B02 is a specific inhibitor of human RAD51 recombinase, blocks HR repair in human embryonic kidney (HEK) and breast cancer cells and increases their sensitivity to a wide range of DNA damaging agents. Also, B02 enhances DNA damage and apoptosis induced by decitabine in MM cells. B02 shows high specificity for RAD51 and does not significantly inhibit RAD54 in the range of concentrations from 0 to 200 μM. B02 shows biological effect in human and mouse cells. In human embryonic kidney (HEK) cells, B02 disrupts RAD51 foci formation in response to DNA damage and inhibited DSB repair and DSB-dependent HR. B02 can also increase the sensitivity of cancer cells to chemotherapeutic DNA damaging agents.
In vivo
B02 significantly increases the anti-tumor activity of cisplatin in vivo. B02 is tolerated by mice at doses up to 50 mg/kg without obvious body weight loss. No detectable morphological changes induced by B02 in kidneys and livers, main organs for detoxification are found.