Substrate-mimetic inhibitors of Akt as potential anti-cancer therapeutics

MEDI 281

Katherine J. Kayser, katherine.kayser@yale.edu1, Matthew P. Glenn, matthew.glenn@yale.edu1, Lin Yang2, Jin Q. Cheng2, and Andrew D. Hamilton, andrew.hamilton@yale.edu1. (1) Department of Chemistry, Yale University, 225 Prospect Street, New Haven, CT 06520, (2) Department of Pathology, University of South Florida College of Medicine, H. Lee Moffitt Cancer Center and Research Institute, SRB-3, 12902 Magnolia Drive, Tampa, FL 33612
Amplification, overexpression, and elevated activation of Akt have been detected in many human malignancies making it a critical target for cancer therapy. The substrate-binding site offers a large number of potential interactions to an appropriately designed small molecule providing an evolutionary handle for the development of selective inhibitors. Here, we report the progression of substrate-mimetic inhibitors towards the development of a potent, small molecule inhibitor of Akt. A simple series of peptidomimetic inhibitors was generated directly from the minimal GSK3 substrate sequence to provide peptidomimetic inhibitors that demonstrate low micromolar activity in vitro, induce apoptosis, and prevent growth in OV3 cancer cells. The first attempt at a completely non-peptidic substrate-mimetic was successful in providing potent, more rigid, lipophilic inhibitors that lack stereocenters and are significantly smaller in size than the GSK3 peptide. Modifications of these inhibitors will provide a useful set of molecular probes to assist in the validation of Akt as a potential target for anticancer drug design.