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NCI Drug Dictionary

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94 results found for: K

Kadcyla
(Other name for: ado-trastuzumab emtansine)
Kadian
(Other name for: morphine sulfate)
kallikrein inhibitor MDPK67b
A recombinant protein-based inhibitor of numerous types of kallikrein-related peptidases (KLKs), with potential antineoplastic activity. Upon administration, KLK inhibitor MDPK67b targets and inhibits various KLKs, including KLK2, KLK4, KLK5 and KLK14. This inhibits KLK-mediated signaling and inhibits the proliferation of tumor cells in which these KLKs are overexpressed. Deregulation of KLKs is associated with some types of cancers.
kanglaite
An injectable microemulsion of a purified oil extracted from the seeds of the traditional Chinese medicinal herb Coix lacryma-jobi (Job's tears), with potential antineoplastic activity. Although the exact mechanism of action is unknown, kanglaite exhibits an antineoplastic effect, potentially via interfering with the cell cycle and halting tumor cells in the G2/M phase, which may eventually inhibit mitosis and proliferation of cancer cells.
kanitinib
A tyrosine kinase inhibitor targeting the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR; MET) and vascular endothelial growth factor receptor 2 (VEGFR2), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, kanitinib targets and binds to c-Met and VEGFR2, thereby disrupting c-Met- and VEGFR2-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met and/or VEGFR2 protein. c-Met and VEGFR2 are both overexpressed in many tumor cell types and play key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
Kanjinti
(Other name for: trastuzumab)
karonudib
An orally available inhibitor of Karolinska nudt1 (MTH1; MutT homologue 1; NUDT1), with potential antineoplastic activity. Upon administration, karonudib targets and binds to the active site of MTH1, thereby preventing the activity of MTH1. This leads to the incorporation of oxidized deoxynucleoside triphosphates (dNTPs) into the DNA of cancer cells, which causes DNA damage, introduces double strand breaks (DSBs), and induces apoptosis in cancer cells. MTH1, a member of the Nudix phosphohydrolase superfamily hydrolyzes oxidized purine nucleoside triphosphates, including 8-oxo-dGTP and 2-OH-dATP, converts them into their corresponding monophosphate forms, and prevents their incorporation into DNA, which allows MTH1-expressing cells to evade cell death. Compared to normal, healthy cells, cancer cells overexpress MTH1, which leads to dysregulation of the cellular redox system and increased reactive oxygen species (ROS) production, which together prevents the incorporation of damaged and oxidized nucleotides into DNA.
KAT2A/KAT2B degrader AUTX-703
An orally bioavailable, small molecule degrader of the histone acetyltransferases and transcriptional activators lysine acetyltransferase 2A (KAT2A) and its paralog lysine acetyltransferase 2B (KAT2B), with potential antineoplastic activity. Upon oral administration, KAT2A/KAT2B degrader AUTX-703 targets, binds to and selectively degrades KAT2A and KAT2B. This prevents the acetylation of non-histone substrates and transcription of certain genes, such as MYC. KAT2A/KAT2B degradation by AUTX-703 reverses the block in differentiation of certain cancer cells, promotes epithelial cell state differentiation towards a more terminally differentiated state, and inhibits proliferation in susceptible tumor cells. In addition, epithelial differentiation induced by AUTX-703 enhances expression of antigen presenting genes in certain tumor cells. KAT2A and KAT2B, epigenetic enzymes involved in normal human development, play a key role in tumor cell plasticity and in creating an altered, de-differentiated, and more proliferative cellular state in certain tumors.
KAT6 inhibitor MEN2312
An orally bioavailable inhibitor of MYST histone acetyltransferase (HAT) KAT6, with potential antineoplastic activity. Upon oral administration, KAT6 inhibitor MEN2312 targets and binds to KAT6, and inhibits the acetylation of histones and other nonhistone substrates. This may disrupt gene expression and inhibit the proliferation of tumors that overexpress KAT6. KAT6A (MOZ; MYST3) and KAT6B (MORF; MOZ2; MYST4), commonly amplified genes in solid tumors, play key roles in cell cycle regulation and in tumorigenesis.
KAT6 inhibitor PF-07248144
An inhibitor of MYST histone acetyltransferase (HAT) KAT6, with potential antineoplastic activity. Upon administration, KAT6 inhibitor PF-07248144 targets and binds to KAT6, and inhibits the acetylation of histones and other nonhistone substrates. This may disrupt gene expression and inhibit the proliferation of tumors that overexpress KAT6. KAT6A (MOZ; MYST3) and KAT6B (MORF; MOZ2; MYST4), commonly amplified genes in solid tumors, play key roles in cell cycle regulation and in tumorigenesis.
Kava-based supplement
A Kava supplement derived from Piper methysticum, with potential cancer preventative activity. Upon oral administration, the kava-based supplement may affect the metabolism of certain carcinogens, presumably because of the kavalactones present in this product.
KDM4 inhibitor TACH101
An orally bioavailable, small-molecule, pan inhibitor of histone lysine (K) demethylase 4 (KDM4), with potential antineoplastic activity. Upon oral administration, KDM4 inhibitor TACH101 specifically targets, binds to and inhibits the catalytic activity of all members of the KDM4 family of proteins. This may prevent KDM4-mediated signaling, epigenetic dysregulation and inhibit the proliferation of tumor cells. The KDM4 family of histone demethylases is frequently upregulated in a variety of cancers and plays an important role in nuclear functions including the regulation of transcription, cell cycle, and DNA replication and repair.
kefir
A fermented milk drink prepared by inoculating cow, goat, or sheep milk with kefir grains.
Keflex
(Other name for: Cephalexin)
Keflin
(Other name for: Cephalothin Sodium)
Kefzol
(Other name for: cefazolin sodium)
Kemstro
(Other name for: baclofen)
Kenalog
(Other name for: triamcinolone acetonide)
Kepivance
(Other name for: palifermin)
Keppra
(Other name for: levetiracetam)
KeraStat
(Other name for: topical keratin)
Ketalar
(Other name for: ketamine hydrochloride)
ketamine hydrochloride
The hydrochloride salt of a synthetic derivative of cyclohexanone with analgesic and anesthetic activities. Although its mechanism of action is not well understood, ketamine appears to non-competitively block N-methyl-D-aspartate (NMDA) receptors and may interact with opioid mu receptors and sigma receptors, thereby reducing pain perception, inducing sedation, and producing dissociative anesthesia.
ketamine/amitriptyline NP-H cream
A topical preparation containing the antidepressant amitriptyline and the excitatory amino acid antagonist ketamine with potential topical analgesic activity. In addition to activating adenosine A1 receptors and inhibiting the neuronal reuptake of norepinephrine and serotonin, amitriptyline produces antinociceptive effects, which appear to be mediated through the modulation of multiple subtypes of glutamate receptors including the N-methyl D-aspartate (NMDA) receptor. Ketamine inhibits biogenic amine uptake, agonistically binds to mu-opioid receptors, and inhibits NMDA receptors. NDMA receptor antagonists such as amitriptyline and ketamine interfere with the role of NMDA receptors in the process of central sensitization in which NMDA receptors on spinal dorsal horn neurons are activated, resulting in an increase in synaptic efficacy and so an amplification of the response to sensory input.
ketoconazole
A synthetic derivative of phenylpiperazine with broad antifungal properties and potential antineoplastic activity. Ketoconazole inhibits sterol 14-a-dimethylase, a microsomal cytochrome P450-dependent enzyme, thereby disrupting synthesis of ergosterol, an important component of the fungal cell wall.
Ketone-IQ
(Other name for: R-1,3-butanediol-based supplement)
ketoprofen
A propionic acid derivate and nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic effects. Ketoprofen inhibits the activity of the enzymes cyclo-oxygenase I and II, resulting in a decreased formation of precursors of prostaglandins and thromboxanes. The resulting decrease in prostaglandin synthesis, by prostaglandin synthase, is responsible for the therapeutic effects of ibuprofen. Ketoprofen also causes a decrease in the formation of thromboxane A2 synthesis, by thromboxane synthase, thereby inhibiting platelet aggregation.
ketorolac
A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.
ketorolac tromethamine
The tromethamine salt of ketorolac, a synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic and antipyretic properties. Ketorolac tromethamine, a non-selective inhibitor of the cyclooxygenases (COX), inhibits both COX-1 and COX-2 enzymes. This agent exerts its anti-inflammatory effect by preventing conversion of arachidonic acid to prostaglandins at inflammation site mediated through inhibition of COX-2, which is undetectable in most tissues but is up-regulated at the inflammation sites. Since COX-1 is expressed virtually in all tissues, inhibition of COX-1 enzyme by this agent prevents normal state production of prostaglandins, which plays housekeeping roles in the protection of the gastrointestinal tract, regulating renal blood flow, and functioning in platelet aggregation. As a result, inhibition of COX-1 is usually associated with adverse effects such as gastrointestinal toxicity and nephrotoxicity.
ketotifen fumarate
The fumarate salt of ketotifen, a cycloheptathiophene derivative with anti-allergic activity. Ketotifen selectively blocks histamine (H1) receptors and prevents the typical symptoms caused by histamine release. This agent also interferes with the release of inflammatory mediators from mast cells involved in hypersensitivity reactions, thereby decreasing chemotaxis and activation of eosinophils.
Kevetrin
(Other name for: thioureidobutyronitrile)
Kevzara
(Other name for: sarilumab)
keyhole limpet hemocyanin
A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins.
keynatinib
A third-generation, orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, keynatinib binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, inhibits the tyrosine kinase activity of EGFR T790M, prevents EGFR T790M-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
Keytruda
(Other name for: pembrolizumab)
Kiacta
(Other name for: eprodisate disodium)
KIF18A inhibitor GH2616
An orally bioavailable inhibitor of the human kinesin-like protein KIF18A, with potential antineoplastic activity. Upon oral administration, KIF18A inhibitor GH2616 selectively binds to and inhibits the activity of KIF18A. This may result in multipolar cell division and inhibit tumor cell proliferation. KIF18A, a mitotic kinesin-8 motor protein, plays an important role in the regulation of chromosome positioning during cell division and is overexpressed in certain cancers. Certain cancer cells with chromosomal instability (CIN) features depend on KIF18A activity for bipolar spindle integrity and cell proliferation.
KIF18A inhibitor VLS-1488
An orally bioavailable inhibitor of the human kinesin-like protein KIF18A, with potential antineoplastic activity. Upon oral administration, KIF18A inhibitor VLS-1488 selectively binds to and inhibits the activity of KIF18A. This may result in multipolar cell division and inhibit tumor cell proliferation. KIF18A, a mitotic kinesin-8 motor protein, plays an important role in the regulation of chromosome positioning during cell division and is overexpressed in certain cancers. Certain cancer cells with chromosomal instability (CIN) features depend on KIF18A activity for bipolar spindle integrity and cell proliferation.
Kimmtrak
(Other name for: tebentafusp-tebn)
kinase inhibitor TQB3912
An orally bioavailable small molecule protein kinase inhibitor, with potential antineoplastic activity. Upon oral administration, kinase inhibitor TQB3912 may target, bind to and inhibit the activity of a protein kinase that plays an important role in tumor cell survival, proliferation, migration, and differentiation.
kinase inhibitor UCT-01-097
An orally bioavailable kinase inhibitor, with potential antineoplastic activity. Upon oral administration, kinase inhibitor UCT-01-097 may target, bind to and inhibit the activity of one or more kinases that play a key role in tumor cell proliferation.
Kineret
(Other name for: anakinra)
Kisqali
(Other name for: ribociclib succinate)
Kisqali Femara Co-Pack
(Other name for: ribociclib succinate/letrozole)
KIT-mutant inhibitor DCC-3009
An orally bioavailable switch-control inhibitor of multiple mutated forms of mast/stem cell factor receptor KIT (c-Kit; SCFR), with potential antineoplastic activity. Upon oral administration, KIT-mutant inhibitor DCC-3009 targets and binds to the switch pocket of c-Kit, thereby inhibiting the activity of specific c-Kit mutants, including primary KIT mutations in exons 9 and 11 and secondary drug-resistant mutations across exons 13, 14, 17, and 18. This may inhibit tumor cell proliferation in cancer cell types that overexpress these c-Kit mutations. c-Kit, a transmembrane protein and receptor tyrosine kinase (RTK) overexpressed in various solid tumors and hematological malignancies, plays a key role in the regulation of cell differentiation and proliferation. Mutant forms of c-Kit are often associated with tumor chemoresistance.
Klebsiella pneumoniae glycoprotein
A glycoprotein complex extracted from Klebsiella pneumoniae K2O1 strain with immunostimulating property. This glycoprotein complex consists of 2 repetitive glycoprotein subunits; P1 comes from the bacterial capsule about 95 kD in molecular mass and F1, having an lipopolysaccharide-related structure (350 kDa), is derived from bacterial external membrane. Although the mechanism of action is not fully elucidated, Klebsiella pneumoniae F1 fraction appears to suppress monocyte apoptosis, hence inducing the differentiation of monocytes into macrophages. Furthermore, this agent also enhances humoral and cell-mediated immune responses, and increases natural killer cell cytotoxicity functions. This glycoprotein has been shown to reduce the incidence of infection.
KLH-FITC
A conjugate consisting of keyhole-limpet hemocyanin (KLH) and fluorescein isothiocyanate (FITC) with potential immunostimulating activity. Vaccination with KLH-FITC may elicit an immune response against fluorescein and the production of anti-fluorescein IgG antibodies. KLH, a natural protein isolated from the marine mollusk keyhole limpet, is an immunostimulant carrier protein.
Komed HC
(Other name for: therapeutic hydrocortisone)
Konakion
(Other name for: Phytonadione)
Korlym
(Other name for: mifepristone)
KOS-953
(Other name for: tanespimycin)
Koselugo
(Other name for: selumetinib sulfate)
KRAS G12C inhibitor BBO-8520
An orally bioavailable, covalent inhibitor of both the active, guanosine triphosphate (GTP)-bound form and the inactive, guanosine diphosphate (GDP)-bound form of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BBO-8520 targets and binds to the switch II pocket in both the GTP-bound (ON) and GDP-bound (OFF) state conformations of KRAS G12C. This modifies and inhibits both the GTP-bound (active) and GDP-bound (inactive) forms of KRAS G12C and prevents KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor BEBT-607
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BEBT-607 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in KRAS G12C mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12C inhibitor BI 1823911
An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BI 1823911 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor BPI-421286
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BPI-421286 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12C inhibitor FMC-376
An orally bioavailable, covalent inhibitor of both the active, guanosine triphosphate (GTP)-bound form and the inactive, guanosine diphosphate (GDP)-bound form of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor FMC-376 targets and covalently binds to cysteine 12 within the switch II pocket in both the GTP-bound (ON) and GDP-bound (OFF) state conformations of KRAS G12C. This modifies and inhibits both the GTP-bound (active) and GDP-bound (inactive) forms of KRAS G12C and prevents KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis. GTP-bound KRAS G12C is upregulated in tumor cells that are resistant to many OFF state KRAS G12C inhibitors.
KRAS G12C inhibitor GEC-255
An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GEC255 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12C inhibitor GH35
An orally bioavailable irreversible inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GH35 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor HBI-2438
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HBI-2438 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12C inhibitor HS-10370
An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HS-10370 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor HYP-2090PTSA
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HYP-2090PTSA selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in KRAS G12C mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis. HYP-2090PTSA may also inhibit phosphatidylinositol 3-kinase (PI3K) activity and PI3K/Akt (protein kinase B)-mediated signaling pathway.
KRAS G12C inhibitor IBI351
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor IBI351 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor JMKX001899
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor JMKX001899 targets and irreversibly binds to the KRAS G12C mutant, and locks it in an inactive state. This inhibits the activity of the KRAS G12C mutant, thereby preventing KRAS G12C mutant-mediated signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis. JMKX001899 is able to penetrate through the blood-brain barrier (BBB).
KRAS G12C inhibitor LY3499446
An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, LY3499446 targets and covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
Kras G12C inhibitor MK-1084
An orally available inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor MK-1084 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12C inhibitor YL-15293
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor YL-15293 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS G12C inhibitor ZG19018
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor ZG19018 selectively targets and irreversibly binds to the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in KRAS G12C mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D degrader ASP3082
A targeted protein degrader (TPD) of the oncogenic KRAS substitution mutation G12D, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. ASP3082 is comprised of an E3 ubiquitin ligase-binding moiety conjugated, via a linker, to a KRAS G12D-binding moiety. Upon administration, KRAS G12D degrader ASP3082 specifically targets and binds, with its KRAS G12D-targeting moiety, to KRAS G12D mutated protein and, with its E3 ligase-binding moiety, to the E3 ubiquitin ligase, thereby forming a ternary complex. This induces E3 ligase ubiquitination and proteasome-mediated degradation of KRAS G12D mutated protein. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D degrader ASP4396
A targeted protein degrader (TPD) of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. ASP4396 is comprised of an E3 ubiquitin ligase-binding moiety conjugated, via a linker, to a KRAS G12D-binding moiety. Upon administration, the KRAS G12D-targeting moiety of KRAS G12D degrader ASP4396 specifically targets and binds to KRAS G12D mutated protein and the E3 ligase-binding moiety targets and binds to the E3 ubiquitin ligase, thereby forming a ternary complex. This induces E3 ligase ubiquitination and proteasome-mediated degradation of KRAS G12D mutated protein. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D inhibitor HRS-4642
An inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon administration, KRAS G12D inhibitor HRS-4642 specifically targets and binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D inhibitor INCB161734
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor INCB161734 specifically targets and binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D inhibitor QLC1101
An orally bioavailable reversible inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor QLC1101 specifically targets and reversibly binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS G12D inhibitor QTX3046
An orally bioavailable allosteric inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor QTX3046 specifically targets and noncovalently binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis. QTX3046 inhibits both the GTP-bound (ON) and GDP-bound (OFF) state conformations of KRAS G12D, and is able to cross the blood-brain barrier (BBB).
KRAS G12D inhibitor TSN1611
An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor TSN1611 specifically targets and binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways and leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRAS inhibitor BI 3706674
An orally bioavailable small molecule inhibitor that targets the oncogenic KRAS wild-type (WT) and various KRAS mutant forms, such as KRAS G12C, with potential antineoplastic activity. Upon oral administration, KRAS inhibitor BI 3706674 selectively binds to KRAS, thereby inhibiting KRAS-dependent signaling and inhibits growth and survival of KRAS-overexpressing and mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS mutant inhibitor ALTA3263
An orally bioavailable non-covalent dual ON/OFF state inhibitor of multiple oncogenic KRAS mutant forms, including KRAS G12V, G12D and G12C, with potential antineoplastic activity. Upon oral administration, KRAS mutant inhibitor ALTA3263 selectively targets and binds to KRAS, thereby inhibiting KRAS-dependent signaling. This inhibits the growth and survival of KRAS-overexpressing and mutated tumor cells. KRAS, a member of the RAS family of oncogenes, plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS mutant inhibitor BBO-11818
An orally bioavailable non-covalent inhibitor of both the active, guanosine triphosphate (GTP)-bound (ON) form and the inactive, guanosine diphosphate (GDP)-bound (OFF) form of multiple oncogenic KRAS substitution mutations, including KRAS G12D, G12V and G12X, with potential antineoplastic activity. Upon oral administration, KRAS mutant inhibitor BBO-11818 selectively targets and binds to KRAS, thereby inhibiting KRAS-dependent signaling. This inhibits the growth and survival of KRAS-overexpressing and mutated tumor cells. KRAS, a member of the RAS family of oncogenes, plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS mutant inhibitor KQB365
An inhibitor of one or more KRAS mutations, with potential antineoplastic activity. Upon administration, KRAS mutant inhibitor KQB365 targets, binds to and inhibits one or more KRAS mutations, thereby inhibiting KRAS mutant-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS mutant inhibitor QTX3034
An orally bioavailable inhibitor of various KRAS mutations, including the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS mutant inhibitor QTX3034 targets, allosterically binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS mutant inhibitor QTX3544
An orally bioavailable allosteric dual ON/OFF state inhibitor of multiple oncogenic KRAS mutant forms, particularly KRAS G12V, with potential antineoplastic activity. Upon oral administration, KRAS mutant inhibitor QTX3544 selectively targets and binds to KRAS, thereby inhibiting KRAS-dependent signaling. This inhibits the growth and survival of KRAS-overexpressing and mutated tumor cells. KRAS, a member of the RAS family of oncogenes, plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
KRAS-G12D inhibitor MRTX1133
An orally bioavailable reversible inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor MRTX1133 specifically targets and noncovalently binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.
KRASG12C inhibitor JNJ-74699157
An orally available, small molecule inhibitor of the oncogenic Kirsten rat sarcoma virus homolog KRAS glycine-to-cysteine substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration JNJ-74699157 targets and binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
Krazati
(Other name for: adagrasib)
KRN5500
A semisynthetic derivative of the nucleoside-like antineoplastic antibiotic spicamycin, originally isolated from the bacterium Streptomyces alanosinicus. KRN 5500 inhibits protein synthesis by interfering with endoplasmic reticulum and Golgi apparatus functions. This agent also induces cell differentiation and caspase-dependent apoptosis.
Krystexxa
(Other name for: pegloticase)
KSP inhibitor ARRY-520
A synthetic, small molecule targeting the kinesin spindle protein (KSP) with potential antineoplastic activity. KSP inhibitor ARRY-520 specifically inhibits KSP (kinesin-5 or Eg5), resulting in activation of the spindle assembly checkpoint, induction of cell cycle arrest during the mitotic phase, and consequently cell death in tumor cells that are actively dividing. Because KSP is not involved in postmitotic processes, such as neuronal transport, this agent does not cause the peripheral neuropathy that is often associated with tubulin-targeting agents. KSP is an ATP-dependent microtubule motor protein that is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis.
KSP inhibitor AZD4877
A synthetic kinesin spindle protein (KSP) inhibitor with potential antineoplastic activity. KSP inhibitor AZD4877 selectively inhibits microtubule motor protein KSP (also called kinesin-5 or Eg5), which may result in the inhibition of mitotic spindle assembly; activation of the spindle assembly checkpoint; induction of cell cycle arrest during the mitotic phase; and cell death in tumor cells that are actively dividing. Because KSP is not involved in postmitotic processes, such as neuronal transport, this agent may be less likely to cause the peripheral neuropathy often associated with the tubulin-targeting agents. Eg5 is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis.
kunecatechins ointment
A topical ointment containing a green tea polyphenol mixture (kunecatechins) with potential antiviral, antibacterial, antioxidant, and chemopreventive activities. Kunecatechins is a partially purified fraction of the aqueous extract of green tea leaves from Camellia sinensis and contains catechins and other green tea components. Catechins, polyphenolic antioxidant plant metabolites or flavonoids, comprise most of the drug substance in kunecatechins with epigallocatechin gallate (EGCG) present as the primary catechin. Catechins may inhibit basic functions of human papillomavirus (HPV), counteract specific changes in tumor cells, affect cell signaling, and stimulate the immune system. Topical application of kunecatechins ointment has been reported to reduce HPV-induced genital and anal warts through a not yet fully understood mechanism, which may involve anti-oxidative activity.
KW-2149
A semisynthetic water-soluble disulfide derivative of the antineoplastic antibiotic mitomycin C. Activated by serum and glutathione, KW-2149 causes interstrand DNA cross-links and DNA-protein cross-links, resulting in single-strand DNA breaks and inhibition of DNA synthesis.
Kybella
(Other name for: deoxycholic acid)
Kymriah
(Other name for: tisagenlecleucel)
Kynacyte
(Other name for: safingol)
Kyprolis
(Other name for: carfilzomib)