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Results for "

FAK-IN-1

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

1

Peptides

1

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-119932
    PROTAC FAK degrader 1
    4 Publications Verification

    		 PROTACs FAK Cancer
    PROTAC FAK degrader 1 is a selective and potent von Hippel-Lindau-based focal adhesion kinase (FAK) degrader with an IC50 of 6.5 nM, DC50 of 3 nM [1].
    PROTAC <em>FAK degrader 1</em>
  • HY-155163
    APG-2449

    		Anaplastic lymphoma kinase (ALK) ROS Kinase FAK Others
    APG-2449 is an orally active ALK/ROS1/FAK inhibitor. APG-2449 shows antitumor activity in mouse models of non-small cell lung cancer (NSCLC) [1].
    APG-2449
  • HY-N0896
    Inulicin
    1 Publications Verification

    1-O-Acetylbritannilactone

    		 NF-κB COX Inflammation/Immunology Cancer
    Inulicin (1-O-Acetylbritannilactone) is an active compound that inhibits VEGF-mediated activation of Src and FAK. Inulicin (1-O-Acetylbritannilactone) inhibits LPS-induced PGE2 production and COX-2 expression, and NF-κB activation and translocation.
    Inulicin
  • HY-145108
    FAK-IN-1

    		FAK Cancer
    FAK-IN-1 is a FAK inhibitor with anticancer activities (WO2020231726 (Example 27)) [1].
    <em>FAK-IN-1</em>
  • HY-P5929
    VnP-16

    		Integrin FAK Inflammation/Immunology
    VnP-16 can promote bone formation by accelerating osteoblast differentiation and activity through direct interaction with β1 integrin followed by FAK activation .
    VnP-16
  • HY-13404
    Capmatinib
    Maximum Cited Publications
    8 Publications Verification

    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 [1] .
    Capmatinib
  • HY-13404B
    Capmatinib hydrochloride

    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 [1] .
    Capmatinib hydrochloride
  • HY-13404C
    Capmatinib dihydrochloride hydrate
    Maximum Cited Publications
    8 Publications Verification

    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 [1] .
    Capmatinib dihydrochloride hydrate
  • HY-13404A
    Capmatinib dihydrochloride

    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 [1] .
    Capmatinib dihydrochloride

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