In Vitro: BML-277 is an ATP-competitive inhibitor of Chk2 that dose dependently protects human CD4+ and CD8+ T-cells from apoptosis due to ionizing radiation. BML-277 efficiently rescues both T-cell populations from radiation-induced apoptosis in a dose-dependent manner with an observed EC50 of 3?7.6 μM. The concentration of BML-277 required for radioprotection is consistent with the biochemical measurement of chk2 inhibition. Providing theKm of ATP for Chk2 is determined to be 99 μM and the Ki for BML-277 is 37 nM, and assuming that the intracellular ATP concentration is 10 mM, a 5 μM concentration of BML-277 would be expected to produce 42% inhibition of intracellular chk2.