Group
KRAS Inhibitors
Study design
RT–Drug Timing Window
Radiobiological rationale for RT–drug interaction
Radiosensitizing selectively in KRAS-mutant (esp. homozygous G12C) tumors by reversing NRF2–53BP1/NHEJ and replication-stress advantages; genotype-dependent and often additive with photons (Laurent et al., Journal of Translational Medicine, 2023; Quevrin et al., Journal for ImmunoTherapy of Cancer, 2026). Because the effect is driver-restricted, an increase in normal-tissue adverse events is theoretically limited.
The data above refer to patients treated with KRAS Inhibitors as the sole drug class,
excluding any concurrent use of drugs from other groups.
Individual Drugs
Select a drug to view its individual evidence base (drug + SBRT, no other concurrent systemic drugs). Drugs without available data are shown greyed out.