Niraparib (PARP inhibitor)

Overview

Niraparib is a highly potent and selective oral, once-daily small molecule poly (ADP-ribose) polymerase 1/2, or PARP 1/2, inhibitor for treatment across multiple solid tumor types. In 2016, Zai Lab obtained an exclusive license for the development and commercialization of niraparib in Chinese mainland, Hong Kong and Macau from TESARO, Inc. We believe that niraparib has the potential to be a best-in-class Category 1 drug in China. Currently we are conducting clinical trials to evaluate niraparib in several indications.

In 2017, ZEJULA® (niraparib) was approved by the FDA and EMA as a maintenance treatment for adult patients with recurrent platinum-sensitive ovarian cancer, regardless of biomarker status. In October 2018, niraparib was approved in Hong Kong (China) as a maintenance treatment for adult patients with recurrent platinum-sensitive ovarian cancer, regardless of biomarker status. In December 2019, the China NMPA approved the NDA for niraparib as a maintenance treatment for adult patients with recurrent platinum-sensitive ovarian cancer, regardless of biomarker status. In April 2020, niraparib was approved by the FDA as a first-line monotherapy maintenance treatment for women with advanced ovarian cancer, regardless of biomarker status. In September 2020, niraparib was approved by the China NMPA as a first-line maintenance treatment of adult patients with recurrent ovarian cancer, regardless of biomarker status. In December 2020, niraparib was included in the China National Reimbursement Drug List (NRDL) as maintenance therapy for adult patients with recurrent platinum-sensitive ovarian cancer. In December 2021, niraparib was included in the China NRDL as a first-line maintenance treatment for adult patients with advanced ovarian cancer.

Mechanism of Action

PARP is a family of proteins playing a key role in the DNA repair pathway. PARP inhibitors appear most effective when used to treat tumors with underlying defects in DNA repair, such as those with homologous recombination deficiencies (HRDs) including BRCA genes mutation. PARP inhibitors also have an additional mechanism of action known as “PARP trapping”, the effect of which is to stabilize PARP-1 and PARP-2 at sites of DNA damage leading to double-strand breaks of DNA during replication and death of tumor cells.