Therapeutic potential and limitations of new FAK inhibitors in the treatment of cancer

Expert Opin Investig Drugs. 2010 Jun;19(6):777-88. doi: 10.1517/13543784.2010.489548.


Importance of the field: Activation of the non-receptor tyrosine kinase focal adhesion kinase (FAK) has been implicated in progression of multiple mesenchymal and epithelial malignant tumors. FAK plays an important role in regulation of proliferation, migration and apoptosis of neoplastic cells.

Areas covered in this review: We review the importance of FAK expression as a prognostic marker in cancer patients, discuss the available small-molecule inhibitors of FAK, summarize the available data from early-phase clinical trials with FAK inhibitors and cover the antiangiogenic properties of FAK inhibitors, as well as their potential to overcome chemoresistance.

What the reader will gain: This review enables the reader to overview current knowledge about FAK inhibition in cancer therapy and its role in the clinical setting. The reader will be able to consider FAK inhibitors not only as direct antitumor but also as antineoangiogenic agents and drugs that can overcome the problem of chemoresistance.

Take home message: Emerging data from early-phase clinical trials with orally available small-molecule inhibitors of FAK are promising. There are early indicators of clinical efficacy. In the future, combination therapy with cytotoxic or antiangiogenic drugs may help to overcome chemoresistance and enhance efficacy of antivascular therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inhibitors / pharmacology
  • Angiogenesis Inhibitors / therapeutic use
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Cell Proliferation / drug effects
  • Clinical Trials as Topic
  • Drug Resistance, Neoplasm
  • Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Humans
  • Neoplasms / blood supply
  • Neoplasms / drug therapy*
  • Neoplasms / physiopathology
  • Neovascularization, Pathologic / drug therapy


  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Focal Adhesion Protein-Tyrosine Kinases