Last reviewed · How we verify

Olaparib 200-300 mg BID, daily

Repare Therapeutics · discontinued Small molecule

Olaparib inhibits PARP enzymes to block DNA single-strand break repair, inducing synthetic lethality in BRCA-mutant and HR-deficient cancers.

Olaparib (200–300 mg BID) is a PARP inhibitor originally developed by AstraZeneca and studied by Repare Therapeutics, now discontinued from Repare's pipeline. The drug inhibits poly(ADP-ribose) polymerase (PARP), a DNA repair enzyme, causing synthetic lethality in BRCA-mutant and homologous recombination-deficient tumors. While olaparib achieved FDA approval under AstraZeneca's Lynparza brand for multiple oncology indications (ovarian, breast, pancreatic, and prostate cancers), Repare's development program has been terminated, indicating the company deprioritized this asset. Clinical trials show olaparib's efficacy in combination regimens (with vorinostat, sapacitabine, radiotherapy, and immunotherapy) across breast, ovarian, and lung cancers, though Repare's Phase 1 combination study with RP-3467 was terminated. The commercial significance lies in olaparib's established market presence under Lynparza (AstraZeneca), which generated substantial revenue; however, Repare's discontinuation suggests limited differentiation or strategic pivot toward proprietary assets.

At a glance

Generic nameOlaparib 200-300 mg BID, daily
Also known asRP-3467 at assigned dose and schedule, Lynparza
SponsorRepare Therapeutics
Drug classPARP inhibitor (DNA damage response inhibitor)
TargetPARP1 and PARP2 (poly(ADP-ribose) polymerase enzymes)
ModalitySmall molecule
Therapeutic areaOncology
Phasediscontinued

Mechanism of action

Olaparib works by blocking poly(ADP-ribose) polymerase (PARP), an enzyme that repairs single-strand DNA breaks. In normal cells, when a single-strand break occurs, PARP detects and repairs it. However, in cancer cells with BRCA1/BRCA2 mutations or other homologous recombination (HR) deficiencies, the cell cannot repair double-strand breaks through the normal HR pathway. When olaparib blocks PARP, single-strand breaks accumulate and convert into lethal double-strand breaks during DNA replication. Because these cancer cells cannot repair double-strand breaks (due to HR deficiency), they die—a phenomenon called synthetic lethality. This mechanism is particularly effective in BRCA-mutant ovarian, breast, and pancreatic cancers, where HR repair is already compromised. Olaparib can also be combined with chemotherapy, radiotherapy, or immunotherapy to enhance DNA damage and overcome resistance mechanisms.

Approved indications

No approved indications tracked.

Pipeline indications

Common side effects

No common side effects on file.

Key clinical trials

Primary sources

Every claim on this page is sourced from regulatory or scientific primary sources. See our editorial policy for full methodology.

SourceUsed for
ClinicalTrials.govTrial enrolment, design, endpoints, results

Competitive intelligence

For the full competitive landscape — auto-detected comparators, recent regulatory actions across the set, upcoming PDUFA, patent timeline, sponsor landscape: