there is two 5 ar isoenzymes,dutasteride block both ,
finasteride just block type 2 (scalp tissue).
acne is type 1 .
5 alpha-Reductase Isoenzyme Inhibition
Both dutasteide and finasteride are 4-azasteroid inhibitors of 5 a -reductase , the enzyme responsible for converting testosterone to dihydrotestosterone (DHT) in the prostate. DHT is the primary androgen int the prostate and has a major role in the development and progression of benign prostatic hyperplasia (BPH) and other prostate diseases (1,2,3,4) as well as androgenetic alopecia (5,6).
Two isoenzymes of 5 a -reductase exist (type 1 and type 2). Type 2 is the dominant isoenzyme in genital tissues including the prostate, but is also present in the skin and liver. Type "1" 5 a -reductase is also found in the skin, liver and prostate, and is the dominant form in sebaceous glands. (1,2,4).
Finasteride is a competitive inhibitor of 5 a -reductase that selectively inhibits the type 2 isoenzyme, with which it forms a stable enzyme complex. this selective activity is attributed to a much lower affinity for the type 1 isoenzyme, and thus a slow rate of type 1 isoenzyme inhibition. In contrast, dutasteride is a competitive inhibitor of both forms of the enzyme, with 45-fold greater potency than finasteride against type 1 and type 2 isoenzymes at clinically used doses. this dual inhibition may potentially be beneficial in prostatic diseased that depend on androgens, since both isoenzymes are up-regulated in BPH while only the type 1 isoenzyme is up-regulated in prostate cancer, as noted above (2,1).
Pharmacogenetic analysis of human steroid 5 alpha reductase type II: comparison of finasteride and dutasteride.
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An update on the use of 5 alpha-reductase inhibitors.
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