Development of Novel Drugs That Target Coactivation Sites of the Androgen Receptor for Treatment of Antiandrogen-Resistant Prostate Cancer

Abstract

Interest in developing androgen receptor (AR) inhibitors with novel mechanism of action is slowly increasing since commercial anti-androgens (Bicalutamide, Flutamide, Nilutamide and Enzalutamide) face therapeutic limitations. Current therapies fail over a period of time because they all target hormone binding pocket on AR to which the receptor has already developed effective resistance mechanisms. One of the promising strategies to combat drug resistance is to develop the inhibitors that target an alternative binding pocket of the AR, called Binding Function 3 (BF3). In the current study, we report indole chemical series, identified through systematic in silico screen, as leading AR BF3 inhibitors. The most potent inhibitor (compound VPC-13566) demonstrated excellent anti-androgen potency, anti-PSA activity and abrogates androgen-induced proliferation of LNCaP and Enzalutamide-resistant prostate cancer cell lines. Moreover, it demonstrated clear reduction of tumour growth in tumor xenograft models in mice. Based on these results new derivatives have been developed to improve stability and better efficacy in in-vivo models. These findings provide evidence that targeting AR BF3 pocket using small molecule inhibitors is a viable therapeutic approach for patients with advanced prostate cancer.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2014
Accession Number
ADA611450

Entities

People

  • Artem Cherkasov
  • Paul Rennie

Organizations

  • University of British Columbia

Tags

DTIC Thesaurus Topics

  • Androgen Receptors
  • Androgens
  • Cell Line
  • Cells
  • Chemistry
  • Drug Resistance
  • Hormones
  • Inhibitors
  • Molecules
  • Neoplasms
  • Prostate
  • Prostate Cancer
  • Resistance
  • Small Molecules
  • Targets
  • Therapy
  • Xenografts

Fields of Study

  • Biology
  • Chemistry
  • Medicine

Readers

  • Prostate Cancer Biology.