Poly(ADP-ribose) polymerase (PARP) enzymes play a huge role in repairing DNA damage and looking after genomic stability. Olaparib, the very first-in-class PARP inhibitor, has proven outstanding clinical benefits in treating BRCA-mutated ovarian or cancer of the breast. However, the undesirable hematological toxicity and pharmacokinetic qualities of olaparib limit its clinical application. Here, we report the very first preclinical portrayal of fluzoparib (code name: SHR-3162), a singular, potent, and orally available inhibitor of PARP. Fluzoparib potently inhibited PARP1 enzyme activity and caused DNA double-strand breaks, G2 /M arrest, and apoptosis in homologous recombination repair (HR)-deficient cells. Fluzoparib preferentially inhibited the proliferation of HR-deficient cells and sensitized both HR-deficient and HR-proficient cells to cytotoxic drugs. Particularly, fluzoparib demonstrated good pharmacokinetic qualities, favorable toxicity profile, and superior antitumor activity in HR-deficient xenografts models. In addition, fluzoparib in conjunction with apatinib or with apatinib plus paclitaxel elicited considerably improved antitumor responses without extra toxicity. According to these bits of information, studies to judge the effectiveness and safety of fluzoparib (phase II) and individuals two combinations (phase I) happen to be initiated. Taken together, our results implicate fluzoparib like a novel attractive PARP inhibitor.