Drug
Defactinib
Drug Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | Other Targeted Agents |
| Group | FAK/Pyk2 inhibitor |
| Mechanism of Action | FAK/Pyk2 inhibitor |
| Half-life | 9 h |
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.
Data on this page refer exclusively to patients treated with
Defactinib combined with SBRT, without concurrent use of
drugs from other classes.
Combination therapy data and pooled group-level evidence are available on the
FAK/Pyk2 inhibitor group page.