About ZEJULA (niraparib)

ZEJULA Inhibits PARP1 and PARP2, Leading to Cancer Cell Death in Pre-Clinical Studies1

Cancer cell death diagram
Cancer cell death diagram

ZEJULA inhibits PARP1 and PARP2, leading to cancer cell death in preclinical studies.4

The clinical significance of in vitro studies is unknown. Mechanism of action statements are not meant to imply clinical efficacy.

PARP, poly (ADP-ribose) polymerase.

ZEJULA is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, PARP1 and PARP2, which play a role in DNA repair.1 In vitro studies suggest that cytotoxic effects of ZEJULA may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complexes resulting in DNA damage, apoptosis, and cell death.1

BRCA1/2, breast cancer susceptibility genes 1 and 2.

Preclinical studies suggest the activity of PARP inhibitors depends on tumor exposure and subsequent PARP1/2 inhibition.5

  • Tumor cells carrying a BRCA mutation have been shown to be significantly more sensitive to PARP inhibition than tumors that do not carry a BRCA mutation6
  • It is hypothesized that in tumors without a BRCA mutation, PARP inhibitors may need to achieve higher tumor concentrations for effect6

ZEJULA has high bioavailability and extensive tissue distribution, as well as a long half-life1

ZEJULA (niraparib) bioavailability
ZEJULA (niraparib) bioavailability

References: 1.  ZEJULA (niraparib). Prescribing Information. GlaxoSmithKline; 2021. 2. Satoh MS, Lindahl T. Role of poly(ADP-ribose) formation in DNA repair. Nature. 1992;356(6367):356-358. 3. Rein ID, Landsverk KS, Micci F, Patzke S, Stokke T. Replication-induced DNA damage after PARP inhibition causes G2 delay, and cell line-dependent apoptosis, necrosis and multinucleation. Cell Cycle. 2015;14(20):‍3248-3260. 4. Data on file, GlaxoSmithKline. 5. Ricks TK, Chiu HJ, Ison G, et al. Successes and challenges of PARP inhibitors in cancer therapy. Front Oncol. 2015;5:222. doi: 10.3389/fonc.2015.00222. 6. Farmer H, McCabe N, Lord CJ, et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature. 2005;434(7035):917-921.

Efficacy Data

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Study Design

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