Sandbox 45673
==Your Heading Here (maybe something like 'Structure')== 0
This is a default text for your page Sandbox 45673. Click above on edit this page to modify. Be careful with the < and > signs. 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. FunctionDiseaseRelevanceStructural highlightsThis is a sample scene created with SAT to color by Group, and another to make a transparent representation of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. MechanismFinasteride 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.(.....) MedicalFinasteride 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).
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