Abstract
Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase with enzymatic and scaffolding functions, composed of a FERM domain, kinase domain, proline-rich regions, and a FAT domain. It interacts with over 50 proteins and plays a key role in cancer progression, metastasis, and recurrence. Although eight FAK inhibitors have entered clinical trials, they primarily block kinase activity and fail to disrupt scaffolding functions. PROTAC technology offers a novel strategy by degrading the entire FAK protein, eliminating both functions. Several FAK-targeting PROTACs have been developed with promising results. Given FAK's critical role in tumor malignancy, combination therapiessuch as dual-target degradation or inhibitor-degrader strategiesmay provide enhanced anticancer efficacy.