RAD51 is a strand exchange protein that is critical for the central steps in homologous recombination (HR) of DNA during double strand break repair. Because HR usually occurs without mutations, it is critically important for maintaining genomic stability. RS-1 is a small molecule that enhances the HR activity of RAD51 by promoting the formation of active presynaptic filaments during repair.1 At low micromolar levels, it was able to increase cellular resistance of neonatal human dermal fibroblasts to the chemotherapeutic agent cisplatin. HR stimulation in various cell types could lead to temporary protection from DNA damaging agents. RS-1 has been used to exploit the RAD51 overexpression in cancerous cells by inducing lethality via genotoxic RAD51 protein complexes.2 RS-1 has also been found to a potent enhancer of CRISPR- and TALEN- based gene editing.3,4
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