Drug
Adagrasib
Drug Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | KRAS inhibitors |
| Group | KRAS Inhibitors |
| Mechanism of Action | KRAS G12C inhibitor |
| Half-life | 23 h (terminal); 17.5 h single-dose |
Study design
RT–Drug Timing Window
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.
Data on this page refer exclusively to patients treated with
Adagrasib combined with SBRT, without concurrent use of
drugs from other classes.
Combination therapy data and pooled group-level evidence are available on the
KRAS Inhibitors group page.