PARP inhibitors

Oral drugs that block a DNA-repair enzyme, PARP, and kill cancer cells that already lack homologous recombination repair, such as BRCA-mutated tumours.

Updated Nov 1, 2026

What they are

Olaparib, niraparib, rucaparib and talazoparib (suffix «-parib») are used in ovarian, breast, prostate and pancreatic cancers with BRCA1/2 mutations or other homologous recombination defects, often as maintenance after a response to platinum chemotherapy.

Mechanism of action

PARP1 and PARP2 detect single-strand DNA breaks and use NAD+ to build poly(ADP-ribose) chains that recruit repair proteins. PARP inhibitors compete with NAD+ at the catalytic site and also trap PARP on the DNA. Unrepaired breaks turn into double-strand breaks during replication. Normal cells fix them by homologous recombination, but cells with faulty BRCA1 or BRCA2 cannot, and they die: two defects together are lethal although each alone is not (synthetic lethality).

Target: Poly(ADP-ribose) polymerases PARP1 and PARP2

Drugs in this class

Test yourself

Think of the answer, then tap the question to see it.

What is synthetic lethality in the context of PARP inhibitors?

Cell death when two repair defects coincide: PARP blocked by the drug and homologous recombination lost through BRCA mutation.

Which cofactor do PARP inhibitors compete with?

NAD+, the donor of ADP-ribose units.

Which haematological malignancies are a class warning for PARP inhibitors?

Myelodysplastic syndrome and acute myeloid leukaemia.

Add to my cards (3)