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Results for "

KRAS wild-type proteins

" in MedChemExpress (MCE) Product Catalog:

8

Inhibitors & Agonists

2

Peptides

2

Click Chemistry

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-148439
    Daraxonrasib
    5+ Cited Publications

    RMC-6236; RAS-IN-2

    		 Ras PERK Cancer
    Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS (ON) inhibitor. Daraxonrasib disrupts the interaction of wild-type or mutant RAS proteins with the RAS binding domain of BRAF, with EC50 values ranging from 28-220 nM for wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. Daraxonrasib inhibits pERK. Daraxonrasib has anti-tumor activity against KRAS mutant tumors .
    Daraxonrasib
  • HY-134813
    MRTX1133
    45+ Cited Publications

    		 Ras Cancer
    MRTX1133 is a noncovalent, potent, and selective alkyne-based KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated KD against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations .
    MRTX1133
  • HY-156498
    RMC-7977
    10+ Cited Publications

    		 Ras ERK Raf Ribosomal S6 Kinase (RSK) AMPK Apoptosis PARP Cancer
    RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (Kd = 195 nM) and KRAS (G12V) (Kd = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRAS G12C cancer models, and demonstrates good tolerability across various RAS cancer models .
    RMC-7977
  • HY-176786
    MCB-36

    		PROTACs Ras Apoptosis PERK p38 MAPK Caspase TNF Receptor Cancer
    MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities Kd ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .
    MCB-36
  • HY-P2265A
    SAH-SOS1A TFA

    		SOS1 Ras Cancer
    SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM). SAH-SOS1A TFA directly and independently blocks nucleotide association. SAH-SOS1A TFA impairs KRAS-driven cancer cell viability and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
    SAH-SOS1A TFA
  • HY-P2265
    SAH-SOS1A

    		SOS1 Ras Cancer
    SAH-SOS1A is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM), directly and independently blocks nucleotide association, impairs KRAS-driven cancer cell viability, and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
    SAH-SOS1A
  • HY-163594
    KRAS-IN-59

    		Ras Cancer
    K-Ras-IN-58 is a K-RAS inhibitor and shows inhibitory activity against KRASG12D, KRASG12C and KRAS WT. K-Ras-IN-58 inhibits proliferation of cancer cells .
    KRAS-IN-59
  • HY-175870A
    (7R)-Eras-4001

    		Ras ERK Cancer
    (7R)-Eras-4001 is an orally active KRAS mutant inhibitor with remarkable selectivity for H-RAS and N-RAS. (7R)-Eras-4001 effectively suppresses cancer cell viability by blocking downstream signaling pathways mediated by RAF family proteins, inhibiting the formation of the KRAS G12D-RAF1 RBD complex and the phosphorylation of ERK1/2. (7R)-Eras-4001 induces tumor growth inhibition and regression in a dose-dependent manner, and also reduces plasma ERK1/2 phosphorylation levels. (7R)-Eras-4001 exerts a synergistic effect with anti-PD-1 Cetuximab (HY-P9905). (7R)-Eras-4001 can be used in research on non-small cell lung cancer, pancreatic cancer, colorectal cancer, and ovarian cancer .
    (7R)-Eras-4001

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