Finax 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, Finax 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 Finax. 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, Finax 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 Finax. Finax 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 Finax 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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The deduced protein sequence of the FAD synthetase shared a homology with those of the protein X of Escherichia coli, which has been reported to have both flavokinase and ATP:FMN adenylyltransferase activities like the FAD synthetase of C. On-column detection of DNA migration in a large number of gel-filled capillaries is carried out using side-entry laser irradiation and with a CCD camera, although it has been considered impossible because the irradiation laser is scattered strongly flucon 150 mg dosis amoxicilina at the surfaces of the first few capillaries. These data indicate that the ACE inhibitor captopril causes an acute and selective enhancement of LV relaxation independent of changes in coronary flow, probably via an endogenous bradykinin/nitric oxide pathway. Here we report that Fas protein is expressed on granulosa and luteal cells but not on oocytes in the ovary.
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