View source for Antiandrogen

{{Short description|Class of pharmaceutical drugs}}
{{Infobox drug class
| Image = Bicalutamide.svg
| ImageClass = skin-invert-image
| Alt =
| Caption = [[Bicalutamide]], a [[nonsteroidal antiandrogen]] and the most widely used [[androgen receptor]] [[receptor antagonist|antagonist]] in the treatment of [[prostate cancer]].
| Width = 250px
| Synonyms = Androgen antagonists; Androgen blockers; Testosterone blockers
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| Use = • Men and boys: [[Prostate cancer]]; [[Benign prostatic hyperplasia]]; [[Scalp hair loss]]; [[Paraphilia]]s; [[Hypersexuality]]; [[Sex offender]]s; [[Precocious puberty]]; [[Priapism]]<br />• Women and girls: [[Acne]]; [[Seborrhea]]; [[Hidradenitis suppurativa]]; [[Hirsutism]]; [[Scalp hair loss]]; [[Hyperandrogenism]]; [[Transgender hormone therapy]]
| ATC_prefix = L02BB
| Biological_target = [[Androgen receptor]]; [[Progesterone receptor]]; [[Estrogen receptor]]; [[Gonadotropin-releasing hormone receptor|{{abbr|GnRH|Gonadotropin-releasing hormone}} receptor]]; [[5α-Reductase]]; [[CYP17A1]] (17α-hydroxylase/<wbr />17,20-lyase); [[P450scc]]; Others
| Chemical_class = [[Steroid]]al; [[Nonsteroidal]]; [[Peptide]]
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| Drugs.com =
| Consumer_Reports =
| medicinenet =
| rxlist =
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| MeshID = D000726
}}

'''Antiandrogens''', also known as '''androgen antagonists''' or '''testosterone blockers''', are a class of [[drug]]s that prevent [[androgen]]s like [[testosterone]] and [[dihydrotestosterone]] (DHT) from mediating their [[biological effect]]s in the body. They act by [[receptor antagonist|blocking]] the [[androgen receptor]] (AR) and/or [[steroidogenesis inhibitor|inhibiting]] or [[antigonadotropin|suppressing]] androgen [[biosynthesis|production]].<ref name = Mowszowicz>{{Cite journal | vauthors = Mowszowicz I | title = Antiandrogens. Mechanisms and paradoxical effects | journal = Ann. Endocrinol. | location = Paris | pages = 50(3):189–99 | year = 1989 | pmid = 2530930 | volume = 50 | issue = 3}}</ref><ref name="Brueggemeier2006">{{cite book| vauthors = Brueggemeier RW |title=Encyclopedia of Molecular Cell Biology and Molecular Medicine|chapter=Sex Hormones (Male): Analogs and Antagonists|year=2006|publisher=Wiley-VCH Verlag GmbH & Co. KGaA |doi=10.1002/3527600906.mcb.200500066|isbn=3527600906}}</ref> They can be thought of as the functional opposites of AR [[agonist]]s, for instance androgens and [[anabolic steroid]]s (AAS) like testosterone, DHT, and [[nandrolone]] and [[selective androgen receptor modulator]]s (SARMs) like [[enobosarm]]. Antiandrogens are one of three types of [[sex-hormonal agent|sex hormone antagonist]]s, the others being [[antiestrogen]]s and [[antiprogestogen]]s.<ref name="Nath2006">{{cite book| vauthors = Nath JL |title=Using Medical Terminology: A Practical Approach|url=https://archive.org/details/usingmedicalterm0000nath|url-access=registration|year=2006|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-4868-1|pages=[https://archive.org/details/usingmedicalterm0000nath/page/977 977]–}}</ref>

Antiandrogens are used to treat an assortment of [[androgen-dependent condition]]s.<ref name="pmid31712062">{{cite journal | vauthors = Student S, Hejmo T, Poterała-Hejmo A, Leśniak A, Bułdak R | title = Anti-androgen hormonal therapy for cancer and other diseases | journal = Eur. J. Pharmacol. | volume = 866 | pages = 172783 | date = January 2020 | pmid = 31712062 | doi = 10.1016/j.ejphar.2019.172783 | doi-access = free }}</ref> In men, antiandrogens are used in the treatment of [[prostate cancer]], [[benign prostatic hyperplasia|enlarged prostate]], [[pattern hair loss|scalp hair loss]], [[hypersexuality|overly high sex drive]], [[paraphilia|unusual and problematic sexual urges]], and [[precocious puberty|early puberty]].<ref name="pmid31712062" /><ref name="pmid16845534">{{Cite journal | vauthors = Gillatt D | title = Antiandrogen treatments in locally advanced prostate cancer: are they all the same? | journal = J Cancer Res Clin Oncol | volume = 1 | pages = S17-26 | year = 2006 | pmid = 16845534 | doi = 10.1007/s00432-006-0133-5| s2cid = 23888640 }}</ref> In women, antiandrogens are used to treat [[acne]], [[seborrhea]], [[hirsutism|excessive hair growth]], scalp hair loss, and [[hyperandrogenism|high androgen levels]], such as those that occur in [[polycystic ovary syndrome]] (PCOS).<ref name="pmid31712062" /> Antiandrogens are also used as a component of [[feminizing hormone therapy]] for [[transgender women]] and as [[puberty blocker]]s in [[transgender youth|transgender girl]]s.<ref name="pmid31712062" />

[[Side effect]]s of antiandrogens depend on the type of antiandrogen and the specific antiandrogen in question. In any case, common side effects of antiandrogens in men include [[breast tenderness]], [[gynecomastia|breast enlargement]], [[feminization (biology)|feminization]], [[hot flash]]es, [[sexual dysfunction]], [[infertility]], and [[osteoporosis]]. In women, antiandrogens are much better [[tolerability|tolerated]], and antiandrogens that work only by directly blocking androgens are associated with minimal side effects. However, because [[estrogen]]s are made from androgens in the body, antiandrogens that suppress androgen production can cause [[hypoestrogenism|low estrogen levels]] and associated symptoms like hot flashes, [[menstrual irregularities]], and osteoporosis in [[premenopause|premenopausal]] women.

There are a few different major types of antiandrogens.<ref name="pmid11502457">{{cite journal | vauthors = Lieberman R | title = Androgen deprivation therapy for prostate cancer chemoprevention: current status and future directions for agent development | journal = Urology | volume = 58 | issue = 2 Suppl 1 | pages = 83–90 | year = 2001 | pmid = 11502457 | doi = 10.1016/s0090-4295(01)01247-x| quote = There are several classes of antiandrogens including (1) antigonadotropins (eg, LHRH agonists/antagonists, synthetic estrogens [diethylstilbestrol]); (2) nonsteroidal androgen-receptor antagonists (eg, flutamide, bicalutamide, nilutamide); (3) steroidal agents with mixed actions (eg, cyproterone acetate); (4) adrenal androgen inhibitors (eg, ketoconazole, hydrocortisone); (5) steroidal agents that inhibit androgen biosynthesis (eg, 5α-reductase inhibitors (type II) and dual-acting 5α-reductase inhibitors); [...]}}</ref> These include AR [[receptor antagonist|antagonist]]s, [[androgen synthesis inhibitor]]s, and [[antigonadotropin]]s.<ref name="pmid11502457" /> AR antagonists work by directly blocking the effects of androgens, while androgen synthesis inhibitors and antigonadotropins work by lowering androgen levels.<ref name="pmid11502457" /> AR antagonists can be further divided into [[steroidal antiandrogen]]s and [[nonsteroidal antiandrogen]]s; androgen synthesis inhibitors can be further divided mostly into [[CYP17A1 inhibitor]]s and [[5α-reductase inhibitor]]s; and antigonadotropins can be further divided into [[gonadotropin-releasing hormone modulator]]s (GnRH modulators), [[progestogen]]s, and [[estrogen (medication)|estrogen]]s.<ref name="pmid11502457" /><ref name="SchröderRadlmaier2009">{{cite book | vauthors = Schröder FH, Radlmaier A | chapter = Steroidal Antiandrogens | pages = [https://archive.org/details/hormonetherapybr00crai/page/n328 325]–346 | doi = 10.1007/978-1-59259-152-7_15 | title = Hormone Therapy in Breast and Prostate Cancer | url = https://archive.org/details/hormonetherapybr00crai | url-access = limited | veditors = Jordan VC, Furr BA | year = 2009 | publisher = Humana Press | isbn = 978-1-60761-471-5}}</ref><ref name="KolvenbagFurr2009">{{cite book | vauthors = Kolvenbag GJ, Furr BJ  | chapter = Nonsteroidal Antiandrogens | pages = [https://archive.org/details/hormonetherapybr00crai/page/n350 347]–368 | doi = 10.1007/978-1-59259-152-7_16 | title = Hormone Therapy in Breast and Prostate Cancer | url = https://archive.org/details/hormonetherapybr00crai | url-access = limited | veditors = Jordan VC, Furr BJ | year = 2009 | publisher = Humana Press | isbn = 978-1-60761-471-5}}</ref>

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==Medical uses==
Antiandrogens are used in the treatment of an assortment of [[androgen-dependent condition]]s in both males and females.<ref name="pmid31712062" /><ref name="pmid2147859">{{cite journal | vauthors = Sciarra F, Toscano V, Concolino G, Di Silverio F | title = Antiandrogens: clinical applications | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 37 | issue = 3 | pages = 349–362 | date = November 1990 | pmid = 2147859 | doi = 10.1016/0960-0760(90)90484-3 | s2cid = 20274398 }}</ref> They are used to treat men with [[prostate cancer]], [[benign prostatic hyperplasia]], [[pattern hair loss]], [[hypersexuality]], [[paraphilia]]s, and [[priapism]], as well as boys with [[precocious puberty]].<ref name="pmid2147859" /><ref name="pmid20092449">{{cite journal | vauthors = Broderick GA, Kadioglu A, Bivalacqua TJ, Ghanem H, Nehra A, Shamloul R | title = Priapism: pathogenesis, epidemiology, and management | journal = The Journal of Sexual Medicine | volume = 7 | issue = 1 Pt 2 | pages = 476–500 | date = January 2010 | pmid = 20092449 | doi = 10.1111/j.1743-6109.2009.01625.x }}</ref><ref name="SteinbergForget2009">{{cite book| vauthors = Steinberg MH, Forget BG, Higgs DR, Weatherall DJ |title=Disorders of Hemoglobin: Genetics, Pathophysiology, and Clinical Management|url=https://books.google.com/books?id=5UcgAwAAQBAJ&pg=PA476|date=17 August 2009|publisher=Cambridge University Press|isbn=978-1-139-48080-2|pages=476–}}</ref> In women and girls, antiandrogens are used to treat [[acne vulgaris|acne]], [[seborrhea]], [[hidradenitis suppurativa]], [[hirsutism]], and [[hyperandrogenism]].<ref name="pmid2147859" /><ref name="pmid16828411">{{cite journal | vauthors = Essah PA, Wickham EP, Nunley JR, Nestler JE | title = Dermatology of androgen-related disorders | journal = Clinics in Dermatology | volume = 24 | issue = 4 | pages = 289–298 | year = 2006 | pmid = 16828411 | doi = 10.1016/j.clindermatol.2006.04.004 }}</ref><ref name="RabeGrunwald2009">{{cite journal| vauthors = Rabe T, Grunwald K, Feldmann K, Runnebaum B |title=Treatment of hyperandrogenism in women|journal=Gynecological Endocrinology|volume=10|issue=sup3|year=2009|pages=1–44|issn=0951-3590|doi=10.3109/09513599609045658}}</ref> Antiandrogens are also used in [[transgender women]] as a component of [[feminizing hormone therapy]] and as [[puberty blocker]]s in [[transgender youth|transgender girl]]s.<ref name="pmid21714669" /><ref name="pmid25404716" />

===Men and boys===

====Prostate cancer====
{{See also|Management of prostate cancer#Hormonal therapy|Androgen deprivation therapy}}

Androgens like testosterone and particularly DHT are importantly involved in the development and progression of prostate cancer.<ref name="pmid27019626">{{cite journal | vauthors = Wadosky KM, Koochekpour S | title = Therapeutic Rationales, Progresses, Failures, and Future Directions for Advanced Prostate Cancer | journal = Int. J. Biol. Sci. | volume = 12 | issue = 4 | pages = 409–26 | year = 2016 | pmid = 27019626 | pmc = 4807161 | doi = 10.7150/ijbs.14090 }}</ref> They act as [[growth factor]]s in the [[prostate gland]], stimulating [[cell division]] and [[tissue growth]].<ref name="pmid27019626" /> In accordance, therapeutic modalities that reduce androgen signaling in the prostate gland, referred to collectively as [[androgen deprivation therapy]], are able to significantly slow the course of prostate cancer and extend life in men with the disease.<ref name="pmid27019626" /> Although antiandrogens are effective in slowing the progression of prostate cancer, they are not generally curative, and with time, the disease adapts and androgen deprivation therapy eventually becomes ineffective.<ref name="pmid21680543">{{cite journal | vauthors = Massard C, Fizazi K | title = Targeting continued androgen receptor signaling in prostate cancer | journal = Clin. Cancer Res. | volume = 17 | issue = 12 | pages = 3876–83 | year = 2011 | pmid = 21680543 | doi = 10.1158/1078-0432.CCR-10-2815 | doi-access = free }}</ref> When this occurs, other treatment approaches, such as [[chemotherapy]], may be considered.<ref name="pmid21680543" />

The most common methods of androgen deprivation therapy currently employed to treat prostate cancer are [[castration]] (with a GnRH modulator or [[orchiectomy]]), nonsteroidal antiandrogens, and the androgen synthesis inhibitor [[abiraterone acetate]].<ref name="pmid27019626" /> Castration may be used alone or in combination with one of the other two treatments.<ref name="pmid27019626" /><ref name="pmid17604502">{{cite journal | vauthors = Msaouel P, Diamanti E, Tzanela M, Koutsilieris M | title = Luteinising hormone-releasing hormone antagonists in prostate cancer therapy | journal = Expert Opin Emerg Drugs | volume = 12 | issue = 2 | pages = 285–99 | year = 2007 | pmid = 17604502 | doi = 10.1517/14728214.12.2.285 | s2cid = 41988320 }}</ref> When castration is combined with a nonsteroidal antiandrogen like [[bicalutamide]], this strategy is referred to as [[combined androgen blockade]] (also known as complete or maximal androgen blockade).<ref name="pmid27019626" /><ref name="pmid21091846">{{Cite journal | vauthors = Akaza H | title = Combined androgen blockade for prostate cancer: review of efficacy, safety, and cost-effectiveness | journal = Cancer Science | volume = 102 | pages = 51–6 |date=Jan 2011 | pmid = 21091846 | doi = 10.1111/j.1349-7006.2010.01774.x | issue = 1| s2cid = 38486547 | doi-access = free }}</ref> [[Enzalutamide]], [[apalutamide]], and abiraterone acetate are specifically approved for use in combination with castration to treat castration-resistant prostate cancer.<ref name="pmid27019626" /><ref name="pmid24390422">{{cite journal | vauthors = Mateo J, Smith A, Ong M, de Bono JS | title = Novel drugs targeting the androgen receptor pathway in prostate cancer | journal = Cancer Metastasis Rev. | volume = 33 | issue = 2–3 | pages = 567–79 | year = 2014 | pmid = 24390422 | doi = 10.1007/s10555-013-9472-2 | s2cid = 13980764 }}</ref> Monotherapy with the nonsteroidal antiandrogen bicalutamide is also used in the treatment of prostate cancer as an alternative to castration with comparable effectiveness but with a different and potentially advantageous side effect profile.<ref name="pmid27019626" /><ref name="pmid11121992" /><ref name="pmid11502439">{{cite journal |vauthors=Kolvenbag GJ, Iversen P, Newling DW | title = Antiandrogen monotherapy: a new form of treatment for patients with prostate cancer | journal = Urology | volume = 58 | issue = 2 Suppl 1 | pages = 16–23 |date=August 2001 | pmid = 11502439 | doi = 10.1016/s0090-4295(01)01237-7}}</ref>

[[High-dose estrogen]] was the first functional antiandrogen used to treat prostate cancer. It was widely used, but has largely been abandoned for this indication in favor of newer agents with improved safety profiles and fewer feminizing side effects.<ref name="pmid12667881">{{cite journal | vauthors = Mcleod DG | title = Hormonal therapy: historical perspective to future directions | journal = Urology | volume = 61 | issue = 2 Suppl 1 | pages = 3–7 | year = 2003 | pmid = 12667881 | doi = 10.1016/s0090-4295(02)02393-2 }}</ref> [[Cyproterone acetate]] was developed subsequently to high-dose estrogen and is the only steroidal antiandrogen that has been widely used in the treatment of prostate cancer,<ref name="SmithWilliams2005">{{cite book | vauthors = Smith HJ, Williams H | title = Smith and Williams' Introduction to the Principles of Drug Design and Action, Fourth Edition |url=https://books.google.com/books?id=P2W6B9FQRKsC&pg=PA489 |date=10 October 2005 |publisher=CRC Press |isbn=978-0-203-30415-0 |pages=489–}}</ref> but it has largely been replaced by nonsteroidal antiandrogens, which are newer and have greater effectiveness, tolerability, and safety.<ref name="ChabnerLongo2010">{{cite book|vauthors=Chabner BA, Longo DL|title=Cancer Chemotherapy and Biotherapy: Principles and Practice|url=https://books.google.com/books?id=WL4arNFsQa8C&pg=PA680|date=8 November 2010|publisher=Lippincott Williams & Wilkins|isbn=978-1-60547-431-1|pages=679–680|quote=From a structural standpoint, antiandrogens are classified as steroidal, including cyproterone [acetate] (Androcur) and megestrol [acetate], or nonsteroidal, including flutamide (Eulexin, others), bicalutamide (Casodex), and nilutamide (Nilandron). The steroidal antiandrogens are rarely used.|access-date=27 December 2016|archive-date=10 January 2023|archive-url=https://web.archive.org/web/20230110224032/https://books.google.com/books?id=WL4arNFsQa8C&pg=PA680|url-status=live}}</ref><ref name="KaliksDel Giglio2008">{{cite journal | vauthors = Kaliks RA, Del Giglio A | title = Management of advanced prostate cancer | journal = Revista da Associação Médica Brasileira | volume = 54 | issue = 2 | pages = 178–82 | year = 2008 | pmid = 18506331 | doi = 10.1590/S0104-42302008000200025 | url = http://www.scielo.br/pdf/ramb/v54n2/a25v54n2.pdf | doi-access = free | access-date = 2016-12-27 | archive-date = 2017-05-10 | archive-url = https://web.archive.org/web/20170510112152/http://www.scielo.br/pdf/ramb/v54n2/a25v54n2.pdf | url-status = live }}</ref> Bicalutamide, as well as enzalutamide, have largely replaced the earlier nonsteroidal antiandrogens [[flutamide]] and [[nilutamide]], which are now little used.<ref name="pmid21091846" /><ref name="HHS2010">{{citation | title = Bicalutamide BPCA Drug Use Review in the Pediatric Population | vauthors = Chang S | publisher = [[United States Department of Health and Human Services|U.S. Department of Health and Human Service]] | date = 10 March 2010 | access-date = 20 July 2016 | url = https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/PediatricAdvisoryCommittee/UCM214400.pdf | archive-date = 24 October 2016 | archive-url = https://web.archive.org/web/20161024181831/https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/PediatricAdvisoryCommittee/UCM214400.pdf | url-status = live }}</ref><ref name="Gulley2011">{{cite book | vauthors = Gulley JL |title=Prostate Cancer |url=https://books.google.com/books?id=WJkjgbRJe3EC&pg=PT81 |year=2011 |publisher=Demos Medical Publishing |isbn=978-1-935281-91-7 |pages=81–}}</ref><ref name="Moser2008">{{cite book |vauthors=Lutz M |title=Controversies in the Treatment of Prostate Cancer |url=https://books.google.com/books?id=4J4OCRyHWRYC&pg=PA41 |date=1 January 2008 |publisher=Karger Medical and Scientific Publishers |isbn=978-3-8055-8524-8 |pages=41–42 |access-date=27 December 2016 |archive-date=12 January 2023 |archive-url=https://web.archive.org/web/20230112173054/https://books.google.com/books?id=4J4OCRyHWRYC&pg=PA41 |url-status=live }}</ref><ref name="Demnos2011">{{cite book |title=Prostate Cancer |url=https://books.google.com/books?id=WJkjgbRJe3EC&pg=PA505 |date=20 December 2011 |publisher=Demos Medical Publishing |isbn=978-1-935281-91-7 |pages=505–}}</ref> The earlier androgen synthesis inhibitors [[aminoglutethimide]] and [[ketoconazole]] have only limitedly been used in the treatment of prostate cancer due to [[toxicity]] concerns and have been replaced by abiraterone acetate.<ref name="FiggChau2010" />

In addition to active treatment of prostate cancer, antiandrogens are effective as [[prophylaxis]] (preventatives) in reducing the risk of ever developing prostate cancer.<ref name="pmid21604953">{{cite journal | vauthors = Rittmaster RS | title = Chemoprevention of prostate cancer | journal = Acta Oncol | volume = 50 | issue = Suppl 1 | pages = 127–36 | year = 2011 | pmid = 21604953 | doi = 10.3109/0284186X.2010.527367 | doi-access = free }}</ref> Antiandrogens have only limitedly been assessed for this purpose, but the 5α-reductase inhibitors [[finasteride]] and [[dutasteride]] and the steroidal AR antagonist [[spironolactone]] have been associated with significantly reduced risk of prostate cancer.<ref name="pmid21604953" /><ref name="pmid27735065">{{cite journal | vauthors = Mackenzie IS, Morant SV, Wei L, Thompson AM, MacDonald TM | title = Spironolactone use and risk of incident cancers: a retrospective, matched cohort study | journal = Br J Clin Pharmacol | volume = 83| issue = 3| pages = 653–663| year = 2016 | pmid = 27735065 | doi = 10.1111/bcp.13152 | pmc = 5306481 }}</ref> In addition, it is notable that prostate cancer is extremely rare in transgender women who have been on feminizing hormone therapy for an extended period of time.<ref name="pmid19509099">{{cite journal | vauthors = Hembree WC, Cohen-Kettenis P, Delemarre-van de Waal HA, Gooren LJ, Meyer WJ, Spack NP, Tangpricha V, Montori VM | title = Endocrine treatment of transsexual persons: an Endocrine Society clinical practice guideline | journal = J. Clin. Endocrinol. Metab. | volume = 94 | issue = 9 | pages = 3132–54 | year = 2009 | pmid = 19509099 | doi = 10.1210/jc.2009-0345 | doi-access = free }}</ref><ref name="pmid24329588">{{cite journal | vauthors = Gooren L, Morgentaler A | title = Prostate cancer incidence in orchidectomised male-to-female transsexual persons treated with oestrogens | journal = Andrologia | volume = 46 | issue = 10 | pages = 1156–60 | year = 2014 | pmid = 24329588 | doi = 10.1111/and.12208 | s2cid = 1445627 | doi-access = free }}</ref><ref name="pmid24032068">{{cite journal | vauthors = Turo R, Jallad S, Prescott S, Cross WR | title = Metastatic prostate cancer in transsexual diagnosed after three decades of estrogen therapy | journal = Can Urol Assoc J | volume = 7 | issue = 7–8 | pages = E544–6 | year = 2013 | pmid = 24032068 | pmc = 3758950 | doi = 10.5489/cuaj.175 }}</ref>

====Enlarged prostate====
{{See also|Benign prostatic hyperplasia#5α-Reductase inhibitors}}

The 5α-reductase inhibitors [[finasteride]] and [[dutasteride]] are used to treat benign prostatic hyperplasia, a condition in which the prostate becomes enlarged and this results in urinary obstruction and discomfort.<ref name="pmid19030020">{{cite journal | vauthors = Dörsam J, Altwein J | title = 5alpha-Reductase inhibitor treatment of prostatic diseases: background and practical implications | journal = Prostate Cancer Prostatic Dis. | volume = 12 | issue = 2 | pages = 130–6 | year = 2009 | pmid = 19030020 | doi = 10.1038/pcan.2008.56 | doi-access = free }}</ref> They are effective because androgens act as growth factors in the prostate gland.<ref name="pmid19030020" /> The antiandrogens [[chlormadinone acetate]] and [[oxendolone]] and the functional antiandrogens [[allylestrenol]] and [[gestonorone caproate]] are also approved in some countries for the treatment of benign prostatic hyperplasia.<ref name="pmid12534901">{{cite journal | vauthors = Ishizuka O, Nishizawa O, Hirao Y, Ohshima S | title = Evidence-based meta-analysis of pharmacotherapy for benign prostatic hypertrophy | journal = Int. J. Urol. | volume = 9 | issue = 11 | pages = 607–12 | year = 2002 | pmid = 12534901 | doi = 10.1046/j.1442-2042.2002.00539.x| s2cid = 8249363 | doi-access = free }}</ref><ref name="RaspéBrosig2013">{{cite book| vauthors = Raspé G, Brosig W |title=International Symposium on the Treatment of Carcinoma of the Prostate, Berlin, November 13 to 15, 1969: Life Science Monographs|url=https://books.google.com/books?id=8RjLBAAAQBAJ&pg=PA165|date=22 October 2013|publisher=Elsevier|isbn=978-1-4831-8711-2|pages=165–}}</ref>

====Scalp hair loss====
{{See also|Management of hair loss#Antiandrogens}}

5α-Reductase inhibitors like finasteride, dutasteride, and [[alfatradiol]] and the [[topical]] nonsteroidal AR antagonist [[topilutamide]] (fluridil) are approved for the treatment of pattern hair loss, also known as scalp hair loss or baldness.<ref name="TrüebLee2014">{{cite book| vauthors = Trüeb RM, Lee WS |title=Male Alopecia: Guide to Successful Management|url=https://books.google.com/books?id=0ue5BAAAQBAJ&pg=PA93|date=13 February 2014|publisher=Springer Science & Business Media|isbn=978-3-319-03233-7|pages=91–93}}</ref> This condition is generally caused by androgens, so antiandrogens can slow or halt its progression.<ref name="BologniaJorizzo">{{cite book| vauthors = Bolognia JL, Jorizzo JL, Rapini RP |title=Dermatology|year=2003 |url=https://books.google.com/books?id=f2IwYiyh3YUC&pg=PT1072|publisher=Gulf Professional Publishing|isbn=9789997638991|pages=1072–}}</ref> Systemic antiandrogens besides 5α-reductase inhibitors are not generally used to treat scalp hair loss in males due to risks like feminization (e.g., gynecomastia) and sexual dysfunction.<ref name="Simpson1989">{{cite book| vauthors = Simpson NB |title=Pharmacology of the Skin II|volume=87 / 2|year=1989|pages=495–508|issn=0171-2004|doi=10.1007/978-3-642-74054-1_37|series=Handbook of Experimental Pharmacology|isbn=978-3-642-74056-5|chapter=The Effect of Drugs on Hair|publisher=Springer }}</ref><ref name="Unger1995">{{cite book| vauthors = Unger WP |chapter=Androgenetic alopecia and its treatment. A historical overview|pages=1–33|title=Hair Transplantation | edition =Third |url=https://books.google.com/books?id=_KxsAAAAMAAJ|date=1 February 1995|publisher=Taylor & Francis|isbn=978-0-8247-9363-0}}</ref><ref name="Rasmusson1986" /><ref name="Cormanevan der Meeren1981" /><ref name="pmid19297634">{{cite journal | vauthors = Giltay EJ, Gooren LJ | title = Potential side effects of androgen deprivation treatment in sex offenders | journal = The Journal of the American Academy of Psychiatry and the Law | volume = 37 | issue = 1 | pages = 53–58 | date = 2009 | pmid = 19297634 }}</ref><ref name="LamHempstead2012">{{cite book| vauthors = Lam SM, Hempstead BR, Williams EF |title=Aesthetic Medicine|chapter=Medical Management Options for Hair Loss|year=2012|pages=529–535|publisher=Springer |doi=10.1007/978-3-642-20113-4_41|isbn=978-3-642-20112-7}}</ref><ref name="Neumann1996" /> However, they have been assessed and reported to be effective for this indication.<ref name="Simpson1989"/><ref name="Unger1995"/><ref name="Coskey1984">{{cite journal | vauthors = Coskey RJ | title = Dermatologic therapy: December, 1982, through November, 1983 | journal = Journal of the American Academy of Dermatology | volume = 11 | issue = 1 | pages = 25–52 | date = July 1984 | pmid = 6376557 | doi = 10.1016/S0190-9622(84)80163-2 }}</ref>

====Acne====
Systemic antiandrogens are generally not used to treat acne in males due to their high risk of feminization (e.g., gynecomastia) and sexual dysfunction.<ref name="PlewigKligman2012">{{cite book| vauthors = Plewig G, Kligman AM |title= ACNE and ROSACEA|url=https://books.google.com/books?id=0cD-CAAAQBAJ&pg=PA687|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-59715-2|pages=687–}}</ref><ref name="AlldredgeCorelli2012">{{cite book| vauthors = Alldredge BK, Corelli RL, Ernst ME |title=Koda-Kimble and Young's Applied Therapeutics: The Clinical Use of Drugs|url=https://books.google.com/books?id=qcVpuHngXK0C&pg=PA952|date=1 February 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-60913-713-7|pages=952–}}</ref> However, they have been studied for acne in males and found to be effective.<ref name="WardBrogden1984">{{cite journal | vauthors = Ward A, Brogden RN, Heel RC, Speight TM, Avery GS | title = Isotretinoin. A review of its pharmacological properties and therapeutic efficacy in acne and other skin disorders | journal = Drugs | volume = 28 | issue = 1 | pages = 6–37 | date = July 1984 | pmid = 6235105 | doi = 10.2165/00003495-198428010-00002 }}</ref><ref name="Rasmusson1986">{{cite book| vauthors = Rasmusson GH |title= Chapter 18. Chemical Control of Androgen Action|volume=21|year=1986|pages=179–188|issn=0065-7743|doi=10.1016/S0065-7743(08)61128-8|series=Annual Reports in Medicinal Chemistry|publisher= Academic Press|isbn=9780120405213}}</ref><ref name="Cormanevan der Meeren1981">{{cite journal| vauthors = Cormane RH, van der Meeren HL |title=Cyproteronacetate in the management of severe acne in males|journal=Archives of Dermatological Research |volume=271 |issue=2 |year=1981 |pages=183–187 |issn=0340-3696|doi=10.1007/BF00412545|s2cid=12153042}}</ref><ref name="pmid2945742">{{cite journal | vauthors = Misch KJ, Dolman WF, Neild V, Rhodes EL | title = Response of male acne to antiandrogen therapy with cyproterone acetate | journal = Dermatologica | volume = 173 | issue = 3 | pages = 139–142 | date = 1986 | pmid = 2945742 | doi = 10.1159/000249236 }}</ref> [[Clascoterone]], a topical antiandrogen, is effective for acne in males and has been approved by the FDA in August 2020.<ref name="pmid31487336">{{cite journal | vauthors = Kircik LH | title = What's new in the management of acne vulgaris | journal = Cutis | volume = 104 | issue = 1 | pages = 48–52 | date = July 2019 | pmid = 31487336 | url = https://www.mdedge.com/dermatology/article/204308/acne/whats-new-management-acne-vulgaris | access-date = 2020-03-30 | archive-date = 2020-10-26 | archive-url = https://web.archive.org/web/20201026050003/https://www.mdedge.com/dermatology/article/204308/acne/whats-new-management-acne-vulgaris | url-status = live }}</ref><ref name="pmid27416311">{{cite journal | vauthors = Hassoun LA, Chahal DS, Sivamani RK, Larsen LN | title = The use of hormonal agents in the treatment of acne | journal = Seminars in Cutaneous Medicine and Surgery | volume = 35 | issue = 2 | pages = 68–73 | date = June 2016 | pmid = 27416311 | doi = 10.12788/j.sder.2016.027 | doi-broken-date = 1 November 2024 }}</ref><ref>{{Cite web |date=2020-08-28 |title=Cassiopea Receives FDA Approval for Winlevi® (clascoterone cream 1%), First-in-Class Topical Acne Treatment Targeting the Androgen Receptor - Cassiopea |url=https://www.cassiopea.com/2020/08/27/cassiopea-receives-fda-approval-for-winlevi-clascoterone-cream-1-first-in-class-topical-acne-treatment-targeting-the-androgen-receptor/ |access-date=2024-04-15 |archive-url=https://web.archive.org/web/20200828021558/https://www.cassiopea.com/2020/08/27/cassiopea-receives-fda-approval-for-winlevi-clascoterone-cream-1-first-in-class-topical-acne-treatment-targeting-the-androgen-receptor/ |archive-date=2020-08-28 }}</ref><ref>{{Cite web |title=Drugs@FDA: FDA-Approved Drugs |url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=213433 |access-date=2024-04-15 |website=www.accessdata.fda.gov |language=en}}</ref>

====Paraphilia====
{{See also|Paraphilia#Antiandrogens|Chemical castration#Treatment for sex offenders}}

Androgens increase [[sex drive]],<ref name="JonesLopez2013">{{cite book| vauthors = Jones RE, Lopez KH |title=Human Reproductive Biology|url=https://books.google.com/books?id=M4kEdSnS-pkC&pg=PA77|date=28 September 2013|publisher=Academic Press|isbn=978-0-12-382185-0|pages=77–}}</ref> and for this reason, antiandrogens are able to reduce sex drive in men.<ref name="pmid11221487">{{cite journal | vauthors = Bradford JM | title = The neurobiology, neuropharmacology, and pharmacological treatment of the paraphilias and compulsive sexual behaviour | journal = Can J Psychiatry | volume = 46 | issue = 1 | pages = 26–34 | year = 2001 | pmid = 11221487 | doi = 10.1177/070674370104600104| doi-access = free }}</ref><ref name="pmid19243704">{{cite journal | vauthors = Guay DR | title = Drug treatment of paraphilic and nonparaphilic sexual disorders | journal = Clin Ther | volume = 31 | issue = 1 | pages = 1–31 | year = 2009 | pmid = 19243704 | doi = 10.1016/j.clinthera.2009.01.009 }}</ref> In accordance, antiandrogens are used in the treatment of conditions such as [[hypersexuality]] (excessively high sex drive) and [[paraphilia]]s (atypical and sometimes societally unacceptable sexual interests) like [[pedophilia]] (sexual attraction to children).<ref name="pmid11221487" /><ref name="pmid19243704" /> They have been used to decrease sex drive in [[sex offender]]s so as to reduce the likelihood of [[recidivism]] (repeat offenses).<ref name="MarshallLaws2013">{{cite book| vauthors = Marshall WL, Laws DR, Barbaree HE |title=Handbook of Sexual Assault: Issues, Theories, and Treatment of the Offender|url=https://books.google.com/books?id=lkf2BwAAQBAJ&pg=PA297|date=21 November 2013|publisher=Springer Science & Business Media|isbn=978-1-4899-0915-2|pages=297–}}</ref> Antiandrogens used for these indications include [[cyproterone acetate]], [[medroxyprogesterone acetate]], and GnRH modulators.<ref name="StunkardBaum1989">{{cite book| vauthors = Stunkard AJ, Baum A |title=Eating, Sleeping, and Sex|url=https://books.google.com/books?id=bf-dRU-Ie9EC&pg=PA209 |year=1989|publisher=Psychology Press|isbn=978-0-8058-0280-1|pages=209–}}</ref><ref name="PhenixHoberman2015">{{cite book| vauthors = Phenix A, Hoberman HM |title=Sexual Offending: Predisposing Antecedents, Assessments and Management|url=https://books.google.com/books?id=NhEpCwAAQBAJ&pg=PA759|date=7 December 2015|publisher=Springer|isbn=978-1-4939-2416-5|pages=759–}}</ref>

====Early puberty====
Antiandrogens are used to treat [[precocious puberty]] in boys.<ref name="pmid18345393">{{cite journal | vauthors = Brito VN, Latronico AC, Arnhold IJ, Mendonça BB | title = Update on the etiology, diagnosis and therapeutic management of sexual precocity | journal = Arq Bras Endocrinol Metabol | volume = 52 | issue = 1 | pages = 18–31 | date = February 2008 | pmid = 18345393 | doi = 10.1590/S0004-27302008000100005 | doi-access = free }}</ref><ref name="pmid6205409">{{cite journal | vauthors = Tindall DJ, Chang CH, Lobl TJ, Cunningham GR | title = Androgen antagonists in androgen target tissues | journal = Pharmacol. Ther. | volume = 24 | issue = 3 | pages = 367–400 | date = 1984 | pmid = 6205409 | doi = 10.1016/0163-7258(84)90010-x}}</ref><ref name="pmid2462132">{{cite journal | vauthors = Namer M | title = Clinical applications of antiandrogens | journal = J. Steroid Biochem. | volume = 31 | issue = 4B | pages = 719–29 | date = October 1988 | pmid = 2462132 | doi = 10.1016/0022-4731(88)90023-4}}</ref><ref name="pmid3109366">{{cite journal | vauthors = Fraser HM, Baird DT | title = Clinical applications of LHRH analogues | journal = Baillière's Clin. Endocrinol. Metab. | volume = 1 | issue = 1 | pages = 43–70 | date = February 1987 | pmid = 3109366 | doi = 10.1016/S0950-351X(87)80052-6}}</ref> They work by opposing the effects of androgens and delaying the development of [[secondary sexual characteristic]]s and onset of changes in [[sex drive]] and [[sexual function|function]] until a more appropriate age.<ref name="pmid18345393" /><ref name="pmid6205409" /> Antiandrogens that have been used for this purpose include [[cyproterone acetate]], [[medroxyprogesterone acetate]], GnRH modulators, [[spironolactone]], [[bicalutamide]], and [[ketoconazole]].<ref name="pmid18345393" /><ref name="pmid3109366" /><ref name="pmid10969925">{{cite journal | vauthors = Laron Z, Kauli R | title = Experience with cyproterone acetate in the treatment of precocious puberty | journal = J. Pediatr. Endocrinol. Metab. | volume = 13 | issue = Suppl 1 | pages = 805–10 | date = July 2000 | pmid = 10969925 | doi = 10.1515/jpem.2000.13.s1.805| s2cid = 25398066 }}</ref><ref name="pmid1838080">{{cite journal | vauthors = Neumann F, Kalmus J | title = Cyproterone acetate in the treatment of sexual disorders: pharmacological base and clinical experience | journal = Exp. Clin. Endocrinol. | volume = 98 | issue = 2 | pages = 71–80 | date = 1991 | pmid = 1838080 | doi = 10.1055/s-0029-1211103 }}</ref><ref name="pmid1903104">{{cite journal | vauthors = Holland FJ | title = Gonadotropin-independent precocious puberty | journal = Endocrinol. Metab. Clin. North Am. | volume = 20 | issue = 1 | pages = 191–210 | date = March 1991 | pmid = 1903104 | doi = 10.1016/s0889-8529(18)30288-3}}</ref><ref name="pmid16361981">{{cite journal | vauthors = Reiter EO, Norjavaara E | title = Testotoxicosis: current viewpoint | journal = Pediatr Endocrinol Rev | volume = 3 | issue = 2 | pages = 77–86 | date = December 2005 | pmid = 16361981 }}</ref> Spironolactone and bicalutamide require combination with an [[aromatase inhibitor]] to prevent the effects of unopposed [[estrogen]]s, while the others can be used alone.<ref name="pmid18345393" /><ref name="pmid1903104" /><ref name="pmid16361981" />

====Long-lasting erections====
Antiandrogens are effective in the treatment of recurrent [[priapism]] (potentially painful [[penile erection]]s that last more than four hours).<ref name="LeveyKutlu2011">{{cite journal | vauthors = Levey HR, Kutlu O, Bivalacqua TJ | title = Medical management of ischemic stuttering priapism: a contemporary review of the literature | journal = Asian Journal of Andrology | volume = 14 | issue = 1 | pages = 156–63 | year = 2012 | pmid = 22057380 | pmc = 3753435 | doi = 10.1038/aja.2011.114 }}</ref><ref name="BroderickKadioglu2010">{{cite journal | vauthors = Broderick GA, Kadioglu A, Bivalacqua TJ, Ghanem H, Nehra A, Shamloul R | title = Priapism: pathogenesis, epidemiology, and management | journal = The Journal of Sexual Medicine | volume = 7 | issue = 1 Pt 2 | pages = 476–500 | year = 2010 | pmid = 20092449 | doi = 10.1111/j.1743-6109.2009.01625.x }}</ref><ref name="ChowPayne2008">{{cite journal | vauthors = Chow K, Payne S | title = The pharmacological management of intermittent priapismic states | journal = BJU International | volume = 102 | issue = 11 | pages = 1515–21 | year = 2008 | pmid = 18793304 | doi = 10.1111/j.1464-410X.2008.07951.x | s2cid = 35399393 | doi-access = free }}</ref><ref name="DahmRao2002">{{cite journal | vauthors = Dahm P, Rao DS, Donatucci CF | title = Antiandrogens in the treatment of priapism | journal = Urology | volume = 59 | issue = 1 | pages = 138 | year = 2002 | pmid = 11796309 | doi = 10.1016/S0090-4295(01)01492-3 }}</ref><ref name="YuanDeSouza2008">{{cite journal | vauthors = Yuan J, Desouza R, Westney OL, Wang R | title = Insights of priapism mechanism and rationale treatment for recurrent priapism | journal = Asian Journal of Andrology | volume = 10 | issue = 1 | pages = 88–101 | year = 2008 | pmid = 18087648 | doi = 10.1111/j.1745-7262.2008.00314.x | doi-access = free }}</ref>

===Women and girls===

====Skin and hair conditions====
{{See also|Acne vulgaris#Hormonal agents|Seborrhoeic dermatitis#Antiandrogens|Hirsutism#Medications}}

Antiandrogens are used in the treatment of androgen-dependent [[skin condition|skin]] and [[hair disease|hair condition]]s including acne, seborrhea, hidradenitis suppurativa, hirsutism, and pattern hair loss in women.<ref name="pmid16828411" /> All of these conditions are dependent on androgens, and for this reason, antiandrogens are effective in treating them.<ref name="pmid16828411" /> The most commonly used antiandrogens for these indications are [[cyproterone acetate]] and [[spironolactone]].<ref name="BaranMaibach1998">{{cite book| vauthors = Baran R, Maibach HI |title=Textbook of Cosmetic Dermatology|url=https://books.google.com/books?id=yIVfq5Lpl2EC&pg=PA388|date=1 October 1998|publisher=CRC Press|isbn=978-1-85317-478-0|pages=388–}}</ref> [[Flutamide]] has also been studied extensively for such uses, but has fallen out of favor due to its association with [[hepatotoxicity]].<ref name="MaibachGorouhi2011">{{cite book| vauthors = Maibach HI, Gorouhi F |title=Evidence Based Dermatology|url=https://books.google.com/books?id=V2L1MAoGHVkC&pg=PA526|year=2011|publisher=PMPH-USA|isbn=978-1-60795-039-4|pages=526–}}</ref> [[Bicalutamide]], which has a relatively minimal risk of hepatotoxicity, has been evaluated for the treatment of hirsutism and found effective similarly to flutamide and may be used instead of it.<ref name="WilliamsBigby2009">{{cite book|vauthors=Williams H, Bigby M, Diepgen T, Herxheimer A, Naldi L, Rzany B|title=Evidence-Based Dermatology|url=https://books.google.com/books?id=SbsQij5xkfYC&pg=PA529|date=22 January 2009|publisher=John Wiley & Sons|isbn=978-1-4443-0017-8|pages=529–|access-date=27 December 2016|archive-date=10 January 2023|archive-url=https://web.archive.org/web/20230110085152/https://books.google.com/books?id=SbsQij5xkfYC&pg=PA529|url-status=live}}</ref><ref name="pmid24455796">{{cite journal | vauthors = Erem C | title = Update on idiopathic hirsutism: diagnosis and treatment | journal = Acta Clin Belg | volume = 68 | issue = 4 | pages = 268–74 | year = 2013 | pmid = 24455796 | doi = 10.2143/ACB.3267 | s2cid = 39120534 }}</ref> In addition to AR antagonists, [[oral contraceptive]]s containing [[ethinylestradiol]] are effective in treating these conditions, and may be combined with AR antagonists.<ref name="Becker2001">{{cite book| vauthors = Becker KL |title=Principles and Practice of Endocrinology and Metabolism |url= https://books.google.com/books?id=FVfzRvaucq8C&pg=PA1004 |year=2001|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-1750-2|pages=1004, 1196}}</ref><ref name="CamachoGharib2012">{{cite book| vauthors = Camacho PM, Gharib H, Sizemore GW |title=Evidence-Based Endocrinology |url=https://books.google.com/books?id=TrLaw_CX1i8C&pg=PA199 |year=2012 |publisher=Lippincott Williams & Wilkins |isbn=978-1-4511-1091-3 |pages=199–}}</ref>

====High androgen levels====
{{See also|Hyperandrogenism#Treatment}}

Hyperandrogenism is a condition in women in which androgen levels are excessively and abnormally high.<ref name="RabeGrunwald2009" /> It is commonly seen in women with PCOS, and also occurs in women with [[intersex condition]]s like [[congenital adrenal hyperplasia]].<ref name="RabeGrunwald2009" /> Hyperandrogenism is associated with [[virilization]] – that is, the development of masculine [[secondary sexual characteristic]]s like male-pattern facial and body hair growth (or hirsutism), [[voice change|voice deepening]], increased [[muscle]] [[lean body mass|mass]] and [[physical strength|strength]], and [[broadening of the shoulders]], among others.<ref name="RabeGrunwald2009" /> Androgen-dependent skin and hair conditions like acne and pattern hair loss may also occur in hyperandrogenism, and [[menstrual irregularity|menstrual disturbance]]s, like [[amenorrhea]], are commonly seen.<ref name="RabeGrunwald2009" /> Although antiandrogens do not treat the underlying cause of hyperandrogenism (e.g., PCOS), they are able to prevent and reverse its manifestation and effects.<ref name="RabeGrunwald2009" /> As with androgen-dependent skin and hair conditions, the most commonly used antiandrogens in the treatment of hyperandrogenism in women are cyproterone acetate and spironolactone.<ref name="RabeGrunwald2009" /> Other antiandrogens, like bicalutamide, may be used alternatively.<ref name="RabeGrunwald2009" />

====Gender-affirming hormone therapy====
{{See also|Feminizing hormone therapy#Antiandrogens}}

Antiandrogens are used to prevent or reverse [[masculinization]] and to facilitate [[feminization (biology)|feminization]] in [[transgender women]] and some nonbinary individuals who are undergoing [[feminizing hormone therapy|hormone therapy]] and who have not undergone [[sex reassignment surgery]] or [[orchiectomy]].<ref name="pmid21714669">{{cite journal | vauthors = Bockting W, Coleman E, De Cuypere G | title = Care of transsexual persons | journal = N. Engl. J. Med. | volume = 364 | issue = 26 | pages = 2559–60; author reply 2560 | year = 2011 | pmid = 21714669 | doi = 10.1056/NEJMc1104884 }}</ref> Besides estrogens, the main antiandrogens that have been used for this purpose are cyproterone acetate, spironolactone, and GnRH modulators.<ref name="pmid21714669" /> Nonsteroidal antiandrogens like bicalutamide are also used for this indication.<ref name="pmid30256230">{{cite journal | vauthors = Randolph JF | title = Gender-Affirming Hormone Therapy for Transgender Females | journal = Clin Obstet Gynecol | volume = 61 | issue = 4 | pages = 705–721 | date = December 2018 | pmid = 30256230 | doi = 10.1097/GRF.0000000000000396 | s2cid = 52821192 }}</ref><ref name="pmid21714669" /> In addition to use in transgender women, antiandrogens, mainly GnRH modulators, are used as [[puberty blocker]]s to prevent the onset of [[puberty]] in [[transgender youth|transgender girl]]s until they are older and ready to begin hormone therapy.<ref name="pmid25404716">{{cite journal | vauthors = Vance SR, Ehrensaft D, Rosenthal SM | title = Psychological and medical care of gender nonconforming youth | journal = Pediatrics | volume = 134 | issue = 6 | pages = 1184–92 | year = 2014 | pmid = 25404716 | doi = 10.1542/peds.2014-0772 | s2cid = 5743822 | url = http://pediatrics.aappublications.org/content/pediatrics/134/6/1184.full.pdf | access-date = 2018-05-14 | archive-date = 2018-05-15 | archive-url = https://web.archive.org/web/20180515045718/http://pediatrics.aappublications.org/content/pediatrics/134/6/1184.full.pdf | url-status = live }}</ref>

===Available forms===
{{See also|Steroidal antiandrogen|Nonsteroidal antiandrogen}}

There are several different types of antiandrogens, including the following:<ref name="pmid11502457" />

* '''Androgen receptor antagonists:''' Drugs that bind directly to and block the AR.<ref name="pmid10637363">{{cite journal | vauthors = Singh SM, Gauthier S, Labrie F | title = Androgen receptor antagonists (antiandrogens): structure-activity relationships | journal = Current Medicinal Chemistry | volume = 7 | issue = 2 | pages = 211–247 | date = February 2000 | pmid = 10637363 | doi = 10.2174/0929867003375371 }}</ref><ref name="ShenTaplin2010">{{cite book| vauthors = Shen HC, Taplin ME, Balk SP |title=Drug Management of Prostate Cancer |chapter=Androgen Receptor Antagonists |year=2010|pages=71–81|publisher=Springer |doi=10.1007/978-1-60327-829-4_6|isbn=978-1-60327-831-7}}</ref> These drugs include the [[steroidal antiandrogen]]s [[cyproterone acetate]], [[megestrol acetate]], [[chlormadinone acetate]], [[spironolactone]], [[oxendolone]], and [[osaterone acetate]] (veterinary) and the [[nonsteroidal antiandrogen]]s [[flutamide]], [[bicalutamide]], [[nilutamide]], [[topilutamide]], [[enzalutamide]], and [[apalutamide]].<ref name="pmid10637363" /><ref name="ShenTaplin2010" /><ref name="SchröderRadlmaier2009" /><ref name="KolvenbagFurr2009" /> Aside from cyproterone acetate and chlormadinone acetate, a few other [[progestin]]s used in [[oral contraceptive]]s and/or in menopausal HRT including [[dienogest]], [[drospirenone]], [[medrogestone]], [[nomegestrol acetate]], [[promegestone]], and [[trimegestone]] also have varying degrees of AR antagonistic activity.<ref>{{cite journal | vauthors = Šauer P, Bořík A, Golovko O, Grabic R, Staňová AV, Valentová O, Stará A, Šandová M, Kocour Kroupová H | display-authors = 6 | title = Do progestins contribute to (anti-)androgenic activities in aquatic environments? | journal = Environmental Pollution | volume = 242 | issue = Pt A | pages = 417–425 | date = November 2018 | pmid = 29990947 | doi = 10.1016/j.envpol.2018.06.104 | bibcode = 2018EPoll.242..417S | s2cid = 51622914 }}</ref><ref name="pmid12600226">{{cite journal | vauthors = Raudrant D, Rabe T | title = Progestogens with antiandrogenic properties | journal = Drugs | volume = 63 | issue = 5 | pages = 463–492 | year = 2003 | pmid = 12600226 | doi = 10.2165/00003495-200363050-00003 | s2cid = 28436828 }}</ref><ref name="pmid14644837">{{cite journal | vauthors = Schneider HP | title = Androgens and antiandrogens | journal = Annals of the New York Academy of Sciences | volume = 997 | issue = 1 | pages = 292–306 | date = November 2003 | pmid = 14644837 | doi = 10.1196/annals.1290.033 | s2cid = 8400556 | bibcode = 2003NYASA.997..292S }}</ref>
* '''Androgen synthesis inhibitors:''' Drugs that directly inhibit the [[enzyme|enzymatic]] [[biosynthesis]] of androgens like testosterone and/or DHT.<ref name="IIIBarbieri2013">{{cite book| vauthors = Strauss III JF, Barbieri RL |title=Yen and Jaffe's Reproductive Endocrinology|url=https://books.google.com/books?id=KZ95AAAAQBAJ&pg=PA90|date=13 September 2013|publisher=Elsevier Health Sciences|isbn=978-1-4557-2758-2|pages=90–}}</ref><ref name="FiggChau2010">{{cite book| vauthors = Figg W, Chau CH, Small EJ |title=Drug Management of Prostate Cancer|url=https://books.google.com/books?id=4KDrjeWA5-UC&pg=PA93|date=14 September 2010|publisher=Springer Science & Business Media|isbn=978-1-60327-829-4|pages=71–72, 75, 91–96}}</ref> Examples include the [[CYP17A1 inhibitor]]s [[ketoconazole]], [[abiraterone acetate]], and [[seviteronel]],<ref name="IIIBarbieri2013" /> the [[CYP11A1]] (P450scc) inhibitor [[aminoglutethimide]],<ref name="IIIBarbieri2013" /> and the [[5α-reductase inhibitor]]s [[finasteride]], [[dutasteride]], [[epristeride]], [[alfatradiol]], and [[saw palmetto extract]] (''[[Serenoa repens]]'').<ref name="pmid19879888">{{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 = 109–53 | year = 2010 | pmid = 19879888 | doi = 10.1016/j.steroids.2009.10.005 | s2cid = 44363501 }}</ref> A number of other antiandrogens, including cyproterone acetate, spironolactone, medrogestone, flutamide, nilutamide, and [[bifluranol]], are also known to weakly inhibit androgen synthesis.
* '''Antigonadotropins:''' Drugs that suppress the [[gonadotropin-releasing hormone]] (GnRH)-induced release of [[gonadotropin]]s and consequent activation of [[gonadal]] androgen production.<ref name="Brueggemeier2006" /><ref name="FarmerWalker2012">{{cite book| vauthors = Farmer PB, Walker JM |title= The Molecular Basis of Cancer|url=https://books.google.com/books?id=Bva8BAAAQBAJ&pg=PA232|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-1-4684-7313-1|pages=232–}}</ref> Examples include [[GnRH modulator]]s like [[leuprorelin]] (a [[GnRH agonist]]) and [[cetrorelix]] (a [[GnRH antagonist]]),<ref name="LemkeWilliams2012" /> [[progestogen]]s like [[allylestrenol]], chlormadinone acetate, cyproterone acetate, [[gestonorone caproate]], [[hydroxyprogesterone caproate]], [[medroxyprogesterone acetate]], megestrol acetate, osaterone acetate (veterinary), and oxendolone,<ref name="pmid10997774" /><ref name="LedgerSchlaff2014">{{cite book| vauthors = Ledger W, Schlaff WD, Vancaillie TG |title=Chronic Pelvic Pain|url=https://books.google.com/books?id=ON-VBQAAQBAJ&pg=PA55|date=11 December 2014|publisher=Cambridge University Press|isbn=978-1-316-21414-5|pages=55–}}</ref> and [[estrogen (medication)|estrogen]]s like [[estradiol (medication)|estradiol]], [[estradiol ester]]s, [[ethinylestradiol]], [[conjugated estrogens]], and [[diethylstilbestrol]].<ref name="Brueggemeier2006" /><ref name="pmid10997774" />
* '''Miscellaneous:''' Drugs that oppose the effects of androgens by means other than the above. Examples include estrogens, especially [[oral administration|oral]] and [[synthetic compound|synthetic]] (e.g., [[ethinylestradiol]], [[diethylstilbestrol]]), which stimulate [[sex hormone-binding globulin]] (SHBG) [[biosynthesis|production]] in the [[liver]] and thereby decrease free and hence [[biological activity|bioactive]] levels of testosterone and DHT; [[anticorticotropin]]s such as [[glucocorticoid]]s, which suppress the [[adrenocorticotropic hormone]] (ACTH)-induced production of [[adrenal androgen]]s; and [[immunogen]]s and [[vaccine]]s against [[androstenedione]] like [[ovandrotone albumin]] and [[androstenedione albumin]], which decrease levels of androgens via the generation of [[antibody|antibodies]] against the androgen and androgen [[precursor (biochemistry)|precursor]] androstenedione (used only in [[veterinary medicine]]).

Certain antiandrogens combine multiple of the above mechanisms.<ref name="pmid11502457" /><ref name="HannaCrosby2015">{{cite book| vauthors = Hanna L, Crosby T, Macbeth F |title=Practical Clinical Oncology|url=https://books.google.com/books?id=wm_OCgAAQBAJ&pg=PA37|date=19 November 2015|publisher=Cambridge University Press|isbn=978-1-107-68362-4|pages=37–}}</ref> An example is the steroidal antiandrogen cyproterone acetate, which is a potent AR antagonist, a potent progestogen and hence antigonadotropin, a weak glucocorticoid and hence anticorticotropin, and a weak androgen synthesis inhibitor.<ref name="pmid11502457" /><ref name="HannaCrosby2015" /><ref name="Weber2015">{{cite book| vauthors = Weber GF |title=Molecular Therapies of Cancer|url=https://books.google.com/books?id=dhs_CgAAQBAJ&pg=PA316|date=22 July 2015|publisher=Springer|isbn=978-3-319-13278-5|pages=314, 316}}</ref><ref name="pmid9592622">{{cite journal | vauthors = Mahler C, Verhelst J, Denis L | title = Clinical pharmacokinetics of the antiandrogens and their efficacy in prostate cancer | journal = Clin Pharmacokinet | volume = 34 | issue = 5 | pages = 405–17 | date = May 1998 | pmid = 9592622 | doi = 10.2165/00003088-199834050-00005 | s2cid = 25200595 }}</ref>

{| class="wikitable sortable mw-collapsible <!--mw-collapsed-->" style="margin-left: auto; margin-right: auto; border: none;"
|+ class="nowrap" | Antiandrogens marketed for clinical or veterinary use
|-
! Generic name !! Class !! Type !! Brand name(s) !! Route(s) !! Launch !! Status !! {{abbr|Hits|Google Search hits (February 2018)}}<sup>a</sup>
|-
| {{No selflink|Abiraterone acetate}} || Steroidal || Androgen synthesis inhibitor || Zytiga || Oral || 2011 || Available || 523,000
|-
| {{No selflink|Allylestrenol}} || Steroidal || Progestin || Gestanin, Perselin || Oral || 1961 || Available<sup>b</sup> || 61,800
|-
| {{No selflink|Aminoglutethimide}} || Nonsteroidal || Androgen synthesis inhibitor || Cytadren, Orimeten || Oral || 1960 || Available<sup>b</sup> || 222,000
|-
| {{No selflink|Apalutamide}} || Nonsteroidal || AR antagonist || Erleada || Oral || 2018 || Available || 50,400
|-
| {{No selflink|Bicalutamide}} || Nonsteroidal || AR antagonist || Casodex || Oral || 1995 || Available || 754,000
|-
| {{No selflink|Chlormadinone acetate}} || Steroidal || Progestin; AR antagonist || Belara, Prostal || Oral || 1965 || Available || 220,000
|-
| {{No selflink|Cyproterone acetate}} || Steroidal || Progestin; AR antagonist || Androcur, Diane || Oral, {{abbr|IM|Intramuscular injection}} || 1973 || Available || 461,000
|-
| {{No selflink|Delmadinone acetate}} || Steroidal || Progestin; AR antagonist || Tardak || Veterinary || 1972 || Veterinary || 42,600
|-
| {{No selflink|Enzalutamide}} || Nonsteroidal || AR antagonist || Xtandi || Oral || 2012 || Available || 328,000
|-
| {{No selflink|Flutamide}} || Nonsteroidal || AR antagonist || Eulexin || Oral || 1983 || Available || 712,000
|-
| {{No selflink|Gestonorone caproate}} || Steroidal || Progestin || Depostat, Primostat || {{abbr|IM|Intramuscular injection}} || 1973 || Available<sup>b</sup> || 119,000
|-
| {{No selflink|Hydroxyprogesterone caproate}} || Steroidal || Progestin || Delalutin, Proluton || {{abbr|IM|Intramuscular injection}} || 1954 || Available || 108,000
|-
| {{No selflink|Ketoconazole}} || Nonsteroidal || Androgen synthesis inhibitor || Nizoral, others || Oral, topical || 1981 || Available || 3,650,000
|-
| {{No selflink|Medroxyprogesterone acetate}} || Steroidal || Progestin || Provera, Depo-Provera || Oral, {{abbr|IM|Intramuscular injection}}, {{abbr|SC|Subcutaneous injection}} || 1958 || Available || 1,250,000
|-
| {{No selflink|Megestrol acetate}} || Steroidal || Progestin; AR antagonist || Megace || Oral || 1963 || Available || 253,000
|-
| {{No selflink|Nilutamide}} || Nonsteroidal || AR antagonist || Anandron, Nilandron || Oral || 1987 || Available || 132,000
|-
| {{No selflink|Osaterone acetate}} || Steroidal || Progestin; AR antagonist || Ypozane || Veterinary || 2007 || Veterinary || 87,600
|-
| {{No selflink|Oxendolone}} || Steroidal || Progestin; AR antagonist || Prostetin, Roxenone || {{abbr|IM|Intramuscular injection}} || 1981 || Available<sup>b</sup> || 36,100
|-
| {{No selflink|Spironolactone}} || Steroidal || AR antagonist || Aldactone || Oral, topical || 1959 || Available || 3,010,000
|-
| {{No selflink|Topilutamide}} || Nonsteroidal || AR antagonist || Eucapil || Topical || 2003 || Available<sup>b</sup> || 36,300
|- class="sortbottom"
| colspan="8" style="width: 1px; background-color:#eaecf0; text-align: center;" | '''Footnotes:''' <sup>a</sup> = Hits = Google Search hits (as of February 2018). <sup>b</sup> = Availability limited / mostly discontinued. '''Class:''' Steroidal = {{No selflink|Steroidal antiandrogen}}. Nonsteroidal = {{No selflink|Nonsteroidal antiandrogen}}. '''Sources:''' See individual articles.
|}

==Side effects==
The side effects of antiandrogens vary depending on the type of antiandrogen – namely whether it is a selective AR antagonist or lowers androgen levels – as well as the presence of [[off-target activity]] in the antiandrogen in question.<ref name="pmid11121992">{{cite journal | vauthors = Iversen P, Melezinek I, Schmidt A | title = Nonsteroidal antiandrogens: a therapeutic option for patients with advanced prostate cancer who wish to retain sexual interest and function | journal = BJU Int. | volume = 87 | issue = 1 | pages = 47–56 | year = 2001 | pmid = 11121992 | doi = 10.1046/j.1464-410x.2001.00988.x| s2cid = 28215804 | doi-access = free }}</ref><ref name="Thomas1997">{{cite book|vauthors=Thomas JA|title=Endocrine Toxicology, Second Edition|url=https://books.google.com/books?id=URc5JMoNirgC&pg=PA152|date=12 March 1997|publisher=CRC Press|isbn=978-1-4398-1048-4|pages=152–|access-date=27 December 2016|archive-date=11 January 2023|archive-url=https://web.archive.org/web/20230111061946/https://books.google.com/books?id=URc5JMoNirgC&pg=PA152|url-status=live}}</ref> For instance, whereas antigonadotropic antiandrogens like GnRH modulators and cyproterone acetate are associated with pronounced [[sexual dysfunction]] and [[osteoporosis]] in men, selective AR antagonists like bicalutamide are not associated with osteoporosis and have been associated with only minimal sexual dysfunction.<ref name="pmid11121992" /><ref name="pmid12603397">{{cite journal | vauthors = Anderson J | title = The role of antiandrogen monotherapy in the treatment of prostate cancer | journal = BJU Int. | volume = 91 | issue = 5 | pages = 455–61 | year = 2003 | pmid = 12603397 | doi = 10.1046/j.1464-410x.2003.04026.x| s2cid = 8639102 | doi-access = free }}</ref><ref name="Priestman2012">{{cite book| vauthors = Priestman T |title=Cancer Chemotherapy in Clinical Practice|url=https://books.google.com/books?id=K41Lf91GULcC&pg=PA97|date=26 May 2012|publisher=Springer Science & Business Media|isbn=978-0-85729-727-3|pages=97–}}</ref> These differences are thought related to the fact that antigonadotropins suppress androgen levels and by extension levels of [[Biological activity|bioactive]] [[metabolite]]s of androgens like [[estrogen]]s and [[neurosteroid]]s whereas selective AR antagonists similarly neutralize the effects of androgens but leave levels of androgens and hence their metabolites intact (and in fact can even increase them as a result of their [[progonadotropic]] effects).<ref name="pmid11121992" /> As another example, the steroidal antiandrogens cyproterone acetate and spironolactone possess off-target actions including [[progestogen]]ic, [[antimineralocorticoid]], and/or [[glucocorticoid]] activity in addition to their antiandrogen activity, and these off-target activities can result in additional side effects.<ref name="Thomas1997" />

In males, the major [[side effect]]s of antiandrogens are [[demasculinization]] and [[feminization (biology)|feminization]].<ref name="pmid12667885">{{cite journal | vauthors = Higano CS | title = Side effects of androgen deprivation therapy: monitoring and minimizing toxicity | journal = Urology | volume = 61 | issue = 2 Suppl 1 | pages = 32–8 | year = 2003 | pmid = 12667885 | doi = 10.1016/S0090-4295(02)02397-X}}</ref> These side effects include [[mastodynia|breast pain/tenderness]] and [[gynecomastia]] ([[breast development]]/[[breast enlargement|enlargement]]), reduced [[body hair]] growth/density, decreased [[muscle mass]] and [[muscle strength|strength]], [[gynoid fat distribution|feminine]] changes in [[body fat percentage|fat mass]] and [[fat distribution|distribution]], and reduced [[human penis size|penile length]] and [[testicle|testicular]] size.<ref name="pmid12667885" /> The rates of gynecomastia in men with selective AR antagonist monotherapy have been found to range from 30 to 85%.<ref name="pmid16321765">{{cite journal | vauthors = Di Lorenzo G, Autorino R, Perdonà S, De Placido S | title = Management of gynaecomastia in patients with prostate cancer: a systematic review | journal = Lancet Oncol. | volume = 6 | issue = 12 | pages = 972–9 | date = December 2005 | pmid = 16321765 | doi = 10.1016/S1470-2045(05)70464-2 }}</ref> In addition, antiandrogens can cause [[infertility]], [[osteoporosis]], [[hot flash]]es, [[sexual dysfunction]] (including loss of [[libido]] and [[erectile dysfunction]]), [[depression (mood)|depression]], [[fatigue (medical)|fatigue]], [[anemia]], and decreased [[Ejaculation#Volume|semen/ejaculate volume]] in males.{{failed verification|reason=source does not attribute antiandrogen as the causative agent of all side effects listed.|date=July 2019}}<ref name="pmid12667885" /> Conversely, the side effects of selective AR antagonists in women are minimal.<ref name="pmid24455796" /><ref name="Shapiro2012">{{cite book| vauthors = Shapiro J |title=Hair Disorders: Current Concepts in Pathophysiology, Diagnosis and Management, An Issue of Dermatologic Clinics|url=https://books.google.com/books?id=9rLeICotHEoC&pg=PT187|date=12 November 2012|publisher=Elsevier Health Sciences|isbn=978-1-4557-7169-1|pages=187–}}</ref> However, antigonadotropic antiandrogens like cyproterone acetate can produce [[hypoestrogenism]], [[amenorrhea]], and osteoporosis in premenopausal women, among other side effects.<ref name="Becker2001" /><ref name="Futterweit2012">{{cite book| vauthors = Futterweit W |title=Polycystic Ovarian Disease|url=https://books.google.com/books?id=siSSBgAAQBAJ&pg=PT282|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-1-4613-8289-8|pages=282–}}</ref><ref name="pmid20082945">{{cite journal | vauthors = Katsambas AD, Dessinioti C | title = Hormonal therapy for acne: why not as first line therapy? facts and controversies | journal = Clin. Dermatol. | volume = 28 | issue = 1 | pages = 17–23 | year = 2010 | pmid = 20082945 | doi = 10.1016/j.clindermatol.2009.03.006 }}</ref> In addition, androgen receptor antagonists can produce unfavorable effects on [[cholesterol]] levels, which long-term may increase the risk of [[cardiovascular disease]].<ref name="pmid28944709">{{cite journal | vauthors = Baldani DP, Skrgatic L, Ougouag R, Kasum M | title = The cardiometabolic effect of current management of polycystic ovary syndrome: strategies of prevention and treatment | journal = Gynecol Endocrinol | volume = 34 | issue = 2 | pages = 87–91 | date = February 2018 | pmid = 28944709 | doi = 10.1080/09513590.2017.1381681 | s2cid = 205631980 | url = }}</ref><ref name="pmid19843067">{{cite journal | vauthors = Nakhjavani M, Hamidi S, Esteghamati A, Abbasi M, Nosratian-Jahromi S, Pasalar P | title = Short term effects of spironolactone on blood lipid profile: a 3-month study on a cohort of young women with hirsutism | journal = Br J Clin Pharmacol | volume = 68 | issue = 4 | pages = 634–7 | date = October 2009 | pmid = 19843067 | pmc = 2780289 | doi = 10.1111/j.1365-2125.2009.03483.x | url = }}</ref><ref name="pmid33334002">{{cite journal | vauthors = Cignarella A, Mioni R, Sabbadin C, Dassie F, Parolin M, Vettor R, Barbot M, Scaroni C | title = Pharmacological Approaches to Controlling Cardiometabolic Risk in Women with PCOS | journal = Int J Mol Sci | volume = 21 | issue = 24 | date = December 2020 | page = 9554 | pmid = 33334002 | pmc = 7765466 | doi = 10.3390/ijms21249554 | url = | doi-access = free }}</ref><ref name="pmid29211888">{{cite journal | vauthors = Moretti C, Guccione L, Di Giacinto P, Simonelli I, Exacoustos C, Toscano V, Motta C, De Leo V, Petraglia F, Lenzi A | title = Combined Oral Contraception and Bicalutamide in Polycystic Ovary Syndrome and Severe Hirsutism: A Double-Blind Randomized Controlled Trial | journal = J. 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A. | last119 = Arcelus | first119 = J. | title = Standards of Care for the Health of Transgender and Gender Diverse People, Version 8 | journal = [[International Journal of Transgender Health]] | date = 19 August 2022 | volume = 23 | issue = Suppl 1 | pages = S1–S259 | issn = 2689-5269 | doi = 10.1080/26895269.2022.2100644 | doi-access=free | pmid = 36238954 | pmc = 9553112 | url = }}</ref><ref name="pmid3318361">{{cite journal | vauthors = Godsland IF, Wynn V, Crook D, Miller NE | title = Sex, plasma lipoproteins, and atherosclerosis: prevailing assumptions and outstanding questions | journal = American Heart Journal | volume = 114 | issue = 6 | pages = 1467–1503 | date = December 1987 | pmid = 3318361 | doi = 10.1016/0002-8703(87)90552-7 }}</ref><ref name="pmid30586774">{{cite journal | vauthors = Grundy SM, Stone NJ, Bailey AL, Beam C, Birtcher KK, Blumenthal RS, Braun LT, de Ferranti S, Faiella-Tommasino J, Forman DE, Goldberg R, Heidenreich PA, Hlatky MA, Jones DW, Lloyd-Jones D, Lopez-Pajares N, Ndumele CE, Orringer CE, Peralta CA, Saseen JJ, Smith SC, Sperling L, Virani SS, Yeboah J | title = 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines | journal = Circulation | volume = 139 | issue = 25 | pages = e1082–e1143 | date = June 2019 | pmid = 30586774 | pmc = 7403606 | doi = 10.1161/CIR.0000000000000625 | url = }}</ref>

A number of antiandrogens have been associated with [[hepatotoxicity]].<ref name="pmid15604569">{{cite journal | vauthors = Thole Z, Manso G, Salgueiro E, Revuelta P, Hidalgo A | title = Hepatotoxicity induced by antiandrogens: a review of the literature | journal = Urol. Int. | volume = 73 | issue = 4 | pages = 289–95 | year = 2004 | pmid = 15604569 | doi = 10.1159/000081585 | s2cid = 24799765 }}</ref> These include, to varying extents, cyproterone acetate, flutamide, nilutamide, bicalutamide, aminoglutethimide, and ketoconazole.<ref name="pmid15604569" /> In contrast, spironolactone, enzalutamide,<ref name="pmid25711765">{{cite journal | vauthors = Keating GM | title = Enzalutamide: a review of its use in chemotherapy-naïve metastatic castration-resistant prostate cancer | journal = Drugs & Aging | volume = 32 | issue = 3 | pages = 243–9 | date = March 2015 | pmid = 25711765 | doi = 10.1007/s40266-015-0248-y | s2cid = 29563345 }}</ref> and other antiandrogens are not associated with significant rates of hepatotoxicity. However, although they do not pose a risk of hepatotoxicity, spironolactone has a risk of [[hyperkalemia]] and enzalutamide has a risk of [[seizure]]s.{{citation needed|date=May 2021}}

In women who are [[pregnancy|pregnant]], antiandrogens can interfere with the androgen-mediated [[sexual differentiation]] of the [[genitalia]] and [[brain]] of male [[fetus]]es.<ref name="LeppertPeipert2004">{{cite book| vauthors = Leppert PC, Peipert JF |title=Primary Care for Women|url=https://books.google.com/books?id=PiiD0iUNhlIC&pg=PA277|year=2004|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-3790-6|pages=277–}}</ref> This manifests primarily as [[ambiguous genitalia]] – that is, undervirilized or feminized genitalia, which, anatomically, are a cross between a [[penis]] and a [[vagina]] – and theoretically also as [[femininity]].<ref name="LeppertPeipert2004" /><ref name="RathusNevid2005">{{cite book|vauthors=Rathus SA, Nevid JS, Fichner-Rathus L|title=Human sexuality in a world of diversity|url=https://books.google.com/books?id=HahZAAAAYAAJ|year=2005|publisher=Pearson Allyn and Bacon|isbn=978-0-205-40615-9|page=313|access-date=2016-12-27|archive-date=2023-02-26|archive-url=https://web.archive.org/web/20230226052955/https://books.google.com/books?id=HahZAAAAYAAJ|url-status=live}}</ref> As such, antiandrogens are [[teratogen]]s, and women who are pregnant should not be treated with an antiandrogen.<ref name="CamachoGharib2012" /> Moreover, women who can or may become pregnant are strongly recommended to take an antiandrogen only in combination with proper [[contraceptive|contraception]].<ref name="CamachoGharib2012" />

==Overdose==
Antiandrogens are relatively safe in acute [[overdose]].{{Citation needed|date=July 2018}}

==Interactions==
[[Enzyme inhibitor|Inhibitor]]s and [[enzyme inducer|inducer]]s of [[cytochrome P450]] [[enzyme]]s may [[drug interaction|interact]] with various antiandrogens.{{Citation needed|date=July 2018}}

==Mechanism of action==

===Androgen receptor antagonists===
{| class="wikitable sortable floatright"
|+ Antiandrogens at steroid hormone receptors
|-
! rowspan="2" | {{No selflink|Antiandrogen}} || colspan="5" | Relative binding affinities
|-
! {{abbrlink|AR|Androgen receptor}} || {{abbrlink|PR|Progesterone receptor}} || {{abbrlink|ER|Estrogen receptor}} || {{abbrlink|GR|Glucocorticoid receptor}} || {{abbrlink|MR|Mineralocorticoid receptor}}
|-
| {{No selflink|Cyproterone acetate}} || 8–10 || 60 || <0.1 || 5 || 1
|-
| {{No selflink|Chlormadinone acetate}} || 5 || 175 || <0.1 || 38 || 1
|-
| {{No selflink|Megestrol acetate}} || 5 || 152 || <0.1 || 50 || 3
|-
| {{No selflink|Spironolactone}} || 7<!--26 for 30 min--> || 0.4<sup>a</sup> || <0.1 || 2<sup>a</sup> || 182
|-
| {{No selflink|Trimethyltrienolone}} || 3.6 || <1 || <1 || <1 || <1
|-
| {{No selflink|Inocoterone}} || 0.8 || <0.1 || <0.1 || <0.1 || <0.1
|-
| {{No selflink|Inocoterone acetate}} || <0.1 || <0.1 || <0.1 || <0.1 || <0.1
|-
| {{No selflink|Flutamide}} || <0.1 || <0.1 || <0.1 || <0.1 || <0.1
|-
| {{No selflink|Hydroxyflutamide}} || 0.5–0.8 || <0.1 || <0.1 || <0.1 || <0.1
|-
| {{No selflink|Nilutamide}} || 0.5–0.8 || <0.1 || <0.1 || <0.1 || <0.1
|-
| {{No selflink|Bicalutamide}} || 1.8 || <0.1 || <0.1 || <0.1 || <0.1
|- class="sortbottom"
| colspan="6" style="width: 1px; background-color:#eaecf0; text-align: center;" | <small>'''Notes:''' (1): Reference [[ligand (biochemistry)|ligand]]s (100%) were [[testosterone (medication)|testosterone]] for the {{abbrlink|AR|androgen receptor}}, [[progesterone (medication)|progesterone]] for the {{abbrlink|PR|progesterone receptor}}, [[estradiol (medication)|estradiol]] for the {{abbrlink|ER|estrogen receptor}}, [[dexamethasone]] for the {{abbrlink|GR|glucocorticoid receptor}}, and [[aldosterone]] for the {{abbrlink|MR|mineralocorticoid receptor}}. (2): Tissues were rat prostate (AR), rabbit uterus (PR), mouse uterus (ER), rat thymus (GR), and rat kidney (MR). (3): Incubation times (0&nbsp;°C) were 24 hours (AR, <sup>a</sup>), 2 hours (PR, ER), 4 hours (GR), and 1 hour (MR). (4): Assay methods were different for bicalutamide for receptors besides the AR. '''Sources:''' <ref name="pmid3059062">{{cite journal | vauthors = Moguilewsky M, Bouton MM | title = How the study of the biological activities of antiandrogens can be oriented towards the clinic | journal = Journal of Steroid Biochemistry | volume = 31 | issue = 4B | pages = 699–710 | date = October 1988 | pmid = 3059062 | doi = 10.1016/0022-4731(88)90021-0 }}</ref><ref name="pmid1992602">{{cite journal | vauthors = Gaillard-Moguilewsky M | title = Pharmacology of antiandrogens and value of combining androgen suppression with antiandrogen therapy | journal = Urology | volume = 37 | issue = 2 Suppl | pages = 5–12 | date = 1991 | pmid = 1992602 | doi = 10.1016/0090-4295(91)80095-O }}</ref><ref name="pmid3009970">{{cite journal | vauthors = Moguilewsky M, Fiet J, Tournemine C, Raynaud JP | title = Pharmacology of an antiandrogen, anandron, used as an adjuvant therapy in the treatment of prostate cancer | journal = Journal of Steroid Biochemistry | volume = 24 | issue = 1 | pages = 139–46 | date = January 1986 | pmid = 3009970 | doi = 10.1016/0022-4731(86)90043-9 }}</ref><ref name="pmid8136296">{{cite journal | vauthors = Teutsch G, Goubet F, Battmann T, Bonfils A, Bouchoux F, Cerede E, Gofflo D, Gaillard-Kelly M, Philibert D | title = Non-steroidal antiandrogens: synthesis and biological profile of high-affinity ligands for the androgen receptor | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 48 | issue = 1 | pages = 111–9 | date = January 1994 | pmid = 8136296 | doi = 10.1016/0960-0760(94)90257-7 | s2cid = 31404295 }}</ref><ref name="RaynaudFortin1986">{{cite book| vauthors = Raynaud JP, Fortin M, Hunt P, Ojasoo T, Doré JC, Surcouf E, Mornon JP | veditors = Gotto AM, O'Malley BW, Liliane FP |chapter=Approaches to drug development using receptors|title=The Role of Receptors in Biology and Medicine: Proceedings of the Ninth Argenteuil Symposium|url=https://books.google.com/books?id=ORFrAAAAMAAJ|year=1986|publisher=Raven Press|isbn=978-0-88167-161-2|pages=65–77}}</ref><ref name="RaynaudOjasoo1981">{{cite book| vauthors = Raynaud JP, Ojasoo T, Labrie F |title=Mechanisms of Steroid Action|chapter=Steroid hormones—agonists and antagonists|year=1981|pages=145–158|publisher=Macmillan Education UK |doi=10.1007/978-1-349-81345-2_11|isbn=978-1-349-81347-6}}</ref><ref name="pmid7421203">{{cite journal | vauthors = Raynaud JP, Bouton MM, Moguilewsky M, Ojasoo T, Philibert D, Beck G, Labrie F, Mornon JP | title = Steroid hormone receptors and pharmacology | journal = Journal of Steroid Biochemistry | volume = 12 | pages = 143–57 | date = January 1980 | pmid = 7421203 | doi = 10.1016/0022-4731(80)90264-2 }}</ref><ref name="pmid359134">{{cite journal | vauthors = Ojasoo T, Raynaud JP | title = Unique steroid congeners for receptor studies | journal = Cancer Research | volume = 38 | issue = 11 Pt 2 | pages = 4186–98 | date = November 1978 | pmid = 359134 | url = http://cancerres.aacrjournals.org/content/38/11_Part_2/4186.short | access-date = 2021-10-31 | archive-date = 2020-11-27 | archive-url = https://web.archive.org/web/20201127182040/https://cancerres.aacrjournals.org/content/38/11_Part_2/4186.short | url-status = live }}</ref><ref name="pmid171505">{{cite journal | vauthors = Raynaud JP, Bonne C, Bouton MM, Moguilewsky M, Philibert D, Azadian-Boulanger G | title = Screening for anti-hormones by receptor studies | journal = Journal of Steroid Biochemistry | volume = 6 | issue = 5 | pages = 615–22 | date = May 1975 | pmid = 171505 | doi = 10.1016/0022-4731(75)90042-4 }}</ref><ref name="pmid14600402">{{cite journal | vauthors = Hanada K, Furuya K, Yamamoto N, Nejishima H, Ichikawa K, Nakamura T, Miyakawa M, Amano S, Sumita Y, Oguro N | title = Bone anabolic effects of S-40503, a novel nonsteroidal selective androgen receptor modulator (SARM), in rat models of osteoporosis | journal = Biol. Pharm. Bull. | volume = 26 | issue = 11 | pages = 1563–9 | date = November 2003 | pmid = 14600402 | doi = 10.1248/bpb.26.1563 | doi-access = free }}</ref></small>
|}
{{Relative potencies of selected antiandrogens in rats}}

AR antagonists act by directly binding to and competitively displacing androgens like testosterone and DHT from the AR, thereby preventing them from activating the receptor and mediating their biological effects.<ref name="pmid10637363" /><ref name="ShenTaplin2010" /> AR antagonists are classified into two types, based on [[chemical structure]]: steroidal and nonsteroidal.<ref name="SchröderRadlmaier2009" /><ref name="KolvenbagFurr2009" /><ref name="pmid10637363" /><ref name="ShenTaplin2010" /><ref name="LemkeWilliams2012">{{cite book| vauthors = Lemke TL, Williams DA |title=Foye's Principles of Medicinal Chemistry|url=https://books.google.com/books?id=Sd6ot9ul-bUC&pg=PA1372|date=24 January 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-60913-345-0|pages=228–231, 1371–1372}}</ref> Steroidal AR antagonists are structurally related to [[steroid hormone]]s like testosterone and [[progesterone]], whereas nonsteroidal AR antagonists are not steroids and are structurally distinct. Steroidal AR antagonists tend to have [[off-target activity|off-target hormonal actions]] due to their structural similarity to other steroid hormones.<ref name="LemkeWilliams2012" /> In contrast, nonsteroidal AR antagonists are selective for the AR and have no off-target hormonal activity.<ref name="LemkeWilliams2012" /> For this reason, they are sometimes described as "pure" antiandrogens.<ref name="LemkeWilliams2012" />

Although they are described as antiandrogens and indeed show only such effects generally, most or all steroidal AR antagonists are actually not [[silent antagonist]]s of the AR but rather are weak [[partial agonist]]s and are able to activate the receptor in the absence of more potent AR agonists like testosterone and DHT.<ref name="pmid10637363" /><ref name="FiggChau2010" /><ref name="PoyetLabrie1985">{{cite journal | vauthors = Poyet P, Labrie F | title = Comparison of the antiandrogenic/androgenic activities of flutamide, cyproterone acetate and megestrol acetate | journal = Molecular and Cellular Endocrinology | volume = 42 | issue = 3 | pages = 283–8 | date = October 1985 | pmid = 3930312 | doi = 10.1016/0303-7207(85)90059-0 | s2cid = 24746807 }}</ref><ref name="pmid2462135">{{cite journal | vauthors = Luthy IA, Begin DJ, Labrie F | title = Androgenic activity of synthetic progestins and spironolactone in androgen-sensitive mouse mammary carcinoma (Shionogi) cells in culture | journal = Journal of Steroid Biochemistry | volume = 31 | issue = 5 | pages = 845–52 | year = 1988 | pmid = 2462135 | doi = 10.1016/0022-4731(88)90295-6}}</ref> This may have clinical implications in the specific context of prostate cancer treatment.<ref name="pmid10637363" /><ref name="PoyetLabrie1985" /> As an example, steroidal AR antagonists are able to increase prostate weight and accelerate prostate cancer cell growth in the absence of more potent AR agonists,<ref name="pmid10637363" /><ref name="PoyetLabrie1985" /> and spironolactone has been found to accelerate progression of prostate cancer in case reports.<ref name="pmid22665559">{{cite journal | vauthors = Sundar S, Dickinson PD | title = Spironolactone, a possible selective androgen receptor modulator, should be used with caution in patients with metastatic carcinoma of the prostate | journal = BMJ Case Rep | volume = 2012 | pages = bcr1120115238| year = 2012 | pmid = 22665559 | pmc = 3291010 | doi = 10.1136/bcr.11.2011.5238 }}</ref><ref name="pmid27641657">{{cite journal | vauthors = Flynn T, Guancial EA, Kilari M, Kilari D | title = Case Report: Spironolactone Withdrawal Associated With a Dramatic Response in a Patient With Metastatic Castrate-Resistant Prostate Cancer | journal = Clin Genitourin Cancer | volume = 15| issue = 1| pages = e95–e97| year = 2016 | pmid = 27641657 | doi = 10.1016/j.clgc.2016.08.006 | s2cid = 38441469 }}</ref> In addition, whereas cyproterone acetate produces ambiguous genitalia via feminization in male fetuses when administered to pregnant animals,<ref name="JamesPasqualini2013">{{cite book | vauthors = James VH, Pasqualini JR | title = Hormonal Steroids: Proceedings of the Sixth International Congress on Hormonal Steroids | url = https://books.google.com/books?id=1VMJAwAAQBAJ&pg=PA391 | date = 22 October 2013 | publisher = Elsevier Science | isbn = 978-1-4831-9067-9 | pages = 391–}}</ref> it has been found to produce masculinization of the genitalia of female fetuses of pregnant animals.<ref name="pmid10637363" /> In contrast to steroidal AR antagonists, nonsteroidal AR antagonists are silent antagonists of the AR and do not activate the receptor.<ref name="pmid9000189">{{cite journal |vauthors=Caubet JF, Tosteson TD, Dong EW, Naylon EM, Whiting GW, Ernstoff MS, Ross SD |title=Maximum androgen blockade in advanced prostate cancer: a meta-analysis of published randomized controlled trials using nonsteroidal antiandrogens |journal=Urology |volume=49 |issue=1 |pages=71–8 |year=1997 |pmid=9000189 |doi=10.1016/S0090-4295(96)00325-1 |quote=Because steroidal antiandrogens such as cyproterone acetate have intrinsic androgenic activity and lower antiandrogenic activity than the NSAAs such as flutamide and nilutamide,39–43 it is not surprising that the two classes of antiandrogens may have different efficacies.}}</ref><ref name="FiggChau2010"/><ref name=SinghGauthier2000>{{cite journal |vauthors=Singh SM, Gauthier S, Labrie F |title=Androgen receptor antagonists (antiandrogens): structure-activity relationships |journal=Current Medicinal Chemistry |volume=7 |issue=2 |pages=211–47 |date=February 2000 |pmid=10637363 |doi=10.2174/0929867003375371}}</ref><ref name="PoyetLabrie1985" /> This may be why they have greater efficacy than steroidal AR antagonists in the treatment of prostate cancer and is an important reason as to why they have largely replaced them for this indication in medicine.<ref name="pmid9000189" /><ref name="FiggChau2010" /><ref name=SinghGauthier2000 /><ref name="PoyetLabrie1985" />

Nonsteroidal antiandrogens have relatively low [[affinity (pharmacology)|affinity]] for the AR compared to steroidal AR ligands.<ref name="FiggChau2010" /><ref name="SinghGauthier2000" /><ref name="pmid2788775v">{{cite journal | vauthors = Ayub M, Levell MJ | title = The effect of ketoconazole related imidazole drugs and antiandrogens on [3H] R 1881 binding to the prostatic androgen receptor and [3H]5 alpha-dihydrotestosterone and [3H]cortisol binding to plasma proteins | journal = J. Steroid Biochem. | volume = 33 | issue = 2 | pages = 251–5 | date = August 1989 | pmid = 2788775 | doi = 10.1016/0022-4731(89)90301-4 }}</ref> For example, bicalutamide has around 2% of the affinity of DHT for the AR and around 20% of the affinity of CPA for the AR.<ref name="pmid2788775v" /> Despite their low affinity for the AR however, the lack of weak partial agonist activity of NSAAs appears to improve their potency relative to steroidal antiandrogens.<ref name="pmid2788775v" /><ref name="pmid14751673">{{cite journal | vauthors = Yamasaki K, Sawaki M, Noda S, Muroi T, Takakura S, Mitoma H, Sakamoto S, Nakai M, Yakabe Y | title = Comparison of the Hershberger assay and androgen receptor binding assay of twelve chemicals | journal = Toxicology | volume = 195 | issue = 2–3 |pages=177–86 |year = 2004 | pmid = 14751673 | doi = 10.1016/j.tox.2003.09.012| bibcode = 2004Toxgy.195..177Y }}</ref> For example, although flutamide has about 10-fold lower affinity for the AR than CPA, it shows equal or slightly greater potency to CPA as an antiandrogen in [[bioassay]]s.<ref name="pmid2788775v" /><ref name="pmid14751673" /> In addition, circulating therapeutic concentrations of nonsteroidal antiandrogens are very high, on the order of thousands of times higher than those of testosterone and DHT, and this allows them to efficaciously compete and block AR signaling.<ref name="Pratt1994">{{cite book| vauthors = Pratt WB |title= The Anticancer Drugs|url=https://books.google.com/books?id=nPR1L4K5HuEC&pg=PA220 |year=1994 |publisher=Oxford University Press |isbn=978-0-19-506739-2 |pages=220– |quote=In patients receiving flutamide at the usual dosage of 250 mg every 8 hours, the minimal plasma concentration of hydroxyflutamide is about 5 uM, which is 5,000 times the plasma concentration of testosterone (1 nM) in patients treated with an LHRH agonist.127 As hydroxyflutamide is only one percent as potent as testosterone in competing for binding to the androgen receptor,126 a plasma level of 5 uM hydroxyflutamide is required to ensure effective competition.127 [...] Both cyproterone acetate and flutamide have been demonstrated to be effective therapy (roughly equivalent to an estrogen) when used alone in the treatment of carcinoma of the prostate.123}}</ref>

AR antagonists may not bind to or block [[membrane androgen receptor]]s (mARs), which are distinct from the classical nuclear AR.<ref name="pmid19931639">{{cite journal | vauthors = Bennett NC, Gardiner RA, Hooper JD, Johnson DW, Gobe GC | title = Molecular cell biology of androgen receptor signalling | journal = Int. J. Biochem. Cell Biol. | volume = 42 | issue = 6 | pages = 813–27 | year = 2010 | pmid = 19931639 | doi = 10.1016/j.biocel.2009.11.013 }}</ref><ref name="pmid25257522">{{cite journal | vauthors = Wang C, Liu Y, Cao JM | title = G protein-coupled receptors: extranuclear mediators for the non-genomic actions of steroids | journal = Int J Mol Sci | volume = 15 | issue = 9 | pages = 15412–25 | year = 2014 | pmid = 25257522 | pmc = 4200746 | doi = 10.3390/ijms150915412 | doi-access = free }}</ref><ref name="pmid23746222">{{cite journal | vauthors = Lang F, Alevizopoulos K, Stournaras C | title = Targeting membrane androgen receptors in tumors | journal = Expert Opin. Ther. Targets | volume = 17 | issue = 8 | pages = 951–63 | year = 2013 | pmid = 23746222 | doi = 10.1517/14728222.2013.806491 | s2cid = 23918273 }}</ref> However, the mARs do not appear to be involved in [[virilization|masculinization]]. This is evidenced by the perfectly [[female]] [[phenotype]] of women with [[complete androgen insensitivity syndrome]].<ref name="PescovitzEugster2004">{{cite book| vauthors = Pescovitz OH, Eugster EA |title=Pediatric Endocrinology: Mechanisms, Manifestations, and Management|url=https://books.google.com/books?id=9gvBlktAT6YC&pg=PA248|year=2004|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-4059-3|pages=248–}}</ref><ref name="BuonocoreBracci2012">{{cite book| vauthors = Buonocore G, Bracci R, Weindling M |title=Neonatology: A Practical Approach to Neonatal Diseases|url=https://books.google.com/books?id=n_L2XpJbhLoC&pg=PA1012|date=28 January 2012|publisher=Springer Science & Business Media|isbn=978-88-470-1405-3|pages=1012–}}</ref> These women have a 46,XY [[karyotype]] (i.e., are genetically "male") and high levels of androgens but possess a defective AR and for this reason never masculinize.<ref name="PescovitzEugster2004" /><ref name="BuonocoreBracci2012" /> They are described as highly feminine, both physically as well as mentally and behaviorally.<ref name="Jordan-Young2011">{{cite book| vauthors = Jordan-Young RM |title=Brain Storm|url=https://books.google.com/books?id=2V9UuOWMXOMC&pg=PA82|date=7 January 2011|publisher=Harvard University Press|isbn=978-0-674-05879-8|pages=82–}}</ref><ref name="BlakemoreBerenbaum2013">{{cite book| vauthors = Blakemore JE, Berenbaum SA, Liben LS |title=Gender Development |url=https://books.google.com/books?id=PQ3Ylt6KnA4C&pg=PT115 |date=13 May 2013|publisher=Psychology Press|isbn=978-1-135-07932-1|pages=115–}}</ref><ref name="Maggi2012">{{cite book| vauthors = Maggi M |title= Hormonal Therapy for Male Sexual Dysfunction|url=https://books.google.com/books?id=o_A9DnMVi3cC&pg=PA6|date=30 January 2012|publisher=John Wiley & Sons|isbn=978-0-470-65760-7|pages=6–}}</ref>

====N-Terminal domain antagonists====
[[Peptide antiandrogen|N-Terminal domain AR antagonist]]s are a new type of AR antagonist that, unlike all currently marketed AR antagonists, bind to the [[N-terminal domain]] (NTD) of the AR rather than the [[ligand-binding domain]] (LBD).<ref name="ImamuraSadar2016">{{cite journal | vauthors = Imamura Y, Sadar MD | title = Androgen receptor targeted therapies in castration-resistant prostate cancer: Bench to clinic | journal = International Journal of Urology | volume = 23 | issue = 8 | pages = 654–665 | date = August 2016 | pmid = 27302572 | pmc = 6680212 | doi = 10.1111/iju.13137 }}</ref> Whereas conventional AR antagonists bind to the LBD of the AR and [[competitive antagonist|competitively]] displace androgens, thereby preventing them from [[Receptor (biochemistry)#Binding and activation|activating]] the receptor, AR NTD antagonists bind [[covalent bond|covalently]] to the NTD of the AR and prevent [[protein–protein interaction]]s subsequent to activation that are required for [[transcription (biology)|transcriptional activity]].<ref name="ImamuraSadar2016" /> As such, they are [[non-competitive antagonist|non-competitive]] and [[irreversible antagonist]]s of the AR.<ref name="De MolFenwick2016">{{cite journal | vauthors = De Mol E, Fenwick RB, Phang CT, Buzón V, Szulc E, de la Fuente A, Escobedo A, García J, Bertoncini CW, Estébanez-Perpiñá E, McEwan IJ, Riera A, Salvatella X | display-authors = 6 | title = EPI-001, A Compound Active against Castration-Resistant Prostate Cancer, Targets Transactivation Unit 5 of the Androgen Receptor | journal = ACS Chemical Biology | volume = 11 | issue = 9 | pages = 2499–2505 | date = September 2016 | pmid = 27356095 | pmc = 5027137 | doi = 10.1021/acschembio.6b00182 }}</ref> Examples of AR NTD antagonists include [[bisphenol A diglycidyl ether]] (BADGE) and its derivatives [[EPI-001]], [[ralaniten]] (EPI-002), and [[ralaniten acetate]] (EPI-506).<ref name="ImamuraSadar2016" /><ref name="pmid26389532">{{cite journal | vauthors = Martinez-Ariza G, Hulme C | title = Recent advances in allosteric androgen receptor inhibitors for the potential treatment of castration-resistant prostate cancer | journal = Pharmaceutical Patent Analyst | volume = 4 | issue = 5 | pages = 387–402 | year = 2015 | pmid = 26389532 | doi = 10.4155/ppa.15.20 }}</ref> AR NTD antagonists are under investigation for the potential treatment of prostate cancer, and it is thought that they may have greater [[efficacy]] as antiandrogens relative to conventional AR antagonists.<ref name="ImamuraSadar2016" /> In accordance with this notion, AR NTD antagonists are active against [[splice variant]]s of the AR, which conventional AR antagonists are not, and AR NTD antagonists are immune to [[gain-of-function mutation]]s in the AR LBD that convert AR antagonists into AR agonists and commonly occur in prostate cancer.<ref name="ImamuraSadar2016" />

====Androgen receptor degraders====
[[Selective androgen receptor degrader]]s (SARDs) are another new type of antiandrogen that has recently been developed.<ref name="pmid27885283">{{cite journal | vauthors = Lai AC, Crews CM | title = Induced protein degradation: an emerging drug discovery paradigm | journal = Nature Reviews. Drug Discovery | volume = 16 | issue = 2 | pages = 101–114 | date = February 2017 | pmid = 27885283 | pmc = 5684876 | doi = 10.1038/nrd.2016.211 }}</ref>  They work by enhancing the [[downregulation|degradation]] of the AR, and are analogous to [[selective estrogen receptor degrader]]s (SERDs) like [[fulvestrant]] (a drug used to treat [[hormone receptor positive breast tumor|estrogen receptor-positive]] [[breast cancer]]).<ref name="pmid27885283" /> Similarly to AR NTD antagonists, it is thought that SARDs may have greater efficacy than conventional AR antagonists, and for this reason, they are under investigation for the treatment of prostate cancer.<ref name="pmid23219429">{{cite journal | vauthors = Lai KP, Huang CK, Chang YJ, Chung CY, Yamashita S, Li L, Lee SO, Yeh S, Chang C | display-authors = 6 | title = New therapeutic approach to suppress castration-resistant prostate cancer using ASC-J9 via targeting androgen receptor in selective prostate cells | journal = The American Journal of Pathology | volume = 182 | issue = 2 | pages = 460–473 | date = February 2013 | pmid = 23219429 | pmc = 3562731 | doi = 10.1016/j.ajpath.2012.10.029 }}</ref> An example of a SARD is [[dimethylcurcumin]] (ASC-J9), which is under development as a [[topical medication]] for the potential treatment of acne.<ref name="AdisInsight-ASC-J9">{{Cite web | url = http://adisinsight.springer.com/drugs/800028542 | title = ASCJ 9 | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2017-12-24 | archive-date = 2018-03-04 | archive-url = https://web.archive.org/web/20180304204526/http://adisinsight.springer.com/drugs/800028542 | url-status = live }}</ref> SARDs like dimethylcurcumin differ from conventional AR antagonists and AR NTD antagonists in that they may not necessarily bind directly to the AR.<ref name="pmid23219429" />

===Androgen synthesis inhibitors===
{{Main|Androgen synthesis inhibitor}}

Androgen synthesis inhibitors are [[enzyme inhibitor]]s that prevent the [[biosynthesis]] of androgens.<ref name="FiggChau2010" /> This process occurs mainly in the [[gonad]]s and [[adrenal gland]]s, but also occurs in other tissues like the [[prostate gland]], [[skin]], and [[hair follicle]]s. These drugs include aminoglutethimide, ketoconazole,<ref name = "pmid2652864">{{cite journal |vauthors=Witjes FJ, Debruyne FM, Fernandez del Moral P, Geboers AD | title = Ketoconazole high dose in management of hormonally pretreated patients with progressive metastatic prostate cancer. Dutch South-Eastern Urological Cooperative Group | journal = Urology | volume = 33 | issue = 5 | pages = 411–5 |date=May 1989 | pmid = 2652864 | doi = 10.1016/0090-4295(89)90037-X }}</ref> and abiraterone acetate.<ref name="IIIBarbieri2013" /><ref name="FiggChau2010" /><ref name="Held-Warmkessel2006">{{cite book| vauthors = Held-Warmkessel J |title= Contemporary Issues in Prostate Cancer: A Nursing Perspective|url=https://books.google.com/books?id=dZe4ZSVDdBsC&pg=PA275|year=2006|publisher=Jones & Bartlett Learning|isbn=978-0-7637-3075-8|pages=275–}}</ref> Aminoglutethimide inhibits cholesterol side-chain cleavage enzyme, also known as P450scc or CYP11A1, which is responsible for the conversion of [[cholesterol]] into [[pregnenolone]] and by extension the production of all steroid hormones, including the androgens.<ref name="IIIBarbieri2013" /> Ketoconazole and abiraterone acetate are inhibitors of the enzyme CYP17A1, also known as 17α-hydroxylase/17,20-lyase, which is responsible for the conversion of [[pregnane]] steroids into androgens, as well as the conversion of [[mineralocorticoid]]s into glucocorticoids.<ref name="IIIBarbieri2013" /><ref name="FiggChau2010" /> Because these drugs all prevent the formation of glucocorticoids in addition to androgens, they must be combined with a glucocorticoid like [[prednisone]] to avoid [[adrenal insufficiency]].<ref name="Held-Warmkessel2006" /> A newer drug currently under development for treatment of prostate cancer, [[seviteronel]], is selective for inhibition of the 17,20-lyase functionality of CYP17A1, and for this reason, unlike earlier drugs, does not require concomitant treatment with a glucocorticoid.<ref name="pmid27154414">{{cite journal | vauthors = Bird IM, Abbott DH | title = The hunt for a selective 17,20 lyase inhibitor; learning lessons from nature | journal = J. Steroid Biochem. Mol. Biol. | volume = 163 | pages = 136–46 | year = 2016 | pmid = 27154414 | doi = 10.1016/j.jsbmb.2016.04.021 | pmc=5046225}}</ref>

====5α-Reductase inhibitors====
5α-Reductase inhibitors such as finasteride and dutasteride are inhibitors of [[5α-reductase]], an enzyme that is responsible for the formation of DHT from testosterone.<ref name = Flores>{{Cite journal |vauthors=Flores E, Bratoeff E, Cabeza M, Ramirez E, Quiroz A, Heuze I | title = Steroid 5alpha-reductase inhibitors | journal = Mini-Reviews in Medicinal Chemistry | volume = 3 | pages = 225–37 |date=May 2003 | pmid = 12570838 | issue = 3 | doi=10.2174/1389557033488196}}</ref> DHT is between 2.5- and 10-fold more potent than testosterone as an androgen<ref name="MozayaniRaymon2011">{{cite book| vauthors = Mozayani A, Raymon L |title=Handbook of Drug Interactions: A Clinical and Forensic Guide|url=https://books.google.com/books?id=NhBJ6kg_uP0C&pg=PA656|date=18 September 2011|publisher=Springer Science & Business Media|isbn=978-1-61779-222-9|pages=656–}}</ref> and is produced in a [[tissue-selective]] manner based on [[gene expression|expression]] of 5α-reductase.<ref name="Bhagavan2002">{{cite book| vauthors = Bhagavan NV |title=Medical Biochemistry|url=https://books.google.com/books?id=b7Dc9bOs9uAC&pg=PA787 |year=2002|publisher=Academic Press|isbn=978-0-12-095440-7|pages=787–}}</ref> Tissues in which DHT forms at a high rate include the [[prostate gland]], [[skin]], and [[hair follicle]]s.<ref name="BologniaJorizzo" /><ref name="Bhagavan2002" /> In accordance, DHT is involved in the [[pathophysiology]] of benign prostatic hyperplasia, pattern hair loss, and hirsutism, and 5α-reductase inhibitors are used to treat these conditions.<ref name="BologniaJorizzo" /><ref name="Bhagavan2002" /><ref name="pmid27672412">{{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 = J Clin Aesthet Dermatol | volume = 9 | issue = 7 | pages = 56–62 | year = 2016 | pmid = 27672412 | pmc = 5023004 }}</ref>

===Antigonadotropins===
[[File:Estradiol and testosterone levels with a single intramuscular injection of 320 mg polyestradiol phosphate in men.png|thumb|right|300px|class=skin-invert-image|Estradiol and testosterone levels following a single intramuscular injection of 320&nbsp;mg [[polyestradiol phosphate]], a [[polymer]]ic estradiol ester and prodrug, in men with prostate cancer.<ref name="pmid8610057">{{cite journal | vauthors = Stege R, Gunnarsson PO, Johansson CJ, Olsson P, Pousette A, Carlström K | title = Pharmacokinetics and testosterone suppression of a single dose of polyestradiol phosphate (Estradurin) in prostatic cancer patients | journal = Prostate | volume = 28 | issue = 5 | pages = 307–10 | year = 1996 | pmid = 8610057 | doi = 10.1002/(SICI)1097-0045(199605)28:5<307::AID-PROS6>3.0.CO;2-8 | s2cid = 33548251 }}</ref>]]
[[File:Testosterone and luteinizing hormone levels with 100 mg per day oral cyproterone acetate in men.png|thumb|right|300px|class=skin-invert-image|Testosterone and luteinizing hormone levels with 100&nbsp;mg/day oral [[cyproterone acetate]] in men.<ref name="FourcadeMcLeod2015">{{cite journal| vauthors = Fourcade RO, McLeod D |title=Tolerability of Antiandrogens in the Treatment of Prostate Cancer|journal=UroOncology|volume=4|issue=1|year=2015|pages=5–13|issn=1561-0950|doi=10.1080/1561095042000191655}}</ref>]]

[[Antigonadotropin]]s are drugs that suppress the GnRH-mediated [[secretion]] of [[gonadotropin]]s from the [[pituitary gland]].<ref name="FarmerWalker2012" /> Gonadotropins include [[luteinizing hormone]] (LH) and [[follicle-stimulating hormone]] (FSH) and are [[peptide hormone]]s that signal the [[gonad]]s to produce [[sex hormone]]s. By suppressing gonadotropin secretion, antigonadotropins suppress gonadal sex hormone production and by extension circulating androgen levels.<ref name="FarmerWalker2012" /> [[GnRH modulator]]s, including both [[GnRH agonist]]s and [[GnRH antagonist]]s, are powerful antigonadotropins that are able to suppress androgen levels by 95% in men.<ref name="Urotext2001">{{cite book|author=Urotext|title=Urotext-Luts: Urology|url=https://books.google.com/books?id=6zjtA37qDsMC&pg=PA71|date=1 January 2001|publisher=Urotext|isbn=978-1-903737-03-3|pages=71–|access-date=2016-12-27|archive-date=2023-01-11|archive-url=https://web.archive.org/web/20230111061908/https://books.google.com/books?id=6zjtA37qDsMC&pg=PA71|url-status=live}}</ref> In addition, estrogens and progestogens are antigonadotropins via exertion of [[negative feedback]] on the [[hypothalamic–pituitary–gonadal axis]] (HPG axis).<ref name="Brueggemeier2006" /><ref name="pmid10997774">{{cite journal |vauthors=de Lignières B, Silberstein S | title = Pharmacodynamics of oestrogens and progestogens | journal = Cephalalgia: An International Journal of Headache | volume = 20 | issue = 3 | pages = 200–7 |date=April 2000 | pmid = 10997774 | doi = 10.1046/j.1468-2982.2000.00042.x| s2cid = 40392817 | doi-access = free }}</ref><ref name="pmid368741">{{cite journal | vauthors = Neumann F | title = The physiological action of progesterone and the pharmacological effects of progestogens--a short review | journal = Postgraduate Medical Journal | volume = 54 | issue = Suppl 2 | pages = 11–24 | year = 1978 | pmid = 368741 }}</ref> High-dose estrogens are able to suppress androgen levels to castrate levels in men similarly to GnRH modulators,<ref name="pmid7000222">{{cite journal | vauthors = Jacobi GH, Altwein JE, Kurth KH, Basting R, Hohenfellner R | title = Treatment of advanced prostatic cancer with parenteral cyproterone acetate: a phase III randomised trial | journal = Br J Urol | volume = 52 | issue = 3 | pages = 208–15 | year = 1980 | pmid = 7000222 | doi = 10.1111/j.1464-410x.1980.tb02961.x}}</ref> while high-dose progestogens are able to suppress androgen levels by up to approximately 70 to 80% in men.<ref name="WeinKavoussi2011">{{cite book|vauthors=Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA|title=Campbell-Walsh Urology: Expert Consult Premium Edition: Enhanced Online Features and Print, 4-Volume Set|url=https://books.google.com/books?id=fu3BBwAAQBAJ&pg=PA2938|date=25 August 2011|publisher=Elsevier Health Sciences|isbn=978-1-4160-6911-9|pages=2938–|access-date=27 December 2016|archive-date=11 January 2023|archive-url=https://web.archive.org/web/20230111061407/https://books.google.com/books?id=fu3BBwAAQBAJ&pg=PA2938|url-status=live}}</ref><ref name="pmid519881">{{cite journal | vauthors = Kjeld JM, Puah CM, Kaufman B, Loizou S, Vlotides J, Gwee HM, Kahn F, Sood R, Joplin GF | title = Effects of norgestrel and ethinyloestradiol ingestion on serum levels of sex hormones and gonadotrophins in men | journal = Clinical Endocrinology | volume = 11 | issue = 5 | pages = 497–504 | year = 1979 | pmid = 519881 | doi = 10.1111/j.1365-2265.1979.tb03102.x| s2cid = 5836155 }}</ref>

Examples of GnRH agonists include [[leuprorelin]] (leuprolide) and [[goserelin]], while an example of a GnRH antagonist is [[cetrorelix]].<ref name="LemkeWilliams2012" /> Estrogens that are or that have been used as antigonadotropins include estradiol, [[estradiol ester]]s like [[estradiol valerate]], [[estradiol undecylate]], and [[polyestradiol phosphate]], conjugated estrogens, ethinylestradiol, diethylstilbestrol (no longer widely used), and [[bifluranol]].<ref name="pmid18268497">{{cite journal | vauthors = Norman G, Dean ME, Langley RE, Hodges ZC, Ritchie G, Parmar MK, Sydes MR, Abel P, Eastwood AJ | title = Parenteral oestrogen in the treatment of prostate cancer: a systematic review | journal = Br. J. Cancer | volume = 98 | issue = 4 | pages = 697–707 | year = 2008 | pmid = 18268497 | pmc = 2259178 | doi = 10.1038/sj.bjc.6604230 }}</ref><ref name="pmid6258683">{{cite journal | vauthors = Dekanski JB | title = Anti-prostatic activity of bifluranol, a fluorinated bibenzyl | journal = Br. J. Pharmacol. | volume = 71 | issue = 1 | pages = 11–6 | year = 1980 | pmid = 6258683 | pmc = 2044395 | doi = 10.1111/j.1476-5381.1980.tb10903.x}}</ref> Progestogens that are used as antigonadotropins include [[chlormadinone acetate]], cyproterone acetate, gestonorone caproate,<ref name="pmid694436">{{cite journal | vauthors = Sander S, Nissen-Meyer R, Aakvaag A | title = On gestagen treatment of advanced prostatic carcinoma | journal = Scand. J. Urol. Nephrol. | volume = 12 | issue = 2 | pages = 119–21 | year = 1978 | pmid = 694436 | doi = 10.3109/00365597809179977}}</ref> [[hydroxyprogesterone caproate]], medroxyprogesterone acetate, [[megestrol acetate]], and oxendolone.<ref name="Brueggemeier2006" /><ref name="PrentkyBurgess2000">{{cite book| vauthors = Prentky RA, Burgess AW |title= Forensic Management of Sexual Offenders|url=https://books.google.com/books?id=-50Of8_n_TAC&pg=PA219 |date=31 July 2000|publisher=Springer Science & Business Media|isbn=978-0-306-46278-8|pages=219–}}</ref><ref name="pmid294107">{{cite journal | vauthors = Sudo K, Yamazaki I, Masuoka M, Nakayama R | title = Anti-androgen TSAA-291. IV. Effects of the anti-androgen TSAA-291 (16 beta-ethyl-17 beta-hydroxy-4-oestren-3-one) on the secretion of gonadotrophins | journal = Acta Endocrinol Suppl (Copenh) | volume = 229 | pages = 53–66 | year = 1979 | pmid = 294107 | doi = 10.1530/acta.0.092s053}}</ref>

===Miscellaneous===

====Sex hormone-binding globulin modulators====
In addition to their antigonadotropic effects, estrogens are also functional antiandrogens by decreasing free concentrations of androgens via increasing the [[liver|hepatic]] production of [[sex hormone-binding globulin]] (SHBG) and by extension circulating SHBG levels.<ref name="NieschlagBehre2012">{{cite book| vauthors = Nieschlag E, Behre HM, Nieschlag S |title=Testosterone: Action, Deficiency, Substitution |url= https://books.google.com/books?id=MkrAPaQ4wJkC&pg=PA62 |date=26 July 2012|publisher=Cambridge University Press|isbn=978-1-107-01290-5|pages=62–}}</ref><ref name="HumansOrganization2007">{{cite book|author1=IARC Working Group on the Evaluation of Carcinogenic Risks to Humans|author2=World Health Organization|author3=International Agency for Research on Cancer|title=Combined Estrogen-progestogen Contraceptives and Combined Estrogen-progestogen Menopausal Therapy|url=https://books.google.com/books?id=aGDU5xibtNgC&pg=PA157|year=2007|publisher=World Health Organization|isbn=978-92-832-1291-1|pages=157–}}</ref><ref name="pmid22294742">{{cite journal | vauthors = Coss CC, Jones A, Parke DN, Narayanan R, Barrett CM, Kearbey JD, Veverka KA, Miller DD, Morton RA, Steiner MS, Dalton JT | title = Preclinical characterization of a novel diphenyl benzamide selective ERα agonist for hormone therapy in prostate cancer | journal = Endocrinology | volume = 153 | issue = 3 | pages = 1070–81 | year = 2012 | pmid = 22294742 | doi = 10.1210/en.2011-1608 | doi-access = free }}</ref> [[Combined oral contraceptive]]s containing ethinylestradiol have been found to increase circulating SHBG levels by 2- to 4-fold in women and to reduce free testosterone concentrations by 40 to 80%.<ref name="HumansOrganization2007" /> However, combined oral contraceptives that contain the particularly androgenic progestin [[levonorgestrel]] have been found to increase SHBG levels by only 50 to 100%,<ref name="HumansOrganization2007" /> which is likely because activation of the AR in the liver has the opposite effect of estrogen and suppresses production of SHBG.<ref name="KrishnaR.2000">{{cite book| vauthors = Krishna UR, Sheriar NK |title=Adolescent Gynecology (pb)|url=https://books.google.com/books?id=B8hcC17D154C&pg=PA121|date=1 January 2000|publisher=Orient Blackswan|isbn=978-81-250-1793-6|pages=121–}}</ref> Levonorgestrel and certain other [[19-nortestosterone]] progestins used in combined oral contraceptives like [[norethisterone]] also directly bind to and displace androgens from SHBG, which may additionally antagonize the functional antiandrogenic effects of ethinylestradiol.<ref name="KrishnaR.2000"/><ref name="FilshieGuillebaud2013">{{cite book| vauthors = Filshie M, Guillebaud J |title=Contraception: Science and Practice|url=https://books.google.com/books?id=Ug3-BAAAQBAJ&pg=PA26 |date=22 October 2013 |publisher=Elsevier Science |isbn=978-1-4831-6366-6 |pages=26–}}</ref> In men, a study found that treatment with a relatively low dosage of 20&nbsp;μg/day ethinylestradiol for 5&nbsp;weeks increased circulating SHBG levels by 150% and, due to the accompanying decrease free testosterone levels, increased total circulating levels of testosterone by 50% (via reduced negative feedback by androgens on the HPG axis).<ref name="NieschlagBehre2012" />

====Corticosteroid-binding globulin modulators====
[[Estrogen (medication)|Estrogens]] at high doses can partially suppress adrenal androgen production.<ref name="Oettel1999">{{cite book | vauthors = Oettel M | title=Estrogens and Antiestrogens II | series=Handbook of Experimental Pharmacology | chapter=Estrogens and Antiestrogens in the Male | publisher=Springer Berlin Heidelberg | publication-place=Berlin, Heidelberg | year=1999 | volume=135 / 2 | issn=0171-2004 | doi=10.1007/978-3-642-60107-1_25 | pages=505–571| isbn=978-3-642-64261-6 }}</ref><ref name="MargiorisChrousos2001">{{cite book| vauthors = Margioris AN, Chrousos GP |title=Adrenal Disorders|url=https://books.google.com/books?id=XB73BwAAQBAJ&pg=PA84|date=20 April 2001|publisher=Springer Science & Business Media|isbn=978-1-59259-101-5|pages=84–}}</ref><ref name="pmid7586614">{{cite journal | vauthors = Polderman KH, Gooren LJ, van der Veen EA | title = Effects of gonadal androgens and oestrogens on adrenal androgen levels | journal = Clin. Endocrinol. (Oxf) | volume = 43 | issue = 4 | pages = 415–21 | date = October 1995 | pmid = 7586614 | doi = 10.1111/j.1365-2265.1995.tb02611.x  | s2cid = 6815423 }}</ref><ref name="pmid2958420">{{cite journal | vauthors = Stege R, Eriksson A, Henriksson P, Carlström K | title = Orchidectomy or oestrogen treatment in prostatic cancer: effects on serum levels of adrenal androgens and related steroids | journal = Int. J. Androl. | volume = 10 | issue = 4 | pages = 581–7 | date = August 1987 | pmid = 2958420 | doi = 10.1111/j.1365-2605.1987.tb00357.x | doi-access = free }}</ref><ref name="pmid2734983">{{cite journal | vauthors = Pousette A, Carlström K, Stege R | title = Androgens during different modes of endocrine treatment of prostatic cancer | journal = Urol. Res. | volume = 17 | issue = 2 | pages = 95–8 | date = 1989 | pmid = 2734983 | doi = 10.1007/BF00262027 | s2cid = 25309877 }}</ref><ref name="pmid7500443">{{cite journal | vauthors = Cox RL, Crawford ED | title = Estrogens in the treatment of prostate cancer | journal = J. Urol. | volume = 154 | issue = 6 | pages = 1991–8 | date = December 1995 | pmid = 7500443 | doi = 10.1016/S0022-5347(01)66670-9 }}</ref> A study found that treatment with a high-dose [[ethinylestradiol]] (100&nbsp;μg/day) reduced levels of major circulating [[adrenal androgen]]s by 27 to 48% in [[transgender women]].<ref name="Oettel1999" /><ref name="MargiorisChrousos2001" /><ref name="pmid7586614" /> Decreased adrenal androgens with estrogens is apparent with [[oral administration|oral]] and [[synthetic compound|synthetic]] estrogens like [[ethinylestradiol]] and [[estramustine phosphate]] but is minimal with [[parenteral administration|parenteral]] [[bioidentical]] [[estradiol (medication)|estradiol]] forms like [[polyestradiol phosphate]].<ref name="pmid2734983" /> It is thought to be mediated via a [[liver|hepatic]] mechanism, probably increased [[corticosteroid-binding globulin]] (CBG) [[biosynthesis|production]] and levels and compensatory changes in adrenal steroid production (e.g., shunting of adrenal androgen synthesis to [[cortisol]] production).<ref name="pmid2734983" /><ref name="pmid7500443" /> It is notable in this regard that oral and synthetic estrogens, due to the oral [[first pass effect|first pass]] and resistance to hepatic [[metabolism]], have much stronger influences on [[liver protein synthesis]] than parenteral estradiol.<ref name="pmid2664738">{{cite journal | vauthors = von Schoultz B, Carlström K, Collste L, Eriksson A, Henriksson P, Pousette A, Stege R | title = Estrogen therapy and liver function--metabolic effects of oral and parenteral administration | journal = Prostate | volume = 14 | issue = 4 | pages = 389–95 | date = 1989 | pmid = 2664738 | doi = 10.1002/pros.2990140410 | s2cid = 21510744 | url = }}</ref> The decrease in adrenal androgen levels with high-dose estrogen therapy may be beneficial in the treatment of [[prostate cancer]].<ref name="pmid7586614" /><ref name="pmid7500443" />

====Anticorticotropins====
[[Anticorticotropin]]s such as [[glucocorticoid]]s and [[mineralocorticoid]]s work by exerting [[negative feedback]] on the [[hypothalamic–pituitary–adrenal axis]] (HPA axis), thereby inhibiting the secretion of [[corticotropin-releasing hormone]] (CRH) and hence [[adrenocorticotropic hormone]] (ACTH; corticotropin) and consequently suppressing the production of [[androgen prohormone]]s like [[dehydroepiandrosterone]] (DHEA), [[dehydroepiandrosterone sulfate]] (DHEA-S), and [[androstenedione]] in the [[adrenal gland]].<ref name="MelmedPolonsky2011">{{cite book| vauthors = Melmed S, Polonsky KS, Larsen PR, Kronenberg HM |title= Williams Textbook of Endocrinology E-Book|url=https://books.google.com/books?id=nbg1QOAObicC&pg=PA753|date=12 May 2011|publisher=Elsevier Health Sciences|isbn=978-1-4377-3600-7|pages=753–}}</ref><ref name="KumarAbbas2009">{{cite book | vauthors = Kumar V, Abbas AK, Fausto N, Aster JC |title=Robbins & Cotran Pathologic Basis of Disease E-Book|url=https://books.google.com/books?id=_1Zmvm4JVNcC&pg=PA1154|date=10 June 2009|publisher=Elsevier Health Sciences|isbn=978-1-4377-2015-0|pages=1154–}}</ref> They are rarely used clinically as functional antiandrogens, but are used as such in the case of [[congenital adrenal hyperplasia]] in girls and women, in which there are excessive production and levels of adrenal androgens due to glucocorticoid deficiency and hence HPA axis overactivity.<ref name="MelmedPolonsky2011" /><ref name="KumarAbbas2009" />

====Insulin sensitizers====
In women with [[insulin resistance]], such as those with [[polycystic ovary syndrome]], androgen levels are often elevated.<ref name="NikolakisKyrgidis2019">{{cite journal | vauthors = Nikolakis G, Kyrgidis A, Zouboulis CC | title = Is There a Role for Antiandrogen Therapy for Hidradenitis Suppurativa? A Systematic Review of Published Data | journal = American Journal of Clinical Dermatology | volume = 20 | issue = 4 | pages = 503–513 | date = August 2019 | pmid = 31073704 | doi = 10.1007/s40257-019-00442-w | s2cid = 149443722 }}</ref> [[Metformin]], an [[insulin-sensitizing medication]], has indirect antiandrogenic effects in such women, decreasing [[testosterone]] levels by as much as 50% secondary to its beneficial effects on insulin sensitivity.<ref name="NikolakisKyrgidis2019" /><ref name="pmid28058854">{{cite journal | vauthors = Patel R, Shah G | title = Effect of metformin on clinical, metabolic and endocrine outcomes in women with polycystic ovary syndrome: a meta-analysis of randomized controlled trials | journal = Current Medical Research and Opinion | volume = 33 | issue = 9 | pages = 1545–1557 | date = September 2017 | pmid = 28058854 | doi = 10.1080/03007995.2017.1279597 | s2cid = 4391302 }}</ref><ref name="pmid33014044">{{cite journal | vauthors = Guan Y, Wang D, Bu H, Zhao T, Wang H | title = The Effect of Metformin on Polycystic Ovary Syndrome in Overweight Women: A Systematic Review and Meta-Analysis of Randomized Controlled Trials | journal = International Journal of Endocrinology | volume = 2020 | issue =  | pages = 5150684 | date = 2020 | pmid = 33014044 | pmc = 7519180 | doi = 10.1155/2020/5150684 | doi-access = free }}</ref>

====Immunogens and vaccines====
[[Ovandrotone albumin]] (Fecundin, Ovastim) and [[Androvax]] (androstenedione albumin) are [[immunogen]]s and [[vaccine]]s against [[4-androstenedione|androstenedione]] that are used in [[veterinary medicine]] to improve [[fecundity]] (reproductive rate) in ewes (adult female sheep).<ref name="SreenanDiskin2012">{{cite book| vauthors = Sreenan JM, Diskin MG |title=Embryonic Mortality in Farm Animals |url= https://books.google.com/books?id=QKFyBgAAQBAJ&pg=PA172 |date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-94-009-5038-2|pages=172–}}</ref><ref name="JindalSharma2010">{{cite book| vauthors = Jindal SK, Sharma MC |title=Biotechnology in Animal Health and Production |url= https://books.google.com/books?id=e9yFom2LWTcC&pg=PA77|year=2010|publisher=New India Publishing|isbn=978-93-80235-35-6|pages=77–}}</ref> The generation of [[antibodies]] against androstenedione by these agents is thought to decrease circulating levels of androstenedione and its metabolites (e.g., testosterone and estrogens), which in turn increases the activity of the HPG axis via reduced negative feedback and increases the rate of [[ovulation]], resulting in greater [[fertility]] and fecundity.<ref name="SreenanDiskin2012" /><ref name="JindalSharma2010" />

==Chemistry==
{{See also|List of antiandrogens|List of steroidal antiandrogens}}

Antiandrogens can be divided into several different types based on [[chemical structure]], including [[steroidal antiandrogen]]s, [[nonsteroidal antiandrogen]]s, and [[peptide]]s. Steroidal antiandrogens include compounds like [[cyproterone acetate]], [[spironolactone]], [[estradiol (medication)|estradiol]], [[abiraterone acetate]], and [[finasteride]]; nonsteroidal antiandrogens include compounds like [[bicalutamide]], [[elagolix]], [[diethylstilbestrol]], [[aminoglutethimide]], and [[ketoconazole]]; and peptides include [[GnRH analogue]]s like [[leuprorelin]] and [[cetrorelix]].{{citation needed|date=May 2021}}

==History==
{{See also|Discovery and development of antiandrogens}}

Antigonadotropins like estrogens and progestogens were both first introduced in the 1930s.<ref name="FritzSperoff2012">{{cite book| vauthors = Fritz MA, Speroff L |title=Clinical Gynecologic Endocrinology and Infertility|url=https://books.google.com/books?id=KZLubBxJEwEC&pg=PA750|date=28 March 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-4511-4847-3|pages=750–751, 963}}</ref> The beneficial effects of androgen deprivation via surgical castration or high-dose estrogen therapy on prostate cancer were discovered in 1941.<ref name="FiggChau2010"/>{{rp|56}}<ref name="KavoussiCostabile2012">{{cite book | vauthors = Kavoussi P, Costabile RA, Salonia A |title=Clinical Urologic Endocrinology: Principles for Men's Health |url=https://books.google.com/books?id=osURyQf4-2EC&pg=PR7 |date=17 October 2012 |publisher=Springer Science & Business Media |isbn=978-1-4471-4404-5 |pages=7–}}</ref> AR antagonists were first discovered in the early 1960s.<ref name="Weber2015" /> The steroidal antiandrogen cyproterone acetate was discovered in 1961. and introduced in 1973. and is often described as the first antiandrogen to have been marketed.<ref name="AcademicPress1997">{{cite book|title=Advances in Drug Research|url=https://books.google.com/books?id=f1aKl17UpxkC&pg=PA34|date=12 August 1997|publisher=Academic Press|isbn=978-0-08-052628-7|pages=34–}}</ref><ref name="StunkardBaum1989" /> However, spironolactone was introduced in 1959.,<ref name="Jugdutt2014">{{cite book|vauthors=Jugdutt BI|title=Aging and Heart Failure: Mechanisms and Management|url=https://books.google.com/books?id=0e23BAAAQBAJ&pg=PA175|date=19 February 2014|publisher=Springer Science & Business Media|isbn=978-1-4939-0268-2|pages=175–|access-date=27 December 2016|archive-date=11 January 2023|archive-url=https://web.archive.org/web/20230111122900/https://books.google.com/books?id=0e23BAAAQBAJ&pg=PA175|url-status=live}}</ref><ref name="Wermuth2011">{{cite book| vauthors = Wermuth CG |title=The Practice of Murl=https://books.google.com/books?id=Qmt1_DQkCpEC&pg=PA34|date=2 May 2011|publisher=Academic Press|isbn=978-0-08-056877-5|pages=34–|author-link = Camille Georges Wermuth}}</ref> although its antiandrogen effects were not recognized or taken advantage of until later and were originally an unintended off-target action of the drug.<ref name="Azziz2007">{{cite book| vauthors = Azziz R |title=Androgen Excess Disorders in Women|url=https://books.google.com/books?id=Ch-BsGAOtucC&pg=PA382|date=8 November 2007|publisher=Springer Science & Business Media|isbn=978-1-59745-179-6|pages=382–}}</ref> In addition to spironolactone, chlormadinone acetate and megestrol acetate are steroidal antiandrogens that are weaker than cyproterone acetate but were also introduced earlier, in the 1960s.<ref name="RunnebaumRabe2012">{{cite book| vauthors = Runnebaum BC, Rabe T, Kiesel L |title=Female Contraception: Update and Trends|url=https://books.google.com/books?id=LtT6CAAAQBAJ&pg=PA136|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-73790-9|pages=136–}}</ref><ref name="OrfanosMontagna2012">{{cite book| vauthors = Orfanos CE, Montagna W, Stüttgen G |title=Hair Research: Status and Future Aspects; Proceedings of the First International Congress on Hair Research, Hamburg, March 13th–16, 1979|url=https://books.google.com/books?id=4gBJCAAAQBAJ&pg=PT587|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-81650-5|pages=587–}}</ref><ref name="Marks2010">{{cite book| vauthors = Marks L |title=Sexual Chemistry: A History of the Contraceptive Pill|url=https://books.google.com/books?id=_i-s4biQs7MC&pg=PA76|year=2010|publisher=Yale University Press|isbn=978-0-300-16791-7|pages=76–78}}</ref> Other early steroidal antiandrogens that were developed around this time but were never marketed include [[benorterone]] (SKF-7690; 17α-methyl-''B''-nortestosterone), [[BOMT]] (Ro 7–2340), [[cyproterone]] (SH-80881), and [[trimethyltrienolone]] (R-2956).<ref name="HorskyPresl2012">{{cite book| vauthors = Horsky J, Presl J |title=Ovarian Function and its Disorders: Diagnosis and Therapy|url=https://books.google.com/books?id=7IrpCAAAQBAJ&pg=PA112|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-94-009-8195-9|pages=112–}}</ref><ref name="AcademicPress1976">{{cite book|title=Vitamins and Hormones|url=https://books.google.com/books?id=5ZbLRONHoDoC&pg=PA682|date=18 May 1976|publisher=Academic Press|isbn=978-0-08-086630-7|pages=682–}}</ref>

The nonsteroidal antiandrogen flutamide was first reported in 1967.<ref name="SmithWilliams2005" /> It was introduced in 1983 and was the first nonsteroidal antiandrogen marketed.<ref name="Neal2012">{{cite book| vauthors = Neal DE |title=Tumours in Urology|url=https://books.google.com/books?id=k28yBwAAQBAJ&pg=PT233|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-1-4471-2086-5|pages=233–}}</ref><ref name="OttowWeinmann2008">{{cite book| vauthors = Ottow E, Weinmann H |title= Nuclear Receptors as Drug Targets|url=https://books.google.com/books?id=iATfLbPgRugC&pg=PA255|date=8 September 2008|publisher=John Wiley & Sons|isbn=978-3-527-62330-3|pages=255–}}</ref> Another early nonsteroidal antiandrogen,<ref name="SinghalThomas1976">{{cite book| vauthors = Singhal RL, Thomas JA |title=Cellular Mechanisms Modulating Gonadal Action|url=https://books.google.com/books?id=2eNqAAAAMAAJ|date=1 January 1976|publisher=University Park Press|isbn=978-0-8391-0776-7|page=239}}</ref> [[DIMP (antiandrogen)|DIMP]] (Ro 7–8117), which is structurally related to [[thalidomide]]<ref name="LiuSu2010">{{cite journal | vauthors = Liu B, Su L, Geng J, Liu J, Zhao G | title = Developments in nonsteroidal antiandrogens targeting the androgen receptor | journal = ChemMedChem | volume = 5 | issue = 10 | pages = 1651–1661 | date = October 2010 | pmid = 20853390 | doi = 10.1002/cmdc.201000259 | s2cid = 23228778 }}</ref> and is a relatively weak antiandrogen,<ref name="HeynsG.1976">{{cite journal | vauthors = Heyns W, Verhoeven G, De Moor P | title = Androgen binding in rat uterus cytosol. Study of the specificity | journal = Journal of Steroid Biochemistry | volume = 7 | issue = 5 | pages = 335–343 | date = May 1976 | pmid = 180344 | doi = 10.1016/0022-4731(76)90092-3 }}</ref><ref>{{cite book|title=Annual Reports in Medicinal Chemistry|url=https://books.google.com/books?id=qsFCGskRHZQC&pg=PA182|date=16 September 1986|publisher=Academic Press|isbn=978-0-08-058365-5|pages=182–}}</ref> was first described in 1973 and was never marketed.<ref name="BorisScott1973">{{cite journal | vauthors = Boris A, Scott JW, DeMartino L, Cox DC | title = Endocrine profile of a nonsteroidal antiandrogen N-(3,5-dimethyl-4-isoxazolylmethyl)phthalimide (DIMP) | journal = Acta Endocrinologica | volume = 72 | issue = 3 | pages = 604–614 | date = March 1973 | pmid = 4739363 | doi = 10.1530/acta.0.0720604 }}</ref> Flutamide was followed by nilutamide in 1989. and bicalutamide in 1995.<ref name="BéguéBonnet-Delpon2008">{{cite book|vauthors=Bégué JP, Bonnet-Delpon D|title=Bioorganic and Medicinal Chemistry of Fluorine|url=https://books.google.com/books?id=QMVSvZ-R7I0C&pg=PA327|date=2 June 2008|publisher=John Wiley & Sons|isbn=978-0-470-28187-1|pages=327–|access-date=27 December 2016|archive-date=12 January 2023|archive-url=https://web.archive.org/web/20230112173104/https://books.google.com/books?id=QMVSvZ-R7I0C&pg=PA327|url-status=live}}</ref> In addition to these three drugs, which have been regarded as first-generation nonsteroidal antiandrogens, the second-generation nonsteroidal antiandrogens [[enzalutamide]] and [[apalutamide]] were introduced in 2012. and 2018.<ref name="pmid23341368">{{cite journal | vauthors = Menon MP, Higano CS | title = Enzalutamide, a second generation androgen receptor antagonist: development and clinical applications in prostate cancer | journal = Current Oncology Reports | volume = 15 | issue = 2 | pages = 69–75 | date = April 2013 | pmid = 23341368 | doi = 10.1007/s11912-013-0293-9 | s2cid = 8725297 }}</ref><ref name="pmid19359544">{{cite journal | vauthors = Tran C, Ouk S, Clegg NJ, Chen Y, Watson PA, Arora V, Wongvipat J, Smith-Jones PM, Yoo D, Kwon A, Wasielewska T, Welsbie D, Chen CD, Higano CS, Beer TM, Hung DT, Scher HI, Jung ME, Sawyers CL | display-authors = 6 | title = Development of a second-generation antiandrogen for treatment of advanced prostate cancer | journal = Science | volume = 324 | issue = 5928 | pages = 787–790 | date = May 2009 | pmid = 19359544 | pmc = 2981508 | doi = 10.1126/science.1168175 | bibcode = 2009Sci...324..787T }}</ref><ref name="FDA2018">{{Cite web|url=https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm596768.htm|title=FDA approves new treatment for a certain type of prostate cancer using novel clinical trial endpoint|website=[[Food and Drug Administration]]|date=24 March 2020|access-date=1 April 2018|archive-date=23 April 2019|archive-url=https://web.archive.org/web/20190423072230/https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm596768.htm|url-status=live}}</ref> They differ from the earlier nonsteroidal antiandrogens namely in that they are much more efficacious in comparison.<ref name="pmid19359544" />

The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960. and 1977., respectively,<ref name="Sneader2005">{{cite book| vauthors = Sneader W |title=Drug Discovery: A History|url=https://books.google.com/books?id=Cb6BOkj9fK4C&pg=PA367|date=23 June 2005|publisher=John Wiley & Sons|isbn=978-0-471-89979-2|pages=367–}}</ref><ref name="Golan2008">{{cite book|vauthors=Golan DE|title=Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy|url=https://books.google.com/books?id=az8uSDkB0mgC&pg=PA624|year=2008|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-8355-2|pages=624–|access-date=2016-12-27|archive-date=2023-01-10|archive-url=https://web.archive.org/web/20230110131048/https://books.google.com/books?id=az8uSDkB0mgC&pg=PA624|url-status=live}}</ref> and the newer drug abiraterone acetate was introduced in 2011.<ref name="Demos2011">{{cite book|title=Prostate Cancer|url=https://books.google.com/books?id=WJkjgbRJe3EC&pg=PA518|date=20 December 2011|publisher=Demos Medical Publishing|isbn=978-1-935281-91-7|pages=518–}}</ref> GnRH modulators were first introduced in the 1980s.<ref name="BowsherCarter2008">{{cite book| vauthors = Bowsher W, Carter A |title= Challenges in Prostate Cancer|url=https://books.google.com/books?id=E3VNhLkqPmUC&pg=PA138|date=15 April 2008|publisher=John Wiley & Sons|isbn=978-1-4051-7177-9|pages=138–}}</ref> The 5α-reductase inhibitors finasteride and dutasteride were introduced in 1992. and 2002. respectively.<ref name="AllahbadiaAgrawal2007">{{cite book| vauthors = Allahbadia G, Agrawal R, Merchant R |title=Polycystic Ovary Syndrome|url=https://books.google.com/books?id=HX0JxcrWJvAC&pg=PA184|year=2007|publisher=Anshan|isbn=978-1-904798-74-3|pages=184–}}</ref><ref name="Bentham2010">{{cite book|title=Frontiers in Medicinal Chemistry|url=https://books.google.com/books?id=b7hCWvdP5OYC&pg=PA329|year=2010|publisher=Bentham Science Publishers|isbn=978-1-60805-208-0|pages=329–}}</ref> [[Elagolix]], the first orally active GnRH modulator to be marketed, was introduced in 2018.<ref name="AdisInsight-Elagolix">{{Cite web | url = https://adisinsight.springer.com/drugs/800020238 | title = Elagolix - Abbvie/Neurocrine Biosciences | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2018-07-30 | archive-date = 2018-09-20 | archive-url = https://web.archive.org/web/20180920082806/https://adisinsight.springer.com/drugs/800020238 | url-status = live }}</ref>

===Timeline===
The following is a timeline of events in the history of antiandrogens:<ref name="pmid29730201">{{cite journal | vauthors = Crawford ED, Schellhammer PF, McLeod DG, Moul JW, Higano CS, Shore N, Denis L, Iversen P, Eisenberger MA, Labrie F | title = Androgen Receptor Targeted Treatments of Prostate Cancer: 35 Years of Progress with Antiandrogens | journal = J. Urol. | volume = 200 | issue = 5 | pages = 956–966 | date = November 2018 | pmid = 29730201 | doi = 10.1016/j.juro.2018.04.083 | s2cid = 19162538 }}</ref>
* 1941: Hudgins and Hodges show that androgen deprivation via high-dose estrogen therapy or surgical castration treats prostate cancer
* 1957: The steroidal antiandrogen spironolactone is first synthesized<ref name="pmid28634268">{{cite journal | vauthors = Kolkhof P, Bärfacker L | title = 30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor antagonists: 60 years of research and development | journal = J. Endocrinol. | volume = 234 | issue = 1 | pages = T125–T140 | date = July 2017 | pmid = 28634268 | pmc = 5488394 | doi = 10.1530/JOE-16-0600 }}</ref>
* 1960: Spironolactone is first introduced for medical use, as an antimineralocorticoid<ref name="pmid28634268" />
* 1961: The steroidal antiandrogen cyproterone acetate is first synthesized<ref name="pmid9476091">{{cite journal | vauthors = Pucci E, Petraglia F | title = Treatment of androgen excess in females: yesterday, today and tomorrow | journal = Gynecol. Endocrinol. | volume = 11 | issue = 6 | pages = 411–33 | date = December 1997 | pmid = 9476091 | doi = 10.3109/09513599709152569 }}</ref>
* 1962: Spironolactone is first reported to produce gynecomastia in men<ref name="pmid28634268" /><ref name="Smith1962">{{cite journal| vauthors = Smith WG |title=Spironolactone and gynaecomastia|journal=The Lancet|volume=280|issue=7261|year=1962|pages=886|issn=0140-6736|doi=10.1016/S0140-6736(62)90668-2}}</ref>
* 1966: Benorterone is the first known antiandrogen to be studied clinically, to treat acne and hirsutism in women<ref name="pmid148431">{{cite journal | vauthors = Stewart ME, Pochi PE | title = Antiandrogens and the skin | journal = Int. J. Dermatol. | volume = 17 | issue = 3 | pages = 167–79 | date = April 1978 | pmid = 148431 | doi = 10.1111/j.1365-4362.1978.tb06057.x | s2cid = 43649686 }}</ref><ref name="pmid4225258">{{cite journal | vauthors = Zarate A, Mahesh VB, Greenblatt RB | title = Effect of an antiandrogen, 17-alpha-methyl-B-nortestosterone, on acne and hirsutism | journal = J. Clin. Endocrinol. Metab. | volume = 26 | issue = 12 | pages = 1394–8 | date = December 1966 | pmid = 4225258 | doi = 10.1210/jcem-26-12-1394 }}</ref>
* 1963: The antiandrogenic activity of cyproterone acetate is discovered<ref name="Neumann1996">{{cite book| vauthors = Neumann F |title=Antiandrogens in Prostate Cancer|chapter=Pharmacology of Cyproterone Acetate — A Short Review|year=1996|pages=31–44|doi=10.1007/978-3-642-45745-6_3|isbn=978-3-642-45747-0}}</ref><ref name="pmid14071315">{{cite journal | vauthors = Hamada H, Neumann F, Junkmann K | title = Intrauterine Antimaskuline Beeinflussung von Rattenfeten Durch ein Stark Gestagen Wirksames Steroid | language = de | journal = Acta Endocrinologica | volume = 44 | issue = 3 | pages = 380–388 | date = November 1963 | pmid = 14071315 | doi = 10.1530/acta.0.0440380 | trans-title = Intrauterine antimasculine influence of Rat Fetuses by Birtue of a Powerful Steroid Acting as a Progestogen }}</ref>
* 1967: A known antiandrogen, benorterone, is first reported to induce gynecomastia in males<ref name="pmid148431" />
* 1967: The first-generation nonsteroidal antiandrogen flutamide is first synthesized
* 1967: Cyproterone acetate was first studied clinically, to treat sexual deviance in men<ref name="pmid20459370">{{cite journal | vauthors = Thibaut F, De La Barra F, Gordon H, Cosyns P, Bradford JM | title = The World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the biological treatment of paraphilias | journal = World J. Biol. Psychiatry | volume = 11 | issue = 4 | pages = 604–55 | date = June 2010 | pmid = 20459370 | doi = 10.3109/15622971003671628 | s2cid = 14949511 }}</ref>
* 1969: Cyproterone acetate was first studied in the treatment of acne, hirsutism, seborrhea, and scalp hair loss in women<ref name="pmid4304873">{{cite journal | vauthors = Hammerstein J, Cupceancu B | title = Behandlung des Hirsutismus mit Cyproteronacetat | trans-title = Management of hirsutism using cyproterone acetate | language = de | journal = Deutsche Medizinische Wochenschrift | volume = 94 | issue = 16 | pages = 829–34 | date = April 1969 | issn = 0012-0472 | pmid = 4304873 | doi = 10.1055/s-0028-1111126 | s2cid = 71214286 }}</ref>
* 1969: The antiandrogenic activity of spironolactone is discovered<ref name="pmid5344274">{{cite journal | vauthors = Steelman SL, Brooks JR, Morgan ER, Patanelli DJ | title = Anti-androgenic activity of spironolactone | journal = Steroids | volume = 14 | issue = 4 | pages = 449–50 | year = 1969 | pmid = 5344274 | doi = 10.1016/s0039-128x(69)80007-3}}</ref>
* 1972: The antiandrogenic activity of flutamide is first reported<ref name="pmid4264731">{{cite journal | vauthors = Neri R, Florance K, Koziol P, Van Cleave S | title = A biological profile of a nonsteroidal antiandrogen, SCH 13521 (4'-nitro-3'trifluoromethylisobutyranilide) | journal = Endocrinology | volume = 91 | issue = 2 | pages = 427–37 | date = August 1972 | pmid = 4264731 | doi = 10.1210/endo-91-2-427 }}</ref><ref name="pmid4116667">{{cite journal | vauthors = Neri RO, Monahan M | title = Effects of a novel nonsteroidal antiandrogen on canine prostatic hyperplasia | journal = Invest Urol | volume = 10 | issue = 2 | pages = 123–30 | date = September 1972 | pmid = 4116667 }}</ref>
* 1973: Cyproterone acetate was first introduced for medical use, to treat sexual deviance<ref name="pmid8005205">{{cite journal | vauthors = Neumann F | title = The antiandrogen cyproterone acetate: discovery, chemistry, basic pharmacology, clinical use and tool in basic research | journal = Exp. Clin. Endocrinol. | volume = 102 | issue = 1 | pages = 1–32 | date = 1994 | pmid = 8005205 | doi = 10.1055/s-0029-1211261 | doi-access = free }}</ref>
* 1977: The first-generation antiandrogen nilutamide is first described<ref name="pmid385986">{{cite journal | vauthors = Raynaud JP, Bonne C, Bouton MM, Lagace L, Labrie F | title = Action of a non-steroid anti-androgen, RU 23908, in peripheral and central tissues | journal = J. Steroid Biochem. | volume = 11 | issue = 1A | pages = 93–9 | year = 1979 | pmid = 385986 | doi = 10.1016/0022-4731(79)90281-4}}</ref>
* 1978: Spironolactone is first studied in the treatment of hirsutism in women<ref name="pmid6205409"/><ref name="pmid717935">{{cite journal | vauthors = Ober KP, Hennessy JF | title = Spironolactone therapy for hirsutism in a hyperandrogenic woman | journal = Ann. Intern. Med. | volume = 89 | issue = 5 Pt 1 | pages = 643–4 | year = 1978 | pmid = 717935 | doi = 10.7326/0003-4819-89-5-643}}</ref>
* 1979: Combined androgen blockade is first studied<ref name="pmid16631454">{{cite journal | vauthors = Klotz L | title = Combined androgen blockade: an update | journal = Urol. Clin. North Am. | volume = 33 | issue = 2 | pages = 161–6, v–vi | date = May 2006 | pmid = 16631454 | doi = 10.1016/j.ucl.2005.12.001 }}</ref><ref name="pmid6819101">{{cite journal | vauthors = Labrie F, Dupont A, Belanger A, Cusan L, Lacourciere Y, Monfette G, Laberge JG, Emond JP, Fazekas AT, Raynaud JP, Husson JM | title = New hormonal therapy in prostatic carcinoma: combined treatment with an LHRH agonist and an antiandrogen | journal = Clin Invest Med | volume = 5 | issue = 4 | pages = 267–75 | date = 1982 | pmid = 6819101 }}</ref>
* 1980: Medical castration via a GnRH analogue is first achieved{{Citation needed|date=March 2020}}
* 1982: The first-generation antiandrogen bicalutamide is first described<ref name="EngelKleemann2014">{{cite book | vauthors = Engel J, Kleemann A, Kutscher B, Reichert D |title=Pharmaceutical Substances: Syntheses, Patents and Applications of the most relevant APIs |edition=5th |year=2009 |url=https://books.google.com/books?id=4lCGAwAAQBAJ&pg=PA153 |publisher=Thieme |isbn=978-3-13-179275-4 |pages=153–154}}</ref>
* 1982: Combined androgen blockade for prostate cancer is developed
* 1983: Flutamide is first introduced, in Chile, for medical use, to treat prostate cancer<ref name="Publishing2013">{{cite book|author=William Andrew Publishing|title=Pharmaceutical Manufacturing Encyclopedia, 3rd Edition|url=https://books.google.com/books?id=_J2ti4EkYpkC&pg=PA1695|date=22 October 2013|publisher=Elsevier|isbn=978-0-8155-1856-3|pages=1695–|access-date=2 January 2019|archive-date=12 January 2023|archive-url=https://web.archive.org/web/20230112173105/https://books.google.com/books?id=_J2ti4EkYpkC&pg=PA1695|url-status=live}}</ref><ref name="Ireland2013">{{cite book|title=The Irish Reports: Containing Reports of Cases Argued and Determined in the Court of Appeal, the High Court of Justice, the Court of Bankruptcy, in Ireland, and the Irish Land Commission|url=https://books.google.com/books?id=FQhMAQAAIAAJ|year=1990|publisher=Incorporated Council of Law Reporting for Ireland|pages=501–502|access-date=2019-01-02|archive-date=2023-01-12|archive-url=https://web.archive.org/web/20230112173103/https://books.google.com/books?id=FQhMAQAAIAAJ|url-status=live}}</ref>
* 1987: Nilutamide is first introduced, in France, for medical use, to treat prostate cancer<ref name="BéguéBonnet-Delpon2008"/>
* 1989: Combined androgen blockade via flutamide and a GnRH analogue is found to be superior to a GnRH analogue alone for prostate cancer
* 1989: Flutamide is first introduced for medical use in the United States, to treat prostate cancer<ref name="Regitz-Zagrosek2012">{{cite book| vauthors = Regitz-Zagrosek V |title=Sex and Gender Differences in Pharmacology |url= https://books.google.com/books?id=J3VxihGDh9wC&pg=PA575| date=2 October 2012 |publisher=Springer Science & Business Media|isbn=978-3-642-30725-6|pages=575–}}</ref>
* 1989: Flutamide is first studied in the treatment of hirsutism in women<ref name="pmid2147859"/>
* 1992: The androgen synthesis inhibitor abiraterone acetate is first described<ref name="ICR2014">{{Cite web|url=https://www.icr.ac.uk/news-features/latest-features/abiraterone-a-story-of-scientific-innovation-and-commercial-partnership|title=Abiraterone: A story of scientific innovation and commercial partnership - the Institute of Cancer Research, London|access-date=2019-01-02|archive-date=2019-01-01|archive-url=https://web.archive.org/web/20190101101202/https://www.icr.ac.uk/news-features/latest-features/abiraterone-a-story-of-scientific-innovation-and-commercial-partnership|url-status=live}}</ref>
* 1995: Bicalutamide is first introduced for medical use, to treat prostate cancer<ref name="BéguéBonnet-Delpon2008" />
* 1996: Nilutamide is first introduced for medical use in the United States, to treat prostate cancer<ref name="AdisInsight-Nilutamide">{{Cite web | url = http://adisinsight.springer.com/drugs/800004379 | title = Nilutamide | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2019-01-02 | archive-date = 2021-05-05 | archive-url = https://web.archive.org/web/20210505173834/https://adisinsight.springer.com/drugs/800004379 | url-status = live }}</ref>
* 2006: The second-generation nonsteroidal antiandrogen enzalutamide is first described<ref name="US20070004753">Sawyers, C., Jung, M., Chen, C., Ouk, S., Welsbie, D., Tran, C., ... & Yoo, D. (2006). U.S. Patent Application No. 11/433,829. https://patents.google.com/patent/US20070004753 [https://patents.google.com/patent/US20070004753]</ref>
* 2007: The second-generation nonsteroidal antiandrogen apalutamide is first described<ref name="WO2007126765">{{Cite web|url=https://worldwide.espacenet.com/publicationDetails/originalDocument?FT=D&date=20071108&DB=EPODOC&locale=en_EP&CC=WO&NR=2007126765A2&KC=A2&ND=6|title=Espacenet - Original document|access-date=2019-01-02|archive-date=2021-11-04|archive-url=https://web.archive.org/web/20211104133256/https://worldwide.espacenet.com/publicationDetails/originalDocument?FT=D&date=20071108&DB=EPODOC&locale=en_EP&CC=WO&NR=2007126765A2&KC=A2&ND=6|url-status=live}}</ref>
* 2011: Abiraterone acetate is first introduced for medical use, to treat prostate cancer<ref name="AdisInsight-Abiraterone-Acetate">{{Cite web|url=https://adisinsight.springer.com/drugs/800005133|title=Abiraterone acetate - Johnson & Johnson|work=AdisInsight|publisher=Springer Nature Switzerland AG|access-date=2019-01-02|archive-date=2019-01-03|archive-url=https://web.archive.org/web/20190103055744/https://adisinsight.springer.com/drugs/800005133|url-status=live}}</ref>
* 2012: Enzalutamide is first introduced for medical use, to treat prostate cancer<ref name="AdisInsight-Enzalutamide">{{Cite web | url = https://adisinsight.springer.com/drugs/800026688 | title = Enzalutamide - Astellas Pharma/Medivation | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2019-01-02 | archive-date = 2018-07-17 | archive-url = https://web.archive.org/web/20180717212735/https://adisinsight.springer.com/drugs/800026688 | url-status = live }}</ref>
* 2018: Apalutamide is first introduced for medical use, to treat prostate cancer<ref name="AdisInsight-Apalutamide">{{Cite web | url = http://adisinsight.springer.com/drugs/800032695 | title = Apalutamide - Janssen Research and Development | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2019-01-02 | archive-date = 2019-01-03 | archive-url = https://web.archive.org/web/20190103110524/https://adisinsight.springer.com/drugs/800032695 | url-status = live }}</ref>
* 2018: Elagolix is the first orally active GnRH antagonist to be introduced for medical use<ref name="AdisInsight-Elagolix" />
* 2019: Relugolix is the second orally active GnRH antagonist to be introduced for medical use<ref name="AdisInsight-Relugolix">{{Cite web | url = https://adisinsight.springer.com/drugs/800028257 | title = Relugolix - Myovant/Takeda | work = AdisInsight | publisher = Springer Nature Switzerland AG | access-date = 2021-08-19 | archive-date = 2021-08-19 | archive-url = https://web.archive.org/web/20210819053135/https://adisinsight.springer.com/drugs/800028257 | url-status = live }}</ref>

==Society and culture==

===Etymology===
The term ''antiandrogen'' is generally used to refer specifically to AR antagonists, as described by Dorfman (1970):<ref name="pmid66176">{{cite journal | vauthors = Neumann F | title = Pharmacology and potential use of cyproterone acetate | journal = Hormone and Metabolic Research | volume = 9 | issue = 1 | pages = 1–13 | date = January 1977 | pmid = 66176 | doi = 10.1055/s-0028-1093574 | s2cid = 7224893 }}</ref><ref name="Dorfman1970">{{cite journal| vauthors = Dorfman RI |title=Biological Activity of Antiandrogens|journal=British Journal of Dermatology|volume=82|issue=s6|year=1970|pages=3|issn=0007-0963|doi=10.1111/j.1365-2133.1970.tb07998.x|s2cid=71393789}}</ref>

{{Blockquote|''Antiandrogens are substances which prevent androgens from expressing their activity at target sites. The inhibitory effect of these substances, therefore, should be differentiated from compounds which decrease the synthesis and/or release of hypothalamic (releasing) factors, from anterior pituitary hormones (gonadotropins, particularly luteinizing hormone) and from material which acts directly on the gonads to inhibit biosynthesis and/or secretion of androgens.''<ref name="pmid66176" /><ref name="Dorfman1970" />}}

However, in spite of the above, the term may also be used to describe ''functional'' antiandrogens like androgen synthesis inhibitors and antigonadotropins, including even estrogens and progestogens.<ref name="Brueggemeier2006" /><ref name="pmid11502457" /><ref name="GräfBrotherton1974">{{cite book| vauthors = Gräf KJ, Brotherton J, Neumann F |title=Androgens II and Antiandrogens / Androgene II und Antiandrogene|chapter=Clinical Uses of Antiandrogens |year=1974 |pages=485–542|publisher=Springer |doi=10.1007/978-3-642-80859-3_7|isbn=978-3-642-80861-6}}</ref> For example, the progestogen and hence antigonadotropin medroxyprogesterone acetate is sometimes described as a steroidal antiandrogen, even though it is not an antagonist of the AR.<ref name="Vogelzang2006">{{cite book| vauthors = Vogelzang N |title=Comprehensive Textbook of Genitourinary Oncology|url=https://books.google.com/books?id=WIsiGZnZ_mgC&pg=PA316 |year=2006 |publisher= Lippincott Williams & Wilkins|isbn=978-0-7817-4984-8|pages=316–}}</ref><ref name="GräfBrotherton1974" />

==Research==
{{See also|List of investigational sex-hormonal agents#Androgenics}}

===Topical administration===
{{Outdated|part=section|date=April 2024|inaccurate=yes|reason=Clascoterone has been approved for acne by the FDA in August 2020, and is considered to be highly effective (>= tretinoin 0.05%)}}
There has been much interest and effort in the development of topical AR antagonists to treat androgen-dependent conditions like acne and pattern hair loss in males.<ref name="HelmsQuan2006">{{cite book| vauthors = Helms RA, Quan DJ |title=Textbook of Therapeutics: Drug and Disease Management|url=https://books.google.com/books?id=aVmRWrknaWgC&pg=PA211|year=2006|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-5734-8|pages=211–}}</ref> Unfortunately, whereas systemic administration of antiandrogens is very effective in treating these conditions, topical administration has disappointingly been found generally to possess limited and only modest effectiveness, even when high-[[affinity (pharmacology)|affinity]] steroidal AR antagonists like cyproterone acetate and spironolactone have been employed.<ref name="HelmsQuan2006" /> Moreover, in the specific case of acne treatment, topical AR antagonists have been found much less effective compared to established treatments like [[benzoyl peroxide]] and [[antibiotic]]s.<ref name="HelmsQuan2006" />

A variety of AR antagonists have been developed for topical use but have not completed development and hence have never been marketed. These include the steroidal AR antagonists [[clascoterone]], [[cyproterone]], [[rosterolone]], and [[topterone]] and the nonsteroidal AR antagonists [[cioteronel]], [[inocoterone acetate]], [[RU-22930]], [[RU-58642]], and [[RU-58841]]. However, one topical AR antagonist, [[topilutamide]] (fluridil), has been introduced in a few European countries for the treatment of pattern hair loss in men.<ref name="TrüebLee2014" /> In addition, a topical 5α-reductase inhibitor and weak estrogen, [[alfatradiol]], has also been introduced in some European countries for the same indication, although its effectiveness is controversial.<ref name="TrüebLee2014" /> [[Spironolactone]] has been marketed in [[Italy]] in the form of a topical cream under the brand name Spiroderm for the treatment of acne and hirsutism, but this formulation was discontinued and hence is no longer available.<ref name="FARIDDiamanti-Kandarakis2009">{{cite book|vauthors=Farid NR, Diamanti-Kandarakis E|title=Diagnosis and Management of Polycystic Ovary Syndrome|url=https://books.google.com/books?id=fgMYVxmPDnMC&pg=PA235|date=27 February 2009|publisher=Springer Science & Business Media|isbn=978-0-387-09718-3|pages=235–|access-date=30 December 2016|archive-date=11 January 2023|archive-url=https://web.archive.org/web/20230111121904/https://books.google.com/books?id=fgMYVxmPDnMC&pg=PA235|url-status=live}}</ref>

===Male contraception===
Antiandrogens, such as cyproterone acetate, have been studied for potential use as [[male hormonal contraceptive]]s.<ref name="pmid793446">{{cite journal | vauthors = Neumann F, Diallo FA, Hasan SH, Schenck B, Traore I | title = The influence of pharmaceutical compounds on male fertility | journal = Andrologia | volume = 8 | issue = 3 | pages = 203–35 | date = 1976 | pmid = 793446 | doi = 10.1111/j.1439-0272.1976.tb02137.x| s2cid = 24859886 | doi-access = free }}</ref><ref name="pmid797248">{{cite journal | vauthors = Prasad MR, Rajalakshmi M | title = Target sites for suppressing fertility in the male | journal = Adv Sex Horm Res | volume = 2 | pages = 263–87 | date = 1976 | pmid = 797248 }}</ref><ref name="pmid206192">{{cite journal | vauthors = Ewing LL, Robaire B | title = Endogenous antispermatogenic agents: prospects for male contraception | journal = Annu. Rev. Pharmacol. Toxicol. | volume = 18 | pages = 167–87 | date = 1978 | pmid = 206192 | doi = 10.1146/annurev.pa.18.040178.001123 }}</ref><ref name="pmid6354690">{{cite journal | vauthors = Gombe S | title = A review of the current status in male contraceptive studies | journal = East Afr Med J | volume = 60 | issue = 4 | pages = 203–11 | date = April 1983 | pmid = 6354690 }}</ref><ref name="pmid6205409"/><ref name="pmid2687939">{{cite book | vauthors = Srivastava RP, Bhaduri AP | title = Progress in Drug Research | chapter = Emerging concepts towards the development of contraceptive agents | series = Progress in Drug Research. Fortschritte der Arzneimittelforschung. Progres des Recherches Pharmaceutiques | volume = 33 | pages = 267–315 | date = 1989 | pmid = 2687939 | doi = 10.1007/978-3-0348-9146-2_9| isbn = 978-3-0348-9925-3 |editor=Ernst Jucker |publisher=Birkhäuser }}</ref><ref name="pmid3075164">{{cite journal | vauthors = Wu FC | title = Male contraception: current status and future prospects | journal = Clin. Endocrinol. (Oxf) | volume = 29 | issue = 4 | pages = 443–65 | date = October 1988 | pmid = 3075164 | doi = 10.1111/j.1365-2265.1988.tb02894.x| s2cid = 36608203 }}</ref><ref name="pmid14667989">{{cite journal | vauthors = Nieschlag E, Zitzmann M, Kamischke A | title = Use of progestins in male contraception | journal = Steroids | volume = 68 | issue = 10–13 | pages = 965–72 | date = November 2003 | pmid = 14667989 | doi = 10.1016/s0039-128x(03)00135-1| s2cid = 22458746 }}</ref> While effective in suppressing [[male fertility]], their use as monotherapies is precluded by side effects, such as [[hypoandrogenism|androgen deficiency]] (e.g., [[demasculinization]], [[sexual dysfunction]], [[hot flash]]es, [[osteoporosis]]) and [[feminization (biology)|feminization]] (e.g., [[gynecomastia]]).<ref name="pmid6205409" /><ref name="pmid2687939" /><ref name="pmid3075164" /><ref name="pmid20933120">{{cite journal | vauthors = Nieschlag E | title = Clinical trials in male hormonal contraception | journal = Contraception | volume = 82 | issue = 5 | pages = 457–70 | year = 2010 | pmid = 20933120 | doi = 10.1016/j.contraception.2010.03.020 | url = http://www.kup.at/kup/pdf/10172.pdf | access-date = 2019-07-08 | archive-date = 2020-12-05 | archive-url = https://web.archive.org/web/20201205082822/https://www.kup.at/kup/pdf/10172.pdf | url-status = live }}</ref> The combination of a primary antigonadotropin such as cyproterone acetate to prevent fertility and an androgen like testosterone to prevent systemic androgen deficiency, resulting in a selective antiandrogenic action locally in the testes, has been extensively studied and has shown promising results, but has not been approved for clinical use at this time.<ref name="pmid3075164" /><ref name="pmid14667989" /><ref name="pmid16313066">{{cite journal | vauthors = Rajalakshmi M | title = Male contraception: expanding reproductive choice | journal = Indian J. Exp. Biol. | volume = 43 | issue = 11 | pages = 1032–41 | date = November 2005 | pmid = 16313066 }}</ref><ref name="pmid27016468">{{cite journal | vauthors = Chao JH, Page ST | title = The current state of male hormonal contraception | journal = Pharmacol. Ther. | volume = 163 | pages = 109–17 | date = July 2016 | pmid = 27016468 | doi = 10.1016/j.pharmthera.2016.03.012 }}</ref><ref name="pmid20933120" /> [[Dimethandrolone undecanoate]] (developmental code name CDB-4521), an [[oral administration|orally active]] dual AAS and progestogen, is under investigation as a potential male contraceptive and as the first male [[birth control pill]].<ref name="pmid16497801">{{cite journal | vauthors = Attardi BJ, Hild SA, Reel JR | title = Dimethandrolone undecanoate: a new potent orally active androgen with progestational activity | journal = Endocrinology | volume = 147 | issue = 6 | pages = 3016–26 | date = June 2006 | pmid = 16497801 | doi = 10.1210/en.2005-1524 | doi-access = free }}</ref><ref name="pmid27907978">{{cite journal | vauthors = Ayoub R, Page ST, Swerdloff RS, Liu PY, Amory JK, Leung A, Hull L, Blithe D, Christy A, Chao JH, Bremner WJ, Wang C | title = Comparison of the single dose pharmacokinetics, pharmacodynamics, and safety of two novel oral formulations of dimethandrolone undecanoate (DMAU): a potential oral, male contraceptive | journal = Andrology | volume = 5 | issue = 2 | pages = 278–285 | date = March 2017 | pmid = 27907978 | pmc = 5352517 | doi = 10.1111/andr.12303 }}</ref>

===Breast cancer===
Antiandrogens such as [[bicalutamide]], [[enzalutamide]], and [[abiraterone acetate]] are under investigation for the potential treatment of [[breast cancer]], including AR-expressing [[triple-negative breast cancer]] and other types of AR-expressing breast cancer.<ref name="pmid24740738">{{cite journal | vauthors = Fioretti FM, Sita-Lumsden A, Bevan CL, Brooke GN | title = Revising the role of the androgen receptor in breast cancer | journal = J. Mol. Endocrinol. | volume = 52 | issue = 3 | pages = R257–65 | date = June 2014 | pmid = 24740738 | doi = 10.1530/JME-14-0030 | doi-access = free }}</ref><ref name="pmid27816190">{{cite journal | vauthors = Gucalp A, Traina TA | title = Targeting the androgen receptor in triple-negative breast cancer | journal = Curr Probl Cancer | volume = 40 | issue = 2–4 | pages = 141–150 | date = 2016 | pmid = 27816190 | pmc = 5580391 | doi = 10.1016/j.currproblcancer.2016.09.004 }}</ref><ref name="pmid24888812">{{cite journal | vauthors = Arce-Salinas C, Riesco-Martinez MC, Hanna W, Bedard P, Warner E | title = Complete Response of Metastatic Androgen Receptor-Positive Breast Cancer to Bicalutamide: Case Report and Review of the Literature | journal = J. Clin. Oncol. | volume = 34 | issue = 4 | pages = e21–4 | date = February 2016 | pmid = 24888812 | doi = 10.1200/JCO.2013.49.8899 }}</ref><ref name="pmid28216075">{{cite journal | vauthors = Héquet D, Mzoughi S, Rouzier R, Guccione E | title = [Androgen receptors in breast cancer: Expression, value and therapeutic prospects] | language = fr | journal = Bull Cancer | volume = 104 | issue = 4 | pages = 363–369 | date = April 2017 | pmid = 28216075 | doi = 10.1016/j.bulcan.2017.01.005 }}</ref><ref name="pmid29940524">{{cite journal | vauthors = Gerratana L, Basile D, Buono G, De Placido S, Giuliano M, Minichillo S, Coinu A, Martorana F, De Santo I, Del Mastro L, De Laurentiis M, Puglisi F, Arpino G | title = Androgen receptor in triple negative breast cancer: A potential target for the targetless subtype | journal = Cancer Treat. Rev. | volume = 68 | pages = 102–110 | date = June 2018 | pmid = 29940524 | doi = 10.1016/j.ctrv.2018.06.005 | doi-access = free | hdl = 11567/914067 | hdl-access = free }}</ref>

===Miscellaneous===
Antiandrogens may be effective in the treatment of [[obsessive–compulsive disorder]].<ref name="pmid31814547">{{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=Curr Med Chem |date=December 2019 |volume=27 |issue=40 |pages=6825–6836 |pmid=31814547 |doi=10.2174/0929867326666191209142209|s2cid=208956450 }}</ref>

==See also==
* [[Androgen insensitivity syndrome]]
* [[Antiandrogens in the environment]]
* [[Androgen replacement therapy]]

==References==
{{Reflist}}

==Further reading==
{{refbegin}}
* {{cite book| vauthors = Neumann F, Steinbeck H |title=Androgens II and Antiandrogens / Androgene II und Antiandrogene|chapter=Antiandrogens|year=1974|pages=235–484|publisher=Springer |doi=10.1007/978-3-642-80859-3_6|isbn=978-3-642-80861-6}}
* {{cite book| vauthors = Gräf KJ, Brotherton J, Neumann F |title=Androgens II and Antiandrogens / Androgene II und Antiandrogene|chapter=Clinical Uses of Antiandrogens|year=1974|pages=485–542|publisher=Springer |doi=10.1007/978-3-642-80859-3_7|isbn=978-3-642-80861-6}}
{{refend}}

{{Androgens and antiandrogens}}
{{Androgen receptor modulators}}
{{Authority control}}

[[Category:Anaphrodisia]]
[[Category:Anti-acne preparations]]
[[Category:Antiandrogens| ]]
[[Category:Hair loss medications]]
[[Category:Hair removal]]
[[Category:Hormonal antineoplastic drugs]]
[[Category:Prostate cancer]]
[[Category:Sex hormones]]
[[Category:Psychoactive drugs]]