View source for Finasteride

{{Short description|Antiandrogen medication}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Use dmy dates|date=October 2022}}
{{Infobox drug
| Watchedfields = changed
| verifiedrevid = 458461973
| image = Finasteride.svg
| image_class = skin-invert-image
| width = 200
| image2 = Finasteride-from-xtal-3D-bs-17.png
| image_class2 = bg-transparent
| width2 = 250
| alt2 = <!-- Clinical data -->
| pronounce = {{IPAc-en|f|ɪ|ˈ|n|æ|s|t|ə|ˌ|r|aɪ|d|audio=LL-Q1860 (eng)-NaomiAmethyst-finasteride.wav}}<br />{{respell|fi|NA|stə|RYDE}}
| tradename = Proscar, Propecia, Finide, others
| Drugs.com = {{drugs.com|monograph|finasteride}}
| MedlinePlus = a698016
| DailyMedID = Finasteride
| pregnancy_AU = X
| pregnancy_category = 
| routes_of_administration = [[By mouth]], [[topical]]
| class = [[5α-Reductase inhibitor]]
| ATC_prefix = G04
| ATC_suffix = CB01
| ATC_supplemental = {{ATC|D11|AX10}}
| legal_AU = S4
| legal_CA = Rx-only
| legal_UK = POM
| legal_UK_comment =<ref>{{Cite web | title = Propecia 1 mg Film-Coated Tablets - Summary of Product Characteristics (SmPC) | date = 27 July 2020 | url = https://www.medicines.org.uk/emc/product/2194/smpc | url-status = live | archive-url = https://web.archive.org/web/20200920055119/https://www.medicines.org.uk/emc/product/2194/smpc | archive-date = 20 September 2020 | access-date = 29 September 2020 | website = (emc) }}</ref><ref>{{Cite web | title = Proscar 5mg film-coated Tablets - Summary of Product Characteristics (SmPC) | date = 10 July 2020 | url = https://www.medicines.org.uk/emc/product/1008/smpc | url-status = live | archive-url = https://web.archive.org/web/20200924060320/https://www.medicines.org.uk/emc/product/1008/smpc | archive-date = 24 September 2020 | access-date = 29 September 2020 | website = (emc) }}</ref>
| legal_US = Rx-only
| legal_US_comment =<ref name="Proscar FDA label">{{Cite web | title = Proscar- finasteride tablet, film coated | date = 15 November 2019 | url = https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7c01f541-1c88-400c-41a9-7cbb9dee50c0 | url-status = live | archive-url = https://web.archive.org/web/20210426231856/https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7c01f541-1c88-400c-41a9-7cbb9dee50c0 | archive-date = 26 April 2021 | access-date = 16 September 2020 | website = DailyMed }}</ref><ref name="Propecia FDA label" />

<!-- Pharmacokinetic data -->| bioavailability = 65%<ref name="Lemke_2008">{{Cite book | vauthors = Lemke TL, Williams DA | title = Foye's Principles of Medicinal Chemistry | pages = 1286– | year = 2008 | url = https://books.google.com/books?id=R0W1ErpsQpkC&pg=PA1286 | publisher = Lippincott Williams & Wilkins | isbn = 978-0-7817-6879-5 | edition = 6th | access-date = 4 December 2017 | archive-url = https://web.archive.org/web/20230110031700/https://books.google.com/books?id=R0W1ErpsQpkC&pg=PA1286 | archive-date = 10 January 2023 | url-status = live }}</ref>
| protein_bound = 90%<ref name="Lemke_2008" />
| metabolism = [[Liver]] ([[CYP3A4]], [[aldehyde dehydrogenase|ALDH]])<ref name="Lemke_2008" />
| elimination_half-life = Adults: 5–6 hours<ref name="Lemke_2008" /><br />Elderly: >8 hours<ref name="Lemke_2008" />
| excretion = [[Feces]]: 57%<ref name="Lemke_2008" /><br />[[Urine]]: 40%<ref name="Lemke_2008" />

<!-- Identifiers -->| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 98319-26-7
| PubChem = 57363
| IUPHAR_ligand = 6818
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB01216
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 51714
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 57GNO57U7G
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D00321
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 5062
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 710
| synonyms = MK-906; YM-152; L-652,931; 17β-(''N''-tert-Butylcarbamoyl)-4-aza-5α-androst-1-en-3-one; ''N''-(1,1-Dimethylethyl)-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide
<!-- Chemical data -->| IUPAC_name = (1S,3aS,3bS,5aR,9aR,9bS,11aS)-''N''-tert-butyl-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecahydroindeno[5,4-f]quinoline-1-carboxamide
| C = 23
| H = 36
| N = 2
| O = 2
| SMILES = O=C(NC(C)(C)C)[C@@H]2[C@]1(CC[C@H]3[C@H]([C@@H]1CC2)CC[C@H]4NC(=O)\C=C/[C@]34C)C
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C23H36N2O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27)/t14-,15-,16-,17+,18+,22-,23+/m0/s1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = DBEPLOCGEIEOCV-WSBQPABSSA-N
}}

<!-- Definition and medical uses -->
'''Finasteride''', sold under the brand names '''Proscar''' and '''Propecia''' among others, is a medication used to treat [[pattern hair loss]] and [[benign prostatic hyperplasia]] (BPH) in men.<ref name="AHFS2019">{{Cite web | title = Finasteride Monograph for Professionals | url = https://www.drugs.com/monograph/finasteride.html | url-status = live | archive-url = https://web.archive.org/web/20180825002456/https://www.drugs.com/monograph/finasteride.html | archive-date = 25 August 2018 | access-date = 5 March 2019 | website = Drugs.com | publisher = American Society of Health-System Pharmacists }}</ref> It can also be used to treat [[hirsutism|excessive hair growth]] in women.<ref name="BlumePeytavi_2008">{{Cite book | vauthors = Blume-Peytavi U, Whiting DA, Trüeb RM | title = Hair Growth and Disorders | page = 369 | date = 26 June 2008 | url = https://books.google.com/books?id=pHrX2-huQCoC&pg=PA369 | publisher = Springer Science & Business Media | isbn = 978-3-540-46911-7 | access-date = 10 December 2016 | archive-url = https://web.archive.org/web/20230110031700/https://books.google.com/books?id=pHrX2-huQCoC&pg=PA369 | archive-date = 10 January 2023 | url-status = live }}</ref> It is usually taken [[oral administration|orally]] but there are [[Topical medication|topical formulations]] for patients with hair loss, designed to minimize systemic exposure by acting specifically on hair follicles.<ref name="Piraccini_2022">{{Cite journal | vauthors = Piraccini BM, Blume-Peytavi U, Scarci F, Jansat JM, Falqués M, Otero R, Tamarit ML, Galván J, Tebbs V, Massana E | title = Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III, randomized, controlled clinical trial | journal = Journal of the European Academy of Dermatology and Venereology  | volume = 36 | issue = 2 | pages = 286–294 | date = February 2022 | pmid = 34634163 | pmc = 9297965 | doi = 10.1111/jdv.17738 }}</ref>

Finasteride is a [[5α-reductase inhibitor]] and therefore an [[antiandrogen]].<ref>{{Cite book | vauthors = Ferri FF | title = Ferri's Clinical Advisor 2015 E-Book: 5 Books in 1 | page = 580 | date = 2014 | url = https://books.google.com/books?id=icTsAwAAQBAJ&pg=PA580 | publisher = Elsevier Health Sciences | isbn = 978-0-323-08430-7 | access-date = 7 May 2020 | archive-url = https://web.archive.org/web/20230110031742/https://books.google.com/books?id=icTsAwAAQBAJ&pg=PA580 | archive-date = 10 January 2023 | url-status = live }}</ref> It works by [[enzyme inhibitor|decreasing]] the [[biosynthesis|production]] of [[dihydrotestosterone]] (DHT) by about 70%.<ref name="AHFS2019" />

In addition to DHT, finasteride also inhibits the production of several anticonvulsant neurosteroids including [[allopregnanolone]], [[androstanediol]], and [[tetrahydrodeoxycorticosterone]].<ref>{{Cite journal | vauthors = Samba Reddy D, Ramanathan G | title = Finasteride inhibits the disease-modifying activity of progesterone in the hippocampus kindling model of epileptogenesis | journal = Epilepsy & Behavior | volume = 25 | issue = 1 | pages = 92–97 | date = September 2012 | pmid = 22835430 | pmc = 3444667 | doi = 10.1016/j.yebeh.2012.05.024 }}</ref>

<!--Adverse effects and mechanism -->
[[Adverse effects]] from finasteride are rare in men with already enlarged prostates;<ref name="Tacklind_2010">{{Cite journal | vauthors = Tacklind J, Fink HA, Macdonald R, Rutks I, Wilt TJ | title = Finasteride for benign prostatic hyperplasia | journal = The Cochrane Database of Systematic Reviews | volume = 2010 | issue = 10 | article-number = CD006015 | date = October 2010 | pmid = 20927745 | pmc = 8908761 | doi = 10.1002/14651858.CD006015.pub3 }}</ref> however, some men experience [[sexual dysfunction]], [[depression (mood)|depression]], and [[gynecomastia|breast enlargement]].<ref name="Zakhem_2019">{{Cite journal | vauthors = Zakhem GA, Goldberg JE, Motosko CC, Cohen BE, Ho RS | title = Sexual dysfunction in men taking systemic dermatologic medication: A systematic review | journal = Journal of the American Academy of Dermatology | volume = 81 | issue = 1 | pages = 163–172 | date = July 2019 | pmid = 30905792 | doi = 10.1016/j.jaad.2019.03.043 | s2cid = 85497115 }}</ref><ref name="Varothai_2014">{{Cite journal | vauthors = Varothai S, Bergfeld WF | title = Androgenetic alopecia: an evidence-based treatment update | journal = American Journal of Clinical Dermatology | volume = 15 | issue = 3 | pages = 217–230 | date = July 2014 | pmid = 24848508 | doi = 10.1007/s40257-014-0077-5 | s2cid = 31245042 }}</ref> In some men, sexual dysfunction may persist after stopping the medication.<ref name="Zakhem_2019a">{{Cite journal | vauthors = Zakhem GA, Goldberg JE, Motosko CC, Cohen BE, Ho RS | title = Sexual dysfunction in men taking systemic dermatologic medication: A systematic review | journal = Journal of the American Academy of Dermatology | volume = 81 | issue = 1 | pages = 163–172 | date = July 2019 | pmid = 30905792 | doi = 10.1016/j.jaad.2019.03.043 | s2cid = 85497115 | quote = In studies addressing reversibility, most of these patients have resolution of sexual adverse effects after discontinuation of finasteride, and many have improvement of adverse effects over time with continued finasteride use. However, some studies describe a subset of patients with persistent adverse effects after discontinuation... Level 1 evidence evaluating sexual dysfunction as a primary outcome was available for finasteride. }}</ref><ref name="Traish_2020">{{Cite journal | vauthors = Traish AM | title = Post-finasteride syndrome: a surmountable challenge for clinicians | journal = Fertility and Sterility | volume = 113 | issue = 1 | pages = 21–50 | date = January 2020 | pmid = 32033719 | doi = 10.1016/j.fertnstert.2019.11.030 | s2cid = 211064052 | doi-access = free }}</ref> It may also hide the early symptoms of certain forms of [[prostate cancer]].<ref name="Varothai_2014" />

<!-- History, society, and culture -->
Finasteride was patented in 1984 and approved for medical use in 1992.<ref name="Fis2006">{{Cite book | vauthors = Fischer J, Ganellin CR | title = Analogue-based Drug Discovery | page = 483 | date = 2006 | url = https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA483 | publisher = John Wiley & Sons | isbn = 978-3-527-60749-5 | access-date = 7 May 2020 | archive-url = https://web.archive.org/web/20230110031701/https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA483 | archive-date = 10 January 2023 | url-status = live }}</ref> It is available as a [[generic medication]].<ref name="Sataloff_2015">{{Cite book | vauthors = Sataloff RT, Sclafani AP | title = Sataloff's Comprehensive Textbook of Otolaryngology: Head & Neck Surgery: Facial Plastic and Reconstructive Surgery | pages = 400– | date = 30 November 2015 | url = https://books.google.com/books?id=acswCwAAQBAJ&pg=PA400 | publisher = JP Medical Ltd | isbn = 978-93-5152-459-5 | access-date = 4 December 2017 | archive-url = https://web.archive.org/web/20230110031702/https://books.google.com/books?id=acswCwAAQBAJ&pg=PA400 | archive-date = 10 January 2023 | url-status = live }}</ref> In 2023, it was the 91st most commonly prescribed medication in the United States, with more than 7{{nbsp}}million prescriptions.<ref name="Top300Drugs">{{cite web | title=Top 300 of 2023 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=12 August 2025 | archive-date=12 August 2025 | archive-url=https://web.archive.org/web/20250812130026/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{Cite web | title = Finasteride Drug Usage Statistics, United States, 2013–2022 | url = https://clincalc.com/DrugStats/Drugs/Finasteride | access-date = 18 August 2025 | website = ClinCalc }}</ref>
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==Medical uses==
Finasteride has been used for the treatment of symptomatic [[benign prostatic hyperplasia]] (BPH)<ref name="Proscar FDA label" /> and for the treatment of male [[pattern hair loss]].<ref name="Propecia FDA label" />

===Enlarged prostate===
Physicians sometimes prescribe finasteride for the treatment of benign prostatic hyperplasia, informally known as an enlarged [[prostate]].<ref>{{Cite journal | vauthors = Smith AB, Carson CC | title = Finasteride in the treatment of patients with benign prostatic hyperplasia: a review | journal = Therapeutics and Clinical Risk Management | volume = 5 | issue = 3 | pages = 535–545 | date = June 2009 | pmid = 19707263 | pmc = 2710385 | doi = 10.2147/tcrm.s6195 | doi-access = free }}</ref> 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.<ref>{{Cite web | title = Benign prostate enlargement | date = 20 October 2017 | 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 }}</ref>

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.<ref name="Corona_2017">{{Cite journal | vauthors = Corona G, Tirabassi G, Santi D, Maseroli E, Gacci M, Dicuio M, Sforza A, Mannucci E, Maggi M | 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 | date = July 2017 | pmid = 28453908 | doi = 10.1111/andr.12353 | s2cid = 3577324 | doi-access = free | hdl = 11380/1132897 | hdl-access = free }}</ref>

===Pattern hair loss===
Finasteride is also used to treat [[pattern hair loss|male pattern baldness]] (androgenic alopecia), a condition that develops in up to 80% of Caucasian men aged 70 and over.<ref name="Kanti_2018">{{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 | 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 | date = January 2018 | pmid = 29178529 | doi = 10.1111/jdv.14624 | doi-access = free }}</ref><ref name="Propecia FDA label">{{Cite web | title = Propecia – finasteride tablet, film coated | date = 15 November 2019 | 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 }}</ref> 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.<ref>{{Cite journal | vauthors = Adil A, Godwin M | 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 | date = July 2017 | pmid = 28396101 | doi = 10.1016/j.jaad.2017.02.054 | s2cid = 46036459 }}</ref> Treatment with finasteride slows further hair loss.<ref name="Habif_2015">{{Cite book | vauthors = Habif TP | title = Clinical Dermatology | pages = 934– | date = 23 April 2015 | url = https://books.google.com/books?id=N_D5CQAAQBAJ&pg=PA934 | publisher = Elsevier Health Sciences | isbn = 978-0-323-26607-9 | 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 }}</ref> Two meta-analyses<ref>{{Cite journal | vauthors = Adil A, Godwin M | 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 | date = 2017-07-01 | pmid = 28396101 | doi = 10.1016/j.jaad.2017.02.054 | url = https://www.jaad.org/article/S0190-9622(17)30306-7/abstract | language = English | issn = 0190-9622 }}</ref><ref>{{Cite journal | vauthors = Gupta A, Mays R, Dotzert M, Versteeg S, Shear N, Piguet V | title = Efficacy of non-surgical treatments for androgenetic alopecia: a systematic review and network meta-analysis | journal = Journal of the European Academy of Dermatology and Venereology  | volume = 32 | issue = 12 | pages = 2112–2125 | date = 2018 | pmid = 29797431 | doi = 10.1111/jdv.15081 | url = https://onlinelibrary.wiley.com/doi/abs/10.1111/jdv.15081 | language = en | issn = 1468-3083 | url-access = subscription }}</ref> found finasteride's efficacy caused about 15% hair regrowth. Specifically oral finasteride was observed to regrow about 18 hair follicles in a square centimeter area of scalp. In comparison a full head of hair usually has 120 hair follicles per square centimeter scalp.<ref>{{Cite journal | vauthors = Han SS, Park YT, Yoo JH, Park TH, Kim KJ | title = Comparative Evaluation of Hair Density and Grouped Hair Unit Pattern between Androgenetic Alopecia and Normal Scalp | journal = Annals of Dermatology | volume = 16 | issue = 1 | pages = 1–8 | date = 2004-01-01 | doi = 10.5021/ad.2004.16.1.1 | language = English | issn = 1013-9087 }}</ref>

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 [[Hair follicle|anagen phase]] by inhibiting and sometimes reversing miniaturization of the hair follicle. Finasteride is most effective on the [[Crown (anatomy)|crown]] but can reduce hair loss in all areas of the scalp.<ref>{{Cite journal | vauthors = Yim E, Nole KL, Tosti A | title = 5α-Reductase inhibitors in androgenetic alopecia | journal = Current Opinion in Endocrinology, Diabetes, and Obesity | volume = 21 | issue = 6 | pages = 493–498 | date = December 2014 | pmid = 25268732 | doi = 10.1097/MED.0000000000000112 | s2cid = 30008068 }}</ref><ref>{{Cite journal | vauthors = Gupta AK, Charrette A | 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 = 156–161 | date = April 2014 | pmid = 23768246 | doi = 10.3109/09546634.2013.813011 | s2cid = 24833568 }}</ref> Finasteride has also been tested for pattern hair loss in women; however, the results were no better than placebo.<ref name="Levy_2013">{{Cite journal | vauthors = Levy LL, Emer JJ | title = Female pattern alopecia: current perspectives | journal = International Journal of Women's Health | volume = 5 | pages = 541–556 | date = August 2013 | pmid = 24039457 | pmc = 3769411 | doi = 10.2147/IJWH.S49337 | doi-access = free }}</ref> Finasteride is less effective in the treatment of scalp hair loss than [[dutasteride]].<ref name="Dhurat_2020">{{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 | title = 5-Alpha reductase inhibitors in androgenetic alopecia: Shifting paradigms, current concepts, comparative efficacy, and safety | journal = Dermatologic Therapy | volume = 33 | issue = 3 | article-number = e13379 | date = May 2020 | pmid = 32279398 | doi = 10.1111/dth.13379 | s2cid = 215748750 | doi-access = free }}</ref><ref name="Zhou_2019">{{Cite journal | vauthors = Zhou Z, Song S, Gao Z, Wu J, Ma J, Cui Y | title = The efficacy and safety of dutasteride compared with finasteride in treating men with androgenetic alopecia: a systematic review and meta-analysis | journal = Clinical Interventions in Aging | volume = 14 | pages = 399–406 | date = 2019 | pmid = 30863034 | pmc = 6388756 | doi = 10.2147/CIA.S192435 | doi-access = free }}</ref>

===Prostate cancer===
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.<ref>{{Cite web | title = Finasteride for Prostate Cancer Prevention | date = 28 August 2013 | 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 }}</ref>

A 2010 review found a 25% reduction in the risk of prostate cancer with 5α-reductase inhibitor.<ref name="Wilt_2010">{{Cite journal | vauthors = Wilt TJ, Macdonald R, Hagerty K, Schellhammer P, Tacklind J, Somerfield MR, Kramer BS | title = 5-α-Reductase inhibitors for prostate cancer chemoprevention: an updated Cochrane systematic review | journal = BJU International | volume = 106 | issue = 10 | pages = 1444–1451 | date = Nov 2010 | pmid = 20977593 | doi = 10.1111/j.1464-410X.2010.09714.x | s2cid = 22178061 | doi-access = free }}</ref> A follow-up study of the [[Medicare (United States)|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.<ref>{{Cite journal | vauthors = Unger JM, Hershman DL, Till C, Tangen CM, Barlow WE, Ramsey SD, Goodman PJ, Thompson IM | 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 | date = March 2018 | pmid = 29534197 | pmc = 6235685 | doi = 10.1093/jnci/djy035 }}</ref> 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.<ref name="Hirshburg_2016">{{Cite journal | vauthors = Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS | title = Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review | journal = The Journal of Clinical and Aesthetic Dermatology | volume = 9 | issue = 7 | pages = 56–62 | date = Jul 2016 | pmid = 27672412 | pmc = 5023004 }}</ref> No impact of 5-α-reductase inhibitor on survival has been found in people with prostate cancer.<ref name="Hirshburg_2016" />

===Excessive hair growth===
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.<ref name="BlumePeytavi_2008" />

==Adverse effects==

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."<ref name="Tacklind_2010" /> {{as of|2016}}, fresh evidence suggested such effects, along with disturbed [[neurosteroid]] production, may persist after finasteride use is stopped.<ref>{{Cite book | vauthors = Patisaul HB, Belcher SM | chapter = Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors | volume = 1 | page = 127 | date = 18 May 2017 | doi = 10.1093/acprof:oso/9780199935734.003.0005 | chapter-url = https://oxford.universitypressscholarship.com/view/10.1093/acprof:oso/9780199935734.001.0001/acprof-9780199935734-chapter-5 | title = Oxford Scholarship Online | publisher = Oxford University Press | isbn = 978-0-19-067852-4 }}</ref>

Finasteride is contraindicated in pregnancy.<ref name="fdapropecia2014">{{Cite web | title = PROPECIA Prescribing Information | url = https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/020788s024lbl.pdf | 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. }}</ref><ref name="fdaproscar2010">{{Cite web | title = PROSCAR Prescribing Information | url = https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020180s037lbl.pdf | 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. }}</ref> 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.<ref>{{Cite web | title = Deferral of Blood and Plasma donors – Medications | date = 28 July 1993 | url = https://www.fda.gov/media/70929/download | 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]] }}</ref>

The FDA has added a warning to [[5α-reductase inhibitor]]s 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.<ref>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 }}</ref><ref name="Walsh_2010">{{Cite journal | vauthors = Walsh PC | title = Chemoprevention of prostate cancer | journal = The New England Journal of Medicine | volume = 362 | issue = 13 | pages = 1237–1238 | date = April 2010 | pmid = 20357287 | doi = 10.1056/NEJMe1001045 }}</ref> Although overall incidence of male breast cancer in clinical trials for finasteride 5&nbsp;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.<ref name="Propecia FDA label" /><ref>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 }}</ref> A 2018 [[meta-analysis]] found no higher risk of breast cancer with 5α-reductase inhibitors.<ref name="Wang_2018">{{Cite journal | vauthors = Wang J, Zhao S, Luo L, Li E, Li X, Zhao Z | title = 5-alpha Reductase Inhibitors and risk of male breast cancer: a systematic review and meta-analysis | journal = International Braz J Urol | volume = 44 | issue = 5 | pages = 865–873 | date = 2018 | pmid = 29697934 | pmc = 6237523 | doi = 10.1590/S1677-5538.IBJU.2017.0531 }}</ref> Some men develop [[gynecomastia]] (breast development or enlargement) following finasteride usage.<ref name="Narula_2014">{{Cite journal | vauthors = Narula HS, Carlson HE | title = Gynaecomastia-pathophysiology, diagnosis and treatment | journal = Nature Reviews. Endocrinology | volume = 10 | issue = 11 | pages = 684–698 | date = August 2014 | pmid = 25112235 | doi = 10.1038/nrendo.2014.139 | url = https://touroscholar.touro.edu/tuncom_pubs/54 | url-status = live | 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 | url-access = subscription }}</ref><ref name="Deepinder_2012">{{Cite journal | vauthors = Deepinder F, Braunstein GD | title = Drug-induced gynecomastia: an evidence-based review. | journal = Expert Opinion on Drug Safety | volume = 11 | issue = 5 | pages = 779–795 | date = Sep 2012 | pmid = 22862307 | doi = 10.1517/14740338.2012.712109 | s2cid = 22938364 }}</ref><ref>{{Cite journal | vauthors = Chung EY, Ruospo M, Natale P, Bolignano D, Navaneethan SD, Palmer SC, Strippoli GF | 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 | article-number = CD007004 | date = October 2020 | pmid = 33107592 | pmc = 8094274 | doi = 10.1002/14651858.CD007004.pub4 }}</ref><ref>{{Cite journal | vauthors = Aiman U, Haseeen MA, Rahman SZ | title = Gynecomastia: An ADR due to drug interaction | journal = Indian Journal of Pharmacology | volume = 41 | issue = 6 | pages = 286–287 | date = December 2009 | pmid = 20407562 | pmc = 2846505 | doi = 10.4103/0253-7613.59929 | doi-access = free }}</ref> The risk of gynecomastia with 5α-reductase inhibitors is low at about 1.5%.<ref name="Trost_2013" /> Depressive symptoms and suicidality have been reported.<ref name="Locci_2017">{{Cite journal | vauthors = Locci A, Pinna G | title = Neurosteroid biosynthesis downregulation and changes in GABAA receptor subunit composition: A biomarker axis in stress-induced cognitive and emotional impairment | journal = British Journal of Pharmacology | volume = 174 | issue = 19 | pages = 3226–3241 | date = Oct 2017 | pmid = 28456011 | pmc = 5595768 | doi = 10.1111/bph.13843 }}</ref>

===Sexual adverse effects===
Use of finasteride is associated with an increased risk of [[sexual dysfunction]] including [[erectile dysfunction]], [[Hypoactive sexual desire disorder|decreased libido]] and ejaculatory dysfunction.<ref name="Lee_2019">{{Cite journal | vauthors = Lee S, Lee YB, Choe SJ, Lee WS | title = Adverse Sexual Effects of Treatment with Finasteride or Dutasteride for Male Androgenetic Alopecia: A Systematic Review and Meta-analysis | journal = Acta Dermato-venereologica | volume = 99 | issue = 1 | pages = 12–17 | date = Jan 2019 | pmid = 30206635 | doi = 10.2340/00015555-3035 | doi-access = free }}</ref><ref name="Zakhem_2019" /> 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.<ref name="Gur_2013">{{Cite journal | vauthors = Gur S, Kadowitz PJ, Hellstrom WJ | 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 | date = January 2013 | pmid = 23173718 | doi = 10.1517/14740338.2013.742885 | s2cid = 11624116 }}</ref>

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

====Finasteride for androgenetic alopecia (hair loss in men)====
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.<ref name="fdapropecia2014" />{{rp|17}}

In addition, finasteride has been reported in [[case reports]] to cause sexual problems that persist after stopping the medication.<ref name="Traish_2020" /><ref name="Zakhem_2019a" /> 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."<ref name="fdapropecia2014" />{{rp|17}}<ref name="Varothai_2014" /><ref>{{Cite web | title = Questions and Answers: Finasteride Label Changes | date = 11 April 2012 | last = FDA | url = https://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm299754.htm | 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 }}</ref><ref name="Trost_2013">{{Cite journal | vauthors = Trost L, Saitz TR, Hellstrom WJ | title = Side Effects of 5-Alpha Reductase Inhibitors: A Comprehensive Review | journal = Sexual Medicine Reviews | volume = 1 | issue = 1 | pages = 24–41 | date = May 2013 | pmid = 27784557 | doi = 10.1002/smrj.3 }}</ref>

In 2025, the [[European Medicines Agency]] confirmed that suicidal thoughts can occur as a side effect of the hair-loss treatment finasteride and similar [[dutasteride]].<ref>{{Cite web | title = Measures to minimise risk of suicidal thoughts with finasteride and dutasteride medicines {{!}} European Medicines Agency (EMA)|date=2025-05-08|url=https://www.ema.europa.eu/en/news/measures-minimise-risk-suicidal-thoughts-finasteride-dutasteride-medicines?utm_campaign=pharmalittle&utm_medium=email&_hsenc=p2ANqtz-9JLW6HNR5XFTP5FkII12F04t1_sJXOIjfq5ZdFFZcUQQDA1tzuHs2UawyLA3ivYCrJM8JBoFNEGMBSR0zTRxOLkSpYBw&_hsmi=360720080&utm_content=360720080&utm_source=hs_email|access-date=2025-05-10|website=www.ema.europa.eu|language=en}}</ref> The majority of these reports involved patients taking the 1&nbsp;mg dosage, typically prescribed for [[androgenetic alopecia]], a hormone-related form of hair loss.<ref>{{Cite news | title = EU drugs regulator confirms suicidal thoughts as side effect of hair loss drug | date = 8 May 2025 | url = https://www.reuters.com/business/healthcare-pharmaceuticals/eu-drugs-regulator-confirms-suicidal-thoughts-side-effect-anti-hair-loss-drug-2025-05-08/ | work = Reuters }}</ref> However, the agency noted that the precise frequency of this adverse effect could not be determined from the data available. In October 2024, the EMA had initiated a review of both finasteride and dutasteride due to concerns over potential links to suicidal ideation.<ref>{{Cite web | title = Meeting highlights from the Pharmacovigilance Risk Assessment Committee (PRAC) 30 September-3 October 2024 {{!}} European Medicines Agency (EMA)|date=2024-10-04|url=https://www.ema.europa.eu/en/news/meeting-highlights-pharmacovigilance-risk-assessment-committee-prac-30-september-3-october-2024|access-date=2025-05-10|website=www.ema.europa.eu|language=en}}</ref> While finasteride—marketed by [[Organon & Co.|Organon]] as Propecia—already includes warnings about possible psychiatric effects, the EMA stated that the evidence did not support a similar link for dutasteride, sold by GSK under the brand name Avodart.<ref>{{Cite web | title = Finasteride- and dutasteride-containing medicinal products - referral {{!}} European Medicines Agency (EMA)|date=2024-10-04|url=https://www.ema.europa.eu/en/medicines/human/referrals/finasteride-dutasteride-containing-medicinal-products|access-date=2025-05-10|website=www.ema.europa.eu|language=en}}</ref>

==== Finasteride for benign prostatic hyperplasia ====
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.<ref name="fdaproscar2010" />{{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.<ref name="Tacklind_2010" />

===Long-term===
Finasteride may cause persistent adverse sexual, neurological, and physical effects in a subset of men.<ref name="Zakhem_2019a" /> A 2019 systematic review 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.<ref name="Zakhem_2019a" /> A separate 2017 retrospective review of nearly 12,000 patients found 1.4% developed persistent (lasting at least 90 days after stopping Finasteride) ED, with this dropping to 0.8% for 16-42 year olds.<ref>{{Cite journal | vauthors = Kiguradze T, Temps WH, Yarnold PR, Cashy J, Brannigan RE, Nardone B, Micali G, West DP, Belknap SM | title = Persistent erectile dysfunction in men exposed to the 5α-reductase inhibitors, finasteride, or dutasteride | journal = PeerJ | volume = 5 | article-number = e3020 | date = 9 March 2017 | pmid = 28289563 | pmc = 5346286 | doi = 10.7717/peerj.3020 | doi-access = free }}</ref>

=== Post-finasteride syndrome ===
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 persistent symptoms.<ref name="Traish_2020" />

Individuals claiming to experience PFS report sexual, neurological, hormonal, and psychological side effects that persist for an extended period after stopping the drug.<ref name="Margo_2012">{{Cite web | vauthors = Margo J | title = Looking at care with a critical eye | date = 26 September 2012 | 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 }}</ref> 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]].<ref name="Maksym_2019" /> 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.<ref name="Pompili_2021">{{Cite journal | vauthors = Pompili M, Magistri C, Maddalena S, Mellini C, Persechino S, Baldessarini RJ | title = Risk of Depression Associated With Finasteride Treatment | journal = Journal of Clinical Psychopharmacology | volume = 41 | issue = 3 | pages = 304–309 | date = 1 May 2021 | pmid = 33814544 | doi = 10.1097/JCP.0000000000001379 | s2cid = 233028103 }}</ref>

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".<ref name="Gray_2019">{{Cite journal | vauthors = Gray SL, Semla TP | title = Post-finasteride syndrome | journal = BMJ | location = Clinical Research Ed. | volume = 366 | article-number = l5047 | date = August 2019 | pmid = 31399423 | doi = 10.1136/bmj.l5047 | s2cid = 199518161 }}</ref> 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.<ref name="Traish_2020" /> There is no known underlying biological mechanism for the proposed syndrome, and its incidence is unclear.<ref name="Gray_2019" /> A lack of clear diagnostic criteria and the variable reporting fraction in different healthcare settings make the problem challenging to evaluate.<ref name="Maksym_2019">{{Cite journal | vauthors = Maksym RB, Kajdy A, Rabijewski M | title = Post-finasteride syndrome – does it really exist? | journal = The Aging Male | volume = 22 | issue = 4 | pages = 250–259 | date = December 2019 | pmid = 30651009 | doi = 10.1080/13685538.2018.1548589 | s2cid = 58569946 | doi-access = free }}</ref>

In 2016 Merck was a defendant in approximately 1,370 [[product liability]] lawsuits which had been filed by customers alleging they had experienced persistent sexual side-effects following cessation of treatment with finasteride.<ref>{{Cite news | vauthors = Marchalik D | title = Watch for these potential side effects in drug Trump reportedly takes for hair loss | date = 4 February 2017 | 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 }}</ref> Most cases had been settled by 2018, when Merck paid a lump sum of US$4.3 million to be distributed. {{As of|September 2019}}, 25 cases remained outstanding in the United States.<ref name="reu">{{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. }}</ref> 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.<ref name="reu" />

==Overdose==
Finasteride has been studied in humans at single doses of up to 400&nbsp;mg and at continuous dosages of up to 80&nbsp;mg/day for three months, without adverse effects observed.<ref name="Propecia FDA label" /><ref name="Proscar FDA label" /><ref name="Frye_2006">{{Cite journal | vauthors = Frye SV | title = Discovery and clinical development of dutasteride, a potent dual 5alpha-reductase inhibitor | journal = Current Topics in Medicinal Chemistry | volume = 6 | issue = 5 | pages = 405–421 | date = 2006 | pmid = 16719800 | doi = 10.2174/156802606776743101 }}</ref> There is no specific recommended [[antidote]] for finasteride overdose.<ref name="Propecia FDA label" /><ref name="Proscar FDA label" />

==Interactions==
No significant [[drug interaction]]s have been observed between finasteride and a limited selection of medications.<ref name="Sudduth_1993">{{Cite journal | vauthors = Sudduth SL, Koronkowski MJ | title = Finasteride: the first 5α-reductase inhibitor | journal = Pharmacotherapy | volume = 13 | issue = 4 | pages = 309–25; discussion 325–9 | date = 1993 | pmid = 7689728 | doi = 10.1002/j.1875-9114.1993.tb02739.x | s2cid = 71103672 }}</ref>

==Pharmacology==

===Pharmacodynamics===
Finasteride is a [[5α-reductase inhibitor]].<ref name="Propecia FDA label" /><ref name="Lemke_2008" /> It is specifically a [[binding selectivity|selective]] [[enzyme inhibitor|inhibitor]] of the [[SRD5A2|type II]] and [[SRD5A3|III]] [[isoform]]s of the [[enzyme]].<ref name="Lemke_2008" /><ref name="Yamana_2010">{{Cite journal | vauthors = Yamana K, Labrie F, Luu-The V | 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 = 293–299 | date = August 2010 | pmid = 25961201 | doi = 10.1515/hmbci.2010.035 | s2cid = 28841145 }}</ref><ref name="Aggarwal_2010">{{Cite journal | vauthors = Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M | title = An overview on 5alpha-reductase inhibitors | journal = Steroids | volume = 75 | issue = 2 | pages = 109–153 | date = February 2010 | pmid = 19879888 | doi = 10.1016/j.steroids.2009.10.005 | s2cid = 44363501 }}</ref> By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the [[potency (pharmacology)|potent]] [[androgen]] [[dihydrotestosterone]] (DHT) from its [[precursor (biochemistry)|precursor]] [[testosterone]] in certain [[tissue (biology)|tissue]]s in the body such as the [[prostate gland]], [[skin]], and [[hair follicle]]s.<ref name="Lemke_2008" /><ref name="Azzouni_2012">{{Cite journal | vauthors = Azzouni F, Godoy A, Li Y, Mohler J | title = The 5 alpha-reductase isozyme family: a review of basic biology and their role in human diseases | journal = Advances in Urology | volume = 2012 | article-number = 530121 | year = 2012 | pmid = 22235201 | pmc = 3253436 | doi = 10.1155/2012/530121 | doi-access = free }}</ref> As such, finasteride is a type of [[antiandrogen]], or more specifically, an [[androgen synthesis inhibitor]].<ref name="Preedy_2012">{{Cite book | vauthors = Preedy VR | title = Handbook of Hair in Health and Disease | pages = 89– | year = 2012 | url = https://books.google.com/books?id=7N3nEX6eL_MC&pg=PA89 | publisher = Springer Science & Business Media | isbn = 978-90-8686-728-8 | 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 }}</ref><ref name="Wu_2012">{{Cite book | vauthors = Wu JJ | title = Comprehensive Dermatologic Drug Therapy E-Book | pages = 361– | date = 18 October 2012 | url = https://books.google.com/books?id=Tqpsm5WKKlcC&pg=PA361 | publisher = Elsevier Health Sciences | isbn = 978-1-4557-3801-4 | 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 }}</ref> However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the [[androgen receptor]].<ref name="Clapauch_2017">{{Cite book | vauthors = Clapauch R, Weiss RV, Rech CM | chapter = Testosterone and Women | title = Testosterone | pages = 319–351 | year = 2017 | doi = 10.1007/978-3-319-46086-4_17 | publisher = Springer | isbn = 978-3-319-46084-0 | quote = Finasteride is not actually an antiandrogen but a 5α-reductase inhibitor. }}</ref>

Finasteride results in a decrease of circulating DHT levels by about 65–70% with an oral dosage of 5&nbsp;mg/day and of DHT levels in the prostate gland by up to 80–90% with an oral dosage of 1 or 5&nbsp;mg/day.<ref name="Yamana_2010" /><ref name="Bartsch_2000">{{Cite journal | vauthors = Bartsch G, Rittmaster RS, Klocker H | title = Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia | journal = European Urology | volume = 37 | issue = 4 | pages = 367–380 | date = April 2000 | pmid = 10765065 | doi = 10.1159/000020181 | s2cid = 25793400 }}</ref><ref name="Kim_2018">{{Cite journal | vauthors = Kim EH, Brockman JA, Andriole GL | 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 | date = January 2018 | pmid = 29379733 | pmc = 5780290 | doi = 10.1016/j.ajur.2017.11.005 }}</ref> 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%.<ref name="Rittmaster_1994">{{Cite journal | vauthors = Rittmaster RS | title = Finasteride | journal = The New England Journal of Medicine | volume = 330 | issue = 2 | pages = 120–125 | date = January 1994 | pmid = 7505051 | doi = 10.1056/NEJM199401133300208 }}</ref><ref name="Libecco_2004">{{Cite journal | vauthors = Libecco JF, Bergfeld WF | title = Finasteride in the treatment of alopecia | journal = Expert Opinion on Pharmacotherapy | volume = 5 | issue = 4 | pages = 933–940 | date = April 2004 | pmid = 15102575 | doi = 10.1517/14656566.5.4.933 | s2cid = 24296644 }}</ref> An oral dosage of finasteride of only 0.2&nbsp;mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2&nbsp;mg/day relative to 72.2% for 5&nbsp;mg/day).<ref name="Libecco_2004" /><ref name="Shapiro_2003">{{Cite journal | vauthors = Shapiro J, Kaufman KD | title = Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss) | journal = The Journal of Investigative Dermatology. Symposium Proceedings | volume = 8 | issue = 1 | pages = 20–23 | date = June 2003 | pmid = 12894990 | doi = 10.1046/j.1523-1747.2003.12167.x | doi-access = free }}</ref> Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the [[SRD5A1|5α-reductase type I]] isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ({{abbrlink|IC<sub>50</sub>|Half-maximal inhibitory concentration}} = 313&nbsp;nM and 11&nbsp;nM, respectively).<ref name="Propecia FDA label" /><ref name="Lemke_2008" /> 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%.<ref name="Yamana_2010" /> In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit [[5β-reductase]] (AKR1D1).<ref name="Drury_2009">{{Cite journal | vauthors = Drury JE, Di Costanzo L, Penning TM, Christianson DW | 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 | date = July 2009 | pmid = 19515843 | pmc = 2740403 | doi = 10.1074/jbc.C109.016931 | author-link4 = David W. Christianson | doi-access = free }}</ref> 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.<ref name="Drury_2009" />

As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear.<ref name="Azzouni_2012" /> This is because different investigators have obtained varying results with different [[reagent]]s, methods, and tissues examined.<ref name="Azzouni_2012" /> However, the different isozymes of 5α-reductase appear to be widely expressed, with notable tissues including the prostate gland, [[seminal vesicle]]s, [[testicle|testes]], [[epididymis|epididymides]], skin, hair follicles, [[liver]], [[kidney]]s, and [[brain]], among others.<ref name="Azzouni_2012" />

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.<ref name="Bostwick_2014">{{Cite book | vauthors = Bostwick DG, Cheng L | title = Urologic Surgical Pathology E-Book | pages = 402– | date = 24 January 2014 | url = https://books.google.com/books?id=wrHQAgAAQBAJ&pg=PA402 | publisher = Elsevier Health Sciences | isbn = 978-0-323-08619-6 }}</ref> Inhibition of 5α-reductase also reduces [[epididymis|epididymal]] weight, and decreases motility and normal morphology of spermatozoa in the epididymis.<ref name="Robaire_2006">{{Cite journal | vauthors = Robaire B, Henderson NA | title = Actions of 5alpha-reductase inhibitors on the epididymis | journal = Molecular and Cellular Endocrinology | volume = 250 | issue = 1–2 | pages = 190–195 | date = May 2006 | pmid = 16476520 | doi = 10.1016/j.mce.2005.12.044 | s2cid = 53464391 }}</ref>

[[Neurosteroid]]s like [[3α-androstanediol]] (derived from DHT) and [[allopregnanolone]] (derived from [[progesterone]]) activate the [[GABAA receptor|GABA<sub>A</sub> 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<sub>A</sub> activity. Reduction of GABA<sub>A</sub> receptor activation by these neurosteroids has been implicated in [[depression (mood)|depression]], [[anxiety]], and [[sexual dysfunction]].<ref name="Finn_2006">{{Cite journal | vauthors = Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM | title = A new look at the 5alpha-reductase inhibitor finasteride | journal = CNS Drug Reviews | volume = 12 | issue = 1 | pages = 53–76 | year = 2006 | pmid = 16834758 | pmc = 6741762 | doi = 10.1111/j.1527-3458.2006.00053.x }}</ref><ref name="Romer_2010">{{Cite journal | vauthors = Römer B, Gass P | title = Finasteride-induced depression: new insights into possible pathomechanisms | journal = Journal of Cosmetic Dermatology | volume = 9 | issue = 4 | pages = 331–332 | date = December 2010 | pmid = 21122055 | doi = 10.1111/j.1473-2165.2010.00533.x | url = https://zenodo.org/record/896024 | url-status = live | 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 }}</ref><ref name="Gunn_2011">{{Cite journal | vauthors = Gunn BG, Brown AR, Lambert JJ, Belelli D | title = Neurosteroids and GABA(A) Receptor Interactions: A Focus on Stress | journal = Frontiers in Neuroscience | volume = 5 | page = 131 | year = 2011 | pmid = 22164129 | pmc = 3230140 | doi = 10.3389/fnins.2011.00131 | doi-access = free }}</ref>

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]].<ref name="Traish_2011">{{Cite journal | vauthors = Traish AM, Hassani J, Guay AT, Zitzmann M, Hansen ML | title = Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients | journal = The Journal of Sexual Medicine | volume = 8 | issue = 3 | pages = 872–884 | date = March 2011 | pmid = 21176115 | doi = 10.1111/j.1743-6109.2010.02157.x }}</ref><ref name="Duskova_2009">{{Cite journal | vauthors = Dusková M, Hill M, Hanus M, Matousková M, Stárka L | title = Finasteride treatment and neuroactive steroid formation | journal = Prague Medical Report | volume = 110 | issue = 3 | pages = 222–230 | date = 2009 | pmid = 19655698 }}</ref><ref name="Duskova_2010">{{Cite journal | vauthors = Dušková M, Hill M, Stárka L | title = The influence of low dose finasteride, a type II 5α-reductase inhibitor, on circulating neuroactive steroids | journal = Hormone Molecular Biology and Clinical Investigation | volume = 1 | issue = 2 | pages = 95–102 | date = January 2010 | pmid = 25961975 | doi = 10.1515/HMBCI.2010.010 | s2cid = 28578077 }}</ref> Pregnanolone acts as a potent GABA<sub>A</sub> receptor positive allosteric modulator similarly to allopregnanolone.<ref name="Reddy_2003">{{Cite journal | vauthors = Reddy DS | title = Pharmacology of endogenous neuroactive steroids | journal = Critical Reviews in Neurobiology | volume = 15 | issue = 3–4 | pages = 197–234 | date = 2003 | pmid = 15248811 | doi = 10.1615/critrevneurobiol.v15.i34.20 }}</ref>

===Pharmacokinetics===
The mean [[oral administration|oral]] [[bioavailability]] of finasteride is approximately 65%.<ref name="Lemke_2008" /> The [[absorption (pharmacokinetics)|absorption]] of finasteride is not affected by food.<ref name="Propecia FDA label" /><ref name="Proscar FDA label" /> At [[steady-state]] with 1&nbsp;mg/day finasteride, mean [[Cmax (pharmacology)|peak]] concentrations of finasteride were 9.2&nbsp;ng/mL (25&nbsp;nmol/L).<ref name="Propecia FDA label" /> Conversely, following a single 5&nbsp;mg dose of finasteride, mean peak levels of finasteride were 37&nbsp;ng/mL (99&nbsp;nmol/L), and plasma concentrations increased by 47–54% following 2.5&nbsp;weeks of continued daily administration.<ref name="Proscar FDA label" /> The [[volume of distribution]] of finasteride is 76&nbsp;L.<ref name="Lemke_2008" /> Its [[plasma protein binding]] is 90%.<ref name="Lemke_2008" /> The drug has been found to cross the [[blood–brain barrier]], whereas levels in [[semen]] were found to be undetectable.<ref name="Lemke_2008" />

Finasteride is extensively [[metabolism|metabolized]] in the [[liver]], first by [[hydroxylation]] via [[CYP3A4]] and then by [[aldehyde dehydrogenase]].<ref name="Lemke_2008" /> It has two major [[metabolite]]s, which are the ''tert''-[[butyl group|butyl]] [[side chain]] monohydroxylated and [[carboxylic acid|monocarboxylic acid]] metabolites.<ref name="Lemke_2008" /> These metabolites show approximately 20% of the inhibitory activity of finasteride on 5α-reductase.<ref name="Lemke_2008" /> Hence, the metabolites of finasteride are not particularly active.<ref name="Lemke_2008" /> The drug has a [[terminal half-life]] of 5 to 6&nbsp;hours in adult men (18–60&nbsp;years of age) and a terminal half-life of 8&nbsp;hours or more in elderly men (more than 70&nbsp;years of age).<ref name="Lemke_2008" /> It is [[elimination (pharmacology)|eliminated]] as its metabolites 57% in the [[feces]] and 40% in the [[urine]].<ref name="Lemke_2008" />

==Chemistry==
{{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 compound|synthetic]] [[androstane]] [[steroid]] and [[4-azasteroid]].<ref name="Sudduth_1993" /><ref name="Tian_1994">{{Cite journal | vauthors = Tian G, Stuart JD, Moss ML, Domanico PL, Bramson HN, Patel IR, Kadwell SH, Overton LK, Kost TA, Mook RA | 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 = 2291–2296 | date = Mar 1994 | pmid = 8117686 | doi = 10.1021/bi00174a041 }}</ref> It is an [[structural analogue|analogue]] of androgen [[steroid hormone]]s like testosterone and DHT.<ref name="Sudduth_1993" /> As an unconjugated steroid, finasteride is a highly [[lipophilic]] compound.<ref name="Sudduth_1993" /><ref name="Azeem_2009">{{Cite journal | vauthors = Azeem A, Khan ZI, Aqil M, Ahmad FJ, Khar RK, Talegaonkar S | title = Microemulsions as a surrogate carrier for dermal drug delivery | journal = Drug Development and Industrial Pharmacy | volume = 35 | issue = 5 | pages = 525–547 | date = May 2009 | pmid = 19016057 | doi = 10.1080/03639040802448646 | s2cid = 205563538 }}</ref>

==History==
In 1942, James Hamilton observed that prepubertal castration prevents the later development of male pattern baldness in mature men.<ref>{{Cite journal | vauthors = Hamilton J | title = Male hormone stimulation is prerequisite and an incitant in common baldness | journal = American Journal of Anatomy | volume = 71 | issue = 3 | pages = 451–480 | year = 1942 | doi = 10.1002/aja.1000710306 }}</ref> 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 [[Ambiguity|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.<ref>{{Cite news | title = The extraordinary case of the Guevedoces | date = 20 September 2015 | 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 }}</ref> Her research group found these children shared a [[genetic mutation]], causing [[5-alpha-reductase deficiency|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.<ref name="ImperatoMcGinley_1974">{{Cite journal | vauthors = Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE | title = Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism | journal = Science | location = New York, N.Y. | volume = 186 | issue = 4170 | pages = 1213–1215 | date = December 1974 | pmid = 4432067 | doi = 10.1126/science.186.4170.1213 | bibcode = 1974Sci...186.1213I | s2cid = 36427689 }}</ref><ref>{{Cite journal | vauthors = Isfort AH, Emerick JE, Paz RA | title = 5-Alpha-Reductase Deficiency | journal = WebMD | date = 11 November 2016 | url = http://emedicine.medscape.com/article/924291-overview#showall | url-status = live | 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 }}</ref>

In 1975, copies of Imperato-McGinley's presentation were seen by [[P. Roy Vagelos]], who was then serving as [[Merck & Co.|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.<ref>{{Cite news | vauthors = Freudenheim M | title = Keeping the Pipeline Filled at Merck | date = 16 February 1992 | 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 }}</ref>

Finasteride was developed by Merck under the code name MK-906.<ref name="Sudduth_1993" /> 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.<ref name="Cordes_2014">{{Cite book | vauthors = Cordes EH | title = Hallelujah Moments: Tales of Drug Discovery | year = 2014 | url = https://books.google.com/books?id=_G9VAgAAQBAJ | publisher = Oxford University Press | isbn = 978-0-19-933714-9 | 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 }}</ref> In 1992, finasteride (5&nbsp;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.<ref name="IPOInventor">{{Cite web | title = Past Inventor of the Year Award Winners | date = 18 March 2013 | 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 }}</ref> In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1&nbsp;mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia.<ref name="Burger_2003">{{Cite book | vauthors = Burger A, Abraham DJ | title = Burger's Medicinal Chemistry and Drug Discovery, Autocoids, Diagnostics, and Drugs from New Biology | page = 439 | date = 20 February 2003 | url = https://books.google.com/books?id=25ZUAAAAMAAJ | publisher = Wiley | isbn = 978-0-471-37030-7 | 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 }}</ref> It was the first 5α-reductase inhibitor to be introduced and was followed by [[dutasteride]] in 2001.<ref name="Doherty_2003">{{Cite book | vauthors = Doherty AM | title = Annual Reports in Medicinal Chemistry | pages = 353– | year = 2003 | url = https://books.google.com/books?id=ECfQ6D5JLusC&pg=PA353 | publisher = Academic Press | isbn = 978-0-12-040538-1 | 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 }}</ref> The first study of finasteride in the treatment of hirsutism in women was published in 1994.<ref name="DiamantiKandarakis_1995">{{Cite journal | vauthors = Diamanti-Kandarakis E, Tolis G, Duleba AJ | title = Androgens and therapeutic aspects of antiandrogens in women | journal = Journal of the Society for Gynecologic Investigation | volume = 2 | issue = 4 | pages = 577–592 | date = 1995 | pmid = 9420861 | doi = 10.1177/107155769500200401 | s2cid = 32242838 }}</ref>

==Society and culture==

===Generic names===
''Finasteride'' is the [[generic term|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}}.<ref name="IndexNominum2000">{{Cite book | title = Index Nominum 2000: International Drug Directory | page = 443 | year = 2000 | url = https://books.google.com/books?id=5GpcTQD_L2oC&pg=PP1 | publisher = Taylor & Francis | isbn = 978-3-88763-075-1 }}</ref><ref name="Morton_2012">{{Cite book | vauthors = Morton IK, Hall JM | title = Concise Dictionary of Pharmacological Agents: Properties and Synonyms | pages = 121– | date = 6 December 2012 | url = https://books.google.com/books?id=tsjrCAAAQBAJ&pg=PA121 | publisher = Springer Science & Business Media | isbn = 978-94-011-4439-1 }}</ref><ref name="Bycroft_2013">{{Cite book | vauthors = Bycroft BW, Payne DJ | title = Dictionary of Antibiotics and Related Substances: with CD-ROM, Second Edition | pages = 816– | date = 9 August 2013 | url = https://books.google.com/books?id=x0hZDwAAQBAJ&pg=PA816 | publisher = CRC Press | isbn = 978-1-4822-8215-3 | 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 }}</ref><ref name="cite0191d294">{{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 }}</ref> It is also known by its former developmental code names ''MK-906'', ''YM-152'', and ''L-652,931''.<ref name="IndexNominum2000" /><ref name="Morton_2012" /><ref name="Bycroft_2013" /><ref name="cite0191d294" />

===Brand names===
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]].<ref name="cite0191d294" /> There is 1&nbsp;mg of finasteride in Propecia and 5&nbsp;mg in Proscar. Merck's patent on finasteride for the treatment of BPH expired in June 2006.<ref>{{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 | 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 }}</ref> Merck was awarded a separate patent for the use of finasteride to treat pattern hair loss and it expired in November 2013.<ref>{{Cite web | title = Patent Expiration for Propecia | last = FDA | url = http://www.accessdata.fda.gov/scripts/cder/ob/docs/patexclnew.cfm?Appl_No=020788&Product_No=001&table1=OB_Rx | 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 }}</ref> Finasteride is also marketed under a variety of other brand names throughout the world.<ref name="cite0191d294" />

===Athletics===
From 2005 to 2009, the [[World Anti-Doping Agency]] banned finasteride because it was discovered that the drug could be used to mask [[anabolic steroids|steroid]] abuse.<ref>{{Cite news | vauthors = Sandomir R | title = Skin Deep; Fighting Baldness, and Now an Olympic Ban | date = 19 January 2006 | 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 }}</ref> It was removed from the list effective 1 January 2009, after improvements in testing methods made the ban unnecessary.<ref name="Staff_2008">{{Cite web | title = WADA removes Finasteride from ban list | date = 28 October 2008 | last = Staff | url = http://www.theaustralian.com.au/archive/news/wada-removes-finasteride-from-ban-list/story-e6frg7mo-1111117876628?nk=0afe1009eb17d32f8f4d47ff9e091a08 | website = The Australian }}</ref> Athletes who used finasteride and were banned from international competition include [[Skeleton (sport)|skeleton racer]] [[Zach Lund]], [[Bobsleigh|bobsledder]] [[Sebastien Gattuso]], [[Football (soccer)|footballer]] [[Romário]], and [[Goaltender|ice hockey goaltender]] [[José Théodore]].<ref name="Staff_2008" /><ref>{{Cite web | title = WADA takes Romario's drug off banned list | date = 9 October 2008 | last = Staff | url = http://www.smh.com.au/zoom/archive/d229652 | 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 }}</ref>

===Miscellaneous===
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.<ref>{{Cite web | title = Deferral of Blood and Plasma donors – Medications | date = 28 July 1993 | url = https://www.fda.gov/downloads/BiologicsBloodVaccines/.../UCM062813.pdf | 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]] }}</ref> The UK also has a one-month deferral period.<ref>{{Cite web | title = Anti-Androgens – Joint United Kingdom Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee | date = 1 June 2007 | 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 }}</ref>

==Research==
Preliminary research suggests that [[topical medication|topical]] finasteride may be effective in the treatment of pattern hair loss.<ref name="Lee_2018">{{Cite journal | vauthors = Lee SW, Juhasz M, Mobasher P, Ekelem C, Mesinkovska NA | 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 | date = April 2018 | pmid = 29601622 | pmc = 6609098 }}</ref><ref name="Marks_2020">{{Cite journal | vauthors = Marks DH, Prasad S, De Souza B, Burns LJ, Senna MM | title = Topical Antiandrogen Therapies for Androgenetic Alopecia and Acne Vulgaris | journal = American Journal of Clinical Dermatology | volume = 21 | issue = 2 | pages = 245–254 | date = April 2020 | pmid = 31832993 | doi = 10.1007/s40257-019-00493-z | s2cid = 209331373 }}</ref> Topical finasteride, like the oral preparation, reduces serum DHT.<ref name="Marks_2020" /><ref name="Lee_2018" />

DHT may be involved in the cause of [[acne]], and 5α-reductase inhibitors might be effective in the treatment of the condition.<ref name="Danby_2015">{{Cite book | vauthors = Danby FW | title = Acne: Causes and Practical Management | pages = 147– | date = 27 January 2015 | url = https://books.google.com/books?id=Z1yFBQAAQBAJ&pg=PA147 | publisher = John Wiley & Sons | isbn = 978-1-118-23277-4 | 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 }}</ref><ref name="Marchetti_2013">{{Cite journal | vauthors = Marchetti PM, Barth JH | title = Clinical biochemistry of dihydrotestosterone | journal = Annals of Clinical Biochemistry | volume = 50 | issue = Pt 2 | pages = 95–107 | date = March 2013 | pmid = 23431485 | doi = 10.1258/acb.2012.012159 | s2cid = 8325257 | doi-access = free }}</ref> A small [[retrospective study]] reported that finasteride was effective in the treatment of acne in women with normal [[testosterone]] levels.<ref name="Hu_2019">{{Cite journal | vauthors = Hu AC, Chapman LW, Mesinkovska NA | title = The efficacy and use of finasteride in women: a systematic review | journal = International Journal of Dermatology | volume = 58 | issue = 7 | pages = 759–776 | date = January 2019 | pmid = 30604525 | doi = 10.1111/ijd.14370 | s2cid = 58555908 }}</ref><ref name="Marchetti_2013" /> 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 [[hyperandrogenism|high androgen levels]].<ref name="Hu_2019" />

[[Androgen]]s and [[estrogen]]s may be involved in the cause of [[hidradenitis suppurativa]] (acne inversa).<ref name="Alikhan_2009">{{Cite journal | vauthors = Alikhan A, Lynch PJ, Eisen DB | title = Hidradenitis suppurativa: a comprehensive review | journal = Journal of the American Academy of Dermatology | volume = 60 | issue = 4 | pages = 539–61; quiz 562–3 | date = April 2009 | pmid = 19293006 | doi = 10.1016/j.jaad.2008.11.911 }}</ref><ref name="Riis_2016">{{Cite journal | vauthors = Riis PT, Ring HC, Themstrup L, Jemec GB | title = The Role of Androgens and Estrogens in Hidradenitis Suppurativa – A Systematic Review | journal = Acta Dermatovenerologica Croatica  | volume = 24 | issue = 4 | pages = 239–249 | date = December 2016 | pmid = 28128074 }}</ref> Two [[case series]] have reported that finasteride is effective in the treatment of hidradenitis suppurativa in girls and women.<ref name="Hu_2019" />

Finasteride and other antiandrogens might be useful in the treatment of [[obsessive–compulsive disorder]] (OCD), but more research is needed.<ref name="Nomani_2019">{{Cite journal | vauthors = Nomani H, Mohammadpour AH, Moallem SM, YazdanAbad MJ, Barreto GE, Sahebkar A | title = Anti-androgen drugs in the treatment of obsessive-compulsive disorder: a systematic review | journal = Current Medicinal Chemistry | volume = 27 | issue = 40 | pages = 6825–6836 | date = December 2019 | pmid = 31814547 | doi = 10.2174/0929867326666191209142209 | s2cid = 208956450 }}</ref>

==References==
{{Reflist}}

{{Androgens and antiandrogens}}
{{Drugs used in benign prostatic hypertrophy}}
{{Other dermatological preparations}}
{{Merck&Co}}
{{Portal bar | Medicine}}

[[Category:Wikipedia medicine articles ready to translate]]
[[Category:5α-Reductase inhibitors]]
[[Category:Androstanes]]
[[Category:Drugs developed by Merck & Co.]]
[[Category:Carboxamides]]
[[Category:Hair loss medications]]
[[Category:Hair removal]]
[[Category:Delta-lactams]]
[[Category:Teratogens]]
[[Category:Tert-butyl compounds]]
[[Category:Heterocyclic compounds with 4 rings]]