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c-Met Inhibitor

" in MedChemExpress (MCE) Product Catalog:

158

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50878
    Crizotinib
    Maximum Cited Publications
    86 Publications Verification

    PF-02341066

    Ligands for Target Protein for PROTAC Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase 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-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-15959
    Savolitinib
    5+ Cited Publications

    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-14721
    Tepotinib
    5+ Cited Publications

    EMD-1214063

    c-Met/HGFR Autophagy Cancer
    Tepotinib (EMD-1214063) is an orally active and highly selective, reversible, ATP-competitive c-Met inhibitor with an IC50 of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib inhibits c-Met phosphorylation and induces autophagy. Tepotinib has antitumor effects .
    Tepotinib
  • 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-50878A
    Crizotinib hydrochloride
    Maximum Cited Publications
    86 Publications Verification

    PF-02341066 hydrochloride

    Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy Cancer
    Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .
    Crizotinib 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-50683
    JNJ-38877605
    5+ Cited Publications

    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-15735
    c-Met inhibitor 1
    1 Publications Verification

    c-Met/HGFR Cancer
    c-Met inhibitor 1 is an orally active c-Met inhibitor. c-Met inhibitor 1 can inhibit c-Met phosphorylation with an IC50 of 0.010 μM. c-Met inhibitor 1 has antitumor activity and can be used for the research of tumors such as gastric cancer, pancreatic cancer and malignant glioma .
    c-Met inhibitor 1
  • 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-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-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-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
  • 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-116000
    Glumetinib
    2 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-15240
    c-Kit-IN-1
    1 Publications Verification

    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-100946
    CEP-40783
    2 Publications Verification

    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-13299
    MK-8033
    3 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-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-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-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-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-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-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-10991

    c-Met/HGFR VEGFR Apoptosis Cancer
    MGCD-265 analog is a potent and oral active inhibitor of c-Met and VEGFR2 tyrosine kinases, with IC50s of 29 nM and 10 nM, respectively. MGCD-265 analog has significant antitumor activity .
    MGCD-265 analog
  • HY-50703
    MK-2461
    1 Publications Verification

    c-Met/HGFR Cancer
    MK-2461 is an ATP-competitive, selective and orally active wild-type and mutant c-Met inhibitor (IC50s: 0.4-2.5 nM). MK-2461 also inhibits Ron (IC50 of 7 nM) and Flt1 (IC50 of 10 nM), MK-2461 shows selective for c-MET over other kinases (lC50s = 22-7800 nM). MK-2461 can be used for the study of cancer, such as gastric cancer .
    MK-2461
  • 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-14721R

    EMD-1214063 (Standard)

    Reference Standards c-Met/HGFR Autophagy Cancer
    Tepotinib (Standard) is the analytical standard of Tepotinib. This product is intended for research and analytical applications. Tepotinib (EMD-1214063) is an orally active and highly selective, reversible, ATP-competitive c-Met inhibitor with an IC50 of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib inhibits c-Met phosphorylation. Tepotinib has antitumor effects .
    Tepotinib (Standard)
  • HY-168135

    PROTACs c-Met/HGFR Cancer
    PROTAC c-Met degrader-1 is a selective and orally active c-Met PROTAC degrader with a DC50 of 6.21 nM against c-Met. PROTAC c-Met degrader-1 induces CRBN-dependent ubiquitination and proteasomal degradation of c-Met. PROTAC c-Met degrader-1 induces G0/G1 phase arrest in c-Met-dependent cancer cells. PROTAC c-Met degrader-1 kills c-Met-dependent cancer cells. PROTAC c-Met degrader-1 inhibits tumor growth in animal models. PROTAC c-Met degrader-1 can be used for the research of gastric cancer .
    PROTAC c-Met degrader-1
  • 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-14721A

    EMD-1214063 hydrochloride

    c-Met/HGFR Autophagy Cancer
    Tepotinib (EMD-1214063) hydrochloride is an orally active and highly selective, reversible, ATP-competitive c-Met inhibitor with an IC50 of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib hydrochloride inhibits c-Met phosphorylation and induces autophagy. Tepotinib hydrochloride has antitumor effects .
    Tepotinib hydrochloride
  • HY-18711

    Metatinib free base; c-Met Inhibitor 2 free base

    c-Met/HGFR VEGFR Cancer
    SCR-1481B1 free base, also known as Metatinib free base, is a small molecule receptor kinase inhibitor that targets both c-MET and vascular endothelial growth factor receptor 2 (VEGFR2) .
    SCR-1481B1 free base
  • HY-126320

    EGFR c-Met/HGFR Cancer
    EGFR-IN-8 is a dual EGFR and c-Met inhibitor, compound 48. EGFR-IN-8 can be a promising candidate for further development to target EGFR TKI-resistant NSCLC .
    EGFR-IN-8
  • 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-133083
    BAY-474
    1 Publications Verification

    c-Met/HGFR Cancer
    BAY-474 is a tyrosine-protein kinase c-Met inhibitor. BAY-474 acts as an epigenetics probe .
    BAY-474
  • HY-N6797

    Bacterial c-Met/HGFR Antibiotic Infection Cancer
    Meleagrin is a roquefortine C-derived alkaloid produced by fungi of the genus Penicillium and has antimicrobial and anti-proliferative activities. Meleagrin is a class of FabI inhibitor. Meleagrin is a lead c-Met inhibitory entity useful for the control of c-Met-dependent metastatic and invasive breast malignancies .
    Meleagrin
  • HY-18307

    c-Met/HGFR Cancer
    SYN1143 is a potent, selective and orally active dual inhibitor of c-Met/RON, with IC50s of 4 and 9 nM, respectively. SYN1143 has weak inhibitory activity on Lck, Tie2, Src, and BTK with IC50s ranging from 160 to 710 nM. SYN1143 can be used for the research of cancers that RON and c-Met are activated .
    SYN1143
  • 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-175320

    PROTACs c-Met/HGFR Apoptosis STAT Cancer
    PROTAC c-Met degrader-5 (Compound D19) is an orally active c-Met PROTAC degrader with DC50s of 0.42 and 0.32 nM in EBC-1 and Hs746T cells, respectively. PROTAC c-Met degrader-5 significantly induces cell apoptosis, G1 cell cycle arrest, and inhibits cell migration and invasion. PROTAC c-Met degrader-5 has potent antiproliferative and degradation efficacy against c-Met-addicted cancer cells and Tepotinib (HY-14721)-resistant cancer cells . Pink: c-Met ligand (HY-W425461); Blue: CRBN ligase ligand (HY-14658); Black: linker
    PROTAC c-Met degrader-5
  • HY-P991565

    c-Met/HGFR Cancer
    CE-355621 is a humanized anti-c-Met IgG1 monoclonal antibody. CE-355621 can effectively bind with human c-Met (KD = 200 pM, IC50 = 466 pM) in A549 cells and cyno c-Met (KD = 610 pM) in cynomolgus kidney cells. CE-355621 inhibits the c-Met signaling pathway by blocking HGF binding. CE-355621 significantly inhibits the growth of tumors dependent on the c-Met/HGF pathway. CE-355621 can be used for research on cancer such as glioblastoma and gastric cancer .
    CE-355621
  • 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-13404R

    INC280 (Standard); INCB28060 (Standard)

    Reference Standards c-Met/HGFR Apoptosis Cancer
    Capmatinib (Standard) is the analytical standard of Capmatinib. This product is intended for research and analytical applications. 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 (Standard)
  • HY-165284

    c-Met/HGFR Anaplastic lymphoma kinase (ALK) Cancer
    CM-118 is a potent and selective c-Met and ALK inhibitor. CM-118 inhibits the HGF-induced c-Met phosphorylation. CM-118 inhibits phosphorylation of ALK, EML4-ALKv1, ALK F1174L, and EMl4-ALKv1 L1196M, with respective IC50 values 0.92, 1.25, 1.9, and 3.5 μM. CM-118 exhibits anticancer activity against cancers dependent on the c-Met or ALK oncogenic pathways .
    CM-118
  • HY-P991589

    NOV-1105

    c-Met/HGFR Cancer
    SFN68 is a humanized IgG1 neutralizing monoclonal antibody targeting HGF. SFN68 significantly inhibits HGF/c-Met interaction, c-Met activation, and, cell scattering and proliferation mediated by HGF. SFN68 can be used for cancers research .
    SFN68
  • HY-107145
    Ningetinib Tosylate
    1 Publications Verification

    TAM Receptor VEGFR c-Met/HGFR Cancer
    Ningetinib Tosylate 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 Tosylate
  • HY-13299A
    MK-8033 hydrochloride
    3 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-50878AS

    PF-02341066-d9 hydrochloride

    c-Met/HGFR Autophagy Anaplastic lymphoma kinase (ALK) ROS Kinase Isotope-Labeled Compounds Cancer
    Crizotinib-d9 hydrochloride is deuterated labeled Crizotinib hydrochloride (HY-50878A). Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .
    Crizotinib-d9 hydrochloride
  • HY-151905

    c-Met/HGFR Cancer
    D6808 is a highly selective and potent c‑Met inhibitor with an IC50 value of 2.9 nM. D6808 induces cell apoptosis and cell cycle arrest. D6808 can be used for the research of NSCLC and gastric cancers .
    D6808
  • HY-174384

    c-Met/HGFR Apoptosis G-quadruplex Cancer
    MET Transcription-IN-1 (Compound C3) is an orally active MET transcription inhibitor. MET Transcription-IN-1 can efficiently bind and stabilize the G-quadruplex in the MET promoter region, thereby inhibiting c-Met expression. MET Transcription-IN-1 can also overcome drug resistance caused by specific c-Met mutations. MET Transcription-IN-1 is capable of inhibiting tumor cell proliferation, migration, and invasion, as well as inducing cell cycle arrest and apoptosis. MET Transcription-IN-1 has antitumor activity, and can be used in the research of tumors such as non-small cell lung cancer .
    MET Transcription-IN-1
  • 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

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