|Systematic (IUPAC) name|
|Trade names||Propecia, Proscar|
|Half-life||Elderly: 8 hours
Adults: 6 hours
|Excretion||Feces (57%) and urine (39%) as metabolites|
|ATC code||G04 D11|
|Mol. mass||372.549 g/mol|
|(what is this?)|
Finasteride (MK-906, 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).
- 1 Medical uses
- 2 Adverse effects
- 3 Mechanism of action
- 4 Vehicle
- 5 History
- 6 See also
- 7 References
- 8 External links
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.
Male pattern baldness
Three Phase 3 clinical trials examined the efficacy of finasteride in the treatment of mild to moderate male pattern baldness. The primary endpoints of each trial were hair count and user self-assessment. Secondary endpoints included investigator assessment and examination of scalp photographs. Each patient also filled out questionairres regarding sexual health and non-scalp body hair growth. These trials enrolled 1879 men and had a duration of one year. Of these 1879 men, 1215 elected to participate in a one year double blind extension trial. Additional extension trials were performed such that 323 men experienced over 4 years of treatment.
Across all three trials, at one year men taking Propecia had 107 more hairs per 1 inch diameter section of scalp (in the area affected by hair loss) than men treated with placebo. At two years the difference was 138 hairs. Maximum hair gain occurred during the first two years, but because hair loss was more rapid in the placebo treated group, the difference between treated and placebo groups increased to 277 hairs per inch circle at 5 years. Self assessment showed that treated patients perceived an improvement in hair density and overall appearance. These results were supported by investigator ratings and by independent readers examining scalp photographs.
At the end of the first year, the sexual health questionaire revealed differences in sexual interest, erections, and perception of sexual problems that favored the placebo group. However, no significant difference was seen in the question on overall satisfaction with sex life.
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.
In a four year controlled clinical study, 3040 patients with symptomatic benign prostatic hyperplasia were treated with 5 mg per day finasteride or placebo. Discontinuation rates due to adverse reactions related to sexual function were 3.7% in the finasteride arm and 2.1% in the placebo arm. Sexual effects were the most common type of adverse reaction.
In 12 month duration double-blind clinical trials including more than 3000 patients, adverse effects included decreased libido (5% in the finasteride group and 3% in the placebo group), erectile dysfunction (8% finasteride, 3% placebo), and ejaculation disorder (2% finasteride, 0.6% placebo).
The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade prostate cancer. While the effect of finasteride on the risk of developing prostate cancer has not been established, evidence suggests it may temporarily reduce the growth and prevalence of benign prostate tumors, but could also mask the early detection of prostate cancer. The primary concern is patients who develop prostate cancer while taking finasteride for benign prostatic hyperplasia, which in turn could delay diagnosis and early treatment of the prostate cancer, thereby potentially increasing the risk of these patients developing high-grade prostate cancer.
The 2005 Prostate Cancer Prevention Trial (PCPT) showed at a dosage of 5 mg per day, as is commonly prescribed for BPH, participants taking finasteride were 25% less likely to have developed prostate cancer at the end of the trial compared to those taking a placebo. It appeared (incorrectly) that finasteride increased the specificity and selectivity of prostate cancer detection, thus creating an apparently increased rate of high Gleason grade tumor. A 2008 update of this study found that finasteride reduces the incidence of prostate cancer by 30%. In the original study, the smaller prostate caused by finasteride facilitated detection of cancer nests and aggressive-looking cells. Most of the men in the study who had both low and high-grade prostate cancer chose to be treated, and many had their prostates removed. A pathologist then carefully examined each of those 500 prostates and compared the kinds of cancers found at surgery to those initially diagnosed at biopsy. This study concluded that finasteride did not increase the risk of high-grade prostate cancer.
Sexual side effects
There are case reports of persistent diminished libido or erectile dysfunction, even after stopping the drug. Prior to 2011, both the Swedish Medical Products agency and the UK's Medical and Healthcare Products Regulatory Agency (MHRA) had both updated their information leaflets to include a statement that "persistence of erectile dysfunction after discontinuation of treatment with Propecia has been reported in post-marketing use."  Despite updating European information leaflets, Merck left the US label unchanged until April 2012, when the FDA added a warning as precaution after reviewing 678 case reports of post-treatment sexual dysfunction received over an 18 year period. 
Anxiety and depression
Mood disorders were not observed as an important adverse effect in the phase 3 trials leading to regulatory approval of finasteride for the treatment of benign prostatic hyperplasia. Nonetheless, a variety of small studies have suggested a possible connection. 
Male breast cancer
In December 2009, the Medicines and Healthcare products Regulatory Agency in the UK announced new drug safety advice on finasteride and the potential risk of male breast cancer. The agency concluded that, although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not significantly increased, a higher risk of male breast cancer with finasteride use cannot be excluded. A warning on this risk will be included in the product information. Merck revised the United States' warning in consumer and medical leaflets to include the risk of male breast cancer.
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.
Interference with doping assays
Many sports organizations have banned finasteride because it can be used to mask steroid abuse. Since 2005, finasteride has been on the World Anti-Doping Agency's list of banned substances. However, it was removed from the list in 2009. Notable athletes who used finasteride for hair loss and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romário and ice hockey goaltender José Théodore.
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 3-10 times 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.
DHT, and neuroactive steroids (NAs) such as allopregnanolone (ALLO) and tetrahydrodeoxycorticosterone (THDOC)—potent positive allosteric modulators of the GABAA receptor (the same site of action of euphoriant and anxiolytic drugs like benzodiazepines and alcohol)—are important endogenous neuroregulators that have been shown to possess powerful antidepressant and anxiolytic effects as well as to play a positive role in sexual function. Their biosynthesis is dependent on both isoforms of 5α-reductase, and accordingly, finasteride has been shown to reduce their formation in the body. As such, this effect of finasteride is a likely cause of the emotional and sexual side effects associated with the drug.
Drug trade names include Propecia and Proscar, the former marketed for male pattern baldness (MPB) and the latter for benign prostatic hyperplasia (BPH), both are products of Merck & Co. There is 1 mg of finasteride in Propecia and 5 mg in Proscar. Merck's patent on finasteride for the treatment of BPH expired on June 19, 2006. Merck was awarded a separate patent for the use of finasteride to treat MPB. This patent is set to expire in November 2013.
Finasteride is lipophilic, and development of a liposomal system of finasteride for topical application has been a subject of recent study. Topical formulations show some effect in reversal of androgenic effects on hair follicles, as well as in hirsutism. More recent studies have looked at microemulsions and liquid crystalline nanoparticles for topical finasteride delivery. In the latter, addition of glycerol, propylene glycol, and polyethylene glycol 400, increased finasteride permeation, while addition of oleic acid made it decrease. Topical finasteride in combination with topical minoxidil is more effective than topical minoxidil alone. Small studies of topical finasteride formulations in combination with other drugs have also been found effective. Surfactants have been shown to aid topical absorption. Topical finasteride gel has been shown an effective route of administration.
In 1974, Julianne Imperato-McGinley of Cornell Medical College in New York attended a conference on birth defects. She reported on a group of intersex children in the Caribbean who appeared sexually ambiguous at birth, and were initially raised as girls, but then grew external male genitalia and other masculine characteristic post-onset of puberty. Her research group found that these children shared a genetic mutation, causing deficiency of the 5α-reductase enzyme and male hormone dihydrotestosterone (DHT), which was found to have been the etiology behind abnormalities in male sexual development. Upon maturation, these individuals were observed to have smaller prostates which were underdeveloped, and were also observed to lack incidence of male pattern baldness.
In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children in order to treat older men who were suffering from benign prostatic hyperplasia.
In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of male pattern baldness (MPB), which was marketed under the brand name Propecia.
- Dutasteride, related 5α-reductase inhibitor (isozyme I, II and III)
- Bexlosteride 5-α reductase inhibitor (isozyme I selective).
- Epristeride (SKF-105657) (SmithKline Beecham)
- Turosteride (FCE-26,073)
- 4-MA steroid not amp
- FCE 28260
- Izonsteride (LY-320,236)
- Lapisteride (INN; CS-891)
- Galeterone (TOK-001 or VN/124-1)
- Ganoderic acid
|“||The two isozymes, usually called Type I and Type II, exhibit differences in their biochemical properties, genetics and pharmacology. Both isozymes are now the subject of considerable research and it has been found that Type I is more prevalent in the scalp, and that Type II is more prevalent in the prostate.||”|
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