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Pathways Recommended: Stem Cell/Wnt Cell Cycle/DNA Damage
Results for "

HMVEC cells

" in MedChemExpress (MCE) Product Catalog:

8

Inhibitors & Agonists

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-107818
    4-Hydroxychalcone
    2 Publications Verification

    ERK Akt Cardiovascular Disease Inflammation/Immunology Endocrinology
    4-Hydroxychalcone is an orally active flavonoid precursor. 4-Hydroxychalcone inhibits VEGF- and bFGF-induced phosphorylation of ERK1/2 and Akt. 4-Hydroxychalcone suppresses resistant hypertension by alleviating hyperaldosteronism, inflammation and renal injury in cryptochrome gene knockout mice. 4-Hydroxychalcone possesses anti-angiogenic activity .\n

    4-Hydroxychalcone
  • HY-16697
    CID 16020046
    2 Publications Verification

    GPR55 Cancer
    CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC50 of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca 2+ signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function .
    CID 16020046
  • HY-108556A

    Protease Activated Receptor (PAR) Apoptosis Cardiovascular Disease
    RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 (HY-108566). RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis .
    RWJ-56110 dihydrochloride
  • HY-108556

    Protease Activated Receptor (PAR) Apoptosis Cardiovascular Disease
    RWJ-56110 is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 (HY-108566). RWJ-56110 inhibits angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 induces cell apoptosis .
    RWJ-56110
  • HY-162621

    Epigenetic Reader Domain Inflammation/Immunology
    BET-IN-25 (compound 7) is an oral bioactive inhibitor of bromodomain (BD1) and BD2, with the IC50s of 0.18 μM and 9.2 μM, respectively .
    BET-IN-25
  • HY-16697R

    GPR55 Cancer
    CID 16020046 (Standard) is the analytical standard of CID 16020046. This product is intended for research and analytical applications. CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC50 of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca2+ signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function .
    CID 16020046 (Standard)
  • HY-108556AR

    Reference Standards Protease Activated Receptor (PAR) Apoptosis Cardiovascular Disease
    RWJ-56110 dihydrochloride (Standard) is the analytical standard of RWJ-56110 (dihydrochloride) (HY-108556A). This product is intended for research and analytical applications. RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 (HY-108566). RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis .
    RWJ-56110 dihydrochloride (Standard)
  • HY-185379

    STING Inflammation/Immunology
    STING antagonist-3 is a potent STING antagonist with an IC50 of 2.3 nM against human wild-type STING. STING antagonist-3 inhibits human wild-type STING and the gain-of-function STING mutants N154S and V155M. STING antagonist-3 suppresses IFN‑α2a production in stimulated human whole blood. STING antagonist-3 inhibits IP-10 production in activated human dermal microvascular endothelial cells (HMVEC-d). STING antagonist-3 can be used for the research of autoimmune diseases, autoinflammatory diseases, interferonopathies, and fibrotic disorders .
    STING antagonist-3

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