About ZEJULA (niraparib)
ZEJULA inhibits PARP1 and PARP2, leading to cancer cell death in pre-clinical studies1
The clinical significance of in vitro studies is unknown. Mechanism of action statements are not meant to imply clinical efficacy.
Single-Strand Break
PARP inhibition interferes with DNA repair, leading to accumulation of single-strand breaks (SSBs).1,2
Double-Strand Break
SSBs become double-strand breaks (DSBs), which are not repaired due to deficient DNA repair pathways present in many ovarian tumors.3
Cell Death
Persistent DSBs that cannot be repaired lead to programmed cell death.3
ZEJULA is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, PARP1 and PARP2, which play a role in DNA repair. In vitro studies suggest that ZEJULA’s cytotoxic effects may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complexes resulting in DNA damage, apoptosis, and cell death.1
Preclinical studies suggest the activity of PARP inhibitors depends on tumor exposure and subsequent PARP1/2 inhibition.4
- 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 mutation5
- It is hypothesized that in tumors without a BRCA mutation, PARP inhibitors may need to achieve higher tumor concentrations for effect5
The clinical significance of in vitro studies is unknown. Mechanism of action statements are not meant to imply clinical efficacy.
ZEJULA has high bioavailability and extensive tissue distribution, as well as a long half-life1
Highly Bioavailable1
Absolute bioavailability
Long Half-life1
Mean half-life, allowing for once-daily dosing
Extensive Tissue Distribution1
Concentrates in tissue
