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RAS mutation

" in MedChemExpress (MCE) Product Catalog:
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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-18707

    Ras Apoptosis Cancer
    K-Ras(G12C) inhibitor 12 is an irreversible inhibitor of K-Ras(G12C). K-Ras(G12C) inhibitor 12 can alter the nucleotide-binding preference of K-Ras and block its interaction with effector proteins. K-Ras(G12C) inhibitor 12 can reduce cell viability and induce apoptosis in lung cancer cell lines with G12C mutations. K-Ras(G12C) inhibitor 12 has anti-tumor activity .
    K-Ras(G12C) inhibitor 12
  • HY-136579
    ASN007
    4 Publications Verification

    ERK-IN-3

    ERK Cancer
    ASN007 (ERK-IN-3) is a potent and orally active inhibitor of ERK. ASN007 inhibits ERK1/2 with low single-digit nM IC50 values. ASN007 can be used for the research of cancers driven by RAS mutations .
    ASN007
  • HY-136579A
    ASN007 benzenesulfonate
    4 Publications Verification

    ERK-IN-3 benzenesulfonate

    ERK Cancer
    ASN007 (ERK-IN-3) benzenesulfonate is a potent and orally active inhibitor of ERK. ASN007 benzenesulfonate inhibits ERK1/2 with low single-digit nM IC50 values. ASN007 benzenesulfonate can be used for the research of cancers driven by RAS mutations .
    ASN007 benzenesulfonate
  • HY-50846
    SCH772984
    Maximum Cited Publications
    142 Publications Verification

    ERK Cancer
    SCH772984 is a highly selective and ATP-competitive ERK inhibitor, with IC50s of 4 and 1 nM for ERK1 and ERK2, respectively. SCH772984 has antitumor activity in MAPK inhibitor-na?ve and MAPK inhibitor-resistant cells containing BRAF or RAS mutations .
    SCH772984
  • HY-132844

    HL-085

    MEK Cancer
    Tunlametinib is a highly selective, orally active MEK1/2 inhibitor (IC50=1.9 nM, MEK1). Tunlametinib blocks the RAS-RAF-MEK-ERK signaling pathway, arrests tumor cell cycle and promotes apoptosis. Tunlametinib potently inhibits the proliferation of RAS/RAF mutant cancer cells (such as BRAF V600E, KRAS G12C mutant cells). Tunlametinib shows synergistic anti-tumor effects with BRAF/KRAS G12C/SHP2 inhibitors, Docetaxel (HY-B0011). Tunlametinib can be used to study targeted therapy for RAS/RAF mutation-driven malignancies (such as melanoma, colorectal cancer, and non-small cell lung cancer) .
    Tunlametinib
  • HY-162460

    ERK Cancer
    ERK1/2 inhibitor 10 (Compound 36c) is a potent ERK1 and ERK2 inhibitor (IC50: 0.11 and 0.08 nM respectively). ERK1/2 inhibitor 10 inhibits ERK1/2 and blocks the phosphorylation expression of their downstream substrates p90RSK and c-Myc. ERK1/2 inhibitor 10 induces cell apoptosis and incomplete autophagy-related cell death. ERK1/2 inhibitor 10 shows potent antitumor efficacy against triple-negative breast cancer and colorectal cancer models harboring BRAF and RAS mutations .
    ERK1/2 inhibitor 10
  • HY-202699

    Ras Apoptosis Cancer
    SHOC2–RAS PPI-IN-1 (compound 6) is a non-covalent competitive inhibitor targeting the interaction between SHOC2 and RAS proteins. SHOC2–RAS PPI-IN-1 has an IC50 of 0.048 μM and a KD of 0.065 μM for NRAS Q61R. SHOC2–RAS PPI-IN-1 can inhibit the activity of the SMP phosphatase complex, leading to increased CRAF S259 phosphorylation levels, thereby blocking the MAPK signaling pathway (such as reducing the levels of pMEK and pERK), inducing tumor cell cycle arrest and apoptosis. SHOC2–RAS PPI-IN-1 can be used for targeted research on malignant tumors such as melanoma and colorectal cancer with NRAS Q61R mutations .
    SHOC2–RAS PPI-IN-1
  • HY-173405

    Ras PI3K Cancer
    VVD-699 is a covalent RAS-PI3K inhibitor. VVD-699 covalently binds to cysteine 242 in the RAS binding domain of PI3K p110α, thereby blocking the ability of RAS to activate PI3K activity. VVD-699 is able to inhibit the growth of RAS-mutated and HER2-overexpressing tumors. VVD-699 can be used to study cancers associated with RAS mutations (e.g., H358 lung cancer cells, A549 cells, FaDu cells) .
    VVD-699
  • HY-173629

    Ras Apoptosis Cancer
    RMC-5127 is an orally active and brain-penetrant mutant-selective tri-complex RAS G12V inhibitor. RMC-5127 non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages RASG12V(ON) to form a high-affinity tri-complex, sterically inhibiting RAS binding . RMC-5127 inhibits the RAS pathway in KRAS G12V mutant cancer cells, reducing cell proliferation and inducing apoptosis. RMC-5127 is promising for research of cancers with RAS mutations, such as non-small cell lung cancer .
    RMC-5127
  • HY-168012

    Ras Phosphatase Cancer
    Pan-RAS-IN-6 (compound 24) is an inhibitor targeting DUSP6, which reduces MAPK activation in the brain of the NCI-H1373-Luc model (DUSP6), at the same time, it shows significant tumor growth inhibition and tumor regression effects in the NSCLC brain metastasis mouse model. Pan-RAS-IN-6 shows high selectivity and strong inhibitory effects, especially in KRAS mutation-related signaling pathways, demonstrating varying inhibitory activity against different KRAS mutants and interacting proteins. The IC50 values for KRAS G12C, G12D, and G12V are 1.3 nM, 4.7 nM, and 0.3 nM, respectively .
    Pan-RAS-IN-6
  • HY-172581

    FLT3 Apoptosis Ras p38 MAPK PI3K Akt JAK STAT Cancer
    Clifutinib (Compound 9e) is an orally active and selective internal tandem duplication mutation of FMS-like tyrosine kinase 3 (FLT3-ITD) inhibitor with an IC50 value of 15.1 nM. Clifutinib inhibits the activity of FLT3-ITD kinase and blocks the downstream RAS/MAPK, PI3K/AKT, and JAK/STAT5 signaling pathways of FLT3. Clifutinib induces apoptosis of acute myeloid leukemia (AML) cells with FLT3-ITD mutations. Clifutinib is promising for research of relapsed/refractory FLT3-ITD-positive acute myeloid leukemia .
    Clifutinib
  • HY-16662

    DNA/RNA Synthesis Ras Apoptosis Cancer
    Oncrasin-1 is an RNA polymerase inhibitor. Oncrasin-1 suppresses the phosphorylation of the largest subunit of RNA polymerase II and the expression of intronless reporter genes in sensitive cells. Oncrasin-1 effectively kills various human lung cancer cells with K-Ras mutations. Oncrasin-1 leads to coaggregation of PKCι and splicing factors into megaspliceosomes. Oncrasin-1 induces malfunction in the RNA processing machinery. Oncrasin-1 is an anti-cancer agent and can therefore be studied in research for lung cancer .
    Oncrasin-1

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