use | CGK733 is an effective ATM/ATR inhibitor that can be used in cancer research. |
storage conditions | -20 ℃, valid for 2 years; Please try to use it within one month after dissolving the solvent at -20 ℃. |
biological activity | CGK 733 is an effective ATM/ATR selective inhibitor with an IC50 of about 200 nM. |
in vitro study | CGK 733 can make aging cells that have stopped proliferation grow strongly. Aging-related β-galactosidase (SA-β-gal) activity disappeared in CGK 733-treated cells. CGK 733 is more effective in inhibiting ATM/ATR(IC50 ~ 5 micron ATM and ATR) than LY294002 (inhibition of ATM and ATR,IC50 is about 5 μM), and is a pan-inhibitor of PI3K and PIKKs. CGK 733 (30 μM) treated senescent MCF-7 cells for 24 hours, causing about 60% cell death. CGK 733(20 μM) acts on MCF-7 and T47D breast cancer cell lines to induce cyclin D1 loss through ubiquitin-proteasome degradation pathway. The concentration of CGK 733 in the range of 0.6-40 μM inhibits the proliferation of MCF-7 and T47D estrogen receptor (ER) positive breast cancer cells, MDA-MB436 ER negative breast cancer cells, LnCap prostate cancer cells, and HCT116 colon cancer cells. In addition, CGK 733 also inhibited the proliferation of non-transformed mouse BALB/c 3T3 embryonic fibroblasts. CGK 733-mediated proliferation inhibition is dose-dependent, with significant effect as low as 2.5 μM. |
target | ATM ATR |
in vivo research | | CGK733 (25 mg/kg, I. p.) increases the ATM reporter activity (reports inactivation of ATM kinase activity) compared to control mice, with 2.4-fold, 3.1-fold, and 1.3-fold changes at 1, 4, and 8 hours, respectively. |