Abstract

Farnesyltransferase (FTase) inhibitors (FTIs) were developed originally as anti-RAS compounds and novel target-based drugs for cancer treatment. The analyses of FTIs continue in the clinic, but the antitumour activity cannot be ascribed simply to inhibition of RAS. Although FTI action is due to inhibition of FTase, and RAS proteins are indeed substrates for this enzyme, the RAS proteins that are most frequently mutated in human cancers escape FTI inhibition. RHOB has been suggested as a target, but is this issue resolved or do the crucial targets of FTIs remain to be identified?

Author affiliations

1. Saïd M. Sebti is at the Drug Discovery Program, H. Lee Moffitt Cancer Center & Research Institute, Department of Oncology, University of South Florida College of Medicine, Tampa, Florida 33612, USA.
2. Channing J. Der is at the Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
   Email: cjder@med.unc.edu