EGFR/VEGFR2-IN-12 

EGFR/VEGFR2-IN-12 (compound 11a) is a dual EGFR/VEGFR2 inhibitor, with an IC₅₀ value of 64 nM against human EGFR and an IC₅₀ value of 74 nM against human VEGFR2. EGFR/VEGFR2-IN-12 inhibits the phosphorylation of EGFR and VEGFR2, induces cell cycle arrest at the G₁/S phase, activates apoptotic pathways, promotes PARP-1 cleavage, exhibits low micromolar antiproliferative activity, and shows much higher selectivity for cancer cells than normal cells. EGFR/VEGFR2-IN-12 is applicable for cancer-related research^[1].

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 (11a) (48 h) shows consistent antiproliferative activity across melanoma and lung cancer cell lines in the five-dose NCI-60 screening assay^[1].
EGFR/VEGFR2-IN-12 (11a) (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 (11a) (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 (11a) 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 (11a) (2.73 μM) induces G0/G1 and S phase cell cycle arrest in HCT-116 colon cancer cells when treated at its IC₅₀ concentration^[1].
EGFR/VEGFR2-IN-12 (11a) (2.73 μM) significantly induces both early and late apoptosis in HCT-116 colon cancer cells when treated at its IC₅₀ concentration, with 19.91% early apoptotic cells and 23.65% late apoptotic cells^[1].
EGFR/VEGFR2-IN-12 (11a) 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].
EGFR/VEGFR2-IN-12 (11a) forms stable, high-affinity interactions with the active sites of both EGFR TK (binding affinity = -15.35 kcal/mol) and VEGFR-2 (binding affinity = -14.21 kcal/mol) via key hydrogen, halogen, and hydrophobic interactions, supporting its dual inhibitory activity^[1].
EGFR/VEGFR2-IN-12 (11a) (100 ns) forms stable complexes with both EGFR TK and VEGFR-2 throughout 100 ns molecular dynamics simulations, maintaining stable protein backbone RMSD values consistent with well-bound, conformationally preserved kinase structures^[1].

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

EGFR/VEGFR2-IN-12 (compound 11a) (100-2000 mg/kg; p.o.; single dose) exhibits low acute oral toxicity in rats, with a calculated LD₅₀ of approximately 1300 mg/kg^[1].

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

552.04

C₃₁H₂₂ClN₃O₃S

O=C(NC1=CC=C(C(/C=C/C2=CC=CC=C2)=O)C=C1)CSC(N3C4=CC=CC=C4)=NC5=C(C=CC(Cl)=C5)C3=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Mansour MA, et al. Rational design of 2-substituted thio-7-chloroquinazolin-4(3H)-one derivatives as dual EGFR/VEGFR-2 inhibitors with broad-Spectrum anticancer and apoptotic activities. Bioorg Chem. 2026 May;172:109562.  [Content Brief]