Abstract
An effective DNA damage response (DDR) is essential for cell survival. Elimusertib inhibits the ataxia-telangiectasia and RAD3-related (ATR) protein kinase, which is activated in response to DNA damage and mediates cell cycle arrest to maintain genomic integrity. Niraparib inhibits poly (ADP-ribose) polymerases 1/2 (PARP-1/2), which bind damaged regions of DNA and facilitate proper repair. Evidence suggests that combined inhibition of parallel DDR pathways act synergistically to improve anti-tumor responses, and the current study begins a clinical investigation of this hypothesis (NCT04267939).
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