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More about Finasteride

What is/are Finasteride?

Finasteride (brand names Proscar and Propecia by Merck, among other generic names) is a synthetic drug for the treatment of benign prostatic hyperplasia (BPH) and male pattern baldness (MPB). It is a type II 5α-reductase inhibitor. 5α-reductase is an enzyme that converts testosterone to dihydrotestosterone (DHT).

Generic Proscar (FINASTERIDE) is an androgen hormone inhibitor used in men to treat Benign Prostatic Hyperplasia (BPH) which is swelling of the prostate. This medicine works by lowering the amount of a hormone in your body called dihydrotestosterone or DHT. Reducing this hormone level in your body may help to reduce the swelling of the prostate and reduce the symptoms of BPH.

Medical uses

Benign prostatic hyperplasia

Physicians use finasteride for the treatment of benign prostatic hyperplasia (BPH), informally known as an enlarged prostate. The FDA-approved dose is 5 mg once a day. Six months or more of treatment with finasteride may be required to determine the therapeutic results of treatment. If the drug is discontinued, any therapeutic benefits reverse within about 6–8 months. Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start of urination, and decreased urinary flow.

Off-label uses

Finasteride is sometimes used in hormone replacement therapy for male-to-female transsexuals in combination with a form of estrogen due to its antiandrogen properties. However, little clinical research of finasteride use for this purpose has been conducted and evidence of efficacy is limited. Indeed, finasteride is a substantially weaker antiandrogen in comparison to conventional antiandrogens like spironolactone and cyproterone acetate. Furthermore, it has been associated with inducing depression and anxiety at a high rate in both male and female patients,ymptoms that are very common in transsexuals, who are already at a high risk. As a result, prescription of finasteride for this indication in male-to-female transsexuals may not be particularly useful, and could put them at risk for detrimental emotional side effects. Finasteride has also been found to mitigate the effects of withdrawal after chronic alcohol use.

Adverse effects

Side effects of finasteride include impotence (1.1% to 18.5%), abnormal ejaculation (7.2%), decreased ejaculatory volume (0.9% to 2.8%), abnormal sexual function (2.5%), gynecomastia (2.2%), erectile dysfunction (1.3%), ejaculation disorder (1.2%) and testicular pain. According to the product package insert, resolution occurred in men who discontinued therapy with finasteride due to these side effects and in most men who continued therapy. The PPI also states that patients have reported persisting erectile dysfunction despite discontinuing the drug. In December 2010, Merck added depression as a side effect of finasteride.

In November 1997, an FDA panel refused to recommend approval of the drug Propecia for male pattern baldness. Although it was not disputing its efficacy, the committee members expressed some concerns about the possibility of long-term side effects on sexual function and possibly even fertility, which arose because of some evidence of diminished ejaculate levels.

Anxiety and depression

Finasteride has been found to robustly induce depressive and anxious behaviors in animals. Accordingly, its clinical use has been associated with depression and anxiety in both men and women in at least several reports in the medical literature. In one study, at a dose of 1 mg per day, finasteride induced moderate to severe depression in 19 of 23 or 83% of participants, notably including all of the female patients. In addition, marked anxiety occurred comorbidly with the depressive symptoms in some cases. Another study with a larger sample size of 128 men, though no women, also at a dose of 1 mg per day, found that finasteride increased both BDI and HADS depression scores significantly. The authors concluded that finasteride should be prescribed cautiously to patients at a high risk of depression.

In late 2010, Merck revised the label of its Propecia formulation of finasteride in the United States and Canada to add depression to the list of possible side effects.

In August 2012, a study of 61 former users of finasteride with persistent sexual side effects found that 75% of them showed significantly higher rates of depressive symptoms relative to a control group. Of the treated men, 36% had severe symptoms, 28% had moderate symptoms, and 11% had mild symptoms. In addition, 44% of these men reported suicidal ideation. In the control group of 29 men, 10% showed depressive symptoms, with all of these cases being mild, and 3% reported thoughts of suicide. It was concluded that finasteride may cause symptoms of depression and suicidal ideation in some persons which can persist even after discontinuation of treatment.


Finasteride is in the FDA pregnancy category X. This means that it is known to cause birth defects in a fetus. Women who are or who may become pregnant must not handle crushed or broken finasteride tablets, because the medication could be absorbed through the skin. Finasteride is known to cause birth defects in a developing male baby. Exposure to whole tablets should be avoided whenever possible, however exposure to whole tablets is not expected to be harmful as long as the tablets are not swallowed. It is not known whether finasteride passes into breast milk, and thus should not be taken by breastfeeding women. Finasteride may pass into the semen of men, but Merck states that a pregnant woman's contact with the semen of a man taking finasteride is not an issue for concern. Finasteride is known to affect blood donations, and potential donors are typically restricted for at least a month after their most recent dose.

Mechanism of action

Testosterone in males is produced primarily in the testicles, but also in the adrenal glands. The majority of testosterone in the body is bound to sex hormone-binding globulin (SHBG), a protein produced in the liver that transports testosterone through the bloodstream, prevents its metabolism, and prolongs its half-life. Once it becomes unbound from SHBG, free testosterone can enter cells throughout the body. In certain tissues, notably the scalp, skin, and prostate, testosterone is converted into 5α-dihydrotestosterone (DHT) by the enzyme 5α-reductase. DHT is a more powerful androgen than testosterone (as it has approximately 3-10x the potency at the androgen receptor, the site of action of the androgen hormones), so 5α-reductase can be thought to amplify the androgenic effect of testosterone in the tissues in which it's found.

Finasteride, a 4-azasteroid and analogue of testosterone, works by acting as a potent and specific, competitive inhibitor of one of the two subtypes of 5α-reductase, specifically the type II isoenzyme. In other words, it binds to the enzyme and prevents endogenous substrates such as testosterone from being metabolized. 5α-reductase type I and type II are responsible for approximately one-third and two-thirds of systemic DHT production, respectively.

Other 5a-reductase substrates include progesterone, androstenedione, epi-testosterone, cortisol, aldosterone, and deoxycorticosterone. The entire physiologic effect of their reduction is unknown, but likely related to their excretion or is itself physiologic. Beyond being a catalyst in the rate-limiting step in testosterone reduction, 5alpha-reductase enzyme isoforms I and II reduce progesterone to dihydroprogesterone (DHP) and deoxycorticosterone to dihydrodeoxycorticosterone (DHDOC). In vitro and animal models suggest subsequent 3alpha-reduction of DHT, DHP and DHDOC lead to steroid metabolites with effect on cerebral function by enhancing gamma-aminobutyric acid GABAergic inhibition. These neuroactive steroid derivatives enhance GABA at GABA(A) receptors and have anticonvulsant, antidepressant and anxiolytic effects, and also alter sexual and alcohol related behavior. 5α-dihydrocortisol is present in the aqueous humor of the eye, is synthesized in the lens, and might help make the aqueous humor itself. Allopregnanolone and THDOC are neurosteroids, with the latter having effects on the susceptibility of animals to seizures. 5α-dihydroaldosterone is a potent antidiuretic agent, although different from aldosterone. Its formation in the kidney is enhanced by restriction of dietary salt, suggesting it may help retain sodium as follows:

            Substrate + NADPH + H+ → 5α-substrate + NADP+

5α-DHP is a major hormone in circulation of normal cycling and pregnant women.

By inhibiting 5a-reductase, finasteride prevents conversion of testosterone to DHT by the type II isoenzyme, resulting in a decrease in serum DHT levels by about 65–70% and in prostate DHT levels by up to 85–90%, where expression of the type II isoenzyme dominates. Unlike dual inhibitors of both isoenzymes of 5α-reductase which can reduce DHT levels in the entire body by more than 99%, finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with 100-fold less affinity for I as compared to II. In addition to blocking the type II isoenzyme, finasteride competitively inhibits the 5β-reductase type II isoenzyme, though this is not believed to affect androgen metabolism.

By blocking DHT production, finasteride reduces androgen activity in the scalp. In the prostate, inhibition of 5α-reductase reduces prostate volume, which improves benign prostatic hyperplasia (BPH) and reduces risk of prostate cancer. 5α-reductase inhibition also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.

This article uses material from the Wikipedia article Finasteride, which is released under the Creative Commons Attribution-Share-Alike License 3.0.

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