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CP-466722 ATM inhibitor,potent and reversible

Catalog No.A8625
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Sample solution is provided at 25 µL, 10mM.

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Chemical structure


Biological Activity

Description CP-466722 is a potent and reversible ATM inhibitor.
Targets ATM          
IC50 0.41 μM          

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Chemical Properties

Cas No. 1080622-86-1 SDF Download SDF
Chemical Name 2-(6,7-dimethoxyquinazolin-4-yl)-5-pyridin-2-yl-1,2,4-triazol-3-amine
Canonical SMILES COC1=C(C=C2C(=C1)C(=NC=N2)N3C(=NC(=N3)C4=CC=CC=N4)N)OC
Formula C17H15N7O2 M.Wt 349.35
Solubility ≥4.36mg/mL in DMSO with ultrasonic and warming Storage Store at -20°C
Physical Appearance A solid Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.


CP-466722 is a selective inhibitor of ATM kinase with IC50 value of 0.41 μM [1].

ATM (ataxia-telangiectasia, mutated) is a serine/threonine protein kinase and plays an important role in the cellular responses to DNA double-strand breaks (DSBs) [2] [3].

CP-466722 is a potent ATM inhibitor and is regareded as a promising drug to increase tumor cells sensitivity to IR. When tested with MCF7 cells, CP-466722 (10 μM) showed inhibition on the pATM and pKAP1 signals which induced by etoposide pre-treatment (25 μM) [1]. In GBM 12 cells, CP-466722 treatment significantly increased the cell sensitivity to TMZ and increased the cell apoptosis which had no effect on the TMZ-resistant GBM12 TMZ cells which indicated that CP-466722 (as an ATM inhibitor) may enhance the efficacy of TMZ in tumors that were inherently sensitive to TMZ [2]. When tested with Hela, MCF-7 and mouse cells pre-treated with IR which induced the increase in ATM-dependent phosphorylation events and then CP-466722 treatment resulted in the disruption of ATM-dependent phosphorylation events and inhibiton of ATM-dependent p53 inducetion at the minimal dose of 6 μM. Further, it was shown that CP-466722 treatment disrupted ATM-dependent cell cycle in increasing the percent in G2/M phase while decreasing the proportion in G1-phase without adverse effects [3].

[1].  Guo, K., et al., Development of a cell-based, high-throughput screening assay for ATM kinase inhibitors. J Biomol Screen, 2014. 19(4): p. 538-46.
[2].  Nadkarni, A., et al., ATM inhibitor KU-55933 increases the TMZ responsiveness of only inherently TMZ sensitive GBM cells. J Neurooncol, 2012. 110(3): p. 349-57.
[3].   Rainey, M.D., et al., Transient inhibition of ATM kinase is sufficient to enhance cellular sensitivity to ionizing radiation. Cancer Res, 2008. 68(18): p. 7466-74.