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Olaparib

Lynparza

PARP inhibitor

Evidence Score

45

theoretical
Mechanism of Action

Inhibits PARP1/2 enzymes involved in DNA single-strand break repair. In cells with elevated ROS (like SDH-deficient cells), increased DNA damage combined with PARP inhibition may create synthetic lethality by overwhelming DNA repair capacity.

Pathway Connections
Oxidative Stress / ROS

Complex II dysfunction causes electron leak in the electron transport chain, increasing reactive oxygen species (ROS). This drives DNA damage but also creates a therapeutic vulnerability.

Upstream event:

Impaired electron flow through Complex II → electron leak

Downstream effects:

Increased ROS productionOxidative DNA damageGenomic instabilityPARP activation for DNA repairTherapeutic vulnerability to further ROS stress
Molecular Targets

PARP1

Poly(ADP-ribose) polymerase 1

synthetic_lethal

DNA repair enzyme activated by ROS-induced damage. PARP inhibition in ROS-elevated cells may cause synthetic lethality.

UniProt: P09874

Quick Facts
FDA Approved

Approved Indications

  • BRCA-mutated ovarian cancer
  • BRCA-mutated breast cancer
  • BRCA-mutated pancreatic cancer
  • HRD-positive prostate cancer
ChEMBL IDCHEMBL521686
PubChem CID23725625
Evidence

Evidence from PubMed, OpenTargets, and ChEMBL will appear here once external data integration is enabled.

Coming in Phase 3

AI Analysis

Have Claude analyze this drug's repurposing potential for SDH-deficient diseases.