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Results for "

Met kinase

" in MedChemExpress (MCE) Product Catalog:

93

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4

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Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-18309

    c-Met/HGFR VEGFR Cancer
    MET kinase-IN-4 is an orally active Met kinase inhibitor. MET kinase-IN-4 has potent Met kinase inhibitory activity with an IC50 value of 1.9 nM. MET kinase-IN-4 can be used for the research of cancer .
    MET kinase-IN-4
  • HY-131065

    c-Met/HGFR Cancer
    MET kinase-IN-2 is a potent, selective, orally bioavailable MET kinase inhibitor with an IC50 of 7.4 nM. MET kinase-IN-2 has antitumor activity .
    MET kinase-IN-2
  • HY-146884

    c-Met/HGFR VEGFR Cancer
    MET kinase-IN-3 (compound 8) is an orally active and potent MET inhibitor, with an IC50 of 9.8 nM. MET kinase-IN-3 shows good and broad-spectrum antiproliferative activity against cancer cell lines .
    MET kinase-IN-3
  • HY-E70754

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET Y1230A is a mutant of MET. MET Y1230A Recombinant Human Active Protein Kinase is a recombinant MET Y1230A protein that can be used to study MET Y1230A-related functions .
    MET Y1230A Recombinant Human Active Protein Kinase
  • HY-E70756

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET Y1230D is a mutant of MET. MET Y1230D Recombinant Human Active Protein Kinase is a recombinant MET Y1230D protein that can be used to study MET Y1230D-related functions .
    MET Y1230D Recombinant Human Active Protein Kinase
  • HY-E70758

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET Y1235D is a mutant of MET. MET Y1235D Recombinant Human Active Protein Kinase is a recombinant MET Y1235D protein that can be used to study MET Y1235D-related functions .
    MET Y1235D Recombinant Human Active Protein Kinase
  • HY-E70749

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET D1228N is a mutant of MET. MET D1228N Recombinant Human Active Protein Kinase is a recombinant MET D1228N protein that can be used to study MET D1228N-related functions .
    MET D1228N Recombinant Human Active Protein Kinase
  • HY-E70748

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET D1228H is a mutant of MET. MET D1228H Recombinant Human Active Protein Kinase is a recombinant MET D1228H protein that can be used to study MET D1228H-related functions .
    MET D1228H Recombinant Human Active Protein Kinase
  • HY-E70755

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET Y1230C is a mutant of MET. MET Y1230C Recombinant Human Active Protein Kinase is a recombinant MET Y1230C protein that can be used to study MET Y1230C-related functions .
    MET Y1230C Recombinant Human Active Protein Kinase
  • HY-E70752

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET L1195V is a mutant of MET. MET L1195V Recombinant Human Active Protein Kinase is a recombinant MET L1195V protein that can be used to study MET L1195V-related functions .
    MET L1195V Recombinant Human Active Protein Kinase
  • HY-E70757

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET Y1230H is a mutant of MET. MET Y1230H Recombinant Human Active Protein Kinase is a recombinant MET Y1230H protein that can be used to study MET Y1230H-related functions .
    MET Y1230H Recombinant Human Active Protein Kinase
  • HY-E70751

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET G1163R is a mutant of MET. MET G1163R Recombinant Human Active Protein Kinase is a recombinant MET G1163R protein that can be used to study MET G1163R-related functions .
    MET G1163R Recombinant Human Active Protein Kinase
  • HY-E70753

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET M1250T is a mutant of MET. MET M1250T Recombinant Human Active Protein Kinase is a recombinant MET M1250T protein that can be used to study MET M1250T-related functions .
    MET M1250T Recombinant Human Active Protein Kinase
  • HY-E70750

    c-Met/HGFR Cancer
    Mesenchymal-to-epithelial transition (MET) is a receptor tyrosine kinase for hepatocyte growth factor (HGF). MET overactivation is strongly associated with angiogenesis, cellular motility, growth, and invasion. Aberrant MET signaling can drive tumorigenesis in several cancer types through various molecular mechanisms, including MET amplification, MET exon 14 skipping mutation, MET overexpression, and MET fusions. MET F1200I is a mutant of MET. MET F1200I Recombinant Human Active Protein Kinase is a recombinant MET F1200I protein that can be used to study MET F1200I-related functions .
    MET F1200I Recombinant Human Active Protein Kinase
  • HY-114357A

    TAM Receptor c-Met/HGFR Trk Receptor Cancer
    DS-1205b free base is a potent and selective inhibitor of AXL kinase, with an IC50 of 1.3 nM. DS-1205b free base also inhibits MER, MET, and TRKA, with IC50s of 63, 104, and 407 nM, respectively. DS-1205b free base can inhibit cell migration in vitro and tumor growth in vivo .
    DS-1205b free base
  • HY-19642

    MGCD265

    TAM Receptor c-Met/HGFR Cancer
    Glesatinib (MGCD265) is an orally active, potent MET/SMO dual inhibitor. Glesatinib, a tyrosine kinase inhibitor, antagonizes P-glycoprotein (P-gp) mediated multidrug resistance (MDR) in non-small cell lung cancer (NSCLC) .
    Glesatinib
  • HY-19642A
    Glesatinib hydrochloride
    2 Publications Verification

    MGCD265 hydrochloride

    TAM Receptor c-Met/HGFR Cancer
    Glesatinib hydrochloride (MGCD265 hydrochloride) is an orally active, potent MET/SMO dual inhibitor. Glesatinib hydrochloride, a tyrosine kinase inhibitor, antagonizes P-glycoprotein (P-gp) mediated multidrug resistance (MDR) in non-small cell lung cancer (NSCLC) .
    Glesatinib hydrochloride
  • 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-174581

    mRNA Cancer
    Human MET mRNA encodes the human MET proto-oncogene, receptor tyrosine kinase (MET) protein, a member of the receptor tyrosine kinase family. MET regulates many physiological processes including proliferation, scattering, morphogenesis and survival.
    Human MET mRNA
  • 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-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-50686
    Tivantinib
    10+ 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-111050

    c-Met/HGFR Cancer
    JNJ-38877618 is a potent, highly selective, orally bioavailable Met kinase inhibitor with IC50s of 2 and 3 nM for wild type and mutant Met, respectively.
    JNJ-38877618
  • HY-18696
    AMG-337
    1 Publications Verification

    c-Met/HGFR Caspase Apoptosis Cancer
    AMG-337 is a potent, orally active, selective MET kinase inhibitor with IC50 values of 1, 1, 4.7, 5, 21.5, 1077 and >4000 nM of WT MET, H1094R MET, M1250T MET, HGF-stimulated pMET (PC3 cells) MET, V1092I MET, Y1230H MET, and D1228H MET, respectively. AMG 337 inhibits the phosphorylation of MET and downstream effectors in MET-amplified cancer cell lines, resulting in an inhibition of MET-dependent cell proliferation and induction of apoptosis .
    AMG-337
  • 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-12017
    PF-04217903
    3 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
    3 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-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-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-164394

    c-Met/HGFR Cancer
    EMD 1204831 is a potent and highly selective c-Met inhibitor which selectively suppresses the c-Met receptor tyrosine kinase activity with an IC50 of 9 nM. EMD 1204831 can be utilized in cancer research .
    EMD 1204831
  • 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-12019
    SGX-523
    5+ Cited Publications

    c-Met/HGFR Cancer
    SGX523 is a exquisitely selective and ATP-competitive MET inhibitor. SGX523 potently inhibits MET with an IC50 of 4 nM and is >1,000-fold selective versus other protein kinases. Antitumor activity .
    SGX-523
  • 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-10338
    Foretinib
    10+ Cited Publications

    XL880; GSK1363089; GSK089; EXEL-2880

    VEGFR c-Met/HGFR Cancer
    Foretinib is a multi-target tyrosine kinase inhibitor with IC50s of 0.4 nM and 0.9 nM for Met and KDR.
    Foretinib
  • 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-174387

    c-Met/HGFR Cancer
    KIN-8741 is a highly selective Type IIb c-Met inhibitor. KIN-8741 has broad activity against c-Met kinase mutations. KIN-8741 shows antitumor activity in MET gene amplified and exon 14 deleted non-small cell lung cancer models. KIN-8741 can be used in the research of c-Met driven cancers, especially advanced tumors carrying MET exon 14 jump mutations, acquired drug resistance mutations, etc .
    KIN-8741
  • HY-50683
    JNJ-38877605
    5 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-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-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
  • HY-76688

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

    c-Met/HGFR 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-146274

    c-Met/HGFR Apoptosis Cancer
    c-Met-IN-10 (compound 26a) is a highly potent c-Met kinase inhibitor with an IC50 value of 16 nM. c-Met-IN-10 has inhibitory activity against cancer cells A549, H460 and HT-29 with IC50s of 0.56 ~ 1.59 μM. c-Met-IN-10 suppresses the colony formation on HT-29 cells, induces HT-29 and A549 cells apoptosis, and inhibits A549 cells motility. c-Met-IN-10 can be used for researching anticancer .
    c-Met-IN-10
  • HY-12076
    BMS 777607
    10+ Cited Publications

    BMS 817378

    c-Met/HGFR TAM Receptor Cancer
    BMS 777607 (BMS 817378) is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50s of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM, respectively, and 40-fold more selective for Met-related targets than Lck, VEGFR-2, and TrkA/B, with more than 500-fold greater selectivity versus all other receptor and non receptor kinases .
    BMS 777607
  • HY-13404A
    Capmatinib dihydrochloride
    20+ Cited Publications

    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-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-13404
    Capmatinib
    20+ 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
    Capmatinib hydrochloride
    20+ Cited Publications

    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-125017
    Bozitinib
    1 Publications Verification

    PLB-1001; CBT-101; Vebreltinib

    c-Met/HGFR Cancer
    Bozitinib (PLB-1001) is a highly selective c-MET kinase inhibitor with blood-brain barrier permeability. Bozitinib (PLB-1001) is a ATP-competitive small-molecule inhibitor, binds to the conventional ATP-binding pocket of the tyrosine kinase superfamily .
    Bozitinib
  • HY-13299
    MK-8033
    2 Publications Verification

    c-Met/HGFR Cancer
    MK-8033 is an orally active ATP competitive c-Met/Ron dual inhibitor (IC50s: 1 nM (c-Met),7 nM (Ron)), with preferential binding to the activated kinase conformation. MK-8033 can be used in the research of cancers, such as breast and bladder cancers, non-small cell lung cancers (NSCLCs) .
    MK-8033
  • HY-13299A
    MK-8033 hydrochloride
    2 Publications Verification

    c-Met/HGFR Cancer
    MK-8033 hydrochloride is an orally active ATP competitive c-Met/Ron dual inhibitor (IC50s: 1 nM (c-Met),7 nM (Ron)), with preferential binding to the activated kinase conformation. MK-8033 hydrochloride can be used in the research of cancers, such as breast and bladder cancers, non-small cell lung cancers (NSCLCs) .
    MK-8033 hydrochloride
  • HY-107145A
    Ningetinib
    1 Publications Verification

    TAM Receptor VEGFR c-Met/HGFR Cancer
    Ningetinib is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC50s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively.
    Ningetinib

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