The brain-penetrant clinical ATM inhibitor AZD1390 radiosensitizes and improves survival of preclinical brain tumor models.

The article presents a study on the primary pharmacology of the clinical-grade ATM inhibitor AZD1390. It found that ATM-dependent DDR pathway activity is blocked by AZD1390 and induces G2 cell cycle phase accumulation, micronuclei, and apoptosis through combining with radiation. It radiosensitizes p53 mutant glioma cells with glioma and lung cancer cell lines.