Molecular Formula | C23H18Cl3FN4O3S |
Molar Mass | 555.84 |
Appearance | Pale yellow solid |
Storage Condition | -20℃,有效期2年;溶入溶剂后-20℃请尽量在一个月内使用。 |
Use | A cell-permeable compound that inhibits kinase activity of ATM / ATR (RETRACTED). |
In vitro study | CGK 733 enables robust growth of senescent cells that have stopped proliferating. Senescence-associated β-galactosidase (SA-β-Gal) activity disappeared in CGK 733 treated cells. CGK 733 is more effective at inhibiting ATM/ATR(IC50 ~ 5 micron ATM and ATR) than LY294002 (inhibits ATM and ATR, with an IC50 of about 5 μm), is a pan-inhibitor of PI3K and PIKKs. Treatment of aged MCF-7 cells with CGK 733 (30 μm) for 24 hours resulted in approximately 60% cell death. CGK 733(20 μm) acts on MCF-7 and T47D breast cancer cell lines to induce loss of cyclin D1 via the ubiquitin-proteasome degradation pathway. CGK 733 inhibited MCF-7 and MDA-MB436 of T47D estrogen receptor (ER)-positive breast cancer cells, of ER-negative breast cancer cells, LnCap prostate cancer cells, and HCT116 colon cancer cell proliferation. In addition, CGK 733 also inhibited the proliferation of non-transformed mouse BALB/c 3T3 embryonic fibroblasts. The 733-mediated inhibition of proliferation by CGK was dose-dependent, with significant effects at doses as low as 2.5 μm. |
In vivo study | 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. |
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. |