Group
FAK/Pyk2 inhibitor
Group Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | Other Targeted Agents |
| Mechanism of Action | FAK/Pyk2 inhibitor |
| Drugs in group | Defactinib |
Study design
RT–Drug Timing Window
Study design
RT–Drug Timing Window
Radiobiological rationale for RT–drug interaction
Radiosensitizing (↓DDR, G2-M arrest, persistent DSBs, disrupts stromal/endothelial NF-κB survival), strongest in mutant-KRAS tumors (Skinner et al., Clinical Cancer Research, 2016; Tang et al., Clinical Cancer Research, 2016). Because FAK-dependent survival is not tumor-exclusive (stroma/endothelium), a theoretical increase in normal-tissue/vascular adverse events is possible.
The data above refer to patients treated with FAK/Pyk2 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.