:Finasteride

Finasteride has been used for the treatment of symptomatic benign prostatic hyperplasia (BPH) and for the treatment of male pattern hair loss in men.

Physicians sometimes prescribe finasteride for the treatment of benign prostatic hyperplasia, informally known as an enlarged prostate.{{Cite journal |vauthors=Smith AB, Carson CC |date=June 2009 |title=Finasteride in the treatment of patients with benign prostatic hyperplasia: a review |journal=Therapeutics and Clinical Risk Management |volume=5 |issue=3 |pages=535–45 |doi=10.2147/tcrm.s6195 |pmc=2710385 |pmid=19707263 |doi-access=free}} Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start and end of urination, and decreased urinary flow.{{Cite web |date=20 October 2017 |title=Benign prostate enlargement |url=https://www.nhs.uk/conditions/prostate-enlargement/ |url-status=live |archive-url=https://web.archive.org/web/20201018014542/https://www.nhs.uk/conditions/prostate-enlargement/ |archive-date=18 October 2020 |access-date=20 October 2020 |website=nhs.uk |language=en}}

The use of the drug showed significant sexual adverse effects such as erectile dysfunction and less sexual desire, in particular when obstructive symptoms due to an enlarged prostate were present.{{Cite journal |display-authors=6 |vauthors=Corona G, Tirabassi G, Santi D, Maseroli E, Gacci M, Dicuio M, Sforza A, Mannucci E, Maggi M |date=July 2017 |title=Sexual dysfunction in subjects treated with inhibitors of 5α-reductase for benign prostatic hyperplasia: a comprehensive review and meta-analysis |journal=Andrology |volume=5 |issue=4 |pages=671–678 |doi=10.1111/andr.12353 |pmid=28453908 |s2cid=3577324 |doi-access=free |hdl=11380/1132897}}

Finasteride is also used to treat male pattern baldness (androgenic alopecia) in men, a condition that develops in up to 80% of Caucasian men aged 70 and over.{{Cite journal |vauthors=Kanti V, Messenger A, Dobos G, Reygagne P, Finner A, Blumeyer A, Trakatelli M, Tosti A, Del Marmol V, Piraccini BM, Nast A, Blume-Peytavi U |date=January 2018 |title=Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men – short version |journal=Journal of the European Academy of Dermatology and Venereology |volume=32 |issue=1 |pages=11–22 |doi=10.1111/jdv.14624 |pmid=29178529 |doi-access=free}}{{Cite web |date=15 November 2019 |title=Propecia – finasteride tablet, film coated |url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4e07adb4-7807-47d3-b9a9-2332a3047410 |url-status=live |archive-url=https://web.archive.org/web/20210606214628/https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4e07adb4-7807-47d3-b9a9-2332a3047410 |archive-date=6 June 2021 |access-date=16 September 2020 |website=DailyMed}} In the United States, finasteride and minoxidil are the only two FDA-approved drugs for the treatment of male pattern hair loss as of 2017.{{Cite journal |vauthors=Adil A, Godwin M |date=July 2017 |title=The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis |journal=Journal of the American Academy of Dermatology |volume=77 |issue=1 |pages=136–141.e5 |doi=10.1016/j.jaad.2017.02.054 |pmid=28396101 |s2cid=46036459}} Treatment with finasteride slows further hair loss{{Cite book |url=https://books.google.com/books?id=N_D5CQAAQBAJ&pg=PA934 |title=Clinical Dermatology |vauthors=Habif TP |date=23 April 2015 |publisher=Elsevier Health Sciences |isbn=978-0-323-26607-9 |pages=934– |access-date=22 October 2016 |archive-url=https://web.archive.org/web/20230110031702/https://books.google.com/books?id=N_D5CQAAQBAJ&pg=PA934 |archive-date=10 January 2023 |url-status=live}} and provides about 30% improvement in hair loss after six months of treatment, with effectiveness persisting as long as the drug is taken.

Taking finasteride leads to a reduction in scalp and serum DHT levels; by lowering scalp levels of DHT, finasteride can maintain or increase the amount of terminal hairs in the anagen phase by inhibiting and sometimes reversing miniaturization of the hair follicle. Finasteride is most effective on the crown but can reduce hair loss in all areas of the scalp.{{Cite journal |vauthors=Yim E, Nole KL, Tosti A |date=December 2014 |title=5α-Reductase inhibitors in androgenetic alopecia |journal=Current Opinion in Endocrinology, Diabetes and Obesity |volume=21 |issue=6 |pages=493–8 |doi=10.1097/MED.0000000000000112 |pmid=25268732 |s2cid=30008068}}{{Cite journal |vauthors=Gupta AK, Charrette A |date=April 2014 |title=The efficacy and safety of 5α-reductase inhibitors in androgenetic alopecia: a network meta-analysis and benefit-risk assessment of finasteride and dutasteride |journal=The Journal of Dermatological Treatment |volume=25 |issue=2 |pages=156–61 |doi=10.3109/09546634.2013.813011 |pmid=23768246 |s2cid=24833568}} Finasteride has also been tested for pattern hair loss in women; however, the results were no better than placebo.{{Cite journal |vauthors=Levy LL, Emer JJ |date=August 2013 |title=Female pattern alopecia: current perspectives |journal=International Journal of Women's Health |volume=5 |pages=541–56 |doi=10.2147/IJWH.S49337 |pmc=3769411 |pmid=24039457 |doi-access=free}} Finasteride is less effective in the treatment of scalp hair loss than dutasteride.{{Cite journal |vauthors=Dhurat R, Sharma A, Rudnicka L, Kroumpouzos G, Kassir M, Galadari H, Wollina U, Lotti T, Golubovic M, Binic I, Grabbe S, Goldust M |date=May 2020 |title=5-Alpha reductase inhibitors in androgenetic alopecia: Shifting paradigms, current concepts, comparative efficacy, and safety |journal=Dermatol Ther |volume=33 |issue=3 |pages=e13379 |doi=10.1111/dth.13379 |pmid=32279398 |s2cid=215748750 |doi-access=free}}{{Cite journal |vauthors=Zhou Z, Song S, Gao Z, Wu J, Ma J, Cui Y |date=2019 |title=The efficacy and safety of dutasteride compared with finasteride in treating men with androgenetic alopecia: a systematic review and meta-analysis |journal=Clin Interv Aging |volume=14 |pages=399–406 |doi=10.2147/CIA.S192435 |pmc=6388756 |pmid=30863034 |doi-access=free}}

In males aged 55 years old and over finasteride decreases the risk of low-grade prostate cancer but may increase the risk of high-grade prostate cancer and has no effect on overall survival.{{Cite web |date=28 August 2013 |title=Finasteride for Prostate Cancer Prevention |url=https://www.cancer.gov/types/prostate/research/finasteride-reduces-low-grade |url-status=live |archive-url=https://web.archive.org/web/20200206153247/https://www.cancer.gov/types/prostate/research/finasteride-reduces-low-grade |archive-date=6 February 2020 |access-date=8 February 2020 |website=National Cancer Institute}}

A 2010 review found a 25% reduction in the risk of prostate cancer with 5α-reductase inhibitor.{{Cite journal |vauthors=Wilt TJ, Macdonald R, Hagerty K, Schellhammer P, Tacklind J, Somerfield MR, Kramer BS |year=2010 |title=5-α-Reductase inhibitors for prostate cancer chemoprevention: an updated Cochrane systematic review |journal=BJU Int. |volume=106 |issue=10 |pages=1444–51 |doi=10.1111/j.1464-410X.2010.09714.x |pmid=20977593 |s2cid=22178061 |doi-access=free}} A follow-up study of the Medicare claims of participants in a 10-year Prostate Cancer Prevention Trial suggests the reduction in prostate cancer is maintained even after discontinuation of treatment.{{Cite journal |vauthors=Unger JM, Hershman DL, Till C, Tangen CM, Barlow WE, Ramsey SD, Goodman PJ, Thompson IM |date=March 2018 |title=Using Medicare Claims to Examine Long-term Prostate Cancer Risk of Finasteride in the Prostate Cancer Prevention Trial |journal=Journal of the National Cancer Institute |volume=110 |issue=11 |pages=1208–1215 |doi=10.1093/jnci/djy035 |pmc=6235685 |pmid=29534197}} However, 5α-reductase inhibitors have been found to increase the risk of developing certain rare but aggressive forms of prostate cancer (27% risk increase), although not all studies have observed this.{{Cite journal |vauthors=Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS |year=2016 |title=Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review |journal=J Clin Aesthet Dermatol |volume=9 |issue=7 |pages=56–62 |pmc=5023004 |pmid=27672412}} No impact of 5-α-reductase inhibitor on survival has been found in people with prostate cancer.

Finasteride has been found to be effective in the treatment of hirsutism (excessive facial or body hair growth) in women. In a study of 89 women with hyperandrogenism due to persistent adrenarche syndrome, finasteride produced a 93% reduction in facial hirsutism and a 73% reduction of bodily hirsutism after 2 years of treatment. Other studies using finasteride for hirsutism have also found it to be effective.

A 2010 Cochrane review of finasteride for BPH found that, in men with a weighted mean age of 62.4, adverse effects are rare in men with already enlarged prostates; "nevertheless, men taking finasteride are at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder, versus placebo." {{asof|2016}}, fresh evidence suggested such effects, along with disturbed neurosteroid production, may persist after finasteride use is stopped.{{Cite book |url=https://oxford.universitypressscholarship.com/view/10.1093/acprof:oso/9780199935734.001.0001/acprof-9780199935734-chapter-5 |title=Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors |vauthors=Patisaul HB, Belcher SM |date=18 May 2017 |work=Oxford Scholarship Online |publisher=Oxford University Press |isbn=9780190678524 |volume=1 |page=127 |doi=10.1093/acprof:oso/9780199935734.003.0005}}

Finasteride is contraindicated in pregnancy.{{Cite web |title=PROPECIA Prescribing Information |url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/020788s024lbl.pdf |url-status=live |archive-url=https://web.archive.org/web/20170210151045/http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/020788s024lbl.pdf |archive-date=10 February 2017 |access-date=30 January 2020 |publisher=US Food & Drug Administration / Merck & Co., Inc.}}{{Cite web |title=PROSCAR Prescribing Information |url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020180s037lbl.pdf |url-status=live |archive-url=https://web.archive.org/web/20170210114729/http://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020180s037lbl.pdf |archive-date=10 February 2017 |access-date=30 January 2020 |publisher=US Food & Drug Administration / Merck & Co., Inc.}} The US Food and Drug Administration (FDA) advises that donation of blood or plasma be deferred for at least one month after taking the last dose of finasteride.{{Cite web |date=28 July 1993 |title=Deferral of Blood and Plasma donors – Medications |url=https://www.fda.gov/media/70929/download |url-status=live |archive-url=https://web.archive.org/web/20191214104503/https://www.fda.gov/media/70929/download |archive-date=14 December 2019 |access-date=30 January 2020 |publisher=FDA}}

The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade prostate cancer, as the treatment of BPH lowers PSA (prostate-specific antigen), which could mask the development of prostate cancer.FDA. Posted 9 June 2011. [https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm258529.htm 5-alpha reductase inhibitors (5-ARIs): Label Change – Increased Risk of Prostate Cancer] {{Webarchive|url=https://web.archive.org/web/20170118091754/http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm258529.htm |date=18 January 2017 }}{{Cite journal |vauthors=Walsh PC |date=April 2010 |title=Chemoprevention of prostate cancer |journal=The New England Journal of Medicine |volume=362 |issue=13 |pages=1237–8 |doi=10.1056/NEJMe1001045 |pmid=20357287}} Although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not increased, there are post-marketing reports of breast cancer in association with its use, though available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers.Medicines and Healthcare products Regulatory Agency Drug Safety Update. December 2009 [http://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON087725 Finasteride: potential risk of male breast cancer] {{Webarchive|url=https://web.archive.org/web/20141025225536/http://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON087725 |date=25 October 2014 }} A 2018 meta-analysis found no higher risk of breast cancer with 5α-reductase inhibitors.{{Cite journal |vauthors=Wang J, Zhao S, Luo L, Li E, Li X, Zhao Z |date=2018 |title=5-alpha Reductase Inhibitors and risk of male breast cancer: a systematic review and meta-analysis |journal=Int Braz J Urol |volume=44 |issue=5 |pages=865–873 |doi=10.1590/S1677-5538.IBJU.2017.0531 |pmc=6237523 |pmid=29697934}} Some men develop gynecomastia (breast development or enlargement) following finasteride usage.{{Cite journal |vauthors=Narula HS, Carlson HE |date=August 2014 |title=Gynaecomastia-pathophysiology, diagnosis and treatment |url=https://touroscholar.touro.edu/tuncom_pubs/54 |url-status=live |journal=Nat Rev Endocrinol |volume=10 |issue=11 |pages=684–698 |doi=10.1038/nrendo.2014.139 |pmid=25112235 |s2cid=40159424 |archive-url=https://web.archive.org/web/20201204085804/https://touroscholar.touro.edu/tuncom_pubs/54/ |archive-date=4 December 2020 |access-date=4 July 2019}}{{Cite journal |vauthors=Deepinder F, Braunstein GD |year=2012 |title=Drug-induced gynecomastia: an evidence-based review. |journal=Expert Opinion on Drug Safety |volume=11 |issue=5 |pages=779–795 |doi=10.1517/14740338.2012.712109 |pmid=22862307 |s2cid=22938364}}{{Cite journal |vauthors=Chung EY, Ruospo M, Natale P, Bolignano D, Navaneethan SD, Palmer SC, Strippoli GF |date=October 2020 |title=Aldosterone antagonists in addition to renin angiotensin system antagonists for preventing the progression of chronic kidney disease |journal=The Cochrane Database of Systematic Reviews |volume=2020 |issue=10 |pages=CD007004 |doi=10.1002/14651858.CD007004.pub4 |pmc=8094274 |pmid=33107592}}{{Cite journal |vauthors=Aiman U, Haseeen MA, Rahman SZ |date=December 2009 |title=Gynecomastia: An ADR due to drug interaction |journal=Indian Journal of Pharmacology |volume=41 |issue=6 |pages=286–7 |doi=10.4103/0253-7613.59929 |pmc=2846505 |pmid=20407562 |doi-access=free}} The risk of gynecomastia with 5α-reductase inhibitors is low at about 1.5%. Depressive symptoms and suicidality have been reported.{{Cite journal |vauthors=Locci A, Pinna G |year=2017 |title=Neurosteroid biosynthesis downregulation and changes in GABAA receptor subunit composition: A biomarker axis in stress-induced cognitive and emotional impairment |journal=Br. J. Pharmacol. |volume=174 |issue=19 |pages=3226–3241 |doi=10.1111/bph.13843 |pmc=5595768 |pmid=28456011}}

Use of finasteride is associated with an increased risk of sexual dysfunction including erectile dysfunction, decreased libido and ejaculatory dysfunction.{{Cite journal |vauthors=Lee S, Lee YB, Choe SJ, Lee WS |year=2019 |title=Adverse Sexual Effects of Treatment with Finasteride or Dutasteride for Male Androgenetic Alopecia: A Systematic Review and Meta-analysis |journal=Acta Derm Venereol |volume=99 |issue=1 |pages=12–17 |doi=10.2340/00015555-3035 |pmid=30206635 |doi-access=free}} Sexual adverse effects of finasteride and dutasteride have been linked to lower quality of life and ability to maintain an intimate relationship, and can cause stress in relationships.{{Cite journal |vauthors=Gur S, Kadowitz PJ, Hellstrom WJ |date=January 2013 |title=Effects of 5-alpha reductase inhibitors on erectile function, sexual desire and ejaculation |journal=Expert Opinion on Drug Safety |volume=12 |issue=1 |pages=81–90 |doi=10.1517/14740338.2013.742885 |pmid=23173718 |s2cid=11624116}}

The adverse effect profiles of finasteride are somewhat different for its indications of hair loss and BPH.{{cn|date=January 2025}}

The most common adverse effects of finasteride taken for hair loss are a decrease in sex drive, erectile dysfunction, and a decrease in the amount of semen.{{rp|17}}

In addition, finasteride has been reported in case reports to cause sexual problems that persist after stopping the medication. A 2012 update to the FDA label noted reports of decreased sex drive, problems with ejaculation and difficulty achieving an erection which continued after stopping the medication. The update also referenced reports of testicular pain and "male infertility and/or poor quality of semen."{{rp|17}}{{Cite web |last=FDA |date=11 April 2012 |title=Questions and Answers: Finasteride Label Changes |url=https://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm299754.htm |url-status=live |archive-url=https://web.archive.org/web/20140818144525/http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm299754.htm |archive-date=18 August 2014 |access-date=26 October 2014 |publisher=US FDA}}{{Cite journal |vauthors=Trost L, Saitz TR, Hellstrom WJ |year=2013 |title=Side Effects of 5-Alpha Reductase Inhibitors: A Comprehensive Review |journal=Sex Med Rev |volume=1 |issue=1 |pages=24–41 |doi=10.1002/smrj.3 |pmid=27784557}}

The most common adverse sexual effects of finasteride for BPH are: trouble getting or keeping an erection, decrease in sex drive, decreased volume of ejaculate, and ejaculation disorders.{{rp|16}}

A 2010 Cochrane review found that men taking finasteride for BPH (with a mean age of 62.4) are at increased risk for impotence, erectile dysfunction (ED), decreased libido, and ejaculation disorder for the first year of treatment. The rates became indistinguishable from placebo after 2–4 years and these side effects usually got better over time.

Finasteride may cause persistent adverse sexual, neurological, and physical effects in a subset of men. A 2019 metastudy surveyed the literature on the reversibility of finasteride's side effects. It identified three studies that demonstrated full reversibility of side effects and eleven that described patients with irreversible adverse events. The findings were most convincing in a retrospective review of about 12,000 patients that 1.4% of the cohort developed persistent ED (ED lasting longer than 90 days post-withdrawal).{{Cite journal |display-authors=6 |vauthors=Kiguradze T, Temps WH, Yarnold PR, Cashy J, Brannigan RE, Nardone B, Micali G, West DP, Belknap SM |date=9 March 2017 |title=Persistent erectile dysfunction in men exposed to the 5α-reductase inhibitors, finasteride, or dutasteride |journal=PeerJ |volume=5 |pages=e3020 |doi=10.7717/peerj.3020 |pmc=5346286 |pmid=28289563 |doi-access=free}}

Reports of long-term, post-discontinuation adverse effects in some fraction of former finasteride users have led to a proposed post-finasteride syndrome (PFS), although some within the medical community question whether there is enough evidence to support a causal relationship between finasteride usage and PFS.

Individuals claiming to experience PFS report sexual, neurological, hormonal, and psychological side effects that persist for an extended period after stopping the drug.{{Cite web |date=26 September 2012 |title=Looking at care with a critical eye |url=http://www.afr.com/p/lifestyle/mens_health/looking_at_care_with_critical_eye_ZRbAzUV4cRxZhspW7YRwBJ |archive-url=https://web.archive.org/web/20121114220945/http://www.afr.com/p/lifestyle/mens_health/looking_at_care_with_critical_eye_ZRbAzUV4cRxZhspW7YRwBJ |archive-date=14 November 2012 |website=Australian Financial Review |vauthors=Margo J}} Reported symptoms include penile atrophy and tissue changes, decreased ejaculate volume and quality, reduced libido, erectile dysfunction, loss of penile sensitivity, decreased orgasm sensation, dry skin, metabolic changes, muscle and strength loss, gynecomastia, depression, anxiety, panic attacks, insomnia, anhedonia, concentration problems, memory impairment and suicidal ideation. A meta-analysis found a significant association between finasteride use and post-discontinuation depression, suicidal ideation, and sexual dysfunction, but the quality of evidence was limited.{{Cite journal |vauthors=Pompili M, Magistri C, Maddalena S, Mellini C, Persechino S, Baldessarini RJ |date=1 May 2021 |title=Risk of Depression Associated With Finasteride Treatment |journal=Journal of Clinical Psychopharmacology |volume=41 |issue=3 |pages=304–309 |doi=10.1097/JCP.0000000000001379 |pmid=33814544 |s2cid=233028103}}

The status of PFS as a legitimate and distinct medical pathology remains a subject of debate. A 2019 editorial in The BMJ called post-finasteride syndrome "ill defined and controversial".{{Cite journal |vauthors=Gray SL, Semla TP |date=August 2019 |title=Post-finasteride syndrome |journal=BMJ |volume=366 |pages=l5047 |doi=10.1136/bmj.l5047 |pmid=31399423 |s2cid=199518161}} Some have argued that it has common features with other self-diagnosed "mystery syndromes" such as Morgellons or multiple chemical sensitivity, while others, including some in the biomedical research community, have concluded based on the available evidence, that it represents a real and serious condition. There is no known underlying biological mechanism for the proposed syndrome, and its incidence is unclear. A lack of clear diagnostic criteria and the variable reporting fraction in different healthcare settings make the problem challenging to evaluate.{{Cite journal |vauthors=Maksym RB, Kajdy A, Rabijewski M |date=December 2019 |title=Post-finasteride syndrome – does it really exist? |journal=The Aging Male |volume=22 |issue=4 |pages=250–259 |doi=10.1080/13685538.2018.1548589 |pmid=30651009 |s2cid=58569946 |doi-access=free}}

As of 2016, Merck was a defendant in approximately 1,370 product liability lawsuits which had been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride.{{Cite news |date=4 February 2017 |title=Watch for these potential side effects in drug Trump reportedly takes for hair loss |url=https://www.miamiherald.com/news/nation-world/national/article130815949.html |url-status=live |archive-url=https://web.archive.org/web/20181207171000/https://www.miamiherald.com/news/nation-world/national/article130815949.html |archive-date=7 December 2018 |access-date=9 December 2018 |work=Miami Herald |vauthors=Marchalik D}} Most cases were settled by 2018 when Merck paid a lump sum of US$4.3 million to be distributed. {{asof|September 2019}}, 25 cases remained outstanding in the United States.{{Cite news |title=U.S. court let Merck hide secrets about popular drug's risks |url=https://www.reuters.com/investigates/special-report/usa-courts-secrecy-propecia/ |url-status=live |archive-url=https://web.archive.org/web/20200212182118/https://www.reuters.com/investigates/special-report/usa-courts-secrecy-propecia/ |archive-date=12 February 2020 |access-date=25 March 2021 |work=Reuters |language=en |quote=these legal briefs filed by plaintiffs' lawyers allege that in revisions to the drug's original 1997 label, Merck understated the number of men who experienced sexual symptoms in clinical trials, and how long those symptoms lasted.}} In 2019, Reuters reported that faulty redactions in court documents revealed allegations from plaintiffs that Merck had known of persistent side effects in their original clinical trials but chose not to disclose them in warning labels.

Finasteride has been studied in humans at single doses of up to 400 mg and at continuous dosages of up to 80 mg/day for three months, without adverse effects observed.{{Cite journal |vauthors=Frye SV |date=2006 |title=Discovery and clinical development of dutasteride, a potent dual 5alpha-reductase inhibitor |journal=Curr Top Med Chem |volume=6 |issue=5 |pages=405–21 |doi=10.2174/156802606776743101 |pmid=16719800}} There is no specific recommended antidote for finasteride overdose.

No significant drug interactions have been observed between finasteride and a limited selection of medications.{{Cite journal |vauthors=Sudduth SL, Koronkowski MJ |date=1993 |title=Finasteride: the first 5α-reductase inhibitor |journal=Pharmacotherapy |volume=13 |issue=4 |pages=309–25; discussion 325–9 |doi=10.1002/j.1875-9114.1993.tb02739.x |pmid=7689728 |s2cid=71103672}}

Finasteride is a 5α-reductase inhibitor. It is specifically a selective inhibitor of the type II and III isoforms of the enzyme.{{Cite journal |vauthors=Yamana K, Labrie F, Luu-The V |date=August 2010 |title=Human type 3 5α-reductase is expressed in peripheral tissues at higher levels than types 1 and 2 and its activity is potently inhibited by finasteride and dutasteride |journal=Hormone Molecular Biology and Clinical Investigation |volume=2 |issue=3 |pages=293–9 |doi=10.1515/hmbci.2010.035 |pmid=25961201 |s2cid=28841145}}{{Cite journal |vauthors=Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M |date=February 2010 |title=An overview on 5alpha-reductase inhibitors |journal=Steroids |volume=75 |issue=2 |pages=109–53 |doi=10.1016/j.steroids.2009.10.005 |pmid=19879888 |s2cid=44363501}} By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the potent androgen dihydrotestosterone (DHT) from its precursor testosterone in certain tissues in the body such as the prostate gland, skin, and hair follicles.{{Cite journal |vauthors=Azzouni F, Godoy A, Li Y, Mohler J |year=2012 |title=The 5 alpha-reductase isozyme family: a review of basic biology and their role in human diseases |journal=Adv Urol |volume=2012 |pages=1–18 |doi=10.1155/2012/530121 |pmc=3253436 |pmid=22235201 |doi-access=free}} As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor.{{Cite book |url=https://books.google.com/books?id=7N3nEX6eL_MC&pg=PA89 |title=Handbook of Hair in Health and Disease |vauthors=Preedy VR |publisher=Springer Science & Business Media |year=2012 |isbn=978-90-8686-728-8 |pages=89– |access-date=6 May 2018 |archive-url=https://web.archive.org/web/20230110031743/https://books.google.com/books?id=7N3nEX6eL_MC&pg=PA89 |archive-date=10 January 2023 |url-status=live}}{{Cite book |url=https://books.google.com/books?id=Tqpsm5WKKlcC&pg=PA361 |title=Comprehensive Dermatologic Drug Therapy E-Book |vauthors=Wu JJ |date=18 October 2012 |publisher=Elsevier Health Sciences |isbn=978-1-4557-3801-4 |pages=361– |access-date=6 May 2018 |archive-url=https://web.archive.org/web/20230110031703/https://books.google.com/books?id=Tqpsm5WKKlcC&pg=PA361 |archive-date=10 January 2023 |url-status=live}} However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor.{{Cite book |title=Testosterone |vauthors=Clapauch R, Weiss RV, Rech CM |publisher=Springer |year=2017 |isbn=978-3-319-46084-0 |pages=319–351 |chapter=Testosterone and Women |doi=10.1007/978-3-319-46086-4_17 |quote=Finasteride is not actually an antiandrogen but a 5α-reductase inhibitor.}}

Finasteride results in a decrease of circulating DHT levels by about 65–70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80–90% with an oral dosage of 1 or 5 mg/day.{{Cite journal |vauthors=Bartsch G, Rittmaster RS, Klocker H |date=April 2000 |title=Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia |journal=European Urology |volume=37 |issue=4 |pages=367–80 |doi=10.1159/000020181 |pmid=10765065 |s2cid=25793400}}{{Cite journal |vauthors=Kim EH, Brockman JA, Andriole GL |date=January 2018 |title=The use of 5-alpha reductase inhibitors in the treatment of benign prostatic hyperplasia |journal=Asian Journal of Urology |volume=5 |issue=1 |pages=28–32 |doi=10.1016/j.ajur.2017.11.005 |pmc=5780290 |pmid=29379733}} In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27–53%.{{Cite journal |vauthors=Rittmaster RS |date=January 1994 |title=Finasteride |journal=N. Engl. J. Med. |volume=330 |issue=2 |pages=120–5 |doi=10.1056/NEJM199401133300208 |pmid=7505051}}{{Cite journal |vauthors=Libecco JF, Bergfeld WF |date=April 2004 |title=Finasteride in the treatment of alopecia |journal=Expert Opin Pharmacother |volume=5 |issue=4 |pages=933–40 |doi=10.1517/14656566.5.4.933 |pmid=15102575 |s2cid=24296644}} An oral dosage of finasteride of only 0.2 mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2 mg/day relative to 72.2% for 5 mg/day).{{Cite journal |vauthors=Shapiro J, Kaufman KD |date=June 2003 |title=Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss) |journal=J. Investig. Dermatol. Symp. Proc. |volume=8 |issue=1 |pages=20–3 |doi=10.1046/j.1523-1747.2003.12167.x |pmid=12894990 |doi-access=free}} Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ({{abbrlink|IC₅₀|Half-maximal inhibitory concentration}} = 313 nM and 11 nM, respectively). This is in contrast to inhibitors of all three isoenzymes of 5α-reductase like dutasteride, which can reduce DHT levels in the entire body by more than 99%. In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1).{{Cite journal |author-link4=David W. Christianson |vauthors=Drury JE, Di Costanzo L, Penning TM, Christianson DW |date=July 2009 |title=Inhibition of human steroid 5beta-reductase (AKR1D1) by finasteride and structure of the enzyme-inhibitor complex |journal=The Journal of Biological Chemistry |volume=284 |issue=30 |pages=19786–19790 |doi=10.1074/jbc.C109.016931 |pmc=2740403 |pmid=19515843 |doi-access=free}} However, its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than for 5α-reductase type I) and hence is unlikely to be of clinical significance.

As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear. This is because different investigators have obtained varying results with different reagents, methods, and tissues examined. However, the different isozymes of 5α-reductase appear to be widely expressed, with notable tissues including the prostate gland, seminal vesicles, testes, epididymides, skin, hair follicles, liver, kidneys, and brain, among others.

By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen signaling in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces the risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia.{{Cite book |url=https://books.google.com/books?id=wrHQAgAAQBAJ&pg=PA402 |title=Urologic Surgical Pathology E-Book |vauthors=Bostwick DG, Cheng L |date=24 January 2014 |publisher=Elsevier Health Sciences |isbn=978-0-323-08619-6 |pages=402–}} Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.{{Cite journal |vauthors=Robaire B, Henderson NA |date=May 2006 |title=Actions of 5alpha-reductase inhibitors on the epididymis |journal=Molecular and Cellular Endocrinology |volume=250 |issue=1–2 |pages=190–5 |doi=10.1016/j.mce.2005.12.044 |pmid=16476520 |s2cid=53464391}}

Neurosteroids like 3α-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABA_A receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABA_A activity. Reduction of GABA_A receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.{{Cite journal |vauthors=Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM |year=2006 |title=A new look at the 5alpha-reductase inhibitor finasteride |journal=CNS Drug Reviews |volume=12 |issue=1 |pages=53–76 |doi=10.1111/j.1527-3458.2006.00053.x |pmc=6741762 |pmid=16834758}}{{Cite journal |vauthors=Römer B, Gass P |date=December 2010 |title=Finasteride-induced depression: new insights into possible pathomechanisms |url=https://zenodo.org/record/896024 |url-status=live |journal=Journal of Cosmetic Dermatology |volume=9 |issue=4 |pages=331–2 |doi=10.1111/j.1473-2165.2010.00533.x |pmid=21122055 |s2cid=24328589 |archive-url=https://web.archive.org/web/20201202011005/https://zenodo.org/record/896024 |archive-date=2 December 2020 |access-date=26 May 2019}}{{Cite journal |vauthors=Gunn BG, Brown AR, Lambert JJ, Belelli D |year=2011 |title=Neurosteroids and GABA(A) Receptor Interactions: A Focus on Stress |journal=Frontiers in Neuroscience |volume=5 |pages=131 |doi=10.3389/fnins.2011.00131 |pmc=3230140 |pmid=22164129 |doi-access=free}}

In accordance with finasteride being a potent 5α-reductase inhibitor but a weak inhibitor of 5β-reductase, the medication decreases circulating levels of 5α-reduced steroids like allopregnanolone but does not reduce concentrations of 5β-reduced steroids like pregnanolone.{{Cite journal |vauthors=Traish AM, Hassani J, Guay AT, Zitzmann M, Hansen ML |date=March 2011 |title=Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients |journal=J Sex Med |volume=8 |issue=3 |pages=872–84 |doi=10.1111/j.1743-6109.2010.02157.x |pmid=21176115}}{{Cite journal |vauthors=Dusková M, Hill M, Hanus M, Matousková M, Stárka L |date=2009 |title=Finasteride treatment and neuroactive steroid formation |journal=Prague Med Rep |volume=110 |issue=3 |pages=222–30 |pmid=19655698}}{{Cite journal |vauthors=Dušková M, Hill M, Stárka L |date=January 2010 |title=The influence of low dose finasteride, a type II 5α-reductase inhibitor, on circulating neuroactive steroids |journal=Horm Mol Biol Clin Investig |volume=1 |issue=2 |pages=95–102 |doi=10.1515/HMBCI.2010.010 |pmid=25961975 |s2cid=28578077}} Pregnanolone acts as a potent GABA_A receptor positive allosteric modulator similarly to allopregnanolone.{{Cite journal |vauthors=Reddy DS |date=2003 |title=Pharmacology of endogenous neuroactive steroids |journal=Crit Rev Neurobiol |volume=15 |issue=3–4 |pages=197–234 |doi=10.1615/critrevneurobiol.v15.i34.20 |pmid=15248811}}

The mean oral bioavailability of finasteride is approximately 65%. The absorption of finasteride is not affected by food. At steady-state with 1 mg/day finasteride, mean peak concentrations of finasteride were 9.2 ng/mL (25 nmol/L). Conversely, following a single 5 mg dose of finasteride, mean peak levels of finasteride were 37 ng/mL (99 nmol/L), and plasma concentrations increased by 47–54% following 2.5 weeks of continued daily administration. The volume of distribution of finasteride is 76 L. Its plasma protein binding is 90%. The drug has been found to cross the blood–brain barrier, whereas levels in semen were found to be undetectable.

Finasteride is extensively metabolized in the liver, first by hydroxylation via CYP3A4 and then by aldehyde dehydrogenase. It has two major metabolites, which are the tert-butyl side chain monohydroxylated and monocarboxylic acid metabolites. These metabolites show approximately 20% of the inhibitory activity of finasteride on 5α-reductase. Hence, the metabolites of finasteride are not particularly active. The drug has a terminal half-life of 5 to 6 hours in adult men (18–60 years of age) and a terminal half-life of 8 hours or more in elderly men (more than 70 years of age). It is eliminated as its metabolites 57% in the feces and 40% in the urine.

{{See also|List of 5α-reductase inhibitors}}

Finasteride, also known as 17β-(N-tert-butylcarbamoyl)-4-aza-5α-androst-1-en-3-one, is a synthetic androstane steroid and 4-azasteroid.{{Cite journal |vauthors=Tian G, Stuart JD, Moss ML, Domanico PL, Bramson HN, Patel IR, Kadwell SH, Overton LK, Kost TA, Mook RA |year=1994 |title=17 beta-(N-tert-butylcarbamoyl)-4-aza-5 alpha-androstan-1-en-3-one is an active site-directed slow time-dependent inhibitor of human steroid 5 alpha-reductase 1 |journal=Biochemistry |volume=33 |issue=8 |pages=2291–6 |doi=10.1021/bi00174a041 |pmid=8117686}} It is an analogue of androgen steroid hormones like testosterone and DHT. As an unconjugated steroid, finasteride is a highly lipophilic compound.{{Cite journal |vauthors=Azeem A, Khan ZI, Aqil M, Ahmad FJ, Khar RK, Talegaonkar S |date=May 2009 |title=Microemulsions as a surrogate carrier for dermal drug delivery |journal=Drug Development and Industrial Pharmacy |volume=35 |issue=5 |pages=525–47 |doi=10.1080/03639040802448646 |pmid=19016057 |s2cid=205563538}}

In 1942, James Hamilton observed that prepubertal castration prevents the later development of male pattern baldness in mature men.{{Cite journal |vauthors=Hamilton J |year=1942 |title=Male hormone stimulation is prerequisite and an incitant in common baldness |journal=American Journal of Anatomy |volume=71 |issue=3 |pages=451–480 |doi=10.1002/aja.1000710306}} 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 after onset of puberty. These children, despite being raised as girls until puberty, were generally heterosexual and were termed "Guevedoces" by their local community, which means "penis at twelve" in Spanish.{{Cite news |date=20 September 2015 |title=The extraordinary case of the Guevedoces |url=https://www.bbc.co.uk/news/magazine-34290981 |url-status=live |archive-url=https://web.archive.org/web/20200813070330/https://www.bbc.co.uk/news/magazine-34290981 |archive-date=13 August 2020 |access-date=3 September 2018 |work=BBC News}} Her research group found 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.{{Cite journal |vauthors=Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE |date=December 1974 |title=Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism |journal=Science |volume=186 |issue=4170 |pages=1213–5 |bibcode=1974Sci...186.1213I |doi=10.1126/science.186.4170.1213 |pmid=4432067 |s2cid=36427689}}{{Cite journal |vauthors=Isfort AH, Emerick JE, Paz RA |date=11 November 2016 |title=5-Alpha-Reductase Deficiency |url=http://emedicine.medscape.com/article/924291-overview#showall |url-status=live |journal=WebMD |series=News & Perspective Drugs & Diseases CME & Education Academy Consult, Drugs & Diseases > Pediatrics: General Medicine |archive-url=https://web.archive.org/web/20200806073933/https://emedicine.medscape.com/article/924291-overview#showall |archive-date=6 August 2020 |access-date=25 October 2014}}

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 that could mimic the condition found in these children to treat older men who had benign prostatic hyperplasia.{{Cite news |date=16 February 1992 |title=Keeping the Pipeline Filled at Merck |url=https://www.nytimes.com/1992/02/16/business/keeping-the-pipeline-filled-at-merck.html |url-status=live |archive-url=https://web.archive.org/web/20170314051749/http://www.nytimes.com/1992/02/16/business/keeping-the-pipeline-filled-at-merck.html |archive-date=14 March 2017 |access-date=16 February 2017 |work=The New York Times |vauthors=Freudenheim M}}

Finasteride was developed by Merck under the code name MK-906. A team led by chemist Gary Rasmusson and biologist Jerry Brooks developed potential 5α-reductase inhibitors based on transition-state inhibitors, using an iterative process of molecular design, testing, and redesign.{{Cite book |url=https://books.google.com/books?id=_G9VAgAAQBAJ |title=Hallelujah Moments: Tales of Drug Discovery |vauthors=Cordes EH |publisher=Oxford University Press |year=2014 |isbn=9780199337149 |access-date=21 June 2020 |archive-url=https://web.archive.org/web/20230110031704/https://books.google.com/books?id=_G9VAgAAQBAJ |archive-date=10 January 2023 |url-status=live}} In 1992, finasteride (5 mg) was approved by the US Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar. Rasmusson and Brooks were awarded IPO's "Inventor of the Year" award in 1993 for their work on finasteride.{{Cite web |title=Past Inventor of the Year Award Winners |url=https://www.ipoef.org/past-ioy-winners |url-status=live |archive-url=https://web.archive.org/web/20200625183234/https://www.ipoef.org/past-ioy-winners/ |archive-date=25 June 2020 |access-date=21 June 2020 |website=ipoef.org |publisher=Intellectual Property Owners Education Foundation}} In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia.{{Cite book |url=https://books.google.com/books?id=25ZUAAAAMAAJ |title=Burger's Medicinal Chemistry and Drug Discovery, Autocoids, Diagnostics, and Drugs from New Biology |vauthors=Burger A, Abraham DJ |date=20 February 2003 |publisher=Wiley |isbn=978-0-471-37030-7 |page=439 |access-date=4 December 2017 |archive-url=https://web.archive.org/web/20230110031744/https://books.google.com/books?id=25ZUAAAAMAAJ |archive-date=10 January 2023 |url-status=live}} It was the first 5α-reductase inhibitor to be introduced and was followed by dutasteride in 2001.{{Cite book |url=https://books.google.com/books?id=ECfQ6D5JLusC&pg=PA353 |title=Annual Reports in Medicinal Chemistry |vauthors=Doherty AM |publisher=Academic Press |year=2003 |isbn=978-0-12-040538-1 |pages=353– |access-date=4 December 2017 |archive-url=https://web.archive.org/web/20230110031703/https://books.google.com/books?id=ECfQ6D5JLusC&pg=PA353 |archive-date=10 January 2023 |url-status=live}} The first study of finasteride in the treatment of hirsutism in women was published in 1994.{{Cite journal |vauthors=Diamanti-Kandarakis E, Tolis G, Duleba AJ |date=1995 |title=Androgens and therapeutic aspects of antiandrogens in women |journal=J. Soc. Gynecol. Investig. |volume=2 |issue=4 |pages=577–92 |doi=10.1177/107155769500200401 |pmid=9420861 |s2cid=32242838}}

Finasteride is the generic name of the drug and its {{abbrlink|INN|International Nonproprietary Name}}, {{abbrlink|USAN|United States Adopted Name}}, {{abbrlink|BAN|British Approved Name}}, and {{abbrlink|JAN|Japanese Accepted Name}}, while finastéride is its {{abbrlink|DCF|Dénomination Commune Française}}.{{Cite book |url=https://books.google.com/books?id=5GpcTQD_L2oC&pg=PP1 |title=Index Nominum 2000: International Drug Directory |publisher=Taylor & Francis |year=2000 |isbn=978-3-88763-075-1 |page=443}}{{Cite book |url=https://books.google.com/books?id=tsjrCAAAQBAJ&pg=PA121 |title=Concise Dictionary of Pharmacological Agents: Properties and Synonyms |vauthors=Morton IK, Hall JM |date=6 December 2012 |publisher=Springer Science & Business Media |isbn=978-94-011-4439-1 |pages=121–}}{{Cite book |url=https://books.google.com/books?id=x0hZDwAAQBAJ&pg=PA816 |title=Dictionary of Antibiotics and Related Substances: with CD-ROM, Second Edition |vauthors=Bycroft BW, Payne DJ |date=9 August 2013 |publisher=CRC Press |isbn=978-1-4822-8215-3 |pages=816– |access-date=6 May 2018 |archive-url=https://web.archive.org/web/20230110031704/https://books.google.com/books?id=x0hZDwAAQBAJ&pg=PA816 |archive-date=10 January 2023 |url-status=live}}{{Cite web |title=Finasteride |url=https://www.drugs.com/international/finasteride.html |url-status=live |archive-url=https://web.archive.org/web/20190408115008/https://www.drugs.com/international/finasteride.html |archive-date=8 April 2019 |access-date=6 December 2017}} It is also known by its former developmental code names MK-906, YM-152, and L-652,931.

Finasteride is marketed primarily under the brand names Propecia, for pattern hair loss, and Proscar, for BPH, both of which 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 in June 2006.{{Cite web |title=Primary Patent Expirations for Selected High Revenue Drugs |url=http://www.rxsolutions.com/c/rxnews/rxnews_view.asp?Article=674&type=19 |url-status=dead |archive-url=https://web.archive.org/web/20080321140432/http://www.rxsolutions.com/c/rxnews/rxnews_view.asp?Article=674&type=19 |archive-date=21 March 2008 |website=RxNews |publisher=Prescription Solutions}} Merck was awarded a separate patent for the use of finasteride to treat pattern hair loss and it expired in November 2013.{{Cite web |last=FDA |title=Patent Expiration for Propecia |url=http://www.accessdata.fda.gov/scripts/cder/ob/docs/patexclnew.cfm?Appl_No=020788&Product_No=001&table1=OB_Rx |url-status=live |archive-url=https://web.archive.org/web/20161026171214/http://www.accessdata.fda.gov/scripts/cder/ob/docs/patexclnew.cfm?Appl_No=020788&Product_No=001&table1=OB_Rx |archive-date=26 October 2016 |access-date=17 August 2007 |website=Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations}} Finasteride is also marketed under a variety of other brand names throughout the world.

From 2005 to 2009, the World Anti-Doping Agency banned finasteride because it was discovered that the drug could be used to mask steroid abuse.{{Cite news |date=19 January 2006 |title=Skin Deep; Fighting Baldness, and Now an Olympic Ban |url=https://query.nytimes.com/gst/fullpage.html?sec=health&res=9F02E2DB153FF93AA25752C0A9609C8B63&n=Top%2fReference%2fTimes%20Topics%2fSubjects%2fO%2fOlympic%20Games |url-status=live |archive-url=https://web.archive.org/web/20171204222824/https://query.nytimes.com/gst/fullpage.html?sec=health&res=9F02E2DB153FF93AA25752C0A9609C8B63&n=Top%2fReference%2fTimes%20Topics%2fSubjects%2fO%2fOlympic%20Games |archive-date=4 December 2017 |access-date=2 May 2010 |work=The New York Times |vauthors=Sandomir R}} It was removed from the list effective 1 January 2009, after improvements in testing methods made the ban unnecessary.{{Cite web |last=Staff |date=28 October 2008 |title=WADA removes Finasteride from ban list |url=http://www.theaustralian.com.au/archive/news/wada-removes-finasteride-from-ban-list/story-e6frg7mo-1111117876628?nk=0afe1009eb17d32f8f4d47ff9e091a08 |website=The Australian}} Athletes who used finasteride and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romário, and ice hockey goaltender José Théodore.{{Cite web |last=Staff |date=9 October 2008 |title=WADA takes Romario's drug off banned list |url=http://www.smh.com.au/zoom/archive/d229652 |url-status=dead |archive-url=https://web.archive.org/web/20150925030419/http://www.smh.com.au/zoom/archive/d229652 |archive-date=25 September 2015 |access-date=25 October 2014 |website=Sydney Morning Herald}}

The US Food and Drug Administration (FDA) advises that donation of blood or plasma be deferred for at least one month after taking the last dose of finasteride.{{Cite web |date=28 July 1993 |title=Deferral of Blood and Plasma donors – Medications |url=https://www.fda.gov/downloads/BiologicsBloodVaccines/.../UCM062813.pdf |url-status=live |archive-url=https://web.archive.org/web/20170208141513/http://www.fda.gov/downloads/BiologicsBloodVaccines/.../UCM062813.pdf |archive-date=8 February 2017 |access-date=4 February 2017 |publisher=FDA}} The UK also has a one-month deferral period.{{Cite web |date=1 June 2007 |title=Anti-Androgens – Joint United Kingdom Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee |url=https://www.transfusionguidelines.org/dsg/wb/guidelines/an027-anti-androgens |url-status=live |archive-url=https://web.archive.org/web/20201112020418/https://www.transfusionguidelines.org/dsg/wb/guidelines/an027-anti-androgens |archive-date=12 November 2020 |access-date=13 May 2020 |website=www.transfusionguidelines.org}}

Preliminary research suggests that topical finasteride may be effective in the treatment of pattern hair loss.{{Cite journal |vauthors=Lee SW, Juhasz M, Mobasher P, Ekelem C, Mesinkovska NA |date=April 2018 |title=A Systematic Review of Topical Finasteride in the Treatment of Androgenetic Alopecia in Men and Women |journal=Journal of Drugs in Dermatology |volume=17 |issue=4 |pages=457–463 |pmc=6609098 |pmid=29601622}}{{Cite journal |vauthors=Marks DH, Prasad S, De Souza B, Burns LJ, Senna MM |date=April 2020 |title=Topical Antiandrogen Therapies for Androgenetic Alopecia and Acne Vulgaris |journal=American Journal of Clinical Dermatology |volume=21 |issue=2 |pages=245–254 |doi=10.1007/s40257-019-00493-z |pmid=31832993 |s2cid=209331373}} Topical finasteride, like the oral preparation, reduces serum DHT.

DHT may be involved in the cause of acne, and 5α-reductase inhibitors might be effective in the treatment of the condition.{{Cite book |url=https://books.google.com/books?id=Z1yFBQAAQBAJ&pg=PA147 |title=Acne: Causes and Practical Management |vauthors=Danby FW |date=27 January 2015 |publisher=John Wiley & Sons |isbn=978-1-118-23277-4 |pages=147– |access-date=24 March 2019 |archive-url=https://web.archive.org/web/20230110031704/https://books.google.com/books?id=Z1yFBQAAQBAJ&pg=PA147 |archive-date=10 January 2023 |url-status=live}}{{Cite journal |vauthors=Marchetti PM, Barth JH |date=March 2013 |title=Clinical biochemistry of dihydrotestosterone |journal=Ann. Clin. Biochem. |volume=50 |issue=Pt 2 |pages=95–107 |doi=10.1258/acb.2012.012159 |pmid=23431485 |s2cid=8325257 |doi-access=free}} A small retrospective study reported that finasteride was effective in the treatment of acne in women with normal testosterone levels.{{Cite journal |vauthors=Hu AC, Chapman LW, Mesinkovska NA |date=January 2019 |title=The efficacy and use of finasteride in women: a systematic review |journal=International Journal of Dermatology |volume=58 |issue=7 |pages=759–776 |doi=10.1111/ijd.14370 |pmid=30604525 |s2cid=58555908}} A randomized controlled trial found that finasteride was less effective than flutamide or an ethinylestradiol/cyproterone acetate birth control pill in the treatment of acne in women with high androgen levels.

Androgens and estrogens may be involved in the cause of hidradenitis suppurativa (acne inversa).{{Cite journal |vauthors=Alikhan A, Lynch PJ, Eisen DB |date=April 2009 |title=Hidradenitis suppurativa: a comprehensive review |journal=J. Am. Acad. Dermatol. |volume=60 |issue=4 |pages=539–61; quiz 562–3 |doi=10.1016/j.jaad.2008.11.911 |pmid=19293006}}{{Cite journal |vauthors=Riis PT, Ring HC, Themstrup L, Jemec GB |date=December 2016 |title=The Role of Androgens and Estrogens in Hidradenitis Suppurativa – A Systematic Review |journal=Acta Dermatovenerol Croat |volume=24 |issue=4 |pages=239–249 |pmid=28128074}} Two case series have reported that finasteride is effective in the treatment of hidradenitis suppurativa in girls and women.

Finasteride and other antiandrogens might be useful in the treatment of obsessive–compulsive disorder (OCD), but more research is needed.{{Cite journal |vauthors=Nomani H, Mohammadpour AH, Moallem SM, YazdanAbad MJ, Barreto GE, Sahebkar A |date=December 2019 |title=Anti-androgen drugs in the treatment of obsessive-compulsive disorder: a systematic review |journal=Curr Med Chem |volume=27 |issue=40 |pages=6825–6836 |doi=10.2174/0929867326666191209142209 |pmid=31814547 |s2cid=208956450}}

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{{Androgens and antiandrogens}}

{{Drugs used in benign prostatic hypertrophy}}

{{Other dermatological preparations}}

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