Drug
Dabrafenib
Drug Profile
| Therapeutic Class | Targeted Therapy |
| Drug Class | BRAF/MEK Pathway Inhibitors |
| Group | BRAF inhibitor |
| Mechanism of Action | BRAF inhibitor |
| Half-life | 10 h |
Study design
RT–Drug Timing Window
Study design
RT–Drug Timing Window
Radiobiological rationale for RT–drug interaction
Potent radiosensitizer in BRAF V600-mutant tumors (G1 arrest, ↓RAD51/BRCA1, ↑apoptosis); MAPK blockade also increases keratinocyte proliferation/radiosensitivity in normal skin, so the effect is not confined to tumor. This provides a strong rationale for increased in-field cutaneous adverse events (radiation dermatitis, radiation-recall reactions) and potential visceral/CNS normal-tissue injury; vemurafenib is mechanistically a stronger radiosensitizer than dabrafenib (Anker et al., Practical Radiation Oncology/ECOG consensus review, 2016).
Data on this page refer exclusively to patients treated with
Dabrafenib combined with SBRT, without concurrent use of
drugs from other classes.
Combination therapy data and pooled group-level evidence are available on the
BRAF inhibitor group page.