In vitro activity: 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.

Kinase Assay: RAD51 Inhibitor B02 (B02) is an inhibitor of human RAD51 with an IC50 of 27.4 μM.

Cell Assay: Cells are exposed for 1 h, then the cells are ished by PBS three times and refreshed by the media containing B02 (5 μM). After 7-10 days, cells are fixed and stained with staining solution (0.05% crystal violet, 50% methanol in PBS); finally cell colonies are counted.