OnCo
pathwaysPathway

KEAP1–NRF2 antioxidant pathway

KEAP1–NRF2 is the cell's antioxidant defence switch. Lung cancers often break the off-switch (KEAP1), leaving NRF2 permanently on, which detoxifies chemotherapy and radiation and makes these tumours resistant to almost everything.

KEAP1 targets NRF2 (NFE2L2) for degradation; oxidative stress or KEAP1 mutation (~20% of lung adenocarcinoma, often with KRAS or STK11) stabilises NRF2, inducing glutathione synthesis, drug efflux, and NADPH production. KEAP1/STK11-mutant NSCLC responds poorly to chemotherapy and immunotherapy. Vulnerabilities: glutaminase dependence (telaglenastat, KEAPSAKE trial negative), NRF2-activated prodrugs (TRC102?), and CDK4/6 dependence; NRF2 also drives ferroptosis resistance.

In one picture

KEAP1–NRF2 is a smoke detector wired to a sprinkler system. Cancers jam the detector on, so the sprinklers run constantly and wash away every poison you throw at them.

Diagram

top
Oxidative stressKEAP1 (mutated)NRF2ARE genes: GSH, NQO1, eff…Chemo/RT/ferroptosis resi…STK11/LKB1 loss (co-mutat…activatesinhibitsdruggable target (click)hit by selected productescape route

How drugs attack it

4top
  • Glutaminase inhibition (negative in KEAPSAKE)
  • NRF2-activated prodrugs and NRF2 inhibitors (preclinical)
  • Biomarker: KEAP1/STK11 status predicts poor IO benefit in NSCLC
  • CDK4/6 and mTOR combinations under study

Notes

top
  • Leading programmes: Papagiannakopoulos (NYU) on KEAP1 in lung cancer; DeNicola (Moffitt); Skoulidis and Heymach (MD Anderson) on STK11/KEAP1 and IO.

Connected

12top