronotropic effects, and leading to a reduction in cardiac output. In addition, both enantiomers of carvedilol bind to and block alpha 1-adrenergic receptors, thereby causing vasodilation and reducing peripheral vascular resistance.
carvedilol phosphate extended-release capsule: An extended-release capsule formulation containing the phosphate salt of carvedilol, a nonselective beta-adrenergic blocking agent with alpha 1-adrenergic blocking activity. Carvedilol is a racemic mixture; the S(-) enantiomer non-selectively binds to and blocks beta-adrenergic receptors, exerting negative inotropic and chronotropic effects, leading to a reduction in cardiac output. Both R(+) and S(-) enantiomers bind to and block alpha 1-adrenergic receptors with equal potency, causing vasodilation and a reduction in peripheral vascular resistance. This agent has no intrinsic sympathomimetic activity.
Carvykti: (Other name for: ciltacabtagene autoleucel)
carzelesin: A cyclopropylpyrroloindole prodrug analogue and DNA minor groove binding agent, with antineoplastic activity. After hydrolysis, the cyclopropyl group of carzelesin alkylates N3-adenine in a sequence-selective fashion. This results in tumor growth inhibition.
casdozokitug: A human immunoglobulin G1 (IgG1) monoclonal antibody against the p28 subunit of the immunosuppressive cytokine interleukin-27 (IL-27p28), with potential immune-activating, pro-inflammatory and antineoplastic activities. Upon administration, casdozokitug targets and binds to IL-27p28, and inhibits the interaction of IL-27 with the IL-27 receptor subunit alpha (IL-27RA). This prevents the activation of IL-27RA and prevents IL-27-mediated signaling. This reduces signal transducer and activator of transcription 1 (STAT1) phosphorylation which leads to increased secretion of pro-inflammatory cytokines, such as interferon-gamma (IFN-g) and tumor necrosis factor-alpha (TNF-a). It also decreases the expression of inhibitory immune checkpoint receptors, such as programmed death-ligand 1 (PD-L1), T cell immunoreceptor with Ig and ITIM domains (TIGIT) and lymphocyte-activation gene 3 (LAG3), on immune cells. This may enhance a T-cell mediated immune response against tumor cells that rely on IL-27 for immune escape. IL-27, a heterodimeric member of the IL-12/IL-23 cytokine family composed of IL-27p28 and Epstein-Barr virus induced gene 3 (EBI3), plays an important role in the immunosuppressive tumor microenvironment (TME). IL-27 signals through the JAK-STAT pathway to limit the duration and intensity of a T cell-mediated immune response during infection and cancer by altering immunoregulatory receptor expression and proinflammatory cytokine secretion.
casein/whey protein/soy protein/pea protein/fat mix/EPA/DHA-based nutritional supplement: A gluten-free, calorie-rich nutritional supplement containing all essential vitamins, minerals, and trace elements, as well as protein, fat and carbohydrates. The protein contained in this supplement is derived from a variety of sources, including casein, whey, soy and pea; it helps maintain digestive health throughout the gastrointestinal tract and reduces the risk of digestive complications. This supplement contains the essential omega-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexanaeoic acid (DHA). DHA and EPA are incorporated into cell membranes and affect the production of pro-inflammatory mediators, eliciting an anti-inflammatory effect. Medium chain triglycerides (MCT) in this supplement enhance fat absorption. Upon oral intake of this nutritional supplement, the ingredients may prevent both malnutrition and weight loss.
caseinate protein isolate: An isolate comprised of the sodium or calcium salt of the glycoprotein casein, the primary protein found in milk and other dairy products, with anti-catabolic activity.
casirivimab: A recombinant, human immunoglobulin G1 (IgG1) kappa monoclonal antibody directed against the spike protein (SP) of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), that can potentially be used for immunization against COVID-19. Upon administration, casirivimab specifically targets and binds to the receptor-binding domain (RBD) of SP, thereby blocking viral attachment and entry into human cells and may thereby neutralize SARS-CoV-2. This may slow the progression of the disease and accelerate recovery, and may potentially provide temporary protection against infection with SARS-CoV-2.
casirivimab/imdevimab: A combination of two monoclonal antibodies, casirivimab and imdevimab, directed against the spike protein (SP) of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), that can potentially be used for immunization against COVID-19. Upon administration, casirivimab and imdevimab specifically target and bind to non-overlapping regions of the receptor-binding domain (RBD) of SP, thereby blocking viral attachment and entry into human cells and may thereby neutralize SARS-CoV-2. This may slow the progression of the disease and accelerate recovery, and may potentially provide temporary protection against infection with SARS-CoV-2. Binding to two distinct regions of the RBD of SP may decrease the potential for virus escape mutants that occur upon treatment with a single SARS-CoV-2 antibody, and may provide enhanced protection against loss of efficacy.
Casodex: (Other name for: bicalutamide)
casopitant mesylate: The mesylate salt of a centrally-acting neurokinin 1 (NK1) receptor antagonist with antidepressant and antiemetic activities. Casopitant competitively binds to and blocks the activity of the NK1 receptor, thereby inhibiting NK1-receptor binding of the endogenous tachykinin neuropeptide substance P (SP), which may result in antiemetic effects. SP is found in neurons of vagal afferent fibers innervating the brain-stem nucleus tractus solitarii and the area postrema, which contains the chemoreceptor trigger zone (CTZ), and may be elevated in response to chemotherapy. The NK1 receptor is a G-protein receptor coupled to the inositol phosphate signal-transduction pathway and is found in both the nucleus tractus solitarii and the area postrema.
caspofungin acetate: The acetate salt of an antimycotic echinocandin lipopeptide, semisynthetically derived from a fermentation product of the fungus Glarea lozoyensis. Caspofungin inhibits 1,3-beta-glucan synthase, resulting in decreased synthesis of beta(1,3)-D-glucan (an essential component of the fungal cell wall), weakening of the fungal cell wall, and fungal cell wall rupture. This agent is active against Aspergillus and Candida species.
Catapres: (Other name for: clonidine hydrochloride)
Catapres-TTS: (Other name for: clonidine)
catequentinib hydrochloride: The hydrochloride salt form of catequentinib, a receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic and anti-angiogenic activities. Upon administration, catequentinib targets multiple RTKs, including vascular endothelial growth factor receptor type 2 (VEGFR2) and type 3 (VEGFR3). This agent may both inhibit angiogenesis and halt tumor cell growth.
cathepsin-activatable Cy5 fluorescent imaging probe LUM015: A cathepsin-activatable fluorescent probe with imaging activity. The cathepsin-activatable fluorescent probe LUM015 contains the Cy5 fluorophore linked, via a pan-cathepsin protease cleavable peptide, to a fluorescent quencher. Upon injection, the peptide in LUM015 can be cleaved by cathepsins overexpressed by tumor cells, which releases the quencher and activates the fluorophore. Upon imaging, tumor cells expressing cathepsin family proteases can be detected.
cathepsin-cleavable NIR substrate probe 6QC-ICG: A fluorescently quenched, cysteine cathepsin-cleavable near infrared (NIR) substrate probe containing the dye indocyanine green (ICG), that may be used for cancer imaging purposes using an NIR imaging system. In 6QC-NIR, the cathepsin-activatable fluorescent probe contains the fluorophore, ICG, linked, via a cathepsin protease cleavable peptide, with a core Cbz-Phe-Lys peptide sequence, to a fluorescent quencher, QC-1. Upon administration of 6QC-NIR, the amide bond of the peptide can be cleaved by cathepsin proteases overexpressed by tumor cells and highly abundant in the tumor microenvironment (TME). Upon proteolysis, the quencher is released, the fluorophore becomes activated and accumulates in the lysosome. Upon clinical NIR imaging, using the da Vinci Si surgical system, tumor cells expressing cathepsin family proteases can be detected which allows for visualization of the tumor.
cathepsin-cleavable NIR substrate probe 6QC-NIR: A cysteine cathepsin-cleavable near infrared (NIR) substrate probe, that may be used for cancer imaging purposes using an NIR imaging system. In 6QC-NIR, the cathepsin-activatable fluorescent probe contains the NIR fluorophore, Dylight 780-B1, linked, via a cathepsin protease cleavable peptide, with a core Cbz-Phe-Lys peptide sequence, to a fluorescent quencher, QC-1. Upon administration of 6QC-NIR, the amide bond of the peptide can be cleaved by cathepsins overexpressed by tumor cells and highly abundant in the tumor microenvironment (TME). Upon cleavage, the quencher is released, the fluorophore becomes activated and accumulates in the lysosome. Upon fluorescence imaging, using the da Vinci Si surgical system, tumor cells expressing cathepsin family proteases can be detected which allows for visualization of the tumor.
cathepsin-targeted fluorescent imaging probe VGT-309: A fluorescently quenched, cathepsin-activatable, near infrared (NIR) probe containing the dye indocyanine green (ICG), that may be used for cancer imaging purposes using an NIR imaging system. Upon administration, cathepsin-targeted fluorescent imaging probe VGT-309 covalently and irreversibly binds to cathepsins overexpressed by tumor cells. This displaces the quencher QC-1 and activates the ICG fluorophore. Upon NIR imaging, cathepsin-expressing tumor cells can be detected which allows for visualization of the tumor.
cationic liposome-encapsulated paclitaxel: A cationic liposome preparation of paclitaxel with antineoplastic activity. Paclitaxel, the active ingredient in cationic liposome-encapsulated paclitaxel, binds to tubulin and inhibits the disassembly of microtubules, resulting in the inhibition of mitosis and cellular proliferation, and apoptosis. Cationic liposome encapsulation of paclitaxel allows the delivery of high doses of paclitaxel to target tissues while minimizing systemic toxicity. Tumor endothelial cells may preferentialy bind and internalize cationic liposomes.
cationic peptide cream Cypep-1: A topical cream containing Cypep-1, a cationic lytic peptide of 27 amino acids, with potential antineoplastic activity. Upon topical administration, Cypep-1 selectively targets tumor cells with negatively charged cell membranes and ruptures the cell membranes. This leads to tumor cell lysis and the release of neoantigens into the tumor microenvironment (TME) and circulation. This elicits a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these neoantigens. Warts are benign skin tumors caused by human papilloma virus (HPV).
catumaxomab: A trifunctional bispecific monoclonal antibody with potential antineoplastic activity. Catumaxomab has two antigen-recognition sites: one for human CD3, a T cell surface antigen; and one for human epithelial cell adhesion molecule (EpCAM), a cell surface antigen expressed by a variety of epithelial tumor cells. In addition, the modified Fc portion of this antibody binds Fc receptors on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs). Catumaxomab brings T cells, EpCAM-expressing epithelial tumor cells and APCs together into tricellular complexes, which may result in a potent cytotoxic T-lymphocyte (CTL) response against EpCAM-expressing epithelial tumor cells. Fc-mediated binding of APCs in the tricellular complex potentiates EpCAM antigen presentation to T cells and the activation of anti-tumor cytotoxic T cell functions.
Cavatak: (Other name for: gebasaxturev)
Caverject: (Other name for: alprostadil)
cavilon durable barrier cream: (Other name for: dimethicone/polymer barrier cream)
Cavrotolimod: A spherical nucleic acid (SN)-based agonist of toll-like receptor 9 (TLR9), with potential immunostimulating activity. Upon administration, cavrotolimod targets and is able to enter various immune cells, including monocytes/macrophages, plasmacytoid dendritic cells (pDCs), natural killer (NK) cells and B cells, through endocytosis. Within the endosome, it binds to and activates TLR9. TLR9 activation induces immune signaling pathways and activates various immune cells, including B cells, pDCs, NKs, and induces both the production of T-helper 1 cells (Th1) and a Th1-mediated immune response as well as a cytotoxic T-lymphocyte (CTL)-based immune response against tumor cells. This results in an inhibition of tumor cell proliferation. TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate and adaptive immune responses. The SNA is a dense, radial arrangement of nucleic acids (DNA) on the surface of liposomal nanoparticles, providing a 3D-construct, that has a high cellular uptake and an increased presentation of the DNA for TLR9 agonism. It also protects against breakdown by nucleases and increases the half-life of the construct compared to linear oligonucleotides that are not in SNA format.
caxmotabart entudotin: An antibody-drug conjugate (ADC) composed of trastuzumab, a humanized monoclonal antibody targeting the tumor-associated antigen (TAA) epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2), site-specifically conjugated, via a tumor-selective beta-glucuronide linker, to the auristatin analog and potent microtubule inhibitor monomethyl auristatin F (MMAF), with potential antineoplastic activity. Upon administration of caxmotabart entudotin, the trastuzumab moiety targets and binds to HER2 expressed on tumor cells. Upon binding, internalization and linker cleavage, MMAF is released. MMAF binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.
CB10-277: A synthetic derivative of dimethylphenyl-triazene related to dacarbazine, with antineoplastic properties. Related to the agent dacarbazine, CB10-277 is converted in vivo to a monomethyl triazene form that alkylates DNA, resulting in inhibition of DNA replication and repair; in addition, this agent may act as a purine analogue, resulting in inhibition of DNA synthesis, and may interact with protein sulfhydryl groups.
CBL-B inhibitor HST-1011: An orally bioavailable, allosteric, small-molecule inhibitor of Casitas B-lineage lymphoma proto-oncogene-b (CBL-B), with potential immunomodulatory and antineoplastic activities. Upon oral administration, CBL-B inhibitor HST-1011 targets, binds to and inhibits the activity of CBL-B, which may result in immune activation, the infiltration of natural killer (NK) cells and activated CD8+ T cells in the tumor microenvironment (TME), and the inhibition of tumor growth. CBL-B, an E3 ubiquitin ligase expressed in all leukocyte subsets including T cells and NK cells, is a negative regulator of immune activation.
CBL-B inhibitor NX-1607: An orally bioavailable, small-molecule inhibitor of Casitas B-lineage lymphoma proto-oncogene-b (CBL-B), with potential immunomodulatory and antineoplastic activities. Upon oral administration, CBL-B inhibitor NX-1607 targets, binds to and inhibits the activity of CBL-B, which may result in immune activation, the infiltration of natural killer (NK) cells and activated CD8+ T cells in the tumor microenvironment (TME), and the inhibition of tumor growth. CBL-B, an E3 ubiquitin ligase expressed in all leukocyte subsets including T cells and NK cells, is a negative regulator of immune activation.
CBL-B inhibitor-treated autologous tumor-infiltrating lymphocytes DeTIL-0255: A preparation of autologous tumor-infiltrating lymphocytes (TILs) derived from a patient's tumor that have been treated ex vivo during cell expansion with NX-0255, an inhibitor of Casitas B-lineage lymphoma proto-oncogene-b (CBL-B), with potential immunomodulating and antineoplastic activities. Upon administration, the CBL-B inhibitor-treated autologous TILs DeTIL-0255 specifically recognize and kill the patient's tumor cells. NX-0255 enhances TIL expansion and the tumor-killing ability of the TILs when returned to the patient.
CBP/beta-catenin modulator E7386: An orally bioavailable, specific inhibitor of the canonical Wnt/beta-catenin signaling pathway, with potential antineoplastic activity. Upon oral administration, CBP/beta-catenin modulator E7386 inhibits beta-catenin and prevents the interaction of beta-catenin with its transcriptional coactivator, CREB (cAMP response element-binding) binding protein (CBP). This prevents binding of beta-catenin/CBP to WRE (Wnt-responsive element), and inhibits the activation of transcription of a wide range of target genes of Wnt/beta-catenin signaling, thereby preventing gene expression of many Wnt-related, pro-survival proteins and suppressing tumor cell growth. The Wnt/beta-catenin signaling pathway regulates cell morphology, motility, and proliferation; aberrant regulation of this pathway leads to neoplastic proliferation. Beta-catenin is frequently mutated in various tumors.
CBP/p300 bromodomain inhibitor AUR-107: An orally bioavailable inhibitor of the bromodomain of the histone acetyltransferase (HAT) paralogs, CREB binding protein (CBP; CREBBP) and p300 (E1A-associated protein p300; p300 HAT), with potential immunomodulating and antineoplastic activities. Upon oral administration, CBP/p300 bromodomain inhibitor AUR-107 targets and binds to the bromodomains of CBP and p300. This disrupts the acetylation of histones and other proteins and decreases regulatory T cells (Tregs) generation, inhibits its suppressive function and causes Tregs apoptosis. This modulates T-helper cells, induces an anti-tumor immune response and decreases tumor growth. The HAT paralogs CBP and p300 are key transcriptional co-activators that are essential for a multitude of cellular processes and play a key role in the regulation of gene expression in both tumor and immune cells.
CBP/p300 bromodomain inhibitor FT-7051: An orally bioavailable inhibitor of the bromodomain of the histone acetyltransferase (HAT) paralogs, CREB binding protein (CBP) and p300 (E1A-associated protein p300; p300 HAT), with potential antineoplastic activity. Upon oral administration, CBP/p300 bromodomain inhibitor FT-7051 targets and binds to the bromodomain of CBP and p300. This disrupts the acetylation of histones and other proteins and prevents the co-activation of the androgen receptor (AR) including AR-v7. This may inhibit tumor cell proliferation in AR-positive tumor cells. The HAT paralogs CBP and p300 are key transcriptional co-activators that are essential for a multitude of cellular processes and are implicated in the progression and therapeutic resistance of certain cancers.
CBP/p300 bromodomain inhibitor OPN-6602: An orally bioavailable small molecule inhibitor of the bromodomain of the histone acetyltransferase (HAT) paralogs, CREB binding protein (CBP) and p300 (E1A-associated protein p300; EP300; p300 HAT), with potential antineoplastic activity. Upon oral administration, CBP/p300 bromodomain inhibitor OPN-6602 targets and binds to the bromodomains of p300 and CBP. This disrupts the acetylation of histones and other proteins, prevents the co-activation of key transcription factors that contribute to tumor progression including the androgen receptor (AR), interferon regulatory factor 4 (IRF4) and Myc proto-oncogene protein (c-Myc), and downregulates AR and IRF4/MYC signaling, thereby inhibiting tumor cell proliferation. The HAT paralogs p300 and CBP are key transcriptional co-activators that are essential for a multitude of cellular processes and are implicated in the progression and therapeutic resistance of certain cancers.
CBP/p300 bromodomain inhibitor TT125-802: An orally bioavailable small molecule inhibitor of the bromodomain of the histone acetyltransferase (HAT) paralogs, CREB binding protein (CBP; CREBBP) and p300 (E1A-associated protein p300; p300 HAT), with potential immunomodulating and antineoplastic activities. Upon oral administration, CBP/p300 bromodomain inhibitor TT125-802 targets and binds to the bromodomains of CBP and p300. This disrupts the acetylation of histones and other proteins and decreases regulatory T cells (Tregs) generation, inhibits its suppressive function and causes Tregs apoptosis. This modulates T-helper cells, induces an anti-tumor immune response and decreases tumor growth. The HAT paralogs CBP and p300 are key transcriptional co-activators that are essential for a multitude of cellular processes and play a key role in the regulation of gene expression in both tumor and immune cells.
CBT-1: (Other name for: MDR modulator CBT-1)
CC-401: A second generation ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor with potential antineoplastic activity. Based on the chemistry of SP600125, another anthrapyrazolone inhibitor of JNK, CC-401 competitively binds the ATP binding site of JNK, resulting in inhibition of the phosphorylation of the N-terminal activation domain of transcription factor c-Jun; decreased transcription activity of c-Jun; and a variety of cellular effects including decreased cellular proliferation.
CC-8490: A benzopyran with potential antineoplastic activity. CC-8490 acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells. This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms.
CCL21-expressing H1944 cell vaccine: A cancer cell vaccine comprised of the allogeneic human lung adenocarcinoma cell line H1944 that has been transduced ex vivo with adenoviral vector encoding human cytokine chemokine C-C motif ligand 21 (CCL21), with potential immunomodulating and antineoplastic activities. Upon administration, CCL21-expressing H1944 cell vaccine expresses the chemokine CCL21, which may induce an antitumoral cytotoxic T-lymphocyte immune response in the tumor microenvironment. CCL21 has been shown to attract antigen presenting cells (APCs), like leukocytes and DCs, and natural killer (NK) cells and their T-cell effectors to induce a cytotoxic immune response. H1944 cells contain tumor-associated antigens (TAAs) overexpressed in non-small cell lung cancer (NSCLC).
CCR2 antagonist CCX872-B: An orally available human C-C chemokine receptor type 2 (CCR2) antagonist, with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist CCX872-B specifically binds to CCR2 and prevents the binding to its cognate endothelium-derived chemokine ligand CCL2 (monocyte chemoattractant protein-1 or MCP1). This may result in the inhibition of both CCR2 activation and CCR2-mediated signal transduction, which may inhibit inflammatory processes, angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, and stimulates their migration and infiltration; it plays a key role in inflammation. CCR2 is overexpressed in certain cancer cell types, where it is involved in angiogenesis, tumor cell migration and proliferation.
CCR2 antagonist PF-04136309: An orally available human chemokine receptor 2 (CCR2) antagonist with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist PF-04136309 specifically binds to CCR2 and prevents binding of the endothelium-derived chemokine ligand CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and signal transduction. This may inhibit inflammatory processes as well as angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.
CCR2/CCR5 antagonist BMS-813160: An antagonist of both human C-C chemokine receptor types 2 (CCR2; CD192) and 5 (CCR5; CD195), with potential immunomodulating and antineoplastic activities. Upon administration, CCR2/CCR5 antagonist BMS-813160 specifically binds and prevents the activation of both CCR2 and CCR5. This inhibits the activation of CCR2/CCR5-mediated signal transduction pathways and may inhibit inflammatory processes, angiogenesis, tumor cell migration, tumor cell proliferation and invasion. The G-protein coupled chemokine receptors CCR2 and CCR5 are expressed on the surface of monocytes and macrophages, and stimulate their migration and infiltration; they play key roles in inflammation and autoimmune disease. CCR2 and CCR5 are overexpressed in certain cancer cell types, and are also involved in angiogenesis, and in tumor cell migration, proliferation and metastasis.
CCR8 inhibitor IPG7236: An orally bioavailable inhibitor of C-C-chemokine receptor 8 (CCR8), with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR8 inhibitor IPG7236 targets, binds to and blocks the activity of CCR8 on CCR8-positive tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and prevents chemokine ligand 1 (CCL1)-CCR8-mediated signaling. This may reactivate antitumor immune responses. CCR8 is specifically expressed by tumor-infiltrating Tregs in multiple types of cancer and plays a key role in immunosuppression, proliferation, resistance, migration and angiogenesis. High expression is correlated with poor prognosis.
CD-expressing bifidobacterium APS001F: A recombinant anaerobic bacterium, Bifidobacterium longum, encoding the cytosine deaminase (CD) gene with potential antineoplastic adjuvant activity. Upon injection, the CD-expressing bifidobacterium preferentially localizes and grows in the hypoxic environment of the tumor and expresses CD, an enzyme that catalyzes the intracellular conversion of the prodrug flucytosine (5-FC) into the antineoplastic agent 5-fluorouracil (5-FU). Upon administration of 5-FC, and subsequent localized conversion into 5-FU and its cytotoxic active metabolites, the tumor is specifically exposed to cytotoxic agents while the exposure to normal tissues is minimal.
CD105/Yb-1/SOX2/CDH3/MDM2-polyepitope plasmid DNA vaccine: A plasmid DNA vaccine containing the mammalian expression vector pUMVC3 (pNGVL3) encoding epitopes of CD105 (Endoglin), Y-box binding protein 1 (Yb-1), SRY-box 2 (SOX2), cadherin 3 (CDH3), and murine double minute 2 (MDM2) proteins, with potential immunomodulating and antineoplastic activities. Upon intradermal administration of pUMVC3-CD105/Yb-1/SOX2/CDH3/MDM2-epitopes plasmid DNA vaccine, the plasmid transfects cells and the peptides are expressed. This generates a specific memory Th1 (T-helper) cell immune response, stimulates secretion of cytokines by the T cells and leads to a cytotoxic T-lymphocyte (CTL) response against CD105/Yb-1/SOX2/CDH3/MDM2-expressing tumor cells. CD105/Yb-1/SOX2/CDH3/MDM2 proteins are highly immunogenic tumor associated antigens that are overexpressed in breast cancer. Additionally, these antigens are associated with breast cancer stem cells and with epithelial to mesenchymal transformation (EMT).
CD11b agonist GB1275: An orally bioavailable small molecule agonist of CD11b (integrin alpha-M; ITGAM; integrin alpha M chain), with potential immunomodulating activity. Upon administration, CD11b agonist GB1275 targets and binds to CD11b, thereby activating CD11b. This leads to CD11b-mediated signaling and promotes pro-inflammatory macrophage polarization while suppressing immunosuppressive macrophage polarization. This reduces influx of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME), promotes anti-tumor immune responses, induces cytotoxic T lymphocytes (CTLs) and suppresses tumor growth. CD11b, a member of the integrin family of cell adhesion receptors highly expressed on immune system cells, is a negative regulator of immune suppression and activates anti-tumor innate immunity.
CD122-selective IL-2/Anti-CD25 antibody-like fusion protein ANV419: A formulation consisting of lipid nanoparticles (LNPs) encapsulating nucleoside-modified messenger RNA (mRNA) encoding the endogenous cytokine interleukin-2 (IL-2), with potential immunostimulating activity. Upon administration, ribocytokine IL-2 BNT153 is taken up by cells and the expressed IL-2 targets and binds to the IL-2 receptor beta subunit (IL2Rb; IL2Rbeta; CD122). The binding of IL-2 to IL2Rb activates IL2Rb-mediated signaling, which activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). The specific induction of T-cell-mediated cytotoxic immune responses against tumor cells causes tumor cell destruction. IL2Rb plays a key role in the proliferation and activation of effector T-cells.
CD123-CD33 compound CAR T cells: A preparation of T lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two distinct units of CARs, one specific for the CD123 (interleukin-3 receptor alpha chain or IL3RA) antigen and one specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, the CD123-CD33 cCAR-T cells specifically and simultaneously target and bind to tumor cells expressing CD123 and/or CD33. This induces selective toxicity in tumor cells that express the CD123 antigen and/or the CD33 antigen. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells. Targeting two different antigens may improve coverage and protect against antigen escape and relapse as it is less likely for tumor cells to lose both antigens. Additionally, the CD123-CD33 cCAR-T cells express CD52 on the cell surface. This allows the depletion of the CD123-CD33 cCAR-T cells with the administration of the anti-CD52 monoclonal antibody alemtuzumab, in case of unacceptable side effects.
CD123-specific adapter SPRX002: A soluble protein antigen-receptor X-linker (sparX) protein containing a CD123 tumor-associated antigen (TAA) binding-domain and a TAG domain, which contains a fragment of human alpha fetoprotein (AFP), with binding ability to CD123-specific tumor cells and universal CAR-modified T cells (antigen-receptor complex-T cells; ARC-T cells), respectively. Upon administration, the CD123-specific adapter SPRX002 targets and binds, with its anti-CD123 binding domain, to CD123-expressing tumor cells and, with its TAG region, targets and binds to the anti-TAG binding domain on the ARC-T-cells. When ARC-T cells bind to the TAG domain of SPRX002 and SPRX002 is bound to CD123-expressing cancer cells, the tricomplex formation leads to T-cell activation, expansion and killing of CD123-expressing cancer cells. The combination of SPRX002 with ARC-T cells is called ACLX002. Since the dose of SPRX002 can be adjusted, it allows for the controllability and adaptability of the ARC-T cells and reduces its potential toxicity .CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.
CD123-specific targeting module TM123: A preparation of soluble adapter molecules consisting of an antigen-binding moiety targeting CD123 linked to a peptide motif recognizable by UniCAR02-T, that may be used to activate UniCAR02-T. Upon administration of CD123-specific targeting module (TM) TM123, and upon co-administration of UniCAR02-T, the antigen-binding moiety of TM123 targets and binds to cancer cells expressing CD123, and the binding domain of UniCAR02-T binds to the nuclear antigen motif of TM123. This activates UniCAR02-T, and induces selective toxicity in and causes lysis of CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.
CD133 antigen peptide-pulsed autologous dendritic cell vaccine: A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A2-restricted peptides derived from the CD133 antigen, with potential antineoplastic activity. Upon intradermal administration, the CD133 antigen peptide-pulsed autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against CD133-expressing tumor cells, resulting in tumor cell lysis. CD133, a cancer stem cell marker, is expressed on hematopoietic stem and progenitor cells and overexpressed on many types of cancer cells; it is associated with resistance to chemotherapy and increased cancer survival. HLA-A2 is an MHC class I molecule that presents antigenic peptides to CD8+ T-cells. Epitope design that is restricted to those epitopes that bind most efficiently to HLA-A2 may improve antigenic peptide immunogenicity.
CD137 agonist: Any agent that targets and activates CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9).
CD137/Nectin-4 bispecific-targeting agent BT748: A synthetic tumor targeted immune cell agonist composed of two bicyclic peptides targeting CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9) linked to a bicyclic peptide targeting the cell adhesion molecule nectin-4 (PVRL4); with potential immunostimulating and antineoplastic activities. Upon administration, CD137/nectin-4 bispecific-targeting agent BT7480 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and nectin-4 expressed on tumor cells. The simultaneous binding to nectin-4 and CD137 allows for conditional stimulation of CD137 signaling within the tumor microenvironment (TME) only upon binding to nectin-4 on tumor cells. CD137 activation results in T-cell stimulation and enhances T-lymphocyte-mediated anti-tumor immune response against nectin-4-expressing tumor cells. Nectin-4, a tumor associated antigen (TAA) belonging to the nectin family, is overexpressed in a variety of cancers, but has a restricted distribution in normal tissue. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.
CD137/PSMA/HSA trispecific-targeting agent CB 307: A trispecific T-cell enabler targeting the human tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA; FOLH1), the co-stimulatory receptor 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) and human serum albumin (HSA), with potential immunostimulating and antineoplastic activities. Upon administration, CD137/PSMA/HSA trispecific-targeting agent CB307 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T lymphocytes, and PSMA expressed on tumor cells. The simultaneous binding to PSMA enables clustering of 4-1BB and thereby allows for conditional stimulation of 4-1BB signaling within the tumor microenvironment (TME) only upon binding to PSMA on tumor cells. 4-1BB activation results in T-cell stimulation and enhances T-lymphocyte-mediated anti-tumor immune response against the PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate tumor cells. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. The albumin-binding domain targets and binds to HSA thereby extending the serum half-life of CB307. The conditional activation of 4-1BB signaling prevents systemic T-cell activation and lowers systemic toxicity.
CD137L/Epstein-Barr virus-targeting autologous dendritic cell vaccine: A cell-based cancer vaccine composed of in vitro generated, highly potent, CD137 ligand (CD137L)-dendritic cells (CD137L-DCs), pulsed with Epstein-Bar Virus (EBV) antigen peptides, with potential antineoplastic and immunostimulatory activities. Upon administration, CD137L-DCs induce potent CD8+ T-cell responses against EBV+ target cells. DCs stimulated with CD137L enhance cytotoxic T-lymphocyte proliferation and activation to a greater extent compared to non-CD137L-stimulated DCs.
CD138CAR-CD137/TCRzeta-expressing T lymphocytes: T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) specific for syndecan-1 (CD138) (CART-138 T cells) coupled to the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD138CAR- CD137/TCRzeta -expressing T lymphocytes direct the T-lymphocytes to syndecan-1-expressing tumor cells and induces selective toxicity in those tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of syndecan-1. Syndecan-1, a type 1 transmembrane proteoglycan and tumor associated antigen, is overexpressed in a variety of cancer cells. It plays a key role in the regulation of cell growth, differentiation, and adhesion, and its expression is correlated with poor prognosis.
CD16-based ROR1-targeted NK cell engager PBA-0405: An engineered natural killer (NK) cell engager comprised of an anti-receptor tyrosine kinase-like orphan receptor 1 (ROR1) antibody, with an increased binding affinity to CD16 Fc receptor, with potential immunostimulating and antineoplastic activities. Upon administration, CD16-based ROR1-targeted NK cell engager PBA-0405 targets and binds to ROR1 expressed on tumor cells and simultaneously binds to the activating CD16 Fc receptor expressed on NK cells, thereby bringing ROR1-expressing tumor cells and NK cells together. This stimulates the NK cells, and results in the selective NK cell-mediated tumor cell lysis of ROR1-expressing tumor cells and antibody-dependent cellular cytotoxicity (ADCC). CD16, also known as Fc-gamma receptor III, is normally expressed on the surface of NK cells, neutrophils, monocytes and macrophages, and plays a key role in initiating ADCC. It is often downregulated in certain cancers, thereby inhibiting the anti-tumor immune response. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is expressed during embryogenesis and in various hematological and solid malignancies. It plays key roles in tumor cell proliferation and survival.
CD16/IL15/CD33 trispecific killer cell engager OXS-3550: A trispecific killer engager (TriKE) molecule containing an anti-cluster of differentiation 16 (CD16; FcgammaRIII) single-chain variable fragment (scFv) to engage natural killer (NK) cells, an anti-CD33 scFv to engage myeloid cells and a human modified interleukin-15 (IL-15) linker, that links the two scFv, with potential immunomodulating and antineoplastic activities against CD33-expressing tumor cells. Upon administration of the CD16/IL15/CD33 TriKE OXS-3550, the simultaneous binding to CD16 on NK cells and CD33 on tumor cells will induce NK cell cytotoxicity specifically against CD33-expressing tumor cells. The cytokine IL-15 linker promotes NK cell proliferation, activity, survival and expansion. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.
CD19-CD34 tagged metabolically programmed CAR T cells: A preparation of a subset of T lymphocytes, that are metabolically enhanced based on selection and purification on CD34 expression and primed to contain T-helper subset 1 and 17 (Th1/17 hybrid cells), that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, CD19-CD34tagged metabolically programmed CAR T cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. These T cells may show enhanced persistence and effector function as compared to other, non-metabolically enhanced, anti-CD19 CAR T cells.
CD19-expressing oncolytic virus CF33: A genetically modified oncolytic virus (OV) composed of CF33, a replication competent orthopoxviral chimera that is engineered to express the tumor-associated antigen (TAA) CD19, with potential oncolytic, immunostimulating and antineoplastic activities. CD19-expressing OV CF33 is used in combination with certain anti-CD19 agents, such as anti-CD19 chimeric antigen receptor (CAR) T cells or anti-CD19 bispecific antibodies. Upon intratumoral (IT) or intravenous (IV) administration of CD19-expressing OV CF33, the oncolytic virus specifically binds to, infects and replicates in tumor cells, leading to 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 CD19 antigen expressed by the OV is specifically delivered to and produced in the infected tumor cells. As CD19 is presented on the tumor cell surface, the tumor cells are tagged with CD19. This allows, upon the administration of certain agents that target CD19, the specific eradication of CD19-expressing tumor cells.
CD19-specific adapter molecule SWI019: A preparation of adapter molecules consisting of an antibody fragment (Fab) targeting CD19 linked to a 14 aa peptide epitope, or peptide neo-epitope (PNE), recognizable by CLBR001, that may be used to activate CLBR001. Upon administration of CD19-specific adapter molecule SWI019, and upon co-administration of CLBR001, the Fab moiety of SWI019 targets and binds to tumor cells expressing CD19, and the PNE of SWI019 binds to the binding domain of CLBR001, thereby activating CLBR001. This induces selective toxicity in and causes lysis of CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.
CD19-targeted 4-1BB ligand RO7227166: An immunotherapeutic agent that targets both CD19 and 4-1BB (CDG5:I9necrosis factor receptor superfamily member 9; TNFRSF9), with potential immunostimulatory and antineoplastic activity. Upon administration, CD19-targeted 4-1BB ligand RO7227166 simultaneously binds to CD19 and 4-1BB, thereby crosslinking CD19 and 4-1BB positive cells. This triggers, through the 4-1BB ligand, the proliferation and activation of natural killer cells (NKs) and T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against CD19-expressing tumor cells. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily (TNFRSF), is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.
CD19-targeted CAR T cells BZ019: A preparation of T lymphocytes that have been genetically modified and transduced with a non-viral vector expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing, as of yet undisclosed co-stimulatory signaling domains, with potential immunostimulating and antineoplastic activities. Upon administration, CD19-targeted CAR T cells BZ019 recognize and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies.
CD19-targeted CAR T2 cells: A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, CD19-targeted CAR T2 cells target and bind to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell-specific cell surface antigen expressed in all B-cell lineage malignancies.
CD19-targeting agent: Any agent targeting CD19.
CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T lymphocytes: A preparation of genetically modified central memory (Tcm) enriched T cells transduced with a replication incompetent lentiviral vector expressing a chimeric antigen receptor (CAR), containing a CD28 signaling domain fused to both CD3 zeta, which targets the CD19 antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T cells are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. The costimulatory signaling domain enhances proliferation of T cells and antitumor activity.
CD19CAR-CD28-CD3zeta-EGFRt-expressing Tn/mem-enriched T lymphocytes: A preparation of genetically modified lymphocytes comprised of CD62L-positive naïve and memory T cells (Tn/mem), that are transduced ex vivo with a self-inactivating (SIN) lentiviral vector expressing a hinge-optimized chimeric antigen receptor (CAR) specific for the CD19 antigen and containing CD28 and CD3 zeta signaling domains, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon isolation of peripheral blood lymphocytes (PBLs), transduction of the CD62L-positive T lymphocytes, expansion ex vivo and administration, the CD19R(EQ)-CD28-CD3zeta-EGFRt-expressing Tn/mem-enriched T cells target CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. Tn/mem T cells include naïve T cells, central memory T cells (Tcm) and stem cell memory T cells (Tscm). CD19R(EQ) contains two point mutations in the immunoglobulin (Ig) G4 spacer region, thereby preventing recognition of the CAR by Fc receptors (FcRs).
CD19CAR-CD28zeta-4-1BB-expressing allogeneic T lymphocytes: Allogeneic T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD28 zeta-4-1BB-expressing allogeneic T lymphocytes directs the T-lymphocytes to and induces selective toxicity in CD19-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity compared to the inclusion of the CD28 costimulatory domain and TCR zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.
CD19CAR-CD3zeta-4-1BB-CD28-expressing autologous T lymphocytes: Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to three co-stimulatory signaling domains derived from CD28, 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, the CD19CAR-CD3zeta-4-1BB-CD28-expressing autologous T-lymphocytes direct the T-lymphocytes to CD19-expressing tumor cells and induce their selective toxicity. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. CD3-zeta is a transmembrane signaling adaptor polypeptide that regulates the assembly of TCR complexes, modulates the expression of the complex on the cell surface and plays a key role in antigen recognition. CD19 antigen, a B-cell specific cell surface antigen, is expressed in all B-cell lineage malignancies.
CD19CAR-CD3zeta-4-1BB-expressing allogeneic T lymphocytes: Allogeneic T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-4-1BB-expressing allogeneic T-lymphocytes direct the T-lymphocytes to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19 and the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.
CD19CAR-CD3zeta-expressing autologous T lymphocytes: Autologous T lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-expressing autologous T lymphocytes are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity only in these tumor cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3-zeta (or CD247) is a transmembrane signaling adaptor polypeptide that regulates the assembly of complete T-cell receptor complexes and their expression on the cell surface.
CD19R(EQ)-CD28-CD3zeta-EGFRt-expressing T lymphocytes: A preparation of genetically modified T cells transduced expressing a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD19 and containing the CD28 signaling domain fused to CD3 zeta, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, CD19R(EQ)-CD28-CD3zeta-EGFRt-expressing T lymphocytes are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response. The costimulatory signaling domain enhances proliferation of T-cells and antitumor activity. CD19R(EQ) contains two-point mutations in the immunoglobulin (Ig) G4 Fc spacer region, thereby preventing recognition of the CAR by Fc gamma receptors (FcgammaRs).
CD19x22 bicistronic CAR T cells: A preparation of T lymphocytes that have that have been transduced with a bicistronic vector encoding two distinct chimeric antigen receptors (CARs), one against the tumor-associated antigen (TAA) CD19 and the other one against the TAA CD22, with potential immunomodulating and antineoplastic activities. Upon administration, the CD19x22 bicistronic CAR T cells target, bind to and induce selective toxicity in tumor cells expressing CD19 and CD22. CD19 and CD22, both transmembrane phosphoglycoproteins expressed on the surface of cells in the B lineage, are often overexpressed on malignant B cells. By simultaneously targeting two B-cell antigens using two different CARs, this preparation may minimize relapse due to single antigen loss in patients with B-cell malignancies.
CD20-CD19 compound CAR-T cells: A preparation of T lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two distinct units of CARs, one specific for the tumor-associated antigen (TAA) cluster of differentiation 20 (CD20) and one specific for the TAA CD19, with potential immunomodulating and antineoplastic activities. Upon administration, the CD20-CD19 cCAR-T cells specifically and simultaneously target and bind to tumor cells expressing CD20 and/or CD19. This induces selective toxicity in tumor cells that express CD20 and/or CD19. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting two different antigens may improve coverage and protect against antigen escape and relapse as it is less likely for tumor cells to lose both antigens.
CD20-targeted Polypeptide TRU-015: A proprietary antibody-based single-chain polypeptide with B cell-depleting activity. Significantly smaller than a whole antibody, CD20-targeted polypeptide TRU-015 binds specifically to the B cell-specific cell surface antigen CD20 with full immunoglobulin Fv fragment-type target binding activity and full immunoglobulin Fc fragment-type effector function. This agent transiently depletes CD20-bearing B cells by inducing B-cell-directed complement dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) and B-cell apoptosis.
CD20/CD47 bispecific fusion protein CPO107: A bispecific fusion protein composed of the anti-CD20 antibody ofatumumab fused to the CD47 binding fragment signal regulatory protein alpha (SIRPalpha), and directed against both the B-cell-specific membrane protein and tumor-associated antigen (TAA) CD20, and the human cell surface antigen CD47, with potential immunostimulating, phagocytosis-inducing and antineoplastic activities. Upon administration of anti-CD47/CD20 bispecific fusion protein CPO107, the anti-CD20 moiety selectively targets and binds to CD20 on CD20-positive tumor cells, thereby inducing antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) in CD20-positive tumor cells, and improving the binding of its SIRPalpha moiety to CD47 expressed by CD20-positive tumor cells. The CD47 binding by CPO107 blocks the interaction of CD47 with endogenous SIRPalpha, an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of the CD20/CD47-expressing tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD20/CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is widely expressed on normal, healthy cells, such as red blood cells and platelets, and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. CD20 is a membrane antigen that is overexpressed in B-cell malignancies. By co-targeting CD47 and CD20, CPO107 has the potential to overcome the limitations of existing CD47-targeted therapies by possibly avoiding the side effects caused by binding to CD47 expressed on healthy hematopoietic stem cells (HSCs).
CD200 activation receptor ligand hP1A8: A humanized peptide ligand of the CD200 activation receptors (CD200ARs), with potential immunostimulating and antineoplastic activities. Upon administration, CD200 activation receptor ligand (CD200AR-L) human P1A8 (hP1A8) targets and binds to CD200ARs complexes on antigen-presenting cells (APCs). This promotes immature dendritic cell (DC) differentiation and cytokine production, and induces a T-cell-mediated immune response against tumor cells. In addition, hP1A8 downregulates the expression of the inhibitory CD200 and PD-1 receptors on APCs and T cells. This inhibits CD200- and PD-1-mediated immunosuppression. CD200, a type 1a transmembrane protein related to the B7 family of co-stimulatory receptors, functions as an immune checkpoint that modulates immune responses through an inhibitory receptor CD200 receptor 1 (CD200R1) and several activation receptors (CD200ARs). It plays an important role in tumor evasion from host immunity.
CD22 immunotoxin: An immunotoxin composed of an anti-CD22 monoclonal antibody and a toxin moiety, which targets antigen-positive cells and causes cytotoxic activity.
CD24 extracellular domain-IgG1 Fc domain recombinant fusion protein CD24Fc: A recombinant fusion protein composed of the extracellular domain of the mature human glycoprotein CD24 linked to a human immunoglobulin G1 (IgG1) Fc domain, with potential immune checkpoint inhibitory, anti-inflammatory and antineoplastic activities. Upon administration, the CD24 extracellular domain-IgG1 Fc domain recombinant fusion protein CD24Fc binds to injured cell components, also called DAMPs (Danger-Associated Molecular Patterns), thereby preventing the interaction of DAMPs with toll-like receptors (TLRs) and inhibiting both nuclear factor-kappa B (NFkB) activation and secretion of inflammatory cytokines. In addition, CD24Fc binds to and activates Siglec G/10, a sialic acid-binding immunoglobulin-type lectin, and stimulates SHP-1-mediated inhibitory signaling, preventing NFkB activation and secretion of inflammatory mediators, which further prevents inflammatory responses. DAMPs activate the innate immune system. CD24 binds to both DAMPs and Siglec G/10 to regulate immune responses.CD24/Siglec G/10 interaction plays a key role in a number of immune-mediated diseases including graft-versus-host disease (GvHD), multiple sclerosis and rheumatoid arthritis.
CD28/ICOS antagonist ALPN-101: An Fc fusion protein comprised of a human inducible T-cell costimulator ligand (ICOSL) variant immunoglobulin domain (vIgD) that binds to both inducible T-cell costimulator (ICOS; CD278) and cluster of differentiation 28 (CD28), with potential immunomodulating activity. Upon administration, CD28/ICOS antagonist ALPN-101 targets and binds to both CD28 and ICOS expressed on certain T cells. This prevents the activation of CD28 and ICOS by its ligands, thereby blocking the two T-cell costimulatory pathways and the resulting T-cell activation. CD28 is involved in initiation of the pathogenic process in graft versus host disease (GVHD). Following initial activation, CD28 is often downregulated while ICOS is upregulated, possibly sustaining GVHD. Dual blockade of CD28 and ICOS may be superior to individual blockade of CD28 or ICOS alone.
CD28CAR/CD137CAR-expressing T lymphocytes: Third generation, chimeric antigen receptor (CAR) cells composed of T-lymphocytes transduced with a lentiviral vector expressing a CAR consisting of an a single chain variable fragment specific for a particular antigen, coupled to the two co-stimulatory signaling domains Cluster of Differentiation 28 (CD28) and Cluster of Differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD28CAR/CD137CAR-expressing T-lymphocytes are directed to, and induce selective toxicity in tumor cells expressing the particular antigen. CD28, a T-cell surface-associated co-stimulatory molecule that is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the antigen. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity when compared to the inclusion of the CD28 co-stimulatory domain and CD3-zeta alone.
CD3+/CD19+ cell-depleted autologous hematopoietic stem cells: A preparation of autologous hematopoietic stem cells (HSCs) that have been selectively depleted of CD3-positive (CD3+) T cells and CD19-positive (CD19+) B cells, with potential immune reconstituting activity. Upon administration, the CD3+/CD19+ cell-depleted autologous HSCs are used for autologous stem cell transplant (ASCT) and may allow for rapid and sustained engraftment and immune reconstitution without the autoreactive CD3+ T cells and CD19+ B cells. This may alleviate manifestations of autoimmune diseases such as systemic lupus erythematosus (SLE) and systemic sclerosis.
CD3+/CD19+ cell-depleted unrelated or partially matched donor-derived allogeneic peripheral blood stem cells: A preparation of allogeneic peripheral blood stem cells (PBSCs) from an unrelated or partially matched related donor that have been selectively depleted of CD3-positive (CD3+) T cells and CD19-positive (CD19+) B cells via leukapheresis with potential immune reconstituting activity. The CD3+/CD19+ cell-depleted PBSCs are used for allogeneic hematopoietic cell transplantation (HCT) and may allow for rapid and sustained engraftment, immune reconstitution, and may prevent or reduce graft-versus-host disease (GvHD) and Epstein-Barr virus (EBV)-driven post-transplant lymphoproliferative disorders.
CD3-activating CD19-bi-specific antibody A-319: A recombinant T-cell activating bispecific antibody directed against the B-cell-specific membrane protein CD19 and the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration, CD3-activating CD19 bi-specific antibody A-319 targets and binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and the CD19 antigen expressed on malignant B cells. This activates and redirects CTLs, bringing CD19-expressing tumor cells and CTLs together, and results in a CTL-mediated immune response against CD19-expressing tumor cells. CD19 is a membrane antigen that is widely expressed during B-cell development, from pro-B cell to early plasma cell stages.
CD3/CD28 costimulated autologous T cells: A population of T cells that have been sensitized to vaccine tumor antigen(s) in vivo; collected from the patient; co-stimulated with antibodies to the T-cell cell surface proteins CD3 and CD28 and expanded ex vivo; and then infused into the same patient. CD3, part of the T-cell receptor complex, and CD28, a T-cell surface-associated co-stimulatory molecule, are both required for full T-cell activation. Adoptive transfer of CD3/CD28 costimulated vaccine-primed autologous T cells may induce the production of interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and associated antitumor effects and a graft-versus-tumor (GVT) response.
CD30 CAR-expressing autologous T lymphocytes: A preparation of autologous T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the CD30 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, the CD30 CAR-expressing autologous T lymphocytes specifically recognize and bind to CD30-expressing tumor cells, resulting in tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies.
CD33-specific CAR lentiviral vector-transduced allogeneic T lymphocytes: A preparation of allogeneic T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, CD33-specific CAR lentiviral vector-transduced allogeneic T lymphocytes target and induce selective toxicity in CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and on myeloid leukemia cells.
CD33-specific CAR lentiviral vector-transduced autologous T lymphocytes: Autologous T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon transfusion, CD33-specific CAR lentiviral vector-transduced autologous T lymphocytes target and induce selective toxicity in CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and on myeloid leukemia cells.
CD33CAR-CD3zeta-4-1BB-expressing autologous T-lymphocytes: Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD33 scFv (single chain variable fragment) coupled to the signaling domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD33-specific CAR retroviral vector-transduced autologous T lymphocytes target CD33-expressing tumor cells and induce selective toxicity in CD33-expressing tumor cells. Following binding to CD33, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells.
CD34/TK75 retroviral vector-transduced donor lymphocytes: A preparation of donor T lymphocytes that are transfected with a retroviral vector encoding a chimeric suicide gene consisting of the extracellular and transmembrane domains of human CD34 and mutant 75 of the herpes simplex virus thymidine kinase (HSV-TK75) with potential controllable immunomodulating activity. Donor T-cell therapy following allogeneic hematopoietic stem cell (HSC) transplantation may result in a graft-versus-leukemia (GVL) and help control transplant-related viral infections. In the event that graft-versus-host disease (GVHD) develops due to donor lymphocyte infusion, CD34/TK75-transduced donor lymphocytes may be selectively eliminated by administration of the prodrug antiviral agent ganciclovir GCV. In CD34/T75-transduced donor lymphocytes, GCV is phosphorylated by expressed HSV-TK75 to its monophosphate form and, subsequently, converted into its active triphosphate form, which specifically kills the donor lymphocytes. The expressed CD34 moiety of the chimeric suicide gene serves as a selection marker; mutant 75 of HSV-TK confers increased GCV sensitivity.
CD371-specific/YSNVz/IL-18 CAR T cells: A preparation of T lymphocytes engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) C-type lectin domain family 12 member A (CLEC12A, CCL1, CD371), and expressing the pro-inflammatory cytokine interleukin 18 (IL-18), with potential antineoplastic activity. Upon intravenous administration, CD371-specific/YSNVz/IL-18 CAR T cells target, bind to, and induce selective toxicity in CD371-expressing tumor cells. IL-18 promotes T-cell persistence and potentiates the immune response against tumor cells. CD371 is expressed on the surface of acute myeloid leukemia (AML) cells and leukemic stem cells, but it is not expressed on normal hematopoietic stem cells (HSCs).
CD38-targeting antibody recruiting molecule KP1237: A synthetic, small, bispecific antibody-redirecting/recruiting molecule (ARM) that recognizes the tumor-associated antigen (TAA) and cell surface glycoprotein CD38 on tumor cells with its target binding terminus (TBT) and, through connection by a tunable linker domain, recognizes endogenous antibodies already present in the patient's blood with its universal antibody binding terminus (uABT), with potential immunomodulating and antineoplastic activities. Upon administration, CD38-targeting ARM KP1237 simultaneously targets and binds to CD38 expressed on tumor cells with its TBT and to endogenous antibodies with its uABT. This recruits immune effector cells, such as the patient's activated natural killer (NK) cells, to eliminate the CD38-expressing tumor cells through antitumoral antibody-dependent cellular cytotoxicity (ADCC). CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies. Its expression has been correlated with poor prognosis.
CD4+ CD25+ regulatory T cells: Regulatory T cells that express CD4 and CD25 (interleukin 2 receptor) antigens, with immunomodulating activity. CD4+CD25+ T regulatory cells (Tregs), a subset of CD4+ T cells expressing high levels of CD25 and the transcription factor Foxp3, are essential in maintaining immunologic homeostasis, preventing autoimmunity by suppressing self-reactive T cells; CD4+CD25+ Tregs may induce tolerance to allogeneic organ transplants such as hematopoetic stem cell transplants (HSCTs).
CD4-specific telomerase peptide vaccine UCPVax: A therapeutic peptide vaccine containing the human telomerase reverse transcriptase catalytic subunit (hTERT)-derived universal cancer peptides 2 (UCP2) and 4 (UCP4), and combined with the immunoadjuvant Montanide ISA 51 VG, with potential immunostimulating and antineoplastic activities. Vaccination with the CD4-specific telomerase peptide vaccine UCPVax activates the immune system to mount a T-helper 1 (TH1) CD4-positive T-lymphocyte immune response against and ultimately killing telomerase-expressing cells. Telomerase, a reverse transcriptase normally repressed in healthy cells, is overexpressed in most cancer cells and plays a key role in cellular proliferation.
CD40 agonist monoclonal antibody CP-870,893: A fully human monoclonal antibody (mAb) agonist of the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Similar to the CD40 ligand (CD40L or CD154), CD40 agonist monoclonal antibody CP-870,893 binds to CD40 on a variety of immune cell types, triggering the cellular proliferation and activation of antigen-presenting cells (APCs), activating B cells and T cells, and enhancing the immune response; in addition, this agent may activate CD40 present on the surfaces of some solid tumor cells, resulting in apoptosis and decreased tumor growth. CD40, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, many B-cell malignancies, and some solid tumors, mediating both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.
CD40L-augmented autologous tumor infiltrating lymphocytes: A preparation of autologous tumor-infiltrating lymphocytes (TILs) derived from a patient's tumor that have been stimulated ex vivo with CD40 ligand (CD40L, tumor necrosis factor superfamily member 5, TNFSF5, CD154, TNF-related activation protein, TRAP, gp39) during cell expansion, with potential immunomodulating and antineoplastic activities. Upon administration, the CD40L-augmented autologous TILs specifically recognize and kill the patient's tumor cells. Stimulation with a CD40L may enhance both the expansion of the TILs and the tumor-killing ability of the TILs when returned to the patient.
CD40L-Fc fusion protein MEDI5083: A fusion protein composed of CD40 ligand (CD40L; CD154; TRAP; TNFSF5) fused to a modified immunoglobulin (Ig) Fc fragment, with potential immunostimulating activity. Upon administration of the CD40L-Fc fusion protein MEDI5083, the CD40L moiety specifically targets, 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 cytotoxic T lymphocytes (CTLs) against tumor cells. Altogether, this may cause tumor cell lysis.
CD44 targeted agent SPL-108: A proprietary agent that targets the cancer stem cell (CSC) antigen CD44, with potential antineoplastic activity. Although the mechanism of action has not been elucidated, following subcutaneous administration, CD44 targeted agent SPL-108 binds to CD44 and prevents the activation of various CD44-mediated signal transduction pathways, which may lead to reduced proliferation of CD44-expressing tumor stem cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types; it plays a key role in the proliferation, migration and survival of tumor cells.
CD44v6-specific CAR-T cells: A preparation of genetically modified T lymphocytes transduced with a lentiviral vector encoding a fourth-generation specific chimeric antigen receptor (4SCAR) specific for CD44 variant domain 6 (CD44v6), with potential immunomodulating and antineoplastic activities. Upon administration, CD44v6-specific CAR T cells specifically recognize and kill CD44v6-expressing tumor cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types. CD44v6, the isoform containing the variant domain 6 of CD44 gene, plays a key role in tumor cell invasion, proliferation and metastasis.
CD45RA-depleted donor T lymphocytes: A preparation of donor lymphocytes that have been depleted of CD45RA-positive cells, that can potentially be used for immune reconstitution purposes. CD45RA depletion results in a cellular product that contains a high amount of memory T cells (Tm). Upon infusion of the allogeneic CD45RA-depleted T lymphocytes after a hematopoietic cell transplantation (HCT), these cells provide Tm recovery and are able to prevent viral infections. The depletion of the CD45RA-positive cells reduces the risk of graft-versus-host disease (GvHD) upon infusion. CD45RA is expressed on naive T cells, whereas Tm cells are CD45RA-negative. Naive T-cells have the potential to induce GvHD.
CD47 antagonist AUR103 calcium: The calcium salt form of AUR103, an orally bioavailable, small molecule antagonist of the human cell surface antigen CD47, with potential phagocytosis-inducing, immunostimulating and antineoplastic activities. Upon oral administration, CD47 antagonist AUR103 calcium binds to CD47 expressed on tumor cells and prevents the interaction of CD47 with its ligand SIRPa, a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of the pro-phagocytic signal calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor cytotoxic T-lymphocyte (CTL) immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.
CD47/SIRPa blocking agent TQB2928: An agent blocking the interaction between the leukocyte surface antigen CD47 and the signal regulatory protein alpha (SIRPalpha; SIRPa), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, CD47/SIRPa blocking agent TQB2928 blocks the interaction between CD47, which is expressed on tumor cells, and SIRPa, which is expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate.
CD56-enriched CD3-positive donor lymphocytes: A population of CD3-positive lymphocytes expressing the CD56 surface antigen, with potential immunomodulating activity. Upon infusion of the CD56-enriched CD3-positive donor lymphocytes, these cells may facilitate the reconstitution of CD4-positive T cells, regulatory T cells (Tregs) and natural killer (NK) cells, which may reduce the incidence of post-transplant graft-versus-host disease (GvHD) following haploidentical stem cell transplant (SCT). CD56 is a transmembrane glycoprotein also known as neural cell adhesion molecule 1 (NCAM-1).
CD73 inhibitor ATG-037: An orally bioavailable inhibitor of the ectoenzyme CD73 (cluster of differentiation 73; 5'-ecto-nucleotidase; 5'-NT; ecto-5'-nucleotidase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CD73 inhibitor ATG-037 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 in the tumor microenvironment (TME). This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells and natural killer (NK) cells. This also activates macrophages and reduces the activity of myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against tumor 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 belonging to the 5'-nucleotidase (NTase) family, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine. It is upregulated in a number of cancer cell types and plays a key role in adenosine-mediated immunosuppression within the TME.
CD73 inhibitor LY3475070: An orally bioavailable inhibitor of the ectoenzyme CD73 (cluster of differentiation 73; 5'-ecto-nucleotidase; 5'-NT; ecto-5'-nucleotidase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CD73 inhibitor LY3475070 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 in the tumor microenvironment (TME). This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells and natural killer (NK) cells. This also activates macrophages and reduces the activity of myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against tumor 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 belonging to the 5'-nucleotidase (NTase) family, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine. It is upregulated in a number of cancer cell types and plays a key role in adenosine-mediated immunosuppression within the TME.
CD73 inhibitor ORIC-533: An orally bioavailable inhibitor of the ectoenzyme CD73 (cluster of differentiation 73; 5'-ecto-nucleotidase; 5'-NT; ecto-5'-nucleotidase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CD73 inhibitor ORIC-533 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 in the tumor microenvironment (TME). This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells and natural killer (NK) cells. This also activates macrophages and reduces the activity of myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against tumor 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 belonging to the 5'-nucleotidase (NTase) family, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine. It is upregulated in a variety of cancer cell types and plays a key role in adenosine-mediated immunosuppression within the TME.
CD8 enriched young autologous tumor-infiltrating lymphocytes: A preparation of autologous young tumor infiltrating lymphocytes (TILs), that are isolated from the patient's tumor tissue that are CD8 enriched and expanded ex vivo, with potential antineoplastic and immunomodulating activities. Upon administration of the CD8 enriched young autologous TILs, the TILs re-infiltrate the tumor, recognize the tumor cells and initiate tumor cell lysis. This inhibits tumor cell growth.
CD8+ and CD4+ donor memory T cells-expressing HA1-specific TCR: A preparation of CD4+ and CD8+ central memory (CM) T lymphocytes isolated from the peripheral blood of a transplant donor and transduced with a lentiviral vector (LV) (pRRLSIN) expressing a minor H antigen (HA-1(H); HA1(H)) T-cell receptor (TCR) containing the suicide gene inducible caspase 9 (iCasp9 or iC9)-HA1 TCR2-RQR-CD8 transgene (pRRLSIN iC9-HA1 TCR2-RQR-CD8; HA-1 TCR LV), with potential immunostimulating and antineoplastic activities. Upon intravenous administration and after allogeneic hematopoietic stem cell transplantation (HSCT), the CD8+ and CD4+ donor memory T cells-expressing HA1-specific TCR are directed to and induce selective toxicity in HA1-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If administration of the T cells lead to unacceptable side effects, a dimerizing agent rimiducid (AP1903), which binds to the FKBP12-F36V drug-binding domain and activates caspase 9, can be administered; caspase-9 activation results in the apoptosis of the administered TCR-modified T cells. HA1(H) is a tumor-associated antigen (TAA) that is selectively and highly expressed on leukemic stem cells and blasts, but not in normal non-hematopoietic cells. RQR includes a CD20 epitope, and a CD34 epitope that facilitates both purification and cell tracking of the transduced T cells with an anti-CD34 monoclonal antibody.
CD8+NKG2D+ AKT cells: A preparation of human CD8-positive tumor-specific T lymphocytes engineered to express the natural killer cell activating receptor group 2D (NKG2D) and the serine/threonine kinase AKT, with potential immunomodulating and antineoplastic activities. Upon administration of CD8+NKG2D+ AKT cells, these cells target and kill tumor cells. AKT-mediated signaling enhances the activation, differentiation, proliferation and cytokine production of tumor specific T cells, which enhances their anti-tumor effects; AKT activity in T cells is often downregulated in the tumor environment. NKG2D, a stimulatory lymphocyte receptor, mediates the recognition of tumors cells and promotes T-cell activation and T-cell-mediated tumor cell killing; NKG2D ligands are expressed on cancer cells, while they are minimally expressed by or absent from normal, healthy cells.
CD8-depleted non-engrafting HLA-mismatched unrelated donor lymphocytes: A preparation of allogeneic lymphocytes from an HLA-mismatched donor that have been selectively depleted of CD8+ T cells, with potential T-cell reconstitution purposes. Upon infusion, the donor-derived CD8+-depleted lymphocytes may increase the levels of CD4+ T cells (Teffs) and promote T-cell reconstitution. The infusion of donor lymphocytes depleted of CD8 T cells may reduce the risk of inducing graft-versus-host disease (GVHD) compared to the infusion of non-CD8-depleted T cells.
CD80 breast cancer vaccine: A vaccine comprised of CD80-transfected allogenic breast cancer cells to induce T-cell response.
CD80-Fc fusion protein ALPN-202: A fusion protein composed of the N-terminal Ig variable-like (IgV) domain of CD80 fused to a human immunoglobulin G1 (IgG1) Fc fragment, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration, CD80-Fc fusion protein ALPN-202 targets and binds to programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) expressed on tumor cells, which blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), and leads to PD-L1-dependent CD28 binding and co-stimulation in the local tumor microenvironment (TME). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling, leads to the co-stimulation of T-cell responses including the activation of naïve and memory T cells in the TME and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, ALPN-202 targets and binds to CTL-associated antigen 4 (CTLA4; CTLA-4) expressed on T cells. This prevents the binding of CTLA-4 to endogenous CD80, thereby enabling CD80-CD28 engagement, CD28 signaling, and T-cell activation. This further promotes T-cell activity. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. CD80 is a co-stimulatory molecule expressed on activated antigen presenting cells (APCs) that plays a key role in T-cell activation upon binding to CD28 on T cells. On the other hand, binding of CD80 to CTLA-4 prevents CD80-CD28 engagement, thereby inhibiting T-cell activity and immune activation. CTLA-4 is a member of the immunoglobulin superfamily (IgSF) and an inhibitory molecule upregulated by T cells following T-cell activation. It plays a key role in the downregulation of the immune system.
CD80-Fc fusion protein FPT155: A recombinant fusion protein composed of the extracellular domain (ECD) of human CD80 (B7.1) fused to a human immunoglobulin G1 (IgG1) Fc fragment, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration of CD80-Fc fusion protein FPT155, the CD80 moiety targets and binds to CD28, which in the presence of antigenic T-cell receptor (TCR) signaling, leads to the co-stimulation of T-cell responses including the activation of naïve and memory T cells. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. FPT155 also targets and binds to CTL-associated antigen 4 (CTLA4; CTLA-4), preventing the binding of CTLA-4 to endogenous CD80, thereby enabling CD80-CD28 engagement, CD28 signaling, and T-cell activation in the tumor microenvironment. CD80 is a co-stimulatory molecule expressed on activated antigen presenting cells that plays a key role in T-cell activation upon binding to CD28 on T cells. On the other hand, binding of CD80 to CTLA-4 prevents CD80-CD28 engagement, thereby inhibiting T-cell activity and immune activation. CTLA-4 is a member of the immunoglobulin superfamily (IgSF) and an inhibitory molecule upregulated by T cells following T-cell activation. It plays a key role in the downregulation of the immune system.
CD80-Fc fusion protein KM602: A recombinant fusion protein composed of the extracellular domain (ECD) of human CD80 (B7.1) fused to a human immunoglobulin G1 (IgG1) Fc fragment, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration of CD80-Fc fusion protein KM602, the CD80 moiety targets and binds to CD28, which 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. KM602 also targets and binds to CTL-associated antigen 4 (CTLA4; CTLA-4), which prevents the binding of CTLA-4 to endogenous CD80 and enables CD80-CD28 engagement, CD28 signaling, and T-cell activation in the tumor microenvironment (TME). In addition, KM602 binds to the immunosuppressive ligand human programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), which prevents the binding of PD-L1 to CD80 and enables CD80-CD28 engagement, CD28 signaling, and T-cell activation in the TME as well as abrogating the binding of PD-L1 to its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279) and preventing PD-L1/PD-1-mediated signaling, which further enhances an anti-tumor immune response. CD80 is a co-stimulatory molecule expressed on activated antigen presenting cells (APCs) that plays a key role in T-cell activation upon binding to CD28 on T cells. On the other hand, binding of CD80 to CTLA-4 prevents CD80-CD28 engagement, thereby inhibiting T-cell activity and immune activation, and T-cell exhaustion. CTLA-4, a member of the immunoglobulin superfamily (IgSF) and an inhibitory molecule, is upregulated by T cells following T-cell activation and plays a key role in the downregulation of the immune system. PD-1, found on activated T cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PD-L1 is often overexpressed on tumor cell types and plays a key role in immune evasion.
CDAC targeting EGFR mutant BG-60366: An orally bioavailable chimeric degradation activation compound (CDAC) targeting mutant epidermal growth factor receptor (EGFR) comprised of an E3 ubiquitin ligase ligand conjugated to an EGFR mutant-binding ligand, with potential antineoplastic activity. Upon oral administration, CDAC targeting EGFR mutant BG-60366 specifically targets and binds, with its mutant EGFR-targeting moiety, to mutant EGFR and the E3 ubiquitin ligase ligand moiety binds to E3 ubiquitin ligase. This catalyzes ubiquitination and proteasome-mediated degradation of mutant EGFR and prevents the activation of the EGFR-mediated signaling pathway. This leads to an inhibition of the growth of EGFR mutant-expressing tumor cells. EGFR is overexpressed or mutated in a variety of cancer cells.
CDC7 inhibitor SGR-2921: An orally bioavailable small molecule inhibitor of cell division cycle 7-related protein kinase (CDC7), with potential antineoplastic activity. Upon oral administration, CDC7 inhibitor SGR-2921 targets, binds to and inhibits the activity of CDC7, which may result in an impaired response to replication stress, DNA damage, and the induction of tumor cell apoptosis. CDC7, a serine-threonine kinase overexpressed in a variety of tumor cell types, plays a key role in DNA replication and DNA damage response by binding to and phosphorylating serine (Ser)-40 and 53 of minichromosome maintenance complex component 2 (MCM2).
CDC7 inhibitor TAK-931: An orally bioavailable inhibitor of cell division cycle 7 (cell division cycle 7-related protein kinase; CDC7), with potential antineoplastic activity. Upon administration, TAK-931 binds to and inhibits CDC7; this prevents the initiation of DNA replication during mitosis, which causes cell cycle arrest and induces apoptosis. This inhibits cell growth in CDC7-overexpressing tumor cells. CDC7, a serine/threonine kinase and cell division cycle protein, is overexpressed in a variety of cancers and plays a key role in the activation of DNA replication and the regulation of cell cycle progression.
CDC7 inhibitor TQB3824: An orally bioavailable inhibitor of cell division cycle 7 (CDC7) kinase, with potential antineoplastic activity. Upon oral administration, CDC7 inhibitor TQB3824 targets, binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. CDC7, a serine-threonine kinase overexpressed in a variety of tumor cell types, plays a key role in DNA replication and DNA damage response by binding to and phosphorylating serine (Ser)-40 and 53 of minichromosome maintenance complex component 2 (MCM2).
CDC7 kinase inhibitor BMS-863233: An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor BMS-863233 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. CDC7, a serine-threonine kinase overexpressed in a variety of tumor cell types, plays an essential role in the initiation of DNA replication by activating origins of replication.
CDC7 kinase inhibitor LY3143921 hydrate: The hydrated form of an orally bioavailable inhibitor of cell division cycle 7 (CDC7) kinase, with potential antineoplastic activity. Upon administration of CDC7 kinase inhibitor LY3143921 hydrate, LY3143921 targets, binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. The serine-threonine kinase CDC7 plays a key role in DNA replication by binding to and phosphorylating serine (Ser)-40 and 53 of MCM2 (minichromosome maintenance complex component 2), which is required for the initiation of DNA replication. Although expressed at low levels in healthy, normal cells, CDC7 is expressed at much higher levels in cancer cells.
CDC7 kinase inhibitor NMS-1116354: An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor NMS-1116354 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. The serine-threonine kinase CDC7 initiates DNA replication by phosphorylating MCM2 (minichromosome maintenance complex component 2) at Ser40 and Ser53.
CDK inhibitor AT7519: An orally bioavailable small molecule with potential antineoplastic activity. AT7519M selectively binds to and inhibits cyclin dependent kinases (CDKs), which may result in cell cycle arrest, induction of apoptosis, and inhibition of tumor cell proliferation. CDKs are serine/threonine kinases involved in regulation of the cell cycle and may be overexpressed in some types of cancer cells.
CDK inhibitor P276-00: A flavone and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. P276-00 selectively binds to and inhibits Cdk4/cyclin D1, Cdk1/cyclin B and Cdk9/cyclin T1, serine/threonine kinases that play key roles in the regulation of the cell cycle and cellular proliferation. Inhibition of these kinases leads to cell cycle arrest during the G1/S transition, thereby leading to an induction of apoptosis, and inhibition of tumor cell proliferation.
CDK Inhibitor R547: An orally bioavailable diaminopyrimidine compound and a cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. CDKs are ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and are frequently overexpressed in cancerous cells. R547 selectively binds to and inhibits CDKs, especially CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclin D1. The inhibition of CDKs results in cell cycle arrest, inhibition of tumor cell proliferation, and induction of apoptosis. By inhibiting CDK activity, R547 also reduces phosphorylation of the retinoblastoma (Rb) protein, thereby preventing activation of transcription factor E2F and leading to further suppression of tumor cell proliferation.
CDK inhibitor SNS-032: A small aminothiazole molecule and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. SNS-032 binds to and prevents the phosphorylation of cyclin-dependent kinases, especially CDK2, 7, and 9 that regulate cell cycle progression. Inhibition of CDKs leads to cell cycle arrest and induces apoptosis. As a result, this agent causes cytotoxicity and prevents further tumor cell growth.
CDK1/2/4 inhibitor AG-024322: A cyclin-dependent kinase (CDK) inhibitor with antineoplastic activity. AG-024322 selectively inhibits cyclin-dependent kinases (particularly CDK1,2 and 4), enzymes that regulate cell cycle progression. Inhibition of CDK may result in cell cycle arrest, induction of apoptosis, and inhibition of DNA replication and tumor cell proliferation.
CDK2 degrader NKT3964: An orally bioavailable, targeted degrader composed of an E3 ubiquitin ligase-binding moiety that is conjugated, via a linker, to a cyclin-dependent kinase 2 (CDK2)-binding moiety using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. Upon oral administration of CDK2 degrader NKT3964, the CDK2-binding moiety specifically targets and binds to CDK2 on tumor cells while the E3 ubiquitin ligase-binding moiety targets and binds to E3 ubiquitin ligase, thereby creating a ternary complex. This induces E3 ligase ubiquitination and proteasome-mediated degradation of CDK2, and inhibits the activity of CDK2. This inhibits retinoblastoma (Rb) phosphorylation and blocks G1/S transition, which leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDK2, in complex with cyclin E1 (CCNE1; CCNE-1), phosphorylates Rb, which leads to E2F target gene expression and G1 to S-phase cell cycle progression. CDK2 and CCNE1 are overexpressed in various tumor cell types. NKT3964 does not cause cyclin E accumulation.
CDK2 inhibitor ARTS-021: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon oral administration, CDK2 inhibitor ARTS-021 selectively targets, reversibly binds to and inhibits the activity of the CDK2/CyclinE1 (CCNE1; CCNE-1) complex. This inhibits retinoblastoma (Rb) phosphorylation and blocks G1/S transition, which leads to cell cycle arrest, the induction of apoptosis, and the inhibition of proliferation in CDK2 and/or CCNE1-overexpressing tumor cells. CDK2, a serine/threonine kinase that plays an important role in the regulation of cell cycle progression and cellular proliferation, is overexpressed in certain tumor cells. CCNE1, a regulatory factor and activator of CDK2 is overexpressed in various tumor cell types and CCNE1 overexpression elevates the activity of CDK2.
CDK2 inhibitor BG-68501: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon oral administration, CDK2 inhibitor BG-68501 selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are frequently overexpressed in tumor cells.
CDK2 Inhibitor BLU-222: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon administration, CDK2 inhibitor BLU-222 selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDK2, a serine/threonine kinase that plays an important role in the regulation of cell cycle progression and cellular proliferation, is overexpressed in certain tumor cells.
CDK2 inhibitor INCB123667: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon oral administration, CDK2 inhibitor INCB123667 selectively targets, binds to and inhibits the activity of CDK2. This inhibits retinoblastoma (Rb) phosphorylation and blocks G1/S transition, which leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDK2, in complex with cyclin E1 (CCNE1; CCNE-1), phosphorylates Rb, which leads to E2F target gene expression and G1 to S-phase cell cycle progression. CDK2 and CCNE1 are overexpressed in various tumor cell types.
CDK2 inhibitor INX-315: An orally bioavailable small molecule inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon oral administration, CDK2 inhibitor INX-315 selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are frequently overexpressed in tumor cells.
CDK2 inhibitor NKT3447: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon oral administration, CDK2 inhibitor NKT3447 selectively targets, reversibly binds to and inhibits the activity of CDK2. This blocks G1/S cell cycle transition, which leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDK2, a serine/threonine kinase that plays an important role in the regulation of cell cycle progression and cellular proliferation, is overexpressed in certain tumor cells.
CDK2 inhibitor PF-07104091: An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon administration, CDK2 inhibitor PF-07104091 selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are frequently overexpressed in tumor cells. CDK2/cyclin E complex plays an important role in retinoblastoma (Rb) protein phosphorylation and the G1-S phase cell cycle transition. CDK2/cyclin A complex plays an important role in DNA synthesis in S phase and the activation of CDK1/cyclin B for the G2-M phase cell cycle transition.
CDK2/4/6 inhibitor NUV-422: An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 2 (CDK2), 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK2/4/6 inhibitor NUV-422 selectively targets and inhibits CDK2, CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types. NUV-422 may be able to penetrate through the blood-brain barrier (BBB).
CDK2/4/6 inhibitor PF-07224826: An orally bioavailable small molecule inhibitor of cyclin-dependent kinase (CDK) types 2 (CDK2), 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK2/4/6 inhibitor PF-07224826 selectively targets and inhibits CDK2, CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types.
CDK2/4/6 inhibitor RGT-419B: An orally bioavailable third-generation inhibitor of cyclin-dependent kinase (CDK) types 2 (CDK2), 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK2/4/6 inhibitor RGT-419B selectively targets and inhibits CDK2, CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types. In addition, RGT-419B may inhibit other kinases.
CDK2/4/6 inhibitor SYH2043: An orally bioavailable small molecule inhibitor of cyclin-dependent kinase (CDK) types 2 (CDK2), 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK2/4/6 inhibitor SYH2043 selectively targets and inhibits CDK2, CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types.
CDK2/4/6/FLT3 inhibitor FN-1501: A small molecule multi-kinase inhibitor of cyclin-dependent kinase (CDK) subtypes 2 (CDK2), 4 (CDK4), and 6 (CDK6) and FMS-related tyrosine kinase 3 (FLT3, FLK2, STK1), with potential antineoplastic activity. Upon intravenous administration, CDK2/4/6/FLT3 inhibitor FN-1501 binds to and inhibits CDK2, CDK4, and CDK6, as well as FLT3. This may induce apoptosis and inhibit tumor cell proliferation in cancer cells that overexpress these kinases. CDKs are serine/threonine kinases that assist in cell cycle regulation and cellular proliferation. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in many cancer types.
CDK4 inhibitor BGB-43395: An orally bioavailable inhibitor of cyclin-dependent kinase 4 (CDK4), with potential antineoplastic activity. Upon oral administration, CDK4 inhibitor BGB-43395 selectively inhibits CDK4, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and inhibits tumor cell proliferation. CDK4, a serine/threonine kinase, is upregulated in many tumor cell types and plays a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4 inhibitor P1446A-05: A protein kinase inhibitor specific for the cyclin-dependent kinase 4 (CDK4) with potential antineoplastic activity. CDK4 inhibitor P1446A-05 specifically inhibits CDK4-mediated G1-S phase transition, arresting cell cycling and inhibiting cancer cell growth. The serine/threonine kinase CDK4 is found in a complex with D-type G1 cyclins and is the first kinase to become activated upon mitogenic stimulation, releasing cells from a quiescent stage into the G1/S growth cycling stage; CDK-cyclin complexes have been shown to phosphorylate the retinoblastoma (Rb) transcription factor in early G1, displacing histone deacetylase (HDAC) and blocking transcriptional repression.
CDK4 inhibitor PF-07220060: An orally bioavailable inhibitor of cyclin-dependent kinase 4 (CDK4), with potential antineoplastic activity. Upon administration, CDK4 inhibitor PF-07220060 selectively inhibits CDK4, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and inhibits tumor cell proliferation. CDK4, a serine/threonine kinase, is upregulated in many tumor cell types and plays a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 degrader BTX-9341: An orally bioavailable bifunctional degrader of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 degrader BTX-9341 targets and binds to CDK4 and CDK6, as well as cereblon (CRBN), a component of the CRL4-CRBN E3 ubiquitin ligase complex that directs proteins for destruction. This leads to ubiquitination and induces proteasome-mediated degradation of CDK4 and CDK6, thereby inhibiting the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, preventing CDK-mediated G1-S-phase transition and leading to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation. BTX-9341 is able to penetrate through the blood-brain barrier (BBB).
CDK4/6 inhibitor BPI-1178: An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor BPI-1178 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation. BPI-1178 may be able to penetrate through the blood-brain barrier (BBB).
CDK4/6 inhibitor BPI-16350: An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor BPI-16350 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor CS3002: An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor CS3002 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor FCN-437: An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor FCN-437 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1/S transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play key roles in the regulation of both cell cycle progression from the G1-phase into the S-phase and cell proliferation.
CDK4/6 inhibitor GLR2007: An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor GLR2007 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor HS-10342: An orally bioavailable, small molecular, selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor HS-10342 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor PRT3645: An orally bioavailable, brain-penetrant, selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor PRT3645 selectively targets and inhibits the activity of CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation. PRT3645 is able to penetrate the brain and could exert its activity against CNS metastases in tumors with CDK4/6 upregulation.
CDK4/6 inhibitor QLS12004: An inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor QLS12004 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types.
CDK4/6 inhibitor SPH4336: An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor SPH4336 selectively targets and inhibits the activity of CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor TQB3303: An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor TQB3303 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor TQB3616: An orally bioavailable, selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor TQB3616 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK4/6 inhibitor UCT-03-008: An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor UCT-03-008 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase and prevents CDK-mediated G1-S-phase transition. This leads to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are upregulated in many tumor cell types.
CDK4/6 inhibitor XZP-3287: An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor XZP-3287 selectively targets and inhibits the activity of CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
CDK7 inhibitor LY3405105: An orally bioavailable, selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, LY3405105 selectively targets, binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. Specifically, inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA Polymerase II, thereby preventing transcription of important cancer-promoting genes. In addition, it prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc and beta-catenin, through the phosphorylation of RNA polymerase II.
CDK7 Inhibitor LY3405105 Besylate: The besylate salt form of LY3405105, an orally bioavailable, selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, LY3405105 selectively targets, binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. Specifically, inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA Polymerase II, thereby preventing transcription of important cancer-promoting genes. In addition, it prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc and beta-catenin, through the phosphorylation of RNA polymerase II.
CDK7 inhibitor Q901: A selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon administration, CDK7 inhibitor Q901 selectively targets, covalently binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. The inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA polymerase II, thereby preventing transcription of important cancer-promoting genes. It prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression and transcriptional regulation, and promotes the expression of key oncogenes through the phosphorylation of RNA polymerase II. It is overexpressed in multiple cancers.
CDK7 inhibitor SY-1365: A selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon administration, SY-1365 binds to and inhibits CDK7, thereby inhibiting CDK7-mediated signal transduction pathways. This inhibits cell growth of CDK7-overexpressing tumor cells. CDK7, a serine/threonine kinase, plays a key role in cell proliferation; CDK7 is overexpressed in a variety of tumor cell types.
CDK7 inhibitor SY-5609: An orally bioavailable, selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, SY-5609 selectively targets, binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. Specifically, inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA Polymerase II, thereby preventing transcription of important cancer-promoting genes. In addition, it prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc and beta-catenin, through the phosphorylation of RNA polymerase II.
CDK7 inhibitor TY-2699a: An orally bioavailable inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, CDK7 inhibitor TY-2699a selectively targets, binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. The inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA polymerase II, thereby preventing transcription of important cancer-promoting genes. The inhibition of CDK7 also prevents the phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression and transcriptional regulation, and promotes the expression of key oncogenes through the phosphorylation of RNA polymerase II. It is overexpressed in multiple cancers.
CDK7 inhibitor XL102: An orally bioavailable, selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, CDK7 inhibitor XL102 selectively targets, covalently binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. The inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA polymerase II, thereby preventing transcription of important cancer-promoting genes. It prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes through the phosphorylation of RNA polymerase II. It's overexpressed in multiple cancers.
CDK8/19 inhibitor RVU120: An orally bioavailable inhibitor of cyclin-dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, CDK8/19 inhibitor RVU120 targets, binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of various tumor-promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDK8/19, serine/threonine kinases involved in the regulation of the cell cycle, are overexpressed in certain cancer cell types and play key roles in tumor cell proliferation.
CDK9 inhibitor AZD4573: A selective, short-acting inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon intravenous administration, AZD4573 binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins. This induces cell cycle arrest and apoptosis, and leads to a reduction in tumor cell proliferation. CDK9 regulates elongation of transcription through phosphorylation of RNA polymerase II at serine 2 (p-Ser2-RNAPII). It is upregulated in various tumor cell types and plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
CDK9 inhibitor GFH009: A selective inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon administration, the CDK9 inhibitor GFH009 targets, binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins. This induces cell cycle arrest and apoptosis and prevents tumor cell proliferation. CDK9 regulates elongation of transcription through phosphorylation of RNA Pol II at serine 2 (p-Ser2-RNAPII). It is upregulated in various tumor cell types and plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
CDK9 inhibitor KB-0742: An orally bioavailable, selective inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon oral administration, CDK9 inhibitor KB-0742 targets, binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins and oncogenic transcription factors including MYC and androgen receptor (AR). This induces cell cycle arrest and apoptosis and prevents tumor cell proliferation. CDK9 regulates elongation of transcription through phosphorylation of RNA Pol II at serine 2 (p-Ser2-RNAPII), and is an important cofactor for various oncogenic transcription factors. It is upregulated in various tumor cell types and plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
CDK9 inhibitor PRT2527: A selective inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon administration, CDK9 inhibitor PRT2527 targets, binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins and oncogenic transcription factors including MYC. This induces cell cycle arrest and apoptosis and prevents tumor cell proliferation. CDK9 regulates elongation of transcription through phosphorylation of RNA Pol II at serine 2 (p-Ser2-RNAPII), and is an important cofactor for various oncogenic transcription factors. It is upregulated in various tumor cell types and plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
Ce-Vi-Sol: (Other name for: ascorbic acid)
CEA-MUC-1-TRICOM vaccine CV301: A cancer prime/boost vaccine-based immunotherapeutic consisting of a prime, which is comprised of a proprietary version of the recombinant vaccinia viral vector, modified vaccinia Ankara-Bavarian Nordic (MVA-BN) and a recombinant fowlpox viral vector, used for the boosts, encoding both the two tumor-associated antigens (TAA), carcinoembryonic antigen (CEA) and mucin-1 (MUC-1), and TRICOM, which is comprised of three immune-enhancing co-stimulatory molecules, B7-1, ICAM-1 and LFA-3, with potential immunostimulatory and antineoplastic activities. The administration of the vaccinia priming dose is followed by multiple boosting doses of the fowlpox vector. CEA-MUC-1-TRICOM vaccine CV301 may enhance presentation of CEA and MUC-1 to antigen-presenting cells (APCs) and may activate a cytotoxic T-lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells. In addition, CV301 upregulates the expression of PD-L1 due to CTL-mediated tumor attack; additionally, when combined with a PD-1 immune checkpoint inhibitor, the antitumor effect may be increased. CEA and MUC-1 are overexpressed in certain cancers.
CEA-Scan: (Other name for: arcitumomab)
CEA-targeting agent RG6123: An agent targeting the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), with potential antineoplastic activity. Upon administration, CEA-targeting agent RG6123 targets and binds to human CEA that is specifically expressed on certain tumor cells. This may, through an as of yet not elucidated mechanism of action, kill CEA-expressing tumor cells. CEA is overexpressed in many cancer cell types.
CEA/tetanus toxoid T helper epitope fusion protein-expressing DNA plasmid vaccine: A plasmid vaccine encoding wild type human carcinoembryonic antigen (CEA) fused to a tetanus toxoid T helper epitope, with potential antineoplastic activity. Upon vaccination and subsequent intradermal electroporation, CEA/tetanus toxoid T helper epitope fusion protein-expressing DNA plasmid vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA, a tumor associated antigen, is overexpressed in a variety of cancer cell types. The tetanus toxoid helper peptide epitope, obtained from the bacterial Clostridium tetani toxoid, binds to class II MHC molecules and increases the helper T-cell response thereby inducing an increased and long-term immune response.
CeaVac: (Other name for: monoclonal antibody 3H1 anti-idiotype vaccine)
CEBPA-targeting saRNA MTL-CEBPA liposome: A lipid-based nanoparticle formulation composed of liposomes encapsulating a small oligonucleotide encoding a small activating RNA (saRNA) targeting the CCAAT enhancer binding protein alpha (CEBPA; C/EBP‐a) gene, with potential antineoplastic activity. Although the exact mechanism of action through which saRNAs exert their effect(s) is still largely being investigated, it appears that, upon administration, the CEBPA-targeting saRNA MTL-CEBPA liposome targets and binds to a specific DNA regulatory target region, most likely the promoter region, for the CEBPA gene. This restores CEBPA gene transcription, and increases both CEBPA mRNA levels and protein expression. This in turn activates the expression of tumor suppressor genes and may halt proliferation of susceptible tumor cells. Specifically, upregulation of CEBPA in liver cells abrogates liver cancer cell proliferation, prevents liver failure and normalizes liver function. CEBPA, a transcription factor that plays a key role in the regulation of the expression of genes with many functions, including those involved in cellular proliferation, metastasis and normal hepatocyte function, is found in many tissues, including liver cells, adipose tissue and myeloid cells. CEBPA is downregulated in certain types of cancer cells, such as liver cancer cells. saRNA is a short, double-stranded RNA that is structurally related to small interfering RNAs (siRNAs); saRNA is most likely to bind to a target site on the promoter of the CEBPA gene and upregulates its gene expression.
cebranopadol: An orally available benzenoid that acts as an opioid peptide receptor agonist for the nociceptin/orphanin FQ peptide receptor (opioid receptor like -1; OPRL1; ORL-1; NOP; kappa-type 3 opioid receptor) and the classical opioid receptors, mu, delta and kappa, with potential anti-nociceptive activity. Upon oral administration, cebranopadol binds to NOP and the mu, delta and kappa opioid receptors, which enhances NOP- and opioid receptor-mediated signaling, interferes with the sensation of pain and results in an analgesic effect. NOP, a member of the opioid receptor family, and its endogenous ligand nociceptin play key roles in the regulation of various brain activities including pain, and some inflammatory and immune responses.
Cecon: (Other name for: ascorbic acid)
cedazuridine: An orally available synthetic nucleoside analog derived from tetrahydrouridine (THU) and cytidine deaminase inhibitor (CDAi), that can potentially be used to prevent the breakdown of cytidines. Upon oral administration, cedazuridine binds to and inhibits CDA, an enzyme primarily found in the gastrointestinal (GI) tract and liver that catalyzes the deamination of cytidine and cytidine analogs. Given in combination with a cytidine, such as the antineoplastic hypomethylating agent decitabine, it specifically prevents its breakdown and increases its bioavailability and efficacy. In addition, this allows for lower doses of decitabine to be administered, which results in decreased decitabine-associated GI toxicity.
cedazuridine/azacitidine combination agent ASTX030: An orally available fixed-dose combination agent containing cedazuridine, a cytidine deaminase (CDA) inhibitor, and the cytidine antimetabolite azacitidine, with potential antineoplastic activity. Upon oral administration of the cedazuridine/azacitidine combination agent ASTX030, cedazuridine binds to and inhibits CDA, an enzyme primarily found in the gastrointestinal (GI) tract and liver that catalyzes the deamination of cytidine and cytidine analogs. This prevents the breakdown of azacitidine, increases its bioavailability and efficacy while decreasing GI toxicity due to the administration of lower doses of azacitidine. Azacitidine exerts its antineoplastic activity through the incorporation of its triphosphate form into DNA, which inhibits DNA methyltransferase (DNMT), thereby blocking DNA methylation and results in hypomethylation of DNA. This interferes with DNA replication and decreases tumor cell growth.
cediranib: An orally bioavailable indole ether quinazoline derivative and vascular endothelial growth factor receptor (VEGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, cediranib binds to and inhibits the three VEGFR subtypes 1 (VEGFR-1), 2 (VEGFR-2) and 3 (VEGFR-3), thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth. Expression of VEGFRs may be upregulated in a variety of tumor cell types.
cediranib maleate: The maleate salt of an indole ether quinazoline derivative with antineoplastic activities. Competing with adenosine triphosphate, cediranib binds to and inhibits all three vascular endothelial growth factor receptor (VEGFR-1,-2,-3) tyrosine kinases, thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth.
Cefamandole: A second-generation cephalosporin antibiotic with bactericidal activity. Cefamandole is active against Haemophilus and gram-negative bacilli susceptible to other cephalosporins. It is also active against many strains resistant to other cephalosporins, such as Enterobacter species and indole-positive Proteus species.
cefazolin: A beta-lactam antibiotic and first-generation cephalosporin with bactericidal activity. Cefazolin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.
cefazolin sodium: The sodium salt of cefazolin, a beta-lactam antibiotic and first-generation cephalosporin with bactericidal activity. Cefazolin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, which results in the weakening of the bacterial cell wall and cell lysis.
cefepime hydrochloride: The hydrochloride salt of a semi-synthetic, beta-lactamase-resistant, fourth-generation cephalosporin antibiotic derived from an Acremonium fungal species with broad-spectrum bactericidal activity. Administered parenterally, cefepime inhibits bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, resulting in a reduction of bacterial cell wall stability and cell lysis. This agent is more active against a variety of Gram-positive pathogens compared to third-generation cephalosporins.
cefixime: A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins.
Ceflatonin: (Other name for: omacetaxine mepesuccinate)
cefmetazole sodium: The sodium salt form of cefmetazole, a second-generation, semi-synthetic, beta-lactam cephalosporin antibiotic with antibacterial activity. Cefmetazole binds to penicillin-binding proteins (PBPs), transpeptidases that are responsible for crosslinking of peptidoglycan. By preventing crosslinking of peptidoglycan, cell wall integrity is lost and cell wall synthesis is halted.
cefotaxime: A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.
cefoxitin sodium: The sodium salt form of cefoxitin, a beta-lactam, second-generation cephalosporin antibiotic with bactericidal activity. Cefoxitin sodium binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.
cefpodoxime proxetil: A third generation semi-synthetic cephalosporin and a beta-lactam antibiotic with bactericidal activity. Cefpodoxime's effect is dependent on its binding to penicillin-binding proteins (PBPs) located in the bacterial cytoplasmic membrane. Binding results in the inhibition of the transpeptidase enzymes, thereby preventing cross-linking of the pentaglycine bridge with the fourth residue of the pentapeptide and interrupting consequent synthesis of peptidoglycan chains. As a result, cefpodoxime inhibits bacterial septum and cell wall synthesis formation.
ceftaroline fosamil: An N-phosphono prodrug of the fifth-generation cephalosporin derivative ceftaroline with antibacterial activity. Ceftaroline fosamil is hydrolyzed to the active form ceftaroline in vivo. Ceftaroline binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.
ceftazidime sodium: The sodium salt of ceftazidime, a third-generation cephalosporin antibiotic with bactericidal activity. Ceftazidime binds to and inactivates penicillin-binding proteins (PBPs), enzymes located on the inner membrane of the bacterial cell wall, resulting in the weakening of the bacterial cell wall and cell lysis. Compared to the second and first generation cephalosporins, ceftazidime is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftazidine also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity.
ceftazidime/avibactam sodium: A combination preparation containing the third-generation cephalosporin ceftazidime and the sodium salt form of avibactam, a non-beta-lactam beta-lactamase inhibitor, with antibiotic and beta-lactamase inhibiting activity, respectively. Upon administration, ceftazidime binds to essential penicillin-binding proteins (PBPs) and inhibits cell wall synthesis in certain bacteria. Avibactam binds to and inactivates beta-lactamases, thereby protecting ceftazidime from degradation and increasing ceftazidime’s efficacy.
ceftobiprole medocaril: A water-soluble prodrug of ceftobiprole, a pyrrolidinone cephalosporin antibiotic, with bactericidal activity. Ceftobiprole binds to and inactivates penicillin-binding proteins (PBPs), enzymes involved in the terminal stages of bacterial cell wall assembly and cell wall reshaping during bacterial growth and division. This agent exhibits a broad spectrum of activity against gram-negative and gram-positive pathogens including methicillin-resistant S. aureus (MRSA), vancomycin-intermediate S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA). Ceftobiprole is refractory to hydrolysis by class A and class C lactamases.
ceftolozane-tazobactam: A combination preparation containing ceftolozane, a semi-synthetic, broad-spectrum, fifth-generation cephalosporin and tazobactam, a beta-lactamase inhibitor, with activity against Gram-negative and Gram-positive bacteria. Upon intravenous administration, ceftolozane binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. This interferes with the final transpeptidation step required to form peptidoglycan chain cross-links, which are a key component of and provide strength and rigidity to the bacterial cell wall. This inhibits bacterial cell wall synthesis and reduces cell wall stability, which weakens the bacterial cell wall and causes bacterial cell lysis. Tazobactam irreversibly inhibits certain penicillinases and cephalosporinases and covalently binds to some chromosomal and plasmid-mediated bacterial beta-lactamases, thereby protecting ceftolozane from degradation and improving ceftolozane’s activity.
ceftriaxone sodium: The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).
Celebrex: (Other name for: celecoxib)
celecoxib: A nonsteroidal anti-inflammatory drug (NSAID) with a diaryl-substituted pyrazole structure. Celecoxib selectively inhibits cyclo-oxygenase-2 activity (COX-2); COX-2 inhibition may result in apoptosis and a reduction in tumor angiogenesis and metastasis.
Celestone: (Other name for: betamethasone)
Celexa: (Other name for: citalopram hydrobromide)
Celiptium: (Other name for: elliptinium acetate)
cell cycle checkpoint/DNA repair antagonist IC83: A proprietary agent with potential antineoplastic activity. IC83 appears to target cell cycle checkpoint/DNA repair enzymes, which are involved in the recognition and repair of damaged DNA and are overexpressed in many types of cancer cells. Inhibition of cell cycle checkpoint/DNA repair enzymes may enhance the cytotoxicity of DNA damaging agents and dissipate tumor cell resistance to chemotherapy and radiation therapy.
cell membrane-anchored/CSV-targeted IL-12-expressing T lymphocytes: A preparation of T lymphocytes engineered to express cell membrane-anchored and cell-surface vimentin (CSV)-targeted interleukin-12 (IL-12), with potential immunostimulatory and antineoplastic activities. Upon administration, the cell membrane-anchored/CSV-targeted IL-12-expressing T lymphocytes are directed to and induce selective toxicity in CSV-expressing tumor cells. The cell membrane-anchored IL-12 cytokine promotes the secretion of interferon-gamma (IFNg), activates natural killer cells (NKs), and induces cytotoxic T-lymphocyte (CTL) responses against tumor cells locally, which may result in immune-mediated tumor cell death and the inhibition of tumor cell proliferation. Vimentin, overexpressed in various tumors, is associated with tumor growth and metastasis. Cell membrane-anchored IL-12 reduces the circulating levels of the inflammatory cytokine and the associated systemic adverse effects.
Cellcept: (Other name for: mycophenolate mofetil)
cemadotin hydrochloride: The hydrochloride salt form of cemadotin, a synthetic dolastatin 15 analogue with potential antineoplastic activity. Cemadotin suppresses spindle microtubule dynamics by binding to tubulin, thereby blocking mitosis.
cemdisiran: A proprietary formulation composed of small-interfering RNAs (siRNAs) directed against terminal complement component 5 (C5) of the complement pathway conjugated to a N-acetylgalactosamine (GalNAc) ligand, which has potential use in the treatment of complement-mediated diseases, such as paroxysmal nocturnal hemoglobinuria (PNH). Upon subcutaneous administration of cemdisiran, the GalNAc ligand moiety specifically binds to and is taken up by the asialoglycoprotein receptor (ASGPR) expressed on hepatocytes. Inside the cell, the siRNAs bind to C5 mRNAs, which results in the inhibition of both the translation and expression of the C5 protein. This lowers plasma C5 levels, prevents C5 cleavage into pro-inflammatory components and blocks complement-mediated hemolysis. C5, a complement pathway protein, is expressed at high levels by the liver.
cemiplimab-rwlc: A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cemiplimab-rwlc binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.
cemsidomide: An orally bioavailable modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon oral administration, cemsidomide specifically binds to cereblon (CRBN), thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T lymphocytes. This also leads to downregulation of the activity of other proteins, some of which play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
cenersen: A phosphorothioate oligonucleotide harboring nucleotide sequences complementary to tumor suppressor p53 mRNA. Cenersen hybridizes with p53 mRNA molecules, and induces Rnase H dependent hydrolysis of p53 transcripts in the double stranded section of the hybrids, thereby resulting in loss of p53 production. Loss of p53 activity leads to sensitization of cancer cells to other therapeutics.
cenisertib: A water-soluble, synthetic small molecule with potential antineoplastic activity. Cenisertib selectively binds to and inhibits aurora kinases (AKs), a family of serine-threonine kinases which are important regulators of cell division and proliferation, and which are overexpressed in certain types of cancer. Inhibition of aurora kinases inhibits cell division and proliferation and induces apoptosis in tumor cells overexpressing AKs.
Cenolate: (Other name for: ascorbic acid)
CENP-E inhibitor GSK-923295A: A small-molecule inhibitor of the mitotic kinesin centromere-associated protein E (CENP-E), with potential antineoplastic activity. Upon administration, GSK-923295A binds to and inhibits CENP-E, thereby preventing cell division, inducing cell cycle arrest, and ultimately leading to an inhibition of cell proliferation. CENP-E, a kinetochore-associated mitotic kinesin, plays an essential role in chromosome movement during mitosis and regulates cell-cycle transition from metaphase to anaphase.
Centella asiatica/melon extract/vitamins supplement: A nutritional supplement composed of Centella asiatica extract, melon extract rich in the antioxidant enzyme superoxide dismutase (SOD), vitamin D3 and the B vitamins B1 (thiamine), B2 (riboflavin) and B6 (pyridoxine), that can potentially be used to reduce edema, paresthesia and pain. Upon oral administration of the centella asiatica/melon extract/vitamins supplement, the Centella asiatica may reduce inflammation, pain and swelling. In addition, Centella asiatica promotes the normal function of the microcirculation, memory and cognitive functions. SOD scavenges superoxide radicals and may protect against oxidative stress-induced damage and exerts anti-inflammatory effects. The B vitamins contribute to the maintenance of the nervous system. Vitamin D3 contributes to the maintenance of muscle and bone health.
Centipeda minima decoction: A traditional Chinese medicine (TCM) formulation containing multiple flavones and their glycosides, phenolic and polyphenolic acids, and sesquiterpene lactones, with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration of Centipeda minima decoction, the active ingredients may modulate the cell cycle, induce apoptosis and inhibit tumor cell proliferation. It may also modulate the immune system by reducing the production of pro-inflammatory cytokines and inhibiting Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling.
cenvacibart: An immunoglobulin G4 (igG4), human anti-factor XI (FXI) antibody, with potential anti-thrombotic activity. Upon administration, cenvacibart targets and binds to the catalytic domain of FXI, thereby preventing the activation of FXI (FXIa). The abrogation of FXI activation prolongs the activated partial thromboplastin time (aPTT) and reduces platelet and fibrin accumulation. This results in the inhibition of contact activation-initiated blood coagulation and prevents thrombus formation. FXI contributes to thrombotic disease while playing a limited role in normal hemostasis. Activation of FXI is essential for thrombus growth and stabilization.
cenzestotug: An agonistic recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody that recognizes the co-stimulatory receptor OX40 (CD134; tumor necrosis factor receptor superfamily member 4; TNFRSF4), with potential immunostimulatory activity. Upon administration, cenzestotug selectively targets, binds to and activates OX40. This may induce the proliferation of memory and effector T lymphocytes and inhibit the function of T-regulatory cells (Tregs) in the tumor microenvironment (TME). This enhances anti-tumor immune responses and prevents Tregs-mediated immune suppression. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and plays an essential role in T-cell activation and differentiation.
Cepacol: (Other name for: dyclonine hydrochloride)
Cephalexin: A beta-lactam, first-generation cephalosporin antibiotic with bactericidal activity. Cephalexin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linking of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to second and third generation cephalosporins, cephalexin is more active against gram-positive and less active against gram-negative organisms.
Cephalothin Sodium: The sodium salt form of cephalothin, a semisynthetic, beta-lactam, first-generation cephalosporin antibiotic with bactericidal activity. Cephalothin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.
Ceplene: (Other name for: histamine dihydrochloride)
ceralasertib: An orally available morpholino-pyrimidine-based inhibitor of ataxia telangiectasia and rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, Ceralasertib selectively inhibits ATR activity by blocking the downstream phosphorylation of the serine/threonine protein kinase CHK1. This prevents ATR-mediated signaling, and results in the inhibition of DNA damage checkpoint activation, disruption of DNA damage repair, and the induction of tumor cell apoptosis. In addition, AZD6738 sensitizes tumor cells to chemo- and radiotherapy. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival; it is activated by DNA damage caused during DNA replication-associated stress.
ceramide: One of a number of a class of sphingolipids, N-acyl derivatives with long chains. Ceramide is the core molecule for the synthesis of sphingomyelin, an essential lipid for myelination and neurotransmission; it may function as a second messenger to stimulate differentiation, inhibit proliferation, and induce apoptosis.
ceramide nanoliposome: A lipid-based nanoparticle formulation composed of the apoptosis-inducing sphingolipid ceramide encapsulated within nanoliposomes, with potential apoptotic and antineoplastic activities. Upon administration, ceramide nanoliposomes accumulate in the tumor environment, due to the unique properties of the tumor vasculature, and easily enter tumor cells. This delivers ceramide inside the tumor cells, where ceramide induces apoptosis. Although the process is not completely understood, ceramide-dependent apoptosis most likely results from the downregulation of nutrient transporter proteins, which prevents cellular access to extracellular nutrients and causes tumor cell starvation. This selectively destroys tumor cells. Ceramide alone is insoluble and has a very short half-life; therefore, the nanoliposome formulation increases its solubility and half-life. Ceramide plays a key role in the regulation of autophagy, apoptosis, survival and proliferation. Serving as a tumor suppressor lipid, the expression of ceramide is inversely correlated with tumor cell growth, survival and metastasis.
ceramide/CLA/cholesterol controlled-release skin barrier emulsion: A lipid-rich emulsion containing ceramide, conjugated linoleic acid (CLA) and cholesterol in an emollient base, with skin protective and healing activities. Upon topical application of the ceramide/CLA/cholesterol controlled-release skin barrier emulsion, the physiological lipids are delivered via a time-release system, and form a skin barrier. This maintains a moist wound and skin environment and enhances healing.
Cerazette: (Other name for: desogestral)
Cerdulatinib: An orally bioavailable dual inhibitor of spleen tyrosine kinase (Syk) and Janus-associated kinases (JAK), with potential anti-inflammatory and antineoplastic activity. Upon oral administration, cerdulatinib specifically binds to and inhibits the activity of Syk, JAK1, and JAK3 with preferential inhibition of JAK1 and JAK3-dependent cytokine-mediated signaling and functional responses. This negatively affects the downstream JAK-STAT (signal transducer and activator of transcription) pathway, and leads to both reduced inflammation in various animal models and enhanced antiproliferative activity towards non-Hodgkin's lymphoma (NHL) cell lines. Syk is a non-receptor cytoplasmic tyrosine kinase involved in signal transduction in cells of hematopoietic origin including B cells, macrophages, basophils and neutrophils. Abnormal function of Syk has been implicated in several hematopoietic malignancies including NHL and chronic lymphocytic leukemia (CLL). The JAK-STAT pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.
cereblon modulator BTX-1188: An orally bioavailable small molecule modulator of cereblon (CRBN), part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CRBN modulator BTX-1188 specifically targets and binds to CRBN, thereby affecting the ubiquitin E3 ligase activity. This leads to ubiquitination and induces proteasome-mediated degradation of the hematopoietic transcription factors Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T cells, and the degradation of the protein neosubstrate G1 to S phase transition 1 (GSPT1), a translation termination factor. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which, may include the activation of T lymphocytes. In addition, the degradation of the proteins IKZF1/3 and GSPT1 may lead to the downregulation of other proteins that play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays an important role in the ubiquitination of certain proteins.
cereblon modulator SP-3164: An orally bioavailable avadomide derivative, which contains the stable, active (S)-enantiomer form of avadomide, and modulator of cereblon (CRBN), which is part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CRBN modulator specifically targets and binds to CRBN, thereby affecting the ubiquitin E3 ligase activity. This leads to ubiquitination and induces proteasome-mediated degradation of the hematopoietic transcription factors Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T lymphocytes. In addition, the degradation of IKZF1 and IKZF3 may lead to the downregulation of other proteins that play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays an important role in the ubiquitination of certain proteins. SP3164 uses deuterium to stabilize the (S)-enantiomer of avadomide and prevent interconversion to the undesired (R)-enantiomer, which increases the binding affinity to CRBN.
cereblon modulator TQB3820: An orally bioavailable modulator of cereblon (CRBN), part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CRBN modulator TQB3820 specifically binds to CRBN, thereby affecting the ubiquitin E3 ligase activity. This leads to ubiquitination and induces proteasome-mediated degradation of the hematopoietic transcription factors Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T lymphocytes. In addition, the degradation of IKZF1 and IKZF3 may lead to the downregulation of other proteins, including interferon regulatory factor 4 (IRF4) and c-Myc, which play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays an important role in the ubiquitination of certain proteins.
Cerebyx: (Other name for: fosphenytoin sodium)
Cereport: (Other name for: lobradimil)
Cerespan: (Other name for: papaverine hydrochloride)
cergutuzumab amunaleukin: A recombinant fusion protein comprised of cergutuzumab, a genetically engineered human immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against carcinoembryonic antigen (CEA, CEACAM5, CD66e), linked to amunaleukin, an engineered, mutated variant form of interleukin-2 (IL-2v), with potential immunostimulating and antineoplastic activities. Upon administration of cergutuzumab amunaleukin, the cergutuzumab moiety recognizes and binds to CEA, thereby specifically targeting IL-2v to CEA-expressing tumor tissue. Subsequently, the IL-2v moiety stimulates a local immune response, which activates both natural killer (NK) cells and cytotoxic T cells, and eventually leads to tumor cell killing. CEA is a cell surface protein that is expressed on a wide variety of cancer cells. The mutations found in IL-2v inhibit its binding to IL-2 receptor-alpha (CD25, IL2Ra), which prevents the activation of regulatory T cells (Tregs); however, IL-2v is able to bind to and induce signaling through IL-2Rbetagamma, which allows the preferential expansion of NK cells and CD8-positive T cells. The Fc domain of cergutuzumab is modified to prevent Fc-gamma binding and downstream effector functions.
ceritinib: An orally available inhibitor of the receptor tyrosine kinase activity of anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, ceritinib binds to and inhibits wild-type ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to both the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types.
certolizumab: A Fab fragment of a recombinant, humanized monoclonal antibody directed against the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), with anti-inflammatory activity. Upon administration, certolizumab binds to TNF-alpha, preventing the interaction of this cytokine with endogenous cell surface receptors, thereby rendering TNF-alpha inactive and inhibiting TNF-mediated inflammatory responses. TNF-alpha is a protein involved in inflammation, cell survival, and apoptosis.
certolizumab pegol: A Fab fragment of a recombinant, humanized monoclonal antibody directed against the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and conjugated to polyethylene glycol (PEG), with anti-inflammatory activity. Upon administration, certolizumab binds to TNF-alpha and prevents the interaction of this cytokine with endogenous cell surface receptors, thereby rendering TNF-alpha inactive and inhibiting TNF-mediated inflammatory responses. TNF-alpha is a protein involved in inflammation, cell survival, and apoptosis. Pegylation of certolizumab allows for an improved pharmacokinetic profile.
Cervarix: (Other name for: recombinant human papillomavirus bivalent vaccine)
Cervene: (Other name for: TGFa-PE38 immunotoxin)
Cervidil: (Other name for: dinoprostone)
cesium Cs 137: A radioactive isotope of cesium with an atomic mass of 139 and potential application in radiotherapy. Cesium Cs 137 is prevalent due to its spontaneous production, which occurs as a result of nuclear fission of other radioactive materials, such as uranium and plutonium. This radionuclide has a relatively long half-life, 30 years, and decays by emitting beta particles. Both Cs 137 and its metastable nuclear isomer, barium-137m, emit gamma radiation of moderate energy and so are used in sterilization procedures in the food industry or in hospital environments.
cesium Cs-131: An unstable radioisotope of cesium (Cs) with radiocytotoxic application. Cs-131 is a gamma photon-emitting radionuclide with high energy and a relatively short half-life of 9.7 days. When used in prostate brachytherapy, Cs-131 demonstrated advantages over other commonly used isotopes.
cEt KRAS antisense oligonucleotide AZD4785: A proprietary formulation composed of a high affinity antisense oligonucleotide (ASO) that contains 2'-4' constrained ethyl residues (cEt) and targets KRAS (K-RAS) transcripts, with potential antineoplastic activity. Upon intravenous administration, cEt KRAS antisense oligonucleotide AZD4785 targets and binds, with high affinity, to a unique genetic sequence within KRAS messenger RNA (mRNA), thereby inhibiting translation of KRAS protein, including forms containing activating mutations. Inhibition of KRAS protein synthesis prevents KRAS-dependent signaling and inhibits the proliferation of KRAS-driven tumor cells. KRAS, a tumor-associated antigen (TAA), is mutated in a variety of tumor cell types. It plays a key role in tumor cell proliferation and survival and is associated with tumor initiation, metastasis and poor prognosis.
Cetacort: (Other name for: therapeutic hydrocortisone)
Cetane: (Other name for: ascorbic acid)
cetrelimab: A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 protein (PD-1, PCDC-1), with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cetrelimab binds to PD-1, and inhibits the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.
cetrorelix: Cetrorelix is a synthetic decapeptide which is structurally related to gonadotrophin-releasing hormone (luteinising-hormone releasing hormone). It acts as an LHRH antagonist. (from ASTA Medica)
cetuximab: A recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR) with antineoplastic activity. Cetuximab binds to the extracellular domain of the EGFR, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition in signal transduction and anti-proliferative effects. This agent may inhibit EGFR-dependent primary tumor growth and metastasis. EGFR is overexpressed on the cell surfaces of various solid tumors.
cetuximab sarotalocan sodium: The sodium salt form of cetuximab sarotalocan, which consists of a chemical conjugate composed of the dye IR700 linked to cetuximab, a monoclonal antibody directed against the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon injection of cetuximab sarotalocan sodium, the cetuximab moiety targets and binds to EGFR-expressing tumor cells, resulting in the internalization of the conjugate. Upon localized application of near-infrared (NIR) light, the IR700 dye becomes activated, disrupts the cell membrane and selectively kills the EGFR-expressing tumor cells. EGFR, a tyrosine kinase receptor, is overexpressed in a variety of cancers.
cetuximab-IRDye 800: An immunoconjugate comprised of the recombinant chimeric monoclonal antibody cetuximab conjugated to the N-hydroxysuccinamide (NHS) ester form of the near-infrared (NIR) fluorescent dye IRDye 800CW (cetuximab-IRDye 800) with potential imaging use. The antibody moiety of cetuximab-IRDye 800 binds to the extracellular domain of the epidermal growth factor receptor (EGFR). Upon binding, IRDye 800 may be detected using NIR imaging, which facilitates the visualization and quantification of EGFR-expressing tumor cells. EGFR is a receptor tyrosine kinase that may be overexpressed on the cell surfaces of various tumor types.
cetuximab-loaded ethylcellulose polymeric nanoparticles decorated with octreotide: A preparation of ethylcellulose polymeric nanoparticles loaded with cetuximab, a recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR), and decorated with the somatostatin analog, octreotide, with potential antineoplastic activity. Upon oral administration, the octreotide moiety directs the nanoparticles, which remain inert until a pH of 6.8 is reached, to somatostatin receptors (SSTRs), which are present on the cell membranes of many neuroendocrine tumor (NET) cells. At this pH, cetuximab is selectively released from the ethylcellulose polymer. Cetuximab may then bind to the extracellular domain of EGFR-expressing tumor cells, thereby preventing the activation and subsequent dimerization of the receptor. This may inhibit signal transduction and inhibit tumor cell proliferation in EGFR-dependent tumor cells. EGFR, a member of the EGFR receptor tyrosine kinase family, may be overexpressed on the cell surfaces of various tumor types.
CEV regimen: A regimen containing carboplatin, etoposide, and vincristine which may be used in the treatment of pediatric retinoblastoma (RB).
Cevalin: (Other name for: ascorbic acid)
cevidoplenib dimesylate: The dimesylate salt of cevidoplenib, an orally available inhibitor of spleen tyrosine kinase (SYK), with potential anti-inflammatory and immunomodulating activities. Upon oral administration, cevidoplenib binds to and inhibits the activity of SYK, blocking Fc receptor and B-cell receptor (BCR)-mediated signaling in inflammatory cells, including macrophages, neutrophils, mast cells, natural killer (NK) cells and B cells. This leads to the inhibition of the activation of these inflammatory cells, and the related inflammatory responses and tissue damage. SYK, a non-receptor cytoplasmic protein tyrosine kinase widely expressed in hematopoietic cells, plays a key role in Fc receptor and B-cell receptor signaling in inflammatory cells. It is involved in coupling activated immunoreceptors, such as Fc receptors and B-cell receptors, to signal downstream events that mediate diverse cellular responses, including proliferation, differentiation, and phagocytosis, which are important for allergic and antibody-mediated immune diseases such as immune thrombocytopenia (ITP).
cevimeline hydrochloride: A cholinergic analogue with glandular secretion stimulatory activity. Cevimeline binds to and activates muscarinic receptors, thereby increasing the secretions in exocrine salivary and sweat glands. This cholinergic agonist also increases the tone of smooth muscle in the gastrointestinal and urinary tracts. Cevimeline is being studied as a treatment for dry mouth caused by radiation therapy to the head and neck.
cevostamab: A proprietary recombinant bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) Fc receptor-like protein 5 (FCRH5; CD307; FCRL5; IRTA2; BXMAS1) and one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of cevostamab, the bispecific antibody binds to both the CD3 antigen on cytotoxic T lymphocytes (CTLs) and FCRH5 found on FCRH5-expressing tumor cells. This activates and crosslinks CTLs with FCRH5-expressing tumor cells, which results in the CTL-mediated cell death of FCRH5-expressing tumor cells. FCRH5, an immune receptor translocation-associated protein/Fc receptor homolog (IRTA/FCRH) family member and a B-cell lineage marker, is overexpressed on myeloma cells.
cFMS tyrosine kinase inhibitor ARRY-382: A small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; cFMS) with potential antineoplastic activity. cFMS tyrosine kinase inhibitor ARRY-382 binds to and inhibits the activity of cFMS. By preventing colony-stimulating factor-1 (CSF-1)-cFMS signaling, this agent may inhibit tumor cell proliferation in cFMS-overexpressing tumor cells. cFMS, a tyrosine kinase receptor, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation and regulation of cell proliferation.
CGP-6809: A water-soluble nitrosourea that cross-links with DNA, causing inhibition of DNA synthesis.
ChAdOx1-PSA/PAP/STEAP1/5T4 prostate cancer vaccine ChAdOx1-PCAQ: A cancer vaccine consisting of recombinant non-replicating chimpanzee adenovirus Oxford 1 (ChAdOx1) viral vector encoding genes for the prostate cancer-associated antigens prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), six-transmembrane epithelial antigen of the prostate 1 (STEAP1), and 5T4 oncofetal antigen, with potential immunostimulatory and antineoplastic activities. Upon administration, ChAdOx1-PSA/PAP/STEAP1/5T4 prostate cancer vaccine ChAdOx1-PCAQ expresses PSA, PAP, STEAP1 and 5T4 peptides, which may elicit humoral and cellular immune responses against prostate cancer cells expressing these antigens.
chamomile: The flower-heads of either the plant Anthemis nobilis or the plant Matricaria chamomilla. Chamomile has a warm aromatic odour and a very bitter taste and contains volatile oils which are a mixture of butyl and amyl angelates and valerates. Due to its coumarin constituents, large doses may interfere with coagulation.
Chantix: (Other name for: varenicline)
checkpoint kinase inhibitor AZD7762: A synthetic small molecule inhibitor of checkpoint kinases (Chks) with potential chemosensitizing activity. AZD7762 binds to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis. This agent may enhance the cytotoxicity of DNA-damaging agents. Chks are protein kinases that regulate either G1/S or G2/M transitions in the cell cycle. In the presence of DNA damage or incomplete DNA replication, Chks become activated and initiate cell cycle arrest to allow DNA repair or the completion of DNA replication.
checkpoint kinase inhibitor XL844: A synthetic small-molecule inhibitor of checkpoint kinases 1 and 2 (Chk1 and Chk2) with potential antineoplastic activity. XL844 binds to and inhibits Chks 1 and 2, resulting in inhibition of cell cycle arrest, progressive DNA damage, inhibition of DNA repair, and, ultimately, tumor cell apoptosis. This agent also inhibits vascular endothelial growth factor receptor 1 (VEGFR1) and vascular endothelial growth factor receptor 3 (VEGFR3), important mediators of tumor angiogenesis and lymphogenesis, respectively. In the presence of extensive damage or absence of timely repair, these checkpoint-signaling pathways may also trigger a pathway that effects apoptosis. Normal functions of Chks involve the initiation of cell-cycle arrest and the up-regulation of transcription genes involved with DNA excision repair and dNTP synthesis.
Chemet: (Other name for: succimer)
chemokine modulation therapy: Therapy used to modulate the activity of chemokine receptors or their ligands, potentially modifying immune response and tumor-related processes, including tumor cell growth, angiogenesis, and metastasis.
Chemophase: (Other name for: recombinant human hyaluronidase)
Chemoplaque: (Other name for: topotecan sustained-release episcleral plaque)
cherry juice: A juice extracted from bitter and sour cherries.
chewing gum: A semi-solid composed of synthetic, polymerized polysaccharide and flavorings, intended to be chewed to release active and/or inert ingredient(s).
chimeric costimulatory converting receptor-modified NK-92 cells: A preparation of genetically-modified natural killer (NK) cells derived from the allogeneic NK-92 cell line that are transduced with an as of yet unspecified chimeric costimulatory converting receptor (CCCR) for cancer retargeting purposes, with potential cytolytic, immunomodulating and antineoplastic activities. Upon infusion of the CCCR-modified NK-92 cells, the redirected NK cells recognize and bind to tumor cells. This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, which results in selective tumor cell lysis. The NK-92 cells are derived from a human cytotoxic cell line composed of allogeneic, activated, interleukin-2-(IL-2) dependent-NK cells from a 50-year old male patient with rapidly progressive non-Hodgkin lymphoma. As NK-92 cells are devoid of killer inhibitory receptors (KIRs; also called killer cell immunoglobulin-like receptors), which are negative regulators of NK cell activity, cancer cells are unable to suppress the cancer cell killing ability of the NK-92 cells.
chimeric humanized anti-CD47 antibody: A humanized, high-chimeric antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, chimeric humanized anti-CD47 antibody selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.
Chinese herbal formulation LC09: A traditional Chinese medicine (TCM) decoction containing Herba Epimedii that can be used for chemotherapy-induced hand-foot syndrome (HFS; Palmar-Plantar Erythrodysesthesia; PPE). Soaking of the affected hands and feet with TCM Formula LC09 may reduce the severity of HFS and may decrease HFS-associated pain.
Chinese herbal formulation PHY906: An oral traditional Chinese herbal formulation in powder form containing a spray-dried preparation of an aqueous extract from the four herbs Scutellaria baicalensis, Glycyrrhiza uralensis, Ziziphus jujuba and Paeonia lactiflora, with potential immunomodulating and chemoprotective activities, and which may be used as an adjuvant for chemotherapeutic agents. Although the mechanisms of action remain to be fully elucidated, PHY906 possesses a wide range of pharmacological activities such as the enhancement of oral uptake of pharmacologically active agents, inhibition of CYP3A4, modulation of certain pro-inflammatory cytokines, enhanced migration of macrophages and lymphocytes, and the inhibition of expression of matrix metalloproteinase (MMP), nuclear factor kappaB (NF-kB), cyclooxygenase (COX), nitric oxide synthase (NOS), beta-glucuronidase, the neurokinin 1 receptor (NK1R; tachykinin receptor 1; TACR1; substance-P receptor) and the delta-opioid receptor. PHY906 may also enhance the anti-tumor effect of other anti-cancer agents, and may protect the gastrointestinal (GI) mucosa against damage and reduce GI symptoms.
Chinese herbal medicine YQ1: A Chinese herbal medicine, with potential immunostimulating and antineoplastic activities. Although the mechanism of action is currently unknown, upon administration, YQ1 may cause an induction of apoptosis and an inhibition of tumor cell proliferation. YQ1 might target cancer stem cells (CSCs).
Chinese herbs: Herbs used in Chinese Herbal Therapy for toxicity attenuation. (NCI)
ChiNing decoction: A decoction of Liang Ge San, a traditional Chinese herbal medicine, with potential anti-inflammatory and anti-stomatitis activities. Although the complete mechanism of action through which the ChiNing decoction works has yet to be fully elucidated, upon oral administration, the active ingredients may inhibit the inflammatory response, possibly by reducing the levels of pro-inflammatory cytokines, such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNFa), in the saliva. This may protect the oral mucosa against these inflammatory mediators, and may reduce and relieve radiation-induced stomatitis and the associated pain.
ChiRhoStim: (Other name for: synthetic human secretin)
Chirocaine: (Other name for: levobupivacaine hydrochloride)
chitin oligosaccharides supplement T-ChOS: A proprietary, nutritional supplement comprised of chitooligosaccharides extracted from deproteinized and demineralized crustacean shells. Upon administration, chitin oligosaccharides supplement T-ChOS may increase stamina and boost energy. In addition, the chitooligosaccharides may stimulate chondrocyte growth.
Chk1 inhibitor BBI-355: An orally bioavailable small molecule inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor BBI-355 selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. BBI-355 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents by targeting extrachromosomal DNA (ecDNA) originating from oncogene amplified cancer cells. Cancer cells that rely on oncogene amplification to grow and survive are highly sensitive to chk1 inhibition. Chk1, an ATP-dependent serine/threonine kinase, mediates cell cycle checkpoint control, is essential for DNA repair, and plays a key role in resistance to chemotherapeutic agents.
Chk1 inhibitor GDC-0425: An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor GDC-0425 selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. GDC-0425 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an ATP-dependent serine/threonine kinase, mediates cell cycle checkpoint control, is essential for DNA repair, and plays a key role in resistance to chemotherapeutic agents.
Chk1 inhibitor GDC-0575: A small molecule inhibitor of cell cycle checkpoint kinase 1 (Chk1), with potential chemosensitization activity. Chk1 inhibitor GDC-0575 specifically binds to and inhibits Chk1; this may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases, which permits the cells to undergo DNA repair prior to entry into mitosis. Therefore, Chk1 inhibition may sensitize tumor cells to the DNA-damaging effects of certain chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that phosphorylates cdc25 phosphatases in response to DNA damage. This results in both inhibitory tyrosine phosphorylation of cyclin-dependent kinase (CDK)-cyclin complexes and cell cycle arrest, which facilitates DNA damage repair.
Chk1 inhibitor LY2880070: An orally bioavailable, selective, adenosine triphosphate (ATP)-competitive inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor LY2880070 selectively binds to chk1, thereby preventing chk1 activity and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. LY2880070 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an ATP-dependent serine/threonine kinase overexpressed in a variety of cancer cell types, mediates cell cycle checkpoint control and is essential for DNA repair; it plays a key role in resistance to chemotherapeutic agents by repairing DNA damage.
CHK1 inhibitor MK-8776: An agent targeting cell cycle checkpoint kinase 1 (Chk1) with potential radiosensitization and chemosensitization activities. Chk1 inhibitor MK-8776 specifically binds to and inhibits Chk1, which may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases to undergo DNA repair prior to entry into mitosis; tumor cells may thus be sensitized to the DNA-damaging effects of ionizing radiation and alkylating chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that in response to DNA damage phosphorylates cdc25 phosphatases, resulting in inhibitory tyrosine phosphorylation of CDK-cyclin complexes and cell cycle arrest.
Chk1 inhibitor PEP07: An orally bioavailable inhibitor of checkpoint kinase 1 (Chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, Chk1 inhibitor PEP07 selectively binds to Chk1, thereby preventing Chk1 activity and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. PEP07 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an adenosine triphosphate (ATP)-dependent serine/threonine kinase overexpressed in a variety of cancer cell types, mediates cell cycle checkpoint control and is essential for DNA repair; it plays a key role in resistance to chemotherapeutic agents by repairing DNA damage.
CHK1 inhibitor PF-477736: A proprietary compound targeting cell cycle checkpoint kinase 1 (chk1) with potential chemopotentiation activity. Chk1 inhibitor PF-477736 inhibits chk1, an ATP-dependent serine-threonine kinase that is a key component in the DNA replication-monitoring S/G2 checkpoint system. By overriding the last checkpoint defense against DNA damaging agent-induced lethal damage, chk1 inhibitor PF-477736 may potentiate the antitumor efficacy of various chemotherapeutic agents against tumor cells with intrinsic checkpoint defects.
Chk1 inhibitor SRA737: An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor SRA737 selectively binds to chk1, thereby preventing chk1 activity and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. SRA737 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an adenosine triphosphate (ATP)-dependent serine/threonine kinase overexpressed in a variety of cancer cell types, mediates cell cycle checkpoint control and is essential for DNA repair; it plays a key role in resistance to chemotherapeutic agents by repairing DNA damage.
chlorambucil: An orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.
chlorambucil/prednisone regimen: A regimen consisting of chlorambucil and prednisone used for the treatment of chronic lymphocytic leukemia.
Chloraprep: (Other name for: chlorhexidine/ethyl alcohol mouthwash)
chlorhexidine: A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.
chlorhexidine gluconate: The gluconate salt form of chlorhexidine, a biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine gluconate is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine gluconate penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.
chlorhexidine gluconate skin cleanser: A skin cleanser containing chlorhexidine gluconate. Chlorhexidine gluconate is a biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine gluconate is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine gluconate penetrates the cell and causes leakage of intracellular components leading to cell death.
chlorhexidine/ethyl alcohol mouthwash: A mouthwash containing the biguanide chlorhexidine and ethyl alcohol, with topical antibacterial activity. Upon rinsing the oral cavity with the chlorhexidine/ethyl alcohol mouthwash, the positively charged chlorhexidine cation exerts its antibacterial activity through binding to the negatively charged microbial cell surface, which destroys the integrity of the cell membrane. This causes leakage of intracellular components leading to cell death. Ethyl alcohol denatures bacterial proteins, and dissolves and disrupts the bacterial lipid membrane, thereby killing the bacteria. This reduces oral colonization with harmful bacteria and may prevent oral mucositis.
chlorine dioxide sterilization: A sterilization process that uses chlorine dioxide at ambient temperatures to kill microorganisms. This process can be used in large spaces.
chlorogenic acid: A polyphenol and the ester of caffeic acid and quinic acid that is found in coffee and black tea, with potential antioxidant and chemopreventive activities. Chlorogenic acid scavenges free radicals, which inhibits DNA damage and may protect against the induction of carcinogenesis. In addition, this agent may upregulate the expression of genes involved in the activation of the immune system and enhances activation and proliferation of cytotoxic T-lymphocytes, macrophages, and natural killer cells. Chlorogenic acid also inhibits the activity of matrix metalloproteinases.
chloroquine: A 4-aminoquinoline with antimalarial, anti-inflammatory, and potential chemosensitization and radiosensitization activities. Although the mechanism is not well understood, chloroquine is shown to inhibit the parasitic enzyme heme polymerase that converts the toxic heme into non-toxic hemazoin, thereby resulting in the accumulation of toxic heme within the parasite. This agent may also interfere with the biosynthesis of nucleic acids. Chloroquine's potential chemosensitizing and radiosensitizing activities in cancer may be related to its inhibition of autophagy, a cellular mechanism involving lysosomal degradation that minimizes the production of reactive oxygen species (ROS) related to tumor reoxygenation and tumor exposure to chemotherapeutic agents and radiation.
chloroquinoxaline sulfonamide: A chlorinated heterocyclic sulfanilamide with potential antineoplastic activity and potential immunosuppressive activity. Chloroquinoxaline sulfonamide poisons topoisomerase II alpha and topoisomerase II beta, thereby causing double-stranded breaks in DNA, accumulation of unrepaired DNA, and apoptosis. This agent also exhibits lymphotoxicity by inhibiting lymphocyte activation in a cell cycle-specific manner.
chlorotoxin (EQ)-CD28-CD3zeta-CD19t-expressing CAR T lymphocytes: A preparation of genetically modified T lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) comprised of a CD28 co-stimulatory signaling domain fused to the zeta chain of the TCR/CD3 complex (CD3zeta), a truncated form of CD19 (CD19t), an immunoglobulin (Ig) G4-Fc (EQ) spacer, and a peptide derived from chlorotoxin (CLTX), with potential imaging and antineoplastic activities. Upon administration, chlorotoxin (EQ)-CD28-CD3zeta-CD19t-expressing CAR T lymphocytes are re-directed to specific tumor cells in the brain inducing selective toxicity in these tumor cells. CLTX, a 36-amino acid peptide found in the venom of the deathstalker scorpion (Leiurus quinquestriatus) and a chloride channel blocker, preferentially binds to glioma (and other neuroectodermal origin) cells via membrane bound forms of the endopeptidase matrix metalloproteinase-2 (MMP-2). This may direct the T lymphocytes to and induce selective toxicity in MMP-2-expressing tumor cells. Additionally, binding to MMP-2 on glioma cells may both interfere with transmembrane chloride exchange and inhibit proteolytic extracellular matrix remodeling by MMP-2, which may further limit the spread of these tumor cells. MMP-2 is specifically upregulated in gliomas and related cancers, but is not normally expressed in brain. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling; its inclusion may increase proliferation of T cells and antitumor activity compared to the inclusion of the CD3 zeta chain alone. IgG4-Fc (EQ) contains two point mutations in its spacer region which prevents recognition of the CAR by Fc receptors (FcRs) without altering the ability of the CAR to mediate antigen-specific lysis. CD19t, which lacks the cytoplasmic signaling tail, provides a non-immunogenic surface marker that allows for accurate measurement, efficient cell tracking and/or imaging of the therapeutic T-cells in vivo following adoptive transfer. Additionally, co-expression of CD19t functions as a "suicide" switch via clinically available antibodies or immunotoxins which can be used to selectively eliminate the genetically modified cells.
Chlorozotocin: A glucose-linked chloroethylnitrosourea with potential antineoplastic activity. Chlorozotocin alkylates DNA and proteins, induces the formation of interstrand DNA and DNA-protein crosslinks, and causes DNA strand breakage, thereby damaging DNA and resulting in cell death. This agent has been shown to exhibit antitumor and immunomodulatory effects in cell lines and animal models. Chlorozotocin is a mutagen and is less myelotoxic than other nitrosoureas.
chlorphenesin carbamate: The carbamate ester form of chlorphenesin, a preservative agent and centrally-acting muscle relaxant with some anti-bacterial and anti-fungal, muscle relaxing and potential antineoplastic activities. Although the exact mechanism of action (MoA) has yet to be fully elucidated, chlorphenesin may inhibit tumor cell proliferation and metastasis.
chlorpromazine: A phenothiazine and traditional antipsychotic agent with anti-emetic activity. Chlorpromazine exerts its antipsychotic effect by blocking postsynaptic dopamine receptors in cortical and limbic areas of the brain, thereby preventing the excess of dopamine in the brain. This leads to a reduction in psychotic symptoms, such as hallucinations and delusions. Chlorpromazine appears to exert its anti-emetic activity by blocking the dopamine receptors in the chemical trigger zone (CTZ) in the brain, thereby relieving nausea and vomiting.
chlorpromazine: A phenothiazine and traditional antipsychotic agent with anti-emetic activity. Chlorpromazine exerts its antipsychotic effect by blocking postsynaptic dopamine receptors in cortical and limbic areas of the brain, thereby preventing the excess of dopamine in the brain. This leads to a reduction in psychotic symptoms, such as hallucinations and delusions. Chlorpromazine appears to exert its anti-emetic activity by blocking the dopamine receptors in the chemical trigger zone (CTZ) in the brain, thereby relieving nausea and vomiting.
chlorpropamide: A long-acting, first-generation sulfonylurea with hypoglycemic activity. Compared to other sulfonylureas, chlorpropamide has an increased risk of prolonged hypoglycemia because of its long half-life.
chlorzoxazone: A benzoxazolone derivative with mild sedative and centrally-acting muscle relaxant activities. Although its exact mechanism of action is unknown, chlorzoxazone (CZ) appears to act at the spinal cord and subcortical levels of the brain to inhibit multisynaptic reflex arcs involved in producing and maintaining muscle spasms. This agent is extensively hydroxylated by cytochrome P450 2E1 (CYP2E1) to 6-hydroxychlorzoxazone (HCZ),11,12 which is subsequently glucuronidated and eliminated renally. Highly selective for CYP2E1, CZ may be used as a selective probe for phenotyping CYP2E1 in humans; the ratio of HCZ-to-CZ plasma concentrations obtained 2 to 4 hours after oral administration of CZ may be used as a phenotypic measure of CYP2E1 enzymatic activity.
chocolate-based dietary supplement: A dietary supplement containing chocolate derived from the cacao bean, with potential vasodilating, anti-inflammatory, antioxidant, cardiovascular protective and neuroprotective activities. Chocolate contains flavonoids, including epicatechin, catechin, procyanidins and xanthines, such as theobromine, and trace minerals. Upon oral administration, the bioactive ingredients in the chocolate-based dietary supplement may inhibit angiotensin-converting enzyme (ACE) and increase the production of nitric oxide (NO) through the activation of endothelial nitric oxide synthase (eNOS). This may result in vasodilation, improve blood flow, and decrease blood pressure. The chocolate-based dietary supplement also may improve insulin sensitivity, enhance cognition, and decrease the production of pro-inflammatory molecules. In addition, chocolate-based dietary may exert antioxidant effects and scavenge reactive oxygen species (ROS), thereby protecting cells from oxidative stress and DNA damage.
cholecalciferol: A steroid hormone produced in the skin when exposed to ultraviolet light or obtained from dietary sources. The active form of cholecalciferol, 1,25-dihydroxycholecalciferol (calcitriol) plays an important role in maintaining blood calcium and phosphorus levels and mineralization of bone. The activated form of cholecalciferol binds to vitamin D receptors and modulates gene expression. This leads to an increase in serum calcium concentrations by increasing intestinal absorption of phosphorus and calcium, promoting distal renal tubular reabsorption of calcium and increasing osteoclastic resorption.
cholecalciferol/d-alpha tocopherol/L-selenomethionine/green tea extract/saw palmetto berry extract/daidzein/genistein/lycopene prostate health supplement: A dietary supplement consisting of a blend of 8 natural ingredients with potential antineoplastic and chemopreventive activities. This dietary supplement contains vitamin D3 (as cholecalciferol), vitamin E (as d-alpha tocopherol), selenium (as L-selenomethionine), epigallocatechin (green tea extract), saw palmetto (berry extract), lycopene, and the isoflavonoids daidzein and genistein. This combination preparation may decrease prostate cell growth and inhibit prostate carcinogenesis.
cholecalciferol/whey protein isolate/EPA/DHA-based nutritional supplement: A gluten-free, energy-rich, non-complete nutritional supplement drink composed of juice from the concentrates of apple pear, pomegranate, purple chokeberry and passion fruit, plus fish oil derived from salmon and cod, the minerals potassium, phosphorus and iodine, whey protein isolate derived from cow’s milk, tocopherols (vitamin E), and cholecalciferol (vitamin D3) with potential anti-cachexic activity. Upon oral intake of the cholecalciferol/whey protein isolate/EPA/DHA-based nutritional supplement, the protein components maintain digestive health throughout the gastrointestinal (GI) tract and reduce the risk of digestive complications. The essential omega-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from the fish oil are incorporated into cell membranes and affect the production of pro-inflammatory mediators, which elicits an anti-inflammatory effect. Cholecalciferol plays an important role in maintaining bone mineralization and regulating blood calcium and phosphorus levels. Tocopherols neutralize free radicals, thereby protecting tissues and organs from oxidative damage. In particular, alpha-tocopherol gets incorporated into biological membranes, maintains cell membrane integrity and protects the cell against damage. This nutritional supplement may prevent both malnutrition and weight loss.
CholestaGel: (Other name for: colesevelam hydrochloride)
cholestyramine: An anion exchange resin with hypolipidemic activity. Cholestyramine resin adsorbs and combines with bile acids in the intestine to form an insoluble complex, which is then excreted in the feces, resulting in an increased oxidation of cholesterol to bile acids, a decrease in low density lipoprotein in the plasma, and a decrease in serum cholesterol levels.
Choletec: (Other name for: technetium Tc 99m mebrofenin)
cholic acid-24-13C: A preparation of carbon C 13-labeled cholic acid with potential diagnostic applications. Upon intravenous administration, cholic acid-24-13C levels may be used to measure first pass hepatic extraction of cholate, which is influenced primarily by portal blood flow and portal-systemic shunt.
cholic-2,2,4,4-D4 acid: A deuterated form of cholic acid with potential diagnostic applications. Upon intravenous administration, cholic-2,2,4,4-D4 acid levels may be used to measure first pass hepatic extraction of cholate, which is influenced primarily by portal blood flow and portal-systemic shunt.
choline kinase alpha inhibitor TCD-717: A small-molecule inhibitor of choline kinase alpha (CHKA), with potential antineoplastic activity. TCD-717 targets and binds to CHKA, an enzyme that plays a key role in the synthesis of phosphatidylcholine, the major phospholipid in eukaryotic cell membranes. Blockade of this enzyme induces cells to activate a different route for phospholipid production which causes a toxic effect and eventually leads to cell destruction. CHKA, overexpressed in human cancer cells while only minimally expressed in normal cells, appears to play a significant role in cellular proliferation, evasion of apoptosis, increased cell motility and metastasis.
choline magnesium trisalicylate: A nonsteroidal anti-inflammatory drug (NSAID) belonging to the salicylate family. Choline magnesium trisalicylate inhibits inflammation-related prostaglandin synthesis. This agent's analgesic effect is mediated through peripheral and central pathways, resulting in a decrease in pain perception; its antipyretic effect is mediated via the hypothalamic heat regulation center.
choline salicylate: The choline salt of salicylic acid, a nonsteroidal anti-inflammatory drug (NSAID), with analgesic, antipyretic, anti-inflammatory, anti-rheumatic and immunomodulating activities. Upon oral administration, salicylic acid irreversibly acetylates cyclooxygenases I and II, thereby inhibiting prostaglandin (PG) synthesis and the PG-associated inflammation, fever and pain. This agent may induce cancer cell apoptosis and modulate the immune response.
Cholybar: (Other name for: cholestyramine)
CHP-HER-2 peptide vaccine: A peptide vaccine, containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the tumor-associated antigen HER-2/neu (ErbB-2), with potential antineoplastic activity. Her-2/neu, a member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumors, including breast, ovarian, and gastric cancers. Vaccination with CHP-HER-2 peptide vaccine may stimulate the host immune system to mount a humoral as well as a cytotoxic T-cell response against tumor cells expressing the HER-2/neu antigen. This results in an inhibition of tumor cell proliferation and tumor cell death. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water.
CHP-NY-ESO-1 peptide vaccine IMF-001: A peptide cancer vaccine containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the cancer-testis antigen NY-ESO-1 protein, with potential immunostimulating and antineoplastic activities. Upon administration, CHP-NY-ESO-1 peptide vaccine IMF-001 may stimulate the host immune system to mount a humoral and cytotoxic T-cell response against tumor cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water. NY-ESO-1, an antigen found in normal testis, is upregulated in various cancers, including bladder, breast, hepatocellular, melanoma, and prostate cancers.
chromomycin A3: A glycosidic antineoplastic antibiotic isolated from the bacterium Streptomyces griseus. Chromomycin A3 reversibly binds to guanine-cytosine (G-C) base pairs in the minor groove of DNA, thereby inhibiting RNA synthesis. This agent is used as a fluorescent chromosome dye.
Chrysanthemum morifolium/Ganoderma lucidum/Glycyrrhiza glabra/Isatis indigotica/Panax pseudoginseng/Rabdosia rubescens/Scutellaria baicalensis/Serona repens supplement: An herbal mixture with potential antineoplastic effects. PC-SPES, an herbal supplement containing extracts from 8 herbs including Chrysanthemum morifolium, Ganoderma lucidum (a root fungus), Glycyrrhiza glabra (Spanish liquorice), Isatis indigotica, Panax pseudoginseng, Rabdosia rubescens, Scutellaria baicalensis, and Serona repens (saw palmetto), with potential antineoplastic and antiproliferative effects, specifically in prostate cancer cells. Its exact pharmacology is not fully understood due to the complexity of the herbal mixture and may involve multiple metabolic pathways. Exposure to PC-SPES in vitro has resulted in a decreased expression of genes encoding cell cycle regulatory proteins as well as an upregulation of genes that modulate apoptosis in both androgen-dependent and androgen-independent cells. The PC in the acronym PC-SPES stands for Prostate Cancer, while SPES is the Latin word for hope.
Cialis: (Other name for: tadalafil)
cibisatamab: An anti-carcinoembryonic antigen (CEA)/anti-CD3 bispecific monoclonal antibody with potential antineoplastic activity. Cibisatamab contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CEA, a tumor-associated antigen that is specifically expressed on certain tumor cells. Upon intravenous administration, cibisatamab binds to both T cells and CEA-expressing tumor cells, which cross-links the T cells with the tumor cells. This may result in a potent cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA is overexpressed in many cancer cell types.
ciclopirox olamine lotion: A lotion preparation of the olamine salt of ciclopirox, a synthetic hydroxypyridone derivative with broad-spectrum antifungal and anti-inflammatory activities. Although its mechanism of action is not well understood, ciclopirox may chelate trivalent cations, such as Fe3+ and Al3+, thereby inhibiting the availability of essential metal co-factors for enzymes, which may result in a loss of enzyme activities that are essential for cellular metabolism, organization of cell wall structure, and other crucial cell functions in a wide variety of fungal species. This agent may also disrupt DNA repair, cell division signals and mitotic spindles as well as some elements of intracellular transport in susceptible fungi. Ciclopirox exhibits anti-inflammatory activity by inhibiting 5-lipoxygenase and cyclooxygenase (COX).
ciclopirox olamine oral: An aqueous suspension of the olamine salt form of ciclopirox, a synthetic, broad-spectrum hydroxypyridone antifungal agent with additional antibacterial and anti-inflammatory activities. Although the exact mechanism of action of ciclopirox has yet to be fully elucidated, this agent is able to chelate trivalent cations, such as Fe3+, thereby inhibiting the availability of essential co-factors for enzymes. This may lead to a loss of activity of enzymes that are essential for cellular metabolism, organization of cell wall structure and other crucial cell functions. In addition, ciclopirox exerts its anti-inflammatory activity by inhibiting 5-lipoxygenase and cyclooxygenase (COX).
Cidan herbal capsule: A capsule-based formulation containing artificial bezoar, Strychni pulveratum (strychnos powder), camphol alcohol (borneol or borneo camphor) and extracts from Zedoary rhizome (Rhizoma curcumae), Pseudobulbus cremastrae seu pleiones (dried pseudobulb of Cremastra appendiculata), Yatantzu (seed of Brucca javanica), beehive, Bombyx mori (Bombyx batryticatus or silkworm), Danshen (dried root of Salvia miltiorrhiza or red sage root), Radix astragali, and Angelica, with potential antineoplastic activity. Upon oral administration of the cidan herbal capsule, the active ingredients in the plant extracts may induce tumor cell apoptosis and reduce tumor cell proliferation.
Cidofovir: A synthetic, acyclic, monophosphate nucleotide analog of deoxycytidine with antiviral activity, and mostly used against cytomegalovirus (CMV). After incorporation into the host cell, cidofovir is phosphorylated by pyruvate kinases to its active metabolite cidofovir diphosphate. Cidofovir diphosphate, bearing structural similarity to nucleotides, competes with deoxycytosine-5-triphosphate (dCTP) for viral DNA polymerase and gets incorporated into the growing viral DNA strands. As a result, it prevents further DNA polymerization and disrupts DNA replication of viruses.
ciforadenant: A small molecule immune checkpoint inhibitor of the adenosine A2A receptor (ADORA2A) with potential antineoplastic activity. Upon oral administration, ciforadenant binds to adenosine A2A receptors expressed on the surface of immune cells, including T-lymphocytes, natural killer (NK) cells, macrophages and dendritic cells (DCs). This prevents tumor-released adenosine from interacting with the A2A receptors on these key immune surveillance cells, thereby abrogating adenosine-induced immunosuppression in the tumor microenvironment. This may stimulate anti-tumor immune responses, resulting in tumor regression.
cifurtilimab: A proprietary, non-fucosylated monoclonal antibody directed against the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, cifurtilimab binds to CD40 on a variety of immune cell types, triggering both cellular proliferation and activation of antigen-presenting cells (APCs), which activates B cells and T cells, and enhances the immune response against tumor cells. In addition, this agent binds to the CD40 antigen present on the surfaces of tumor cells, which induces antibody-dependent cytotoxicity (ADCC), and eventually inhibits the proliferation of CD40-expressing tumor cells. CD40, a stimulatory receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, such as macrophages, dendritic cells and various tumor cell types; it plays a key role in the activation of the immune system. The non-fucosylated antibody shows increased efficacy as compared to its fucosylated counterpart.
cilastatin sodium: The sodium salt form of cilastatin, a renal dehydropeptidase inhibitor, that can be used to inhibit the activity of renal dehydropeptidase. Upon administration of cilastatin sodium, cilastatin targets, binds to and inhibits the activity of renal dehydropeptidase. This reduces the breakdown of drugs, such as the broad spectrum beta-lactam carbapenem imipenem, by renal dehydropeptidase, and thereby increases the activity and therapeutic effect of such drugs that would otherwise be metabolized by renal dehydropeptidase.
cilengitide: A cyclic Arg-Gly-Asp peptide with potential antineoplastic activity. Cilengitide binds to and inhibits the activities of the alpha(v)beta(3) and alpha(v)beta(5) integrins, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis.
cilgavimab/tixagevimab: A combination of two neutralizing human monoclonal antibodies cilgavimab and tixagevimab, that are isolated from convalescent patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, and directed against the spike (S) protein, that can potentially be used for passive immunization against Coronavirus disease 2019 (COVID-19). Upon administration of cilgavimab/tixagevimab, both antibodies specifically target and bind to the SARS-CoV-2 S protein, thereby blocking viral attachment and entry into human cells and may thereby neutralize SARS-CoV-2. This may slow the progression of the disease and accelerate recovery, and may potentially provide temporary protection against infection with SARS-CoV-2. S protein, usually found on the surface of SARS-CoV-2, plays an essential role in the infection pathway of the SARS-CoV-2 virus.
cilostazol: A quinolinone derivative and cellular phosphodiesterase inhibitor, more specific for phosphodiesterase III (PDE III). Although the exact mechanism of action of is unknown, cilostazol and its metabolites appears to inhibit PDE III activity, thereby suppressing cyclic adenosine monophosphate (cAMP) degradation. This results in an increase in cAMP in platelets and blood vessels, leading to inhibition of platelet aggregation and vasodilation.
ciltacabtagene autoleucel: A preparation of autologous T lymphocytes that are transduced, ex vivo, with LCAR-B38M, a lentiviral vector expressing a chimeric antigen receptor (CAR) containing two bispecific anti-B-cell maturation antigen (BCMA) variable fragments of llama heavy-chain murine antibodies fused to the signaling domain of 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. The antigen-binding region of the CAR is a non-scFv structure targeting two distinct regions of BCMA. Upon intravenous administration back into the patient, ciltacabtagene autoleucel are directed to cells expressing BCMA, bind to two different epitopes on BCMA and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-associated antigen (TAA) and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is overexpressed on malignant plasma cells.
ciltistotug: A humanized agonistic antibody targeting the immune checkpoint human B-cell surface antigen CD40, with potential immunostimulatory and antineoplastic activities. Upon administration, ciltistotug targets and binds to CD40 on a variety of immune cell types. This induces CD40-dependent signaling pathways, triggers the proliferation and activation of antigen-presenting cells (APCs) and activates T cells. This results in an enhanced cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD40, a cell surface receptor and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on various immune cells, such as dendritic cells (DCs), macrophages and B cells, and plays a key role in the activation of the immune system.
cimdelirsen: An antisense oligonucleotide targeting the growth hormone receptor (GHR; somatotropin receptor) mRNA, with potential somatotropin-inhibiting activity. Upon subcutaneous administration, cimdelirsen hybridizes with GHR mRNA, which blocks translation of the GHR protein. Reduction of GHR levels in turn decreases the circulating level of insulin-like growth factor-1 (IGF-1). IGF-1 is a hormone that plays an important role in childhood growth and has anabolic effects in adults. Excess production of IGF-1 results in various disease states including acromegaly.
cimetidine: A histamine H(2)-receptor antagonist. Enhancing anti-tumor cell-mediated responses, cimetidine blocks histamine's ability to stimulate suppressor T lymphocyte activity and to inhibit natural killer (NK) cell activity and interleukin-2 production. Cimetidine also may inhibit tumor growth by suppressing histamine's growth-factor activity and blocking histamine-induced stimulation of vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor.
Cimzia: (Other name for: certolizumab pegol)
cinacalcet hydrochloride: The orally bioavailable hydrochloride salt of the calcimimetic cinacalcet. Cinacalcet increases the sensitivity of calcium-sensing receptors on chief cells in the parathyroid gland to extracellular calcium, thereby reducing parathyroid hormone (PTH) secretion. A reduction in PTH levels inhibits osteoclast activity, which may result in a decrease in cortical bone turnover and bone fibrosis, and normalization of serum calcium and phosphorus levels. In addition, by reducing PTH levels, cinacalcet may reduce PSA levels; PTH appears to raise PSA levels and may increase prostate cancer cell growth.
Cinnamomum cassia capsules: A nutritional supplement composed of the blue-green microalgae spirulina. Spirulina is high in protein and contains significant amounts of calcium, niacin, potassium, magnesium, B vitamins, vitamin E, iodine, iron, beta-carotene, phycocyanin and chlorophyll. The spirulina dietary supplement may affect the cardiovascular, digestive and immune systems and may improve diabetes and high cholesterol. In addition, spirulina contains antioxidants and may protect against cellular DNA damage by reactive oxygen species (ROS). As spirulina has a high concentration of iodine and contains the amino acid tyrosine, it may improve thyroid function, and ameliorate the size of benign thyroid nodules.
cinobufagin: A bufadienolide compound extracted from the dried venom secreted by the parotid glands of toads and one of the glycosides in the traditional Chinese medicine ChanSu, with potential antineoplastic activity. Although the mechanism of action of cinobufagin is still under investigation, it has been found to suppress cancer cell proliferation and cause apoptosis in cancer cells via a sequence of apoptotic modulators that include mitochondrial Bax and cytosolic chromosome c, and caspases 3, 8, and 9. Possible upstream mediators of cinobufagin-induced apoptosis include Fas and p53.
cinobufotalin: A bufadienolide isolated from toad venom and utilized in traditional Chinese medicine (TCM) for its cardiotonic, diuretic and hemostatic effects, with potential cytotoxic and antineoplastic activities. Upon administration and although the exact mechanism of action(s) (MoAs) through which this agent exerts its effects have yet to be fully discovered, cinobufotalin causes DNA fragmentation, decreases mitochondrial membrane potential (MMP), increases intracellular calcium (Ca2+) ion concentrations and reactive oxygen species (ROS) production, upregulates Fas protein and activates cytochrome C, various caspases, Bid and Bax. This causes cell cycle arrest, induces apoptosis and inhibits tumor cell growth and survival. In addition, cinobufotalin inhibits the activity of sphingosine kinase 1 (SphK1) and induces pro-apoptotic ceramide production, which further promotes tumor cell apoptosis. Cinobufotalin also induces mitochondrial protein cyclophilin D (Cyp-D)-dependent opening of the mitochondrial permeability transition pore (mPTP), which may contribute to cinobufotalin-induced non-apoptotic death of certain tumor cells.
cinrebafusp alfa: A bivalent, bispecific fusion protein comprised of an anti-human epidermal growth factor receptor (HER2) monoclonal antibody linked to a CD137-targeting anticalin with potential immunostimulatory and antineoplastic activities. Upon administration of cinrebafusp alfa, CD137 clustering is promoted by bridging CD137-positive T-cells with HER2-positive tumor cells, leading to the recruitment of tumor antigen-specific cytotoxic T lymphocytes (CTLs). This may result in potent CTL-mediated lysis of HER2-expressing tumor cells. HER2 plays a key role in tumor cell proliferation and tumor vascularization. CD137 is a costimulatory immunoreceptor and a member of the tumor necrosis factor receptor superfamily (TNFRSF). Anticalins are synthetic antigen-binding proteins derived from lipocalins. Structurally dissimilar to antibodies, anticalins are able to bind to smaller antigens and exhibit improved tissue penetration.
cintirorgon: An orally bioavailable agonist of retinoic acid-related orphan receptor gamma (RORg), with potential immunomodulatory and antineoplastic activities. Upon oral administration of cintirorgon, this agent selectively binds to the nuclear receptor transcription factor RORg, forming a receptor complex that translocates to the nucleus, and binds to ROR response elements (ROREs), enhancing the function, proliferation and survival of type 17 T cells, including Th17 (helper T cells) and Tc17 (cytotoxic T cells). This may increase the expression of co-stimulatory molecules and decrease the expression of co-inhibitory molecules on T cells leading to increased production of cytokines and chemokines by T cells, decreased proliferation of regulatory T cells (Tregs), and abrogation of tumor-induced immunosuppression. This ultimately induces a T-cell-mediated immune response against cancer cells and leads to a reduction in tumor cell growth. RORg, the nuclear receptor transcription factor that is involved in Th17/Tc17 differentiation, plays a key role in immune activation.
cintredekin besudotox: A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R).The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis.
Cinvanti: (Other name for: aprepitant)
cipepofol: A 2,6-disubstituted alkylphenol and structural analog of propofol, that may potentially be used for the induction of sedation and hypnosis during general anesthesia. Upon intravenous administration, cipepofol facilitates inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA). This induces and maintains sedation and hypnosis.
Cipro: (Other name for: ciprofloxacin)
ciprofloxacin: A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria.
Circadin: (Other name for: therapeutic melatonin)
cirmtuzumab: A humanized monoclonal antibody against the extracellular domain of the human receptor tyrosine kinase-like orphan receptor 1 (ROR1), with potential antineoplastic activity. Upon administration, cirmtuzumab binds to ROR1 and blocks ROR1-mediated signaling. This prevents tumor cell proliferation in cancer cells overexpressing ROR1. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is normally expressed during embryogenesis. It is overexpressed in certain leukemias and solid tumors, but minimally expressed in healthy cells.
cis-urocanic acid: A derivative of the amino acid histidine, formed in the mammalian skin from trans-urocanic acid upon ultraviolet radiation, and protodynamic agent, with potential anti-inflammatory and antiproliferative activity. Upon intravesical instillation of cis-urocanic acid (cis-UCA), this agent is protonated at the imidazolyl moiety in the mildly acidic extracellular tumor environment and penetrates into the cancer cell. Once inside the cell and due to the slightly alkaline pH inside the tumor cell, cis-UCA is deprotonated, i.e. the imidazolyl proton is released into the cytosol which eventually raises the intracellular acidity. This acidification impairs many cellular processes, such as metabolic activity, and may lead to cell cycle arrest, an induction of cellular apoptosis and necrotic cell death. In addition, cis-UCA enhances ERK and JNK signaling pathways by inhibiting the activity of serine/threonine and tyrosine phosphatases.
cisapride: A substituted piperidinyl benzamide prokinetic agent. Cisapride facilitates release of acetylcholine from the myenteric plexus, resulting in increased gastrointestinal motility. In addition, cisapride has been found to act as a serotonin agonist, stimulating type 4 receptors, and a serotonin 5-HT3 receptor antagonist. (NCI)
cisatracurium besylate: The besylate salt form of cisatracurium, a non-depolarizing skeletal muscle relaxant of the benzylisoquinolinium class, with skeletal muscle relaxing activity. Cisatracurium besylate acts as a competitive acetylcholine antagonist that binds to nicotinic receptors at the neuromuscular junction. This blocks neuromuscular transmission and causes neuromuscular relaxation.
cisplatin: An alkylating-like inorganic platinum agent (cis-diamminedichloroplatinum) with antineoplastic activity. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.
cisplatin liposomal: A synthetic formulation in which the antineoplastic agent cisplatin is encapsulated in lipids. Cisplatin liposomal consists of small aggregates of cisplatin covered by a single lipid bilayer. Encasement in liposomes improves cisplatin's tumor bioavailability and toxicity profile. Liposomal encapsulation does not affect the pharmacological properties of cisplatin directly. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.
cisplatin micelle formulation HA132: A micelle formulation containing the inorganic platinum agent cisplatin, with potential antineoplastic activity. Upon administration, cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and growth inhibition of tumor cells.
cisplatin nano-engineered intraoperative system PRV211: A nano-engineered intraoperative system containing a liquid permeation enhancer (PE) and a patch composed of nanoparticles loaded with the inorganic platinum agent cisplatin, with potential antineoplastic and immunomodulating activities. Immediately following surgical tumor resection, the cisplatin nano-engineered intraoperative system PRV211 is applied intraoperatively; the PE is brushed onto the resected tumor bed and then the cisplatin patch is applied onto the same tumor site. Upon subsequent long-lasting and controlled release from the patch and penetration into the tumor bed, cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and growth inhibition of tumor cells. Cisplatin may reach regional lymph nodes and may trigger anti-tumor immune responses. Administration of PRV211 may eliminate any remaining micro metastases or close margins that could not be fully resected while avoiding system circulation. This may prevent systemic side effect and cancer recurrence.
cisplatin transmucosal patch: A transmucosal patch containing cisplatin, an inorganic platinum agent, with potential antineoplastic activity. Upon mucosal application to the tumor site in the oral cavity, and upon subsequent release from the patch, cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and growth inhibition of tumor cells.
cisplatin-E therapeutic implant: An injectable gel comprised of a collagen matrix containing the inorganic platinum (Pt) agent cisplatin and the sympathomimetic agent epinephrine with potential antineoplastic activity. After intratumoral injection, cisplatin forms highly reactive, positively charged, platinum complexes, which covalently bind to nucleophilic groups in DNA, preferably at the N7 position of guanine bases. This induces both intra- and inter-strand DNA cross-links. In addition, cisplatin forms DNA-Pt-protein cross-links. Cross-link formation results in both the induction of apoptosis and cell growth inhibition. Epinephrine, a potent vasoconstrictor, is added to the gel to both enhance the penetration of cisplatin into tumor tissue and reduce its dispersion into the surrounding tissues. Intratumoral injection of cisplatin-E therapeutic implant may increase local chemotherapeutic efficacy, as compared to the systemic administration of cisplatin, while reducing its systemic toxicity.
Cisplatin/Gemcitabine Regimen: A regimen consisting of cisplatin and gemcitabine that can be used in the treatment of biliary tract, bladder, cervical, kidney, occult primary, pancreatic, ovarian, fallopian tube, primary peritoneal, and vulvar cancers, peritoneal and pleural mesothelioma, non-small cell lung cancer (NSCLC), gestational trophoblastic neoplasia (GTN), cancer of the nasopharynx, and ampullary adenocarcinoma.
cisplatin/vinblastine/cell penetration enhancer formulation INT230-6: A formulation composed of three agents in a fixed ratio: two chemotherapeutic agents, the platinum compound cisplatin and the vinca alkaloid vinblastine, and a proprietary amphiphilic excipient that acts as a penetration enhancer, with potential antineoplastic activity. Upon intra-tumoral (IT) injection of INT230-6, the dispersion/cell penetration enhancer excipient of INT230-6 facilitates dispersion of the two drugs throughout the tumor tissue and enables increased cellular uptake of these agents into tumor cells. Once inside the cell, cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, which results in apoptosis and cell growth inhibition. Vinblastine kills the tumor cells through binding to tubulin and thereby inhibits microtubule formation, resulting in disruption of the mitotic spindle assembly and cell cycle arrest of tumor. In addition, the tumor cell killing leads to recruitment of dendritic cells (DCs) and induces a tumor-specific T-cell-mediated immune response that attacks both the injected tumor and distant tumor lesions. Local administration of both cisplatin and vinblastine, without the diffusion/penetration enhancer, results in to poor diffusion and a lack of cellular uptake of the agents; INT230-6 increases the intracellular concentration of cisplatin and vinblastine, thereby improving efficacy.
Cistane: (Other name for: isotretinoin)
citalopram hydrobromide: The orally bioavailable hydrobromide salt of the racemic bicyclic phthalene derivative citalopram with antidepressant activity. As a selective serotonin reuptake inhibitor (SSRI), citalopram selectively inhibits the CNS neuronal reuptake of serotonin, thereby potentiating serotonergic activity in the central nervous system (CNS). This agent has minimal effects on the CNS neuronal reuptake of norepinephrine (NE) and dopamine (DA).
Citanest: (Other name for: prilocaine hydrochloride)
citarinostat: An orally available histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon oral administration, citarinostat inhibits the activity of HDACs; this results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes, which inhibit tumor cell division and induce tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.
citatuzumab bogatox: A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody Fab fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a modified bouganin cytotoxin with potential antineoplastic activity. Citatuzumab bogatox binds to EpCAM, delivering modified bouganin cytotoxin directly to EpCam-positive tumor cells, which may result in the inhibition of tumor cell protein synthesis and tumor cell death. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers. Bouganin is a plant-derived ribosome-inactivating protein (RIP), a toxic plant N-glycosidase that depurinates the universally conserved alpha-sarcin loop of ribosomal rRNA, inactivating the ribosome and preventing protein synthesis. Compared to unmodified bouganins, modified bouganins may have a reduced propensity to activate human T cells.
Citicoline: A nutritional supplement and source of choline and cytidine with potential neuroprotective and nootropic activity. Citicoline, also known as cytidine-5-diphosphocholine or CDP-choline, is hydrolyzed into cytidine and choline in the intestine. Following absorption, both cytidine and choline are dispersed, utilized in various biosynthesis pathways, and cross the blood-brain barrier for resynthesis into citicoline in the brain, which is the rate-limiting product in the synthesis of phosphatidylcholine. This agent also increases acetylcholine (Ach), norepinephrine (NE) and dopamine levels in the central nervous system (CNS). In addition, citicoline is involved in the preservation of sphingomyelin and cardiolipin and the restoration of Na+/K+-ATPase activity. Citicoline also increases glutathione synthesis and glutathione reductase activity, and exerts antiapoptotic effects.
Citracal: (Other name for: calcium citrate)
citric acid monohydrate: A tricarboxylic acid found in citrus fruits. Citric acid is used as an excipient in pharmaceutical preparations due to its antioxidant properties. It maintains stability of active ingredients and is used as a preservative. It is also used as an acidulant to control pH and acts as an anticoagulant by chelating calcium in blood.
Citroma: (Other name for: magnesium citrate)
citrulline: A non-essential amino acid. In hepatocytes, L-citrulline is synthesized in the urea cycle by the addition of carbon dioxide and ammonia to ornithine. L-citrulline is converted into L-arginine by the enzymes argininosuccinate synthetase and argininosuccinate lyase in the presence of L-aspartate and ATP. Subsequently, L-arginine is converted to nitric oxide by nitric oxide synthase and L-citrulline is regenerated as a by-product.
Civacir: (Other name for: hepatitis C immune globulin intravenous)
cixutumumab: A fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor (IGF-1R) with potential antineoplastic activity. Cixutumumab selectively binds to membrane-bound IGF-1R, thereby preventing the binding of the natural ligand IGF-1 and the subsequent activation of PI3K/AKT signaling pathway. Downregulation of the PI3K/AKT survival pathway may result in the induction of cancer cell apoptosis and may decrease cancer cellular proliferation. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily overexpressed by many cancer cell types, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been implicated in tumorigenesis and metastasis.
CK1 alpha degrader CC-91633: An orally bioavailable degrader of casein kinase 1 alpha (CK1alpha; CK1a), with potential antineoplastic activity. Upon oral administration, CK1a degrader CC-91633 binds to and degrades CK1a, thereby inhibits the activity of CK1a. This prevents the enhanced binding of murine double minute X (MDMX) to p53, reduces the formation of CK1a and MDM2 complex, and prevents the interaction of MDM2 with p53. This prevents the inhibition of p53 and increases p53 activity. This induces p53-mediated cell cycle arrest, thereby inhibiting tumor cell proliferation. CK1a, a serine/threonine kinase and a leukemic stem cell target, acts as a tumor suppressor in several cancers through the negative regulation of Wnt/beta-catenin signaling and p53. It negatively regulates p53 by phosphorylating MDMX, thus enhancing binding of MDMX to p53, as well as by forming a complex with MDM2.
CK1 alpha degrader GLB-001: An orally bioavailable molecular glue degrader of casein kinase 1 alpha (CK1alpha; CK1a), with potential antineoplastic activity. Upon oral administration, CK1a degrader GLB-001 targets and binds to CK1a, and to E3 ubiquitin ligase, thereby creating a ternary complex. This induces E3 ligase ubiquitination and proteasome-mediated degradation of CK1a, and inhibits the activity of CK1a. This prevents the enhanced binding of murine double minute X (MDMX) to p53, reduces the formation of CK1a and MDM2 complex, and prevents the interaction of MDM2 with p53. This prevents the inhibition of p53 and increases p53 activity. This induces p53-mediated cell cycle arrest, thereby inhibiting tumor cell proliferation. CK1a, a serine/threonine kinase and a leukemic stem cell target, acts as a tumor suppressor in several cancers through the negative regulation of Wnt/beta-catenin signaling and p53. It negatively regulates p53 by phosphorylating MDMX, thus enhancing binding of MDMX to p53, as well as by forming a complex with MDM2.
CK1alpha/CDK7/CDK9 inhibitor BTX-A51: The ditosylated salt of A51, an orally bioavailable inhibitor of casein kinase 1alpha (CK1alpha) and cyclin-dependent kinases 7 and 9 (CDK7 and CDK9), with potential antineoplastic activity. Upon administration, BTX-A51 binds to and inhibits the activity of CK1alpha, CDK7, and CDK9. Blocking the phosphorylation and kinase activity of CK1alpha prevents the enhanced binding of murine double minute X (MDMX) to p53, the formation of CK1alpha and MDM2 complex, and the resulting inhibition of p53. This induces p53-mediated cell cycle arrest, slowing tumor cell proliferation. Blocking the phosphorylation and kinase activity of CDK7 and CDK9 prevents the positive transcription elongation factor b (PTEFb)-mediated activation of RNA polymerase II (RNA Pol II) and leads to the inhibition of gene transcription of various anti-apoptotic proteins. This also induces cell cycle arrest and apoptosis, slowing tumor cell proliferation. CK1alpha, a serine/threonine kinase and a leukemic stem cell target, acts as a tumor suppressor in several cancers through the negative regulation of Wnt/beta-catenin signaling and p53. It negatively regulates p53 by phosphorylating MDMX, thus enhancing binding of MDMX to p53, as well as by forming a complex with MDM2. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc through the phosphorylation of RNA Pol II. CDK9, also a serine/threonine kinase, regulates elongation of transcription through phosphorylation of RNA Pol II at serine 2 (p-Ser2-RNAPII). It is upregulated in various tumor cell types and plays a key role in the regulation of RNA Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
CK2-targeting synthetic peptide CIGB-300: A synthetic peptide targeting the substrates of casein kinase 2 (CK2), with potential antineoplastic activity. Upon administration and nucleolar localization, CK2-targeting synthetic peptide CIGB-300 binds to phosphoacceptor sites on the CK2 substrates, in particular the oncoprotein nucleophosmin (B23 or NPM1). This blocks the activation of B23 and induces apoptosis, thereby inhibiting tumor cell growth in susceptible tumor cells. CK2, a protein kinase often overexpressed in a variety of cancer cell types, appears to be correlated with malignant transformation, tumor growth and survival. Overexpression of B23 has been correlated with increased cellular growth and proliferation as well as inhibition of differentiation and apoptosis.
CL 246738: An immunomodulator, 3,6-bis(2-piperidinoethoxy) acridine trihydrochloride, used in a phase I study for possible immunostimulatory effects in colorectal cancer. (NCI)
cladribine: A purine nucleoside antimetabolite analogue. Cladribine triphosphate, a phosphorylated metabolite of cladribine, incorporates into DNA, resulting in single-strand breaks in DNA, depletion of nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP), and apoptosis. Because this agent is resistant to adenosine deaminase, an enzyme that inactivates some antineoplastic agents, it is selectively toxic to lymphocytes and monocytes which exhibit little deoxynucleotide deaminase activity.
Claravis: (Other name for: isotretinoin)
Clarinol: (Other name for: conjugated linoleic acid)
clarithromycin: A semisynthetic 14-membered ring macrolide antibiotic. Clarithromycin binds to the 50S ribosomal subunit and inhibits RNA-dependent protein synthesis in susceptible organisms. Clarithromycin has been shown to eradicate gastric MALT (mucosa-associated lymphoid tissue) lymphomas, presumably due to the eradication of tumorigenic Helicobacter pylori infection. This agent also acts as a biological response modulator, possibly inhibiting angiogenesis and tumor growth through alterations in growth factor expression.
Claritin: (Other name for: loratadine)
CLARIX CORD 1K: (Other name for: cryopreserved umbilical cord allograft)
Class 1 PI3K family inhibitor XL147: An orally bioavailable small molecule, targeting the class I phosphatidylinositol 3 kinase (PI3K) family of lipid kinases, with potential antineoplastic activity. Class 1 PI3K kinase family inhibitor XL147 reversibly binds to class 1 PI3Ks in an ATP-competitive manner, inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K signaling pathway; this may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents including genotoxic agents and receptor tyrosine kinase inhibitors.
clavulanic acid: A semisynthetic beta-lactamase inhibitor isolated from Streptomyces. Clavulanic acid contains a beta-lactam ring and binds strongly to beta-lactamase at or near its active site, thereby hindering enzymatic activity. This protects other beta-lactam antibiotics from beta-lactamase catalysis, thereby enhancing their antibacterial effects. This agent is used in conjunction with beta-lactamase susceptible antibiotics, such as penicillins and cephalosporins, to treat infections caused by beta-lactamase producing organisms.
clazakizumab: A humanized monoclonal antibody directed against the pro-inflammatory cytokine interleukin-6 (Il-6) with potential immunomodulating activity. Upon administration, clazakizumab binds to and blocks the activity of IL-6, which may mitigate the catabolic effects of IL-6.
CLEC12A-targeting CCR/anti-ADGRE2 CAR T cells ADCLEC.syn1: A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the human myeloid-restricted adhesion G protein-coupled receptor E2 (ADGRE2; EGF-like module receptor 2; EMR2; CD312), and a chimeric costimulatory receptor (CCR) targeting C-type lectin domain family 12 member A (CLEC12A, C-type-lectin-like molecule-1; CLL-1; CLL1), with potential immunomodulating and antineoplastic activities. Upon administration, CLEC12A-targeting CCR/anti-ADGRE2 CAR T cells ADCLEC.syn1 target and bind to ADGRE2- and CLEC12A-expressing tumor cells. This induces selective toxicity in tumor cells that express a high level of ADGRE2, and tumor cells that express both ADGRE2 and CLEC12A. ADGRE2 is expressed mainly on myeloid cells and is overexpressed on leukemic stem cells (LSCs) in acute myeloid leukemia (AML). CLEC12A, a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily, is overexpressed on LSCs and plays an important role in disease progression and relapse for myeloid malignancies. ADGRE2 and CLEC12A are highly co-expressed in AML and not in normal tissues. Targeting both ADGRE2 and CLEC12A may improve efficacy and reduce adverse effects.
clemizole hydrochloride: The hydrochloride salt form of clemizole, an orally bioavailable histamine H1 antagonist, with potential anti-tumor and anti-allergic activities. Upon oral administration, clemizole binds to and blocks the H1 receptor, thereby preventing the interaction between histamine and the H1 receptor and inhibiting H1-mediated signaling. This may inhibit or prevent the symptoms that are caused by histamine activity and rescues or prevents allergic reactions. Although the exact mechanism of action by which clemizole appears to exert its antineoplastic effect is yet to be elucidated, clemizole inhibits the proliferation of certain tumor cell types.
clevudine: A synthetic pyrimidine analogue with activity against hepatitis B virus (HBV). Intracellularly, clevudine is phosphorylated to its active metabolites, clevudine monophosphate and triphosphate. The triphosphate metabolite competes with thymidine for incorporation into viral DNA, thereby causing DNA chain termination and inhibiting the function of HBV DNA polymerase (reverse transcriptase). Clevudine has a long half-life and shows significant reduction of covalently closed circular DNA (cccDNA), therefore the patient is less likely to have a relapse after treatment is discontinued.
clifutinib besylate: The besylate salt form of clifutinib, an orally bioavailable, selective, small molecule inhibitor of FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential antineoplastic activity. Upon oral administration, clifutinib targets, binds to and inhibits the activity of FLT3. This inhibits the proliferation of FLT3-expressing cancer cells. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias.
Climara: (Other name for: therapeutic estradiol)
clindamycin phosphate: The phosphate salt form of clindamycin, a semi-synthetic, chlorinated broad spectrum antibiotic produced by chemical modification of lincomycin. Clindamycin phosphate is used in topical preparations.
clindamycin/hydrocortisone lotion: A topical lotion, containing clindamycin and hydrocortisone, with antibacterial and anti-inflammatory activities. Clindamycin, a lincomycin antibiotic, binds to the 50S subunit of the bacterial ribosome, thereby inhibiting bacterial protein synthesis. As a glucocorticoid agonist, hydrocortisone promotes protein catabolism, gluconeogenesis, capillary wall stability, renal excretion of calcium, and suppression of immune and inflammatory responses.
Clino-San vaginal lubricant: A vaginal lubricant formulated as a topical gel used to prevent and treat vaginal dryness. With a pH similar to that of normal vaginal discharge, Clino-San vaginal lubricant may reduce dryness, pain and irritation often caused by insufficient vaginal discharge due to atrophy of the vulvovaginal mucosa.
ClinOleic: (Other name for: olive oil/soya oil/egg lecithin-based emulsion)
Clinoril: (Other name for: sulindac)
Clioquinol: An orally bioavailable, lipophilic, copper-binding, halogenated 8-hydroxyquinoline with antifungal, antiparasitic and potential antitumor activities. Clioquinol forms a stable chelate with copper (copper (II) ions), which inhibits the chymotrypsin-like activity of the proteasome; consequently, ubiquitinated proteins may accumulate in tumor cells, followed by tumor cell apoptosis and the inhibition of tumor angiogenesis. In addition, the clioquinol-copper complex appears to decrease the expression of androgen receptors (AR) in human copper-enriched prostate cancer cells. Serum levels of copper are often elevated in patients with cancer; copper chelation may inhibit copper-dependent endothelial cell proliferation and tumor secretion of angiogenic factors.
CLK inhibitor BH-30236: An orally bioavailable macrocyclic ATP-competitive inhibitor of CDC2-like kinase (CLK) family kinases, including CLK1, CLK2 and CLK4, with potential antineoplastic activity. Upon oral administration, CLK inhibitor BH-30236 targets, binds to and inhibits the activity of CLK1/2/4, thereby inhibiting the phosphorylation of serine/arginine-rich (SR) domain-containing splicing factors (SFs). This modulates RNA splicing, prevents the expression of certain tumor-associated genes, and inhibits tumor cell proliferation. In many cancer cells, core spliceosome proteins, including SF3B1, U2 small nuclear ribonucleoprotein auxiliary factor 1 (U2AF1), serine/arginine-rich splicing factor 2 (SRSF2) and U2 small nuclear ribonucleoprotein auxiliary factor subunit-related protein 2 (ZRSR2), are mutated and aberrantly activated leading to a dysregulation of mRNA splicing. CLK family kinases, an evolutionarily conserved group of kinases, phosphorylates various SR proteins including SR domain-containing SFs.
CLK inhibitor CTX-712: An orally bioavailable inhibitor of CLK family kinases, with potential antineoplastic activity. Upon oral administration, CLK inhibitor CTX-712 binds to and inhibits the activity of CLK family kinases, thereby inhibiting the phosphorylation of serine/arginine-rich (SR) domain-containing splicing factors (SFs). This modulates RNA splicing, prevents the expression of certain tumor-associated genes, and inhibits tumor cell proliferation. In many cancer cells, core spliceosome proteins, including SF3B1, U2 small nuclear ribonucleoprotein auxiliary factor 1 (U2AF1), serine/arginine-rich splicing factor 2 (SRSF2) and U2 small nuclear ribonucleoprotein auxiliary factor subunit-related protein 2 (ZRSR2), are mutated and aberrantly activated leading to a dysregulation of mRNA splicing. CLK family kinases, an evolutionarily conserved group of kinases, phosphorylates various SR proteins including SR domain-containing SFs.
clobetasol: A topical synthetic corticosteroid with anti-inflammatory, anti-pruritic, and vasoconstrictive properties. Upon topical administration, clobetasol binds to cytoplasmic glucocorticoid receptors (GRs) and activates GR-mediated gene expression. This results in synthesis of certain anti-inflammatory proteins, while inhibiting the synthesis of certain inflammatory mediators. Specifically, clobetasol induces phospholipase A2 inhibitory proteins, thereby controlling the release of the inflammatory precursor arachidonic acid from membrane phospholipids by phospholipase A2. This inhibits skin inflammation, and reduces swelling, redness, itching and rashes.
clobetasol propionate: The propionate salt form of clobetasol, a topical synthetic corticosteroid with anti-inflammatory, anti-pruritic, and vasoconstrictive properties. Clobetasol propionate exerts its effect by binding to cytoplasmic glucocorticoid receptors and subsequently activates glucocorticoid receptor mediated gene expression. This results in synthesis of certain anti-inflammatory proteins, while inhibiting the synthesis of certain inflammatory mediators. Specifically, clobetasol propionate appears to induce phospholipase A2 inhibitory proteins, thereby controlling the release of the inflammatory precursor arachidonic acid from membrane phospholipids by phospholipase A2.
clodronate disodium: The disodium salt of a nitrogen-free bisphosphonate analog of naturally occurring pyrophosphate. Clodronate binds to calcium and inhibits osteoclastic bone resorption and hydroxyapatite crystal formation and dissolution, resulting in a reduction of bone turnover. This agent may control malignancy-associated hypercalcemia, inhibit osteolytic bone metastasis and decrease pain.
clofarabine: A second generation purine nucleoside analog with antineoplastic activity. Clofarabine is phosphorylated intracellularly to the cytotoxic active 5'-triphosphate metabolite, which inhibits the enzymatic activities of ribonucleotide reductase and DNA polymerase, resulting in inhibition of DNA repair and synthesis of DNA and RNA. This nucleoside analog also disrupts mitochondrial function and membrane integrity, resulting in the release of pre-apoptotic factors, including cytochrome C and apoptotic-inducing factors, which activate apoptosis.
clofazimine: A phenazine dye with anti-mycobacterial and anti-inflammatory activities. The exact mechanism through which clofazimine exerts its effect is unknown. However, it binds preferentially to mycobacterial DNA, thereby inhibiting DNA replication and cell growth. Clofazimine has a slow bactericidal effect on Mycobacterium leprae and is active against various other Mycobacteria.
clofibrate: An aryloxyisobutyric acid derivate with antihyperlipidemic activity. Although the exact mechanism of action has not been fully characterized, clofibrate may enhance the conversion of very-low-density lipoprotein (VLDL) to low-density lipoprotein (LDL), decreasing the production of hepatic VLDL, inhibiting cholesterol production, and increasing fecal excretion of neutral sterols.
Clolar: (Other name for: clofarabine)
Clomid: (Other name for: clomiphene citrate)
clomiphene citrate: The citrate salt form of clomiphene, a triphenylethylene nonsteroidal ovulatory stimulant evaluated for antineoplastic activity against breast cancer. Clomiphene has both estrogenic and anti-estrogenic activities that compete with estrogen for binding at estrogen receptor sites in target tissues. This agent causes the release of the pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to ovulation.
clonidine: An imidazoline derivate and centrally-acting alpha-adrenergic agonist, with antihypertensive activity. Clonidine binds to and stimulates central alpha-2 adrenergic receptors, thereby reducing the amount of norepinephrine (NE) release and thus decreasing sympathetic outflow to the heart, kidneys, and peripheral vasculature. The reduction in sympathetic outflow leads to decreased peripheral vascular resistance, decreased blood pressure, and decreased heart rate. In addition, clonidine binds to imidazoline receptor subtype 1 (I1), which may also contribute to a reduction in blood pressure.
clonidine hydrochloride: The hydrochloride salt form of clonidine, an imidazoline derivate and centrally-acting alpha-adrenergic agonist as well as antagonist with antihypertensive activity. Clonidine hydrochloride binds to and stimulates central alpha-2 adrenergic receptors, thereby decreasing sympathetic outflow to the heart, kidneys, and peripheral vasculature. The reduction in sympathetic outflow, leads to decreased peripheral vascular resistance, decreased blood pressure, and decreased heart rate.
Clonidine Lauriad: (Other name for: clonidine-containing mucoadhesive buccal tablet)
clonidine-containing mucoadhesive buccal tablet: An extended release, proprietary mucoadhesive buccal tablet formulation containing the hydrochloride salt form of clonidine, the imidazoline derivative and adrenergic alpha 2 receptor agonist, with anti-inflammatory activity. Upon contact of the tablet with the buccal mucosa, clonidine binds to the adrenergic receptors on macrophages and lymphocytes and may reduce the release of pro-inflammatory mediators such as tumor necrosis factor alpha (TNFalpha). As a result, this agent may prevent chemoradiation therapy-induced mucositis.
clopidogrel: A thienopyridine, with antiplatelet activity. Clopidogrel targets, irreversibly binds to and alters the platelet receptor for adenosine diphosphate (ADP), thereby blocking the binding of ADP to its receptor, inhibiting ADP-mediated activation of the glycoprotein complex GPIIb/IIIa, and inhibiting fibrinogen binding to platelets and platelet adhesion and aggregation. This results in increased bleeding time.
clopidogrel bisulfate: A thienopyridine with antiplatelet activity. Clopidogrel bisulfate irreversibly alters the platelet receptor for adenosine diphosphate (ADP), thereby blocking the binding of ADP to its receptor, inhibiting ADP-mediated activation of the glycoprotein complex GPIIb/IIIa, and inhibiting fibrinogen binding to platelets and platelet adhesion and aggregation.
Cloretazine: (Other name for: laromustine)
clostridia strain formulation VE303: An orally bioavailable formulation composed of eight nonpathogenic, nontoxigenic, commensal strains of Clostridia derived from healthy human stool samples and manufactured from clonal cell banks, for the potential prevention of recurrent Clostridium difficile (C. difficile) infections. Upon oral administration of the Clostridia strain formulation VE303, the microbiota populates the gastrointestinal (GI) tract. The transplanted microbiota allows re-population of the patient's microbiome with diverse protective microorganisms that competitively exclude C. difficile. This may prevent recurrent C. difficile infections.
Clostridioides difficile toxin B-binding proteins/endolysin combination LMN-201: An orally bioavailable combination agent composed of a whole, dried, non-viable biomass of spirulina (Arthrospira platensis) grown from four separate strains expressing three toxin-binding proteins targeting Clostridioides difficile toxin B (TcdB) and a phage-derived endolysin, with potential antibacterial activity. Upon oral administration of C. difficile TcdB-binding proteins/endolysin combination LMN-201, the C. difficile TcdB-binding proteins bind to distinct epitopes of the TcdB, thereby preventing the binding of the toxin to target host cells. TcdB is one of two exotoxins responsible for the symptoms of Clostridium difficile infections. In addition, the phage-derived endolysin degrades the cell wall of C. difficile, resulting in bacterial cell lysis. Altogether, this may prevent or treat C. difficile infection.
Clostridium butyricum CBM 588 probiotic strain: A probiotic containing a specific strain of the anaerobic, butyric acid-forming Gram-positive bacterium Clostridium butyricum (C. butyricum), with potential immunomodulatory, anti-inflammatory and antineoplastic activities. Clostridium butyricum MIYAIRI (CBM) 588 is the 588th MIYAIRI strain, isolated from a soil sample in Japan in 1963. Upon oral administration of C. butyricum CBM 588 probiotic strain, C. butyricum modulates the composition of the normal gastrointestinal (GI) microflora, by increasing the beneficial bacteria and decreasing the harmful bacteria, and helps maintain adequate colonization of the GI tract, thereby improving digestion and preventing GI disturbances. These bacteria and the butyric acid produced by them create an environment unfavorable to pathogens by adhering to human epithelial cells and forming a protective mucosal barrier. This prevents attachment of pathogens and reduces the risk of infection. By restoring gut microbiota, these bacteria may restore or enhance intestinal immune responses. C. butyricum induces interleukin-10-producing macrophages in inflamed mucosa via the Toll-like receptor 2 (TLR2)/myeloid differentiation primary response gene 88 (MyD88) pathway, thereby decreasing inflammatory responses. In addition, CBM588 may exert antineoplastic activity by inducing the release of the endogenous cytokine tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) from intracellular stores in polymorphonuclear neutrophils (PMNs), most likely involving matrix metalloproteinase 8 (MMP-8) and the Toll-like receptors (TLR)2/4 signaling pathways. This results in TRAIL-mediated induction of apoptosis in susceptible tumor cells.
Clostridium butyricum-containing probiotic: A probiotic containing the anaerobic, butyric acid-forming Gram-positive bacterium Clostridium butyricum (C. butyricum), with potential immunomodulatory activity. Upon oral administration of C. butyricum-containing probiotic, C. butyricum modulates the composition of the normal gastrointestinal (GI) microflora and help maintain adequate colonization of the GI tract, thereby improving digestion and preventing GI disturbances. This bacterium creates an environment unfavorable to pathogens by adhering to human epithelial cells, thereby forming a protective mucosal barrier. This prevents attachment of pathogens and reduces the risk of infection. Dietary supplementation with this bacterium may restore or enhance intestinal immunity.
clostridium Novyi-NT spores: Spores of the bacterial strain Clostridium novyi-NT, the attenuated obligate anaerobic C. novyi, with potential immunostimulating, bacteriolytic, and antineoplastic activities. Upon intravenous administration, Clostridium novyi-NT spores germinate exclusively in hypoxic tissue, such as avascular regions of tumors. Germination results in lysis and destruction of surrounding viable tumor cells. Due to their anaerobic nature, C. novyi-NT spores do not proliferate in oxygenated tumor regions. However, this agent may stimulate the immune system to exert a cellular immune response, resulting in additional killing of tumor cells not lysed by the bacteria, including those in the well-oxygenated tumor area.
clotrimazole: A synthetic, imidazole derivate with broad-spectrum, antifungal activity. Clotrimazole inhibits biosynthesis of sterols, particularly ergosterol, an essential component of the fungal cell membrane, thereby damaging and affecting the permeability of the cell membrane. This results in leakage and loss of essential intracellular compounds, and eventually causes cell lysis.
clove oil: The essential oil extracted from Syzygium aromaticum. Clove oil has both analgesic and antiseptic properties and is commonly used to treat tooth and gum pain.
cloxacillin: A semisynthetic beta-lactamase resistant penicillin antibiotic with antibacterial activity. Cloxacillin binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall, thereby preventing the cross-linkage of peptidoglycans, which are critical components of the bacterial cell wall. This leads to an interruption of the bacterial cell wall and causes bacterial cell lysis.
clozapine: A synthetic dibenzo-diazepine derivative, atypical antipsychotic Clozapine blocks several neurotransmitter receptors in the brain (dopamine type 4, serotonin type 2, norepinephrine, acetylcholine, and histamine receptors). Unlike traditional antipsychotic agents, it weakly blocks dopamine type 2 receptors. It relieves schizophrenic symptoms (hallucinations, delusions, dementia).
cMet CAR-mRNA electroporated autologous T lymphocytes: A preparation of autologous T-lymphocytes that have been electroporated with an mRNA encoding a chimeric antigen receptor (CAR) consisting of an anti-human hepatocyte growth factor receptor (HGFR or cMet) scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta) coupled to the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activities. Upon intratumoral administration, cMet CAR-mRNA electroporated autologous T lymphocytes direct T-cells to cMet-expressing tumor cells, which induces a selective toxicity in cMet-expressing tumor cells and causes tumor cell lysis. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of cMet. The inclusion of the 4-1BB signaling domain may increase the antitumor activity as compared to the inclusion of the CD3-zeta chain alone. The mRNA CAR is expressed for a limited amount of time, which can prevent serious, unforeseen side effects. cMet, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.
CMF regimen: A regimen consisting of cyclophosphamide, methotrexate and fluorouracil, used as a neoadjuvant or adjuvant treatment for breast cancer; also used for the treatment of recurrent and metastatic breast cancer.
CMV pentamer complex proteins/gB-encoding mRNA vaccine mRNA-1647: A messenger RNA (mRNA) vaccine consisting of six mRNAs five of which encode the human cytomegalovirus (CMV) subunits that form the membrane-bound pentamer protein complex and one that encodes the full-length membrane-bound glycoprotein B (gB), with potential immunostimulatory activity against CMV. Upon intramuscular (IM) administration of the CMV pentamer complex proteins/gB-encoding mRNA vaccine mRNA-1647, the mRNAs are translated by the cellular protein translation machinery to produce the proteins. This exposes the immune system to the six peptides, activates both humoral and cellular immune responses, and may provide active immunization against both the pentamer proteins and gB and therefore against CMV infection. Both the pentamer, consisting of gH, gL, UL128, UL130 and UL131 proteins, and gB are essential for CMV to infect barrier epithelial surfaces. CMV can cause significant disease in immunocompromised patients.
CMV pp65 mRNA lipid particle vaccine: An off-the-shelf (OTS) lipid particle (LP)-based cancer priming vaccine containing messenger RNA (RNA) encoding the human cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83), with potential immunostimulatory and antineoplastic activities. Upon administration of CMV pp65 mRNA LP vaccine, the mRNA is taken up, translated and presented by antigen presenting cells (APCs), mainly dendritic cells (DCs). This may result in a specific cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells leading to tumor cell lysis. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.
CMV pp65 peptide: A peptide derived from cytomegalovirus (CMV) internal matrix protein pp65. CMV pp65 peptide antigen is used in recombinant vaccinia virus as an HLA-A-restricted epitope to produce vaccines and specific CD8+ and CD4+ cell responses against CMV infection, a serious complication of allogeneic bone marrow transplantation (BMT). In BMT, CMV infection may be prevented by passive immunization with donor-derived CMV-pp65-specific T-cell clones if provided early post-BMT.
CMV pp65 peptide-loaded alpha-type-1 polarized dendritic cell vaccine: A dendritic cell (DC)-based cancer vaccine composed of mature polarized DCs (alpha-type-1 polarized DCs) loaded with the human cytomegalovirus (CMV) phosphoprotein pp65 (UL83), with potential immunostimulatory and antineoplastic activities. Upon administration, the CMV pp65 peptide-loaded alpha-type-1 polarized DC vaccine exposes the immune system to the CMV pp65 peptide, which may result in a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells leading to tumor cell lysis. The CMV pp65 protein is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types.
CMV/EBV/ADV/BKV-specific cytotoxic T lymphocytes: A population of cytotoxic T lymphocytes (CTLs) specifically reactive to cytomegalovirus (CMV), Epstein-Barr virus (EBV), adenovirus (ADV) and BK virus (BKV), with potential antiviral and protective activities. T cells derived from peripheral blood mononuclear cells (PBMCs) are exposed to and activated by dendritic cells (DCs) that are loaded with specific peptides from CMV, EBV, ADV and BKV. Upon infusion of the CMV/EBV/ADV/BKV-specific CTLs, these lymphocytes target and cause lysis of CMV-, EBV-, ADV- and/or BKV-infected cells and may prevent infection and complications from CMV-, EBV-, ADV- and BKV-driven viral diseases. Opportunistic infections caused by these viruses are often seen in immunosuppressed patients.
CMVpp65-A*0201 peptide vaccine: A peptide-based cancer vaccine containing a mutated form of the HLA-A*0201-restricted cytomegaloviral epitope CMVpp65(495-503) with potential immunostimulatory and antitumor activities. Upon subcutaneous administration, CMVpp65-A*0201 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CMV-positive cells, resulting in cell lysis. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity. CMVpp65, a tegument protein of the herpes virus CMV, is the main viral antigen found in peripheral blood mononuclear cells (PBMCs) after viral infection and may activate cell-mediated immunity.
CMVpp65/gB plasmid vaccine ASP0113: A poloxamer-formulated, bivalent DNA vaccine containing two plasmids encoding both the human cytomegaloviral (CMV) tegument phosphoprotein 65 (pp65), a major internal matrix protein, and glycoprotein B (gB), an important CMV component responsible for attachment and entry into cells, with potential immunostimulatory properties. Upon intramuscular injection of CMVpp65/gB plasmid vaccine ASP0113, the expressed proteins may activate the immune system to mount both cellular and humoral immune responses against CMV-positive cells. This results in cell lysis of CMV-infected cells and prevents both viral replication and the development of CMV disease. This vaccine also provides active immunization and protective immunity against CMV infection in CMV-negative patients exposed to infected donor cells or tissues in transplant recipients. CMV infection can cause serious complications in patients receiving either allogeneic hematopoietic cell transplants (HCT) or solid organ transplants. The poloxamer-based delivery system enhances DNA delivery.
CNDO-109-activated allogeneic natural killer cells: A preparation of non-interleukin-2 primed, tumor activated allogeneic natural killer (NK) cells with potential immunostimulating activity. The allogeneic NK cells obtained from a first or second degree relative of the patient are co-incubated with a lysate from the CTV-1 cell line, a minimally differentiated myeloid line derived from an acute myelogenous leukemia patient. Infusion of CNDO-109-activated allogeneic NK cells may be able to lyse and destroy NK-resistant tumor cells and a broad spectrum of tumor cells.
CNGRC peptide-TNF alpha conjugate: A cytokine-peptide conjugate composed of the cytokine tumor necrosis factor alpha (TNF-alpha) chemically linked to the peptide CNGRC. The peptide moiety CNGRC, a ligand for the membrane-bound metalloprotease CD13, binds to endothelial cells of the angiogenic vasculature that express CD13 (also known as aminopeptidase N); subsequently, the TNF-alpha moiety induces apoptosis in endothelial cells expressing CD13, thereby inhibiting tumor-associated angiogenesis.
cobalamin: An essential nutrient and natural water-soluble vitamin of the B-complex family that must combine with an intrinsic factor for absorption by the intestine, Vitamin B12 (cyanocobalamin) is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions.
Cobavite: (Other name for: cyanocobalamin)
cobicistat: A cytochrome P450 3A (CYP3A) inhibitor that can be used to enhance the pharmacokinetic profile of certain anti-HIV-1 agents. Upon administration, cobicistat inhibits the liver enzyme CYP3A4 and limits the breakdown of co-administered agents that are metabolized by CYP3A4, and increases the concentration, systemic exposure and efficacy of the co-administered agent.
cobimetinib fumarate: The fumarate salt of an orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.
cobiprostone spray: A topical spray formulation containing the prostone cobiprostone, a type 2 chloride channel (ClC-2) agonist, with potential mucosal protective and anti-mucositis activities. Upon administration of cobiprostine via a spray into the oral cavity, cobiprostone specifically binds to and activates the ClC2 channel located on the mucosal membrane. This activates the epithelial ClC2 channel, enhances secretion of chloride, and promotes epithelial barrier repair. This prevents or reduces mucosal injury and reduces mucositis. ClC2 plays a key role in the protection of mucosal barrier function.
cobolimab: A monoclonal antibody against the inhibitory T-cell receptor, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cobolimab binds to TIM-3 expressed on certain T cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.
cobomarsen: A locked nucleic acid (LNA)-based oligonucleotide inhibitor of microRNA (miRNA) 155 (miR-155), with potential antineoplastic activity. Upon administration, cobomarsen targets, binds to and inhibits miR-155. This silences miR-155 and prevents the translation of certain tumor promoting genes, which leads to the induction of cancer cell apoptosis and the inhibition of tumor cell growth. miR-155, an oncogenic single-stranded, non-coding RNA that is critical to the regulation of gene expression, is overexpressed in certain tumor cell types. Up-regulation of miR-155 plays a key role in increased tumor cell proliferation and survival. The LNA is an RNA analog in which the ribose ring is locked in a particular confirmation that increases stability. Compared to the unmodified oligonucleotide, the LNA-modified oligonucleotide shows increased affinity for its target miR-155.
cocculus/Nux vomica/tabacum/petroleum extract: A homeopathic herbal formulation with potential anti-emetic activity. Cocculus/nux vomica/tabacum/petroleum extract contains equal homeopathic units of the following extracts: extract of Cocculus indicus (fish berry), the fruit of the southeast Asian/Indian climbing plant Anamirta cocculus; extract of the seeds of Strychnos nux vomica (poison nut), an evergreen tree native to southeast Asia; extract of Nicotiana tabacum (tobacco); and petroleum. Although the exact mechanism(s) of action for this formulation has yet to be fully elucidated, alkaloids in these plant extracts have been shown to relieve nausea, vomiting, and, in some cases, dizziness.
cocoa extract: A dietary supplement containing cocoa extract derived from the cacao bean, with potential vasodilating, anti-inflammatory, cardiovascular protective, neuroprotective, cognition enhancing and chemopreventive activities. Cocoa extract contains flavonoids, including high levels of epicatechin, catechin, procyanidins and xanthines, such as theobromine. Upon oral administration, the bioactive ingredients in the cocoa extract inhibit angiotensin-converting enzyme (ACE) and increase the production of nitric oxide (NO) through the activation of endothelial nitric oxide synthase (eNOS). This causes vasodilation, improves blood flow, and decreases blood pressure. The cocoa extract also improves insulin sensitivity, enhances cognition, and decreases the production of pro-inflammatory molecules. In addition, this extract exerts antioxidant effects and is able to scavenge reactive oxygen species (ROS). As a result, healthy cells are protected from oxidative stress and DNA damage.
CodaLytic: (Other name for: oncolytic influenza A virus)
codeine phosphate: The phosphate salt of codeine, a naturally occurring phenanthrene alkaloid and opioid agonist with analgesic, antidiarrheal and antitussive activities. Codeine mimics the actions of endogenous opioids by binding to the opioid receptors at many sites within the central nervous system (CNS). Stimulation of mu-subtype opioid receptors results in a decrease in the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline; in addition, the codeine metabolite morphine induces opening of G-protein-coupled inwardly rectifying potassium (GIRK) channels and blocks the opening of N-type voltage-gated calcium channels, resulting in hyperpolarization and reduced neuronal excitability. Stimulation of gut mu-subtype opioid receptors results in a reduction in intestinal motility and delayed intestinal transit times. Antitussive activity is mediated through codeine’s action on the cough center in the medulla.
Codonopsis pilosula supplement: A traditional Chinese medicine composed of the roots of Codonopsis pilosula, with potential immunostimulatory, anti-inflammatory and antioxidant activities. Codonopsis pilosula contains the oligosaccharide inulin, various polysaccharides, sterols, alkaloids and triterpenoids. Upon administration, Codonopsis pilosula supplement may exert immunostimulatory, anti-inflammatory and antioxidant effects, and enhance immunity and improve hematopoietic functions.
codrituzumab: A humanized monoclonal antibody directed against the cell surface oncofetal protein glypican-3 (GPC3) with potential antineoplastic activity. Anti-GPC3 monoclonal antibody GC33 binds to GPC3 and triggers a host immune response against GPC3-expressing tumor cells, which may result in tumor cell death. GPC3, a heparin sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma and mesoderm-derived organs such as the liver, lungs, and kidney.
coenzyme Q10: A naturally occurring benzoquinone important in electron transport in mitochondrial membranes. Coenzyme Q10 functions as an endogenous antioxidant; deficiencies of this enzyme have been observed in patients with many different types of cancer and limited studies have suggested that coenzyme Q10 may induce tumor regression in patients with breast cancer. This agent may have immunostimulatory effects.
CoFactor: (Other name for: folitixorin)
cofetuzumab pelidotin: An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody against human inactive tyrosine-protein kinase 7 (PTK7) linked, via a cleavable valine-citrulline linker, to an analog of the auristatin microtubule inhibitor dolastatin 10, auristatin-0101, with potential antineoplastic activity. Upon administration, cofetuzumab pelidotin targets and binds to PTK7 expressed on tumor cells. Upon binding, internalization and cleavage, auristatin-0101 binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and apoptosis of PTK7-expressing tumor cells. PTK7, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells.
Coffea arabica extract: An orally bioavailable dietary supplement composed of an extract from the beans of green coffee (Coffea arabica), which are unprocessed and unroasted, with potential anti-inflammatory, antioxidant and chemopreventive activities. Coffea arabica extract contain high amounts of phenolic compounds and their derivatives, such as chlorogenic acid (CGA), and alkaloids, such as caffeine. As many of the active components in the Coffea arabica are antioxidant compounds, upon administration, they scavenge free radicals, protect against oxidation of low-density lipoprotein (LDL), and inhibit cell damage due to reactive oxygen species (ROS). This inhibits oxidative stress and protects against DNA damage. The components in the extract also inhibit enzymes involved in inflammation, cell replication and DNA synthesis, and induce the expression of antioxidant enzymes. They also induce anti-inflammatory-mediated pathways, decrease nuclear factor Kappa-B (NF-kB) activation and decrease the expression of pro-inflammatory cytokines. This may inhibit growth and induce apoptosis of cancer cells. In addition, Coffea arabica extract upregulates the expression of anti-inflammatory adipokines (adipocytokines), such as adiponectin, and reduces the expression of pro-inflammatory adipokines, such as tumor necrosis factor-alpha (TNF-a), leptin and interleukin 6 (IL-6), thereby further preventing inflammation and inflammation-induced cancer. Adipokines are normally secreted by adipose tissue and play a key role in the regulation of glucose and fat metabolism, insulin sensitivity and inflammation.
coffee dietary supplement: A dietary supplement containing coffee, with potential gastrointestinal (GI) tract stimulating activity. Following consumption of the dietary supplement, the coffee may both stimulate peristalsis and may increase bowel movement. The supplement also may stimulate the central nervous system, suppress appetite and cause weight loss.
colchicine: An alkaloid isolated from Colchicum autumnale with anti-gout and anti-inflammatory activities. The exact mechanism of action by which colchicine exerts its effect has not been completely established. Colchicine binds to tubulin, thereby interfering with the polymerization of tubulin, interrupting microtubule dynamics, and disrupting mitosis. This leads to an inhibition of migration of leukocytes and other inflammatory cells, thereby reducing the inflammatory response to deposited urate crystals. Colchicine may also interrupt the cycle of monosodium urate crystal deposition in joint tissues, thereby also preventing the resultant inflammatory response. Overall, colchicine decreases leukocyte chemotaxis/migration and phagocytosis to inflamed areas, and inhibits the formation and release of a chemotactic glycoprotein that is produced during phagocytosis of urate crystals.
cold contaminant-free Iobenguane I-131: An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine, manufactured with a proprietary process, with radioisotopic and potential antineoplastic activities. Cold contaminant-free iobenguane I 131 (MIBG) localizes to adrenergic tissue and may be used to image or eradicate tumor cells that accumulate and metabolize norepinephrine. This agent is manufactured using a technology that avoids the production of unwanted "cold contaminants" (i.e., carrier molecules), which may cause undesirable side effects and compete with MIBG for binding on target receptor sites.
COLD-fX: (Other name for: North American ginseng extract AFX-2)
colesevelam hydrochloride: A hydrochloride salt form of colesevelam, a non-absorbed polymer that binds bile acids in the intestine and lowers serum lipids.
colestipol: A positively charged, non-digestible, triamine and epoxypropane copolymer anion-exchange resin that binds to bile acids in the intestine to form an insoluble complex, which is excreted in the feces.
colistimethate sodium: The sodium salt of colistimethate, a broad-spectrum polymyxin antibiotic against most aerobic Gram-negative bacteria except Proteus bacteria. Colistimethate sodium contains the pentasodium salt of the penta(methanesulfonic acid) derivative of colistin A as the major component and a small proportion of the petasodium salt of the pentamethanesulfonate derivative of colistin B. Colistins are cyclic polypeptides produced from Bacillus colistinus or B. polymyxa and function as a surfactant which penetrates into and disrupts the bacterial cell membrane, thereby resulting in bactericidal effect.
colistin sulfate: Cyclic polypeptide antibiotic from Bacillus colistinus. It is composed of Polymyxins E1 and E2 (or Colistins A, B, and C) which act as detergents on cell membranes. Colistin is less toxic than Polymyxin B, but otherwise similar; the methanesulfonate is used orally. (Medical Dictionary Online)
collagen/aloe vera/vitamin E/lidocaine topical hydrogel: A topical preparation containing collagen, aloe vera, vitamin E, and lidocaine hydrochloride with wound-healing activity. The four ingredients of collagen/aloe vera/vitamin E/lidocaine topical hydrogel may promote wound repair and new tissue growth in which : collagen, a structural protein in connective tissue, provides a connective tissue matrix for the attachment of various cells involved in wound repair; aloe vera carbohydrate polymers provide a moist wound environment; vitamin E promotes blood vessel formation; and lidocaine acts as a local anesthetic.
collagenase: Collagenases are enzymes that degrade collagen fibers. These enzymes play an important role in connective tissue metabolism and are produced by specific cells involved in both repair and remodeling processes.
collagenase clostridium histolyticum EN3835: An injectable formulation composed of the enzyme collagenase produced by the bacterium Clostridium histolyticum and containing a fixed ratio of purified class I (AUX-I) and class II (AUX-II) collagenases, with enzymatic debriding activity. Upon injection of collagenase clostridium histolyticum (CCH) EN3835 to the affected area(s), the collagenase hydrolyzes collagen in the collagen triple helix structure resulting in lysis and solubilization of collagen deposits and plaques. This may promote healing and reduce symptoms caused by excessive collagen deposits and accumulation, such as stiffness of the tissue and pain.
colloidal bismuth pectin granules: A granule-based formulation containing colloidal bismuth pectin (CBP), with potential cytoprotective activities. Upon oral administration of the colloidal bismuth, bismuth inhibits peptic activity, increases mucosal secretions of prostaglandins and bicarbonate and acts as a barrier to prevent damage by acids. It also prevents adhesion of Helicobacter (H.) pylori to epithelial cells and can inhibit enzymes secreted by H. pylori. This protects against ulcer formation and may help heal existing ulcers.
colloidal gold-bound tumor necrosis factor: A nanoparticle delivery system for recombinant human tumor necrosis factor (TNF) consisting of recombinant TNF bound to pegylated colloidal gold nanoparticles with potential antineoplastic activity. Upon intravenous administration, colloidal gold-bound recombinant human TNF travels through the bloodstream, avoiding immune detection and uptake by the reticuloendothelial system because of nanoparticle pegylation. Due to their size, the colloidal gold nanoparticles exit the circulatory system only at hyperpermeable tumor neovasculature sites; TNF then binds to and activates tumor cell TNF receptors, which may result in an increase in tumor cell apoptosis and a reduction in tumor cell proliferation. Compared to the administration of unbound TNF, colloidal gold-bound TNF may improve the efficacy and safety of TNF administration by delivering TNF specifically to tumor tissue.
colloidal modified fluid gelatin plasma substitute: A colloidal, isotonic, physiologically balanced, plasma volume substitute containing succinylated gelatine and electrolytes, with potential nephroprotective properties. Upon intravenous administration, colloidal modified fluid gelatin plasma substitute expands the blood volume, restores intravascular volume and increases blood flow, thereby preventing hypovolemia, hypotension and shock and may decrease the accumulation of nephrotoxic agents in the kidneys.
colloidal oatmeal cream: A colloidal oatmeal-based skin cream with potential moisturizing and skin protecting activity. Upon application to the skin, colloidal oatmeal cream forms a protective barrier and thereby prevents water loss, provides moisture to the skin and protects the skin from damage.
colorectal cancer peptide vaccine PolyPEPI1018: A peptide cancer vaccine consisting of a combination of six synthetic polypeptides directed against cancer testis antigens (CTAs) frequently expressed in colorectal cancers, with potential antineoplastic and immunostimulatory activities. Colorectal cancer peptide vaccine PolyPEPI1018 potentially elicits a cytotoxic T-lymphocyte response against colorectal tumors expressing the CTAs associated with the vaccine, which may result in a reduction in tumor cell proliferation.
colorectal tumor-associated peptides vaccine IMA910: A synthetic tumor-associated peptide (TUMAP)-based cancer vaccine directed against colorectal cancer with potential immunostimulatory and antineoplastic activities. Synthetic colorectal tumor-associated peptides vaccine IMA910 contains 13 different synthetic TUMAPs, each of which represents a tumor associated antigen (TAA) specific for colorectal cancer. Upon administration, this agent may elicit a cytotoxic T-lymphocyte (CTL) response against colorectal tumors expressing these TAAs, which may result in a reduction in colorectal tumor cell proliferation.
Colprosterone: (Other name for: therapeutic progesterone)
coltuximab ravtansine: An immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Coltuximab ravtansine targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells.
Columvi: (Other name for: glofitamab-gxbm)
Coly-Mycin: (Other name for: colistimethate sodium)
Coly-Mycin S: (Other name for: colistin sulfate)
Combidex: (Other name for: ferumoxtran-10)
Combotox: (Other name for: deglycosylated ricin A chain-conjugated anti-CD19/anti-CD22 immunotoxins)
combretastatin A1 diphosphate: The diphosphate prodrug of the stilbenoid combretastatin A1, originally isolated from the plant Combretum caffrum, with vascular-disrupting and antineoplastic activities. Upon administration, combretastatin A1 diphosphate (CA1P) is dephosphorylated to the active metabolite combretastatin A1 (CA1), which promotes rapid microtubule depolymerization; endothelial cell mitotic arrest and apoptosis, destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis may ensue. In addition, orthoquinone intermediates, metabolized from combretastatin A1 by oxidative enzymes found to be elevated in some tumor types, may bind to tumor cell thiol-specific antioxidant proteins and DNA, and stimulate oxidative stress by enhancing superoxide/hydrogen peroxide production. CA1 binds to tubulin at the same site as colchicine but with higher affinity.
Cometriq: (Other name for: cabozantinib S-malate)
commensal bacterial strain formulation BMC128: An oral formulation composed of four unique and live commensal bacterial strains that are natural inhabitants of the human intestinal tract, with potential immunostimulating and antineoplastic activities. Upon administration of the commensal bacterial strain formulation BMC128, the bacterial strains may promote intra-tumoral lymphocytic infiltration and increase the population of natural killer (NK) cells, and cytotoxic CD4+ and CD8+ T cells. This may enhance anti-tumor immune response and may eradicate tumor cells.
commensal bacterial strain formulation VE800: An orally bioavailable formulation composed of eleven alive, distinct nonpathogenic, nontoxigenic, human commensal bacterial strains, isolated from healthy human donor feces, with potential immunostimulating and antineoplastic activities. Upon administration of the commensal bacterial strain formulation VE800, the bacterial strains induce an interferon-gamma (IFN-g)-producing CD8-positive T-cell-mediated immune response in the intestines. This may activate an IFN-g-expressing CD8+ T-cell -mediated anti-cancer immune response and may eradicate tumor cells.
Commit: (Other name for: nicotine lozenge)
compound Kushen injection: A traditional Chinese medicine (TCM) formulation composed of compound Kushen injection (CKI) containing aqueous extracts from the roots of Kushen (Radix Sophorae Flavescentis) and Baituling (Rhizoma Smilacis Glabrae), with potential antineoplastic and immunomodulating activities. CKI contains numerous chemicals including alkaloids, such as matrine and oxymatrine, flavonoids, alkylxanthones, quinones, triterpene glycosides, fatty acids, and essential oils. Although the exact mechanism(s) of action through which CKI exerts its effects has yet to be fully elucidated, CKI is able to interfere with the activation of various signal transduction pathways, such as the Wnt/beta-catenin signaling pathway, inhibit nuclear factor-kappa B (NF-κB) activation, and block the activity of multiple receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR). CKI induces apoptosis in and inhibits proliferation, migration, invasion and adhesion of tumor cells. CKI also modulates the production of inflammatory mediators.
compound sodium lactate solution: A multiple electrolyte, isotonic, crystalloid solution for intravenous infusion containing sodium chloride, potassium chloride, calcium chloride dihydrate, and sodium lactate, which can restore the electrolyte balance, normalize pH, and provide water for hydration. Upon intravenous administration, the compound sodium lactate solution will replace any lost body fluids and electrolytes thereby providing hydration as well as normalizing electrolyte concentrations. In addition, conversion of sodium lactate to bicarbonate increases plasma bicarbonate levels, which facilitates the removal of hydrogen ions from the blood stream, raises blood pH and normalizes the acid-base balance.
Comtan: (Other name for: entacapone)
conatumumab: A fully human monoclonal agonist antibody directed against the extracellular domain of human TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptor 2 (TR-2) with potential antineoplastic activity. Conatumumab mimics the activity of native TRAIL, binding to and activating TR-2, thereby activating caspase cascades and inducing tumor cell apoptosis. TR-2 is expressed by a variety of solid tumors and cancers of hematopoietic origin.
conbercept: A recombinant, soluble, vascular endothelial growth factor receptor (VEGFR) protein composed of the second immunoglobulin (Ig) domain of VEGFR-1, the third and fourth Ig domains of VEGFR-2, and the constant region (Fc) of human immunoglobulin G1 (IgG1) with potential anti-angiogenic activities. Upon intravitreal injection, conbercept, functioning as a soluble decoy receptor, binds with high affinity to all VEGF-A isoforms, VEGF-B, as well as placenta growth factor (PlGF)-1 and PlGF-2. This prevents the binding of these growth factors to their endogenous receptors, potentially inhibiting angiogenesis and tumor cell growth.
Concentraid: (Other name for: desmopressin acetate)
concentrated beet crystals: A formulation containing concentrated beetroot crystals, with potential antioxidant and protective activities. Concentrated beetroot crystals contain antioxidants, including betacyanin, which scavenge free radicals, and high levels of nitrates and folic acid. Intake of concentrated beetroot crystals leads to the conversion of nitrate to nitric oxide (NO). This may have a beneficial effect on blood flow and blood pressure through the stimulation of NO-mediated vasodilation. Additionally, this agent may decrease fatigue and increase physical performance.
concentrated fortified collagen protein hydrolysate liquid supplement: A liquid-based nutritional supplement containing enzyme-hydrolyzed concentrated protein derived from collagen, and fortified with L-tryptophan, with potential anti-cachexic and wound-healing activities. The concentrated, fortified, collagen protein hydrolysate liquid supplement contains all essential and non-essential amino acids. Upon oral administration, this supplement may improve both gastric functioning and gastrointestinal (GI) health, thereby reducing vomiting and diarrhea. The hydrolyzed protein helps to alleviate the digestive burden and allows for fast and efficient absorption and utilization of the protein. This may prevent both malnutrition and weight loss.
concentrated lingzhi mushroom extract: A nutritional supplement and traditional Chinese medicine (TCM) composed of a highly concentrated extract of the fruiting body of the red reishi mushroom Ganoderma lucidum (G. lucidum; lingzhi), with potential immunomodulating activities. Upon administration, the concentrated lingzhi mushroom extract may support the body's immune function and may support the immune system to eliminate tumor cells. The lingzhi mushroom extract contains high amounts of G. lucidum polysaccharides and G. lucidum triterpenoids (GLTs).
Concerta: (Other name for: methylphenidate hydrochloride)
conditionally replicative adenovirus 5/3-delta24: A replication competent, oncolytic adenovirus serotype 5 (Ad5) with its knob domain of fiber protein substituted by that of the serotype 3 (Ad5/3-delta24), with potential oncolytic activity. Upon administration, oncolytic adenovirus Ad5/3-delta24 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. 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 replacement of the Ad5 fiber knob, which mediates viral-cell receptor binding, allows for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells; CAR expression is often deficient on cancer cells.
conditionally-activated anti-EpCAM antibody-drug conjugate CX-2051: An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epithelial cell adhesion molecule (Ep-CAM; EpCAM; CD326), linked to a proprietary masking peptide through a protease-cleavable linker, and conjugated to a derivative of camptothecin, with potential antineoplastic activity. Upon administration of conditionally-activated anti-EpCAM ADC CX-2051, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment (TME), the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the TME, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables the binding of the unmasked, fully active anti-EpCAM antibody moiety of CX-2051 to EpCAM-expressing tumor cells. Upon binding and internalization, the camptothecin derivative is released. The camptothecin derivative inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of EpCAM-expressing tumor cells. EpCAM, a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells.
conjugated estrogens: Purified orally bioavailable female sex hormones isolated from pregnant mare urine or synthetically derived from plant materials and primarily conjugated as sulfate esters. Estrogen binds to and activates specific nuclear receptors, which, in turn, bind to estrogen response elements (EREs) in target genes, resulting in histone acetylation, alteration of chromatin conformation, and initiation of transcription.
conjugated estrogens/bazedoxifene: A combination preparation of conjugated estrogens and the selective estrogen receptor modulator (SERM) bazedoxifene that can be used for hormone replacement purposes. The conjugated estrogens increase the diminishing levels of estrogen in menopausal and postmenopausal women by binding to and activating estrogen receptors (ERs), which, in turn, bind to estrogen response elements (EREs) in target genes; this results in the transcription of estrogen-regulated genes. Maintaining adequate estrogen levels decreases symptoms such as hot flashes, night sweats, irregular menstruation, fat redistribution, mood swings, sleep disorders, vaginal dryness and osteoporosis. Bazedoxifene specifically binds to and activates ERs in certain tissues, including liver, bone, breast, and endometrium, and also promotes the transcription of estrogen-regulated genes in these tissues. However, bazedoxifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the proliferative effects of estrogen-binding to ER-positive cells in these tissues.
conjugated linoleic acid: A slightly altered form of linoleic acid, which is an omega-6 fatty acid important to human health. It is found in beef and dairy fats.
Constant-T: (Other name for: theophylline)
contrast agent CS-1000: An aqueous colloidal nanoemulsion containing perfluorocarbon (PFC) polymers that can be used as a tracer for cell tracking purposes during fluorine-19 (19F) magnetic resonance imaging (MRI). Upon administration of the contrast agent CS-1000 to cells ex vivo, this agent freely enters the cells. Upon introduction of these cells into the patient and subsequent 19F MRI, the amount of fluorine can be detected and cellular persistence, survival and distribution of the treated cells can be assessed. The emulsion allows for fast entry of the fluorinated polymers into cells; the polymers do not degrade and remain in the cells.
Contrave: (Other name for: naltrexone hydrochloride/bupropion hydrochloride)
contusugene ladenovec: A replication-defective adenoviral-CMV vector that encodes a wild-type p53 gene. Contusugene ladenovec induces tumor cells that have been transfected with the vector to produce wild-type p53, a tumor suppressor gene that is deleted or mutated in a significant number of cancers. In transfected tumor cells, the wild-type p-53 gene product exerts an antitumor effect by blocking cell cycle progression at the G1/S regulation point, activating DNA repair proteins in the presence of DNA damage, and initiating apoptosis when DNA damage is irreparable.
convalescent plasma: Plasma derived from patients who have recovered from an illness.
ConvitVax: (Other name for: autologous tumor cells/bacillus Calmette-Guérin/formalin-based vaccine)
copanlisib: A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Copanlisib inhibits the activation of the PI3K signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
copanlisib hydrochloride: The dihydrochloride salt form of copanlisib, a phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Copanlisib inhibits the activation of the PI3K signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
Coparvax: (Other name for: attenuated corynebacterium parvum)
COPDAC regimen: A chemotherapy regimen consisting of cyclophosphamide, vincristine sulfate, prednisone and dacarbazine used for the treatment of male children with classical Hodgkin lymphoma (HL).
Copegus: (Other name for: ribavirin)
Copiktra: (Other name for: duvelisib)
copovithane: A synthetic polymer (copolymer of 1,3-bis(methylaminocarboxyl)-2-methylenepropanecarbamate and N-vinyl pyrrolidone) of low molecular weight which acts as a nonspecific immune modulator and has been shown to have significant antitumor activity in vitro and in vivo in preclinical and some early clinical studies. The mechanism of action is unknown. Immunologic evaluation revealed some improvement in helper and suppressor T cell ratio, in vitro cytotoxicity tests, and lymphocyte blastogenic response. (NCI)
COPP regimen: A regimen that is a derivative of the original MOPP regimen consisting of cyclophosphamide, vincristine, procarbazine and prednisone used as an initial treatment for Hodgkin lymphoma. Also used for the treatment of non-Hodgkin lymphoma.
COPP-ABV regimen: A regimen consisting of cyclophosphamide, vincristine, prednisone and procarbazine (COPP) alternating with doxorubicin, bleomycin and vinblastine (ABV), used in combination with radiation therapy for the treatment of low-risk, childhood Hodgkin's lymphoma.
copper: An element with atomic symbol Cu, atomic number 29, and atomic weight 63.
copper 64 Cu-labeled macrophage-targeted nanoparticle: A radioconjugate composed of macrophage-targeted polyglucose nanoparticle, labeled with the radioisotope copper Cu 64, with potential use as a tracer for macrophages including tumor-associated macrophages (TAMs) during positron emission tomography (PET). Upon administration of copper Cu 64-labeled macrophage-targeted nanoparticle, the macrophage-targeted nanoparticle is taken up by macrophages, including TAMs in the tumor microenvironment (TME). Upon PET imaging, the macrophages can be detected. The accumulation of macrophages is present in various inflammatory diseases and tumors.
copper chloride formulation: A formulation containing the compound copper chloride (CuCl2), that can potentially be used to enhance Cu levels in cancer cells in order to elevate the antitumor activity of chemotherapeutic agents that are dependent on Cu for their activity. Upon intravenous administration of CuCl2, the mineral Cu is selectively taken up by and accumulates in cancer cells. In the presence of certain chemotherapeutic agents whose mechanism of action (MoA) is dependent on Cu, this formulation may enhance their cytotoxic activity.
copper Cu 61-ATSM: A lipophilic copper(II)bis(thiosemicarbazone) labeled with the positron-emitting isotope (61)Cu with hypoxia-selective and radioisotopic activities. With a high membrane permeability and redox potential, (61)Cu-ATSM easily enters and selectively resides in hypoxic cells. The extent of (61)Cu-ATSM retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia with positron emission tomography (PET).
copper Cu 62 ethylglyoxal bis(thiosemicarbazone): A radiopharmaceutical composed of the nonspecific perfusion agent ethylglyoxal bis(thiosemicarbazone) (ETS) linked to the beta-emitting, radioisotope copper Cu 62, with potential tumor imaging activity upon positron emitting tomography (PET). Upon injection, copper Cu 62-ETS distributes to various organs, especially the kidneys and the myocardium. Upon PET imaging, tumor blood flow can be visualized and the efficacy of antineoplastic and anti-angiogenic chemotherapeutics can be assessed. Cu62-ETS has a short half life of 9.74 minutes. ETS has an enhanced hyperemic response compared to other perfusion agents.
copper Cu 62-ATSM: A radioconjugate consisting of a lipophilic, neutral, bioreductive copper-bis(thiosemicarbazone) complex, copper-diacetyl-bis(N4-methylthiosemicarbazone) (Cu-ATSM), labeled with the beta-emitting radioisotope copper Cu 62, with hypoxia-selective and positron emitting tomography (PET) radioimaging activities. With a high membrane permeability and low reduction potential, copper Cu 62-ATSM easily enters cells. This agent can only be reduced by mitochondria found in hypoxic cells with abnormally high electron concentrations. This chemical reaction traps Cu 62-ATSM in the cell, which allows for the selective accumulation of this agent in hypoxic cells compared to normoxic cells. The extent of copper Cu 62-ATSM retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia with PET. This provides information about diagnosis, prognosis, treatment options and outcomes for certain cancers. The short half-life of copper Cu 62 (9.7 minutes) reduces the amount of radiation a patient is subjected to and allows for several imaging studies to be performed. Hypoxic tumors are associated with increased malignancy and resistance to radiation and chemotherapy.
copper Cu 62-PTSM: A radioconjugate consisting of a lipophilic, bioreductive copper(II)bis(thiosemicarbazone) complex, copper-pyruvaldehyde-bis(N4-methylthiosemicarbazone) (Cu-PTSM), linked to the beta-emitting, radioisotope copper Cu 62, with potential perfusion and positron emitting tomography (PET) tumor imaging activities. Upon injection, the distribution of copper Cu 62-PTSM correlates with blood flow. This agent’s high membrane permeability allows for rapid diffusion into cells. Once it enters the cell, 62Cu-PTSM is then reduced by the mitochondria, which prevents diffusion of the agent out of the cell. Upon PET imaging, tumor blood flow can be visualized and tumor perfusion can be assessed. Compared with other copper radionuclides, the short half-life of copper Cu 62 (9.7 minutes) reduces the amount of radiation a patient is subjected to and allows for several imaging studies to be performed. PTSM lacks selectivity for hypoxic cells.
copper Cu 64 anti-CEA monoclonal antibody M5A: A radioimmunoconjugate consisting of a humanized monoclonal antibody directed against the human carcinoembryonic antigen, carcinoembryonic antigen-related cell adhesion molecule 5 (CEA or CEACAM5), which is conjugated with the radioisotope copper Cu 64 via the chelator tetra-azacyclododecanetetra-acetic acid (DOTA), with potential use as an imaging agent during positron emission tomography (PET). Upon administration, the antibody moiety of copper Cu 64 anti-CEA monoclonal antibody M5A specifically binds to cells expressing CEA. Upon binding, the radioisotope moiety can be detected using PET, thereby allowing the imaging and quantification of CEA-expressing tumor cells. CEA, a tumor associated antigen and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion, and cell adhesion and is overexpressed by a variety of cancer types.
copper Cu 64 DOTA-daratumumab: A radioimmunoconjugate containing daratumumab, a human immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against the cell surface glycoprotein CD38, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging. The monoclonal antibody moiety of copper Cu 64-DOTA-daratumumab specifically targets and binds to cell surface antigen CD38. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CD38-expressing tumor cells. CD38, a cell surface glycoprotein, is expressed on various hematopoietic cells and is overexpressed on multiple myeloma (MM) cells.
copper Cu 64 dotatate: A radioconjugate consisting of the somatostatin analog tyrosine-3-octreotate (Tyr3-octreotate or TATE) labeled, via the macrocyclic chelating agent 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra-acetic acid (DOTA), with the positron emission tomography (PET) tracer copper Cu 64, which may be used to image somatostatin receptor (SSTR)-expressing neuroendocrine tumors (NETs) upon PET. Upon administration of copper Cu 64 Dotatate, the TATE moiety targets and binds to SSTRs, with a much higher affinity for type 2 SSTR, present on the cell membranes of many types of NETs. This allows for visualization of SSTR-positive tumor cells upon PET. SSTR subtypes have been shown to be present in large numbers on NETs and their metastases, while most other normal tissues express low levels of SSTR subtypes.
copper Cu 64 EB-ss-CPT: A radioconjugate composed of the amphiphilic camptothecin (CPT) prodrug EB-ss-CPT, labeled with the radioisotope copper Cu 64, with potential use as a tracer for tumor cells during positron emission tomography (PET). EB-ss-CPT is composed of CPT conjugated, via a redox-responsive disulfide linker, to an albumin-binding Evans blue (EB) derivative. Upon administration of copper Cu 64 EB-ss-CPT, the EB-ss-CPT moiety binds to endogenous albumin and the resulting albumin-bound nanocomplex accumulates in tumor cells. This allows the detection and visualization of tumor cells upon PET imaging.
copper Cu 64 FAP-2286: A radioconjugate composed of FAP-2286, a fibroblast activation protein (FAP)-targeted peptide, labeled with the radioisotope copper Cu 64, with potential use as a tracer for FAP-expressing cells during positron emission tomography (PET). Upon administration of copper Cu 64 FAP-2286, the FAP-2286 moiety targets and binds to FAP-expressing cancer-associated fibroblasts (CAFs) and FAP-expressing tumor cells. Upon binding, FAP-expressing cells can be detected during PET imaging. FAP, a cell surface protein, is overexpressed on CAFs in the tumor microenvironment (TME) and certain tumor cells.
copper Cu 64 FBP8: A radioconjugate consisting of fibrin binding probe 8 (FBP8), a fibrin-targeting cyclic peptide, labeled with the radioisotope copper Cu 64, which may be used to image fibrin upon positron emission tomography (PET)/magnetic resonance (MR) imaging. Upon administration of copper Cu 64 FBP8, the FBP8 moiety selectively targets and binds to fibrin. This allows for visualization of fibrin-containing thrombus and emboli upon PET/MR imaging and may help in the diagnosis of arterial thrombosis, deep vein thrombosis (DVT) and pulmonary embolism (PE).
copper Cu 64 GRIP B: A radioconjugate composed of granzyme targeting restricted interaction peptide specific to family member B (GRIP B), a nontoxic antimicrobial peptide (AMP), labeled with the radioisotope copper Cu 64 linked to a peptide masking domain via a granzyme B (GZMB) cleavage site, with potential use as a tracer for GZMB activity during positron emission tomography (PET). Upon administration of copper Cu 64 GRIP B and its cleavage by GZMB, the radiolabeled AMP is released, adopts its preferred helical conformation, and binds to nearby phospholipid bilayers such as the plasma membrane of tumor cells. This allows the detection and visualization of GZMB activity upon PET imaging. GZMB, a pro-apoptotic serine protease, is released by cytotoxic lymphocytes and plays an important role in cytotoxicity against virus-infected and tumor cells.
copper Cu 64 LNTH-1363S: A radioconjugate composed of LNTH-1363S, a fibroblast activation protein (FAP) binding ligand and inhibitor (FAPi) chelated to the radionuclide copper Cu 64, and an albumin-binding moiety, with potential use as a tracer for FAP-expressing cancer-associated fibroblasts (CAFs) during positron emission tomography/computed tomography (PET/CT). Upon administration of copper Cu 64 LNTH-1363S, the LNTH-1363S moiety selectively targets and binds to FAP-expressing CAFs. Upon binding, FAP-expressing cells can be detected and LNTH-1363S binding can be assessed during PET/CT imaging. FAP, a membrane-bound dipeptidyl peptidase, is overexpressed on CAFs in the tumor microenvironment (TME) and activated fibroblasts in tissues undergoing extracellular matrix remodeling due to chronic inflammation, fibrosis or wound healing. Its expression is low in normal tissues.
copper Cu 64 NODAGA-TTX-MC138: A radioconjugate comprised of the microRNA-10b (miR-10b)-inhibitor TTX-MC138, which consists of an anti-miR10b antagomir conjugated to ultrasmall iron oxide nanoparticles, chelated with 1,4,7-triazacyclononane,1-glutaric acid-4,7 acetic acid (NODAGA) and radiolabeled with the radiotracer copper Cu 64, that may be used as an imaging agent for miR-10b-overexpressing tumor cells upon positron emission tomography (PET)-magnetic resonance imaging (PET-MRI). Upon administration of copper Cu 64 NODAGA- TTX-MC138, the TTX-MC138 moiety targets and binds to miR-10b inside tumor cells. This allows for visualization of miR-10b-overexpressing tumor cells upon imaging with PET-MRI. miR-10b, a mRNA that is highly expressed in a variety of metastatic tumor cells, plays a key role in tumor cell migration, invasion and metastasis.
copper Cu 64 NOTA-PSMAi-PEG-Cy5.5-C' dots: An imaging agent composed of silica-based nanoparticles labeled with a near-infrared (NIR) fluorophore, cyanine 5.5 (Cy5.5), and surrounded by polyethylene glycol (PEG) chains attached to a human prostate-specific membrane antigen (PSMA) inhibitor (PSMAi) and labeled with, via the macrocyclic chelating agent 1,4,7-triazacyclononane-N,N',N''-triacetic acid (NOTA), the radioisotope copper Cu 64, with potential tumor-selective diagnostic properties upon positron emission tomography (PET) imaging. Upon administration of the copper Cu 64 NOTA-PSMAi-PEG-Cy5.5-C' dots, the PSMAi moiety selectively targets and binds to PSMA expressed on tumor cells. Upon PET imaging, PSMA-expressing tumor cells can be visualized and assessed. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells. The nanoparticle formulation may allow for enhanced uptake in PSMA-positive tumors.
copper Cu 64 plerixafor: A radioconjugate labeled with the positron-emitting radioisotope, copper Cu 64, and also composed of plerixafor, a bicyclam and hematopoietic stem cell-mobilizing agent that targets the chemokine receptor CXCR4, with tumor imaging potential using positron emission tomography (PET)/computed tomography (CT). Upon administration, the plerixafor moiety blocks the binding of stromal cell-derived factor-1alpha (SDF-1alpha or CXCL12) to the cellular receptor CXCR4. In turn, the CXCR4-expressing tumor cells can be visualized using PET/CT and the resulting images could be used to predict a tumor's response to certain treatments. The expression of CXCR4 on cancer cells has been correlated with increased tumor cell survival, tumor progression, and increased metastatic potential.
copper Cu 64 SAR-bisPSMA: A radioconjugate composed of two human prostate-specific membrane antigen (PSMA) binding motifs linked to a SAR chelator and labeled with the positron emission tomography (PET) tracer copper Cu 64, with potential use as a tracer for PSMA-expressing tumors during positron emission tomography (PET)/computed tomography (CT). Upon administration of copper Cu 64 SAR-bisPSMA, the PSMA binding motifs target and bind to PSMA-expressing tumor cells. Upon binding, PSMA-expressing tumor cells can be detected during PET/CT imaging. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells.
copper Cu 64 SAR-bombesin: A radioconjugate containing bombesin (BBN), a tetra-decapeptide that binds with high affinity to the gastrin-releasing peptide receptor (GRPR), and linked, by the sarcophagine chelator (SAR), to the radionuclide copper Cu 64, with potential use in diagnostic imaging using positron emission tomography/computed tomography (PET/CT). Upon administration of copper Cu 64 SAR-BBN, the BBN moiety targets and binds to GRPR. Upon PET/CT, GRPR-expressing tumor cells can be visualized. GRPR, also called bombesin receptor 2 (BB2), is a seven-transmembrane G protein-coupled receptor belonging to the bombesin receptor family. It is overexpressed in certain types of cancers.
copper Cu 64 TP3805: A peptide analog of pituitary adenylate cyclase-activating peptide (PACAP) radiolabeled with the positron-emitting radioisotope copper Cu 64, with potential diagnostic ability upon positron emission tomography (PET) imaging. The peptide moiety of copper Cu 64 TP3805 is able to bind to vasoactive intestinal peptide/pituitary adenylate cyclase activating peptide receptors 1 (VPAC1). Upon PET imaging, the cancer cells expressing VPAC1 can be visualized and this may allow for early detection. The oncogenic product VPAC1 is overexpressed in a variety of cancer cell types, moreover, it is overexpressed in 100% of breast tumors at the onset of the cancer. Compared to other positron-emitting radioisotopes, Cu 64 has a longer half life.
copper Cu 64 trastuzumab: A diagnostic radioimmunoconjugate comprised of the recombinant humanized monoclonal antibody trastuzumab conjugated with the positron-emitting radioisotope copper Cu 64. Copper Cu 64 trastuzumab binds to the extracellular domain of human epidermal growth factor receptor 2 (HER2), allowing the detection of HER2 distribution using positron emission tomography (PET).
copper Cu 64 ucasareotide dasaroxetan: A radioconjugate consisting of the tyrosine-containing somatostatin analog Tyr3-octreotate (TATE) conjugated with the bifunctional chelator 5-(8-methyl-3,6,10,13,16,19-hexaaza-bicyclo[6.6.6]icosan-1-ylamino)-5-oxopentanoic acid (MeCOSar) and labeled with the positron emission tomography (PET) tracer copper Cu 64, which may be used to image somatostatin receptor (SSTR)-expressing neuroendocrine tumors (NETs) upon PET. Upon administration of copper Cu 64 ucasareotide dasaroxetan, the TATE moiety targets and binds to SSTRs, with high affinity for type 2 SSTR, present on the cell membranes of many types of NETs. This allows for visualization of SSTR-positive tumor cells upon PET. TATE is an octreotide derivative in which phenylalanine at position 3 is substituted by tyrosine and position 8 threoninol is replaced with threonine. SSTRs have been shown to be present in large numbers on NETs and their metastases, while most other normal tissues express low levels of SSTRs.
copper Cu 64-ATSM: A radioconjugate consisting of a lipophilic copper(II)bis(thiosemicarbazone) labeled with the positron- and beta-emitting isotope (64)Cu with hypoxia-selective and antineoplastic activities. With a high membrane permeability and redox potential, copper Cu 64-ATSM is preferentially taken up by hypoxic cells compared to normoxic cells; the extent of retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia by positron emission tomography (PET). In addition, the radioactive copper moiety of this agent may deliver a selective cytotoxic dose of beta radiation to hypoxic tumor cells.
copper Cu 64-CB-TE1A1P-PEG4-LLP2A: A radioconjugate containing LLP2A, a high-affinity peptidomimetic ligand for the tumor-associated antigen (TAA) very-late-antigen-4 (VLA-4; VLA 4; alpha4beta1 integrin; CD49d/CD29), conjugated, via the chelator 1,4,8,11-tetraazacyclotetradecane-1-(methane phosphonic acid)-8-(methane carboxylic acid) (CB-TE1A1P), to the radioisotope copper Cu 64, and conjugated to polyethylene glycol (PEG) chains that can potentially be used as a diagnostic imaging agent of VLA-4-expressing tumor cells using positron-emitting tomography (PET). Upon administration, copper Cu 64-CB-TE1A1P-PEG4-LLP2A targets, binds to and is taken up by VLA-4-expressing tumor cells. Upon PET, the VLA-4-expressing tumor cells can be visualized, and the tumor can be assessed. VLA-4, a transmembrane adhesion receptor overexpressed and activated on various tumor cell types and surrounding stroma, plays an important role in tumor growth, angiogenesis, metastasis, drug resistance and immune responses. Pegylation optimizes the pharmacokinetic profile of 64Cu-LLP2A.
copper Cu 64-DOTA B-Fab: A radioimmunoconjugate containing a bivalent monospecific tandem immunoglobulin fragment (B-Fab) derived from the humanized monoclonal antibody DS6 targeting the tumor-associated mucin-1 (MUC1)-sialoglycotope CA6 conjugated with the bifunctional, macrocyclic chelating agent 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with potential use as an imaging agent for CA6-expressing tumors using positron emission tomography (PET). The B-Fab moiety of copper Cu 64-DOTA B-Fab binds, with high affinity, to the cell surface antigen CA6. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CA6-expressing tumor cells. This tracer could be used to select patients who could benefit from and to monitor efficacy of CA6-targeted anti-cancer therapies. Compared to DS6, the antibody fragment allows for increased tumor penetration, faster blood clearance, and more rapid renal elimination. The CA6 epitope is found on a variety of solid tumors.
copper Cu 64-DOTA-AE105: A radiotracer composed of AE105, a urokinase-type plasminogen activator receptor (uPAR) peptide antagonist, conjugated with DOTA and labeled with the radionuclide copper Cu 64, with potential imaging activity upon positron emission tomography (PET). Upon administration, the AE105 moiety of copper Cu 64-DOTA-AE105 targets and binds to uPAR-expressing tumor cells. Upon PET imaging, the copper Cu 64 moiety can be visualized, uPAR-expressing tumor cells can be quantified and the degree of tumor aggressiveness can be assessed. uPAR expression is correlated with increased tumor invasiveness and aggressiveness as well as a poor prognosis.
copper Cu 64-DOTA-anti-HER3 monoclonal antibody U3-1287: A radioimmunoconjugate of the fully human monoclonal antibody against the third member of the epidermal growth factor receptor (EGFR), HER3 or ERBB3, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging and antineoplastic activity. The antibody moiety of copper Cu 64-DOTA-anti-HER3 monoclonal antibody U3-1287 binds to and blocks the activation of HER3, thereby resulting in the inhibition of EGFR-dependent PI3K/AKT signaling and the subsequent inhibition of cellular proliferation and differentiation. The Cu 64 moiety may be detected using positron emission tomography (PET), thereby allowing the imaging and quantification of HER3-expressing tumor cells. HER3, which lacks the kinase domain conveying ligand-binding signaling by forming heterodimers with other EGFR members that have kinase activity, is frequently overexpressed in solid tumors.
copper Cu 64-DOTA-ECL1i: A radiotracer composed of ECL1i (extracellular loop 1 inverso; d(LGTFLKC)), an allosteric peptidic modulator of CC chemokine receptor type 2 (CCR2), conjugated with 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radionuclide copper Cu 64, with potential imaging activity upon positron emission tomography (PET). Upon administration, the ECL1i moiety targets and allosterically binds to CCR2 expressing tumor cells. Upon PET imaging, the copper Cu 64 moiety can be visualized, thereby allowing the quantification of CCR2-expressing cells. CCR2, a G-protein coupled receptor expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays a significant role in angiogenesis, inflammation, tumor cell migration, and proliferation. Quantification of CCR2 may help predict chemotherapy resistance and identify early metastatic disease in certain cancers.
copper Cu 64-DOTA-pembrolizumab: A radioimmunoconjugate composed of pembrolizumab, a humanized monoclonal immunoglobulin (Ig) G4 antibody directed against the human cell surface receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed cell death-1), conjugated with the bifunctional, macrocyclic chelating agent 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging. Upon administration, the monoclonal antibody moiety of copper Cu 64-DOTA-pembrolizumab specifically binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands. Upon PET imaging, PD-1-expressing T cells, as well as pembrolizumab biodistribution, can be visualized and the expected response to treatment with pembrolizumab, as well as selection of patients that would respond to pembrolizumab, can be assessed. The ligands for PD-1 include programmed cell death-1 ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death-1 ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.
copper Cu 64-DOTA-rituximab: A radioimmunoconjugate containing rituximab, a recombinant chimeric murine/human antibody directed against the human CD20 antigen, conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with potential diagnostic properties upon positron emission tomography (PET) imaging. The monoclonal antibody moiety of copper Cu 64-DOTA-Rituximab specifically binds to cell surface antigen CD20. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of CD20-expressing tumor cells. CD20 is a non-glycosylated phosphoprotein that is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.
copper Cu 64-DOTA-TLX592: A radioimmunoconjugate containing an engineered monoclonal antibody targeting the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA), conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), and labeled with the radioisotope copper Cu 64, with potential diagnostic properties upon positron emission tomography (PET) imaging. Upon administration of copper Cu 64-DOTA-TLX592, the monoclonal antibody moiety TLX592 targets and specifically binds to PSMA on tumor cells. Upon binding, the radioisotope moiety may be detected using PET, thereby allowing the imaging and quantification of PSMA-expressing tumor cells and the biodistribution of TLX592. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.
copper Cu 64-DOTA-trastuzumab: A radioimmunoconjugate containing the recombinant humanized monoclonal antibody trastuzumab conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64 with radioisotopic activity and potential use as an imaging agent. The trastuzumab moiety of copper Cu 64-DOTA-trastuzumab binds with high affinity to the extracellular domain of human epidermal growth factor receptor 2 (HER2). Upon binding, the radioisotope moiety may be detected using positron emission tomography (PET), thereby allowing the imaging and quantification of HER2-expressing tumor cells. HER2, a tyrosine kinase and client protein of heat shock protein 90 (Hsp90), may be overexpressed on the cell surfaces of various tumor cell types.
copper Cu 64-GRIP B: An imagining agent composed of granzyme targeted restricted interaction peptide (RIP) specific to family member B (GRIP B) and radiolabeled with the radioisotope copper Cu 64, that can potentially be used to detect granzyme B (GZMB) activity upon positron emission tomography (PET). RIP consists of three domains, including a) Temporin L, an antimicrobial peptide (AMP) and membrane binding domain that is coupled to copper-64, b) a specific GZMB substrate and endoprotease cleavage binding domain, and c) a peptide masking domain that prevents the AMP from adopting its preferred helical conformation. Upon administration of copper Cu 64-GRIP B, the protease cleavage binding domain of RIP is specifically cleaved by extracellular GZMB, and upon cleavage, the AMP changes conformation and the radiolabeled activated AMP targets and irreversibly binds to adjacent phospholipid bilayers within any nearby membranes, thereby sequestering the radioisotope to nearby tumor cells. Upon PET, tissue biodistribution of the radioisotope can be assessed and the accumulated radioisotope in tissues reflects the proteolytic activity of secreted GZMB. GZMB secretion and activity is correlated with immune cell activation and can be enhanced by certain immune checkpoint inhibitors.
copper Cu 64-PSMA-I&T: A radioconjugate composed of PSMA-I&T, a human prostate-specific membrane antigen (PSMA)-targeting ligand linked to the bifunctional, macrocyclic chelating agent 1,4,7,10-tetraazacyclododecane-1-(glutamic acid)-4,7,10-triacetic acid (DOTAGA; DOTA-GA), labeled with the positron emission tomography (PET) tracer copper Cu 64, with potential use as a tracer for PSMA-expressing tumors during positron emission tomography (PET)/computed tomography (CT). Upon administration of copper Cu 64-PSMA-I&T, PSMA-I&T targets and binds to PSMA-expressing tumor cells. Upon binding, PSMA-expressing tumor cells can be detected during PET/CT imaging. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.
copper Cu 64-Tz-SarAr: A radioconjugate composed of a tetrazine-based molecule linked to a SarAr chelator and labeled with the radionuclide copper Cu 64, with potential use as a tracer during positron emission tomography (PET). Upon administration, copper Cu 64-Tz-SarAr binds to the trans-cyclooctene (TCO) moiety of a pre-administered TCO-bearing immunoconjugate, which is bound to an antigen of interest via an antibody moiety. The immunoconjugate localizes the radionuclide to and allows the imaging of target cells expressing the antigen of interest upon PET.
copper Cu 67 SAR-bisPSMA: A radioconjugate composed of two human prostate-specific membrane antigen (PSMA)-binding motifs linked to a sarcophagine (SAR)-based chelator and radiolabeled with the beta-emitting radioisotope copper Cu 67, with potential antineoplastic activity. Upon administration of copper Cu 67 SAR-bisPSMA, the PSMA-binding motifs target and bind to PSMA-expressing tumor cells, thereby delivering a cytotoxic dose of beta radiation to PSMA-expressing tumor cells. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells as well as a variety of other solid tumors.
copper Cu 67 SAR-bombesin: A radioconjugate composed of bombesin (BBN), a tetra-decapeptide that binds with high affinity to the gastrin-releasing peptide receptor (GRPR), linked by the sarcophagine chelator (SAR) and radiolabeled with the beta-emitting radioisotope copper Cu 67, with potential antineoplastic activity. Upon administration of copper Cu 67 SAR-BBN, the BBN moiety targets and binds to GRPR, thereby delivering a cytotoxic dose of beta radiation to GRPR-expressing tumor cells. GRPR, also called bombesin receptor 2 (BB2), is a seven-transmembrane G protein-coupled receptor belonging to the bombesin receptor family. It is overexpressed in certain types of cancers.
copper Cu 67 ucasareotide dasaroxetan: A radioconjugate consisting of the tyrosine-containing somatostatin analog Tyr3-octreotate (TATE) conjugated with the bifunctional chelator 5-(8-methyl-3,6,10,13,16,19-hexaaza-bicyclo[6.6.6]icosan-1-ylamino)-5-oxopentanoic acid (MeCOSar) and radiolabeled with the beta-emitting radioisotope copper Cu 67, with potential antineoplastic activity. Upon administration, copper Cu 67 ucasareotide dasaroxetan binds to somatostatin receptors (SSTRs), with high affinity to type 2 SSTR, present on the cell membranes of many types of neuroendocrine tumor (NET) cells. Upon binding and internalization, this radioconjugate specifically delivers a cytotoxic dose of beta radiation to SSTR-positive cells. TATE is an octreotide derivative in which phenylalanine at position 3 is substituted by tyrosine and position 8 threoninol is replaced with threonine. SSTRs have been shown to be present in large numbers on NET and their metastases, while most other normal tissues express low levels of SSTRs.
copper Cu-64-DOTA-alendronate: A radioconjugate containing the biphosphonate alendronate conjugated with the bifunctional, macrocyclic chelating agent 1,4,7,10-tetra-azacyclododecane-1,4,7,10-tetra-acetic acid (DOTA) and labeled with the radioisotope copper Cu 64, with potential use as an imaging agent for microcalcifications in mammary tumors using positron emission tomography (PET). Upon administration of the copper Cu-64 alendronate, the alendronate moiety targets and binds to hydroxyapatite crystals found in malignant tumors. Upon binding and PET imaging, the radioisotope moiety is detected, thereby allowing differentiation between malignant tumors, benign tumors and normal tissue, as the highest uptake of 64Cu-DOTA-alendronate occurs in malignant tumors while the lowest uptake occurs in benign tumors and normal mammary tissue.
copper gluconate: The orally bioavailable copper salt of D-gluconic acid. In addition to its roles as an enzyme cofactor for cytochrome C oxidase and superoxide dismutase, copper forms complexes with the thiocarbamate disulfiram (DSF) forming DSF-copper complexes, which enhances the DSF-mediated inhibition of the 26S proteasome; proteasome inhibition may result in inhibition of cellular protein degradation, cessation of cell cycle progression, inhibition of cellular proliferation, and the induction of apoptosis in susceptible tumor cell populations.
cord blood-derived CAR T cells: A preparation of umbilical cord blood (CB)-derived T lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) that targets an as of yet unidentified tumor-associated antigen (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration of the cord blood derived CAR T cells, the T cells target, bind to and induce selective cytotoxicity in tumor cells expressing the TAA.
cord blood-derived CMV/AdV/EBV/BKV-specific cytotoxic T lymphocytes: A population of allogeneic expanded cord blood (CB)-derived cytotoxic T lymphocytes (CTLs) that are specifically reactive to cytomegalovirus (CMV), Epstein-Barr virus (EBV), adenovirus (AdV), and human polyomavirus type I (BKV), with potential antiviral activity. Infusion of the CB-derived CMV/AdV /EBV/BKV-specific CTLs into CB hematopoietic stem cell transplant (HSCT) recipients may provide virus-specific cellular immunity, thereby preventing the infection or reactivation of certain viral-associated diseases.
cord blood-derived expanded allogeneic natural killer cells: A preparation of human umbilical cord blood (UCB)-derived and ex vivo-expanded allogeneic natural killer (NK) cells, with immunomodulating and cytotoxic activities. Upon infusion of the cord blood-derived expanded allogeneic NK cells, these cells recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which cause cancer cell lysis.
cord blood-derived expanded natural killer cells PNK-007: A population of allogeneic lytic natural killer (NK) cells derived from human umbilical cord blood (UCB), with potential cytotoxic activity. Hematopoietic stem cells (HSC) are isolated from human UCB; this is followed by ex vivo differentiation into mature, highly lytic, NK cells, and expansion. Upon administration, the CB-derived expanded NK cells PNK-007 may lyse cancer cells.
Cordarone: (Other name for: amiodarone hydrochloride)
cordycepin: A purine nucleoside antimetabolite and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic, antioxidant, and anti-inflammatory activities. Cordycepin is an inhibitor of polyadenylation, activates AMP-activated protein kinase (AMPK) and reduces mammalian target of rapamycin (mTOR) signaling, which may result in both the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase belonging to the phosphatidylinositol 3-kinase (PI3K)-related kinase (PIKK) family, plays an important role in the PI3K/AKT/mTOR signaling pathway that regulates cell growth and proliferation, and its expression or activity is frequently dysregulated in human cancers.
Coreg: (Other name for: carvedilol)
Coreg CR: (Other name for: carvedilol phosphate extended-release capsule)
CoREST inhibitor TNG260: An orally bioavailable small molecule inhibitor of the histone deacetylase 1 (HDAC1)-containing co-repressor of repressor element-1 silencing transcription (CoREST) complex, with potential immunomodulating activity. Upon oral administration, CoREST inhibitor TNG260 binds to CoREST complex and inhibits the catalytic activity of HDAC1, which results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This may reverse immune evasion and resistance to immune checkpoint inhibitors caused by serine-threonine kinase 11 (STK11) mutations. Loss-of-function mutations in STK11 is associated with immune checkpoint inhibitor resistance.
Corgard: (Other name for: nadolol)
Coriolus versicolor extract: An extract derived from the mushroom Coriolus versicolor, containing polysaccharide K (PSK) and polysaccharide-peptide (PSP), with potential immunomodulating and antineoplastic activities. Coriolus versicolor extract has been shown to stimulate the production of lymphocytes and cytokines, such as interferons and interleukins, and may exhibit antioxidant activities. However, the precise mechanism of action(s) of this agent is unknown.
Coriolus versicolor-based vaginal gel: A vaginal gel consisting of hyaluronic acid niosomes, beta-glucan niosomes, alpha-oligoglycan, Coriolus versicolor, Azadirachta indica extract, Centella asiatica and Aloe vera, with protective and repairing activities. Upon vaginal administration, the Coriolus versicolor-based vaginal gel may repair and improve re-epithelization of the cervical-vaginal mucosa with lesions that were caused by human papillomavirus (HPV) and may aid in the clearance of HPV-induced lesions. This may normalize HPV-dependent cervical lesions, prevent integration of HPV and HPV infection. It may also re-balance the vaginal microbiota and improve vaginal health.
Corlanor: (Other name for: ivabradine hydrochloride)
corn starch: A starch derived from corn grain and used as food or food ingredient, with potential anti-hypoglycemic activity. Upon ingestion, corn starch is broken down and releases glucose in the gastrointestinal (GI) tract. Glucose is taken up in the bloodstream and maintains as well as stabilizes glucose levels. This may prevent or improve hypoglycemia in patients with glycogen storage disease or insulinomas.
Cort-Dome: (Other name for: therapeutic hydrocortisone)
Cortalone: (Other name for: prednisolone)
Cortef: (Other name for: therapeutic hydrocortisone)
Cortenema: (Other name for: therapeutic hydrocortisone)
corticorelin acetate: The acetate salt form of coticorelin, a synthetic peptide of neurohormone corticotropin-releasing factor (CRF), with potential antitumor and antiangiogenesis activities. Upon administration, corticorelin stimulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary gland. In turn, ACTH stimulates cortisol production from the adrenal cortex and is regulated by a negative feedback mechanism. Corticorelin appears to inhibit swelling around brain tumors through reduction in vascular leakage and maintenance of endothelial cell integrity. This agent potentially suppresses vascularization and tumor cell growth through reduction of vascular endothelial growth factor (VEGF) that appears to be via activation of corticotrophin-releasing factor receptor 2 (CRFR2), a G protein-coupled receptor.
corticorelin ovine triflutate: A trifluoroacetate salt of ovine corticotropin-releasing hormone (CRH), a 41 amino acids peptide similar to human CRH, used as a diagnostic agent. Corticorelin ovine triflutate is a potent stimulator of adrenocorticotropic hormone (ACTH), secreted from the anterior pituitary gland. In turn, ACTH stimulates cortisol production from the adrenal cortex and is regulated by a negative feedback mechanism. Corticorelin ovine triflutate is used as a diagnostic tool in differentiating pituitary and ectopic production of ACTH.
corticosteroid-containing eye drop: A sterile ophthalmic solution containing a corticosteroid, with anti-inflammatory activity. Upon application of the corticosteroid-containing eye drop into the eye, the corticosteroid binds to cytoplasmic receptors, translocates to the nucleus and subsequently initiates the transcription of glucocorticoid-responsive genes such as lipocortins to inhibit phospholipase A2. This prevents the release of arachidonic acid, a precursor to prostaglandins and leukotrienes, both important mediators in the pro-inflammatory response mechanism.
corticotropin-releasing hormone: A hormone synthesized in the hypothalamus and regulates the secretion of adrenocorticotropic hormone (ACTH).
Cortispray: (Other name for: therapeutic hydrocortisone)
Cortril: (Other name for: therapeutic hydrocortisone)
Corynebacterium granulosum P40: An insoluble fraction isolated from the bacterium Corynebacterium granulosum with potential cancer immunotherapeutic activity. As a non-specific immunostimulant, Corynebacterium granulosum P40 activates the reticuloendothelial system, induces the production of certain cytokines, enhances macrophage activity, and potentiates a delayed-type hypersensitivity response when co-administered with an antigen.
Corynebacterium parvum, Burroughs: (Other name for: attenuated corynebacterium parvum)
Corynebacterium parvum, Merieux: (Other name for: attenuated corynebacterium parvum)
Cosentyx: (Other name for: secukinumab)
cosibelimab-ipdl: An immunoglobulin G1 (IgG1), human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cosibelimab-ipdl specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death protein 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T cells.
cositecan: A synthetic silicon-containing agent related to camptothecin with antineoplastic properties. Cositecan stabilizes the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks and consequently triggering apoptosis. Because it is lipophilic, cositecan exhibits enhanced tissue penetration and bio-availability compared to water-soluble camptothecins.
Cosmegen: (Other name for: dactinomycin)
cosyntropin: A synthetically-derived subunit of the endogenous peptide pituitary hormone adrenocorticotropic hormone (ACTH). Consisting of the first 24 amino acids from the amino terminal of ACTH, Cortrosyn is usually prepared for injection and intended for diagnostic and not therapeutic use. Similar to endogenous ACTH, this agent stimulates the adrenal secretion of specific adrenal steroids that can be measured in the plasma.
Cotara: (Other name for: iodine I 131 monoclonal antibody TNT-1/B)
Cotellic: (Other name for: cobimetinib fumarate)
Cotrim: (Other name for: Trimethoprim-Sulfamethoxazole)
cotsiranib: A polypeptide nanoparticle (PNP)-based small interfering RNA (siRNA) therapeutic directed against transforming growth factor-beta 1 (TGF-beta 1) and cyclo-oxygenase-2 (COX-2), with potential antineoplastic activity. Upon intralesional administration, cotsiranib binds to both TGF-beta 1 and COX-2 messenger RNAs (mRNAs), preventing the translation and expression of TGF-beta 1 and COX-2 proteins. This inhibits TGF-beta 1-mediated signaling and abrogates TGF-beta 1-mediated immunosuppression, which may enhance anti-tumor immunity in the tumor microenvironment (TME) and promote a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. The inhibition of COX-2 prevents COX-2-mediated signaling, which may result in apoptosis and a reduction in tumor cell proliferation, tumor angiogenesis and metastasis.
Coumadin: (Other name for: warfarin sodium)
coumarin: O hydroxycinnamic acid. Pleasant smelling compound found in many plants and released on wilting. Has anticoagulant activity by competing with Vitamin K.
Coversin: (Other name for: nomacopan)
COVID-19 convalescent plasma: Plasma that has been collected from patients who have recovered from the novel coronavirus disease, COVID-19. This plasma contains antibodies developed against the SARS-CoV-2 virus and is being investigated for the treatment of COVID-19.
COVID-19 vaccine Ad26.COV2.S: A coronavirus vaccine composed of a genetically engineered, replication-incompetent, adenovirus serotype 26 (Ad26) vector expressing the stabilized pre-fusion spike (S) protein of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), with potential immunomodulating and anti-COVID-19 activities. Upon intramuscular administration of the COVID-19 vaccine Ad26.COV2.S, the Ad26 infects human cells, which produces SARS-CoV-2 S protein. The released S protein activates the immune system to induce a humoral and cell-mediated immune response against SARS-CoV-2. This may prevent SARS-CoV-2 infection and inhibit viral replication. S protein, usually found on the surface of SARS-CoV-2, plays an essential role in the infection pathway of the SARS-CoV-2 virus.
COX-2 inhibitor ECP-1014: An orally bioavailable inhibitor of the enzyme cyclooxygenase-2 (COX-2), with potential analgesic, anti-inflammatory and antineoplastic activities. Upon oral administration, COX-2 inhibitor ECP-1014 inhibits COX-2, thereby inhibiting the conversion of arachidonic acid to prostaglandins, including prostaglandin E2 (PGE2). This may reduce pain and inflammation. The COX-2/PGE 2 pathway may also play an important role in tumor proliferation, angiogenesis, metastasis and immune suppression in the tumor microenvironment (TME). COX-2 is overexpressed in certain tumor cells.
Cozaar: (Other name for: losartan potassium)
CP-609,754: A quinolinone derivative that inhibits farnesyl protein transferase, an enzyme that mediates the farnesylation of RAS, causing possible inhibition of the RAS pathway.
CP-724,714: An orally bioavailable quinazoline with potential antineoplastic activity. CP-724,714 selectively binds to the intracellular domain of HER2, reversibly inhibiting its tyrosine kinase activity and resulting in suppression of tumor cell growth. HER2, a member of the epidermal growth factor receptor (EGFR) family, is overexpressed in many adenocarcinomas, particularly breast cancers.
CpG oligodeoxynucleotide GNKG168: A synthetic, 21-mer, unmethylated CpG motif-based oligodeoxynucleotide (ODN), with immunostimulatory activity. CpG oligodeoxynucleotide GNKG168 binds to and activates Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines, such as immunoglobulins (Igs), interferons (IFNs), interleukins (ILs) and tumor necrosis factor (TNF). Through activation of TLR9, this ODN can directly stimulate B-lymphocytes, dendritic and natural killer (NK) cells, resulting in an increase in innate immunity and antibody-dependent cellular cytotoxicity (ADCC). In addition, through the release of IL-12 and IFN, this agent may induce a preferential shift to the T-helper 1(Th1) phenotype resulting in enhanced CD8+ T cell-mediated antitumor cytotoxicity.
CpG oligodeoxynucleotide TLR9 agonist DV281: A proprietary synthetic, aerosolized C-class CpG oligodeoxynucleotide-based (ODN) agonist of toll-like receptor 9 (TLR9), with potential immunostimulating activity. Upon inhalation, CpG ODN TLR9 agonist DV281 specifically targets, binds to and activates TLR9 expressed by plasmacytoid dendritic cells (pDCs) and B-cells. This initiates immune signaling pathways and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against antigens expressed by lung cancer cells. TLR9, a member of the TLR family, plays a fundamental role in pathogen recognition and activation of the innate immune system.
CpG-28 oligodeoxynucleotide: A synthetic oligodeoxynucleotide, containing unmethylated CpG motifs derived from bacterial DNA, with immunostimulatory activities. A CpG oligodeoxynucleotide (CpG ODN) binds to and activates a Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines. Through activation of TLR9, a CpG ODN can directly stimulate B-lymphocytes, dendritic and NK cells, resulting in an increase in innate immunity and antibody-dependant cell cytotoxicity (ADCC). Additionally, a CpG ODN can indirectly modulate T-cell responses, through the release of cytokines (IL-12 and IFN gamma), to induce a preferential shift to the Th1 (helper) phenotype resulting in enhanced CD8+ cellular cytotoxicity.
CpG-STAT3 siRNA CAS3/SS3: A Toll-like receptor 9 (TLR9) agonist/STAT3 siRNA conjugate composed of a CpG oligodeoxynucleotide (ODN) and a short interfering RNA (siRNAs) directed against signal transducer and activator of transcription 3 (STAT3), with potential immunostimulating and antineoplastic activities. Upon administration of CpG-STAT3 siRNA CAS3/SS3, the CpG ODN moiety binds to and activates TLR9, and the conjugate is internalized by various antigen-presenting cells (APCs), including dendritic cells (DCs), macrophages and B cells. This activates numerous signaling transduction pathways which results in the release of multiple cytokines, such as immunoglobulins (Igs), interferons (IFNs), interleukins (ILs) and tumor necrosis factor (TNF) and induces innate and adaptive immune responses. In addition, the internalization results in the delivery of anti-STAT siRNA moiety into myeloid and B-cells. The siRNA binds to STAT mRNA and inhibits both the translation and expression of the STAT protein. This prevents STAT3 binding to responsive gene promoters and blocks STAT3-mediated regulation of gene expression. STAT3 regulates the transcription of genes involved in several cellular functions. It is constitutively activated in a variety of human cancers and plays a key role in neoplastic transformation, uncontrolled tumor cell proliferation, resistance to apoptosis, metastasis, immune evasion, tumor angiogenesis, epithelial-mesenchymal transition (EMT) and the Warburg effect. Altogether, this may result in tumor cell death and inhibit tumor cell proliferation, angiogenesis and metastasis.
cPLA2 Inhibiting silicone-based gel AVX001: A topical preparation composed of a silicone gel containing a docosahexaenoic acid derivative and cytosolic group IVA phospholipase A2 alpha (cytosolic phospholipase A2 group IVA; cPLA2a; GIVA cPLA2; Group IVA cPLA2) inhibitor, with potential anti-inflammatory activity. Upon topical application to the affected site(s), the cPLA2 inhibiting silicone-based gel AVX001 binds to and inhibits the activity of cPLA2alpha. This may inhibit cPLA2alpha-mediated inflammation. cPLA2alpha catalyzes the release of arachidonic acid from glycerophospholipids and plays a key role in various inflammatory diseases. It is overexpressed in certain cancer cells and may play a key role in proliferation, migration, and chemo-resistance.
CR2-fH fusion protein TT30: A recombinant, chimeric human fusion protein consisting of the iC3b/C3d-binding region of human complement receptor type 2 (CR2/CD21) linked to the alternative complement pathway (ACP) inhibitory domain of human factor H (fH) (CR2-fH), with potential complement system inhibiting activity. Via its C3 binding domain, TT30 selectively binds to complement activated cell surfaces and via its fH binding domain regulates ACP activity. This suppresses excessive complement activity and may result in an inhibition of ACP-mediated hemolysis of paroxysmal nocturnal hemoglobinuria (PNH) red blood cells (RBCs) as well as preventing ACP-induced tissue damage. Factor H is a key regulator in the activation of ACP.
creatine monohydrate: The monohydrate form of creatine similar or identical to endogenous creatine produced in the liver, kidneys, and pancreas. Creatine, in phosphate form, helps supply energy to muscle cells for contraction. After intense effort, when ATP deposits are depleted, creatine phosphate donates phosphate groups toward the fast synthesis of ATP. Dietary supplementation with creatine may improve muscle wasting associated with cancer and other chronic diseases.
crelosidenib: An orally available inhibitor of mutant form of the isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble), including the substitution mutation at arginine (R) in position 132, IDH1(R132), with potential antineoplastic activity. Upon oral administration, crelosidenib specifically and covalently binds to and modifies a single cysteine (Cys269) in the allosteric binding pocket of mutant forms of IDH1, thereby inactivating IDH1. This inhibits the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This depletes 2-HG levels, prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing mutant forms of IDH1. In addition, crelosidenib has the ability to cross the blood-brain barrier (BBB). IDH1 mutations, including 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.
crenigacestat: An orally available inhibitor of the integral membrane protein gamma-secretase (GS), with potential antineoplastic activity. Upon administration, crenigacestat binds to the GS protease complex, thereby blocking the proteolytic cleavage and release of the Notch intracellular domain (NICD), which would normally follow ligand binding to the extracellular domain of the Notch receptor. This prevents both the subsequent translocation of NICD to the nucleus to form a transcription factor complex and the expression of Notch-regulated genes. This results in the induction of apoptosis and the inhibition of growth in tumor cells that overexpress Notch. Overexpression of the Notch signaling pathway plays an important role in tumor cell proliferation and survival.
crenolanib: An orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.
crenolanib besylate: The besylate salt form of crenolanib, an orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.
Creon: (Other name for: pancrelipase)
Cresemba: (Other name for: isavuconazonium sulfate)
Crestor: (Other name for: rosuvastatin calcium)
cretostimogene grenadenorepvec: A recombinant oncolytic adenovirus encoding the immunohematopoietic cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential antineoplastic activity. Upon administration, cretostimogene grenadenorepvec selectively infects and replicates in tumor cells, which may result in tumor cells lysis. Synergistically, GM-CSF expressed by the oncolytic adenovirus may promote a cytotoxic T cell response against tumor cells harboring the oncolytic adenovirus, resulting in an immune-mediated tumor cell death.
cridanimod sodium: The sodium salt form of cridanimod, a small molecule that can increase progesterone receptor (PR) expression, with potential antineoplastic adjuvant activity. Upon intramuscular administration, cridanimod is able to induce the expression of PR in endometrial cancer. This could increase the sensitivity of endometrial cancer cells to progestin monotherapy. In combination with a progestin, cancer cells could be eradicated through increased PR-mediated signaling, leading to an inhibition of luteinizing hormone (LH) release from the pituitary gland, via a negative feedback mechanism, and, eventually, an inhibition of estrogen release from the ovaries. This leads to an inhibition of cellular growth in estrogen-dependent tumor cells. In addition, this agent is able to increase the production and release of interferon (IFN) alpha and beta. PR is often downregulated in endometrial cancer and makes it resistant to progestin-mediated hormone therapy.
crisaborole ointment: A topical ointment formulation composed of crisaborole, a boron-containing phosphodiesterase 4 (PDE4) inhibitor, with potential immunomodulating activity. Upon topical administration of the crisaborole ointment to the affected area(s), crisaborole targets, binds to and inhibits PDE4, which increases intracellular cyclic adenosine monophosphate (cAMP) levels. This decreases inflammation in the skin. PDE4 inhibition may reduce cetuximab-related skin toxicity and atopic dermatitis.
Crispact: (Other name for: Lactobacillus crispatus M247 supplement)
CRISPR-Cas9-engineered TGFbRII-deleted anti-EGFR CAR T cells: A preparation of human T lymphocytes genetically engineered to express an anti-epidermal growth factor receptor (EGFR) chimeric antigen receptor (CAR) gene and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of transforming growth factor-beta receptor II (TGFbRII), with potential immunostimulatory and antineoplastic activities. Upon administration, the CRISPR-Cas9 engineered TGFbRII-deleted anti-EGFR CAR T cells target and bind to the EGFR antigen on tumor cell surfaces; subsequently, EGFR-expressing tumor cells may be lysed. EGFR, overexpressed by a variety of cancer cell types, plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance. By knocking out the expression of TGFbRII, the immunosuppressive cytokine TGF-beta is unable to bind to the T cells and prevent the activation of the T cells. TGF-beta contributes to the immunosuppressive nature of the tumor microenvironment (TME), and plays a key role in promoting tumor initiation, metastasis, and suppressing anti-tumor immunity.
CRISPR/Cas9-edited HPV16/18 E6/E7 plasmid: A plasmid encoding for clustered regularly interspaced short palindromic repeats (CRISPR) targeting the promoters for the human papillomavirus (HPV) type 16 (HPV16) and 18 (HPV18) epitopes E6 and E7, and coupled to the endonuclease cas9, with potential antineoplastic activities. Upon administration and transfection of the CRISPR/Cas9-edited HPV16/18 E6/E7 plasmid, the guide RNA (gRNA) of the CRISPR moiety specifically targets and binds to complementary sites on the HPV 16/18 promoter regions for E6 and E7. Cas9 cleaves these specific DNA sites, thereby disrupting HPV16/18 E6/E7 transcription. Decreased expression of E6 and E7 induces apoptosis and decreases tumor cell proliferation in HPV-driven tumor cells. This induces the expression of certain tumor suppressor genes, such as p53 and retinoblastoma 1 (RB1), which induces tumor cell apoptosis and inhibits tumor cell proliferation.
CRISPR/Cas9-mediated PD-1 and TCR gene-deleted anti-mesothelin CAR-T cells: A preparation of human T lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) mesothelin and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR and programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) expression, with potential immunostimulating and antineoplastic activities. The CRISPR guide RNA (gRNA) specifically targets and binds to complementary sites on TCRalpha, TCRbeta and PD-1. In turn, Cas9 cleaves these specific DNA sites, thereby disrupting transcription. Upon isolation, transduction, electroporation with TCRalpha, TCRbeta and PD-1 gRNAs, which are complexed to Cas9 RNA to disrupt expression of endogenous TCRalpha, TCRbeta and PD-1, expansion ex vivo, and introduction into the patient, the CRISPR-Cas9-mediated PD-1 and TCR gene-deleted anti-mesothelin CAR T cells recognize and bind to mesothelin-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of mesothelin-positive tumor cells. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the mesothelin-expressing tumor cells. Removal of endogenous TCR reduces TCR competition for expression, increases the persistence and function of the expressed transgenic TCR, enhances resistance to T-cell exhaustion and increases T-cell activity. Mesothelin is upregulated on a variety of tumor cell types.
Crixivan: (Other name for: indinavir sulfate)
crizanlizumab: A humanized monoclonal immunoglobulin G1 anti-P-selectin antibody with vaso-protective and anti-vaso-occlusive properties. Upon administration, crizanlizumab binds to P-selectin and blocks its interaction with P-selectin glycoprotein ligand-1 (PSGL-1; SELPLG) on neutrophils and monocytes. P-selectin, a glycoprotein that functions as a cell adhesion molecule (CAM), translocates to the surface of activated endothelial cells and platelets, upon stimulation, where it binds to its ligand and mediates the rolling of platelets and neutrophils on activated endothelial cells. Therefore, blockade of p-selectin may inhibit platelet aggregation, maintain blood flow and minimize sickle cell-related pain crises (SCPC).
crizotinib: An orally available aminopyridine-based inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the c-Met/hepatocyte growth factor receptor (HGFR) with antineoplastic activity. Crizotinib, in an ATP-competitive manner, binds to and inhibits ALK kinase and ALK fusion proteins. In addition, crizotinib inhibits c-Met kinase, and disrupts the c-Met signaling pathway. Altogether, this agent inhibits tumor cell growth. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.
CRL 1005: A nonionic block copolymer adjuvant used to enhance viral or non-viral polynucleotide delivery in gene therapy vaccines.
CRL4-CRBN modulator KPG-818: An orally bioavailable modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CRL4-CRBN modulator KPG-818 specifically targets and binds to cereblon (CRBN) of the E3 ubiquitin ligase (CRL4-CRBN) complex, thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces proteasome-mediated degradation of certain transcription factors, some of which are transcriptional repressors in T cells. This leads to modulation of the immune system, including activation of T lymphocytes, and downregulation of the activity of other proteins, some of which play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
crofelemer: An oligomeric proanthocyanidin extracted from the latex produced by the tree Croton lechleri (Euphorbiaceae), with antidiarrheal, and potential antiviral and antimicrobial activities. Upon oral administration, crofelemer acts locally within the gastrointestinal (GI) tract by inhibiting both the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion (Cl-) channel and the calcium-activated Cl- channel (CaCC) expressed on the luminal surface of enterocytes. This inhibits the secretion of chloride ions into the intestinal lumen and prevents high volume water loss. By normalizing Cl- and water balance in the intestines, crofelemer relieves secretory diarrhea.
crolibulin: A small molecule tubulin polymerization inhibitor with potential antineoplastic activity. Microtubulin inhibitor EPC2407 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of tubulin into microtubules, which may result in cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. As a vascular disruption agent (VDA), this agent also disrupts tumor neovascularization, which may result in a reduction in tumor blood flow and tumor hypoxia and ischemic necrosis.
cromolyn sodium inhalant PA101: A solution containing a high concentration of cromolyn sodium, with potential mast cell stabilizing, anti-tussive and anti-inflammatory activities. Upon inhalation of PA101 via a nebulizer, cromolyn blocks calcium ion influx into mast cells, thereby preventing the degranulation of mast cells in the lungs. This blocks the release of pro-inflammatory mediators from mast cells, such as histamine and slow-reacting substance of anaphylaxis (SRS-A), and prevents both bronchoconstriction and an inflammatory response. In indolent systemic mastocytosis (ISM), PA101 may be able to reduce the symptoms associated with this disease.
crotoxin: A toxic protein complex isolated from Crotalus durissus terrificus (South American rattlesnake) venom that is comprised of a basic neurotoxic subunit with phospholipase A2 (PLA2) activity and an acidic non-enzymatic, non-toxic subunit called crotapotin, with anticoagulant and immunomodulatory activities. The PLA2 subunit of crotoxin hydrolyzes the acyl groups in phosphoglycerides, acts as an anticoagulant by inhibiting the prothrombinase activity of coagulation factor Xa (F10a) and increases chloride-dependent current modulated by the cystic fibrosis transmembrane conductance regulator (CFTR). The PLA2 subunit may also metabolize eicosanoids, forming products that cause sequestration of lymphocytes in the lymph nodes and inhibit the spreading and phagocytic activity of macrophages. Crotoxin down-modulates the immune system, leading to the inhibition of both humoral and cellular immune responses.
crovalimab: A humanized recycling monoclonal antibody directed against the complement pathway protein C5, with potential complement pathway inhibitory and immunomodulating activities. Upon administration, crovalimab targets and binds to a specific C5 epitope, thereby preventing C5 convertase-mediated cleavage of C5, inhibiting the formation of C5a and C5b, and the C5b6 deposition on membranes. This inhibits C5-mediated signal transduction, the formation of the membrane attack complex (MAC) and the activation of the terminal complement pathway. This results in the prevention and/or inhibition of both complement-mediated inflammation and cell destruction of red blood cells (RBCs) as seen in paroxysmal nocturnal hemoglobinuria (PNH). C5 plays a key role in the activation of the complement cascade. Crovalimab is engineered with sequential monoclonal antibody recycling technology (SMART).
CRTH2 antagonist ACT-774312: An orally bioavailable, selective antagonist of the chemoattractant receptor‐homologous molecule expressed on T-helper (Th) 2 cells (CRTH2; prostaglandin D2 receptor 2; G-protein coupled receptor 44), with potential anti-allergic and anti-inflammatory activities. Upon administration, CRTH2 antagonist ACT-774312 selectively binds to and prevents the activation of CRTH2 by prostaglandin D2 (PGD2). This may inhibit the recruitment of eosinophils, basophils, innate lymphoid cells type 2 (ILC2), and Th2 cells, thereby reducing the number of inflammatory cells within the affected tissue. Additionally, this may reduce the release of cytokines at the site of allergen entry and block type 2 cytokine-mediated effects such as tissue remodeling. CRTH2, a G-protein-coupled receptor, is mainly expressed on eosinophils, basophils, macrophages, monocytes, mast cells, Th2 cells, ILC2 and dendritic cells (DCs).
cryopreserved umbilical cord allograft: An allograft composed of cryopreserved, ultra-thick umbilical cord tissue in which the natural structural and biological characteristics of the native placental tissue has been preserved, that may potentially be used to improve wound healing and nerve regeneration. The cryopreserved umbilical cord allograft retains the heavy chain hyaluronic acid/pentraxin3 (HC-HA/PTX3) complex and growth factors that minimize inflammation, reduce scar tissue formation, and promote nerve and tissue healing. Upon placement of the allograft to the relevant area(s) at the surgical site, the allograft may aid in improving nerve regeneration and wound healing.
crystalline genistein formulation AXP107-11: The sodium salt dihydrate form of crystalline genistein, a soy-derived isoflavone and phytoestrogen, with potential antineoplastic, chemosensitizing, and antioxidant activities. Upon administration, crystalline genistein formulation AXP107-11 binds to and modulates the activities of the nuclear estrogen receptors ERalpha (ESR1) and ERbeta (ESR2), and activates the G-coupled estrogen receptor 1 (GPER1). In addition, this agent increases the expression of phosphatase and tensin homolog (PTEN), which deactivates protein kinase Akt and mitogen-activated protein kinases (MAPK1 and 3; ERK2 and 1), thereby disrupting PI3K/Akt signal transduction and inducing apoptosis. AXP107-11 also induces antioxidant enzymes through AMP-activated protein kinase (AMPK) activation, inhibits nuclear factor kappa-B (NF-kB) activation and decreases inflammation response, thereby sensitizing tumors to chemotherapy. Compared to genistein itself, which has poor oral availability, this crystalline formulation shows improved solubility and bioavailability.
Crysvita: (Other name for: burosumab)
CSF-1R inhibitor BLZ945: An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF-1R; CSF1R), with potential antineoplastic activity. CSF1R inhibitor BLZ945 selectively binds to CSF1R expressed on tumor-associated macrophages (TAMs), blocks the activity of CSF1R, and inhibits CSF1R-mediated signal transduction pathways. This inhibits the activity and proliferation of TAMs, and reprograms the immunosuppressive nature of existing TAMs. Altogether, this reduces TAM-mediated immune suppression in the tumor microenvironment, re-activates the immune system, and improves anti-tumor cell responses mediated by T-cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand, colony stimulating factor 1 (CSF1); this receptor is overexpressed by TAMs in the tumor microenvironment, and plays a major role in both immune suppression and the induction of tumor cell proliferation.
CSF-1R/DDR1/VEGFR2 inhibitor C019199: An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), discoid domain receptor type 1 (DDR1) and vascular endothelial growth factor receptor type 2 (VEGFR2), with potential antineoplastic activity. Upon oral administration, CSF-1R/DDR1/VEGFR2 inhibitor C019199 targets, binds to and inhibits the activity of CSF-1R. This inhibits CSF1R activation and CSF1R-mediated signaling, thereby inhibiting the activities of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), and preventing immune suppression in the tumor microenvironment (TME). This enhances antitumor T-cell immune responses and inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor that plays major roles in tumor cell proliferation and metastasis. C019199 also targets, binds to and inhibits the activity of DDR1 and VEGFR2. Blocking DDR1, a protein expressed on tumor cells that binds collagen to make a minimally permeable physical barrier that blocks immune cells in the TME from interacting with and attacking the tumor, causes the collagen fibers to lose alignment and loosen. This creates gaps in the tumor barrier, thereby allowing cytotoxic T-cells to enter and attack the tumor. Blocking VEGFR2 results in the inhibition of tumor angiogenesis and tumor cell proliferation.
CSF1-targeting agent: Any agent targeting the cytokine colony stimulating factor 1 (CSF1; CSF-1; macrophage colony-stimulating factor; M-CSF).
CSF1R inhibitor HMPL-653: An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), with potential immunomodulatory and antineoplastic activities. Upon oral administration, CSF1R inhibitor HMPL-653 targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activities of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), and prevents immune suppression in the tumor microenvironment (TME). This enhances antitumor T-cell immune responses and inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor that plays major roles in tumor cell proliferation and metastasis.
CSF1R inhibitor PLX73086: An inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R), with potential antineoplastic activity. Upon administration, CSF1R inhibitor PLX73086 targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activity of tumor-associated macrophages (TAMs) in the tumor tissue and prevents TAM-related tumor cell growth. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1) and plays major roles in tumor cell proliferation and metastasis.
CSF1R-targeting agent: Any agent targeting the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; C-FMS; CD115; M-CSFR).
CT2584: A lipid metabolism and phosphatidic acid modulator, with potential antineoplastic activity. Upon administration, CT-2584 inhibits phospholipid signaling which may inhibit tumor cell proliferation.
CTP-37-DT vaccine: A vaccine composed of synthetic peptides derived from beta-human chorionic gonadotropin (hCG) conjugated to diphtheria toxoid. Vaccination with this peptide may elicit the host immune response against hCG-producing cancer cells.
Cubicin: (Other name for: daptomycin)
cudarolimab: An agonistic fully human anti-OX40 (tumor necrosis factor receptor superfamily member 4; TNFRSF4; CD134; OX40L receptor) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cudarolimab selectively binds to and activates OX40. Receptor activation induces proliferation of memory and effector T lymphocytes and results in a T-cell-mediated immune response against tumor cells, which leads to tumor cell lysis. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes and provides a co-stimulatory signal that promotes both the proliferation and survival of activated T-cells.
cultured Lentinula edodes mycelia extract: An orally bioavailable capsule-based formulation of a standardized extract of cultured Lentinula edodes (Shiitake mushroom) mycelia (ECLM), which is high in the polysaccharides beta- and alpha-glucans, with potential antioxidant, immunomodulating and antineoplastic activities. Upon oral administration, the cultured Lentinula edodes mycelia extract activates the immune system, by binding to toll-like receptors (TLRs), specifically TLR-4, and induces the activation of dendritic cells (DCs), natural killer (NK) cells, macrophages and T cells and the release of cytokines. This may clear human papillomavirus (HPV) infections.
Culturelle: (Other name for: Lactobacillus rhamnosus GG)
cumin/ginger extract-based artificial saliva spray: An artificial saliva spray formulation containing cumin and ginger extract, that has potential anti-xerostomia activity. Upon direct oral application of the cumin/ginger extract-based artificial saliva spray, a protective film of moisture is deposited over the mucous membranes of the mouth, which relieves dryness of the mucous membranes and increases salivary flow. Ginger and cumin may increase salivation and reduce xerostomia. In addition, this artificial saliva spray may help prevent chemotherapy- or radiotherapy-induced oral mucositis.
Cuprenil: (Other name for: penicillamine)
Cuprimine: (Other name for: penicillamine)
Curcuma xanthorrhiza oil: The oil extracted from the root tuber of Curcuma xanthorrhiza. Curcuma xanthorrhiza oil is used primarily in skincare preparations.
curcumin: A phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a variety of pharmacologic properties. Curcumin blocks the formation of reactive-oxygen species, possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation; and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C. These effects may play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell proliferation and suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer.
curcumin C3 complex: (Other name for: curcumin/demethoxycurcumin/bisdemethoxycurcumin-containing supplement)
curcumin-based gel: A proprietary topical gel formulation containing an extract of curcumin, the polyphenol derived from the plant Curcuma longa, with potential anti-inflammatory, antioxidant, and wound healing activities. Upon topical administration to the affected areas, curcumin inhibits a variety of pro-inflammatory enzymes and reduces the production of certain pro-inflammatory mediators. Curcumin also blocks the formation of reactive oxygen species (ROS), neutralizes free radicals and prevents oxidative stress and DNA damage. In addition, curcumin inhibits phosphorylase kinase (PhK) in the skin, which prevents multiple PhK-mediated signal transduction pathways that are induced upon skin injury. This further prevents inflammation, promotes healing and reduces scar tissue formation. The proprietary curcumin-based gel also provides moisture to the skin and contains tetrahydropiperine (THP), which is derived from black pepper fruit and increases skin uptake of curcumin.
curcumin/chondroitin sulfate/hyaluronic acid/quercetin soft gels: An orally available preparation containing curcumin, quercetin, hyaluronic acid, and chondroitin sulfate with potential radioprotective activity. Upon administration, the glycosaminoglycans may improve barrier function and reduce inflammation and irritation in the genitourinary tract caused by radiotherapy.
curcumin/demethoxycurcumin/bisdemethoxycurcumin-containing supplement: A mixture composed of curcuminoid phenols extracted from the plant Curcuma longa (turmeric root) with potent antioxidant and anti-inflammatory properties. Curcumin/demethoxycurcumin/bisdemethoxycurcumin-containing supplement is a unique combination of three phenols: curcumin, demethoxycurcumin and bisdemethoxycurcumin. This agent may both prevent the formation of free radicals and neutralize free radicals. Curcuminoids may have chemopreventive and antiproliferative properties.
curcumin/doxorubicin-encapsulating nanoparticle IMX-110: A water-soluble, nano-sized formulation composed of nanoparticles encapsulating the poorly water-soluble curcumin, a signal transducer and activator of transcription 3 (Stat3), nuclear factor Kappa B (NF-kB) and poly-tyrosine kinase inhibitor (TKI), and the antineoplastic anthracycline antibiotic doxorubicin, with potential antineoplastic activity. Upon administration of the curcumin/doxorubicin-encapsulating nanoparticle IMX-110, the curcumin moiety targets and inhibits the activation of STAT3 and NF-kB and prevents STAT3- and NF-kB-mediated signaling pathways, both of which are activated in a variety of human cancers and plays a key role in neoplastic transformation, uncontrolled tumor cell proliferation, tumor resistance to apoptosis, metastasis and immune evasion. The doxorubicin moiety intercalates into DNA and interferes with topoisomerase II activity. This inhibits DNA replication and RNA synthesis, leading to tumor cell growth inhibition and apoptosis. This agent also interacts with cell membrane lipids causing lipid peroxidation. Delivery of doxorubicin in nanoparticles may improve drug penetration into tumors and curcumin, by inhibiting NFkB and STAT3 activity, may circumvent the tumor cells multidrug resistance mechanisms and may therefore be effective in chemoresistant tumor cells. Chemotherapeutic agents, such as doxorubicin, upregulate the expression of NF-kB in tumor cells which generates chemotherapy-resistant tumor cells.
curcumin/green tea extract/Polygonum cuspidatum extract/soybean extract capsule: An oral capsule containing curcumin, green tea extract, Polygonum cuspidatum extract, and soybean extract, with antioxidant and potential chemopreventive activities. The antioxidants in curcumin/green tea extract/Polygonum cuspidatum extract/soybean extract capsule bind to and neutraliize free-radicals, which may prevent their genotoxic and carcinogenic effects.
curcumin/polyphenols-containing botanical agent APG-157: An orally bioavailable botanically-based formulation containing multiple polyphenols, including curcumin, the polyphenol derived from the plant Curcuma longa that is also known as turmeric, with potential anti-inflammatory, immunomodulatory and antineoplastic activities. Upon oral administration of curcumin/polyphenols-containing botanical agent APG-157, the curcumin and polyphenols in APG-157 may exert anti-inflammatory activity by decreasing the production of inflammation mediators, such as interleukin (IL) 1-beta, IL-6 and IL-8. The curcumin and polyphenols may also promote T-cell recruitment to the tumor microenvironment (TME) and cytotoxic effects against cancer cells.
cusatuzumab: A defucosylated, humanized IgG1 monoclonal antibody directed against the extracellular domain of the human CD70 molecule with potential antineoplastic activity. Upon administration, cusatuzumab selectively binds to, and neutralizes the activity of CD70, which may also induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on a number of solid and hematological tumors. Its overexpression may play an important role in evasion of immune surveillance.
custirsen sodium: The eicosasodium salt of a mixed-backbone antisense oligodeoxynucleotide with chemosensitizing properties. Custirsen inhibits testosterone-repressed prostate message-2 (TRPM-2). Administration of custirsen abrogates the anti-apoptotic effect of TRPM-2, thereby sensitizing cells to chemotherapy and resulting in tumor cell death. TRPM-2 is an anti-apoptotic clusterin that is overexpressed by prostate cancer cells and is associated with chemoresistance.
CUX1 wt allele: Human CUX1 wild-type allele is located in the vicinity of 7q22.1 and is approximately 468 kb in length. This allele, which encodes homeobox protein cut-like 1 and protein CASP, plays a role in both the regulation of transcription and intra-Golgi vesicle transport.
CVP Regimen: A regimen consisting of cyclophosphamide, vincristine and prednisone that may be used to treat Castleman disease, post-transplant lymphoproliferative disorders, indolent forms of non-Hodgkin lymphoma and chronic lymphocytic leukemia.
Cx43 agonistic monoclonal antibody ALMB-0168: A humanized agonistic monoclonal antibody targeting connexin43 (Cx43; gap junction alpha-1 protein) hemichannels, with potential antineoplastic activity. Upon administration, Cx43 agonistic monoclonal antibody ALMB-0168 binds to the extracellular domain of Cx43 and activates the Cx43 hemichannels expressed on osteocytes, but not those in gap junctions. This causes the Cx43 hemichannels to open and release several factors including adenosine triphosphate (ATP) into the extracellular environment in the bone and tumor-inhibiting cytokines. This may inhibit tumor cell growth and migration in the bone. Cx43, mechanosensitive hemichannels highly expressed in osteocytes, plays important roles in osteocytes functions by mediating the release of various signaling molecules.
CXC chemokine receptor 2 antagonist AZD5069: An orally bioavailable, selective and reversible antagonist of CXC chemokine receptor 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration, CXC chemokine receptor 2 antagonist AZD5069 directly binds to CXCR2 and inhibits its activation. This inhibits CXCR2-mediated signaling and may inhibit tumor cell proliferation in CXCR2-overexpressing tumor cells. In addition, AZD5069 reduces both neutrophil recruitment and migration from the systemic circulation into sites of inflammation, including the lung mucosa; it may also prevent neutrophil migration from the bone marrow. This results in the reduction of inflammation, mucus production, and neutrophil proteinase-mediated tissue destruction in the lung. CXCR2, a G protein-coupled receptor protein also known as IL-8 receptor B (IL-8RB), is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation and progression; it is known to be elevated in several inflammatory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and fibrotic pulmonary disorders.
CXCR1/2 inhibitor RP72: A small molecular weight protein and an inhibitor of CXC chemokine receptor types 1 (CXCR1) and 2 (CXCR2), with potential immunomodulating, anti-inflammatory and antineoplastic activities. Upon administration, CXCR1/2 inhibitor RP72 targets and binds to CXCR1 and CXCR2 and prevents CXCR1 and CXCR2 activation by its ligand interleukin 8 (IL-8 or CXCL8). This blocks CXCL8-mediated signal transduction and may cause cancer stem cell (CSC) apoptosis. This may also reduce both recruitment and migration of immunosuppressive myeloid-derived suppressor cells (MDSCs) and neutrophils in the tumor microenvironment (TME), inhibits inflammatory processes and abrogates the immunosuppressive-induced nature of the TME. This allows effector cells, such as natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), to kill and eliminate cancer cells. Altogether, blocking CXCL8-mediated signal transduction may inhibit tumor cell migration, metastasis, angiogenesis and tumor cell proliferation. CXCR1 and CXCR2, G protein-coupled receptors located on myeloid cells and certain tumor cells, play key roles in CSC survival and the ability of CSC to self-renew, the immunosuppressive nature of the TME, tumor cell proliferation and metastasis, and resistance to chemotherapeutic agents.
Cxcr1/2 inhibitor SX-682: An orally bioavailable, selective and reversible antagonist of C-X-C motif chemokine receptors 1 (CXCR1) and 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration CXCR1/2 inhibitor SX-682 selectively and allosterically binds to CXCR 1 and 2 and inhibits their activation by tumor-secreted chemokines. This inhibits CXCR1/2-mediated signaling, reduces both recruitment and migration of immunosuppressive myeloid-derived suppressor cells (MDSCs) and neutrophils in the tumor microenvironment (TME), inhibits inflammatory processes and abrogates the immunosuppressive-induced nature of the TME. This allows effector cells, such as natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), to kill and eliminate cancer cells. This inhibits tumor cell migration, metastasis, angiogenesis and tumor cell proliferation. CXCR1 and 2, G protein-coupled receptor proteins located on myeloid cells and certain tumor cells, play key roles in the immunosuppressive nature of the TME, tumor metastasis, therapy-resistance and myeloid cell suppression. They play a key role in inflammation and their expression is elevated in several inflammatory-driven diseases.
CXCR2 agonist MGTA-145: An agonist of CXC chemokine receptor type 2 (CXCR2), with potential hematopoietic stem cell (HSC) mobilization activity. Upon administration, CXCR2 agonist MGTA-145 binds to and activates CXCR2. This releases matrix metalloproteinase-9 (MMP-9), resulting in hematopoietic stem cell (HSC) release from bone marrow and HSC movement into the peripheral circulation. The HSCs can be collected for autologous and allogeneic stem cell transplantation.
CXCR2 antagonist QBM076: An orally available small molecule antagonist of the G protein-coupled receptor, C-X-C motif chemokine receptor 2 (CXCR2), with potential immunomodulating and antineoplastic activities. Upon administration, QBM076 binds to and inhibits the activation of CXCR2, resulting in reduced neutrophil recruitment, myeloid-derived suppressor cell (MDSC) accumulation, and may potentially slow tumorigenesis and metastatic processes. CXCR2 is upregulated in a variety of cancer types, predominately in neutrophils/MDSCs rather than tumor cells, and is thought to contribute to tumor cell proliferation, invasion, and metastasis.
CXCR2-transduced autologous tumor infiltrating lymphocytes: A preparation of autologous tumor infiltrating lymphocytes (TILs) that are transduced, ex vivo, with a retroviral vector encoding a gene for CXC chemokine receptor 2 (CXCR2), with potential antineoplastic activity. Upon administration of the CXCR2-transduced autologous TILs, the CXCR2-expressing T cells selectively migrate toward tumor cells expressing CXCR2 ligands, which leads to tumor cell killing. CXCR2 expression allows for optimal TIL migration towards tumor cells and enhances the TILs anti-tumor activity. This leads to a reduction in both tumor cell proliferation and survival. CXCR2, a transmembrane protein also known as IL-8 receptor B (IL-8RB), plays a key role in inflammation and cancer progression. Certain CXCR2 ligands, such as CXCL1 and CXCL8 (IL-8), are expressed by tumor cells.
CXCR3/IL-12/TGFb1 inhibitor engineered oncolytic vaccinia Virus VET3-TGI: An oncolytic vaccinia virus (VV) genetically engineered to express C-X-C chemokine receptor type 3 (CXCR3), the human pro-inflammatory cytokine interleukin-12 (IL-12), and an inhibitor of transforming growth factor (TGF)-beta 1 (TGFb1; TGF-b1), with potential immunomodulating and antineoplastic activities. Upon administration of CXCR3/IL-12/TGFb1 inhibitor engineered oncolytic VV VET3-TGI, the virus preferentially targets, infects and replicates in tumor cells, particularly tumor cells expressing CXCR3 ligands, causing oncolysis. In turn, the lysed tumor cells release various tumor-associated antigens (TAAs), which induce an immune response against the tumor cells. In addition, CXCR3/IL-12/TGFb1 inhibitor engineered oncolytic VV VET3-TGI promotes the secretion of IL-12 and the TGFb1 inhibitor in the tumor microenvironment (TME). IL-12 activates natural killer cells (NKs), induces the secretion of interferon-gamma (IFNg) and promotes CD8 cytotoxic T-lymphocyte (CTL) responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. The inhibition of TGFb1 prevents TGFb1-mediated signaling. This abrogates TGFb1-mediated immunosuppression, enhances anti-tumor immunity in the TME and further promotes CTL-mediated immune response against tumor cells. The TGF-beta signaling pathway is often deregulated in tumors and plays a key role in immunosuppression in the TME. TGFb1 is the predominant isoform in many tumors.
CXCR4 antagonist BL-8040: An orally bioavailable inhibitor of CXC Chemokine Receptor 4 (CXCR4) with potential antineoplastic activity. CXCR4 antagonist BL-8040 selectively binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation, which may result in decreased tumor cell proliferation and migration. In addition, inhibition of CXCR4 may induce mobilization of hematopoietic cells from the bone marrow into blood. The G protein-coupled receptor CXCR4 plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; SDF-1/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.
CXCR4 antagonist USL311: An orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic activity. Upon administration, USL311 binds to CXCR4, thereby preventing the binding of stromal-cell derived factor-1 (SDF-1 or CXCL12) to CXCR4 and inhibiting CXCR4 activation, which may result in decreased proliferation and migration of CXCR4-expressing tumor cells. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays an important role in chemotaxis and angiogenesis, and is upregulated in several tumor cell types.
CXCR4 inhibitor GPC-100: An inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential hematopoietic stem cell (HSC)-mobilizing activity. Upon administration, CXCR4 inhibitor GPC-100 targets and binds to CXCR4, thereby preventing the binding of stromal-cell derived factor-1 (SDF-1; C-X-C motif chemokine ligand 12; CXCL12) to CXCR4. This results in HSC release from the bone marrow and HSC movement into the peripheral circulation. The CXCL12/CXCR4 signaling pathway plays an important role in the migration and retention of HSC in the bone marrow.
CXCR4 inhibitor Q-122: An orally bioavailable inhibitor of CXCR4 with potential antineoplastic and antiviral activities. CXCR4 inhibitor MSX-122 binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1) to the CXCR4 receptor and receptor activation, which may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the GPCR (G protein-coupled receptor) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; it is also a co-receptor for HIV entry into T cells.
CXCR4 peptide antagonist LY2510924: An inhibitor of CXC chemokine receptor 4 (CXCR4), with potential antineoplastic activity. Upon subcutaneous administration, CXCR4 inhibitor LY2510924 binds to the chemokine receptor CXCR4, thereby preventing CXCR4 binding to its ligand, stromal derived factor-1 (SDF-1), and subsequent receptor activation. This may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types.
CXCR4-modified anti-BCMA CAR T cells: A preparation of T lymphocytes that have been genetically engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; TNFRSF17) with modification of the C-X-C chemokine receptor type 4 (CXCR4), with potential immunomodulating and antineoplastic activities. Upon administration, the CXCR4-modified anti-BCMA CAR T cells target and bind to tumor cells expressing BCMA and induce selective cytotoxicity in those tumor cells. The modification of the stromal-cell derived factor-1 (SDF-1 or CXCL12) receptor CXCR4 may improve the penetration of CAR T cells into the tumor microenvironment (TME). BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival.
CXCR4/E-selectin antagonist GMI-1359: An antagonist of both the C-X-C chemokine receptor type 4 (CXCR4) and E-selectin (CD62E), with potential antineoplastic activity. Upon administration, CXCR4/E-selectin antagonist GMI-1359 binds to both CXCR4 and E-selectin expressed on endothelial cells. The binding to CXCR4 prevents the binding of stromal-cell derived factor-1 (SDF-1; CXCL12) to CXCR4 and inhibits CXCR4 activation, which may result in decreased proliferation and migration of CXCR4-expressing tumor cells. The binding to E-selectin expressed on endothelial cells prevents their interaction with E-selectin ligand-expressing cancer cells. This may prevent tumor cell activation, migration and metastasis. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays an important role in chemotaxis and angiogenesis, and is upregulated in several tumor cell types. E-selectin is a cell adhesion molecule involved in cell rolling, signaling and chemotaxis. Its overexpression has been associated with tumor angiogenesis and metastasis in several cancers.
cyanide antidote package: (Other name for: sodium thiosulfate)
cyanocobalamin: A cobalt-containing coordination compound generated by intestinal microbes, and a natural water-soluble vitamin of the B-complex family that must combine with Intrinsic Factor for absorption by the intestine. Cyanocobalamin is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions.
cyanocobalamin/dexamethasone/gentamicin/procaine formulation: A quadruple mixture composed of the corticosteroid dexamethasone, the aminoglycoside antibiotic gentamicin, the vitamin cyanocobalamin (vitamin B12), and the local anesthetic agent procaine, with antimucositis activity. Upon oral administration of the cyanocobalamin/dexamethasone/gentamicin/procaine formulation, the active ingredients prevent or inhibit inflammation and infection of the oral mucosa and reduce the associated pain. This may prevent or treat radiation-induced oral mucositis (OM).
cyclin A/B RxL inhibitor CID-078: An orally bioavailable macrocycle inhibitor of cyclin A and B RxL, with potential antineoplastic activity. Upon oral administration, cyclin A/B RxL inhibitor CID-078 selectively targets and binds to the hydrophobic patch (HP) of cyclins A and B and prevents cyclin A and B substrates containing RxL motifs from binding to cyclins A and B, thereby preventing their interaction, including the interaction of the cyclin A substrate E2F1 with cyclin A-cyclin-dependent kinase 2 (CDK2) and the cyclin B substrate Myt1 with cyclin B-CDK1. This may lead to DNA cell damage and cell cycle arrest during the G1/S transition, induce apoptosis, and inhibit proliferation of susceptible tumor cells. Cyclins A and B play a key role in the regulation and progression of the cell cycle and their function is dysregulated in certain tumor cell types.
cyclin B1 peptide-pulsed autologous dendritic cell vaccine: A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with cyclin B1 peptide, with potential immunostimulatory and antineoplastic activities. Upon administration, cyclin B1 peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and anti-cyclin B1 antibody responses against cyclin B1-expressing cancer cells, resulting in tumor cell lysis. Cyclin B1, a key regulator of the cell cycle and cell division, is overexpressed in a variety of cancer cells.
cyclin-dependent kinase 4 inhibitor: Any agent that inhibits the serine/threonine kinase cyclin-dependent kinase 4 (CDK4).
cyclin-dependent kinase 6 inhibitor: Any agent that inhibits the serine/threonine kinase cyclin-dependent kinase 6 (CDK6).
cyclin-dependent kinase 8/19 inhibitor BCD 115: An orally bioavailable inhibitor of cyclin dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, CDK8/19 inhibitor BCD 115 binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of certain tumor promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDKs are serine/threonine kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. CDK8 plays a key role in transcription regulation and is an important oncogenic driver in a variety of cancer cell types.
cyclin-dependent kinase inhibitor PF-06873600: An orally bioavailable, cyclin-dependent kinase (CDK) inhibitor, with potential antineoplastic activity. Upon administration, PF-06873600 selectively targets, binds to and inhibits the activity of CDKs. Inhibition of these kinases leads to cell cycle arrest, induction of apoptosis and inhibition of tumor cell proliferation. CDKs, ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation, are frequently overexpressed in tumor cells.
cyclobenzaprine hydrochloride: A centrally acting muscle relaxant, chemically similar to amitriptyline hydrochloride with antidepressant activity. The exact mechanism of action of cyclobenzaprine hydrochloride has not been fully determined. However, it primarily acts at the brain stem to reduce tonic somatic motor activity, influencing both gamma and alpha motor neurons. This leads to a reduction in muscle spasms.
Cyclodynone: (Other name for: Vitex agnus-castus fruit extract)
Cycloflex: (Other name for: cyclobenzaprine hydrochloride)
cycloleucine: A non-metabolizable synthetic amino acid, formed through the cyclization of the amino acid leucine, with immunosuppressive, antineoplastic, and cytostatic activities. Cycloleucine competitively inhibits the enzyme methionine adenosyltransferase, resulting in the inhibition of S-adenosylmethionine (SAM) synthesis from methionine and ATP, and subsequent nucleic acid methylation and polyamine production; RNA, and perhaps to a lesser extent, DNA biosyntheses and cell cycle progression are finally disrupted. This agent is also a competitive inhibitor at the glycine modulatory site of the N-methyl-D-aspartate (NMDA) receptor.
Cyclopentenyl Cytosine: A pro-drug carbocyclic analogue of cytidine with antineoplastic and antiviral activities. Cyclopentenyl cytosine (CPEC) is converted to the active metabolite cyclopentenyl cytosine 5'-triphosphate (CPEC-TP); CPEC-TP competitively inhibits cytidine triphosphate (CTP) synthase, thereby depleting intracellular cytidine pools and inhibiting DNA and RNA synthesis. This agent may also induce differentiation of some tumor cell types. The antiviral activity of this agent is broad-spectrum.
cyclophosphamide: A synthetic alkylating agent chemically related to the nitrogen mustards with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to the active metabolites aldophosphamide and phosphoramide mustard, which bind to DNA, thereby inhibiting DNA replication and initiating cell death.
CycloSam: (Other name for: samarium Sm 153-DOTMP)
cycloserine: An analogue of the amino acid D-alanine with broad-spectrum antibiotic and glycinergic activities. D-cycloserine interferes with bacterial cell wall synthesis by competitively inhibiting two enzymes, L-alanine racemase and D-alanine:D-alanine ligase, thereby impairing peptidoglycan formation necessary for bacterial cell wall synthesis. This agent may be bactericidal or bacteriostatic, depending on its concentration at the infection site and the susceptibility of the organism. In addition, D-cycloserine is an excitatory amino acid and partial agonist at the glycine binding site of the NMDA receptor in the central nervous system (CNS); binding to the central NMDA receptor may result in amelioration of neuropathic pain.
cyclosporine: A natural cyclic polypeptide immunosuppressant isolated from the fungus Beauveria nivea. The exact mechanism of action of cyclosporine is not known but may involve binding to the cellular protein cytophilin, resulting in inhibition of the enzyme calcineurin. This agent appears to specifically and reversibly inhibit immunocompetent lymphocytes in the G0-or G1-phase of the cell cycle. T lymphocytes are preferentially inhibited with T-helper cells as the primary target. Cyclosporine also inhibits lymphokine production and release.
cyclosporine ophthalmic emulsion: An topical ophthalmic formulation containing cyclosporine, an undecapeptide produced by the fungus Beauveria nivea, with immunosuppressant and anti-inflammatory activities. The exact therapeutic mechanism of action of cyclosporine is not known but may involve binding to the cellular protein cytophilin, resulting in inhibition of the enzyme calcineurin. This agent appears to specifically and reversibly inhibit immunocompetent lymphocytes in the G0-or G1-phase of the cell cycle. T-lymphocytes are preferentially inhibited with T-helper cells as the primary target. Cyclosporine also inhibits lymphokine production and release.
Cycrin: (Other name for: medroxyprogesterone acetate)
Cyklokapron: (Other name for: tranexamic acid)
CYL-02 plasmid DNA: A gene transfer preparation of a plasmid DNA encoding mouse somatostatin receptor subtype 2 (sst2) and a fusion protein of human deoxycytidine kinase (DCK) and uridine monophosphate kinase (UMK), complexed to a synthetic polycationic carrier, polyethylenimine, with antineoplastic adjuvant application. Upon administration, CYL-02 plasmid DNA expresses DCK::UMK fusion protein that converts gemcitabine into its toxic phosphorylated metabolite. Expression of sst2 protein by this agent could induce both antioncogenic and local antitumor bystander effects. A loss of sst2 gene expression often is found in pancreatic and colorectal cancers, and is the receptor for somatostatin which negatively regulates a number of processes such as epithelial cell proliferation. Combination effects of these gene products allows for less chemotherapy to cause tumor cell lysis in not only the original tumor, but in distant tumors as well.
Cymbalta: (Other name for: duloxetine hydrochloride)
Cynviloq™: (Other name for: paclitaxel polymeric micelle formulation NANT-008)
CYP11A1 inhibitor ACE-232: An orally bioavailable inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc) (CYP11A1; P450 11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor ACE-232 selectively targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit the proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone, which is the first rate-limiting step in steroid hormone biosynthesis.
CYP11A1 inhibitor INV-9956: An orally bioavailable inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc) (CYP11A1; P450 11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor INV-9956 selectively targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit the proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone, which is the first rate-limiting step in steroid hormone biosynthesis.
CYP11A1 inhibitor ODM-209: An orally bioavailable inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc)(CYP11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor ODM-209 targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit the proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone (Preg), which is the first rate-limiting step in steroid hormone biosynthesis.
CYP17 lyase inhibitor ASN001: An orally available non-steroidal, lyase-selective inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential anti-androgenic and antineoplastic activities. Upon oral administration, CYP17 lyase inhibitor ASN001 selectively binds to and inhibits the lyase activity of CYP17A1 in both the testes and adrenal glands, resulting in a significant reduction in androgen production to castrate-range levels. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities; it plays a key role in the steroidogenic pathway. The selective inhibition of CYP17A1 lyase activity by ASN001 prevents the increased synthesis of mineralocorticoids that is normally seen with non-selective CYP17 inhibitors, which also inhibit the 17-alpha-hydroxylase activity of CYP17A1.
CYP17/androgen receptor inhibitor ODM 204: An orally available inhibitor of both the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17) and androgen receptor (AR), with potential anti-androgen and antineoplastic activities. Upon oral administration, CYP17/AR inhibitor ODM 204 selectively inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. In addition, ODM 204 binds to ARs in target tissues and inhibits androgen-induced receptor activation and AR nuclear translocation, which prevents the binding to and transcription of AR-responsive genes. This leads to an inhibition of growth in AR-expressing prostate cancer cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities.
CYP17/CYP11B2 Inhibitor LAE001: An orally bioavailable, non-steroidal, potent, reversible, dual inhibitor of cytochrome P450 17 (CYP17 or CYP17A1) and CYP11B2, with potential antiandrogen and antineoplastic activities. Upon oral administration, LAE001 inhibits the enzymatic activity of CYP17A1 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. LAE001 also inhibits the enzymatic activity of CYP11B2, thereby inhibiting aldosterone production. This may reduce the elevated aldosterone levels resulting from CYP17 inhibition and androgen deprivation, leading to a reduction in mineralocorticoid side effects including cardiovascular complications. The cytochrome P450 enzyme CYP17A1, localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones. The cytochrome P450 enzyme CYP11B2, aldosterone synthase, is an enzyme that plays a key role in aldosterone biosynthesis.
CYP3A4 substrate: Any substance that is metabolized by cytochrome P450 3A4.
cyproheptadine hydrochloride: The hydrochloride salt of a synthetic methyl-piperidine derivative with antihistaminic and anti-serotoninergic properties. Cyproheptadine competes with free histamine (HA) for binding at HA-receptor sites, thereby competitively antagonizing histamine stimulation of HA-receptors in the gastrointestinal tract, large blood vessels, and bronchial smooth muscle. This agent also competes with free serotonin for binding at serotonin receptor sites. Cyproheptadine exhibits anticholinergic and sedative properties and has been shown to stimulate appetite and weight gain.
cyproterone acetate: The acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.
Cyramza: (Other name for: ramucirumab)
Cyren A: (Other name for: diethylstilbestrol)
Cysteine-Rich Non-Denatured Whey Protein Isolate IMN1207: A biologically active, cysteine-rich, undenatured, bovine whey-based protein isolate with potential anti-cachexia and glutathione-enhancing properties. Upon administration of cysteine-rich whey protein isolate, cystine and glutamylcystine are taken up by cells and release free cysteine. The available cysteine allows cells to synthesize glutathione (GSH), a tripeptide made from amino acids glycine, glutamate and cysteine, thereby maintaining and increasing intracellular GSH concentrations. GSH plays a major role as an antioxidant, thereby protecting cells from oxidative damage due to harmful substances such as free radicals and reactive oxygen compounds. As IMN 1207 is rich in protein, this agent may prevent weight loss and increase body weight and strength.
cystemustine: A chloroethylating nitrosourea that causes DNA cross-linking, inhibiting DNA replication. (NCI)
Cysview: (Other name for: hexaminolevulinate hydrochloride)
cytadine analogue RX-3117: An orally available small molecule and nucleoside antimetabolite with potential antineoplastic activity. Upon administration, the cytidine analogue RX-3117 is taken up by cells through a carrier-mediated transporter, phosphorylated by uridine cytidine kinase (UCK) and then further phosphorylated to its diphosphate (RX-DP) and triphosphate forms (RX-TP). The triphosphate form is incorporated into RNA and inhibits RNA synthesis. The diphosphate RX-DP is reduced by ribonucleotide reductase (RR) to dRX-DP; its triphosphate form (dRX-TP) is incorporated into DNA. In addition, RX-3117 also inhibits DNA methyltransferase 1 (DNMT1). This eventually leads to cell cycle arrest and the induction of apoptosis. UCK is the rate-limiting enzyme in the pyrimidine-nucleotide salvage pathway.
Cytadren: (Other name for: aminoglutethimide)
Cytalux: (Other name for: pafolacianine sodium)
cytarabine: An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair.
cytarabine liposome: A liposomal intrathecal formulation of the antimetabolite cytarabine. As an S-phase-specific antimetabolite, cytarabine is phosphorylated by deoxycytidine kinase to a triphosphate form which competes with thymidine for incorporation into DNA; the incorporation of cytarabine triphosphate into DNA appears to inhibit DNA polymerase and so DNA synthesis, resulting in cell death.
cytarabine monophosphate prodrug MB07133: A prodrug of the monophosphate (MP) form of the antimetabolite cytarabine (araCMP), an analogue of cytidine with a modified sugar moiety (arabinose instead of ribose), with potential antineoplastic activity. Upon administration of the cytarabine MP prodrug MB07133, the targeting moiety of this agent specifically delivers the cytarabine moiety to the liver. In turn, araCMP is selectively converted to araC triphosphate (araCTP) by a liver kinase, where it binds to and competes with cytidine for incorporation into DNA, thereby inhibiting DNA polymerase, and DNA synthesis. This leads to the inhibition of tumor cell proliferation and destruction of liver cancer cells. The liver is not able to convert araC into araCMP; araCMP is not converted into araCTP in tissues other than the liver. This enhances efficacy and minimizes systemic toxicity.
Cytembena: A cytostatic agent that interferes with DNA synthesis.
cytochlor: A radio-sensitizing pyrimidine nucleoside with potential antineoplastic activity. Cytochlor is metabolized first to a phosphate derivative, CldCMP, by the enzyme deoxycytidine kinase and then to the active uracyl derivative, CldUMP, by the enzyme dCMP deaminase; deoxycytidine kinase and dCMP deaminase have been found in abnormally high concentrations in most cancers. CldUMP, the active metabolite, incorporates into DNA and, upon exposure to radiation, induces the formation of uracil radicals and double-strand DNA breaks.
cytokine-based biologic agent IRX-2: A cell-free mixture comprised of a variety of naturally-derived cytokines obtained from normal, unrelated donor lymphocytes with potential immunostimulatory activity. The cytokines in IRX-2, including interleukin (IL)-1, -2, -6, -8, -10, -12, tumor necrosis factor alpha (TNF-a), interferon-gamma (IFN-g) and colony stimulating factors (CSFs), play vital roles in regulating cellular immunity and may synergistically stimulate a cellular immune response against tumor cells.
cytokine-induced killer cells: A preparation of cytokine-induced killer (CIK) cells, with potential immunopotentiating and antineoplastic activities. CIK cells are generated from peripheral blood lymphocytes (PBLs) by sequential ex vivo incubation with a monoclonal antibody against CD3 (anti-CD3), interferon-gamma (IFN-g) and interleukin-2 (IL-2), followed by expansion. CIK cells are heterogeneous cells comprising CD3+CD56- T cells, CD3-CD56+ natural killer (NK) cells, and CD3+CD56+ natural killer T (NKT) cells. Upon administration of the CIK cells into the patient, the terminally differentiated CD3- and CD56-positive subset of the CIK cells primarily exert the direct MHC-unrestricted tumor killing activity.
cytokine-treated veto cells: A preparation of activated veto cells, with potential immunostimulating and antineoplastic activities. White blood cells (WBCs), taken from either the patient or a healthy third-party donor, are processed and ex-vivo treated with an as of yet not disclosed mix of cytokines to activate specific cytotoxic veto cells. Upon administration, the veto cells specifically target and bind to tumor or foreign cells, thereby inducing apoptosis. Veto cells are able to selectively activate the immune system to only attack and kill tumor or foreign cells upon transplantation to prevent graft-versus-host disease (GvHD).
cytomegalovirus IE-1-specific cytotoxic T lymphocytes: Cytotoxic T-lymphocytes (CTLs), specifically reactive to the cytomegalovirus (CMV) immediate early-1 (IE-1) protein, with immunomodulating activity. Adoptive immunotherapy with cytomegalovirus IE-1-specific cytotoxic T lymphocytes may help reconstitute CD8+ cytomegalovirus-specific CTL responses in CMV-infected immunocompromised hosts. IE-1 is one of the first CMV antigens expressed by CMV-infected cells, predominantly inducing a CD8+ CTL response.
cytomegalovirus pp65-specific cytotoxic T lymphocytes: Cytotoxic T lymphocytes (CTLs) specifically reactive to the cytomegalovirus (CMV) phosphoprotein pp65 with potential antiviral activity. To prepare CMV pp65-specific cytotoxic T lymphocytes in vitro, dendritic cells (DCs) are pulsed with CMV pp65 epitopes and then used to stimulate and propagate CMV pp65-specific cytotoxic T lymphocytes from peripheral blood mononuclear cells (PBMNCs); the CMV pp65-specific cytotoxic T lymphocyte population is then expanded so as to be sufficient for use in adoptive T lymphocyte therapy. When administered into a patient post-allogeneic hematopoietic stem cell transplantation, this agent may elicit a specific CTL response against CMV-infected host cells, which may result in the resolution of CMV infection. The CMV pp65 protein (65 kDa lower matrix phosphoprotein), the primary component of the enveloped subviral particle, is an immunodominant target for helper and cytotoxic T lymphocyte responses to CMV.
Cytomel: (Other name for: liothyronine sodium)
cytotoxic agent-LAT1 substrate QBS10072S: A blood-brain-barrier (BBB) penetrative agent composed of a cytotoxic chemotherapeutic domain, tertiary N-bis(2-chloroethyl)amine, linked to the structural features of a selective large amino acid transporter 1 (LAT1) substrate, with potential antineoplastic activity. Upon administration of QBS10072S, the LAT1 substrate binds to LAT1 expressed on the BBB and in LAT1-expressing cancer cells, such as glioblastoma multiforme (GBM). After entering the brain and binding to LAT1-expressing tumor cells, the cytotoxic domain in turn binds to DNA, causing cell cycle arrest and induces apoptosis. LAT1 is expressed at much lower levels in normal brain tissue and QBS10072S may therefore potentially target brain tumors while avoiding uptake by healthy, normal tissue.