Drug
Capivasertib
Drug Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | PI3K/AKT/mTOR Pathway Inhibitors |
| Group | AKT inhibitor |
| Mechanism of Action | AKT inhibitor |
| Half-life | 8.3 h; popPK ~10 h (7–15 h) |
Study design
RT–Drug Timing Window
Study design
RT–Drug Timing Window
Radiobiological rationale for RT–drug interaction
Radiosensitizing (PI3K/AKT/PTEN blockade impairs NHEJ and HR; ↑apoptosis/senescence), strongest in PTEN-deficient tumors (Holler et al., PLoS One, 2016; Kao et al., Journal of Biological Chemistry, 2007; Toulany and Rodemann, Seminars in Cancer Biology, 2015). Because DNA-repair inhibition is not tumor-selective, a theoretical increase in acute in-field mucocutaneous/GI adverse events is plausible, potentially compounded by class hyperglycemia, diarrhea, and rash.
Data on this page refer exclusively to patients treated with
Capivasertib combined with SBRT, without concurrent use of
drugs from other classes.
Combination therapy data and pooled group-level evidence are available on the
AKT inhibitor group page.