产品
编 号：F754728
分子式：C28H28Cl2N6O
分子量：535.47
分子式：C28H28Cl2N6O
分子量：535.47
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CAS No: 2699877-43-3
产品详情
生物活性：
EGFR-IN-60 (Compound 7d) shows obvious inhibition of EGFRWT, EGFRT790M, EGFRL858R and JAK3 with IC50s of 83, 26, 53, and 69 nM, respectively. EGFR-IN-60 potently inhibits the growth of H1975 cells harboring EGFRT790M mutation (IC50=1.32 μM) over A431 cells overexpressing EGFRWT (IC50=4.96 μM). EGFR-IN-60 exhibits good oral absorption, potent and safe antitumor activity. EGFR-IN-60 induces cell death through apoptosis supported by increased Bax/Bcl-2 ratio.
体外研究：
EGFR-IN-60 (compound 7d) (3.25-88.46 μM, 48 hours) shows well antitumor activity against hepatocellular (HepG2), colorectal (HCT-116) and breast (MCF-7) cancer cells.EGFR-IN-60 (compound 7d) (0.49-86.4 μM, 48 hours) shows cytotoxic activity against cancer cells. EGFR-IN-60 (compound 7d) (0-5.27 μM, 24 hours) induces an increase in G2/M phase cells and induces apoptosis in HepG2, HCT-116, and MCF-7 cell lines.EGFR-IN-60 (compound 7d) (0 μM, 10 μM, 24 hours) can induce apoptosis through up-regulation of Bax and down-regulation of Bcl-2.
EGFR-IN-60 (Compound 7d) shows obvious inhibition of EGFRWT, EGFRT790M, EGFRL858R and JAK3 with IC50s of 83, 26, 53, and 69 nM, respectively. EGFR-IN-60 potently inhibits the growth of H1975 cells harboring EGFRT790M mutation (IC50=1.32 μM) over A431 cells overexpressing EGFRWT (IC50=4.96 μM). EGFR-IN-60 exhibits good oral absorption, potent and safe antitumor activity. EGFR-IN-60 induces cell death through apoptosis supported by increased Bax/Bcl-2 ratio.
体外研究：
EGFR-IN-60 (compound 7d) (3.25-88.46 μM, 48 hours) shows well antitumor activity against hepatocellular (HepG2), colorectal (HCT-116) and breast (MCF-7) cancer cells.EGFR-IN-60 (compound 7d) (0.49-86.4 μM, 48 hours) shows cytotoxic activity against cancer cells. EGFR-IN-60 (compound 7d) (0-5.27 μM, 24 hours) induces an increase in G2/M phase cells and induces apoptosis in HepG2, HCT-116, and MCF-7 cell lines.EGFR-IN-60 (compound 7d) (0 μM, 10 μM, 24 hours) can induce apoptosis through up-regulation of Bax and down-regulation of Bcl-2.
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