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c-Met inhibitor

" in MedChemExpress (MCE) Product Catalog:

96

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2

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Isotope-Labeled Compounds

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Click Chemistry

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-15735

    c-Met/HGFR Cancer
    c-Met inhibitor 1 is an inhibitor of the c-Met receptor signaling pathway useful for the treatment of cancer including gastric, glioblastoma, and pancreatic cancer.
    <em>c-Met</em> <em>inhibitor</em> 1
  • HY-18711A

    Metatinib anhydrous; c-Met inhibitor 2

    c-Met/HGFR VEGFR Cancer
    SCR-1481B1 (Metatinib anhydrous) is a potent compound that has activity against cancers dependent upon Met activation and also has activity against cancers as a VEGFR inhibitor.
    SCR-1481B1
  • HY-115937

    c-Met/HGFR Apoptosis Cancer
    c-Met-IN-9, a 4-phenoxypyridine derivative, is a c-Met kinas inhibitor with an IC50 of 12 nM. c-Met-IN-9 induces cells apoptosis, and has antitumor activities .
    c-Met-IN-9
  • HY-157302

    c-Met/HGFR Cancer
    c-Met-IN-21 (compound 54) is a c-met inhibitor with an IC50 value of 0.45? nM, and shows anti-tumor efficacy in vivo .
    c-Met-IN-21
  • HY-147694

    c-Met/HGFR VEGFR Cancer
    c-Met-IN-11 (compound 3) is a potent c-MET and VEGFR-2 inhibitor, with IC50 values of 41.4 and 71.1 nM, respectively .
    c-Met-IN-11
  • HY-153831

    c-Met/HGFR Cancer
    c-Met-IN-17 is a potent c-Met kinase inhibitor with an IC50 of 0.031 μM. c-Met-IN-17 can be used in anticancer research. . c-Met-IN-17 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    c-Met-IN-17
  • HY-147695

    c-Met/HGFR Cancer
    c-Met-IN-12 (compound 4r) is an orally active, potent and selective type II c-Met kinase inhibitor, with an IC50 of 10.6 nM. c-Met-IN-12 displays high inhibitory effects (inhibition rate > 80% in 1 μM) against AXL, Mer and TYRO3 kinases. c-Met-IN-12 can be used a scaffold for further kinase selectivity enhancement. c-Met-IN-12 shows antitumor efficacy .
    c-Met-IN-12
  • HY-148279

    c-Met/HGFR Cancer
    c-Met-IN-15 (compound S3) is a c-Met kinase inhibitor. c-Met-IN-15 inhibits c-Met kinase activity of 21.1% at the concentration of 10 μM .
    c-Met-IN-15
  • HY-161141

    c-Met/HGFR Cancer
    EGFR/ C-Met-in-2 (Compound H-22) is a dual inhibitor of EGFR/c-Met. EGFR/c-Met-IN-2 inhibits cell proliferation by arresting G2/M phase. EGFR/c-Met-IN-2 has antitumor activity .
    EGFR/c-Met-IN-2
  • HY-15959
    Savolitinib
    5 Publications Verification

    Volitinib; HMPL-504; AZD-6094

    c-Met/HGFR Cancer
    Savolitinib (AZD-6094) is a potent, highly selective, and orally bioavailable c-Met inhibitor with IC50 s of 5 nM and 3 nM for c-Met and p-Met, respectively. Savolitinib (AZD-6094) selectively binds to and inhibits the activation of c-Met in an ATP-competitive manner, and disrupts c-Met signal transduction pathways. Antineoplastic activity .
    Savolitinib
  • HY-161353

    c-Met/HGFR P-glycoprotein Cancer
    c-Met-IN-23 (Compound 12g) is a c-Met inhibitor (IC50 = 0.052 μM for c-Met). c-Met-IN-23 also inhibits MDR1 and MRP1/2 pumps in the cancerous HepG2 and BxPC3 cells. c-Met-IN-23 is an anticancer agent .
    c-Met-IN-23
  • HY-124267

    SOMG-833

    c-Met/HGFR Cancer
    Zgwatinib (SOMG-833) is a potent, selective, and ATP-competitive c-MET inhibitor, with an IC50 of 0.93 nM against c-MET, over 10,000-fold more potent compared with 19 tyrosine kinases (including c-MET family members and highly homologous kinases). Zgwatinib potently inhibits c-MET-driven cell proliferation. Zgwatinib as a potential candidate agent for c-MET-driven human cancers research .
    Zgwatinib
  • HY-14723

    c-Met/HGFR Cancer
    AMG-458 is a potent, selective and orally bioavailable c-Met inhibitor, with Ki values of 1.2 nM and 2.0 nM for human and mouse c-Met, respectively .
    AMG-458
  • HY-120908

    c-Met/HGFR Cancer
    c-Met-IN-16 is a c-Met inhibitor that can be used for cancer research .
    c-Met-IN-16
  • HY-149880

    c-Met/HGFR Cancer
    c-Met-IN-18 is ATP competitive type-III c-MET inhibitor of WT and D1228V mutant c-MET. c-Met-IN-18 has inhibitory for WT/D1228V with an IC50 value of 0.013/0.20 e.c-Met-IN-18 can be used for the research of c-MET driven cancers . c-Met-IN-18 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    c-Met-IN-18
  • HY-147259

    c-Met/HGFR Cancer
    Dalmelitinib is an orally active selective c-Met kinase inhibitor (IC50: 2.9 nM) that binds to the ATP-binding region of c-Met. Dalmelitinib induces the phosphorylation of MET, partially or completely inhibits the phosphorylation of AKT and ERK. Dalmelitinib potently inhibits cancer cell (c-Met oncogene amplification) proliferation, and is used for the research of cancers like human non-small cell lung cancer (NSCLC) .
    Dalmelitinib
  • HY-150004

    c-Met/HGFR HDAC Apoptosis Cancer
    c-Met/HDAC-IN-3 (Compound 15f) is a dual c-Met and HDAC inhibitor with IC50 values of 12.50 nM and 26.97 nM against c-Met and HDAC1, respectively. c-Met/HDAC-IN-3 induces apoptosis and cause cell cycle arrest in G2/M phase .
    c-Met/HDAC-IN-3
  • HY-101773

    c-Met/HGFR Cancer
    c-Met-IN-2 is a potent, selective and orally available c-Met inhibitor, with an IC50 of 0.6 nM, with antitumor activity.
    c-Met-IN-2
  • HY-50683
    JNJ-38877605
    3 Publications Verification

    c-Met/HGFR Metabolic Disease Cancer
    JNJ-38877605 is an orally active ATP-competitive inhibitor of c-Met with an IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases . JNJ-38877605 inhibits c-Met phosphorylation and regulates lipid accumulation. JNJ-38877605 can be used for tumor and metabolic disease reseach .
    JNJ-38877605
  • HY-163006

    EGFR c-Met/HGFR Cancer
    EGFR/c-Met-IN-1 (compound TS-41) is a dual-target inhibitor of EGFR/c-Met. The IC50 for inhibiting EGFR L858R and c-Met is 68.1 nM and 0.26 nM respectively. . EGFR/c-Met-IN-1 induces apoptosis and cell cycle arrest in A549-P cells, downregulating the phosphorylation of EGFR, c-Met, and downstream AKT. EGFR/c-Met-IN-1 inhibits tumor growth in vitro and in vivo .
    EGFR/c-Met-IN-1
  • HY-116000
    Glumetinib
    1 Publications Verification

    Gumarontinib; SCC244

    c-Met/HGFR Cancer
    Glumetinib (SCC244) is a highly selective, orally bioavailable, ATP-competitive c-Met inhibitor with an IC50 of 0.42 nM. Glumetinib has greater than 2400-fold selectivity for c-Met over those 312 kinases evaluated, including the c-Met family member RON and highly homologous kinases Axl, Mer, TyrO3. Antitumor activity .
    Glumetinib
  • HY-101031

    c-met-IN-1 (compound 16) is a potent and selective c-Met inhibitor, with IC50 of 1.1 nM, with antitumor activity. .
    c-Met-IN-1
  • HY-14721
    Tepotinib
    5 Publications Verification

    EMD-1214063

    c-Met/HGFR Autophagy Cancer
    Tepotinib (EMD-1214063) is a potent and highly selective c-Met inhibitor with an IC50 of 4 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Antitumor effects .
    Tepotinib
  • HY-50686
    Tivantinib
    5+ Cited Publications

    ARQ 197; (3R,4R)-ARQ 198

    c-Met/HGFR Apoptosis Cancer
    Tivantinib is a highly selective c-Met tyrosine kinase inhibitor with a Ki of 355 nM.
    Tivantinib
  • HY-150582

    c-Met/HGFR c-Kit FLT3 Apoptosis Cancer
    c-Met-IN-14 (compound 26af) is a selective inhibitor of c-Met kinase from N-sulfonylamidine-based derivatives, with an IC50 value of 2.89 nM. c-Met-IN-14 shows anticancer activity by blocking phosphorylation of c-Met, and arrests cell cycle at G2/M phase. c-Met-IN-14 induces apoptosis of A549 cells in a dose-dependent manner .
    c-Met-IN-14
  • HY-13404
    Capmatinib
    5+ Cited Publications

    INC280; INCB28060

    c-Met/HGFR Apoptosis Cancer
    Capmatinib (INC280; INCB28060) is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib is largely metabolized by CYP3A4 and aldehyde oxidase .
    Capmatinib
  • HY-13404B

    INC280 hydrochloride; INCB-28060 hydrochloride

    c-Met/HGFR Apoptosis Cancer
    Capmatinib (INC280; INCB28060) hydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib hydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib hydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib hydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase .
    Capmatinib hydrochloride
  • HY-13404C

    INC280 dihydrochloride hydrate; INCB-28060 dihydrochloride hydrate

    c-Met/HGFR Apoptosis Cancer
    Capmatinib (INC280; INCB28060) dihydrochloride hydrate is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride hydrate can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride hydrate potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride hydrate is largely metabolized by CYP3A4 and aldehyde oxidase .
    Capmatinib dihydrochloride hydrate
  • HY-13404A

    INC280 dihydrochloride; INCB28060 dihydrochloride

    c-Met/HGFR Apoptosis Cancer
    Capmatinib (INC280; INCB28060) dihydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase .
    Capmatinib dihydrochloride
  • HY-157387

    c-Met/HGFR Apoptosis Cancer
    c-Met-IN-22 (compound 51am) is an orally active inhibitor against c-Met with an IC50 value of 2.54 nM. c-Met-IN-22 has antiproliferative and antitumor activities. c-Met-IN-22 induces cell apoptosis .
    c-Met-IN-22
  • HY-12017
    PF-04217903
    2 Publications Verification

    c-Met/HGFR Cancer
    PF-04217903 is a potent ATP-competitive c-Met kinase inhibitor with Ki of 4.8 nM for human c-Met. PF-04217903 shows more than 1,000-fold selectivity relative to 208 kinases. Antiangiogenic properties .
    PF-04217903
  • HY-12017A
    PF-04217903 mesylate
    2 Publications Verification

    c-Met/HGFR Cancer
    PF-04217903 mesylate is a potent ATP-competitive c-Met kinase inhibitor with Ki of 4.8 nM for human c-Met. PF-04217903 mesylate shows more than 1,000-fold selectivity relative to 208 kinases. Antiangiogenic properties .
    PF-04217903 mesylate
  • HY-143462

    HDAC c-Met/HGFR Apoptosis Cancer
    c-Met/HDAC-IN-2 is a highly potent c-Met and HDAC dual inhibitor with IC50s of 18.49 nM and 5.40 nM for HDAC1 and c-Met, respectively. c-Met/HDAC-IN-2 has antiproliferative activities against certain cancer cell lines. c-Met/HDAC-IN-2 can cause G2/M-phase arrest and induce apoptosis in HCT-116. c-Met/HDAC-IN-2 can be used for researching anti-cancer resistance .
    c-Met/HDAC-IN-2
  • HY-150576

    c-Met/HGFR Cancer
    c-Met-IN-13 is a potent c-Met inhibitor with an IC50 value of 2.43 nM. c-Met-IN-13 shows excellent cytotoxicity for cancer cells. c-Met-IN-13 shows antiproliferative activity in a concentration- and time- dependent manner. c-Met-IN-13 has the potential for the research of cancer .
    c-Met-IN-13
  • HY-12017B

    c-Met/HGFR Cancer
    PF-04217903 phenolsulfonate is a potent ATP-competitive c-Met kinase inhibitor with Ki of 4.8 nM for human c-Met. PF-04217903 phenolsulfonate shows more than 1,000-fold selectivity relative to 208 kinases. Antiangiogenic properties .
    PF-04217903 phenolsulfonate
  • HY-147040

    c-Met/HGFR Cancer
    ABN401 is a highly potent and selective ATP-competitive c-MET inhibitor with an IC50 value of 10 nM. ABN401 has cytotoxic activity against MET-addicted cancer cells. ABN401 can inhibit c-MET phosphorylation in tumor tissues. ABN401 can be used for researching anticancer .
    ABN401
  • HY-15240

    c-Kit c-Met/HGFR Cancer
    c-Kit-IN-1 is a potent inhibitor of c-Kit and c-Met with IC50s of <200 nM.
    c-Kit-IN-1
  • HY-50703
    MK-2461
    1 Publications Verification

    c-Met/HGFR Cancer
    MK-2461 is a novel ATP-competitive multitargeted inhibitor of activated c-Met with a mean IC50 of 2.5 nM.
    MK-2461
  • HY-100946

    RXDX-106

    TAM Receptor c-Met/HGFR Cancer
    CEP-40783 is a potent, selective and orally available inhibitor of AXL and c-Met with IC50 values of 7 nM and 12 nM, respectively.
    CEP-40783
  • HY-133083

    c-Met/HGFR Cancer
    BAY-474 is a tyrosine-protein kinase c-Met inhibitor. BAY-474 acts as an epigenetics probe .
    BAY-474
  • HY-P99196

    c-Met/HGFR Cancer
    Ficlatuzumab is a monoclonal antibody (McAb) targeting human hepatocyte growth factor (HGF). Ficlatuzumab blocks the activation of the HGF/c-Met signaling pathway, and inhibits c-Met receptor-mediated cancer cell proliferation, migration, and invasion .
    Ficlatuzumab
  • HY-50878
    Crizotinib
    Maximum Cited Publications
    61 Publications Verification

    PF-02341066

    Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy Cancer
    Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .
    Crizotinib
  • HY-50878B

    PF-02341066 acetate

    Anaplastic lymphoma kinase (ALK) ROS Kinase c-Met/HGFR Cancer
    Crizotinib (PF-02341066) acetate is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib acetate inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib acetate is also a ROS1 inhibitor. Crizotinib acetate has effective tumor growth inhibition .
    Crizotinib acetate
  • HY-13068
    Golvatinib
    4 Publications Verification

    E-7050

    c-Met/HGFR VEGFR Cancer
    Golvatinib (E-7050) is a potent dual inhibitor of both c-Met and VEGFR2 kinases with IC50s of 14 and 16 nM, respectively.
    Golvatinib
  • HY-12035
    AMG-208
    1 Publications Verification

    c-Met/HGFR Cytochrome P450 Cancer
    AMG-208 is an orally active c-Met/RON dual selective inhibitor with an IC50 of 9 nM for c-Met. AMG-208 is a CYP3A4 inhibitor with an IC50 of 32 μM. AMG-208 has anti-cancer activity .
    AMG-208
  • HY-149675

    VEGFR c-Met/HGFR Cancer
    VEGFR-2/c-Met-IN-2 (compound 3e) is a VEGFR-2/c-Met inhibitor, with IC50 values of 83 and 48 nM, respectively. VEGFR-2/c-Met-IN-2 exhibits cytotoxic activity against HCT-116 cell line (IC50: 3.403 µM) .
    VEGFR-2/c-Met-IN-2
  • HY-76688

    (Rac)-ARQ 197; (Rac)-ARQ 198

    Others Cancer
    (Rac)-Tivantinib is the isomer of Tivantinib (HY-50686), and can be used as an experimental control. Tivantinib is a highly selective c-Met tyrosine kinase inhibitor with a Ki of 355 nM.
    (Rac)-Tivantinib
  • HY-50878S

    PF-02341066-d5

    Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy Cancer
    Crizotinib-d5 is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .
    Crizotinib-d5
  • HY-156098

    c-Met/HGFR Cancer
    c-Met-IN-19 (Compound 21j) is a c-Met inhibitor (IC50: 1.99 nM). c-Met-IN-19 shows cytotoxicity against A549, HT-29, SGC-7901, MDA-MB-231 cells with IC50s of 0.25, 0.36, 0.98, 0.76 μM .
    c-Met-IN-19
  • HY-11107
    PHA-665752
    10+ Cited Publications

    c-Met/HGFR Autophagy Apoptosis Cancer
    PHA-665752 is a selective, ATP-competitive, and active-site inhibitor of the catalytic activity of c-Met kinase (Ki=4 nM; IC50=9 nM). PHA-665752 exhibits >50-fold selectivity for c-Met compared with a panel of diverse tyrosine and serine-threonine kinases. PHA-665752 induces apoptosis and cell cycle arrest, and exhibits cytoreductive antitumor activity .
    PHA-665752

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