NCI Drug Dictionary

453 results found for: B

B-GOS: (Other name for: galacto-oligosaccharide prebiotic supplement)
B-Raf/VEGFR-2 inhibitor RAF265: An orally bioavailable small molecule with potential antineoplastic activity. CHIR-265 binds and inhibits Raf kinases, which may result in a reduction of tumor cell growth and proliferation, and tumor cell death. In addition, this agent inhibits vascular endothelial growth factor receptor type 2 (VEGFR-2), thereby disrupting tumor angiogenesis. Raf kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are frequently upregulated in neoplasms.
B. infantis-based formulation PBCLN-014: An orally bioavailable formulation containing the naturally occurring lactic acid-producing gut bacteria Bifidobacterium longum subspecies infantis (B. infantis), with potential immunomodulating activity. Upon oral administration, B. infantis-based formulation PBCLN-014 may restore the unhealthy, altered gut microbiome, enhance the microbial diversity and function in the gastrointestinal (GI) tract and may re-establish a healthy microbiome in the GI tract. This may improve intestinal barrier function, suppress inflammation, enhance the patients' immunological activity and lower the risk of GI antibiotic-resistant bacterial infections, bacteremia and graft-versus-host disease (GvHD) in patients undergoing solid organ and allogeneic stem cell transplantation.
B16alphaGal melanoma vaccine: A whole cell melanoma cancer vaccine with potential immunostimulating and antineoplastic activities. B16alphaGal melanoma vaccine contains three types of human melanoma cell lines that are genetically engineered to express the alpha(1,3)-galactosyl (alphaGal) epitope on cell surfaces. The agent stimulates a hyperacute rejection of whole melanoma cancer cells expressing alphaGal epitopes, initiated by opsonization by anti-alphaGal antibodies and followed by antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis. This results in the stimulation of a broader cytotoxic T-lymphocyte response (CTL) directed against tumor antigens on melanoma cells that do not express alphaGal. AlphaGal is not normally expressed in humans because alpha(1,3)-galactosyltransferase (Alpha-GT), the enzyme that catalyzes the synthesis of alphaGal epitopes on glycoproteins and glycolipids, is not naturally present in humans and other primates.
B43-Genistein immunoconjugate: An immunoconjugate comprised of an anti-CD19 monoclonal antibody conjugated with Genistein selectively targeting B-lineage progenitor cells and inhibiting protein tyrosine kinase, causing apoptosis.
B43-PAP immunotoxin: A mouse-derived anti-human CD19 monoclonal antibody linked to pokeweed (Phytolacca americana) antiviral protein (PAP) with antileukemic activity. The monoclonal antibody portion specifically binds to the CD19 antigen, a cell surface molecule normally expressed only by B lymphocytes and follicular dendritic cells and over-expressed in B-lineage lymphocytic leukemia cells. Following internalization, PAP, a plant hemitoxin and a ribosome-inactivating protein, is cleaved from the immunoconjugate and released into the cytoplasm where it enzymatically removes a single adenine base from a conserved, surface exposed loop sequence of rRNA leading to inhibition of protein synthesis and cell growth, but not necessarily cell death.
B7-DC cross-linking antibody rHIgM12B7: A recombinant form of the monoclonal IgM antibody M12 isolated from a Waldenstrom macroglobulinaemia patient (rHIgM12) with potential immunomodulating activity. B7-DC cross-linking antibody rHIgM12B7 binds and crosslinks the B7 co-stimulatory family member B7-DC (PD-L2) on dendritic cells (DCs), antigen presenting cells (APCs) that play a crucial role in the human immune response. This results in enhanced activation of DCs; enhanced antigen-presenting activity; and increased production of immunomodulatory cytokines (especially interleukin 12); and may potentiate a specific cytotoxic T lymphocyte (CTL) response against Waldenstrom macroglobulinaemia B cells.
B7-H4-targeting agent: Any agent that targets the T-cell checkpoint ligand B7-H4 (B7H4; V-set domain-containing T-cell activation inhibitor 1; VTCN1; B7x; B7S1).
B7H3/CD3-targeting T-cell engaging molecule TAK-280: A T-cell engaging bispecific antibody and Conditional Bispecific Redirected Activation (COBRA) protein targeting both the tumor-associated antigen (TAA) and immunoregulatory protein B7-homologue 3 (B7-H3, CD276) and the T-cell surface antigen CD3, with potential immunostimulating and antineoplastic activities. Upon intravenous administration, B7H3/CD3-targeting T-cell engaging molecule TAK-280 is cleaved by proteases in the tumor microenvironment (TME). Upon cleavage, TAK-280 is activated and binds to both CD3 on cytotoxic T lymphocytes (CTLs) and B7H3 on B7H3-expressing tumor cells. This activates and redirects CTLs to B7H3-expressing tumor cells, leading to a CTL-mediated killing of B7H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of T-cell activation and its overexpression plays a key role in tumor cell invasion and metastasis.
babaodan capsule: An orally available mixed powder of traditional Chinese medicine containing eight constituents including natural calculus bovis, snake gall, antelope horn, pearl, musk, radix notoginseng, and other as of yet not disclosed ingredients, with potential antifibrotic, immunomodulatory, and antineoplastic activities. Upon oral administration, babaodan may ameliorate substance-induced liver injury and fibrosis, and inhibit lipopolysaccharide (LPS)-induced hepatic stellate cell (HSC) activation and proliferation through toll-like receptor 4 (TLR4)/nuclear factor-kappa B and TLR4/extracellular-signal-regulated kinase (ERK) pathways. Babaodan may, through an as of yet not elucidated mechanism, enhance the efficacy of chemotherapeutic drugs and may inhibit the occurrence and development of certain tumor types.
bacitracin: A complex of cyclic polypeptide antibiotics, mainly bacitracin A, produced by spore-forming organisms belonging to the licheniformin group of the Bacillus subtilis with antibacterial activity. Bacitracin binds to C55-isoprenyl pyrophosphate, a biphosphate lipid transport molecule that carries the building blocks of the peptidoglycan bacterial cell wall. The binding interferes with the enzymatic dephosphorylation of the C55-isoprenyl pyrophosphate and prevents peptidoglycan synthesis, thereby inhibiting bacterial cell growth.
baclofen: A synthetic chlorophenyl-butanoic acid derivative used to treat spasms due to spinal cord damage and multiple sclerosis. Muscle-relaxing Baclofen acts as a gamma-aminobutyric acid (GABA) agonist specific for GABA-B receptors. It acts at spinal and supraspinal sites, reducing excitatory transmission.
baclofen/amitriptyline/ketamine gel: A topical preparation of baclofen, amitriptyline, and ketamine compounded in a penetration-enhancing polaxamer-lecithin organogel (PLO) with potential antineuralgic activity. The gamma-aminobutyric acid (GABA) analogue baclofen appears to activate the inhibitory GABA(B) receptor, a G protein-coupled receptor, which may result in hyperpolarization of the neuronal cell membrane and inhibition of neurotransmitter release. Amitriptyline likely produces antineuralgic effects via modulation of multiple subtypes of glutamate (Glu) receptors, independent of its antidepressant actions. Ketamine displays complex pharmacologic actions including biogenic amine uptake inhibition, interaction with opioid receptors, and inhibition of N-methyl D-aspartate (NMDA) receptors. Stimulation of GABA(B) receptor activity, modulation of Glu receptor activity, and inhibition of NMDA receptor activity may be of benefit in managing neuropathic pain.
bacterial type III secretion-based agent T3P-Y058-739: A therapeutic based on a genetically-modified, live attenuated strain of the bacterium Yersinia enterocolitica that is able to deliver a combination of as of yet undisclosed type I interferons (IFN) and toll-like receptor (TLR) protein payloads, with potential immunomodulating and antineoplastic activities. Upon administration, bacterial type III secretion (T3S)-based agent T3P-Y058-739 may selectively target tumor cells, colonize and deliver the protein payloads into tumor cells. This may activate type I IFN- and TLR-mediated signaling, thereby activating an immune response and killing tumor cells.
bacteriophage phi X 174 vaccine: A vaccine composed of the bacteriophage phi X 174, a virus that infects the bacterium Escherichia coli (E. coli), that can be used as a diagnostic agent to measure immune function of immunocompromised patients. Upon administration of the bacteriophage phi X 174 vaccine, the bacteriophage may activate the immune system to induce bacteriophage phi X174 specific antibody responses. The clearance of phage from the blood and the measurement of phage neutralization by antibodies can be used to assess the immune status of patients with suspected antibody-mediated immunodeficiency and to measure the response to certain therapies.
Bactrim: (Other name for: Trimethoprim-Sulfamethoxazole)
Bactrim DS: (Other name for: Trimethoprim-Sulfamethoxazole)
bafetinib: An orally active 2-phenylaminopyrimidine derivative with potential antineoplastic activity. INNO-406 specifically binds to and inhibits the Bcr/Abl fusion protein tyrosine kinase, an abnormal enzyme produced by Philadelphia chromosomal translocation associated with chronic myeloid leukemia (CML). Furthermore, this agent also inhibits the Src-family member Lyn tyrosine kinase, upregulated in imatinib-resistant CML cells and in a variety of solid cancer cell types. The inhibitory effect of INNO-406 on these specific tyrosine kinases decreases cellular proliferation and induces apoptosis. A high percentage of CML patients are refractory to imatinib, which sometimes results from point mutations occurring in the kinase domain of the Bcr/Abl fusion product. Due to its dual inhibitory activity, INNO-406 has been shown to overcome this particular drug resistance and to be a potent and effective agent in the treatment of imatinib-resistant CML.
bafisontamab: A human, Fabs-in-tandem immunoglobulin (FIT-Ig)-based, tetravalent, bispecific antibody targeting both the epidermal growth factor receptor EGFR and the hepatocyte growth factor receptor (HGFR;; cMet; c-Met), with potential antineoplastic activity. Upon administration, bafisontamab simultaneously targets and binds to wild-type or certain mutant forms of both EGFR and c-Met expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and c-Met-mediated signaling pathways and results in the inhibition of tumor cell proliferation. EGFR and c-Met, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation. In bafisontamab, the two antigen-binding fragments (Fabs) are fused directly in a crisscross orientation resulting in four active and independent antigen binding sites.
Bag Balm: (Other name for: 8-hydroxyquinoline sulfate ointment)
balanced crystalloid solution: A multiple electrolyte, isotonic, crystalloid solution for intravenous infusion containing sodium chloride, sodium gluconate, sodium acetate, potassium chloride and magnesium chloride, which can restore electrolyte balance, normalize pH, and provide hydration. Upon intravenous administration, the balanced crystalloid solution will replace lost body fluids and electrolytes thereby providing hydration, normalizing electrolyte concentrations and regulating acid-base balance.
balixafortide: An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. Balixafortide binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. 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; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.
baloramotide: A genetically engineered synthetic protein, recombinant NY-ESO-1 protein (cancer-testis tumor antigen family) elicits strong humoral and cellular immune responses to NY-ESO-1-expressing cancers and is used to produce specific vaccines to increase the immune response against tumors. NY-ESO-1 epitopes presented by human HLA are recognized by CD4(+) T lymphocytes in patients with NY-ESO-1-expressing melanoma.
baloxavir marboxil: An orally bioavailable prodrug and influenza cap-dependent endonuclease (CEN) inhibitor, with antiviral activity. Upon administration of baloxavir marboxil, the agent is converted by hydrolysis to its active metabolite baloxavir. Baloxavir targets, binds to and inhibits the CEN activity of the influenza polymerase acidic (PA) protein, an influenza virus-specific enzyme in the viral RNA polymerase complex required for the initiation of influenza gene transcription. By inhibiting PA endonuclease, influenza virus mRNA replication is halted. This reduces viral load and prevents further influenza infection.
balstilimab: A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks 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.
baltaleucel-T: A preparation of autologous Epstein-Barr virus (EBV)-specific cytotoxic T lymphocytes (CTLs), which have specific reactivity to the EBV antigens, latent membrane proteins (LMP) 1 (LMP1) and 2 (LMP2), EBV nuclear antigen (EBNA) and BamHI-A rightward frame-1 (BARF1), with potential immunomodulating and antineoplastic activities. Upon administration, baltaleucel-T targets and binds to EBV-expressing cancer cells specifically expressing the targeted antigens. This may kill LMP1/LMP2/EBNA/BARF1-expressing EBV-associated cancer cells. LMP1, LMP2, EBNA and BARF1 are tumor-associated antigens (TAAs) that are specifically associated with EBV infection, and play key roles in the proliferation of a variety of tumors.
Balversa: (Other name for: erdafitinib)
Balziva: (Other name for: ethinyl estradiol/norethindrone)
banoxantrone: A bioreductive, alkylaminoanthraquinone prodrug with antineoplastic activity. Under hypoxic conditions, often seen in solid tumors, banoxantrone (AQ4N) is converted and activated by cytochrome P450 enzymes, which are upregulated in certain tumors, to the cytotoxic DNA-binding agent AQ4. Banoxantrone intercalates into and crosslinks DNA, and inhibits topoisomerase II. This results in an inhibition of DNA replication and repair in tumor cells. Combined with conventional therapeutic agents, both oxygenic and hypoxic regions of tumors can be targeted.
bapotulimab: A mouse/human cross-reactive immunoglobulin G2 (IgG2) monoclonal antibody against the immune checkpoint immunoglobulin-like domain containing receptor 2 (ILDR2; Chromosome 1 Open Reading Frame 32; C1orf32), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, bapotulimab targets, binds to and inhibits ILDR2, thereby blocking the immunosuppressive activity of ILDR2. This prevents ILDR2-mediated inhibition of T-cell activities and induces a cytotoxic T-lymphocyte (CTL) response against tumor cells. ILDR2, a type I transmembrane protein belonging to the B7 family of immunomodulatory receptors, negatively regulates T-cell responses.
Baraclude: (Other name for: entecavir)
barasertib: An orally bioavailable, small-molecule, dihydrogen phosphate prodrug of the pyrazoloquinazoline Aurora kinase inhibitor AZD1152-hydroxyquinazoline pyrazol anilide (AZD1152-HQPA) with potential antineoplastic activity. Upon administration and rapid conversion from the prodrug form in plasma, AZD1152-HQPA specifically binds to and inhibits Aurora kinase B, which results in the disruption of spindle checkpoint functions and chromosome alignment and, so, the disruption of chromosome segregation and cytokinesis. Consequently, cell division and cell proliferation are inhibited and apoptosis is induced in Aurora kinase B-overexpressing tumor cells. Aurora kinase B, a serine/threonine protein kinase that functions in the attachment of the mitotic spindle to the centromere, is overexpressed in a wide variety of cancer cell types.
bardoxolone: A synthetic triterpenoid compound with potential antineoplastic and anti-inflammatory activities. Bardoxolone blocks the synthesis of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), two enzymes involved in inflammation and carcinogenesis. This agent also inhibits the interleukin-1 (IL-1)-induced expression of the pro-inflammatory proteins matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13) and the expression of Bcl-3; Bcl-3 is an IL-1-responsive gene that preferentially contributes to MMP-1 gene expression.
bardoxolone methyl: The methyl ester form of bardoxolone, a synthetic triterpenoid compound with potential antineoplastic and anti-inflammatory activities. Bardoxolone blocks the synthesis of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), two enzymes involved in inflammation and carcinogenesis. This agent also inhibits the interleukin-1 (IL-1)-induced expression of the pro-inflammatory proteins matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13) and the expression of Bcl-3; Bcl-3 is an IL-1-responsive gene that preferentially contributes to MMP-1 gene expression.
barecetamab: A fully human antibody directed against the receptor tyrosine-protein kinase erbB-3 (ErbB3; HER3) with potential antineoplastic activity. Upon intravenous administration, barecetamab targets and binds to domain 3 and weakly interacts with domain 1 of ErbB3. This prevents heregulin (HRG) binding and blocks dimerization of ErbB3, thereby inactivating ErbB3 downstream signaling. ISU104 may also elicit the internalization of ErbB3 from the plasma membrane and downregulate ErbB3 expression. This inhibits cellular proliferation and survival of ErbB3-expressing tumor cells. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in a variety of tumors and its overexpression generally correlates with poor prognosis and tumor resistance.
baricitinib: An orally bioavailable inhibitor of Janus kinases 1 and 2 (JAK1/2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, baricitinib binds to JAK1/2, which inhibits JAK1/2 activation and leads to the inhibition of the JAK-signal transducers and activators of transcription (STAT) signaling pathway. This decreases the production of inflammatory cytokines and may prevent an inflammatory response. In addition, baricitinib may induce apoptosis and reduce proliferation of JAK1/2-expressing tumor cells. JAK kinases are intracellular enzymes involved in cytokine signaling, inflammation, immune function and hematopoiesis; they are also upregulated and/or mutated in various tumor cell types.
barium sulfate: The sulfate salt of barium, an alkaline, divalent metal. Barium sulfate is quite insoluble in water, and is used as a radiopaque agent to diagnose gastrointestinal medical conditions. Barium sulfate is taken by mouth or given rectally.
Barrigel: (Other name for: hyaluronic acid-based gel)
Barseb HC: (Other name for: therapeutic hydrocortisone)
base edited natural killer cells NK510: A preparation of natural killer (NK) cells derived from human peripheral blood and base-edited for as of yet not elucidated modifications, with potential cytolytic and antineoplastic activities. Upon administration, base edited NK cells NK510 recognize and lyse cancer cells. The NK cells also secrete pro-inflammatory cytokines, which further stimulate an anti-tumor immune response.
Basen: (Other name for: voglibose)
basiliximab: A recombinant, chimeric, human-murine monoclonal antibody directed against the alpha subunit of the interleukin-2 receptor (IL-2R alpha) with immunosuppressant activity. Basiliximab selectively binds to and blocks IL-2R alpha, expressed on the surface of activated T-lymphocytes, thereby preventing interleukin-2 binding and inhibiting the interleukin-2-mediated activation of lymphocytes.
basiliximab-IR700 RM-1995: An antibody-dye conjugate composed of basiliximab, a chimeric monoclonal antibody directed against the alpha subunit of interleukin-2 receptor (IL-2R alpha, CD25 or Tac antigen), and conjugated to the light-activatable phthalocyanine dye IR700 (IRDye 700DX), with potential antineoplastic activity. Upon intravenous administration of basiliximab-IR700 RM-1995, the basiliximab moiety targets and binds to IL-2R alpha expressed on the surface of activated regulatory T lymphocytes (Tregs) in the tumor microenvironment (TME). Upon binding and localized application of 690nm nonthermal red light using the PIT690 laser system, the IR700 dye transiently becomes activated, disrupts the cell membrane and selectively kills the IL-2R alpha-expressing Tregs. This may abrogate the Tregs-mediated immunosuppressive nature of the TME and may result in systemic anti-cancer immune activation. This may activate a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD25-positive Tregs inhibit antitumor immune responses and enhance tumor growth.
basroparib: An orally bioavailable inhibitor of the poly (ADP-ribose) polymerase (PARP) enzyme tankyrase, with potential antineoplastic activity. Upon administration, basroparib selectively binds to and inhibits the activity of tankyrase. This may block the tankyrase-mediated poly(ADP-ribosyl)ation of multiple target proteins including various tumor suppressors. This may include the blockage of the poly(ADP-ribosyl)ation and destabilization of AXIN, a negative regulator of beta-catenin, and prevents Wnt/beta-catenin signaling. This may inhibit 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. Tankyrase, a member of the PARP family, plays an important role in the regulation of the Wnt/beta-catenin signaling pathway, tumor suppressors, as well as telomere maintenance and mitosis regulation.
batabulin sodium: The sodium salt form of batabulin, a synthetic pentafluorophenylsulfonamide with potential antineoplastic activity. Batabulin covalently binds to and selectively modifies the beta 1, beta 2, beta 3, and beta 4 isotypes of beta tubulin at a conserved cysteine residue, resulting in disruption of microtubule polymerization, collapse of the cytoskeleton, an increase in chromosomal ploidy, cell cycle arrest, and tumor cell apoptosis.
batanopride: A serotonin antagonist having antiemetic properties.
batiraxcept: A soluble fusion protein comprised of the extracellular domain of the receptor tyrosine kinase (RTK) AXL (UFO) fused to a human immunoglobulin G1 (IgG1) Fc domain, with potential antineoplastic activity. Upon administration, batiraxcept selectively binds to growth arrest-specific protein 6 (GAS6), the endogenous ligand for AXL. This may inhibit GAS6/AXL-mediated signaling, which plays a key role in tumor cell proliferation, survival, invasion and metastasis, as well as immune evasion and resistance to other anticancer agents. AXL, a member of the Tyro3, AXL and Mer (TAM) family of RTKs, is overexpressed by many tumor cell types and its expression is associated with drug resistance and poor prognosis.
batoclimab: A human monoclonal antibody directed against the neonatal crystallizable fragment receptor (FcRn), with potential immunomodulating activity. Upon administration, batoclimab targets and binds to FcRn at the immunoglobulin G (IgG) binding site, thereby preventing the interaction between FcRn and the serum protein IgG. By preventing FcRn/IgG binding, batoclimab blocks the FcRn-mediated rescue of IgG, enables IgG degradation and prevents IgG-mediated inflammation. IgG plays a key role in many autoimmune diseases and is an important factor in inflammatory processes.
batoprotafib: An inhibitor of protein tyrosine phosphatase (PTP) non-receptor type 11 (SHP2; src homology region 2 domain phosphatase; PTPN11), with potential antineoplastic activity. Upon oral administration,batoprotafib binds to and inhibits SHP2. This prevents SHP2-mediated signaling, inhibits MAPK signaling and prevents growth of SHP2-expressing tumor cells. SHP2, an oncoprotein overexpressed in a variety of cancer cell types, regulates cell survival, differentiation and proliferation through activation of the RAS-RAF-ERK signaling pathway. SHP2 also regulates programmed cell death 1 (PD-1)-mediated signal transduction and is involved in immune checkpoint modulation.
bavdegalutamide: An orally available selective androgen receptor (AR)-targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. Bavdegalutamide is composed of an AR ligand attached to an E3 ligase recognition moiety. Upon oral administration, bavdegalutamide targets and binds to the AR ligand binding domain. E3 ligase is recruited to the AR by the E3 ligase recognition moiety and the AR target protein is tagged by ubiquitin. This causes ubiquitination and degradation of AR by the proteasome. This prevents the expression of AR target genes and halts AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. In addition, the degradation of the AR protein releases the ARV-110 is released and can bind to additional AR target proteins. AR plays a key role in the proliferation of castration-resistant prostate cancer cells (CRPC).
Bavencio: (Other name for: Avelumab)
bavituximab: A chimeric, IgG1 monoclonal antibody directed against anionic phospholipids with potential antineoplastic activity. Bavituximab binds to anionic phospholipids in a beta 2-glycoprotein I-dependent manner, inhibiting tumor growth by stimulating antibody-dependent cellular cytotoxicity (ADCC) to tumor vessels.
Baycadron: (Other name for: dexamethasone)
BayGam: (Other name for: therapeutic immune globulin)
bazedoxifene: An indole derivative and third-generation selective estrogen receptor modulator (SERM) with potential antineoplastic activity. Upon administration, bazedoxifene specifically binds to estrogen receptors in responsive tissues, including liver, bone, breast, and endometrium. The resulting ligand-receptor complex is translocated to the nucleus where, depending on the tissue type, it either promotes or suppresses the transcription of estrogen-regulated genes. 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. Bazedoxifene functions as an estrogen agonist in lipid metabolism, thereby decreasing total and LDL cholesterol levels. In bone, it decreases bone resorption and bone turnover and increases bone mineral density.
Bazlitoran: An oligonucleotide targeted to the mRNA of MYD88 L265P, a mutant form of the linker protein MYD88, with potential antitumor activity. Bazlitoran binds to and inhibits the translation of mutated MYD88 L265P mRNA. This prevents overactivation of signaling pathways mediated by toll-like receptors (TLRs) 7, 8, and 9, nuclear factor-kappa B (NF-kB) activity, Janus-associated kinases-signal transducer and activator of transcription (JAK-STAT) signaling and the production of various cytokines. Together, this leads to an induction of apoptosis and an inhibition of tumor cell proliferation in MYD88 L265P-expressing tumor cells. MYD88, a key adaptor protein in the TLR signaling pathway, is mutated in a variety of B-cell lymphomas, including Waldenstrom's macroglobulinemia (WM) and activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL).
BC-819 plasmid/polyethylenimine complex: A plasmid DNA encoding for the A fragment of Diphtheria Toxin (DTA) under the control of the H19 gene promoter (BC-819 or DTA-H19) and mixed with the transfectant polyethylenimine (PEI), with potential antineoplastic activity. Upon administration, the PEI moiety enhances the entry of the agent into rapidly dividing cells. Upon cell entry, activation of the H19 gene promoter-containing plasmids and DTA expression are limited to tumor cells, as high levels of H19 expression are only found in tumor cells. DTA disrupts protein synthesis. Tumor-cell selective expression of this toxin leads to the selective destruction of the tumor while sparing healthy, normal cells. H19, an oncofetal, regulatory RNA, is overexpressed in certain cancer cells while its expression in normal cells is minimal or absent; it plays a key role in cancer progression, angiogenesis and metastasis.
BCG solution: A solution containing an attenuated, live culture preparation of the Bacillus Calmette Guerin (BCG) strain of Mycobacterium bovis with potential immunostimulating activity. Although the precise mechanism of action is unknown, upon intravesical administration, attenuated, live BCG bacteria in the solution come into direct contact with the bladder wall, inciting an antitumor granulomatous inflammatory reaction.
BCG Tokyo-172 strain solution: A solution containing an attenuated, live culture preparation of the bacillus Calmette-Guerin (BCG) strain of Mycobacterium bovis obtained from the Pasteur Institute in 1924, with potential immunostimulating and antineoplastic activities. Although the precise mechanism of action is unknown, upon intravesical instillation through a catheter, the attenuated, live BCG bacteria in the BCG Tokyo-172 strain solution come into direct contact with the bladder wall and elicits a local, multifaceted immune response against the BCG antigens, which kills the bladder cancer cells. Previous vaccination with a systemic BCG vaccine may enhance the immune system's response against the BCG antigens.
BCG Tokyo-172 strain vaccine: A vaccine containing bacillus Calmette-Guerin (BCG), a live, attenuated strain of Mycobacterium bovis obtained from the Pasteur Institute in 1924, with non-specific immunoadjuvant and immunotherapeutic activities. Upon intradermal administration, BCG Tokyo-172 strain vaccine activates the immune system and enhances a specific, systemic BCG antigen immune response. This results in active immunization against tuberculosis and primes the immune system against future administered BCG antigens.
BCG vaccine: A vaccine containing bacillus Calmette-Guerin (BCG), an attenuated strain of Mycobacterium bovis, with non-specific immunoadjuvant and immunotherapeutic activities. Although the mechanism of its anti-tumor activity is unclear, immunization with BCG vaccine likely activates a Th1 cytokine response that includes the induction of interferon. Vaccination with BCG vaccine may be immunoprotective against infection with Mycobacterium tuberculosis.
Bcl-2 family protein inhibitor: Any agent that inhibits any of the Bcl-2 family members.
BCL-2 inhibitor ABBV-453: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor ABBV-453 targets, binds to and inhibits the activity of Bcl-2. This restores caspase-mediated apoptosis in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis. Its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor ABBV-623: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor ABBV-623 targets, binds to and inhibits the activity of Bcl-2. This restores caspase-mediated apoptosis in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis. Its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor BCL201: A selective inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon administration, Bcl-2 inhibitor BCL201 binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor BGB-21447: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor BGB-21447 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
BCL-2 inhibitor ICP-248: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor ICP-248 targets, binds to and inhibits the activity of Bcl-2. This restores caspase-mediated apoptosis in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis. Its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor LOXO-338: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor LOXO-338 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor LP-108: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor LP-108 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor TGRX-814: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor TGRX-814 targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2 inhibitor TQB3909: An orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2 inhibitor TQB3909 targets, binds to and inhibits the activity of Bcl-2. This restores caspase-mediated apoptosis in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis. Its expression is associated with increased drug resistance and tumor cell survival.
Bcl-2/Bcl-XL inhibitor LP-118: An orally bioavailable inhibitor of the anti-apoptotic proteins B-cell lymphoma-2 (Bcl-2) and Bcl-extra large (Bcl-XL), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, Bcl-2/Bcl-XL inhibitor LP-118 selectively targets, binds to and inhibits the activity of Bcl-2 and Bcl-XL. This restores apoptotic processes in tumor cells. Bcl-2 and Bcl-XL, Bcl-2 family proteins overexpressed in many cancers, play important roles in the negative regulation of apoptosis. Their expression is associated with increased drug resistance and tumor cell survival.
Bcl-XL proteolysis targeting chimera DT2216: An anti-apoptotic protein B-cell lymphoma-extra large (Bcl-XL) targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential pro-apoptotic, immunomodulating and antineoplastic activities. DT2216 is composed of a Bcl-XL ligand attached to a Von Hippel-Lindau (VHL) E3 ligase ligand. Upon administration of DT2216, the Bcl-XL binding moiety specifically targets and binds to Bcl-XL which is expressed on tumor-infiltrating regulatory T cells (Tregs) in the tumor microenvironment (TME) and cancer cells that are dependent on Bcl-XL for their survival, such as certain Bcl-XL-dependent T-cell malignancies. In turn, the VHL E3 ligase ligand is recruited to the endoplasmic reticulum (ER) and Bcl-XL is tagged by ubiquitin. This causes ubiquitination and proteasome-mediated degradation of Bcl-XL. The degradation of Bcl-XL leads to an inhibition of the anti-apoptotic activity of Bcl-XL and restores apoptotic processes in and causes depletion of Bcl-XL-expressing Tregs and Bcl-XL-dependent cancer cells. Reduction of Tregs may activate anti-tumor CD8-positive-mediated immune responses. This leads to the inhibition of tumor growth. Bcl-XL, a protein belonging to the Bcl-2 family, plays an important role in the negative regulation of apoptosis. Their expression in tumors is associated with increased Tregs survival. Tregs play a key role in cancer progression and tumor immunosuppression. Compared to other Bcl-XL inhibitors, DT2216 does not cause platelet toxicity as the VHL E3 ligase is not highly expressed in platelets.
BCL2 inhibitor VOB560: An inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon intravenous administration, Bcl-2 inhibitor VOB560 binds to and inhibits the activity of Bcl-2, thereby restoring apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in many cancer types and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.
BCL6 degrader ARV-393: An orally bioavailable, targeted degrader composed of an E3 ubiquitin ligase-binding moiety that is conjugated, via a linker, to a B-cell lymphoma 6 protein (BCL6; BCL-6)-binding moiety using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. Upon oral administration of BCL6 degrader ARV-393, the BCL6-binding moiety specifically targets and binds to BCL6 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 BCL6. This prevents BCL6-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress BCL6. BCL6, a transcriptional repressor overexpressed in certain tumor cells, serves an important role in cell signaling and tumor cell proliferation.
BCL6 degrader BMS-986458: An orally bioavailable ligand directed degrader (LDD) composed of an E3 ubiquitin ligase-binding moiety that is conjugated, via a linker, to a B-cell lymphoma 6 protein (BCL6; BCL-6)-binding moiety, with potential antineoplastic activity. Upon oral administration, BCL6 degrader BMS-986458 specifically and simultaneously targets and binds to BCL6 on tumor cells and to E3 ubiquitin ligase, thereby creating a ternary complex. This induces E3 ligase ubiquitination and proteasome-mediated degradation of BCL6. This prevents BCL6-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress BCL6. BCL6, overexpressed in certain tumor cells, serves an important role in cell signaling and tumor cell proliferation.
BCMA CART cells secreting mutant PD-1Fc fusion protein: A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; TNFRSF17) and secrete a fusion protein composed of programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) and a human immunoglobulin Fc region, with potential immunomodulating and antineoplastic activities. Upon administration of the BCMA CAR T cells secreting mutant PD-1Fc fusion protein, these T cells target and bind to tumor cells expressing BCMA and induce selective cytotoxicity in those tumor cells. The expressed PD-1-Fc fusion protein targets and binds to programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells, thereby halting PD-1/PD-L1-mediated signaling. This may decrease T-cell exhaustion and may enhance T-cell activity against the PD-L1-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA is found on the surfaces of plasma cells, is overexpressed on malignant plasma cells and plays a key role in plasma cell proliferation and survival. PD-1, an immune checkpoint receptor expressed on T cells, plays a key role in tumor immune evasion by binding to its ligand PD-L1 expressed on tumor cells.
BCMA-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) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and one specific for the TAA CD19, with potential immunomodulating and antineoplastic activities. Upon administration, the BCMA-CD19 cCAR T cells specifically and simultaneously target and bind to tumor cells expressing BCMA and/or CD19. This induces selective toxicity in tumor cells that express BCMA and/or CD19. BCMA, a tumor-specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in the survival of B lymphocytes and plasma cells. BCMA is found on the surfaces of B cells and is overexpressed on malignant plasma cells. CD19 is a B-cell-specific cell surface antigen overexpressed in B-cell lineage malignancies. 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.
BCMA-specific universal CAR-expressing T lymphocytes LCAR-BCX: A preparation of universal T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, BCMA-specific universal CAR-expressing T lymphocytes LCAR-BCX are directed to cells expressing BCMA and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is overexpressed on malignant plasma cells.
BCMA-targeted LCAR-BCDR cells: A preparation of T lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17), with potential immunostimulating and antineoplastic activities. Upon administration, BCMA-targeted LCAR-BCDR cells specifically recognize and kill BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.
BCMA-TGF-beta insensitive armored CAR T cells: A preparation of human T lymphocytes genetically engineered to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; tumor necrosis factor receptor superfamily member 17; TNFRSF17) and armored to be insensitive to the immunosuppressive cytokine transforming growth factor-beta (TGF-beta), with potential immunostimulating and antineoplastic activities. Upon administration, BCMA-TGF-beta insensitive armored CAR T cells specifically recognize and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). BCMA, found on the surfaces of plasma cells and overexpressed on malignant plasma cells, plays a key role in plasma cell proliferation and survival. Though the nature of the TGF-beta armor has yet to be fully elucidated, it prevents the binding of TGF-beta to the CAR T-cells. TGF-beta negatively regulates T-cell proliferation and activation, 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.
BCMA/CD3e tri-specific T-cell activating construct HPN217: A recombinant antibody derivative composed of tri-specific T-cell activating construct (TriTAC) directed against the human tumor-associated antigen (TAA) B-cell maturation antigen (BCMA; TNFRSF17), the epsilon domain of CD3 antigen (CD3e) found on T lymphocytes, and albumin, with potential immunostimulating and antineoplastic activities. Upon administration, BCMA/CD3e TriTAC HPN217 targets and binds to BCMA on tumor cells and CD3e on cytotoxic T lymphocytes (CTLs), thereby bringing BCMA-expressing tumor cells and CTLs together, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. The albumin-binding domain targets and binds to serum albumin, thereby extending the serum half-life of HPN217. BCMA, a member of the tumor necrosis factor receptor superfamily (TNFRSF), is overexpressed on malignant plasma cells and plays a key role in plasma cell survival.
BCR signaling pathway inhibitor DZD8586: An inhibitor of the B-cell antigen receptor (BCR) signaling pathway, with potential antineoplastic activity. Upon administration, BCR signaling pathway inhibitor DZD8586 blocks signaling through the BCR signaling pathway. This prevents the proliferation of malignant B cells in which the BCR signaling pathway is overactivated. DZD8586 is able to cross the blood-brain barrier (BBB) and thus potentially useful in the treatment of central nervous system (CNS) metastases.
bcr-abl (b2a2)-derived peptide vaccine: A peptide vaccine consisting of the bcr-abl b2a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b2a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b2a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.
bcr-abl (b3a2)-derived peptide vaccine: A peptide vaccine consisting of the bcr-abl b3a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b3a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b3a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.
BCR-ABL inhibitor ELVN-001: An orally bioavailable, selective, active-form inhibitor of tyrosine kinase BCR-ABL fusion oncoprotein, with potential antineoplastic activity. Upon oral administration, BCR-ABL inhibitor ELVN-001 specifically targets and binds to the ATP-binding site in the kinase domain of activated BCR-ABL1, thereby inhibiting the activity of both wild-type BCR-ABL and certain mutation forms, including the T315I mutation. This binding results in the inhibition of BCR-ABL-mediated proliferation and enhanced apoptosis of Philadelphia chromosome-positive (Ph+) hematological malignancies. The BCR-ABL fusion protein tyrosine kinase is an abnormal enzyme produced by leukemia cells that contain the Philadelphia chromosome. The T315I mutation, the most common BCR-ABL mutation, shows resistance to nearly all commonly used tyrosine kinase inhibitors (TKIs).
BCR-ABL inhibitor HS-10382: An orally bioavailable, allosteric tyrosine kinase inhibitor of the BCR-ABL fusion oncoprotein, with potential antineoplastic activity. Upon oral administration, BCR-ABL inhibitor HS-10382 targets and binds to the ABL myristoyl pocket, locking BCR-ABL into an inactive conformation, thereby inhibiting the activity of BCR-ABL and decreasing the proliferation of tumor cells. BCR-ABL fusion protein is an aberrantly activated tyrosine kinase produced by certain leukemia cells.
BCR-ABL inhibitor TGRX-678: An orally bioavailable inhibitor of the tyrosine kinase BCR-ABL fusion oncoprotein, with potential antineoplastic activity. Upon oral administration, BCR-ABL inhibitor TGRX-678 specifically targets and binds to the myristate site at the C-terminal of the kinase domain, which results in the cross-linking of SH3 and SH2 domains to the kinase domain, and locks the kinase in its inactive state. This inhibits the activity of BCR-ABL, including the T315I gatekeeper residue mutation. The binding results in the inhibition of BCR-ABL-mediated proliferation and enhanced apoptosis of Philadelphia chromosome-positive (Ph+) hematological malignancies. The BCR-ABL fusion protein tyrosine kinase is an abnormal enzyme produced by leukemia cells that contain the Philadelphia chromosome. The T315I mutation, the most common BCR-ABL mutation, shows resistance to nearly all commonly used tyrosine kinase inhibitors (TKIs).
Bcr-Abl kinase inhibitor K0706: An orally bioavailable, Bcr-Abl tyrosine kinase inhibitor (TKI), with potential antineoplastic activity. Upon administration, Bcr-Abl kinase inhibitor K0706 selectively targets and binds to the Bcr-Abl fusion oncoprotein, including various Bcr-Abl mutant forms, such as those with the ‘gatekeeper’ resistance mutation T315I. This inhibits proliferation of Bcr-Abl-expressing tumor cells. The Bcr-Abl fusion protein is an aberrantly activated tyrosine kinase produced by certain leukemia cells. T315I, a threonine (T) to isoleucine (I) amino acid substitution at position 315 in the tyrosine-protein kinase ABL1 portion of the Bcr-Abl fusion protein, plays a key role in resistance to certain chemotherapeutic agents, and its expression is associated with poor prognosis.
Bcr-Abl kinase inhibitor PF-114: An orally bioavailable, Bcr-Abl tyrosine kinase inhibitor, with potential antineoplastic activity. Designed to overcome resistance of tumor cells to second generation Bcr-Abl inhibitors, PF-114 targets and binds to the Bcr-Abl fusion oncoprotein, including those fusion proteins with the ‘gatekeeper’ resistance mutation T315I, an amino acid substitution at position 315 in Bcr-Abl from a threonine (T) to an isoleucine (I). This inhibits Bcr-Abl-mediated proliferation of, and enhances apoptosis in, Philadelphia chromosome-positive (Ph+) hematologic malignancies. The Bcr-Abl fusion protein is an aberrantly activated tyrosine kinase produced by leukemia cells that contain the Philadelphia chromosome.
BCR-ABL p210-b3a2 breakpoint-derived pentapeptide vaccine: A multipeptide vaccine consisting of five peptides derived from the bcr-abl p210-b3a2 breakpoint fusion protein with potential antineoplastic activity. Vaccination with bcr-abl p210-b3a2 breakpoint-derived multipeptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl p210-b3a2 breakpoint fusion protein. In chronic myelogenous leukemia (CML), fusion genes typically result from the fusion of either bcr exon b2 or exon b3 to abl exon a2, resulting in either a b3a2 or a b2a2 gene fusion product.
bcr-abl peptide vaccine: A multivalent antineoplastic vaccine comprised of the bcr-abl oncogene breakpoint fusion peptide that elicits a bcr-abl specific T-cell immune response.
BD2-selective BET inhibitor NUV-868: An orally bioavailable BD2-selective inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, BD2-selective BET inhibitor NUV-868 primarily targets and binds to the BD2 domain of the BRD4 BET protein, thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and suppresses the expression of certain oncogenes, resulting in the inhibition of tumor cell growth. BRD4, a transcriptional regulator, plays an important role in the modulation of gene expression during tumor cellular growth. NUV-868 is designed to be more selective for BD2 than BD1 to avoid the therapeutic limiting toxicities of other non-selective BD1/2 BRD4 inhibitors, such as gastrointestinal (GI) and bone marrow toxicities.
BEACOPP regimen: A regimen consisting of bleomycin, etoposide, doxorubicin hydrochloride (Adriamycin), cyclophosphamide, vincristine (Oncovin), procarbazine and prednisone, used for the treatment of advanced-stage Hodgkin lymphoma.
Bead Block Compressible Microspheres: (Other name for: PVA microporous hydrospheres)
becatecarin: A synthetic diethylaminoethyl analogue of the indolocarbazole glycoside antineoplastic antibiotic rebeccamycin. Becatecarin intercalates into DNA and stabilizes the DNA-topoisomerase I complex, thereby interfering with the topoisomerase I-catalyzed DNA breakage-reunion reaction and initiating DNA cleavage and apoptosis.
beclabuvir: A non-nucleoside, polymerase inhibitor of the hepatitis C virus (HCV) nonstructural protein 5B (NS5B), a RNA-dependent RNA polymerase, with potential activity against HCV. Upon administration and after intracellular uptake, beclabuvir allosterically binds to the non-catalytic Thumb 1 site of viral HCV NS5B polymerase and causes a decrease in viral RNA synthesis and replication. The HCV NS5B protein is essential for the replication of the viral HCV RNA genome. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family.
beclomethasone dipropionate: The dipropionate ester of a synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, beclomethasone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production.
Beclovent: (Other name for: beclomethasone dipropionate)
Beconase: (Other name for: beclomethasone dipropionate)
becotatug: A human immunoglobulin G1 (IgG1) monoclonal antibody directed against human epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon administration, becotatug targets, binds to and prevents the activation of EGFR. This inhibits EGFR-mediated signaling and proliferation of EGFR-expressing tumor cells. In addition, JMT101 may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against EGFR-expressing tumor cells. EGFR, a member of the epidermal growth factor receptor family, is overexpressed on various tumor cell types.
bedaquiline: An orally bioavailable diarylquinoline antimycobacterial agent, that can be used in the treatment of pulmonary multi-drug resistant tuberculosis (MDR-TB). Upon oral administration, bedaquiline specifically binds to subunit c of Mycobacterium tuberculosis (M. tuberculosis) adenosine 5'-triphosphate (ATP) synthase, thereby preventing ATP synthase activity. This inhibits ATP synthesis in M. tuberculosis, thereby blocking its energy metabolism and killing M. tuberculosis.
bedaquiline fumarate: The fumarate salt form of bedaquiline, an orally bioavailable diarylquinoline antimycobacterial agent, that can be used in the treatment of pulmonary multi-drug resistant tuberculosis (MDR-TB). Upon oral administration, bedaquiline specifically binds to subunit c of Mycobacterium tuberculosis (M. tuberculosis) adenosine 5'-triphosphate (ATP) synthase, thereby preventing ATP synthase activity. This inhibits ATP synthesis in M. tuberculosis, thereby blocking its energy metabolism and killing M. tuberculosis.
Beesix: (Other name for: pyridoxine hydrochloride)
BeetElite NeoShot: (Other name for: concentrated beet crystals)
beetroot juice: The juice of the beetroot, with potential antioxidant and protective activities. Beetroot juice contains antioxidants, including betacyanin, which scavenge free radicals. In addition, beetroot contains high levels of nitrates and folic acid. Consumption of beetroot juice leads to the conversion of nitrate to nitric oxide (NO) in the body. This juice may have a beneficial effect on blood flow and blood pressure through the induction of NO-mediated vasodilation. Additionally, this agent may decrease fatigue and increase physical performance.
befotertinib: An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, befotertinib specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. Compared to some other EGFR inhibitors, befotertinib may have therapeutic benefits in tumors with T790M-mediated drug resistance. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
Begedina: (Other name for: begelomab)
begelomab: A monoclonal antibody against the human dipeptidyl peptidase 4 (dipeptidylpeptidase IV, DPPIV, DPP4; CD26), with potential activity against graft-versus-host disease (GvHD). Upon administration, begelomab binds to CD26 expressed on T cells. This inhibits the stimulation of T cells and may prevent GvHD. CD26, a membrane-bound glycoprotein with dipeptidyl peptidase activity, plays a key role in T-cell activation and immune regulation.
belagenpumatucel-L: A transforming growth factor beta2 (TGF-beta2) antisense gene-modified allogeneic tumor cell vaccine with potential immunostimulatory and antineoplastic activities. Belagenpumatucel-L is prepared by transfecting allogeneic non-small cell lung cancer (NSCLC) cells with a plasmid containing a TGF-beta2 antisense transgene, expanding the cells, and then irradiating and freezing them. Upon administration, this agent may elicit a cytotoxic T lymphocyte (CTL) response against host NSCLC cells, resulting in decreased tumor cell proliferation; vaccine immunogenicity may be potentiated by suppression of tumor TGF-beta2 production by antisense RNA expressed by the vaccine plasmid TGF-beta2 antisense transgene. Elevated levels of TGF-beta2 are frequently linked to immunosuppression in cancer patients and may be inversely correlated with prognosis in patients with NSCLC.
belantamab mafodotin-blmf: An antibody-drug conjugate (ADC) consisting of belantamab, an afucosylated, humanized monoclonal antibody, directed against the B-cell maturation antigen (BCMA), conjugated to mafodotin, an auristatin analogue and microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. Upon administration of belantamab mafodotin, the anti-BCMA antibody moiety selectively binds to BCMA on tumor cell surfaces. Upon internalization, the MMAF moiety binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces tumor cell apoptosis. In addition, belantamab mafodotin-blmf induces antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of cellular proliferation in tumor cells that overexpress BCMA. BCMA, a receptor for a proliferation-inducing ligand and B-cell activating factor, is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma cell survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. Afucosylation of the antibody moiety increases ADCC.
belapectin: A carbohydrate-based galectin inhibitor, with potential antineoplastic activity. Belapectin binds to the carbohydrate-binding domain of galectins, especially galectin-3, and may result in an induction of apoptosis mediated through activation of both mitochondria and caspases. This may reduce tumor growth in galectin-overexpressing tumor cells. Galectins, often overexpressed on tumor cells, play a key role in cancer cell proliferation, apoptosis, tumor angiogenesis and evasion of immune responses.
Beleodaq: (Other name for: belinostat)
belimumab: A fully human IgG1 monoclonal antibody directed against B-Lymphocyte stimulator protein (BlyS or TNFSF13B) with potential immunomodulating activity. Belimumab specifically recognizes and inhibits the biological activity of BlyS, thereby preventing the binding of BlyS to B lymphocytes. This inhibits the maturation of B-lymphocytes and may induce apoptosis in B-lymphocytes. In addition, it may decrease B-lymphocyte proliferation and/or survival. BlyS, a member of TNF family supporting B-lymphocyte maturation and survival, has been implicated in the pathogenesis of autoimmune diseases and B-lymphocyte malignancies.
belinostat: A novel hydroxamic acid-type histone deacetylase (HDAC) inhibitor with antineoplastic activity. Belinostat targets HDAC enzymes, thereby inhibiting tumor cell proliferation, inducing apoptosis, promoting cellular differentiation, and inhibiting angiogenesis. This agent may sensitize drug-resistant tumor cells to other antineoplastic agents, possibly through a mechanism involving the down-regulation of thymidylate synthase.
belotecan hydrochloride: The hydrochloride salt of the semi-synthetic camptothecin analogue belotecan with potential antitumor activity. Belotecan binds to and inhibits the activity of topoisomerase I, stabilizing the cleavable complex of topoisomerase I-DNA, which inhibits the religation of single-stranded DNA breaks generated by topoisomerase I; lethal double-stranded DNA breaks occur when the topoisomerase I-DNA complex is encountered by the DNA replication machinery, DNA replication is disrupted, and the tumor cell undergoes apoptosis. Topoisomerase I is an enzyme that mediates reversible single-strand breaks in DNA during DNA replication.
Belrapzo: (Other name for: bendamustine hydrochloride)
belrestotug: A human immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and anti-tumor activities. Upon administration, belrestotug targets and binds to TIGIT expressed on various immune cells, including tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. In addition, belrestotug may preferentially deplete immunosuppressive, TIGIT-expressing regulatory T-cells (Tregs) through Fc gamma receptor interaction and antibody-dependent cellular cytotoxicity (ADCC). This may further enhance anti-tumor activity. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.
Belsomra: (Other name for: suvorexant)
belumosudil: An orally bioavailable inhibitor of Rho-associated coiled-coil kinase 2 (ROCK2; ROCK-II), with potential immunomodulating activity. Upon oral administration, belumosudil binds to and inhibits the serine/threonine kinase activity of ROCK2. This inhibits ROCK2-mediated signal transduction pathways and modulates various pro- and anti-inflammatory immune cell responses through the regulation of signal transducer and activator of transcription 3 and 5 (STAT3/STAT5) phosphorylation. This downregulates pro-inflammatory Th17 cells and increases regulatory T (Treg) cells. Belumosudil also inhibits ROCK2-mediated fibrotic processes, including stress fiber formation, myofibroblast activation and pro-fibrotic gene transcription. ROCK2 is upregulated in various diseases, including various fibrotic, neurodegenerative and autoimmune diseases.
belumosudil mesylate: The mesylate salt form of belumosudil, an orally bioavailable inhibitor of Rho-associated coiled-coil kinase 2 (ROCK2; ROCK-II), with potential immunomodulating activity. Upon oral administration, belumosudil binds to and inhibits the serine/threonine kinase activity of ROCK2. This inhibits ROCK2-mediated signal transduction pathways and modulates various pro- and anti-inflammatory immune cell responses through the regulation of signal transducer and activator of transcription 3 and 5 (STAT3/STAT5) phosphorylation. This downregulates pro-inflammatory Th17 cells and increases regulatory T (Treg) cells. Belumosudil also inhibits ROCK2-mediated fibrotic processes, including stress fiber formation, myofibroblast activation and pro-fibrotic gene transcription. ROCK2 is upregulated in various diseases, including various fibrotic, neurodegenerative and autoimmune diseases.
belvarafenib: An orally available inhibitor of members of the Raf family of serine/threonine protein kinases, with potential antineoplastic activity. Upon administration, belvarafenib binds to and inhibits the B-Raf mutant V600E and C-Raf. This inhibits B-Raf V600E- and C-Raf-mediated signal transduction pathways, thereby inhibiting tumor cell growth of susceptible tumor cells. In addition, belvarafenib may also inhibit mutated Ras proteins. Raf protein kinases play a key role in the Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. The Raf mutation B-Raf V600E, where the valine at residue 600 is substituted for glutamic acid, is frequently overexpressed in a variety of human tumors and results in the constitutive activation of the Raf/MEK/ERK signaling pathway.
belzupacap sarotalocan: A formulation composed of nanoparticles derived from the human papillomavirus (HPV-NPs) and conjugated to the infrared (IR)-activated fluorescent dye IR700 (IR-700), with potential antineoplastic activity. Upon intravitreal injection of belzupacap sarotalocan, the HPV-NPs target and bind to heparan-sulfated proteoglycans (HSPG) expressed by ocular melanoma cells. Upon irradiation with near-IR (NIR) light, the photosensitizer IR700 becomes activated, generates reactive oxygen species (ROS) and selectively damages the melanoma cell membrane, which induces necrosis of the melanoma cells while sparing the surrounding, healthy non-HSPG-expressing tissue, and potentially preserving vision. HSPGs are overexpressed on a variety of cancer cell types.
belzutifan: An orally active, small molecule inhibitor of hypoxia inducible factor (HIF)-2alpha (HIF-2a), with potential antineoplastic activity. Upon oral administration, belzutifan binds to and blocks the function of HIF-2alpha, thereby preventing HIF-2alpha heterodimerization and its subsequent binding to DNA. This results in decreased transcription and expression of HIF-2alpha downstream target genes, many of which regulate hypoxic signaling. This inhibits cell growth and survival of HIF-2alpha-expressing tumor cells. HIF-2alpha, the alpha subunit for the heterodimeric transcription factor HIF-2, is overexpressed in many cancers and promotes tumorigenesis.
bemarituzumab: A glycoengineered, humanized monoclonal antibody directed against the fibroblast growth factor receptor type 2b (FGFR2b), with potential antineoplastic activity. Upon administration, bemarituzumab specifically binds to and inhibits FGFR2b on tumor cell surfaces, which prevents FGFR2 from binding to its ligands, FGFR2b activation and the activation of FGFR2b-mediated signal transduction pathways. The binding of bemarituzumab to FGFR2b protein also induces antibody-dependent cell-mediated cytotoxicity (ADCC) against FGFR2b-expressing tumor cells. This results in the inhibition of cell proliferation and the induction of cell death of FGFR2-expressing tumor cells. FGFR2b, a specific isoform of the receptor tyrosine kinase FGFR2 upregulated in many tumor cell types, is essential to tumor proliferation, differentiation and survival. Glycoengineering enhances the FPA144-mediated ADCC.
bemcentinib: An orally available and selective inhibitor of the AXL receptor tyrosine kinase (UFO), with potential antineoplastic activity. Upon administration, bemcentinib targets and binds to the intracellular catalytic kinase domain of AXL and prevents its activity. This blocks AXL-mediated signal transduction pathways and inhibits the epithelial-mesenchymal transition (EMT), which, in turn, inhibits tumor cell proliferation and migration. In addition, bemcentinib enhances chemo-sensitivity. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.
bemiparin sodium: The sodium salt of bemiparin, a second generation, synthetic, low-molecular-weight heparin (LMWH) with anticoagulant activity. Derived, after depolymerisation and fractionation, from medical-grade porcine unfractionated heparin (UFH), bemiparin has an average molecular weight of 3,600 daltons and has a higher anti-factor Xa/anti-factor IIa ratio (8:1) than first-generation LMWHs. This anticoagulant binds to antithrombin III, thereby enhancing the inactivation of activated Factor X (Factor Xa) and, to a lesser extent, activated factor II (Factor IIa). Compared to unfractionated heparins, the use of bemiparin is associated with lower incidences of major bleeding, osteoporosis, and heparin-induced thrombocytopenia. Bemiparin also promotes a greater release of tissue factor pathway inhibitor than UFH or dalteparin.
bempegaldesleukin: A recombinant form of the endogenous cytokine interleukin-2 (IL-2) conjugated to six releasable polyethylene glycol (PEG) chains, with potential immunostimulating activity. Upon administration of bempegaldesleukin, the IL-2 moiety 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 primarily causes tumor cell destruction. IL2Rb plays a key role in the proliferation and activation of effector T cells. PEG conjugation prevents IL-2 binding to the IL2Ralpha subunit (IL2Ra) because signaling through IL2Ra activates CD4-positive regulatory, immunosuppressive T cells (Tregs), which would suppress tumor cell killing.
Benadryl: (Other name for: diphenhydramine hydrochloride)
benazepril hydrochloride: The hydrochloride salt of benazepril, a carboxyl-containing angiotensin-converting enzyme (ACE) inhibitor with antihypertensive activity. As a prodrug, benazepril is metabolized to its active form benazeprilat. Benazeprilat competitively binds to and inhibits ACE, thereby blocking the conversion of angiotensin I to angiotensin II. This prevents the potent vasoconstrictive actions of angiotensin II, resulting in vasodilation. Benazeprilat also decreases angiotensin II-induced aldosterone secretion by the adrenal cortex, which leads to an increase in sodium excretion and subsequently increases water outflow.
bendamustine hydrochloride: The hydrochloride salt of bendamustine, a bifunctional mechlorethamine derivative with alkylator and antimetabolite activities. Bendamustine possesses three active moieties: an alkylating group; a benzimidazole ring, which may act as a purine analogue; and a butyric acid side chain. Although its exact mechanism of action is unknown, this agent appears to act primarily as an alkylator. Bendamustine metabolites alkylate and crosslink macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis. Bendamustine may differ from other alkylators in that it may be more potent in activating p53-dependent stress pathways and inducing apoptosis; it may induce mitotic catastrophe; and it may activate a base excision DNA repair pathway rather than an alkyltransferase DNA repair mechanism. Accordingly, this agent may be more efficacious and less susceptible to drug resistance than other alkylators.
bendamustine-containing nanoparticle-based formulation RXDX-107: A nanoparticle-based formulation containing the alkyl ester of bendamustine, a bifunctional mechlorethamine derivative, encapsulated in human serum albumin (HSA), with potential alkylating and antineoplastic activities. Upon administration of the alkyl ester bendamustine-containing nanoparticle formulation RXDX-107, the nanoparticle formulation permits high concentrations of the alkyl ester of bendamustine be localized at the tumor site. The modified bendamustine alkylates and crosslinks macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis.
Bendeka: (Other name for: bendamustine hydrochloride)
Bendopa: (Other name for: levodopa)
Benefin: (Other name for: shark cartilage)
Benemid: (Other name for: probenecid)
Beneo Synergy 1: (Other name for: oligofructose-enriched inulin)
Benlysta: (Other name for: belimumab)
benmelstobart: A humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, benmelstobart specifically targets and binds to PD-L1, preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
Benoquin: (Other name for: monobenzone)
benralizumab: An afucosylated, humanized monoclonal antibody against the alpha chain of the interleukin-5 receptor (IL-5Ra), with potential anti-asthmatic activity. Upon administration, benralizumab binds to IL-5Ra and elicits an antibody-directed cell cytotoxicity (ADCC) against IL-5Ra-expressing cells. This induces apoptosis in IL-5Ra-expressing cells and may reduce asthmatic episodes. IL-5Ra, expressed on both eosinophils and basophils, plays a key role in asthma.
benzaldehyde dimethane sulfonate: A dimethane sulfonate derivative and alkylating agent with a structure similar to other alkylating agents such as chlorambucil, busulfan and melphalan, with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, benzaldehyde dimethane sulfonate alkylates DNA, which results in DNA double strand breaks, inhibition of DNA replication, cell cycle arrest and cell death. In addition, this agent is metabolized by the enzyme aldehyde dehydrogenase (ALDH) into the active carboxylic acid metabolite benzoic acid dimethane sulfonate (BA), which further contributes to its alkylating activity. Unlike other alkylating agents, benzaldehyde dimethane sulfonate has demonstrated antitumor activity in renal cell carcinoma.
benznidazole: A nitroimidazole derivative having an antiprotozoal activity by interfering with parasite protein biosynthesis, influencing cytokines production and stimulating host phagocytosis. (NCI)
benzoylphenylurea: A low molecular weight agent with antineoplastic activity. Benzoylphenylurea binds to the colchicine binding site on tubulin, thereby blocking tubulin polymerization and disrupting mitotic function. This agent also inhibits DNA polymerase, and has been shown to arrest leukemia cells in the G1-S transition phase of the cell cycle.
benzydamine hydrochloride: An indazole non-steroidal anti-inflammatory drug (NSAID) with analgesic, antipyretic, and anti-edema properties. Unlike other NSAIDs, benzydamine hydrochloride does not inhibit cyclooxygenases (COX) but stabilizes membranes, resulting in local anesthesia; inhibits the production of pro-inflammatory cytokines; inhibits the generation of reactive oxygen species by neutrophils; inhibits leukocyte aggregation and adhesion; and exhibits antimicrobial properties.
BEP regimen: A regimen consisting of bleomycin, etoposide and cisplatin that may be used for the treatment of gestational trophoblastic neoplasia (GTN), malignant sex cord-stromal tumors, ovarian and testicular cancer, including ovarian and testicular germ cell tumors (GCTs).
berberine chloride: The orally bioavailable, hydrochloride salt form of berberine, a quaternary ammonium salt of an isoquinoline alkaloid and active component of various Chinese herbs, with potential antineoplastic, radiosensitizing, anti-inflammatory, anti-lipidemic and antidiabetic activities. Although the mechanisms of action through which berberine exerts its effects are not yet fully elucidated, upon administration this agent appears to suppress the activation of various proteins and/or modulate the expression of a variety of genes involved in tumorigenesis and inflammation, including, but not limited to transcription factor nuclear factor-kappa B (NF-kB), myeloid cell leukemia 1 (Mcl-1), B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xl), cyclooxygenase (COX)-2, tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), C-X-C motif chemokine 2 (CXCL2), cyclin D1, activator protein (AP-1), hypoxia-inducible factor 1 (HIF-1), signal transducer and activator of transcription 3 (STAT3), peroxisome proliferator-activated receptor (PPAR), arylamine N-acetyltransferase (NAT), and DNA topoisomerase I and II. The modulation of gene expression may induce cell cycle arrest and apoptosis, and inhibit cancer cell proliferation. In addition, berberine modulates lipid and glucose metabolism.
bermekimab: A human immunoglobulin (Ig) G1 monoclonal antibody directed against interleukin-1 alpha (IL-1a) and derived from human B lymphocytes that were obtained from a natural human immune response against IL-1a, with potential antineoplastic, anti-inflammatory, anti-cachectic and anti-angiogenic activities. Upon administration, bermekimab targets, binds to and neutralizes IL-1a thereby preventing IL-1a activity. This prevents IL-1a-mediated inflammation, tumorigenesis and angiogenesis. In addition, bermekimab may abrogate IL-1a-mediated cachexia and stimulate metabolic activity in the central nervous system (CNS). IL-1a, an inflammatory mediator expressed on monocytes, platelets and overexpressed by certain tumors, plays a key role in the promotion of tumor cell growth, metastasis and invasion.
bersanlimab: A fully human IgG1 monoclonal antibody directed against intercellular adhesion molecule-1 (ICAM-1 or CD54), with potential antineoplastic activity. Bersanlimab selectively binds to the adhesion protein ICAM-1, which may result in antibody-dependent cellular cytotoxicity (ADCC), hyper-cross-linking-induced apoptosis, and a decrease in cellular proliferation of ICAM-1-expressing tumor cells. ICAM-1, normally expressed on leukocytes and endothelial cells, may be overexpressed in a variety of cancers.
berubicin hydrochloride: The hydrochloride salt of the anthracycline derivative berubicin with potential antineoplastic activity. Berubicin intercalates into DNA and interrupts topoisomerase II activity, resulting in the inhibition of DNA replication and repair, and RNA and protein synthesis. Unlike other anthracycline derivatives, this agent crosses the blood-brain barrier (BBB).
Berubigen: (Other name for: cyanocobalamin)
berzosertib: An inhibitor of ataxia telangiectasia and rad3-related (ATR) kinase, a DNA damage response kinase, with potential antineoplastic activity. Upon administration, berzosertib selectively binds to and inhibits ATR kinase activity and prevents ATR-mediated signaling in the ATR-checkpoint kinase 1 (Chk1) signaling pathway. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, and induces 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.
Besponsa: (Other name for: inotuzumab ozogamicin)
Besremi: (Other name for: ropeginterferon alfa-2B)
besufetamig: A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the T-cell surface antigen CD3, with potential immunomodulatory and antineoplastic activities. Upon administration, besufetamig binds to both PD-1 expressed on activated T and B cells and certain malignant T cells and CD3 antigen on cytotoxic T lymphocytes (CTLs). This may activate and redirect CTLs to PD-1-expressing cells, resulting in CTL-mediated killing of these cells. This may lead to anti-tumor activity in some T-cell lymphomas, and immunomodulatory activity in some autoimmune diseases.
BET bromodomain inhibitor ZEN-3694: An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ZEN-3694 binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.
BET inhibitor ABBV-744: An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ABBV-744 preferentially binds to the second bromodomain (BD2) of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that contain two homologous bromodomains, the BD1 and BD2 domains. They play an important role during development and cellular growth.
BET inhibitor BAY1238097: An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BAY1238097 binds to the acetylated lysine recognition motifs on the BRD of BET proteins, thereby preventing the interaction between BET proteins and histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes. This leads to an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.
BET inhibitor BMS-986158: An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BMS-986158 binds to the acetyl-lysine binding site in the BRD of BET proteins, thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes, resulting in an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.
BET inhibitor FT-1101: An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor FT-1101 binds to the acetylated lysine recognition motifs in the bromodomain sites of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to the inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.
BET inhibitor GSK2820151: An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor GSK2820151 binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.
BET inhibitor INCB054329: An inhibitor of the bromodomain and extra-terminal (BET) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor INCB054329 binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, BET proteins, BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular growth.
BET inhibitor INCB057643: An inhibitor of the Bromodomain (BRD) and Extra-Terminal (BET) family of BRD-containing proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor INCB057643 binds to the acetylated lysine recognition motifs found in the BRD of BET proteins, thereby preventing the interaction between the BET proteins and acetylated lysines on histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes, such as c-Myc-dependent target genes, may lead to an inhibition of tumor cell growth. BET proteins are transcriptional regulators that are overexpressed in certain tumor cells and play an important role in cellular growth.
BET inhibitor JAB-8263: An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic and anti-fibrotic activities. Upon oral administration, BET inhibitor JAB-8263 targets and binds to bromodomain-containing proteins 2, 3, and 4 (BRD2, BRD3, and BRD4) as well as bromodomain testis-specific protein (BRDT), thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and suppresses the expression of certain oncogenes and profibrotic genes, including Myc and other transcriptional regulators. Preventing the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth and fibrosis. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.
BET inhibitor RO6870810: A small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor RO6870810 binds to the acetylated lysine recognition motifs found in the bromodomain of BET proteins, which prevents the interaction between BET proteins and acetylated histones. This interaction disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.
BET inhibitor TQB3617: An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, BET inhibitor TQB3617 targets and binds to the acetyl-lysine binding site in the bromodomains (BRDs), thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and suppresses the expression of certain oncogenes, resulting in the inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role in the modulation of gene expression during cellular growth and development.
BET-bromodomain inhibitor ODM-207: An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ODM-207 binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression of oncogenic drivers that are important for cell proliferation and survival. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that bind to acetylated lysine residues in histones and play an important role during development and cellular growth. In tumor cells, BET proteins play a key role in the regulation of oncogene transcription and tumor cell proliferation.
BET/CBP/p300 inhibitor EP31670: An orally bioavailable inhibitor of the bromodomains (BRDs) of the bromodomain and extra-terminal (BET) family of proteins and the histone acetyltransferase (HAT) paralogs CREB binding protein (CBP) and p300 (E1A-associated protein p300; p300 HAT), with potential antineoplastic activity. Upon oral administration, BET/CBP/p300 inhibitor EP31670 targets and binds to the BET proteins bromodomain-containing proteins 2, 3, and 4 (BRD2, BRD3, and BRD4) and bromodomain testis-specific protein (BRDT), as well as the BRD of CBP and p300. This prevents the interaction between BET proteins and acetylated histones, disrupts chromatin remodeling and suppresses the expression of certain oncogenes, resulting in the inhibition of tumor cell growth. BET proteins are transcriptional regulators that play an important role in the modulation of gene expression during cellular growth and development. In addition, this prevents the co-activation of the androgen receptor (AR) including AR-v7 by CBP and p300, which 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.
beta alethine: A disulfide agent that stimulates T and B-cell functions and exhibits anti-tumor and immunostimulant activity. (NCI)
beta carotene: A naturally-occurring retinol (vitamin A) precursor obtained from certain fruits and vegetables with potential antineoplastic and chemopreventive activities. As an anti-oxidant, beta carotene inhibits free-radical damage to DNA. This agent also induces cell differentiation and apoptosis of some tumor cell types, particularly in early stages of tumorigenesis, and enhances immune system activity by stimulating the release of natural killer cells, lymphocytes, and monocytes.
beta endorphin: An endogenous opioid-like substance found in the hypothalamus and pituitary gland that produces a sense of well-being, euphoria, and can reduce physical and emotional pain.
beta tubulin polymerization inhibitor CCI-001: A colchicine derivative and beta tubulin polymerization inhibitor, with potential antineoplastic activity. Upon administration, beta tubulin polymerization inhibitor CCI-001 targets, binds to and inhibits beta-III tubulin (TUBB3), and prevents tubulin polymerization and destabilizes microtubules, ultimately leading to cell cycle arrest, blockage of cell division and an induction of cell death in cancer cells. TUBB3, overexpressed in many cancers, is associated with poor outcomes and a reduced response to taxane-based microtubule-targeting antineoplastic agents.
beta-catenin inhibitor FOG-001: A conformationally stabilized alpha-helical polypeptide and direct inhibitor of the oncogenic driver beta-catenin, with potential immunomodulating and antineoplastic activities. Upon administration, beta-catenin inhibitor FOG-001 penetrates into the cell where it targets and binds to beta-catenin, thereby preventing the interaction of beta-catenin with the transcriptional factor T-cell factor (TCF). This disrupts beta-catenin-dependent oncogenic signaling and prevents the transcription of Wnt target genes that regulate the proliferation, migration, invasion, and the metastatic potential of tumor cells, as well as genes regulating the immunosuppression of the tumor microenvironment (TME). Dysregulation of the Wnt/beta-catenin signaling pathway is found in a variety of tumors and drives oncogenesis.
beta-elemene: One of the isomers of elemene, a lipid soluble sesquiterpene and the active component isolated from the Chinese medicinal herb Rhizoma zedoariae with potential antineoplastic and chemopreventive activities. Although the exact mechanism of action through which beta-elemene exerts its effect has yet to be fully elucidated, this agent appears to induce apoptosis through different mechanisms of action and induces cell cycle arrest at different stages based on the tumor cell type involved. Beta-elemene may sensitize cancer cells to other chemotherapeutic agents.
beta-glucan: A polysaccharide isolated from the cell walls of bacteria, plants, and fungi with immunostimulant and antineoplastic activities. In a solubilized form, beta-glucan binds to a lectin site within complement receptor 3 (CR3) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to complement 3 (iC3b)-coated tumors. Thus, the attachment of beta-glucan to CR3 of circulating leukocytes simulates leukocytes to kill iC3b-coated tumor cells in the same way as they kill iC3b-coated yeast.
beta-glucan MM-10-001: A powder formulation containing a triple helix beta-glucan, isolated from the cell walls of the shiitake mushroom (Lentinula edodes), with potential immunostimulating activity. The beta-glucan in beta-glucan MM-10-001 binds to a lectin site within the complement receptor 3 (CR3 or iC3b receptor) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to iC3b-opsonized tumor cells. iC3b is the proteolyticly inactive product of the complement cleavage fragment C3b.
beta-glucan/alginate/hyaluronic acid/squalene/avocado oil-containing emulsion: A topical emulsion containing beta-glucan (5%), alginate, hyaluronic acid, squalene and avocado oil, with cutaneous protective activity. Upon topical application of beta-glucan/alginate/hyaluronic acid/squalene/avocado oil-containing emulsion, the naturally-occurring polysaccharide beta-glucan acts as an immunomodulator by activating the innate immune response, in particular through the activation of macrophages and migration of neutrophils. Alginate acts as a moisturizer and supports skin healing. Hyaluronic acid, squalene and avocado oil provide barrier protection, help maintain skin integrity and are natural emollients and moisturizers. This emulsion may accelerate wound healing and may prevent radiation-induced dermatitis.
beta-glucan/dexpanthenol/glutamine in mucoadhesive polymer hydrogel: A water soluble, hydrogel-based formulation containing beta-glucan, a polysaccharide isolated from the cell walls of bacteria, plants, and fungi, dexpanthenol, an alcohol derivative of pantothenic acid, the nonessential amino acid glutamine, and preserved water, that can potentially be used to treat mucositis. Upon oral administration of the beta-glucan/dexpanthenol/glutamine in mucoadhesive polymer hydrogel, the mucoadhesive polymer hydrogel interacts with the oral mucosa and promotes contact time between the active ingredients and the mucous membranes in the mouth while also providing moisture and serving as a protective barrier. The additional preserved water may also keep the oral mucosa moisturized. Dexpanthenol is converted to pantothenic acid (vitamin B5) which is required for coenzyme A synthesis as well as for the metabolism of proteins, carbohydrates, and fats. Coenzyme A is involved in fatty acids and sphingolipids synthesis crucial for cell membrane integrity. Dexpanthenol may promote cell proliferation and epithelial remodeling and may provide a protective and healing effect on the oral mucosa. Beta-glucan may stimulate the immune system, may protect against pathogens and may prevent inflammation. Glutamine may also help maintain the integrity of the oral mucosa, prevent cellular damage, and improve cellular recovery. Altogether, this may prevent or reduce radiation/chemotherapy-induced mucositis.
beta-glucan/Lactobacillus casei/Bifidobacterium lactis-based supplement: A synbiotic supplement containing beta-1,3-glucan, bacteria Lactobacillus casei (L. casei) and Bifidobacterium lactis (B. lactis), with potential immunomodulating activity. The naturally-occurring bacterial components in this dietary supplement may improve digestion and help maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. During colonization of the GI tract, the bacteria may form a protective intestinal barrier, thereby preventing attachment of potential pathogens. Both the probiotics and beta-glucan have been shown to stimulate the immune system. This supplement also contains several vitamins and other insoluble polysaccharides.
beta-hydroxy-beta-methylbutyrate supplement: A nutritional supplement containing the active metabolite of the essential amino acid leucine, with potential anti-catabolic and anabolic activities. Upon oral administration of beta-hydroxy-beta-methylbutyrate (HMB), this leucine metabolite may decrease protein breakdown and increase protein synthesis thereby increasing muscle strength and mass. Although the exact mechanisms remain to be fully elucidated, multiple mechanisms have been proposed: 1) HMB is a precursor of cholesterol synthesis in skeletal muscle cells thereby increasing sarcolemmal integrity; 2) HMB may inhibit the ubiquitin-proteasome proteolytic pathway responsible for the specific degradation of intracellular proteins, thereby preventing muscular proteolysis; and/or 3) HMB may stimulate protein synthesis through a mammalian target of rapamycin (mTOR)-mediated mechanism.
beta-lapachone: A poorly soluble, ortho-naphthoquinone with potential antineoplastic and radiosensitizing activity. Beta-lapachone (b-lap) is bioactivated by NAD(P)H:quinone oxidoreductase-1 (NQO1), creating a futile oxidoreduction that generates high levels of superoxide. In turn, the highly reactive oxygen species (ROS) interact with DNA, thereby causing single-strand DNA breaks and calcium release from endoplasmic reticulum (ER) stores. Eventually, the extensive DNA damage causes hyperactivation of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme facilitating DNA repair, accompanied by rapid depletion of NAD+/ATP nucleotide levels. As a result, a caspase-independent and ER-stress induced mu-calpain-mediated cell death occurs in NQO1-overexpressing tumor cells. NQO1, a flavoprotein and two-electron oxidoreductase, is overexpressed in a variety of tumors.
beta-lapachone prodrug ARQ 761: A synthetic, soluble prodrug of beta-lapachone, a poorly soluble, ortho-naphthoquinone with potential antineoplastic and radiosensitizing activity. ARQ 761 is converted to beta-lapachone (b-lap) in vivo. When b-lap is activated by NAD(P)H:quinone oxidoreductase-1 (NQO1) this agent creates a futile oxidoreduction, generating highly reactive oxygen species (ROS) that results in DNA damage. The activation of b-lap also causes hyperactivation of poly (ADP-ribose) polymerase-1 (PARP-1), an enzyme that facilitates DNA repair, accompanied by rapid depletion of NAD+/ATP nucleotide levels. As a result, a caspase-independent and endoplasmic reticulum (ER) stress-induced mu-calpain-mediated cell death occurs in NQO1-overexpressing tumor cells. In addition, b-lap induces expression of the checkpoints activator E2F transcription factor 1 (E2F1) and thereby activates the E2F1-mediated checkpoint pathway that directly triggers apoptosis. As ARQ 761 is soluble and requires less solvent, this formulation may cause less hemolytic anemia associated with administration of the synthetic b-lap ARQ 501.
beta-thioguanine deoxyriboside: A thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication. This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo. Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells.
Betadine: (Other name for: povidone-iodine solution)
Betadine Solution: (Other name for: povidone-iodine solution)
betaglucin gel: A soluble gel containing the beta-glucan betaglucin, with potential immunostimulating activity. Upon topical administration of the betaglucin gel, betaglucin is able to increase the number of macrophages and natural killer (NK) cells. NK cells and macrophages may kill a variety of tumor cells, and virally infected cells. This may treat human papillomavirus (HPV)-related anogenital warts.
betahistine hydrochloride nasal spray: A nasal spray containing the hydrochloride salt form of betahistine, a histamine analog with weak histamine H1 agonistic and more potent histamine H3 antagonistic properties. Upon intranasal administration, betahistine binds to histamine H1 and H3 receptors and exerts its agonistic and antagonistic actions locally and centrally. This promotes cochlear, vestibular and cerebral blood flow, decreases neuronal firing in the vestibular nuclei and increases histamine synthesis and release in the brain which facilitates vestibular compensation.
Betalin 12: (Other name for: cyanocobalamin)
BetaLT: (Other name for: beta alethine)
BetaMarc: (Other name for: formoterol fumarate/roxithromycin)
betamethasone: A synthetic glucocorticoid with metabolic, immunosuppressive and anti-inflammatory activities. Betamethasone binds to specific intracellular glucocorticoid receptors and subsequently binds to DNA to modify gene expression. The synthesis of certain anti-inflammatory proteins is induced while the synthesis of certain inflammatory mediators is inhibited. As a result, there is an overall reduction in chronic inflammation and autoimmune reactions.
Betathine: (Other name for: beta alethine)
bethanechol chloride: A synthetic quaternary ammonium base derivative, parasympathomimetic bethanechol is a slowly hydrolyzed muscarinic agonist with no nicotinic effects. Generally used to increase smooth muscle tone, bethanechol is used to treat reflux esophagitis and to initiate urination after surgery, in urinary infections, or for enlarged prostate. It may cause hypotension, cardiac rate changes, and bronchial spasms.
betibeglogene autotemcel: A preparation of autologous, CD34-positive hematopoietic stem cells (HSCs) transduced ex vivo with the BB305 recombinant replication-defective, self-inactivating lentiviral vector encoding for an engineered form of human beta-globin (hemoglobin-beta, HBB) gene, beta-A-T87Q (b-A-T87Q) where the threonine at position 87 has been substituted with glutamine, with potential to restore beta-globin expression and function. Autologous CD34-positive stem cells are isolated from the patient's own bone marrow and the cells are transduced with the lentiviral vector. Upon re-infusion of betibeglogene autotemcel back into the patient, these cells express b-A-T87Q-globin, thereby allowing the body to make normal hemoglobin and thus normal, healthy red blood cells. Beta-globin, the beta-chain of the most common form of hemoglobin, is encoded by the HBB gene; mutations in this gene prevent normal beta-globin production and are associated with beta-thalassemia and sickle cell anemia. The b-A-T87Q form of beta-globin has increased antisickling activity compared to the wild type protein.
betifisolimab: A second-generation, humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Betifisolimab contains a unique, not as of yet elucidated, pH-dependent antigen binding property allowing the antibody to only bind to PD-L1 within the acidic tumor microenvironment (TME), while it is not able to bind to PD-L1 in normal, healthy tissue. Upon administration, once able to bind to PD-L1 in the TME, betifisolimab blocks the binding of PD-L1 to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on activated T-cells suppresses the immune system and results in immune evasion. PD-1 negatively regulates T-cell activation.
betrixaban: An orally active inhibitor of coagulation factor Xa (activated factor X) with anticoagulant activity. Betrixaban is primarily excreted unchanged in the bile and has a half life of about 19 hours.
betulinic acid: A pentacyclic lupane-type triterpene derivative of betulin (isolated from the bark of Betula alba, the common white birch) with antiinflammatory, anti-HIV and antineoplastic activities. Betulinic acid induces apoptosis through induction of changes in mitochondrial membrane potential, production of reactive oxygen species, and opening of mitochondrial permeability transition pores, resulting in the release of mitochondrial apogenic factors, activation of caspases, and DNA fragmentation. Although originally thought to exhibit specific cytotoxicity against melanoma cells, this agent has been found to be cytotoxic against non-melanoma tumor cell types including neuroectodermal.and brain tumor cells.
bevacizumab: A recombinant humanized monoclonal antibody directed against the vascular endothelial growth factor (VEGF), a pro-angiogenic cytokine. Bevacizumab binds to VEGF and inhibits VEGF receptor binding, thereby preventing the growth and maintenance of tumor blood vessels.
bevacizumab-IRDye 800CW: An immunoconjugate and a fluorescent tracer consisting of the recombinant humanized anti-vascular endothelial growth factor (VEGF) monoclonal antibody bevacizumab conjugated to the N-hydroxysuccinamide (NHS) ester form of the near-infrared (NIR) fluorescent dye IRDye 800CW, that may be used for VEGF-specific tumor imaging. Upon administration, the bevacizumab moiety of bevacizumab-IRDye 800CW binds to VEGF and the fluorescent signal can be visualized using NIR fluorescence imaging (700–1,000 nm).
bevacizumab/carboplatin/paclitaxel regimen: A regimen consisting of bevacizumab, carboplatin and paclitaxel that can be used in the treatment of endometrial, ovarian, fallopian tube and primary peritoneal, vulvar and cervical cancers and non-small cell lung cancer (NSCLC).
bevifimod: A proprietary formulation containing a highly purified form of Staphylococcal protein A (SpA; protein A), with potential immunomodulating activity. Upon administration of bevifimod, this protein is able to specifically bind to both the subset of B-lymphocytes that express the heavy chain variable region 3 (VH3)-encoded immunoglobulin (Ig) (VH3-B-cells) and macrophages. This prevents B-cell activation, induces apoptosis, prevents VH3-derived antibody formation, antibody-mediated immune responses, and destruction by macrophages. This may modulate specific immune signaling pathways and restore normal immune system functions caused by certain immune-mediated inflammatory diseases. In patients with the autoimmune-mediated disease immune thrombocytopenia (ITP), PRTX-100 prevents destruction of platelets, increases platelet production and platelet blood levels, and decreases the risk of bleeding. SpA, a 42 kDa bacterial membrane protein produced by Staphylococcus aureus bacteria, consists of five nearly identical Ig binding domains; each SpA domain binds with high affinity to the Igs containing regions encoded by the VH3 gene family. B-lymphocytes that express VH3-encoded Igs are specifically involved in various auto-immune diseases.
bevonescein: A synthetic, peptide-dye conjugate composed of an undisclosed, proprietary peptide conjugated to a fluorescent dye, that can potentially be used for the intraoperative fluorescence detection and localization of nerve tissue. Upon administration of bevonescein, the peptide moiety binds to the extracellular matrix of nerves independent of myelin. Upon fluorescence imaging, nerve tissues are illuminated and detected.
Bevyxxa: (Other name for: betrixaban)
bexarotene: A synthetic retinoic acid agent with potential antineoplastic, chemopreventive, teratogenic and embryotoxic properties. Bexarotene selectively binds to and activates retinoid X receptors (RXRs), thereby inducing changes in gene expression that lead to cell differentiation, decreased cell proliferation, apoptosis of some cancer cell types, and tumor regression.
bexirestrant: An orally bioavailable selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, bexirestrant specifically targets and binds to both wild-type and mutant forms of the estrogen receptor (ER; ERalpha), including the somatic mutations Y537S and D538G. This induces a conformational change that results in ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells. Somatic mutations in the ER gene ESR1, especially Y537S and D538G, have been associated with acquired antiestrogen drug resistance.
bexmarilimab: A monoclonal antibody directed against common lymphatic endothelial and vascular endothelial receptor-1 (CLEVER-1; stabilin-1; FEEL-1), with potential immunomodulatory and antineoplastic activities. Upon administration, bexmarilimab targets and binds to CLEVER-1 that is expressed on tumor endothelial cells. This prevents the recruitment, infiltration and attachment of tumor-associated macrophages (TAMs) at the tumor site. By preventing the binding of TAMs to tumor cells, the infiltration of activated T-regulatory cells (Tregs) to the tumor and the TAM-mediated immune suppression is abrogated, leading to the polarization of TAM from the immunosuppressive M2 macrophages to the anti-inflammatory and immunostimulatory M1 macrophages. This leads to the activation of the immune system, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response and inhibition of tumor cell growth and metastasis. CLEVER-1 is an endothelial cell surface molecule involved in immune suppression, cancer growth and metastasis.
Bextra: (Other name for: valdecoxib)
Bexxar: (Other name for: tositumomab and iodine I 131 tositumomab)
bezlotoxumab: A human monoclonal antibody directed against Clostridium difficile Toxin B (TcdB), with anti-toxin activity. Upon intravenous infusion, the two Fab regions of bezlotoxumab bind to two distinct epitopes within the N-terminal half of the TcdB combined repetitive oligopeptide (CROP) domain, blocking the carbohydrate binding pockets of the toxin and preventing binding of the toxin to target host cells. TcdB is one of two exotoxins responsible for the symptoms of Clostridium difficile infections.
bezuclastinib: An orally bioavailable protein tyrosine kinase inhibitor of mutated forms of the tumor-associated antigen mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, bezuclastinib binds to and inhibits specific c-Kit mutants. This may result in an inhibition of tumor cell proliferation in cancer cell types that overexpress these c-Kit mutations. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.
BF-200 gel formulation: A topical nanoemulsion-based gel formulation containing 5-aminolevulinic acid (ALA), a metabolic precursor of the photosensitizer protoporphyrin IX, with a potential application for enhanced photodynamic therapy (PDT) for various precancerous and malignant skin lesions. After topical administration of a thick layer of the ALA-based BF-200 gel formulation to the affected area, ALA penetrates the skin and is intracellularly converted to protoporphyrin IX (PpIX). Exposure of PpIX to the proper excitation wavelength of light generates singlet oxygen molecules, resulting in a local cytotoxic effect.
BH3 mimetic ABT-737: An orally bioavailable, selective small molecule B-cell lymphoma 2 (Bcl-2) Homology 3 (BH3) mimetic, with potential pro-apoptotic and antineoplastic activities. ABT-737 binds to the hydrophobic groove of multiple members of the anti-apoptotic Bcl-2 protein family, including Bcl-2, Bcl-xl and Bcl-w. This inhibits the activity of these pro-survival proteins and restores apoptotic processes in tumor cells, via activation of Bak/Bax-mediated apoptosis. The pro-survival Bcl-2 proteins are overexpressed in many cancers and play important roles in the regulation of apoptosis. Their expression is associated with increased drug resistance and tumor cell survival. ABT-737 does not inhibit the pro-survival proteins Mcl-1, Bcl-B, Bfl-1 (A1); therefore, tumors that overexpress these Bcl-2 family proteins are resistant to ABT-737.
BI 2536: A small molecule compound with potential antineoplastic activities. BI 2536 binds to and inhibits Polo-like kinase 1 (Plk1), resulting in mitotic arrest, disruption of cytokinesis, and apoptosis in susceptible tumor cell populations. Plk1, a serine/threonine-protein kinase, is a key regulator of multiple processes fundamental to mitosis and cell division.
bi-sialidase fusion protein E-602: A fusion protein composed of two engineered human sialidase molecules fused to an Fc antibody domain, with potential immunomodulating and antineoplastic activities. Upon administration, bi-sialidase fusion protein E-602 targets and binds to sialoglycans overexpressed on the cell surface of certain tumor cells and immune cells, such as exhausted T cells. This degrades the immunosuppressive sialoglycans and allows for the re-activation of the immune system, thereby inducing an anti-tumor immune response. Sialidase is an enzymatic degrader of immunosuppressive sialoglycans. E-602 is based on the enzyme-antibody glyco-ligand editing (EAGLE) platform. The Fc domain enhances retention in the tumor, half-life and manufacturability.
Biaxin: (Other name for: clarithromycin)
bicalutamide: A synthetic, nonsteroidal antiandrogen. Bicalutamide competitively binds to cytosolic androgen receptors in target tissues, thereby inhibiting the receptor binding of androgens. This agent does not bind to most mutated forms of androgen receptors.
Bicitra: (Other name for: sodium citrate)
BiCNU: (Other name for: carmustine)
bictegravir: A human immunodeficiency virus type 1 (HIV-1) integrase strand transfer inhibitor (INSTI), that is used to treat HIV infection. Upon oral administration, bictegravir inhibits the strand transfer activity of HIV-1 integrase, an HIV-1 coded enzyme that is necessary for viral replication. Inhibition of integrase prevents the integration of linear HIV-1 DNA into host genomic DNA.
Bifidobacterium animalis ssp. lactis probiotic supplement: An orally bioavailable, probiotic supplement containing the non-pathogenic microorganism Bifidobacterium animalis subspecies lactis, with potential immunomodulating and mucosal protective activities. Upon oral rinsing with a solution of the capsule contents in water and oral administration, the probiotic bacteria in Bifidobacterium animalis ssp. lactis probiotic supplement may help to maintain adequate colonization of the gastrointestinal (GI) tract, including the oral mucosa, by modulating the composition of the normal microflora. During colonization in the GI tract, the bacteria may form a protective intestinal barrier that may prevent both damage to the mucosal epithelia caused by toxins and attachment of potential pathogens, thereby protecting against bacterial translocation and infection. In addition, the probiotic bacteria may potentiate immunity. Altogether, this may increase immunity and prevent mucosal damage.
Bifidobacterium animalis/Lactobacillus rhamnosus probiotic supplement: An orally bioavailable, probiotic supplement containing the non-pathogenic microorganisms Bifidobacterium animalis and Lactobacillus rhamnosus subspecies lactis with potential immunomodulating, anti-diarrheal and mucosal protective activities. Upon oral ingestion, the naturally-occurring bacterial components in Bifidobacterium animalis/Lactobacillus rhamnosus subspecies lactis probiotic supplement (BB-12/LGG) may improve digestion and help to maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. They produce lactic acid, hydrogen peroxide and other substances during fermentation, thereby creating an acidic environment that is unfavorable for pathogens. During colonization in the GI tract, the bacteria may also form a protective intestinal barrier, which may prevent damage to the mucosal epithelium, maintains the integrity of the epithelial barrier from potential damage by toxins and certain chemicals, and reduces the potential for attachment of pathogens. This further protects against bacterial translocation and infection. In addition, this agent may reduce the secretion of pro-inflammatory cytokines and may potentiate natural and acquired immunity. Altogether, this may increase immunity, prevent GI mucosal damage, malabsorption, inflammation, and reduce diarrhea, such as diarrhea induced by inflammation and GI mucosa-damaging agents. BB-12 and LGG are registered trademarks of Chr. Hansen A/S in the United States and other jurisdictions.
Bifidobacterium lactis/Lactobacillus acidophilus/inulin probiotic supplement: A tablet probiotic supplement containing the polysaccharide inulin and the non-pathogenic microorganisms Bifidobacterium lactis and Lactobacillus acidophilus, with potential anti-inflammatory, immunomodulating and protective activities. Upon oral administration of B. lactis/L. acidophilus/inulin probiotic supplement, the bacterial components in this dietary supplement may improve digestion and promote adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. During colonization in the GI tract, the bacteria may form a protective intestinal barrier that may prevent both damage to the mucosal epithelia caused by toxins and attachment of potential pathogens, which protects against bacterial translocation and infection. In addition, this agent may both reduce the secretion of pro-inflammatory cytokines, including interleukin-10, and potentiate natural and acquired immunity. In colon cancer patients, these probiotic bacteria may favorably modulate the composition of the colon cancer-associated microbiota and may increase expression of tumor-suppressing genes. Inulin promotes growth and activity of beneficial GI bacteria, thereby altering the endogenous flora further.
Bifidobacterium lactis/Lactobacillus acidophilus/L. plantarum/L. salivarius probiotic supplement: An orally available, probiotic supplement containing the non-pathogenic microorganisms Lactobacillus acidophilus, L. plantarum, L. salivarius and Bifidobacterium lactis, with potential anti-inflammatory, immunomodulating and protective activities. Upon oral ingestion, the naturally-occurring bacterial components in this dietary supplement may improve digestion and help maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. During colonization in the GI tract, the bacteria may form a protective intestinal barrier that may prevent both damage to the mucosal epithelia caused by toxins and attachment of potential pathogens, which protects against bacterial translocation and infections. In addition, this agent may both reduce the secretion of pro-inflammatory cytokines, including interleukin-10, and potentiate natural and acquired immunity.
Bifidobacterium longum/Lactobacillus acidophilus/Enterococcus faecalis probiotic supplement: An orally bioavailable, probiotic supplement containing the microorganisms Bifidobacterium longum (B. longum), Lactobacillus acidophilus (L. acidophilus) and Enterococcus faecalis (E. faecalis), with potential immunomodulating, anti-diarrheal and mucosal protective activities. Upon oral ingestion, the naturally-occurring bacterial components in B. longum/L. acidophilus/E. faecalis probiotic supplement may improve digestion and help to maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. They produce lactic acid, hydrogen peroxide and other substances during fermentation, thereby creating an acidic environment that is unfavorable for pathogens. During colonization in the GI tract, the bacteria may also form a protective intestinal barrier, which may prevent damage to the mucosal epithelium, maintain the integrity of the epithelial barrier from potential damage by toxins and certain chemicals, and reduce the potential for attachment of pathogens. This further protects against bacterial translocation and infection. In addition, this agent may reduce the secretion of pro-inflammatory cytokines and may potentiate natural and acquired immunity. Altogether, this may increase immunity, prevent GI mucosal damage, malabsorption, inflammation, and reduce diarrhea.
bifikafusp alfa: An immunoconjugate consisting of the recombinant form of the cytokine interleukin-2 (IL-2) fused to a human single-chain Fv (scFv) antibody fragment directed against the extra-domain B (ED-B) of fibronectin (L19), with potential immunopotentiating and antineoplastic activities. The L19 moiety of bifikafusp alfa binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. In turn, the IL-2 moiety may locally activate natural killer (NK) cells and macrophages, and may induce T cell cytotoxic immune responses against ED-B fibronectin-expressing tumor cells. This may specifically decrease the proliferation of ED-B-expressing tumor cells. ED-B is predominantly expressed during angiogenesis and tumor growth.
bifunctional expression vector plasmid DNA-bi-shRNA EWS/FLI1 type 1 lipoplex: A proprietary plasmid DNA expression vector encoding bi-functional short hairpin RNAs (bi-shRNAs) targeting the identical type 1 translocation junction region of the human fusion oncogene Ewing sarcoma (EWS)/Ets family transcription factor Friend leukemia virus integration 1 (FLI1) and are encapsulated in liposomal delivery vehicle (lipoplex; LPX), with potential antineoplastic activity. pbi-shRNA EWS/FLI1 type 1 contains 2 stem-loop structures encoded by a plasmid vector: one cleavage-dependent unit with perfectly matched passenger- and guide-strand, which is the small interfering RNA (siRNA)-like component, and one cleavage-independent unit composed of a strategically mismatched double strand, which is the microRNA (miRNA)-like component. Upon intratumoral administration and transcription into tumor cells, one shRNA unit with an imperfectly matched sequence causes inhibition of EWS/FLI1 messenger RNA (mRNA) translation (through mRNA sequestration and cleavage-independent degradation) while the other unit with a perfectly matched sequence promotes EWS/FLI1 mRNA degradation (through cleavage-dependent mRNA silencing). This prevents EWS/FLI1 expression in tumor cells, which results in a reduction of tumor cell proliferation. The EWS/FLI1 type 1 fusion gene product is overexpressed in type 1 Ewing’s sarcoma and correlates with increased tumor proliferation and poor prognosis.
bifunctional TGF-beta antagonist/IL-15 protein complex HCW9218: A heterodimeric, bifunctional fusion protein composed of the ectodomains of the transforming growth factor (TGF) beta (TGF-beta; TGFb) receptor II (TGFbRII;TGFBR2) fused to a human immunostimulatory cytokine interleukin-15 (IL-15)/ IL-15 receptor alpha complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the bifunctional TGF-beta antagonist/IL-15 protein complex HCW9218, the TGFbRII moiety specifically and selectively targets, binds to and neutralizes TGF-beta, an immunosuppressive cytokine secreted by tumors. This prevents TGF-beta from binding to TGF receptors and prevents TGFb-mediated signaling. This abrogates TGFb-mediated immunosuppression in the tumor microenvironment (TME), enhances immune cell infiltration and anti-tumor immunity in the TME, and promotes a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells leading to tumor cell death. This may lead to a reduction in TGFb-dependent proliferation of cancer cells. The IL-15 moiety stimulates the proliferation and cytotoxic activity of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the TME, which further induces an anti-tumor immune response, and increases tumor cell killing. In addition, by stimulating the immune system and NK cell activation, HCW9218 may eliminate chemotherapy-induced senescent cells in tumors and normal tissues, may reduce senescence-associated secretory phenotype (SASP) factor activity, and may reduce therapy-induced senescence (TIS)-mediated proinflammatory side effects in normal tissues. TGFb, overproduced in many types of cancer, plays a key role in immunosuppression in the TME, enhances tumor cell proliferation, and promotes cancer progression. IL-15 regulates CD8+ T and NK cell development, activation and proliferation.
bimagrumab: A human monoclonal antibody directed against type II activin receptors (ActRII; ActR2), with potential muscle-sparing and anti-cachectic activities. Upon administration, bimagrumab binds to ActRII, which prevents the binding of the natural ligands, myostatin and activin, to activin receptors and blocks ActRII-mediated signaling. This increases protein synthesis, decreases protein degradation, stimulates skeletal muscle cell growth, and increases muscle function and strength. Overstimulation of the ActRII-mediated signaling pathway is associated with muscle loss and weakness.
bimatoprost ophthalmic solution: A sterile ophthalmic solution containing 0.03% of a synthetic prostaglandin analog bimatoprost with hair-growing and anti-glaucoma activities. Applied once daily to the upper eyelid margin at the base of the eyelashes and, optionally, to the eyebrows, bimatoprost penetrates into the hair follicle and may, through a mechanism that has yet to be fully understood, stimulate the transition of hair follicles from the telogen phase into the anagen phase and may increase the duration of the time follicles spend in anagen. By increasing the numbers of hair follicles in and duration of anagen phase, bimatoprost may help increase eyebrow and eyelash growth and appearance, including their length, thickness and darkness.
bimiralisib: An orally bioavailable pan inhibitor of phosphoinositide-3-kinases (PI3K) and inhibitor of the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. Bimiralisib inhibits the PI3K kinase isoforms alpha, beta, gamma and delta and, to a lesser extent, mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy. As mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase. By inhibiting mTOR to a lesser extent than PI3K, PQR309 does not interfere with the mTOR-mediated negative feedback loop on PI3K signaling. Blocking the negative feedback loop would potentially increase PI3K signaling and decrease therapeutic efficacy.
Bimuno: (Other name for: galacto-oligosaccharide prebiotic supplement)
Bina-Skin: (Other name for: pregnenolone)
binetrakin: A recombinant agent chemically identical to or similar to the endogenous cytokine interleukin-4 (IL-4). Produced primarily by activated T cells, IL-4 binds to and activates its cell-surface receptor, stimulating the proliferation and differentiation of activated B cells and enhancing their ability to present antigens to T cells. As a potential immunotherapeutic agent, binetrakin also augments the effects of other cytokines on dendritic cells (DC), cytotoxic T lymphocytes (CTL), and tumor-infiltrating lymphocytes (TIL).
binimetinib: An orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.
Binosto: (Other name for: alendronate sodium)
bintrafusp alfa: A bifunctional fusion protein composed of an anti-programmed death ligand 1 (PD-L1) human monoclonal antibody, bound to the soluble extracellular domain of human transforming growth factor beta (TGFbeta) receptor type II (TGFbetaRII), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, bintrafusp alfa binds to and neutralizes activated TGFbeta and binds to PD-L1. This prevents TGFbeta- and PD-L1-mediated signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This inhibits tumor cell proliferation in susceptible tumor cells. TGFbeta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.
bio-enhanced curcumin extract formulation: A bio-enhanced extract-based preparation containing curcumin, a poorly water-soluble phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a variety of pharmacologic properties, including antineoplastic, chemopreventive, antioxidant, anti-angiogenic, neuroprotective and anti-inflammatory activities. Upon oral administration, curcumin blocks the formation of reactive-oxygen species, neutralizes free radicals, and prevents oxidative stress and DNA damage. Curcumin also possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation. It disrupts various cell signal transduction pathways involved in carcinogenesis and prevents the expression of many transcription factors. In addition, curcumin modulates phase II enzymes. Altogether, this prevents and/or inhibits tumor cell formation and proliferation. Compared to the very poorly absorbed curcumin alone, this extract formulation, by micronizing curcumin and adding turmeric essential oils, has a much greater bioavailability, an improved pharmacokinetic profile and increased efficacy.
bioadhesive nanoparticles-encapsulating avobenzone/octocrylene plus diosmin/ferulic acid/cytisine/trans-resveratrol sunscreen: A sunscreen formulation containing bioadhesive nanoparticles (BNP) encapsulating the broad-spectrum ultraviolet radiation (UVR) protectors avobenzone and octocrylene plus additional naturally-occurring active ingredients, including the flavonoid diosmin, the phenolic phytochemical ferulic acid, the alkaloid cytisine and the polyphenol trans-resveratrol, with potential free radical scavenging, anti-oxidant and skin protective activities. Upon topical application of the BNP-encapsulating avobenzone/octocrylene plus diosmin/ferulic acid/cytisine/trans-resveratrol sunscreen, avobenzone and octocrylene absorb UVR and prevent exposure of the skin to UVR, thereby preventing the formation of UVR-induced reactive oxygen species (ROS). This prevents oxidative damage to DNA, double-stranded DNA breaks and cellular skin damage. The other active ingredients may protect the skin through their ability to scavenge ROS. BNP prevents penetration of the UVR protectors into the skin.
Biocurcumax: (Other name for: bio-enhanced curcumin extract formulation)
Biomed 101: An agent binding to the leukotriene B4 receptor, leading to reduced interleukin-2 mediated hypoxia. Biomed 101 does not affect interleukin-2 antitumor activity.
Bioperine: (Other name for: piperine extract (standardized))
BioResponse DIM: (Other name for: oral microencapsulated diindolylmethane)
Biostim: (Other name for: Klebsiella pneumoniae glycoprotein)
Biotest-HCIG: (Other name for: hepatitis C immune globulin intravenous)
birabresib: A synthetic, small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins 2, 3 and 4 with potential antineoplastic activity. Upon administration, birabresib binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes, including c-Myc-dependent target genes, may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, the BET proteins BRD2, BRD3, BRD4 are transcriptional regulators that play an important role in cellular growth.
biricodar dicitrate: The dicitrate salt of a synthetic pipecolinate derivative with potential chemosensitizing activity. Biricodar binds directly to the plasma membrane drug-efflux pumps P-glycoprotein (Pgp) and multidrug resistance protein 1 (MRP-1) and inhibits their activities, which may result in increased intracellular accumulation and retention of cytotoxic agents.
birinapant: A synthetic small molecule that is both a peptidomimetic of second mitochondrial-derived activator of caspases (SMAC) and inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins, with potential antineoplastic activity. As a SMAC mimetic and IAP antagonist, birinapant selectively binds to and inhibits the activity of IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 (cIAP1) and 2 (cIAP2), with a greater effect on cIAP1 than cIAP2. Since IAPs shield cancer cells from the apoptosis process, this agent may restore and promote the induction of apoptosis through apoptotic signaling pathways in cancer cells and inactivate the nuclear factor-kappa B (NF-kB)-mediated survival pathway. IAPs are overexpressed by many cancer cell types. They are able to suppress apoptosis by binding to, via their baculoviral lAP repeat (BIR) domains, and inhibiting active caspases-3, -7 and -9. IAP overexpression promotes both cancer cell survival and chemotherapy resistance.
biropepimut-S: A proprietary, peptide cancer vaccine comprised of multiple peptides derived from human melanoma antigen A3 (MAGE-A3; MAGEA3), with potential immunostimulating and antineoplastic activities. Upon administration, biropepimut-S may stimulate the immune system to mount specific responses from B-cells, and CD4-positive and CD8-positive cells against tumor cells expressing MAGE-A3, resulting in tumor cell lysis. MAGE-A3, a tumor-associated antigen (TAA), is overexpressed by a variety of cancer cell types.
birtamimab: A monoclonal antibody against amyloid with potential use in the treatment of amyloid light chain (AL) and AA amyloidosis. Upon intravenous administration, birtamimab specifically binds to amyloid fibrils. This prevents the formation of amyloid deposits in certain organs and facilitates their clearance. It also reduces the level of amyloid deposits in organs and prevents organ dysfunction.
bisacodyl: A synthetic pyridinylmethylene-diacetate ester derivative stimulant laxative, Bisacodyl acts with a parasympathetic effect directly on mucosal sensory nerves, increasing peristaltic contractions. It is used for occasional constipation, in pre- and postoperative treatment, and in conditions that require facilitation of defecation.
bisantrene hydrochloride: The hydrochloride salt of an anthracenyl bishydrazone with antineoplastic activity. Bisantrene intercalates with and disrupts the helical structure of DNA, resulting in DNA single-strand breaks, DNA-protein crosslinking, and inhibition of DNA replication. This agent is similar to doxorubicin in activity, but unlike doxorubicin, does not exhibit cardiotoxicity.
bismuth Bi213 monoclonal antibody M195: A radioimmunoconjugate consisting of murine monoclonal antibody (M195) and bismuth 213 (Bi213). Monoclonal antibody M195 binds to CD33, a surface antigen expressed by myelogenous leukemia cells. Bismuth 213 is an isotope that emits short-ranged high-energy alpha particles. This radioimmunoconjugate selectively delivers alpha particle-mediated cytotoxicity to leukemic cells, thereby limiting the exposure of normal tissues to ionizing radiation.
bismuth subcitrate: A mineral compound that is used to treat duodenal and gastric ulcers associated with Helicobacter pylori.
bismuth subsalicylate: A bismuth salt of salicylic acid. Little absorbed from the gastrointestinal tract, bismuth subsalicylate exerts a local effect on the gastric mucosa, coating it and protecting it from the corrosive effects of acid and pepsin. This agent also has local antimicrobial properties.
bisoprolol fumarate: The fumarate salt of a synthetic phenoxy-2-propanol-derived cardioselective beta-1 adrenergic receptor antagonist with antihypertensive and potential cardioprotective activities. Devoid of intrinsic sympathomimetic activity, bisoprolol selectively and competitively binds to and blocks beta-1 adrenergic receptors in the heart, decreasing cardiac contractility and rate, reducing cardiac output, and lowering blood pressure. In addition, this agent may exhibit antihypertensive activity through the inhibition of renin secretion by juxtaglomerular epithelioid (JGE) cells in the kidney, thus inhibiting activation of the renin-angiotensin system (RAS). Bisoprolol has been shown to be cardioprotective in animal models.
bispecific antibody 2B1: A monoclonal antibody with potential antineoplastic activity. Specific for both the immunoglobulin G (IgG) receptor CD16 and c-erbB-2, bispecific antibody 2B1 may enhance cellular immune responses against c-erbB-2-positive cells, resulting in increased tumor cell lysis.
bispecific antibody 4G7xH22: A bispecific antibody containing a 4G7 hybridoma secreting IgG1 antibody specific for B-lymphocytes and a monoclonal antibody targeting Fc gamma RI-expressing cells.
bispecific antibody AGEN1223: A bispecific antibody that simultaneously binds to two different and as of yet undisclosed antigens co-expressed specifically on tumor-infiltrating regulatory T cells (Tregs), with potential immunomodulating and antineoplastic activities. Upon administration, AGEN1223 targets and binds to the two antigens co-expressed specifically on tumor-infiltrating Tregs. This leads to the selective depletion of immunosuppressive Tregs in the tumor microenvironment (TME), while sparing peripheral Tregs and effector T cells, enhancing the overall antitumor response. AGEN1223 may also co-stimulate antigen-specific effector T cells, resulting in tumor cell death.
bispecific antibody AMG 509: A bispecific antibody that simultaneously binds to two different and as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, AMG 509 targets and binds to the two antigens. This may modulate the tumor microenvironment (TME) and may enhance an immune-mediated antitumor response.
bispecific antibody AMG 994: A bispecific antibody, with potential antineoplastic activity. Upon intravenous administration, bispecific antibody AMG 994 targets and binds to two as of yet undisclosed targets. This may inhibit tumor cell proliferation.
bispecific antibody JNJ-70218902: A T-cell redirecting agent and bispecific antibody targeting an as of yet undisclosed tumor-associated antigen (TAA) expressed on tumor cells and the CD3 receptor complex expressed on T cells, with potential immunomodulating and antineoplastic activities. Upon administration, bispecific antibody JNJ-70218902 binds to both CD3 on T cells and a TAA expressed on tumor cells. The resulting cross-linkage activates and redirects T cells to the TAA-expressing tumor cells. This results in T-cell-mediated lysis of tumor cells.
bispecific antibody MDX-H210: A humanized bivalent antibody directed against both cytotoxic effector cells expressing Fc gamma receptor type I (Fc gammaRI, or CD64) and HER2/neu-overexpressing tumor cells with potential antineoplastic activity. Bispecific antibody MDX-H210 was constructed by chemically linking Fab' fragments of the anti-HER2/neu-specific monoclonal antibody 520C9 and the Fab' fragments of the anti-Fc gammaRI-specific monoclonal antibody H22. This agent selectively binds to both HER2/neu-expressing tumor cells and Fc gammaRI-expressing cytotoxic effector cells, which may trigger antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis of HER2/neu-expressing tumor cells. While HER2/neu is overexpressed in a variety of epithelial malignancies, expression of Fc gammaRI is primarily found in cytotoxic immune cells, including monocytes, macrophages, and cytokine-activated polymorphonuclear (PMN) cells.
bispecific antibody MDX447: An antibody with potential antineoplastic activity. Specific for both the high-affinity immunoglobulin G (IgG) receptor CD64 and epidermal growth factor receptor (EGFR), bispecific antibody MDX447 may enhance cellular immune responses against EGFR positive cells, resulting in increased tumor cell lysis.
bispecific antibody QLF3108: A bispecific antibody that simultaneously binds to two different and as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, bispecific antibody QLF3108 targets and binds to the two antigens expressed on T cells and tumor cells respectively. This may activate T cells to kill tumor cells expressing the specific tumor-associated antigen (TAA).
bispecific CD80-lgG4Fc-IL-2v fusion protein GI-101: A bi-specific Fc fusion protein composed of the N-terminal extracellular domain (ECD) of human CD80 (B7.1) fused to a human immunoglobulin G4 (IgG4) Fc fragment and linked to an interleukin (IL)-2 variant (IL-2v) as a C-terminal moiety, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration of bispecific CD80-IgG4Fc-IL-2v fusion protein GI-101, the CD80 moiety 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, enables the binding of CD80 to CD28, which leads to CD28-mediated signaling, and results in the activation of T cells in the tumor microenvironment (TME). This promotes T-cell activity. The IL-2 moiety may stimulate a local immune response and activate natural killer (NK) cells and cytotoxic T cells. This may enhance the activity of neoantigen specific T cells and potentiates the T-cell-mediated immune response against tumor cells. 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. IL-2v cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T cells (Tregs).
bispecific CD80-lgG4Fc-IL-2v fusion protein GI-102: A bi-specific Fc fusion protein composed of the N-terminal ectodomain of human CD80 (B7.1) fused to a human immunoglobulin G4 (IgG4) Fc fragment and linked to an interleukin (IL)-2 variant (IL-2v) as a C-terminal moiety, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration of bispecific CD80-IgG4Fc-IL-2v fusion protein GI-102, the CD80 moiety targets and binds to cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) expressed on T cells. This prevents the binding of CTLA-4 to endogenous CD80, enables the binding of CD80 to CD28, which leads to CD28-mediated signaling, and results in the activation of T cells in the tumor microenvironment (TME). This promotes T-cell activity. The IL-2v moiety may stimulate a local immune response and activate natural killer (NK) cells and cytotoxic T cells. This may enhance the activity of neoantigen specific T cells and potentiates the T-cell-mediated immune response against tumor cells. 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. The IL-2v moiety cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T cells (Tregs).
bispecific ligand-drug conjugate CBP-1018: A bispecific ligand-drug conjugate targeting two as of yet undisclosed receptors and conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of bispecific ligand-drug conjugate CBP-1018, the bispecific ligand moiety targets and binds to one or both of the two as of yet undisclosed receptors expressed in certain tumor types. After internalization of the agent, the cytotoxic moiety is released and kills the cancer cells expressing the receptor(s), through an as of yet unknown mechanism of action.
bispecific ligand-drug conjugate CBP-1019: A bispecific ligand-drug conjugate targeting two as of yet undisclosed receptors and conjugated to a topoisomerase inhibitor, with potential antineoplastic activity. Upon administration of bispecific ligand-drug conjugate CBP-1019, the bispecific ligand moiety targets and binds to one or both of the two as of yet undisclosed receptors expressed in certain tumor types. After internalization of the agent, the topoisomerase inhibitor inhibits DNA topoisomerase activity, thereby inhibiting DNA replication which results in cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of cancer cells expressing the receptor(s).
bispecific monoclonal antibody ASP2074: A bispecific monoclonal antibody directed against as of yet unknown targets, with potential antineoplastic activity. Upon administration, bispecific monoclonal antibody ASP2074 may, through as of yet unelucidated mechanisms of action, enhance cellular immune responses against susceptible tumor cells, resulting in increased tumor cell lysis.
bisthianostat: An orally bioavailable pan-inhibitor of human histone deacetylase (HDAC), with potential antineoplastic activity. Upon administration, bisthianostat selectively binds to and inhibits HDACs, which inhibits deacetylation of histone proteins and leads to the accumulation of highly acetylated histones. This may result in an induction of chromatin remodeling, the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes. This prevents cell division, induces cell cycle arrest and apoptosis. This may inhibit the proliferation of susceptible tumor cells. HDACs, upregulated in many tumor cell types, are a family of enzymes that deacetylate histone proteins.
BiTE antibody AMG 910: A half-life extended (HLE), bispecific T-cell engager (BiTE) antibody that simultaneously binds to two different and as of yet undisclosed antigens, with potential immunomodulating and antineoplastic activities. Upon administration, AMG 910 targets and binds to the two antigens. This may modulate the tumor microenvironment (TME) and may enhance an immune-mediated antitumor response.
bivalent BRD4 inhibitor AZD5153: An orally bioavailable bivalent inhibitor of bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon oral administration, the BRD4 inhibitor AZD5153 selectively binds to the acetylated lysine recognition motifs in two bromodomains in the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and dysregulates expression of target genes, which leads to the downregulation of the expression of certain growth-promoting genes, induces apoptosis and inhibits the proliferation of BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.
bivalent HPV16/18 therapeutic cervical cancer vaccine: A bivalent human papillomavirus (HPV) therapeutic vaccine containing recombinant inactivated adenylate cyclase (CyaA) from Bordetella pertussis carrying a sequence encoding the E7 antigen of both HPV16 and 18, with potential immunostimulatory and antiviral properties. Upon administration of bivalent HPV16/18 therapeutic cervical cancer vaccine, the expressed proteins may activate cell-mediated immunity and induce both cytotoxic CD8+ T cells and CD4+ helper T cells against the target antigens HPV16-E7 and HPV18-E7, which leads to HPV viral clearance. Adenylate cyclase is a virulence factor of Bordetella pertussis. Its ability to bind to CD11b-expressing dendritic cells and deliver antigens directly to the cytosol allows the activation and induction of T-cell immunity. CyaA may also induce a B cell response.
bizalimogene ralaplasmid: A DNA vaccine consisting of plasmids encoding the E6 and E7 genes of human papilloma virus (HPV) subtypes 16 and 18, respectively, with potential immunostimulating and antineoplastic activities. Administered via intramuscular electroporation, bizalimogene ralaplasmid expresses E6 and E7 proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response against cervical cancer cells expressing E6 and E7 proteins, resulting in tumor cell lysis. HPV type 16 and HPV type 18 are the most common HPV types involved in cervical carcinogenesis.
bizaxofusp: A fusion protein consisting of the cytokine interleukin-4 (IL-4) linked to a truncated form of Pseudomonas exotoxin with potential antineoplastic activity. Upon specific, high-affinity binding to IL-4 receptors located on the tumor cell surface., bizaxofusp is internalized; the exotoxin moiety then binds to translation elongation factor 2 (EF-2), which may result in ADP ribosylation, deactivation of EF-2, inhibition of protein synthesis, and tumor cell apoptosis. The Pseudomonas exotoxin moiety of this agent has been engineered to reduce non-specific binding to cells expressing its receptor, the multiligand cell surface receptor alpha 2-macroglobulin receptor/low-density lipoprotein receptor-related protein (alpha 2MR/LRP). IL-4R is a type I transmembrane protein that binds IL-4 and IL-13 and may be overexpressed by cancers such as renal cell carcinoma and glioma.
bizelesin: A synthetic cyclopropylpyrroloindole antineoplastic antibiotic. Bizelesin binds to the minor groove of DNA and induces interstrand cross-linking of DNA, thereby inhibiting DNA replication and RNA synthesis. Bizelesin also enhances p53 and p21 induction and triggers G2/M cell-cycle arrest, resulting in cell senescence without apoptosis.
Bizengri: (Other name for: zenocutuzumab-zbco)
BL22 immunotoxin: A recombinant immunotoxin consisting of the Fv portion of the anti-CD22 antibody RFB4 fused to a fragment of Pseudomonas exotoxin-A with potential antineoplastic activity. BL22 immunotoxin binds to CD22, an antigen expressed in B-cell malignancies, thereby delivering its toxin directly to tumor cells. The toxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also blocks translational elongation via binding to elongation factor-2 in eukaryotic cells.
black cohosh: A triterpene-containing herb isolated from the roots and rhizomes of the plant Cimicifuga racemosa (also known as Actaea racemosa). While the mechanism of action of black cohosh is not completely understood, it appears to act as a selective estrogen receptor modulator. In vitro, this preparation has been shown to induce cell cycle arrest and caspase-dependent apoptosis of estrogen-sensitive breast cancer cells.
black currant juice: The juice from the berries of the black currant (Ribes nigrum L.) shrub belonging to the family Grossulariaceae, with potential antioxidant and protective activities. Black currant juice contains a variety of nutrients, including vitamin C, iron, potassium, manganese, anthocyanins, including delphinidin-3-O-glucoside, delphinidin-3-O-rutinoside, cyanidin-3-O-glucoside, and cyanidin-3-O-rutinoside. The antioxidants in black currant juice scavenge free radicals, thereby protecting cells from damage.
black raspberry nectar: A concentrated fruit juice containing black raspberries, with potential antioxidant, pro-apoptotic, anti-angiogenic and chemopreventive activities. In addition to vitamins, minerals and phytosterols, black raspberries are rich in phenolic acids, such as gallic acid, ellagic acid, anthocyanidins, and flavonoids. Upon oral administration, the phytochemicals in the black raspberry nectar inhibit the activation of several signal transduction pathways involved in carcinogenesis and the expression of downstream target genes that are upregulated in a variety of cancer cell types. In addition, the phytochemicals in black raspberry may protect the oral microbiome and may enhance the bacterial defense against pathogens.
black seed oil extract supplement: An oral supplement composed of the oil extracted from the seeds of Nigella sativa, also known as black seed or black cumin, with potential anti-oxidant, anti-inflammatory, hepatoprotective and immunomodulatory activities. Upon administration of black seed oil extract supplement, the main constituent thymoquinone may stimulate various cytoprotective antioxidant enzymes. Thymoquinone may also exert anti-inflammatory activity by decreasing the production of inflammation mediators, such as tumor necrosis factor (TNF)-alpha, interleukin (IL) 1-beta and IL-6, and inhibiting pro-inflammatory enzymes, including cyclooxygenase (COX). In addition, thymoquinone may modulate the activity of various immune cells such as T cells, B cells, macrophages, neutrophils, natural killer (NK) cells, and dendritic cells (DCs) in the tumor microenvironment (TME) and may enhance anticancer immune responses.
black tea: Black tea is an infusion of dried leaves from plants of the Theaceae family. Due to the alkaloid caffeine, its main effect is stimulation. Black teas also contain other phytochemicals such as flavonoid and flavonoid-related compounds with strong antioxidant effects. They also attenuate atherosclerotic inflammation, reduce thrombosis, promote normal endothelial function, and block expression of cellular adhesion molecules. Black tea may reduce the risk of cancer, heart diseases, infectious diseases, and degenerative diseases.
Blenrep: (Other name for: belantamab mafodotin-blmf)
bleomycin: A mixture of glycopeptide antineoplastic antibiotics isolated from the bacterium Streptomyces verticillus. Bleomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.
bleomycin sulfate: A mixture of the sulfate salts of basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus. Bleomycin sulfate forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.
BLI850: An oral laxative containing sodium sulfate, potassium sulfate, magnesium sulfate and sucralose. Oral sulfate-based laxative BLI850 exhibits osmotic activity, attracting water into the intestinal tract from tissues and increasing the volume and the water content of the stool; gastrointestinal motility is stimulated, resulting in defecation. Sucralose, an artificial sweetener, may contribute to the laxative effect.
blinatumomab: A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B lymphocytes.
Blincyto: (Other name for: blinatumomab)
Blopress: (Other name for: Candesartan Cilexetil)
blue citrus-based herbal capsule: An oral capsule formulation of a traditional Chinese herbal medicine with potential analgesic activity. In addition to other herbs, seeds and fruits, blue citrus-based herbal capsule contains the Chinese herb blue citrus (qing pi), which is produced from the dried immature green peel of the tangerine Citrus reticulata Blanco. Blue citrus contains large amounts of limonene, citral and synephrine, which may attribute to its analgesic activity. However, due to the complexity of its chemical components, the exact mechanism of action of this agent remains to be determined.
blueberry powder supplement: An orally available, dietary supplement consisting of lyophilized blueberry powder, with antioxidant and potential chemopreventive and chemosensitizing activity. In addition to vitamins and minerals, blueberries are rich in phytonutrients, such as proanthocyanidins, anthocyanins (e.g. malvidin, delphinidin, pelargonidin, cyanidin, petunidin, and peonidin), hydroxycinnamic acids, hydroxybenzoic acids, pterostilbene, resveratrol, and flavonols (e.g. kaempferol, quercetin and myricetin). Although the exact mechanism of action through which blueberries may exert their anti-tumor effect has yet to be fully elucidated, the effects of blueberry powder on cancer cells may be attributable to the phytonutrient’s antioxidant and pro-apoptotic activities.
BMS-184476: A 7-methylthiomethyl ether derivative of paclitaxel with antineoplastic activity. BMS-184476 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)
BMS-188797: An analog of paclitaxel with antineoplastic activity. BMS-188797 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)
BMS-214662: A nonsedating benzodiazepine derivative with potential antineoplastic activity. Farnesyltransferase inhibitor BMS-214662 inhibits the enzyme farnesyltransferase and the post-translational farnesylation of number of proteins involved in signal transduction, which may result in the inhibition of Ras function and apoptosis in susceptible tumor cells. This agent may reverse the malignant phenotype of H-Ras-transformed cells and has been shown to be active against tumor cells with and without Ras mutations.
BMS-275183: An orally available, C-4 methyl carbonate analog of paclitaxel with potential antineoplastic activity. Like paclitaxel, BMS-275183 binds to tubulin and stabilizes microtubules, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and an induction of apoptosis.
Boanmycin Hydrochloride: The hydrochloride salt form of boanmycin (aka bleomycin A6), a component of the antibiotic bleomycin produced by Streptomyces species, with potential antineoplastic activity. Upon administration, boanmycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals. This causes single- and double-stranded DNA breaks which eventually leads to cell death. Compared to bleomycin, boanmycin appears to have a more favorable toxicity profile.
boceprevir: An orally bioavailable, synthetic tripeptide inhibitor of the nonstructural protein 3 and 4A complex (NS3/NS4A), with potential activity against hepatitis C virus (HCV) genotype 1. Upon administration, boceprevir reversibly binds to the active center of the HCV NS3/NS4A and prevents NS3/NS4A protease-mediated polyprotein maturation. This disrupts the processing of viral proteins and the formation of a viral replication complex, which inhibits viral replication in HCV genotype 1-infected host cells. NS3, a serine protease, is essential for the proteolytic cleavages within the HCV polyprotein and plays a key role during HCV viral RNA replication. NS4A is an activating factor for NS3. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family.
bocodepsin besylate: The besylate form of bocodepsin, an orally bioavailable inhibitor of the histone deacetylase (HDAC) subtypes 1 and 4, with potential antineoplastic activity. Upon administration,bocodepsin targets, binds to and inhibits the activity of HDAC1/4. This results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This consequently results in a selective transcription of tumor suppressor genes, tumor suppressor protein-mediated inhibition of tumor cell division and an induction of apoptosis in tumor cells that overexpress HDAC1/4. HDAC, which is upregulated in many tumor cell types, deacetylates chromatin histone proteins and plays a key role in transcriptional regulation and cell cycle progression.
boditrectinib: An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, boditrectinib specifically targets and binds to TRK, TRK mutations and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.
bomedemstat: An orally available, irreversible inhibitor of lysine-specific demethylase 1 (LSD1), with potential antineoplastic activity. Upon administration, bomedemstat binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the di- and mono-methylated forms of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor suppressor genes. In addition, LSD1 demethylates mono- or di-methylated H3K9 which increases gene expression of tumor promoting genes; thus, inhibition of LSD1 also promotes H3K9 methylation and decreases transcription of these genes. Altogether, this may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. LSD1, an enzyme belonging to the flavin adenine dinucleotide (FAD)-dependent amine oxidase family is overexpressed in certain tumor cells and plays a key role in the regulation of gene expression, tumor cell growth and survival.
bone metastasis targeting peptide-11: A peptide that mimics naturally occurring interleukin-11 (IL-11) with interleukin receptor binding activity. Upon administration, bone metastasis targeting peptide-11 (BMTP-11) binds to interleukin-11 receptor alpha (IL-11Ra) BMTP-11. This agent might be used to deliver therapeutic agents specifically to IL-11Ra-expressing tumor cells while sparing normal cells. IL-11Ra is a cell surface receptor that may be overexpressed by osteosarcoma cells and by prostate cancer cells in prostate cancer bone metastases.
Bonine: (Other name for: meclizine hydrochloride)
Boniva: (Other name for: ibandronate sodium)
Boost: (Other name for: nutritional supplement drink)
Boost Breeze: (Other name for: whey protein isolate-based nutritional supplement)
borofalan (10B): A boronated phenylalanine and boron (boron-10) carrier that may be used in boron neutron capture therapy (BNCT), with potential antineoplastic activity. Upon administration, borofalan (10B) is absorbed mostly by tumor cells. When exposed to neutron irradiation, borofalan (10B) absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radiotargeting of tumor cells spares adjacent normal tissues.
boron-based gel: A boron-based topical gel formulation containing sodium pentaborate pentahydrate, with potential antioxidant, protective, and wound healing activities. Upon topical administration, boron-based topical gel may prevent oxidative stress and damage by increasing the activity of glutathione. It may also promote wound healing by regulating the levels of certain cytokines and enzymes, such as tumor necrosis factor-alpha (TNF-alpha), cathepsin D, collagenase and matrix metalloproteinases (MMPs). In addition, it may improve skin hydration which may help protect against skin irritation.
boron-dipyrromethene-modified olaparib fluorescent imaging agent: A poly (ADP-ribose) polymerase type 1 (PARP1) fluorescence imaging agent based on the PARP1 inhibitor olaparib, in which the cyclopropane group of olaparib is replaced by the green fluorescent dye boron-dipyrromethene (BODIPY) fluorophore (FL), with potential fluorescent imaging activity. Upon administration of the fluorescent PARP1 inhibitor PARPi-FL, the olaparib binding moiety specifically targets and binds to PARP1, which is often overexpressed on cancer cells. Upon fluorescent imaging, the PARP1-expressing cancer cells can be visualized. PARP1, the nuclear enzyme that catalyzes post-translational ADP-ribosylation of nuclear proteins, is activated by single-strand (SS) DNA breaks and overexpressed in certain tumor cells; it plays a key role in DNA repair, tumor cell resistance and survival.
boronophenylalanine-fructose complex: A boronated phenylalanine complexed with fructose to increase its solubility. When exposed to neutron irradiation, boronophenylalanine absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radiotargeting of tumor cells, known as boron neutron capture therapy (BNCT), spares adjacent normal tissues.
bortezomib: A dipeptide boronic acid analogue with antineoplastic activity. Bortezomib reversibly inhibits the 26S proteasome, a large protease complex that degrades ubiquinated proteins. By blocking the targeted proteolysis normally performed by the proteasome, bortezomib disrupts various cell signaling pathways, leading to cell cycle arrest, apoptosis, and inhibition of angiogenesis. Specifically, the agent inhibits nuclear factor (NF)-kappaB, a protein that is constitutively activated in some cancers, thereby interfering with NF-kappaB-mediated cell survival, tumor growth, and angiogenesis. In vivo, bortezomib delays tumor growth and enhances the cytotoxic effects of radiation and chemotherapy.
bosentan: A sulfonamide-derived, competitive and specific endothelin receptor antagonist with a slightly higher affinity for the endothelin A receptor than endothelin B receptor. Bosentan blocks the action of endothelin 1, an extremely potent endogenous vasoconstrictor and bronchoconstrictor, by binding to endothelin A and endothelin B receptors in the endothelium and vascular smooth muscle. Bosentan decreases both pulmonary and systemic vascular resistance and is particularly used in the treatment of pulmonary arterial hypertension.
boserolimab: A humanized agonistic monoclonal antibody targeting the cell surface antigen CD27, with potential immunostimulatory and antineoplastic activities. Upon administration, boserolimab targets and binds to CD27 on a variety of immune cell types, including most T-lymphocytes. This induces CD27-dependent signaling pathways and enhances T-cell-mediated responses, including the expansion of antigen-activated T cells and the cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. CD27, a co-stimulatory molecule and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T lymphocytes, memory B cells and natural killer (NK) cells. It plays an important role in NK cell-mediated cytolytic activity and T- and B-lymphocyte proliferation and activation. It is overexpressed in certain tumor cell types.
bosmolisib: An orally bioavailable inhibitor of phosphoinositide 3-kinase delta (PI3-kinase subunit delta; PI3K-delta; PI3Kdelta) and DNA-dependent protein kinase (DNA-PK), with potential antineoplastic and immunomodulating activities. Upon oral administration, bosmolisib inhibits the activity of both PI3K-delta and DNA-PK. This prevents PI3K-mediated signaling pathways and may lead to the inhibition of cancer cell growth in PI3K-overexpressing tumor cells. Specifically, since PI3K regulates c-myc expression, inhibition of PI3K signaling may lead to a decrease in proliferation of c-myc-expressing tumor cells. Also, by inhibiting the activity of DNA-PK, bosmolisib interferes with the non-homologous end joining (NHEJ) process and prevents the repair of DNA double strand breaks (DSBs) caused by ionizing radiation or chemotherapeutic treatment. This increases chemo- and radiotherapy cytotoxicity by inhibiting the ability of tumor cells to repair damaged DNA. The PI3K pathway is upregulated in a variety of tumors and plays an important role in regulating cancer cell proliferation, growth, and survival. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks. The enhanced ability of tumor cells to repair DSBs plays a major role in the resistance of tumor cells to chemo- and radiotherapy. In addition, bosmolisib is able to decrease Tregs and increase CD8 lymphocytes.
Bosulif: (Other name for: bosutinib)
bosutinib: A synthetic quinolone derivative and dual kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Unlike imatinib, bosutinib inhibits the autophosphorylation of both Abl and Src kinases, resulting in inhibition of cell growth and apoptosis. Because of the dual mechanism of action, this agent may have activity in resistant CML disease, other myeloid malignancies and solid tumors. Abl kinase is upregulated in the presence of the abnormal Bcr-abl fusion protein which is commonly associated with chronic myeloid leukemia (CML). Overexpression of specific Src kinases is also associated with the imatinib-resistant CML phenotype.
Boswellia serrata extract: A standardized extract derived from the plant Boswellia serrata of the family Burseraceae with anti-inflammatory activity. Boswellia serrata extract contains terpenoid boswellic acids, which are potent inhibitors of 5-lipoxygenase activity and, so, leukotriene synthesis.
botanical agent BEL-X-HG: An orally available botanically-based agent with potential antineoplastic activity. Upon oral administration, the components in BEL-X-HG may exert cytotoxic effects against cancer cells.
botanical agent LEAC-102: A botanical-based formulation derived from the Taiwanese mushroom Antrodia cinnamomea, with potential antineoplastic activity, Upon administration, the components in LEAC-102 may exert cytotoxic effects against cancer cells.
botanical extract DCB-BO1301: A proprietary botanical, galactolipid-enriched extract derived from the edible plant Crassocephalum crepidioides (Zhaohe Cao), with potential anti-inflammatory and antineoplastic activities. Upon oral administration, DCB-BO1301 may inhibit the growth of certain types of tumor cells, although the exact mechanism of action has yet to be fully elucidated.
botanical extracts rinse IZN-6N4: An oral rinse containing 1% of botanical extracts with potential anti-inflammatory and antimucositis activity. Upon rinsing with botanical extracts rinse IZN-6N4 in the oral cavity, this agent may prevent inflammation of the mucosal membranes and may decrease chemotherapy- and/or radiation-induced oral mucositis.
botanical lotion CG428: A proprietary lotion containing a blend of the four botanicals Allium cepa L. (Onion), Citrus limon L. (Citrus), Theobroma cacao L. (Cocoa), Paullinia cupana (Guarana), with potential activity against chemotherapy-induced alopecia (CIA). Upon administration to the scalp, botanical lotion CG428 may normalize the apoptotic process of hair follicular cells and reduce inflammation in the scalp. This may reverse chemotherapy-induced alopecia (CIA), restore the natural hair cycle, improve hair regrowth, and improve the psychosocial well-being of the affected patient.
botanical-based agent NBT-NM108: An orally administered, botanical-based drinkable formula, with potential immunomodulatory activity. Upon oral administration, botanical-based agent NBT-NM108 may modulate the gut microbiota, restore the unhealthy, altered gut microbiome, enhance the microbial diversity and function in the gastrointestinal (GI) tract and may re-establish a healthy microbiome in the GI tract. This may enhance the patients' immunological activity against various opportunistic pathogens and may decrease pathogen-induced inflammation.
botanically-derived agent RH324: An orally bioavailable, botanically-derived substance, with potential antineoplastic activity. Though the nature of the plant has yet to be fully elucidated, the botanically-derived agent RH324 contains all the plant's natural constituents, including proteins, amino acids, various fatty acids, carbohydrates, vitamins, minerals, and phytochemicals. Upon oral administration, the botanically-derived agent RH324 may exert its activity by a variety of as of yet not elucidated mechanisms of action.
botensilimab: An Fc-engineered recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody botensilimab binds to CTLA-4 expressed on T cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system. The engineered Fc domain increases the stability and half-life of the antibody.
BOTOX: (Other name for: botulinum toxin type A)
Botox cosmetic: (Other name for: botulinum toxin type A)
botulinum toxin E EB-001: An injectable formulation containing the bacterial Clostridium botulinum type E neurotoxin, with neuromuscular transmission inhibitory and analgesic activities. Upon injection of botulinum toxin E EB-001 into the muscles of the affected area, the heavy chain portion of botulinum toxin type E binds to the cell membrane of the presynaptic nerve terminal and is internalized via endocytosis. Upon entry into the cytoplasm, the light chain portion of the toxin binds to and cleaves synaptosomal-associated protein 25 (SNAP-25), thereby preventing the fusion of acetylcholine (ACh)-containing synaptic vesicles with the cell membrane and, thus the release of the neurotransmitter ACh into the neuromuscular junction. This prevents the binding of ACh to the motor end-plate nicotinic acid receptors and ACh-mediated muscle contraction. This causes flaccid paralysis and may decrease musculoskeletal pain and may improve wound healing and reduce scar formation due to the absence of muscle contractions. In addition, EB-001 may inhibit the release of neuropeptides, such as substance P and glutamate, which may contribute to its analgesic activity. Compared to other botulinum toxin types, type E has the fastest onset and the shortest duration of action.
botulinum toxin type A: An injectable formulation of a neurotoxin derived through the fermentation of the Hall strain of Clostridium botulinum type A with neuromuscular transmission inhibitory and analgesic activities. Upon injection into the affected muscle, the heavy chain portion of botulinum toxin type A (BTX-A) binds to the cell membrane of the motor nerve and is internalized via endocytosis. Upon entry, the light chain portion of the toxin is activated and cleaves the protein SNAP-25, thereby preventing the fusion of acetylcholine (ACh)-containing synaptic vesicles with the cell membrane and, so, the release of ACh into the neuromuscular junction; subsequent binding of ACH to motor end-plate nicotinic acid receptors and ACh-mediated muscle contraction are thus blocked. In addition to ACh, BTX-A may inhibit the release of neuropeptides, such as substance P and glutamate, which may contribute to its analgesic activity.
bovine cartilage: Cartilage extracted from various parts of a cow and is proposed to stimulate the immune system and inhibit tumor cell growth. It was used in the 1950s and 60s to enhance wound healing. (NCI)
bovine lactoferrin supplement: A supplement containing lactoferrin derived from bovine milk with potential chemopreventive, immunostimulating, and antimicrobial activity. Upon administration, lactoferrin binds to metal in the oral cavity and may prevent metal-induced oxidation of lipids. This may reduce the metallic taste and taste disturbances induced by certain metal-containing chemotherapeutics; metal-induced lipid oxidation, and the subsequent production of aldehydes and ketones attribute to the metallic smell. Lactoferrin, a glycoprotein belonging to the transferrin family of metal-binding proteins, can be found in milk and other secretory fluids as well as in polymorphonuclear cells and leukocytes; lactoferrin plays a role in the innate defense of mucosal surfaces and its iron-binding activity is associated with the antibacterial activity.
Bowman-Birk inhibitor concentrate: An extract of soybeans enriched in Bowman-Birk inhibitor (BBI), a soybean-derived, 71-amino acid, polypeptide and serine protease inhibitor with potential chemopreventive activity. Bowman-Birk inhibitor contains distinct inhibitory sites for trypsin and chymotrypsin. Although the exact mechanism by which BBI suppresses carcinogenesis is unknown, its antiproliferative activity appears to be linked to the chymotrypsin inhibitory region.
BP-Cx1-platinum complex BP-C1: A combination agent composed of the benzo-poly-carbonic-acid polymer BP-Cx1 chelated to platinum with potential antineoplastic activity. Upon intramuscular injection, the polymer moiety of BP-Cx1-Platinum Complex BP-C1 (BP-C1) alters the permeability of the cell membranes, which allows for increased penetration of platinum into tumor cells. In turn, platinum binds to nucleophilic groups such as GC-rich sites in DNA and induces intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition. In addition, the BP-Cx1 ligand is able to stimulate the innate immune system and upregulates a variety of cytokines including interferon, tumor necrosis factor-alpha (TNF-alpha), granulocyte macrophage-colony stimulating factor (GM-CSF), and various interleukins (ILs) such as IL-6 and IL-25. In comparison to cisplatin and other platinum–based compounds, treatment with BP-C1 allows for less platinum administration, which reduces platinum-associated systemic toxicity and side effects, and enhances the safety profile while maintaining or improving its efficacy.
BR96-doxorubicin immunoconjugate: An antibody-drug conjugate composed of the chimeric monoclonal antibody BR96 chemically linked to the cytotoxic drug doxorubicin. The antibody moiety of BMS-182248-1 binds to Lewis Y, a cell surface antigen expressed on many solid tumor types. Thus, the doxorubicin conjugate is targeted specifically to Lewis Y-expressing tumor cells, where it intercalates with DNA, thereby inhibiting DNA replication and repair, RNA synthesis and protein synthesis. (NCI)
brachyury-expressing modified vaccinia Ankara-TRICOM vaccine: A cancer vaccine composed of a replication-deficient, attenuated derivative of the vaccinia virus strain Ankara expressing both a CD8+ T-cell epitope from the brachyury protein and a triad of T-cell co-stimulatory molecules (MVA Brachyury-TRICOM), with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration of the brachyury-expressing modified vaccinia Ankara (MVA)-TRICOM vaccine, the expressed brachyury protein induces specific CD8+ and CD4+ T-cell responses against brachyury-expressing tumor cells. This causes both tumor cell lysis and a decrease in the growth of brachyury-expressing tumor cells. Brachyury, a member of the T-box family of transcription factors that is overexpressed in numerous cancer cell types, is correlated with increased epithelial-mesenchymal transition (EMT), cancer resistance and cancer progression. TRICOM, a triad of three human T-cell co-stimulatory molecules, B7.1, ICAM-1 and LFA-3, enhances antigen-specific T-cell activation.
brachyury-expressing yeast vaccine GI-6301: A cancer vaccine composed of a heat-killed, recombinant form of the yeast Saccharomyces cerevisiae that is genetically modified to express the transcription factor brachyury protein, with potential antineoplastic activity. Upon subcutaneous administration, the brachyury-expressing yeast vaccine GI-6301 is recognized by dendritic cells, processed, and presented by Class I and II MHC molecules on the dendritic cell surface. This elicits a targeted CD4+ and CD8+ T-lymphocyte-mediated immune response. This process kills brachyury-expressing tumor cells. Brachyury is overexpressed in a variety of tumor types and plays an important role in cancer progression and metastasis.
BRAF inhibitor ARQ 736: An orally bioavailable, highly soluble phosphate prodrug of B-raf (BRAF) protein kinase with potential antineoplastic activity. BRAF inhibitor ARQ 736 is converted into its active form ARQ 680 in the presence of phosphatases. In turn, ARQ 680 selectively binds to and inhibits the activity of oncogenic B-raf, which may inhibit the proliferation of tumor cells expressing mutated B-raf gene. B-raf belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations. The valine to glutamic acid substitution at residue 600 (V600E) accounts for about 90% of BRAF gene mutations.
BRAF inhibitor LUT014: A topically bioavailable small molecule inhibitor of serine/threonine-protein kinase B-raf (BRAF) protein with potential chemoprotective activity. Upon topical administration, BRAF inhibitor LUT014 targets and binds BRAF and, through the paradoxical effect of BRAF inhibition, induces mitogen-activated protein kinase (MAPK) signaling, which leads to the proliferation and migration of healthy human keratinocytes. This decreases dermal toxicities associated with epidermal growth factor (EGFR) inhibitor therapy. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of MAPK/extracellular signal-regulated kinase (ERK) signaling pathways.
BRAF inhibitor PF-07284890: An antibody targeting human signal-regulatory protein alpha (SIRPa; CD172a), with potential immune checkpoint inhibitory, phagocytosis-inducing and antineoplastic activities. Upon administration, anti-SIRPa antibody FSI-189 targets and binds to SIRPa, a cell surface protein expressed on macrophages, thereby blocking the interaction between SIRPa and cluster of differentiation 47 (CD47) expressed on tumor cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. SIRPa, also known as tyrosine-protein phosphatase non-receptor type substrate 1, mediates negative regulation of phagocytosis, mast cell activation and dendritic cell activation. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.
BRAF inhibitor PF-07799933: An orally bioavailable class 1 and 2 inhibitor of the serine/threonine-protein kinase B-raf (BRAF) protein, with potential antineoplastic activity. Upon oral administration, BRAF inhibitor PF-07799933 selectively binds to and inhibits the activity of class 1 and 2 BRAF alterations. This inhibits the proliferation of tumor cells which express these BRAF alterations. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) signaling pathways, which may be constitutively activated due to BRAF gene mutations. Mutated forms and fusions of BRAF are associated with a number of neoplastic diseases.
BRAF V600E degrader CFT1946: An orally bioavailable heterobifunctional protein degrader of the v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mutant V600E, with potential antineoplastic activity. CFT1946 is comprised of a cereblon (CRBN)-binding moiety and a BRAF V600E-binding moiety. Upon oral administration, BRAF V600E degrader CFT1946 targets and binds to BRAF V600E with its BRAF V600E-binding moiety. Upon BRAF V600E binding, the CRBN-binding moiety binds to CRBN, a component of the CRL4-CRBN E3 ubiquitin ligase complex, which directs proteins for destruction, resulting in the proteasome-mediated degradation of BRAF V600E. This leads to the inhibition of an over-activated MAPK signaling pathway downstream in BRAF V600E-expressing tumor cells and a reduction in tumor cell proliferation. BRAF belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway. The valine to glutamic acid substitution at residue 600 accounts for the majority of BRAF gene mutations. The oncogenic product, BRAF V600E, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway.
BRAF V600E inhibitor HLX208: An orally bioavailable, small molecule inhibitor of the v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mutant V600E, with potential antineoplastic activity. Upon oral administration, BRAF V600E inhibitor HLX208 selectively binds to and inhibits the activity of BRAF V600E kinase, which may result in the inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. BRAF belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway. The valine to glutamic acid substitution at residue 600 accounts for the majority of BRAF gene mutations. The oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway.
BRAF(V600E) kinase inhibitor ABM-1310: An orally bioavailable, small molecule inhibitor of mutant (V600E) v-raf murine sarcoma viral oncogene homolog B1 (BRAF) with potential antineoplastic activity. Upon oral administration, BRAF(V600E) kinase inhibitor ABM-1310 selectively binds to and inhibits the activity of BRAF(V600E) kinase, which may result in the inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. BRAF belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway. The valine to glutamic acid substitution at residue 600 accounts for about 90% of BRAF gene mutations. The oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) mutation has been found to occur in about 8% of all tumors.
BRAF(V600E) kinase inhibitor RO5212054: An orally available small-molecule inhibitor of mutant (V600E) v-raf murine sarcoma viral oncogene homolog B1 (BRAF) with potential antineoplastic activity. BRAF(V600E) kinase inhibitor RO5212054 selectively binds to the ATP-binding site of BRAF(V600E) kinase and inhibits its activity, which may result in an inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. The valine to glutamic acid substitution at residue 600 accounts for about 90% of BRAF gene mutations; the oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) mutation has been found to occur in approximately 60% of melanomas, and in about 8% of all solid tumors.
BRAF/EGFR inhibitor BGB-283: An inhibitor of the serine/threonine protein kinase B-raf (BRAF) and epidermal growth factor receptor (EGFR), with potential antineoplastic activity. BRAF/EGFR inhibitor BGB-283 selectively binds to and inhibits the activity of BRAF and certain BRAF mutant forms, and EGFR. This prevents BRAF- and EGFR-mediated signaling and inhibits the proliferation of tumor cells that either contain a mutated BRAF gene or express over-activated EGFR. In addition, BGB-283 inhibits mutant forms of the Ras proteins K-RAS and N-RAS. BRAF and EGFR are mutated or upregulated in many tumor cell types.
BRAF585-614 (V600E) peptide: A mutated neoantigen peptide consisting of amino acids 585 through 614 of the v-raf murine sarcoma viral oncogene homolog B1 (BRAF; B-raf) and containing the specific mutation V600E, and to which a histidine has been added to the N-terminus, with potential immunostimulating and antineoplastic activities. Upon administration, the BRAF585-614 (V600E) peptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells expressing the mutated BRAF V600E. BRAF, a serine/threonine protein kinase, plays a key role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations, including the BRAF(V600E) mutation, in which valine (V) is substituted by glutamic acid (E) at amino acid 600.
Braftovi: (Other name for: encorafenib)
BRAFV600/PI3K inhibitor ASN003: A selective inhibitor of mutated forms of B-RAF kinase at amino acid position 600 (BRAFV600), including BRAFV600E, the alpha, delta and, to a lesser extent, beta isoforms of phosphatidylinositide 3-kinase (PI3K), including mutated forms of PI3KCA, which encodes the p110-alpha catalytic subunit of the class I PI3K, and the phosphatase and tensin homologs (PTEN) with loss-of-function mutation, with potential antineoplastic activity. Upon administration of ASN003, this agent selectively targets, binds to and inhibits the activity of BRAFV600 mutants as well as mutated isoforms of PI3K. This inhibits signaling through B-RAF- and PI3K/mechanistic target of rapamycin (mTOR)-mediated pathways and inhibits cellular proliferation in tumor cells with BRAFV600 mutations, those expressing PI3K and/or those driven by PTEN. Dysregulation of the B-RAF- and PI3K-mediated pathways is frequently seen in a variety of tumors and results in increased tumor cell growth and survival. Dual targeting of both pathways may increase efficacy and anti-tumor potential compared to the targeting of just one pathway by a selective B-RAF inhibitor or selective PI3K pathway inhibitor alone.
brain tumor initiating cell vaccine: A cell-based cancer vaccine comprised of brain tumor initiating cells (BTICs), with potential immunostimulating and antineoplastic activity. BITCs are from the glioblastoma multiforme (GBM) cell line GBM-6 and contain glioma stem-like cell-associated antigens. Upon administration, the BITC vaccine may stimulate a specific anti-tumoral cytotoxic T –lymphocyte (CTL) response against brain tumor cancer cells and brain tumor stem like cells, resulting in tumor cell lysis. BITC have unique antigenicity and have the ability to self-renew; vaccination against BITC antigens may kill these cells and may prevent tumor recurrences.
Brakiva: (Other name for: liposomal topotecan hydrochloride)
branched-chain amino acid supplement: A nutritional supplement containing essential branched-chain amino acids (BCAAs), including leucine, isoleucine and valine, with potential anti-cachectic, antiangiogenic, hepatocellular carcinoma (HCC) inhibiting and hepatoprotective activities. Upon oral administration, BCAAs inhibit the expression of both hypoxia-inducible factor 1-alpha subunit (HIF-1a) and vascular endothelial growth factor (VEGF), which prevents VEGF-mediated angiogenesis in HCC cells. In addition, BCAAs inhibit proliferation and induce apoptosis of HCC cells by both suppressing the expression of insulin-like growth factor (IGF), and inhibiting the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. BCAAs also correct the plasma amino acid imbalance and promote protein metabolism, including the synthesis of albumin and glycogen. They reduce oxidative stress by inducing the activation of genes involved in antioxidant defenses, which prevent the production of reactive oxygen species (ROS). BCAAs also strengthen the immune system by increasing hepatic lymphocytes and stimulating natural killer (NK) cell activity. This supplement is able to improve insulin resistance and promote ammonia detoxification through increased glutamine (Gln) production.
brassica vegetable: A vegetable belonging to the Brassicaceae family of plants with potential chemopreventive activity. Brassica vegetables, including broccoli, cabbage, kale, Brussels sprouts, turnip and cauliflower, contain a significant amount of glucosinolates. Glucosinolate metabolites, such as sulforaphane and indole-3-carbinol, act as antioxidants and may stimulate endogenous phase II detoxifying enzymes, including glutathione S-transferase and quinone reductase. These biotransformation enzymes play major roles in the detoxification of carcinogenic agents.
BRD4 inhibitor PLX2853: An orally bioavailable inhibitor of the bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon oral administration, the BRD4 inhibitor PLX2853 binds to the acetylated lysine recognition motifs in the bromodomains of the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and dyregulates gene expression. This may lead to the downregulation of the expression of certain growth-promoting genes, which may induce apoptosis and inhibit the proliferation of BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.
BRD4 inhibitor PLX51107: An inhibitor of the bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon administration, the BRD4 inhibitor PLX51107 binds to the acetylated lysine recognition motifs in the bromodomains of the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an induction of apoptosis and an inhibition of proliferation in BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.
BRD4 protein degrader RNK05047: A small molecule, chaperone-mediated protein degrader of bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon intravenous administration of BRD4 protein degrader RNK05047, a BRD4-binding moiety targets and binds to BRD4, and a chaperone-binding moiety targets and binds to the chaperone protein heat shock protein 90 (Hsp90). This results in the Hsp90-mediated proteasomal degradation of BRD4 by the ubiquitin-proteasome system, and dysregulates gene expression. This may lead to the downregulation of the expression of certain growth-promoting genes, which may induce apoptosis and inhibit the proliferation of BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation. Hsp90 is upregulated in a variety of tumor cells and regulates the folding, stability, and degradation of many oncogenic signaling proteins.
BRD9 degrader CFT8634: An orally bioavailable heterobifunctional protein degrader of bromodomain-containing protein 9 (BRD9; sarcoma antigen NY-SAR-29; rhabdomyosarcoma antigen MU-RMS-40.8), with potential antineoplastic activity. CFT8634 is comprised of an E3 ligase-binding moiety and a BRD9-binding moiety. Upon oral administration, BRD9 degrader CFT8634 targets and binds to BRD9 with its BRD9-binding moiety. Upon BRD9 binding, the E3 ligase-binding moiety binds to cereblon (CRBN), a component of the CRL4-CRBN E3 ubiquitin ligase complex, which directs proteins for destruction, resulting in the proteasome-mediated degradation of BRD9. This leads to an inhibition of the growth of tumor cells that rely on BRD9 for survival. BRD9, a component of one form of the Brg/Brahma-Associated Factor (BAF) complex, is needed for the survival of certain cancer cells due to mutations.
BRD9 degrader FHD-609: A protein degrader of bromodomain-containing protein 9 (BRD9; sarcoma antigen NY-SAR-29; rhabdomyosarcoma antigen MU-RMS-40.8), with potential antineoplastic activity. FHD-609 is comprised of an E3 ligase-binding moiety and a BRD9-binding moiety. Upon administration, BRD9 degrader FHD-609 targets and binds to BRD9 with its BRD9-binding moiety. Upon BRD9 binding, the E3 ligase-binding moiety binds to a receptor on the E3 ligase complex which directs proteins for destruction, resulting in the degradation of BRD9. This leads to an inhibition of the growth of tumor cells that rely on BRD9 for survival. BRD9, a component of one form of the Brg/Brahma-Associated Factor (BAF) complex, is needed for the survival of certain cancer cells due to mutations.
brentuximab: A genetically-engineered, chimeric mouse-human, anti-CD30 monoclonal antibody with potential antineoplastic activity. Brentuximab specifically binds to the receptor CD-30, a member of the tumor necrosis factor receptor super-family, which may be overexpressed on the surfaces of Hodgkin lymphoma cells and anaplastic-large cell lymphoma cells. After binding to CD30, this agent interferes with the G1 phase of the cell cycle, thereby inducing growth arrest and apoptosis in susceptible tumor cell populations.
brentuximab vedotin: An antibody-drug conjugate (ADC) directed against the tumor necrosis factor (TNF) receptor CD30 with potential antineoplastic activity. Brentuximab vedotin is generated by conjugating the chimeric anti-CD30 monoclonal antibody SGN-30 to the cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline peptide linker. Upon administration and internalization by CD30-positive tumor cells, brentuximab vedotin undergoes enzymatic cleavage, releasing MMAE into the cytosol; MMAE binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8;TNFRSF8) may be constitutively expressed in hematologic malignancies including Hodgkin lymphoma and some T-cell non-Hodgkin lymphomas. The linkage system in brentuximab vedotin is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells.
brepocitinib: An orally available, selective inhibitor of non-receptor tyrosine-protein kinase TYK2 (tyrosine kinase 2) and tyrosine-protein kinase JAK1 (Janus kinase 1; JAK1) with potential immunomodulatory and anti-inflammatory activities. Upon oral administration, brepocitinib selectively binds to and inhibits the activation of TYK2 and JAK1, thereby disrupting TYK2 and JAK-1-dependent cytokine signaling. This may reduce inflammatory responses and prevent inflammation-induced damage caused by certain immunological diseases. TYK2 and JAK-1 are members of the Janus kinase family of non-receptor tyrosine kinases and are involved in signaling pathways affecting hematopoiesis, immunity and inflammation.
brequinar: A synthetic quinolinecarboxylic acid analogue with antineoplastic properties. Brequinar inhibits the enzyme dihydroorotate dehydrogenase, thereby blocking de novo pyrimidine biosynthesis. This agent may also enhance the in vivo antitumor effect of antineoplastic agents such as 5-FU.
Brevicon: (Other name for: ethinyl estradiol/norethindrone)
brexucabtagene autoleucel: A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion and re-introduction of abrexucabtagene autoleucel into the patient, these cells bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen that is expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it regulates both the assembly and cell surface expression of TCR complexes. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development. KTE-X19 has the same construct as axicabtagene ciloleucel, but differs in the manufacturing process in that KTE-X19 includes specific T-cell selection and lymphocyte enrichment necessary for activity against certain B-cell malignancies.
Breyanzi: (Other name for: lisocabtagene maraleucel)
BRG1/BRM inhibitor FHD-286: An orally bioavailable, allosteric, small molecule inhibitor of transcription activator BRG1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 4; SMARCA4) and BRM (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2; SMARCA2), with potential antineoplastic activity. Upon oral administration, BRG1/BRM inhibitor FHD-286 targets, binds to, and inhibits the activity of BRG1 and/or BRM, the primary ATPase components and mutually exclusive subunits of the BRG1/BRM-associated factor (BAF) complexes. This may lead to the inhibition of the SWI/SNF chromatin remodeling complex, disrupt chromatin remodeling and gene expression, and result in the downregulation of oncogenic pathways and the inhibition of tumor cell proliferation. BAF is an important regulator of transcriptional programs and gene expression. Mutations in BAF or its transcription factor partners are found in certain diseases including cancers.
Bria-IMT: (Other name for: allogeneic GM-CSF-secreting breast cancer vaccine SV-BR-1-GM)
briciclib sodium: A benzyl styryl sulfone analog, and a disodium phosphate ester prodrug of ON 013100, with potential antineoplastic activity. Upon hydrolysis, briciclib is converted to ON 013100, which blocks cyclin D mRNA translation and decreases protein expression of cyclin D. This may induce cell cycle arrest and apoptosis in cancer cells overexpressing cyclin D and eventually decrease tumor cell proliferation. This agent may exhibit synergistic antitumor activity in combination with other chemotherapeutic agents. Cyclin D, a member of the cyclin family of cell cycle regulators, plays a key role in cell cycle division and is often overexpressed in a variety of hematologic and solid tumors and is correlated with poor prognosis.
Bridion: (Other name for: sugammadex sodium)
brigatinib: An orally available inhibitor of receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Brigatinib binds to and inhibits ALK kinase and ALK fusion proteins as well as EGFR and mutant forms. This leads to the inhibition of ALK kinase and EGFR kinase, disrupts their signaling pathways and eventually inhibits tumor cell growth in susceptible tumor cells. In addition, AP26113 appears to overcome mutation-based resistance. 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. EGFR is overexpressed in a variety of cancer cell types.
brigimadlin: An orally available inhibitor of murine double minute 2 (MDM2), with potential antineoplastic activity. Upon oral administration, brigimadlin binds to MDM2 protein and prevents its binding to the transcriptional activation domain of the tumor suppressor protein p53. By preventing MDM2-p53 interaction, the transcriptional activity of p53 is restored. This leads to p53-mediated induction of tumor cell apoptosis. Compared to currently available MDM2 inhibitors, the pharmacokinetic properties of BI 907828 allow for more optimal dosing and dose schedules that may reduce myelosuppression, an on-target, dose-limiting toxicity for this class of inhibitors.
brilacidin oral rinse: An oral rinse containing brilacidin, a defensin mimetic, with potential antimicrobial and anti-mucositic activities. Upon rinsing with the brilacidin oral rinse, brilacidin imitates defensin as a human host defense protein (HDP), and binds to and disrupts the bacterial cell membrane. This causes bacterial cell membrane lysis and leakage of cellular cytoplasmic contents. This inhibits bacterial activity and may prevent or treat radiation-induced mucositis. Defensins, a family of antimicrobial and cytotoxic peptides expressed mainly by epithelial cells and neutrophils, play a key role in the natural human innate immunity against pathogens.
brilanestrant: An orally available, nonsteroidal selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, brilanestrant binds to the estrogen receptor and induces a conformational change that results in the degradation of the receptor. This may inhibit the growth and survival of ER-expressing cancer cells.
Brimarafenib: An orally available inhibitor of both monomer and dimer forms of activating mutations of the serine/threonine-protein kinase BRAF (B-raf) protein, including V600 BRAF mutations, non-V600 BRAF mutations, and RAF fusions, with potential antineoplastic activity. Upon administration, brimarafenib targets and binds to both monomeric and dimeric forms of activating BRAF mutations and fusions. This may result in the inhibition of BRAF-mediated signaling and inhibit proliferation in tumor cells expressing BRAF mutations and fusions. BRAF belongs to the RAF family of serine/threonine protein kinases and plays a role in regulating the mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. BRAF mutations and fusions have been identified in a number of solid tumors and are drivers of cancer growth.
Brimonidine Tartrate: The tartrate salt form of brimonidine, an imidazole derivative and a selective alpha-2 adrenergic receptor agonist. Upon ocular administration, brimonidine tartrate acts on the blood vessels causing them to constrict which leads to a decrease in the production of aqueous humor. Brimonidine tartrate also enhances the outflow of aqueous humor. This drug is used in the treatment of glaucoma to reduce intraocular pressure.
brimonidine tartrate nanoemulsion OCU-300: An ophthalmic nanoemulsion consisting of the tartrate salt form of brimonidine, an imidazole derivative and selective alpha-adrenergic receptor agonist, with potential anti-inflammatory and vasoconstrictive activities. Upon ophthalmic instillation, brimonidine tartrate nanoemulsion OCU-300 reduces intraocular pressure by promoting the outflow and decreasing the production of aqueous humor and may reduce ocular erythema through direct vasoconstriction. Additionally, brimonidine may disrupt leukocyte extravasation into the ocular tissue, inhibit nociception and reduce inflammation associated with ocular graft-versus-host disease (oGvHD). The nanoemulsion formulation may enhance distribution of brimonidine to target tissues, thereby allowing more of the active drug to reach underlying ocular tissue.
brincidofovir: An alkoxyalkyl ester prodrug containing the synthetic, acyclic nucleoside monophosphate analog cidofovir linked, through its phosphonate group, to a lipid, 3-hexadecyloxy-1-propanol, with antiviral activity against double-stranded DNA viruses. Upon oral administration, brincidofovir crosses the intestinal wall and penetrates target viral-infected cells before being cleaved to the free antiviral agent cidofovir. In turn, 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. Compared to cidofovir, which is given intravenously, hexadecyloxypropyl-cidofovir shows better oral bioavailability, less toxicity and enhanced cellular penetration.
Brintellix: (Other name for: vortioxetine hydrobromide)
briquilimab: A humanized monoclonal antibody directed against CD117 (tyrosine-protein kinase KIT; c-Kit; mast/stem cell growth factor receptor; SCFR), that can potentially be used to deplete hematopoietic stem cells (HSCs). Upon administration, briquilimab targets and binds to CD117. This prevents the binding of stem cell factor (SCF) to its receptor CD117 on HSCs. As CD117 binding to SCF is critical for survival and maintenance of blood forming stem cells, blocking this interaction causes the HSCs that are present in the bone marrow niches to be depleted. Briquilimab can potentially be used as a conditioning regimen to prepare patients for hematopoietic stem cell transplantation.
brivanib: A pyrrolotriazine-based compound and an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antineoplastic activity. BMS-540215 specifically targets and binds strongly to human VEGFR-2, a tyrosine kinase receptor and pro-angiogenic growth factor expressed almost exclusively on vascular endothelial cells. Blockade of VEGFR-2 by this agent may lead to an inhibition of VEGF-stimulated endothelial cell migration and proliferation, thereby inhibiting tumor angiogenesis.
brivanib alaninate: The alaninate salt of a vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor with potential antineoplastic activity. Brivanib strongly binds to and inhibits VEGFR2, a tyrosine kinase receptor expressed almost exclusively on vascular endothelial cells; inhibition of VEGFR2 may result in inhibition of tumor angiogenesis, inhibition of tumor cell growth, and tumor regression.
brivaracetam: An orally bioavailable levetiracetam derivative, with anticonvulsant activity. Although the exact mechanism through which brivaracetam exerts its effects is not fully known, this agent targets and binds to synaptic vesicle protein 2A (SV2A) in the brain. This prevents synaptic vesicle exocytosis and the synaptic release of certain, as of yet not fully known, excitatory neurotransmitters. This may inhibit impulse conduction across synapses, decrease neuronal (hyper-)excitability, and may modulate epileptogenesis. SV2A, a membrane glycoprotein present in neuronal synaptic vesicles, plays a key role in action potential-induced neurotransmitter release in the brain.
Briviact: (Other name for: brivaracetam)
brivudine phosphoramidate: A small molecule phosphoramidate derivative of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVdU) with potential antineoplastic activity. Selectively active against tumor cells expressing high levels of thymidylate synthase (TS), brivudine is converted intracellularly by TS to bromovinyldeoxyuridine monophosphate (BVdUMP) which competes with the natural substrate, deoxyuridine monophosphate, for binding to TS. Unlike TS inhibitors, this agent is a reversible substrate for TS catalysis. Thus, TS retains activity and converts BVdUMP into cytotoxic metabolites. As key enzyme in the de novo synthesis of dTMP, TS is an enzyme critical to DNA biosynthesis and is overexpressed in many solid tumors.
broad-spectrum human papillomavirus vaccine V505: A non-infectious recombinant cancer vaccine prepared from the human papillomavirus (HPV) with potential immunoprophylactic activity. Vaccination with broad-spectrum human papillomavirus vaccine V505 may stimulate the host immune system to mount humoral and cytotoxic T lymphocyte (CTL) responses against HPV-infected cells. HPV infection, the cause of genital warts, is a risk factor for the development of cancers of the cervix, vagina, vulva, anus, and penis.
broccoli sprout extract: A cruciferous vegetable extract with potential chemopreventive activities. Broccoli sprout extract contains a high amount of sulforaphane, a naturally occurring isothiocyanate. Sulforaphane activates the transcription factor NF-E2-related factor 2 (Nrf2), a member of the basic leucine zipper family, which binds to and activates antioxidant-response elements (AREs). Subsequently, activated AREs mediate the transcription of antioxidant enzymes (particularly glutathione-S-transferase and quinone oxidoreductase), resulting in the detoxification of highly reactive carcinogens. AREs are cis-acting regulatory enhancer elements found in the 5’ flanking region of many phase II detoxification enzymes.
broccoli sprout/broccoli seed extract supplement: A tablet-based nutritional supplement composed of a mixture of sprout and seed extracts of the cruciferous vegetable broccoli, with potential chemopreventive and antioxidant activities. Broccoli sprout/broccoli seed extract contains a high amount of both the glycosinolate glucoraphanin and the enzyme myrosinase, which catalyzes the production of glucoraphanin to sulforaphane. Upon administration of the broccoli sprout/broccoli seed extract, sulforaphane activates the transcription factor NF-E2-related factor 2 (Nrf2), a member of the basic leucine zipper family, which binds to and activates antioxidant-response elements (AREs). Subsequently, activated AREs promote the transcription of antioxidant and detoxifying enzymes, particularly glutathione-S-transferase and NAD(P)H dehydrogenase [quinone] 1 (NAD(P)H:quinone oxidoreductase; NQO1), resulting in the detoxification of highly reactive carcinogens. This accelerates the elimination of carcinogens, may protect against cellular damage, and prevents cancer formation. AREs are cis-acting regulatory enhancer elements found in the 5' flanking region of many phase II detoxification enzymes.
bromelains: A proteolytic enzyme obtained from the pineapple plant that cleaves sulfhydryl groups. The enzyme is adsorbed intact through the gastrointestinal tract and has demonstrated therapeutic benefit. Bromelain has the ability to modulate cytokines, and has also demonstrated anti-inflammatory activity, immune response activity, and fibrinolytic activity.
bromelains/Boswellia serrata supplement: A nutritional supplement composed of bromelains, enzymes found in pineapple juice and in the pineapple stem, and an extract from the Boswellia serrata tree, that can potentially be used to reduce edema, paresthesia and pain. Upon oral administration of bromelains/Boswellia serrata supplement, the bromelains may reduce inflammation, pain and swelling. The Boswellia serrata extract containing active boswellic acids, appears to have anti-inflammatory effects, may suppress pain and reduce edema, and may promote tissue regeneration.
bromocriptine mesylate: The mesylate salt of bromocriptine, a semisynthetic ergot alkaloid with dopaminergic, antidyskinetic, and antiprolactinemic activities. Bromocriptine selectively binds to and activates postsynaptic dopamine D2 receptors in the corpus striatum of the central nervous system (CNS). Activation of these D2 receptors activate inhibitory G-proteins, which inhibit adenylyl cyclase, preventing signal transduction mediated via cAMP and resulting in the inhibition of neurotransmission and an antidyskinetic effect. This agent also stimulates dopamine D2 receptors in the anterior pituitary gland, which results in the inhibition of prolactin secretion and lactation and may inhibit the proliferation of prolactin-dependent breast cancer cells.
bromovinyl-deoxyuridine: A uridine derivative and nucleoside analog with pro-apoptotic and chemosensitizing properties. In vitro, bromovinyl-deoxyuridine (BVDU) has been shown to downregulate the multifunctional DNA repair enzyme APEX nuclease 1, resulting in the inhibition of DNA repair and the induction of apoptosis. In addition, this agent may inhibit the expression of STAT3 (signal transducer and activator of transcription 3), which may result in the downregulation of vascular endothelial growth factor (VEGF). BVDU has also been found to inhibit the upregulation of chemoresistance genes (Mdr1 and DHFR) during chemotherapy. Overall, the gene expression changes associated with BVDU treatment result in the decrease or prevention of chemoresistance. In addition, this agent has been shown to enhance the cytolytic activity of NK-92 natural killer cells towards a pancreatic cancer cell line in vitro.
brontictuzumab: A humanized monoclonal antibody directed against the Notch-1 receptor with potential antineoplastic activity. Upon administration, brontictuzumab binds to Notch-1 on the cell surface, thereby inhibiting Notch-mediated signaling and tumor cell proliferation. Notch 1, a type 1 transmembrane protein belonging to the Notch family, functions as a receptor for membrane bound ligands and has various roles during development; dysregulated Notch signaling is associated with increased cell growth and chemoresistance in cancers.
bropirimine: An oral immunostimulant that causes the body to produce interferon and other substances.
brostallicin: A synthetic, alpha-bromoacrylic, second-generation minor groove binder (MGB), related to distamycin A, with potential antineoplastic activity. Brostallicin binds to DNA minor groove DNA, after having formed a highly reactive glutathione (GSH)-brostallicin complex in the presence of the enzyme glutathione S-transferase (GST), which is overexpressed in cancer cells; DNA replication and cell division are inhibited, resulting in tumor cell death. Compared to typical MGBs, this agent appears to bind covalently to DNA in a different manner and its activity does not depend on a functional DNA mismatch repair (MMR) mechanism. Accordingly, brostallicin may be effective against MMR-defective tumors that are refractory to various anticancer agents.
Broxine: (Other name for: broxuridine)
broxuridine: A halogenated thymidine analogue with potential antineoplastic and radiosensitizing activities. Bromodeoxyuridine competes with thymidine for incorporation into DNA, resulting in DNA mutation and the inhibition of cell proliferation. As a radiosensitizer, this agent is associated with the inhibition of repair of radiation-induced DNA double-strand breaks.
Bruceantin: A triterpene quassinoid antineoplastic antibiotic isolated from the plant Brucea antidysenterica. Bruceantin inhibits the peptidyl transferase elongation reaction, resulting in decreased protein and DNA synthesis. Bruceantin also has antiamoebic and antimalarial activity.
Brukinsa: (Other name for: zanubrutinib)
Brussels sprout: A leafy green vegetable and a member of the Gemmifera group of cabbages that contains high amounts of phytochemicals, with potential chemopreventive activity. Brussels sprouts contain high amounts of the glycosinolate glucobrassicin. Upon consumption of brussels sprouts, the phytochemicals in the vegetable, and some of their metabolites, are able to induce the expression of various hepatic cytochrome P450 monooxygenases, scavenge free radicals and may inhibit the activation of various signal transduction pathways.
bryostatin 1: A macrocyclic lactone isolated from the bryozoan Bugula neritina with antineoplastic activity. Bryostatin-1 binds to and inhibits the cell-signaling enzyme protein kinase C, resulting in the inhibition of tumor cell proliferation, the promotion of tumor cell differentiation, and the induction of tumor cell apoptosis. This agent may act synergistically with other chemotherapeutic agents.
BTK degrader ABBV-101: An orally bioavailable, targeted degrader of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) comprised of an E3 ubiquitin ligase binding moiety conjugated, via a linker, to a BTK-binding moiety, with potential antineoplastic activity. Upon oral administration of BTK degrader ABBV-101, the BTK-targeting moiety targets and binds to BTK, and the E3 ligase-binding moiety targets and binds to E3 ubiquitin ligase. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK degrader AC0676: An orally bioavailable chimeric degrader of Bruton's tyrosine kinase (BTK) comprised of an E3 ubiquitin ligase ligand conjugated to a BTK-binding ligand, with potential antineoplastic activity. Upon oral administration, BTK degrader AC0676 specifically targets and binds to, with its BTK-targeting moiety, wild-type (WT) and various mutant forms, including, but not limited to, C481S and L528W. Upon binding, the E3 ubiquitin ligase ligand moiety binds to E3 ubiquitin ligase. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK degrader BGB-16673: An orally bioavailable, targeted degrader of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) by using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. BGB-16673 is comprised of an E3 ubiquitin ligase binding moiety conjugated, via a linker, to a BTK-binding moiety. Upon oral administration, BTK degrader BGB-16673 targets and binds to BTK with its BTK-targeting moiety, thereby inhibiting its activity. Upon binding, the E3 ligase-binding moiety binds to cereblon (CRBN), a component of the CRL4-CRBN E3 ubiquitin ligase complex. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. Compared to BTK inhibitors, BGB-16673 may overcome tumor resistance associated with BTK inhibitor-induced resistance mutations, including the BTK C481S mutation, a resistance mutation in the BTK active site in which cysteine is substituted for serine at residue 481.
BTK degrader HSK29116: An orally bioavailable chimeric targeting molecule (CTM) and targeted degrader of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase) by using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. HSK29116 is comprised of an E3 ubiquitin ligase binding moiety conjugated, via a linker, to a BTK-binding moiety. Upon oral administration, BTK degrader HSK29116 targets and binds to BTK with its BTK-targeting moiety, thereby inhibiting its activity. Upon binding, the E3 ligase-binding moiety binds to cereblon (CRBN), a component of the CRL4-CRBN E3 ubiquitin ligase complex. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. Compared to BTK inhibitors, HSK29116 may overcome tumor resistance associated with BTK inhibitor-induced resistance mutations, including the BTK C481 mutation, a resistance mutation in the BTK active site in which cysteine is substituted for serine at residue 481.
BTK degrader NX-2127: An orally bioavailable chimeric targeting molecule (CTM) and targeted degrader of Bruton's tyrosine kinase (BTK), with potential immunomodulatory drug (IMiD) and antineoplastic activities. NX-2127 is comprised of a cereblon (CRBN)-binding moiety conjugated, via a linker, to a BTK-binding moiety. Upon administration, BTK degrader NX-2127 targets and binds to BTK with its BTK-targeting moiety. Upon binding, the CRBN-binding moiety recruits CRBN, a component of the CRL4-CRBN E3 ubiquitin ligase complex. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. In addition, NX-2127 catalyzes the degradation of CRBN neosubstrates Aiolos (IKZF3) and Ikaros (IKZF1), two transcription factors regulating T-cell function. This modulates the activity of the immune system and increases the activation of T lymphocytes, thereby increasing T-cell-mediated anti-tumor effects. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins. Compared to BTK inhibitors, NX-2127 may overcome tumor resistance associated with BTK inhibitor-induced resistance mutations.
BTK degrader NX-5948: An orally bioavailable chimeric targeting molecule (CTM) and targeted degrader of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. NX-5948 is comprised of a cereblon (CRBN)-binding moiety conjugated, via a linker, to a BTK-binding moiety. Upon oral administration, BTK degrader NX-5948 targets and binds to BTK with its BTK-targeting moiety. Upon binding, the CRBN-binding moiety recruits CRBN, a component of the CRL4-CRBN E3 ubiquitin ligase complex. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. NX-5948 does not catalyze the degradation of CRBN neosubstrates and transcription factors Aiolos (IKZF3) and Ikaros (IKZF1), and does not possess immunomodulatory activity. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins. NX-5948 may overcome tumor resistance associated with BTK inhibitor-induced resistance mutations. In addition, NX-5948 is able to cross the blood-brain barrier (BBB) and thus potentially useful in the treatment of central nervous system (CNS) metastases.
BTK degrader UBX-303061: An orally bioavailable chimeric degrader of Bruton's tyrosine kinase (BTK) comprised of an E3 ubiquitin ligase ligand conjugated to a BTK-binding ligand, with potential antineoplastic activity. Upon oral administration, BTK degrader UBX-303061 specifically targets and binds, with its BTK-targeting moiety, to BTK and the E3 ubiquitin ligase ligand moiety binds to E3 ubiquitin ligase. This catalyzes ubiquitination and proteasome-mediated degradation of BTK, and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor ABBV-992: An orally bioavailable and irreversible covalent inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon oral administration, BTK inhibitor ABBV-992 targets, binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies. It plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor CC-292: An orally bioavailable, selective inhibitor of Bruton’s agammaglobulinemia tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, AVL-292 targets and covalently binds to BTK, thereby preventing its activity. By irreversibly inhibiting BTK, administration of this agent may lead to an inhibition of B cell receptor (BCR) signaling and may inhibit cell proliferation of B-cell malignancies. BTK, a cytoplasmic tyrosine kinase and member of the Tec family of kinases, plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor CT-1530: An inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, CT-1530 binds to and inhibits the activity of BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
BTK inhibitor DTRMWXHS-12: An orally available inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, DTRMWXHS-12 inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
BTK inhibitor GB5121: An orally bioavailable, central nervous system (CNS)-penetrating, irreversible covalent inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon oral administration, BTK inhibitor GB5121 selectively targets, irriversibly binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies. It plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. GB5121 is able to penetrate the blood-brain-barrier (BBB) and may thereby treat BTK-driven CNS tumors and metastasis.
BTK inhibitor GDC-0853: An orally available inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, GDC-0853 inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways, which leads to the inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor HMPL-760: A third-generation, reversible inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, BTK inhibitor HMPL-760 non-covalently binds to and inhibits the activity of both wild-type and the C481S mutated form of BTK, a resistance mutation in the BTK active site in which cysteine is substituted for serine at residue 481. This prevents the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK or the C481S mutated form. BTK C481S mutation plays an important role in resistance to certain BTK inhibitors; HMPL-760 may be able to overome this resistance. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
BTK inhibitor HZ-A-018: An orally bioavailable inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, BTK inhibitor HZ-A-018 targets, binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor JNJ-64264681: An orally bioavailable and irreversible covalent inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, BTK inhibitor JNJ-64264681 targets, binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor TL-895: An orally bioavailable, selective inhibitor of Bruton's tyrosine kinase (BTK), with potential antineoplastic activity. Upon oral administration, BTK inhibitor TL-895 targets and covalently binds to BTK, thereby preventing its activity. This leads to an inhibition of B cell receptor (BCR) signaling and inhibits cell proliferation of B-cell malignancies. BTK, a cytoplasmic tyrosine kinase and member of the Tec family of kinases, plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.
BTK inhibitor TQB3702: An orally bioavailable inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon oral administration, BTK inhibitor TQB3702 targets, binds to and inhibits the activity of BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
BTK inhibitor TT-01488: An orally bioavailable reversible inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon oral administration, BTK inhibitor TT-01488 non-covalently binds to and inhibits the activity of BTK, including the C481S mutated form, a resistance mutation in the BTK active site in which cysteine is substituted for serine at residue 481. This prevents the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes. BTK C481S mutation plays an important role in resistance to certain BTK inhibitors.
budesonide: A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. Upon administration, budesonide binds to intracellular glucocorticoid receptors (GRs) and induces the expression of glucocorticoid-responsive genes that encode for anti-inflammatory mediators, such as certain anti-inflammatory cytokines, including interleukin 10 (IL-10), and lipocortins. Lipocortins inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and preventing the synthesis of prostaglandins and leukotrienes, both mediators of inflammation. In addition, budesonide prevents the release of pro-inflammatory cytokines from epithelial cells and macrophages, including interleukin 6 (IL-6), IL-8, interferon-beta (IFNb), and inhibits nuclear factor kappa-B (NF-kB) activation thereby decreasing NF-kB-mediated inflammation.
budesonide/formoterol fumarate dihydrate inhalation aerosol: An inhalation aerosol formulation containing budesonide and the fumarate dihydrate salt of formoterol with anti-inflammatory and bronchial smooth muscle-relaxing activities. The synthetic corticosteroid steroid budesonide binds to intracellular glucocorticosteroid receptors (GRs), exhibiting inhibitory activities against multiple cell types and mediators associated with allergic inflammation. The long-acting beta-adrenergic receptor agonist formoterol selectively binds to beta-2 adrenergic receptors in bronchial smooth muscle, activating intracellular adenyl cyclase, an enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP); increased intracellular cAMP result in the relaxation of bronchial smooth muscle and inhibition of the cellular release of mediators of immediate hypersensitivity, especially from mast cells.
budigalimab: A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, budigalimab targets and binds to PD-1, thereby blocking its binding to the PD-1 ligand, programmed cell death-1 ligand 1 (PD-L1), and preventing the activation of PD-1/PD-L1 downstream signaling pathways. This may restore immune function through the activation of cytotoxic T lymphocytes (CTLs). 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.
buffered lidocaine: A solution of 1% lidocaine, an aminoethylamide and a prototypical member of the amide class anesthetics, buffered with 8.4% sodium bicarbonate in a 3:1 ratio, with anesthetic activity. Upon local injection of the buffered lidocaine, lidocaine interacts with voltage-gated Na+ channels in the nerve cell membrane and blocks the transient increase in permeability of excitable membranes to Na+. This prevents the generation and conduction of nerve impulses and produces a reversible loss of sensation. Buffered lidocaine may reduce the pain of the local injection more than unbuffered lidocaine, may reduce the onset time of anesthesia and may increase its duration of action.
buformin hydrochloride: The hydrochloride salt form of buformin, an agent belonging to the biguanide class of antidiabetics with antihyperglycemic activity. Buformin is not metabolized and is excreted in the urine. This agent has an elevated risk of causing lactic acidosis, and has been withdrawn from the market.
Bulkamid: (Other name for: polyacrylamide hydrogel)
bumetanide: A potent sulfamoylanthranilic acid derivative belonging to the class of loop diuretics. In the brain, bumetanide may prevent seizures in neonates by blocking the bumetanide-sensitive sodium-potassium-chloride cotransporter (NKCC1), thereby inhibiting chloride uptake thus, decreasing the internal chloride concentration in neurons and may block the excitatory effect of GABA in neonates.
Bumex: (Other name for: bumetanide)
buparlisib: An orally bioavailable specific oral inhibitor of the pan-class I phosphatidylinositol 3-kinase (PI3K) family of lipid kinases with potential antineoplastic activity. Buparlisib specifically inhibits class I PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway in an ATP-competitive manner, thereby inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate 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.
Buphenyl: (Other name for: sodium phenylbutyrate)
bupivacaine: An amide-type, long-acting local anesthetic. Bupivicaine reversibly binds to specific sodium ion channels in the neuronal membrane, resulting in a decrease in the voltage-dependent membrane permeability to sodium ions and membrane stabilization; inhibition of depolarization and nerve impulse conduction; and a reversible loss of sensation.
bupivacaine hydrochloride: A long-acting, amide-type local anesthetic. Bupivicaine reversibly binds to specific sodium ion channels in the neuronal membrane, resulting in a decrease in the voltage-dependent membrane permeability to sodium ions and membrane stabilization; inhibition of depolarization and nerve impulse conduction; and a reversible loss of sensation.
bupivacaine hydrochloride liposome injectable suspension: A liposome-encapsulated formulation of bupivacaine, which is an amide-type, long-acting local anesthetic. Upon administration, bupivacaine reversibly binds to specific sodium ion channels in the neuronal membrane, resulting in both a decrease in the voltage-dependent membrane permeability to sodium ions and membrane stabilization. This leads to inhibition of both depolarization and nerve impulse conduction, and a reversible loss of sensation. Compared to bupivacaine alone, liposomal delivery increases the duration of local anesthetic action and delays the peak plasma concentration of bupivacaine due to its slow release from the liposome.
buprenorphine: A synthetic phenanthrene and partial agonist at the mu-opioid receptor and antagonist at the kappa-opioid receptor, with analgesic and sedative activities, and potential antidepressant activity and anti-hyperalgesic effect. Buprenorphine binds to and activates the mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of the endogenous opiates. Binding to opioid receptors stimulates exchange of GTP for GDP, inhibits adenylate cyclase, and decreases intracellular cAMP. This inhibits the release of various nociceptive neurotransmitters, such as substance P, gamma-aminobutyric acid (GABA), dopamine, acetylcholine, noradrenaline, vasopressin, and somatostatin. In addition, buprenorphine closes N-type voltage-gated calcium channels and opens calcium-dependent inwardly rectifying potassium channels, resulting in hyperpolarization, reduced neuronal excitability, analgesia and sedation. Buprenorphine also acts as an antagonist at the kappa-opioid receptor, which may result in antidepressant activity and anti-hyperalgesic effect.
buprenorphine transdermal matrix patch: A transdermal matrix patch containing the synthetic opioid buprenorphine with analgesic and sedative activities. Buprenorphine binds to and activates the mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of the endogenous opiates. Binding to opioid receptors stimulates exchange of GTP for GDP, inhibits adenylate cyclase, and decreases intracellular cAMP. This inhibits the release of various nociceptive neurotransmitters, such as substance P, gamma-aminobutyric acid (GABA), dopamine, acetylcholine, noradrenaline, vasopressin, and somatostatin. In addition, buprenorphine closes N-type voltage-gated calcium channels and opens calcium-dependent inwardly rectifying potassium channels, resulting in hyperpolarization, reduced neuronal excitability, analgesia and sedation. Buprenorphine is a partial agonist at the mu-opioid receptor and an antagonist at the kappa-opioid receptor in the CNS.
bupropion: An aminoketone with antidepressant activity. The molecular mechanism of the antidepressant effect of bupropion is unknown. This agent does not inhibit monoamine oxidase and, compared to classical tricyclic antidepressants, is a weak blocker of the neuronal uptake of serotonin and norepinephrine. Buproprion also weakly inhibits the neuronal re-uptake of dopamine.
bupropion hydrochloride: The hydrochloride salt of the aminoketone bupropion, with antidepressant activity and for potential use in promoting smoking cessation and improving sexual desire. Bupropion is a weak blocker of the neuronal uptake of serotonin, dopamine and norepinephrine and is a central nicotinic acetylcholine receptor antagonist.
bupropion hydrochloride controlled-release: A controlled-release tablet formulation containing the hydrochloride salt of the aminoketone bupropion, with antidepressant activity and for potential use in promoting smoking cessation, improving sexual desire, and improving cancer-related fatigue. Bupropion is a weak blocker of the neuronal uptake of serotonin, dopamine and norepinephrine and is a central nicotinic acetylcholine receptor antagonist. Bupropion may also reduce circulating levels of tumor necrosis factor (TNF) and normalize hypothalamic-pituitary-adrenal (HPA) axis functioning, which is dysregulated in certain cases of cancer-related fatigue. The controlled-release formulation results in a higher concentration of the drug in the body over an extended period, thereby permitting a reduction in the frequency of dosing.
burixafor: An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. Burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation; this may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. 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; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.
burixafor hydrobromide: The hydrobromide salt form of burixafor, an orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with hematopoietic stem cell (HSC)-mobilization and chemosensitizing activities. Upon administration, burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal cell-derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into the peripheral circulation. Additionally, burixafor-mediated mobilization of disseminated tumor cells (DTCs) from the bone marrow into the blood may make these metastatic tumor cells more susceptible to the actions of chemotherapeutic agents. 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. CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.
burosumab: An orally bioavailable recombinant human immunoglobulin G1 monoclonal antibody directed against human fibroblast growth factor 23 (FGF23), that can be used to increase serum phosphate levels. Upon subcutaneous administration, burosumab binds to and inhibits FGF23, thereby interfering with FGF23 signaling. This increases tubular phosphate reabsorption, decreases excretion of phosphate, and increases serum phosphate levels, resulting in enhanced bone mineralization. FGF23, a member of the fibroblast growth factor (FGF) family produced by osteocytes, plays a key role in hypophosphatemic rickets/osteomalacia, such as X-linked hypophosphatemia (XLH) and tumor-induced rickets/osteomalacia. Increased FGF23 levels lead to decreased expression of the sodium-phosphate co-transporters in the proximal tubules, reduced renal phosphate reabsorption, increased excretion by the kidneys, and low serum phosphate concentration.
buserelin: A synthetic analog of gonadotropin-releasing hormone (GnRH). Buserelin binds to and activates pituitary gonadotropin releasing hormone (GnRH) receptors. Prolonged administration of buserelin results in sustained inhibition of gonadotropin production, suppression of testicular and ovarian steroidogenesis, and reduced levels of circulating gonadotropin and gonadal steroids. Buserelin is more potent that GnRH.
Bushen Culuan decoction: A traditional Chinese medicine (TCM) decoction containing a mixture of ten Chinese herbs including Tusizi, Yinyanghuo, Xianmao, Xuduan, Gouqizi, Nvzhenzi, Zelan, Shengpuhuang, Xiangfu and Chuanshanlong, with potential to induce ovulation. Upon oral administration, Bushen Culuan decoction may, through a not yet fully elucidated mechanism, depress follicle-stimulating hormone (FSH) levels, elevate anti-Mullerian hormone (AMH) levels, and increase the number of antral follicle counts (AFCs), thereby promoting ovulation.
Bushen-Jianpi decoction: A traditional Chinese medicine (TCM) that is used for Yin deficiency of the liver, kidney and spleen, with potential immunomodulating and antineoplastic activities. Bushen-Jianpi decoction (BSJPD; BJD) consists of various herbs, including, but not limited to, Radix Codonopsis (Dang Shen), Fructus Lycii (the fruit of Chinese wolfberry), Rhizoma Atractylodis Macrocephalae (Baishu; Bai Zhu), Fructus Ligustri Lucidi, Cuscuta chinensis (Chinese dodder) seed, and Psoralea corylifolia Linn. As a TCM, Bushen-Jianpi is used as an antineoplastic agent as it is thought to invigorate the spleen and tonify the kidney, which presumably prevents or treats a variety of cancers. Upon administration of Bushen-Jianpi decoction, the ingredients in the decoction may affect signaling pathways involved in carcinogenesis and enhance the immune system by increasing the levels of numerous cytokines and a variety of immune cells, such as cytotoxic T lymphocytes (CTLs), natural killer cells (NKs) and macrophages. It may also reduce the expression of various proteins involved in tumorigenesis.
Buspirone Hydrochloride: The hydrochloride salt of an anxiolytic agent chemically and pharmacologically unrelated to benzodiazepines, barbiturates, or other sedative/hypnotic drugs. Although its exact mechanism of action is unknown, buspirone may exert its anti-anxiety effects via serotonin (5-HT1A) and dopamine receptors (D2) and may indirectly affect other neurotransmitter systems. Unlike typical benzodiazepine anxiolytics, this agent does not exert anticonvulsant or muscle relaxant effects and lacks prominent sedative effects.
busulfan: A synthetic derivative of dimethane-sulfonate with antineoplastic and cytotoxic properties. Although its mechanism of action is not fully understood, busulfan appears to act through the alkylation of DNA. Following systemic absorption of busulfan, carbonium ions are formed, resulting in DNA alkylation and DNA breaks and inhibition of DNA replication and RNA transcription.
busulfan/melphalan regimen: A regimen composed of busulfan and melphalan used as a conditioning regimen for stem cell transplantation (SCT).
Busulfex: (Other name for: busulfan)
buthionine sulfoximine: A synthetic amino acid. Buthionine sulfoximine irreversibly inhibits gamma-glutamylcysteine synthase, thereby depleting cells of glutathione, a metabolite that plays a critical role in protecting cells against oxidative stress, and resulting in free radical-induced apoptosis. Elevated glutathione levels are associated with tumor cell resistance to alkylating agents and platinum compounds. By depleting cells of glutathione, this agent may enhance the in vitro and in vivo cytotoxicities of various chemotherapeutic agents in drug-resistant tumors. Buthionine sulfoximine may also exhibit antiangiogenesis activity.
butylscopolamine bromide: An orally available bromide salt form of butylscopolamine, a quaternary ammonium derivative of the alkaloid scopolamine, with anticholinergic property. Upon oral administration, hyoscine butylbromide binds to and blocks muscarinic receptors located on postganglionic parasympathetic nerve endings and on smooth muscle cells. This blocks the activity of acetylcholine (Ach) and causes its antispasmodic effect in the gastrointestinal (GI), urinary, uterine, and biliary tracts. This agent may also facilitate radiologic visualization of the GI tract.
BW A773U: The hydrochloride salt form of 73U82, a three substituted fluoranthene derivative of the 2-(arylmethylamino)-1,3-propanediol family, with potential antineoplastic activity. Upon administration, BW-A-773U intercalates with DNA, causing inhibition of DNA synthesis.
BXQ-350 nanovesicle formulation: A stable, nanovesicle formulation composed of a synthetic form of the human glycoprotein saposin C (SapC) linked to the phospholipid dioleoylphosphatidylserine (DOPS), with potential antineoplastic activity. Upon intravenous administration, the BXQ-350 nanovesicle formulation selectively targets and preferentially accumulates in tumor vessels and cells, due to the leaky nature of tumor vasculature and the presence of phosphatidylserine (PS) lipids in tumor cell membranes. Upon binding to the phospholipids in the tumor cell membrane, SapC fuses with the membrane and is internalized leading to its accumulation within the internal membrane. SapC becomes active in the acidic tumor microenvironment and as a lysosomal sphingolipid activator protein, activates lysosomal enzymes, such as beta-glucosidase, acid sphingomyelinase, and beta-galactosylceramidase. This leads to the degradation of glucosylceramide and sphingomyelin, and the conversion of galactosylceramide to ceramide, respectively. This elevates intracellular ceramide levels, activates caspases and induces ceramide-mediated apoptosis, which together lead to an inhibition of tumor cell growth. SapC plays key roles in lipid transport and organization of biological membranes and has strong lipid membrane binding activity.
Byetta: (Other name for: exenatide)
Bystolic: (Other name for: nebivolol)
BZLF1 peptide vaccine OSU-2131: A cancer preventive vaccine composed of the synthetic peptide RAKFKQLL, which is derived from the Epstein-Barr virus (EBV) immediate-early protein and transcriptional activator BZLF1, and complexed with the recombinant human heat shock protein Hsc70, with potential immunoactivating and antineoplastic activities. Upon subcutaneous administration of the BZLF1 peptide vaccine OSU-2131, the immune system may exert a cytotoxic T-lymphocyte (CTL)-mediated immune response against BZLF1-expressing and EBV-infected cells. This may prevent EBV infections and the development of EBV-driven cancer cells. The Hsc70 may enhance the T-cell responses against the BZLF1 peptide.