Effects of some novel inhibitors of C17,20-lyase and 5alpha-reductase in vitro and in vivo and their potential role in the treatment of prostate cancer

Cancer Res. 1998 Sep 1;58(17):3826-32.

Abstract

The effects of some novel steroidal compounds were evaluated against both human C17,20-lyase and 5alpha-reductase in vitro and also against androgen synthesis in normal male rats. L-2, L-36, L-37, and I-41 showed potent inhibition of human testicular C17,20-lyase, with IC50s of 43, 39, 42, and 58 nM, respectively. In contrast, ketoconazole, a competitive inhibitor of C17,20-lyase, had an IC50 of 76 n.M. L-36 also showed potent inhibitory activity against 5a-reductase in human prostatic microsomes, with an IC50 of approximately 31 nM. The inhibitory activities of L-2 and 1-41 on 5alpha-reductase were moderate, with IC50s of 75 and 151 nM, respectively, whereas L-37 showed little inhibitory activity against this enzyme. In comparison, finasteride, a potent inhibitor of 5alpha-reductase, had an IC50 of 33 nM. When normal male rats were treated with these novel compounds (50 or 100 mg/kg/day) for 14 consecutive days, the wet weight of the prostate was significantly reduced by L-36, L-37, and I-41, compared to the control group. Testosterone levels in rat serum were also reduced by L-36 (55%), L-37 (86%), and I-41 (53%). The concentrations of testosterone in rat testes were reduced by these novel compounds by 13-74%. The compounds also reduced the concentration of testosterone in rat prostates by 35-75%. Similarly, dihydrotestosterone (DHT) concentration in rat serum was reduced 30-89% by these compounds, compared to the control group. Prostatic DHT levels were also lower in rats treated with L-36 (48%), L-37 (54%), or I-41 (26%). In contrast, L-2 enhanced serum testosterone and prostatic DHT concentrations by >50%. These findings suggest that the dual activities of several of these novel inhibitors of C17,20-lyase and 5alpha-reductase accounts for the diminished levels of circulating androgens in vivo.

Publication types

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

MeSH terms

  • Androgens / biosynthesis
  • Animals
  • Cholestenone 5 alpha-Reductase
  • Dihydrotestosterone / metabolism
  • Enzyme Inhibitors / therapeutic use*
  • Finasteride / pharmacology
  • Humans
  • Ketoconazole / pharmacology
  • Male
  • Organ Size / drug effects
  • Oxidoreductases / antagonists & inhibitors*
  • Prostate / drug effects
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Steroid 17-alpha-Hydroxylase / antagonists & inhibitors*
  • Testosterone / metabolism

Substances

  • Androgens
  • Enzyme Inhibitors
  • Dihydrotestosterone
  • Testosterone
  • Finasteride
  • Oxidoreductases
  • Steroid 17-alpha-Hydroxylase
  • Cholestenone 5 alpha-Reductase
  • Ketoconazole