|Creation Date||2006-05-22 14:17:30 UTC|
|Update Date||2013-05-29 19:33:10 UTC|
|Secondary Accession Numbers|
|Description||Finasteride is only found in individuals that have used or taken this drug. Finasteride is an androgen antagonist. It is an orally active testosterone 5-alpha-reductase inhibitor. Finasteride is one of the currently available pharmacologic treatment modalities with proven efficacy for treatment of androgenetic alopecia. The mechanism of action has not been fully determined, but finasteride has shown to decrease scalp DHT concentration to the levels found in hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss. Androgenetic alopecia (AGA), or male pattern hair loss, affects approximately 50% of the male population. AGA is an androgen-related condition in genetically predisposed individuals. There is no treatment to completely reverse AGA in advanced stages, but with medical treatment (e.g., finasteride), the progression can be arrested and partly reversed in the majority of patients who have mild to moderate AGA. Finasteride is also used as a surgical alternative for treatment of benign prostatic hyperplasia. [PubChem]The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5a-reductase through the formation of a stable complex with the enzyme. Inhibition of Type II 5a-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations, minimal to moderate increase in serum testosterone concentrations, and substantial increases in prostatic testosterone concetrations. As DHT appears to be the principal androgen responsible for stimulation of prostatic growth, a decrease in DHT concentrations will result in a decrease in prostatic volume (approximately 20-30% after 6-24 months of continued therapy). Finasteride may increase the sensitivity of prostate specific antigen to detect prostate cancer. At present, finasteride remains the only intervention shown in long-term prospective phase III clinical trials to reduce the incidence of prostate cancer. (PMID: 18044109 , 17543725 , 17414641 , 17415094 , 17394699 ).|
|Average Molecular Weight||372.5441|
|Monoisotopic Molecular Weight||372.277678406|
|Traditional IUPAC Name||finasteride|
|CAS Registry Number||98319-26-7|
- Aliphatic Heteropolycyclic Compounds
- Carboxamide Group
- Secondary Carboxylic Acid Amide
|Status||Expected and Not Quantified|
- Anti-baldness Agents
- Antihyperplasia Agents
- Cell signalling
- Enzyme Inhibitors
- Fuel and energy storage
- Fuel or energy source
- Hormones, Membrane component
- Membrane integrity/stability
- Skin and Mucous Membrane Agents
- Surfactants and Emulsifiers
|Melting Point||252 - 254 °C||Not Available|
|Boiling Point||Not Available||Not Available|
|Water Solubility||1.98e-03 g/L||Not Available|
|LogP||3.03||HANSCH,C ET AL. (1995)|
- Smith AB, Carson CC: Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Ther Clin Risk Manag. 2009 Jun;5(3):535-45. Epub 2009 Jul 12.
- Suzuki R, Satoh H, Ohtani H, Hori S, Sawada Y: Saturable binding of finasteride to steroid 5alpha-reductase as determinant of nonlinear pharmacokinetics. Drug Metab Pharmacokinet. 2010;25(2):208-13.
- Trueb RM: Pharmacologic interventions in aging hair. Clin Interv Aging. 2006;1(2):121-9.
- Otberg N, Finner AM, Shapiro J: Androgenetic alopecia. Endocrinol Metab Clin North Am. 2007 Jun;36(2):379-98.
- Lin AM, Small EJ: Prostate cancer update: 2006. Curr Opin Oncol. 2007 May;19(3):229-33.
- Dunn BK, Ford LG: Hormonal interventions to prevent hormonal cancers: breast and prostate cancers. Eur J Cancer Prev. 2007 Jun;16(3):232-42.
- Thorpe JF, Jain S, Marczylo TH, Gescher AJ, Steward WP, Mellon JK: A review of phase III clinical trials of prostate cancer chemoprevention. Ann R Coll Surg Engl. 2007 Apr;89(3):207-11.