Premium
Comparison of finasteride (proscar®), a 5α reductase inhibitor, and various commercial plant extracts in in vitro and in vivo 5α reductase inhibition
Author(s) -
Rhodes Linda,
Primka Raymond L.,
Berman Charles,
Vergult Gerard,
Gabriel Munir,
PierreMalice Marie,
Gibelin Bruno
Publication year - 1993
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.2990220107
Subject(s) - finasteride , in vivo , 5 alpha reductase inhibitor , in vitro , reductase , pharmacology , enzyme , medicine , biology , biochemistry , microbiology and biotechnology , prostate , cancer
Human prostate was used as a source of 5α reductase. Compounds were incubated with an enzyme preparation and [ 3 H]testosterone. [ 3 H]‐dihydrotestosterone production was measured to calculate 5ã reductase activity. IC 50 values (ng/ml) were finasteride = 1; Permixon = 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T) or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton, inhibited T stimulated prostate growth, while none of the three compounds inhibited DHT stimulated growth. These results demonstrate that finasteride inhibits 5α reductase, while Permixon and Bazoton have neither anti‐androgen nor 5α reductase inhibitory activity. In addition, in a 7 day human clinical trial, finasteride, but not Permixon or placebo, decreased serum DHT in men, further confirming the lack of 5α reductase inhibition by Permixon. Finasteride and the plant extracts listed above do not inhibit the binding of DHT to the rat prostatic androgen receptor (concentrations to 100 μg/ml). Based on these results, it is unlikely that these plant extracts would shrink the prostate by inhibiting androgen action or 5α reductase. © 1993 Wiley‐Liss, Inc.