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Results for "

RAS-effector

" in MedChemExpress (MCE) Product Catalog:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-153346
    Elironrasib
    2 Publications Verification

    RMC-6291

    		 Ras ERK Apoptosis Cancer
    Elironrasib is an orally active and covalent inhibitor of KRAS G12C(ON). Elironrasib forms a tri-complex within tumor cells between KRAS G12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRAS G12C(ON) from signaling via steric blockade of RAS effector binding. Elironrasib inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. Elironrasib also inhibits the proliferation of KRAS G12C mutant cells with a median IC50 of 0.11 nM .
    Elironrasib
  • HY-122862
    RAS inhibitor Abd-7
    3 Publications Verification

    		 Ras Cancer
    RAS inhibitor Abd-7, a potent RAS-binding compound (Kd=51 nM), is a RAS-effector protein-protein interaction (PPI) inhibitor. RAS inhibitor Abd-7 interacts with RAS inside the cells, prevents RAS-effector interactions and inhibits endogenous RAS-dependent signaling. RAS inhibitor Abd-7 impairs the PPI of various mutant KRAS proteins with PI3K, CRAF and RALGDS as well as NRAS Q61H and HRAS G12V .
    RAS inhibitor Abd-7
  • HY-162321
    ZINC57632462

    		Ras Cancer
    ZINC57632462 (ACA-6) is a non-covalent allosteric KRAS inhibitor. ZINC57632462 disrupts nucleotide exchange and inhibits RAS-effector interaction. ZINC57632462 can be used for the research of cancer .
    ZINC57632462
  • HY-164645
    pan-KRAS-IN-16

    		Ras Cancer
    pan-KRAS-IN-16 (Compound 3344) is an anti-RAS small molecule derived from an intracellular antibody fragment with pan-RAS-effector protein-protein interaction inhibitor properties. pan-KRAS-IN-16 binds to a hydrophobic pocket near to the effector-binding switch regions of RAS. pan-KRAS-IN-16 prevents endogenous RAS-dependent signaling in tumor cell lines .
    pan-KRAS-IN-16
  • HY-186086
    RM-041

    		Ras Cancer
    RM-041 is a selective, orally active KRAS G13C (ON) inhibitor that forms a covalent complex with KRAS G13C (ON) and Cyclophilin A. RM-041 blocks the binding of RAS effector proteins via steric hindrance, and then covalently binds to Cys-13 to form an irreversible inhibitory complex, thereby inhibiting the proliferation of KRAS G13C mutant cancer cells. RM-041 induces regression of KRAS G13C tumors in cellular and xenograft tumor models. RM-041 exerts a synergistic effect when combined with upstream node inhibitors (such as SHP2 inhibitors). RM-041 can be used for the research of non-small cell lung cancer .
    RM-041

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