EGFR/VEGFR2-IN-12

EGFR/VEGFR2-IN-12 (compound 11a) (10 μM; 48 h) exhibits potent broad-spectrum antiproliferative activity against the full NCI-60 human tumor cell line panel at 10 μM, with a mean GI% of 115% and exceptional activity across lung, colon, CNS, melanoma, ovarian, renal, prostate, and breast cancer cell lines^[1].
EGFR/VEGFR2-IN-12 (96 h) potently inhibits the growth of HepG-2, HCT-116, and MCF-7 cancer cells with IC₅₀ values of 8.26 μM, 2.73 μM, and 6.72 μM respectively, while showing low cytotoxicity against normal WI-38 and MCF-10A cells, resulting in high selectivity indices^[1].
EGFR/VEGFR2-IN-12 (30-40 min) acts as a potent dual inhibitor of wild-type EGFR TK (IC₅₀ = 64 nM) and VEGFR-2 (IC₅₀ = 74 nM), and also inhibits clinically relevant EGFR mutants including L858R (IC₅₀ = 90 nM), T790M (IC₅₀ = 241 nM), and C797S (IC₅₀ = 649 nM)^[1].
EGFR/VEGFR2-IN-12 suppresses EGFR and VEGFR-2 phosphorylation and induces PARP1 cleavage, indicating inhibition of oncogenic signaling and activation of apoptosis in MDA-MB-231 breast cancer cells^[1].
EGFR/VEGFR2-IN-12 (2.73 μM) can induce G0/G1 and S phase cell cycle arrest in HCT-116 colon cancer cells at its IC₅₀ concentration; it can also significantly induce early and late apoptosis in HCT-116 colon cancer cells^[1].
EGFR/VEGFR2-IN-12 promotes apoptosis in MDA-MB-231 breast cancer cells by upregulating pro-apoptotic BAX, caspase-3, caspase-7, and caspase-9, and downregulating anti-apoptotic BCL-2^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.