Abstract
The advent of poly(ADP-ribose) polymerase (PARP) inhibitors has resulted in a significant paradigm shift in ovarian cancer treatment. Niraparib, a potent PARP inhibitor, has demonstrated substantial efficacy in both first-line and recurrent disease settings. By targeting homologous recombination DNA repair, a pathway frequently disrupted in ovarian cancer, particularly in the context of BRCA mutations, niraparib induces synthetic lethality. Pivotal clinical trials, including PRIMA, ENGOT-OV16/NOVA, and QUADRA, have solidified niraparib's role in the treatment paradigm. While sharing a common mechanism of action with other PARP inhibitors, niraparib exhibits a distinct toxicity profile. Notably, hematologic toxicities, particularly thrombocytopenia, and hypertension have been observed at Grade 3-4 levels. A comprehensive understanding of niraparib's efficacy and safety is essential for optimal patient selection and management.