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Finasteride pharmacodynamics

Whether the pharmacodynamic advantages of dutasteride confer clinical advantages over finasteride is unknown. Dutasteride inhibits types I and II 5a-reductase, whereas finasteride inhibits only type II. Dutasteride more quickly and completely suppresses intraprostatic DHT (vs. 80% to 90% for finasteride) and decreases serum DHT by 90% (versus 70%). [Pg.947]

Steiner JF. Clinical pharmacokinetics and pharmacodynamics of finasteride. Clin Pharmacokinet 1996 30(l) 16-27. [Pg.156]

Because finasteride and dutasteride are metabolized primarily by CYP3A4, the CYP3A4 inhibitors, such as ritonavir, ketoconazole, verapamil, diltiazem, cimetidine, and ciprofloxacin, may increase the drugs blood levels and, possibly, cause drug-drug interactions. Clinical drug interaction studies have shown no pharmacokinetic or pharmacodynamic interactions between dutasteride and tamsulosin or terazosin, warfarin, digoxin, and cholestyramine. [Pg.2025]

Finasteride 5 mg daily for 10 days caused no change in the pharmacokinetics or pharmacodynamics of a single 80-mg dose of propranolol in healthy subjects. Further, the manufacturers say that finasteride was used with beta blockers in clinical studies without any evidence of an interaction. Similarly, dutasteride , (p.l2S7) does not appear to interact with beta blockers. [Pg.843]


See other pages where Finasteride pharmacodynamics is mentioned: [Pg.208]    [Pg.1540]    [Pg.54]    [Pg.87]   
See also in sourсe #XX -- [ Pg.150 , Pg.151 ]




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Finasteride

Pharmacodynamic

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