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Olaparib Oral Product

Duke University · discontinued Small molecule

Olaparib inhibits poly-ADP-ribose polymerase (PARP) enzymes to impair DNA repair in cancer cells with BRCA mutations or homologous recombination deficiency.

Olaparib oral product is a PARP (poly-ADP-ribose polymerase) inhibitor developed by Duke University, currently in discontinued status. The drug works by inhibiting PARP enzymes, which are critical for DNA repair in cancer cells, particularly those with BRCA1/2 mutations or homologous recombination deficiency (HRD). While no FDA-approved indications are listed for the Duke formulation, olaparib has extensive clinical trial activity across 50 trials spanning Phase 1–4, with notable studies in BRCA-mutated breast and ovarian cancers, prostate cancer, and combination therapies with immunotherapies and targeted agents. The clinical pipeline demonstrates broad oncology application, though the discontinued status suggests Duke may have deprioritized development in favor of the commercially available AstraZeneca olaparib (Lynparza®). Competitive positioning is challenged by the established market presence of Lynparza and other PARP inhibitors (rucaparib, niraparib), which have secured multiple regulatory approvals and substantial market penetration in HRD-positive and BRCA-mutated malignancies.

At a glance

Generic nameOlaparib Oral Product
Also known asOlaparib tablet
SponsorDuke University
Drug classPARP inhibitor (DNA repair inhibitor)
TargetPARP-1 and PARP-2 (poly-ADP-ribose polymerase enzymes)
ModalitySmall molecule
Therapeutic areaOncology
Phasediscontinued

Mechanism of action

Olaparib works by blocking PARP enzymes, which are responsible for repairing single-strand DNA breaks in cells. In normal cells, this repair mechanism is redundant—cells can use homologous recombination (HR) as an alternative pathway. However, cancer cells with BRCA1/2 mutations or other HR deficiencies cannot use this backup pathway. When olaparib blocks PARP, these deficient cancer cells accumulate unrepaired DNA damage, leading to cell death. This creates a synthetic lethal interaction: the drug is selectively toxic to HR-deficient tumors while sparing most normal cells that retain functional HR. The oral formulation allows convenient at-home dosing compared to intravenous alternatives.

Approved indications

No approved indications tracked.

Pipeline indications

Common side effects

No common side effects on file.

Key clinical trials

Primary sources

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

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