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

H1373 cells

" in MedChemExpress (MCE) Product Catalog:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-130149
    Adagrasib
    55+ Cited Publications

    MRTX849

    Ras Cancer
    Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction .
    Adagrasib
  • HY-173259

    PARP Cancer
    PARP7-IN-23 (compound 56) is a potent PARP7 inhibitor with an EC50 of 0.915 nM for pSTAT1 in NCI-H1373 cells. PARP7-IN-23 has the potential for cancer research .
    PARP7-IN-23
  • HY-173262

    PARP Cancer
    PARP7-IN-24 (compound 44) is a potent PARP7 inhibitor with an EC50 of 0.375 nM for pSTAT1 in NCI-H1373 cells. PARP7-IN-24 has the potential for cancer research .
    PARP7-IN-24
  • HY-179312

    PARP Cancer
    PARP7-IN-25 is a PARP7 inhibitor with an IC50 of 1.582 nM.PARP7-IN-25 inhibits enzymatic activity of PARP7. PARP7-IN-25 inhibits proliferation of lung cancer cells.PARP7-IN-25 can be used for the research of PARP7-related cancer .
    PARP7-IN-25
  • HY-181815

    ULK Beclin1 Autophagy MHC Caspase Apoptosis Cancer
    SBP-5147 is an orally active ULK1/ULK2 inhibitor, with an IC50 of 2 nM against ULK1 and an IC50 of 53 nM against ULK2. SBP-5147 inhibits the phosphorylation of Beclin-1 and Vps34, reduces autophagy flux, downregulates the expression of ATG13 and ATG101, upregulates the expression of MHC-I, induces caspase-dependent apoptosis, and decreases the viability of non-small cell lung cancer cells. SBP-5147 is applicable to research related to non-small cell lung cancer [1] .
    SBP-5147
  • HY-181964

    Cancer
    KRAS G12C-IN-77 is an orally active and selective KRAS G12C covalent dual-state inhibitor that binds with high affinity to both GDP-bound (inactive state) and GTP-bound (active state) KRAS G12C (IC50 = 133 nM). KRAS G12C-IN-77 rapidly inhibits ERK1/2 phosphorylation, induces the formation of covalent adducts with endogenous KRAS G12C, suppresses the expression of MAPK pathway genes, and inhibits the proliferation of KRAS G12C-mutant cells. KRAS G12C-IN-77 is applicable to research related to KRAS G12C-mutant solid tumors, including pancreatic ductal adenocarcinoma and non-small cell lung cancer .
    KRAS G12C-IN-77

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