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Finpecia (Finasteride)
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Finasteride

Finpecia works by inhibiting type II 5-alpha reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT). This converted form of testosterone stimulates development of the penis, testes and scrotum, as well as other male sexual characteristics such as body hair and pubic hair. DHT also promotes growth of the prostate. In 1992, Finpecia 5 mg per day was approved by the U.S. Food and Drug Administration (FDA) as a treatment for benign prostatic hyperplasia. The agent was marketed by Merck under the name Finpecia. Patients need to allow at least 6 months for the therapeutic effects to be determined. Symptoms that may improve include difficulty urinating, increased urination frequency and decreased urinary flow. If the therapy is discontinued, symptoms will return within around 6 to 8 months. In 1997, Finpecia 1 mg per day was approved by the FDA as a treatment for male pattern baldness and this time the agent was market by Merck as Finpecia. Finpecia 1 mg per day was shown to benefit men with mild to moderate hair loss in a five-year study. Two thirds of the men who took the medication on a daily basis saw some regrowth of their hair, while those who did not take the medication experienced further hair loss. Analysis showed that for all five years of the study, the average hair count remained above baseline among the Finpecia group and was increased compared to those who did not take the treatment. The medication is only effective for as long as it is used, with the therapeutic effects being lost within 6 to 12 months after discontinuation of the therapy.

Other names for this medication:
Finasteride, Androfin, Avertex, Daric, Fenered, Finahair, Finalo, Finalop, Finar, Finara, Finast, Finax, Fincar, Finpecia, Firide, Monast, Prohair, Propecia, Proscalpin, Proscar, Prosteride, Reduprost, Renacidin, Sutrico, Symasteride, Tealep, Tensen,

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Angiotensin-II-induced expression of proto-oncogene (c-fos, jun-B and c-jun) mRNA in bovine adrenocortical fasciculata cells (BAC) is mediated by AT-1 receptors. Determinants of obstetric outcomes: a study of primiparae in central Saudi Arabia. Aldehydo-D-galactose heptaacetate and aldehydo-D-xylose hexaacetate form acetolysis of guaran and xylan. Our results showed that nadolol (NAD), a beta2-adrenergic antagonist, did not reverse the RST-induced suppression of EAE. Thirty patients with positive family history of migraine were selected and sequencing analysis after DNA extraction was performed.

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