Sandbox 45673

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You may include any references to papers as in: the use of JSmol in Proteopedia ^[1] or to the article describing Jmol ^[2] to the rescue.

Function

Disease

Relevance

Structural highlights

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Mechanism

Finasteride is a 5-alpha reductase inhibitor. There are two isoforms of the 5alpha-reductase enzyme, type I and II, and while the drug has a higher affinity for the type II enzyme, it also inhibits the function of the type I. (.....) Typically 5 alpha-redcutase turns testosterone into Dihydrotestosterone(DHT), but the enzyme will accept Finasteride as an alternate substrate; turning it into dihydrofinasteride through an enzyme bound, NADP-dihydrofinasteride adduct. Finasteride is similar in structure to testosterone and 5alpha-reductase has almost the same affinity for both molecules. However, Finasteride , having a high affinity for 5 alpha-reductase, covalently binds to the enzyme as a Michael acceptor, through a functionally irreversible reaction. However, the NADP-dihydrofinasteride complex breaks down with a half life of about 1 month at 37˚C., which is why patients must continue taking the drug.(.....) http://pubs.acs.org/doi/pdf/10.1021/ja953069t

Medical

Finasteride is used to shrink an enlarged prostate, also known as benign prostatic hyperplasia (BPH), in adult men. This medication works by inhibiting 5a-reductase, which prevents conversion of testosterone to the natural body hormone, dihydrosestosterone (DHT) that causes growth of the prostate. Finasteride is specific for type II isoenzymes, resulting in a decline in serum DHT levels by 65-70% and in prostate DHT levels by up to 80-90% (source).