Recent advances in our understanding of the molecular biology of epithelial 
ovarian cancer have led to the development of a number of targeted therapies, 
including poly-ADP-ribose polymerase (PARP) inhibitors. PARP inhibitors are a 
novel class of therapeutic agents that target tumors with deficiencies in the 
homologous recombination DNA repair pathway. Early studies have shown 
significant efficacy for PARP inhibitors in patients with germline BRCA1/2 
mutations. It has become evident that BRCA wild-type patients with other defects 
in the homologous recombination repair pathway benefit from this therapeutic 
approach. Importantly, companion homologous recombination deficiency scores are 
being developed to help guide the selection of patients most likely to gain 
clinical benefit from PARP inhibition. Olaparib, the first and most extensively 
investigated PARP inhibitor, is now licensed in Europe for maintenance treatment 
of patients with platinum-sensitive relapsed BRCA-mutated (germline or somatic) 
high-grade serous ovarian cancer who have responded to platinum-based 
chemotherapy. In the United States, olaparib is licensed for treatment of 
patients with germline BRCA-mutated ovarian cancer who have received 3 or more 
lines of chemotherapy. There are a number of other PARP inhibitors in late phase 
clinical development in ovarian cancer including rucaparib, niraparib, 
veliparib, and talazoparib. This review will focus on the current evidence for 
PARP inhibitors in ovarian cancer and discuss ongoing clinical trials and future 
research directions in this rapidly evolving area.