TLDR Finasteride poorly inhibits type 1 5AR, affecting its effectiveness.
The paper discusses the time-dependent inhibition of human steroid 5a-reductase by finasteride, a specific 5AR inhibitor used to treat benign prostatic hyperplasia. The study found that the limited efficacy of finasteride in vivo is due to poor inhibition of type 1 5AR. The rate of inhibition is important for both potency and selectivity, and the document analyzes the in vivo factors affecting these rates. The study concludes that time-dependent inhibitors have potential for potent inhibition of target enzymes, but their potency may not be observed in vivo unless the rate of inhibition is faster than the rate of inhibitor elimination.
Cited in this study
4 / 4 results
70 citations
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June 1993 in “Biochemistry” Finasteride slowly binds to 5-alpha-reductase, affecting enzyme stability and inhibitor potency.
147 citations
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April 1990 in “The Journal of Clinical Endocrinology and Metabolism” Finasteride safely lowers DHT levels without affecting testosterone.
55 citations
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March 1990 in “The Journal of Clinical Endocrinology and Metabolism” Finasteride may treat baldness but less effective for those with 5α-reductase deficiency.
193 citations
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August 1985 in “Endocrinology” Different animals have unique versions of the enzyme that changes testosterone into another hormone, which is important for creating effective treatments for prostate and hair loss conditions.
29 citations
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January 1996 in “Journal of Pharmaceutical Sciences” Finasteride poorly inhibits type 1 5AR, affecting its effectiveness.
30 citations
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August 1992 in “The Journal of Clinical Endocrinology and Metabolism” Finasteride doesn't affect hormone levels in normal men.