Group
AKT inhibitor
Group Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | PI3K/AKT/mTOR Pathway Inhibitors |
| Mechanism of Action | AKT inhibitor |
| Drugs in group | Capivasertib |
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.
The data above refer to patients treated with AKT inhibitor 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.