Drexel researchers have developed small molecule therapeutics overcoming drug resistance mechanisms in certain types of ovarian and breast cancers. These compounds are specific inhibitors of human RAD51, a protein that plays a critical role in the repair of DNA double-strand breaks (DSB) and inter-strand cross links (ICL), the types of DNA damage caused by ionizing radiation or chemotherapies like cisplatin and doxorubicin. The ability to repair such DNA damage is a main form of cancer cells’ resistance to treatment, and is mediated by homologous recombination, a highly conserved mechanism of maintaining genome’s integrity. RAD51 plays a crucial role in homologous recombination and is vital for cell survival. RAD51 is overexpressed in a variety of cancer cells, which makes it a particularly attractive target for cancer therapeutics inhibiting RAD51. The combination of the newly discovered inhibitors of RAD51 with platinum chemotherapeutics or radiation therapy may significantly increase the potency of anti-cancer treatments in certain types of ovarian and breast cancer. In mouse xenograft model of breast cancer Drexel’s RAD51 inhibitor has significantly enhanced the therapeutic activity of cisplatin.