Antiandrogen

Antiandrogens, also known as androgen antagonists or testosterone blockers, are a class of drugs that prevent androgens like testosterone and dihydrotestosterone (DHT) from mediating their biological effects in the body. They act by blocking the androgen receptor (AR) and/or inhibiting or suppressing androgen production.[1][2] They can be thought of as the functional opposites of AR agonists, for instance androgens and anabolic steroids (AAS) like testosterone, DHT, and nandrolone and selective androgen receptor modulators (SARMs) like enobosarm. Antiandrogens are one of three types of sex hormone antagonists, the others being antiestrogens and antiprogestogens.[3]

Antiandrogens are used to treat an assortment of androgen-dependent conditions.[4] In men, antiandrogens are used in the treatment of prostate cancer, enlarged prostate, scalp hair loss, overly high sex drive, unusual and problematic sexual urges, and early puberty.[4][5] In women, antiandrogens are used to treat acne, seborrhea, excessive hair growth, scalp hair loss, and high androgen levels, such as those that occur in polycystic ovary syndrome (PCOS).[4] Antiandrogens are also used as a component of feminizing hormone therapy for transgender women and as puberty blockers in transgender girls.[4]

Side effects 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, breast enlargement, feminization, hot flashes, sexual dysfunction, infertility, and osteoporosis. In women, antiandrogens are much better tolerated, and antiandrogens that work only by directly blocking androgens are associated with minimal side effects. However, because estrogens are made from androgens in the body, antiandrogens that suppress androgen production can cause low estrogen levels and associated symptoms like hot flashes, menstrual irregularities, and osteoporosis in premenopausal women.

There several major classes of antiandrogens.[6] These include AR antagonists, androgen synthesis inhibitors, and antigonadotropins.[6] AR antagonists work by directly blocking the effects of androgens, while androgen synthesis inhibitors and antigonadotropins work by lowering androgen levels.[6] AR antagonists can be further divided into steroidal antiandrogens and nonsteroidal antiandrogens; androgen synthesis inhibitors can be further divided mostly into CYP17A1 inhibitors and 5α-reductase inhibitors; and antigonadotropins can be further divided into gonadotropin-releasing hormone modulators (GnRH modulators), progestogens, and estrogens.[6][7][8]

## Contents

* 1 Medical uses
* 1.1 Males
* 1.1.1 Prostate cancer
* 1.1.2 Enlarged prostate
* 1.1.3 Scalp hair loss
* 1.1.4 Acne
* 1.1.5 Paraphilias
* 1.1.6 Early puberty
* 1.1.7 Long-lasting erections
* 1.2 Women and girls
* 1.2.1 Skin and hair conditions
* 1.2.2 High androgen levels
* 1.2.3 Transgender hormone therapy
* 1.3 Available forms
* 2 Side effects
* 3 Overdose
* 4 Interactions
* 5 Mechanism of action
* 5.1 Androgen receptor antagonists
* 5.1.1 N-Terminal domain antagonists
* 5.1.2 Androgen receptor degraders
* 5.2 Androgen synthesis inhibitors
* 5.2.1 5α-Reductase inhibitors
* 5.3 Antigonadotropins
* 5.4 Miscellaneous
* 5.4.1 Sex hormone-binding globulin modulators
* 5.4.2 Corticosteroid-binding globulin modulators
* 5.4.3 Anticorticotropins
* 5.4.4 Insulin sensitizers
* 5.4.5 Immunogens and vaccines
* 6 Chemistry
* 7 History
* 7.1 Timeline
* 8 Society and culture
* 8.1 Etymology
* 9 Research
* 9.1 Topical administration
* 9.2 Male contraception
* 9.3 Breast cancer
* 9.4 Miscellaneous
* 10 See also
* 11 References
* 12 Further reading

## Medical uses

Antiandrogens are used in the treatment of an assortment of androgen-dependent conditions in both males and females.[4][9] They are used to treat men with prostate cancer, benign prostatic hyperplasia, pattern hair loss, hypersexuality, paraphilias, and priapism, as well as boys with precocious puberty.[9][10][11] In women and girls, antiandrogens are used to treat acne, seborrhea, hidradenitis suppurativa, hirsutism, and hyperandrogenism.[9][12][13] Antiandrogens are also used in transgender women as a component of feminizing hormone therapy and as puberty blockers in transgender girls.[14][15]

### Males

#### Prostate cancer

Androgens like testosterone and particularly DHT are importantly involved in the development and progression of prostate cancer.[16] They act as growth factors in the prostate gland, stimulating cell division and tissue growth.[16] 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 males with the disease.[16] 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.[17] When this occurs, other treatment approaches, such as chemotherapy, may be considered.[17]

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.[16] Castration may be used alone or in combination with one of the other two treatments.[16][18] 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).[16][19] Enzalutamide, apalutamide, and abiraterone acetate are specifically approved for use in combination with castration to treat castration-resistant prostate cancer.[16][20] 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.[16][21][22]

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.[23] 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,[24] but it has largely been replaced by nonsteroidal antiandrogens, which are newer and have greater effectiveness, tolerability, and safety.[25][26] Bicalutamide, as well as enzalutamide, have largely replaced the earlier nonsteroidal antiandrogens flutamide and nilutamide, which are now little used.[19][27][28][29][30] 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.[31]

In addition to active treatment of prostate cancer, antiandrogens are effective as prophylaxis (preventatives) in reducing the risk of ever developing prostate cancer.[32] 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.[32][33] 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.[34][35][36]

#### Enlarged prostate

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.[37] They are effective because androgens act as growth factors in the prostate gland.[37] 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.[38][39]

#### Scalp hair loss

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.[40] This condition is generally caused by androgens, so antiandrogens can slow or halt its progression.[41] 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.[42][43][44][45][46][47][48] However, they have been assessed and reported to be effective for this indication.[42][43][49]

#### 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.[50][51] However, they have been studied for acne in males and found to be effective.[52][44][45][53] Clascoterone, a topical antiandrogen, is effective for acne in males, albeit modestly,[54] and has been approved by the FDA in August 2020.[55][56][57][58]

#### Paraphilias

Androgens increase sex drive,[59] and for this reason, antiandrogens are able to reduce sex drive in males.[60][61] In accordance, antiandrogens are used in the treatment of conditions such as hypersexuality (excessively high sex drive) and paraphilias (atypical and sometimes societally unacceptable sexual interests) like pedophilia (sexual attraction to children).[60][61] They have been used to decrease sex drive in sex offenders so as to reduce the likelihood of recidivism (repeat offenses).[62] Antiandrogens used for these indications include cyproterone acetate, medroxyprogesterone acetate, and GnRH modulators.[63][64]

#### Early puberty

Antiandrogens are used to treat precocious puberty in males.[65][66][67][68] They work by opposing the effects of androgens and delaying the development of secondary sexual characteristics and onset of changes in sex drive and function until a more appropriate age.[65][66] Antiandrogens that have been used for this purpose include cyproterone acetate, medroxyprogesterone acetate, GnRH modulators, spironolactone, bicalutamide, and ketoconazole.[65][68][69][70][71][72] Spironolactone and bicalutamide require combination with an aromatase inhibitor to prevent the effects of unopposed estrogens, while the others can be used alone.[65][71][72]

#### Long-lasting erections

Antiandrogens are effective in the treatment of recurrent priapism (potentially painful penile erections that last more than four hours).[73][74][75][76][77]

### Women and girls

#### Skin and hair conditions

Antiandrogens are used in the treatment of androgen-dependent skin and hair conditions including acne, seborrhea, hidradenitis suppurativa, hirsutism, and pattern hair loss in women.[12] All of these conditions are dependent on androgens, and for this reason, antiandrogens are effective in treating them.[12] The most commonly used antiandrogens for these indications are cyproterone acetate and spironolactone.[78] Flutamide has also been studied extensively for such uses, but has fallen out of favor due to its association with hepatotoxicity.[79] 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.[80][81] In addition to AR antagonists, oral contraceptives containing ethinylestradiol are effective in treating these conditions, and may be combined with AR antagonists.[82][83]

#### High androgen levels

Hyperandrogenism is a condition in women in which androgen levels are excessively and abnormally high.[13] It is commonly seen in women with PCOS, and also occurs in women with intersex conditions like congenital adrenal hyperplasia.[13] Hyperandrogenism is associated with virilization – that is, the development of masculine secondary sexual characteristics like male-pattern facial and body hair growth (or hirsutism), voice deepening, increased muscle mass and strength, and broadening of the shoulders, among others.[13] Androgen-dependent skin and hair conditions like acne and pattern hair loss may also occur in hyperandrogenism, and menstrual disturbances, like amenorrhea, are commonly seen.[13] Although antiandrogens do not treat the underlying cause of hyperandrogenism (e.g., PCOS), they are able to prevent and reverse its manifestation and effects.[13] 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.[13] Other antiandrogens, like bicalutamide, may be used alternatively.[13]

#### Transgender hormone therapy

Antiandrogens are used to prevent or reverse masculinization and to facilitate feminization in transgender women and some non-binary transfeminine individuals who are undergoing hormone therapy and who have not undergone sex reassignment surgery or orchiectomy.[14] Besides estrogens, the main antiandrogens that have been used for this purpose are cyproterone acetate, spironolactone, and GnRH modulators.[14] Nonsteroidal antiandrogens like bicalutamide are also used for this indication.[84][14] In addition to use in transgender women, antiandrogens, mainly GnRH modulators, are used as puberty blockers to prevent the onset of puberty in transgender girls until they are older and ready to begin hormone therapy.[15]

### Available forms

See also: Biology:Steroidal antiandrogen and Nonsteroidal antiandrogen

There are several different types of antiandrogens, including the following:[6]

* Androgen receptor antagonists: Drugs that bind directly to and block the AR.[85][86] These drugs include the steroidal antiandrogens cyproterone acetate, megestrol acetate, chlormadinone acetate, spironolactone, oxendolone, and osaterone acetate (veterinary) and the nonsteroidal antiandrogens flutamide, bicalutamide, nilutamide, topilutamide, enzalutamide, apalutamide, and darolutamide.[85][86][7][8] Aside from cyproterone acetate and chlormadinone acetate, a few other progestins used in oral contraceptives and/or in menopausal HRT including dienogest, drospirenone, medrogestone, nomegestrol acetate, promegestone, and trimegestone also have varying degrees of AR antagonistic activity.[87][88][89]
* Androgen synthesis inhibitors: Drugs that directly inhibit the enzymatic biosynthesis of androgens like testosterone and/or DHT.[90][31] Examples include the CYP17A1 inhibitors ketoconazole, abiraterone acetate, and seviteronel,[90] the CYP11A1 (P450scc) inhibitor aminoglutethimide,[90] and the 5α-reductase inhibitors finasteride, dutasteride, epristeride, alfatradiol, and saw palmetto extract (Serenoa repens).[91] 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 gonadotropins and consequent activation of gonadal androgen production.[2][92] Examples include GnRH modulators like leuprorelin (a GnRH agonist) and cetrorelix (a GnRH antagonist),[93] progestogens like allylestrenol, chlormadinone acetate, cyproterone acetate, gestonorone caproate, hydroxyprogesterone caproate, medroxyprogesterone acetate, megestrol acetate, osaterone acetate (veterinary), and oxendolone,[94][95] and estrogens like estradiol, estradiol esters, ethinylestradiol, conjugated estrogens, and diethylstilbestrol.[2][94]
* Miscellaneous: Drugs that oppose the effects of androgens by means other than the above. Examples include estrogens, especially oral and synthetic (e.g., ethinylestradiol, diethylstilbestrol), which stimulate sex hormone-binding globulin (SHBG) production in the liver and thereby decrease free and hence bioactive levels of testosterone and DHT; anticorticotropins such as glucocorticoids, which suppress the adrenocorticotropic hormone (ACTH)-induced production of adrenal androgens; and immunogens and vaccines against androstenedione like ovandrotone albumin and androstenedione albumin, which decrease levels of androgens via the generation of antibodies against the androgen and androgen precursor androstenedione (used only in veterinary medicine).

Certain antiandrogens combine multiple of the above mechanisms.[6][96] 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.[6][96][97][98]

Antiandrogens marketed for clinical or veterinary use  Generic name | Class | Type | Brand name(s) | Route(s) | Launch | Status | Hitsa

|
|
|
|
|
|
|

Abiraterone acetate | Steroidal | Androgen synthesis inhibitor | Zytiga | Oral | 2011 | Available | 523,000
Allylestrenol | Steroidal | Progestin | Gestanin, Perselin | Oral | 1961 | Availableb | 61,800
Aminoglutethimide | Nonsteroidal | Androgen synthesis inhibitor | Cytadren, Orimeten | Oral | 1960 | Availableb | 222,000
Apalutamide | Nonsteroidal | AR antagonist | Erleada | Oral | 2018 | Available | 50,400
Bicalutamide | Nonsteroidal | AR antagonist | Casodex | Oral | 1995 | Available | 754,000
Chlormadinone acetate | Steroidal | Progestin; AR antagonist | Belara, Prostal | Oral | 1965 | Available | 220,000
Cyproterone acetate | Steroidal | Progestin; AR antagonist | Androcur, Diane | Oral, IM | 1973 | Available | 461,000
Darolutamide | Nonsteroidal | AR antagonist | Nubeqa | Oral | 2019 | Available | ?
Delmadinone acetate | Steroidal | Progestin; AR antagonist | Tardak | Veterinary | 1972 | Veterinary | 42,600
Enzalutamide | Nonsteroidal | AR antagonist | Xtandi | Oral | 2012 | Available | 328,000
Flutamide | Nonsteroidal | AR antagonist | Eulexin | Oral | 1983 | Available | 712,000
Gestonorone caproate | Steroidal | Progestin | Depostat, Primostat | IM | 1973 | Availableb | 119,000
Hydroxyprogesterone caproate | Steroidal | Progestin | Delalutin, Proluton | IM | 1954 | Available | 108,000
Ketoconazole | Nonsteroidal | Androgen synthesis inhibitor | Nizoral, others | Oral, topical | 1981 | Available | 3,650,000
Medroxyprogesterone acetate | Steroidal | Progestin | Provera, Depo-Provera | Oral, IM, SC | 1958 | Available | 1,250,000
Megestrol acetate | Steroidal | Progestin; AR antagonist | Megace | Oral | 1963 | Available | 253,000
Nilutamide | Nonsteroidal | AR antagonist | Anandron, Nilandron | Oral | 1987 | Available | 132,000
Osaterone acetate | Steroidal | Progestin; AR antagonist | Ypozane | Veterinary | 2007 | Veterinary | 87,600
Oxendolone | Steroidal | Progestin; AR antagonist | Prostetin, Roxenone | IM | 1981 | Availableb | 36,100
Spironolactone | Steroidal | AR antagonist | Aldactone | Oral, topical | 1959 | Available | 3,010,000
Topilutamide | Nonsteroidal | AR antagonist | Eucapil | Topical | 2003 | Availableb | 36,300
Footnotes: a = Hits = Google Search hits (as of February 2018). b = Availability limited / mostly discontinued. Class: Steroidal = Steroidal antiandrogen. Nonsteroidal = Nonsteroidal antiandrogen. Note: For other antiandrogens not included in the table like 5α-reductase inhibitors, GnRH modulators, and estrogens, see elsewhere. 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.[21][99] 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.[21][100][101] These differences are thought related to the fact that antigonadotropins suppress androgen levels and by extension levels of bioactive metabolites of androgens like estrogens and neurosteroids 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).[21] As another example, the steroidal antiandrogens cyproterone acetate and spironolactone possess off-target actions including progestogenic, antimineralocorticoid, and/or glucocorticoid activity in addition to their antiandrogen activity, and these off-target activities can result in additional side effects.[99]

In males, the major side effects of antiandrogens are demasculinization and feminization.[102] These side effects include breast pain/tenderness and gynecomastia (breast development/enlargement), reduced body hair growth/density, decreased muscle mass and strength, feminine changes in fat mass and distribution, and reduced penile length and testicular size.[102] The rates of gynecomastia in men with selective AR antagonist monotherapy have been found to range from 30 to 85%.[103] In addition, antiandrogens can cause infertility, osteoporosis, hot flashes, sexual dysfunction (including loss of libido and erectile dysfunction), depression, fatigue, anemia, and decreased semen/ejaculate volume in males. [102] Conversely, the side effects of selective AR antagonists in women are minimal.[81][104] However, antigonadotropic antiandrogens like cyproterone acetate can produce hypoestrogenism, amenorrhea, and osteoporosis in premenopausal women, among other side effects.[82][105][106] In addition, androgen receptor antagonists can produce unfavorable effects on cholesterol levels, which long-term may increase the risk of cardiovascular disease.[107][108][109][110][111][112][113]

A number of antiandrogens have been associated with hepatotoxicity.[114] These include, to varying extents, cyproterone acetate, flutamide, nilutamide, bicalutamide, aminoglutethimide, and ketoconazole.[114] In contrast, spironolactone, enzalutamide,[115] 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 seizures. In women who are pregnant, antiandrogens can interfere with the androgen-mediated sexual differentiation of the genitalia and brain of male fetuses.[116] 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.[116][117] As such, antiandrogens are teratogens, and women who are pregnant should not be treated with an antiandrogen.[83] Moreover, women who can or may become pregnant are strongly recommended to take an antiandrogen only in combination with proper contraception.[83]

## Overdose

## Interactions

## Mechanism of action

### Androgen receptor antagonists

Antiandrogens at steroid hormone receptors  Antiandrogen | Relative binding affinities

|

AR | PR | ER | GR | MR
Cyproterone acetate | 8–10 | 60 | <0.1 | 5 | 1
Chlormadinone acetate | 5 | 175 | <0.1 | 38 | 1
Megestrol acetate | 5 | 152 | <0.1 | 50 | 3
Spironolactone | 7 | 0.4a | <0.1 | 2a | 182
Trimethyltrienolone | 3.6 | <1 | <1 | <1 | <1
Inocoterone | 0.8 | <0.1 | <0.1 | <0.1 | <0.1
Inocoterone acetate | <0.1 | <0.1 | <0.1 | <0.1 | <0.1
Flutamide | <0.1 | <0.1 | <0.1 | <0.1 | <0.1
Hydroxyflutamide | 0.5–0.8 | <0.1 | <0.1 | <0.1 | <0.1
Nilutamide | 0.5–0.8 | <0.1 | <0.1 | <0.1 | <0.1
Bicalutamide | 1.8 | <0.1 | <0.1 | <0.1 | <0.1
v * d * e Relative potencies of selected antiandrogens  Antiandrogen | Relative potency

|

Bicalutamide | 4.3
Hydroxyflutamide | 3.5
Flutamide | 3.3
Cyproterone acetate | 1.0
Zanoterone | 0.4
Description: Relative potencies of orally administered antiandrogens in antagonizing 0.8 to 1.0 mg/kg s.c. testosterone propionate-induced ventral prostate weight increase in castrated immature male rats. Sources: See template.

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.[85][86] AR antagonists are classified into two types, based on chemical structure: steroidal and nonsteroidal.[7][8][85][86][93] Steroidal AR antagonists are structurally related to steroid hormones like testosterone and progesterone, whereas nonsteroidal AR antagonists are not steroids and are structurally distinct. Steroidal AR antagonists tend to have off-target hormonal actions due to their structural similarity to other steroid hormones.[93] In contrast, nonsteroidal AR antagonists are selective for the AR and have no off-target hormonal activity.[93] For this reason, they are sometimes described as "pure" antiandrogens.[93]

Although they are described as antiandrogens and indeed show only such effects generally, most or all steroidal AR antagonists are actually not silent antagonists of the AR but rather are weak partial agonists and are able to activate the receptor in the absence of more potent AR agonists like testosterone and DHT.[85][31][118][119] This may have clinical implications in the specific context of prostate cancer treatment.[85][118] 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,[85][118] and spironolactone has been found to accelerate progression of prostate cancer in case reports.[120][121] In addition, whereas cyproterone acetate produces ambiguous genitalia via feminization in male fetuses when administered to pregnant animals,[122] it has been found to produce masculinization of the genitalia of female fetuses of pregnant animals.[85] In contrast to steroidal AR antagonists, nonsteroidal AR antagonists are silent antagonists of the AR and do not activate the receptor.[123][31][124][118] 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.[123][31][124][118]

Nonsteroidal antiandrogens have relatively low affinity for the AR compared to steroidal AR ligands.[31][124][125] 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.[125] 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.[125][126] 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 bioassays.[125][126] 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.[127]

AR antagonists may not bind to or block membrane androgen receptors (mARs), which are distinct from the classical nuclear AR.[128][129][130] However, the mARs do not appear to be involved in masculinization. This is evidenced by the perfectly female phenotype of women with complete androgen insensitivity syndrome.[131][132] 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.[131][132] They are described as highly feminine, both physically as well as mentally and behaviorally.[133][134][135]

#### N-Terminal domain antagonists

N-Terminal domain AR antagonists 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).[136] Whereas conventional AR antagonists bind to the LBD of the AR and competitively displace androgens, thereby preventing them from activating the receptor, AR NTD antagonists bind covalently to the NTD of the AR and prevent protein–protein interactions subsequent to activation that are required for transcriptional activity.[136] As such, they are non-competitive and irreversible antagonists of the AR.[137] Examples of AR NTD antagonists include bisphenol A diglycidyl ether (BADGE) and its derivatives EPI-001, ralaniten (EPI-002), and ralaniten acetate (EPI-506).[136][138] 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.[136] In accordance with this notion, AR NTD antagonists are active against splice variants of the AR, which conventional AR antagonists are not, and AR NTD antagonists are immune to gain-of-function mutations in the AR LBD that convert AR antagonists into AR agonists and commonly occur in prostate cancer.[136]

#### Androgen receptor degraders

Selective androgen receptor degraders (SARDs) are another new type of antiandrogen that has recently been developed.[139] They work by enhancing the degradation of the AR, and are analogous to selective estrogen receptor degraders (SERDs) like fulvestrant (a drug used to treat estrogen receptor-positive breast cancer).[139] 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.[140] An example of a SARD is dimethylcurcumin (ASC-J9), which is under development as a topical medication for the potential treatment of acne.[141] SARDs like dimethylcurcumin differ from conventional AR antagonists and AR NTD antagonists in that they may not necessarily bind directly to the AR.[140]

### Androgen synthesis inhibitors

Androgen synthesis inhibitors are enzyme inhibitors that prevent the biosynthesis of androgens.[31] This process occurs mainly in the gonads and adrenal glands, but also occurs in other tissues like the prostate gland, skin, and hair follicles. These drugs include aminoglutethimide, ketoconazole,[142] and abiraterone acetate.[90][31][143] 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.[90] 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 mineralocorticoids into glucocorticoids.[90][31] 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.[143] 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.[144]

#### 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.[145] DHT is between 2.5- and 10-fold more potent than testosterone as an androgen[146] and is produced in a tissue-selective manner based on expression of 5α-reductase.[147] Tissues in which DHT forms at a high rate include the prostate gland, skin, and hair follicles.[41][147] 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.[41][147][148]

### Antigonadotropins

Estradiol and testosterone levels following a single intramuscular injection of 320 mg polyestradiol phosphate, a polymeric estradiol ester and prodrug, in men with prostate cancer.[149] Testosterone and luteinizing hormone levels with 100 mg/day oral cyproterone acetate in men.[150]

Antigonadotropins are drugs that suppress the GnRH-mediated secretion of gonadotropins from the pituitary gland.[92] Gonadotropins include luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and are peptide hormones that signal the gonads to produce sex hormones. By suppressing gonadotropin secretion, antigonadotropins suppress gonadal sex hormone production and by extension circulating androgen levels.[92] GnRH modulators, including both GnRH agonists and GnRH antagonists, are powerful antigonadotropins that are able to suppress androgen levels by 95% in men.[151] In addition, estrogens and progestogens are antigonadotropins via exertion of negative feedback on the hypothalamic–pituitary–gonadal axis (HPG axis).[2][94][152] High-dose estrogens are able to suppress androgen levels to castrate levels in men similarly to GnRH modulators,[153] while high-dose progestogens are able to suppress androgen levels by up to approximately 70 to 80% in men.[154][155]

Examples of GnRH agonists include leuprorelin (leuprolide) and goserelin, while an example of a GnRH antagonist is cetrorelix.[93] Estrogens that are or that have been used as antigonadotropins include estradiol, estradiol esters like estradiol valerate, estradiol undecylate, and polyestradiol phosphate, conjugated estrogens, ethinylestradiol, diethylstilbestrol (no longer widely used), and bifluranol.[156][157] Progestogens that are used as antigonadotropins include chlormadinone acetate, cyproterone acetate, gestonorone caproate,[158] hydroxyprogesterone caproate, medroxyprogesterone acetate, megestrol acetate, and oxendolone.[2][159][160]

### 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 hepatic production of sex hormone-binding globulin (SHBG) and by extension circulating SHBG levels.[161][162][163] Combined oral contraceptives 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%.[162] However, combined oral contraceptives that contain the particularly androgenic progestin levonorgestrel have been found to increase SHBG levels by only 50 to 100%,[162] which is likely because activation of the AR in the liver has the opposite effect of estrogen and suppresses production of SHBG.[164] 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.[164][165] In men, a study found that treatment with a relatively low dosage of 20 μg/day ethinylestradiol for 5 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).[161]

#### Corticosteroid-binding globulin modulators

Estrogens at high doses can partially suppress adrenal androgen production.[166][167][168][169][170][171] A study found that treatment with a high-dose ethinylestradiol (100 μg/day) reduced levels of major circulating adrenal androgens by 27 to 48% in transgender women.[166][167][168] Decreased adrenal androgens with estrogens is apparent with oral and synthetic estrogens like ethinylestradiol and estramustine phosphate but is minimal with parenteral bioidentical estradiol forms like polyestradiol phosphate.[170] It is thought to be mediated via a hepatic mechanism, probably increased corticosteroid-binding globulin (CBG) production and levels and compensatory changes in adrenal steroid production (e.g., shunting of adrenal androgen synthesis to cortisol production).[170][171] It is notable in this regard that oral and synthetic estrogens, due to the oral first pass and resistance to hepatic metabolism, have much stronger influences on liver protein synthesis than parenteral estradiol.[172] The decrease in adrenal androgen levels with high-dose estrogen therapy may be beneficial in the treatment of prostate cancer.[168][171]

#### Anticorticotropins

Anticorticotropins such as glucocorticoids and mineralocorticoids 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 prohormones like dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione in the adrenal gland.[173][174] 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.[173][174]

#### Insulin sensitizers

In women with insulin resistance, such as those with polycystic ovary syndrome, androgen levels are often elevated.[175] 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.[175][176][177]

#### Immunogens and vaccines

Ovandrotone albumin (Fecundin, Ovastim) and Androvax (androstenedione albumin) are immunogens and vaccines against androstenedione that are used in veterinary medicine to improve fecundity (reproductive rate) in ewes (adult female sheep).[178][179] 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.[178][179]

## Chemistry

## History

See also: Medicine:Discovery and development of antiandrogens

Antigonadotropins like estrogens and progestogens were both first introduced in the 1930s.[180] The beneficial effects of androgen deprivation via surgical castration or high-dose estrogen therapy on prostate cancer were discovered in 1941.[31]: 56 [181] AR antagonists were first discovered in the early 1960s.[97] 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.[182][63] However, spironolactone was introduced in 1959,[183][184] although its antiandrogen effects were not recognized or taken advantage of until later and were originally an unintended off-target action of the drug.[185] 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.[186][187][188] 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).[189][190]

The nonsteroidal antiandrogen flutamide was first reported in 1967.[24] It was introduced in 1983 and was the first nonsteroidal antiandrogen marketed.[191][192] Another early nonsteroidal antiandrogen,[193] DIMP (Ro 7–8117), which is structurally related to thalidomide[194] and is a relatively weak antiandrogen,[195][196] was first described in 1973 and was never marketed.[197] Flutamide was followed by nilutamide in 1989, and bicalutamide in 1995.[198] 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, respectively.[199][200][201] They differ from the earlier nonsteroidal antiandrogens namely in that they are much more efficacious in comparison.[200]

The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960 and 1977, respectively,[202][203] and the newer drug abiraterone acetate was introduced in 2011.[204] GnRH modulators were first introduced in the 1980s.[205] The 5α-reductase inhibitors finasteride and dutasteride were introduced in 1992. and 2002. respectively.[206][207] Elagolix, the first orally active GnRH modulator to be marketed, was introduced in 2018.[208]

### Timeline

The following is a timeline of events in the history of antiandrogens:[209]

* 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[210]
* 1960: Spironolactone is first introduced for medical use, as an antimineralocorticoid[210]
* 1961: The steroidal antiandrogen cyproterone acetate is first synthesized[211]
* 1962: Spironolactone is first reported to produce gynecomastia in men[210][212]
* 1966: Benorterone is the first known antiandrogen to be studied clinically, to treat acne and hirsutism in women[213][214]
* 1963: The antiandrogenic activity of cyproterone acetate is discovered[48][215]
* 1967: A known antiandrogen, benorterone, is first reported to induce gynecomastia in males[213]
* 1967: The first-generation nonsteroidal antiandrogen flutamide is first synthesized
* 1967: Cyproterone acetate was first studied clinically, to treat sexual deviance in men[216]
* 1969: Cyproterone acetate was first studied in the treatment of acne, hirsutism, seborrhea, and scalp hair loss in women[217]
* 1969: The antiandrogenic activity of spironolactone is discovered[218]
* 1972: The antiandrogenic activity of flutamide is first reported[219][220]
* 1973: Cyproterone acetate was first introduced for medical use, to treat sexual deviance[221]
* 1977: The first-generation antiandrogen nilutamide is first described[222]
* 1978: Spironolactone is first studied in the treatment of hirsutism in women[66][223]
* 1979: Combined androgen blockade is first studied[224][225]
* 1982: The first-generation antiandrogen bicalutamide is first described[226]
* 1982: Combined androgen blockade for prostate cancer is developed
* 1983: Flutamide is first introduced, in Chile, for medical use, to treat prostate cancer[227][228]
* 1987: Nilutamide is first introduced, in France, for medical use, to treat prostate cancer[198]
* 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[229]
* 1989: Flutamide is first studied in the treatment of hirsutism in women[9]
* 1992: The androgen synthesis inhibitor abiraterone acetate is first described[230]
* 1995: Bicalutamide is first introduced for medical use, to treat prostate cancer[198]
* 1996: Nilutamide is first introduced for medical use in the United States, to treat prostate cancer[231]
* 2006: The second-generation nonsteroidal antiandrogen enzalutamide is first described[232]
* 2007: The second-generation nonsteroidal antiandrogen apalutamide is first described[233]
* 2011: Abiraterone acetate is first introduced for medical use, to treat prostate cancer[234]
* 2012: Enzalutamide is first introduced for medical use, to treat prostate cancer[235]
* 2018: Apalutamide is first introduced for medical use, to treat prostate cancer[236]
* 2018: Elagolix is the first orally active GnRH antagonist to be introduced for medical use[208]
* 2019: Relugolix is the second orally active GnRH antagonist to be introduced for medical use[237]
* 2019: Darolutamide is first introduced for medical use, to treat prostate cancer[238]

## Society and culture

### Etymology

The term antiandrogen is generally used to refer specifically to AR antagonists, as described by Dorfman (1970):[239][240]

> 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.[239][240]

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.[2][6][241] 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.[242][241]

## Research

### Topical administration

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.[243] 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 steroidal AR antagonists like cyproterone acetate and spironolactone have been employed.[243] 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 antibiotics.[243]

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 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.[40] 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.[40] 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.[244]

Topical clascoterone, brand name Winlevi, was approved to treat acne in males and females in the United States in 2020.[245][246] However, although significantly more effective than placebo, topical clascoterone, like previous topical antiandrogens that have been developed, showed modest effectiveness in treating acne in clinical trials, and it appeared to be far less effective than systemic spironolactone.[54]

### Male contraception

Antiandrogens, such as cyproterone acetate, have been studied for potential use as male hormonal contraceptives.[247][248][249][250][66][251][252][253] While effective in suppressing male fertility, their use as monotherapies is precluded by side effects, such as androgen deficiency (e.g., demasculinization, sexual dysfunction, hot flashes, osteoporosis) and feminization (e.g., gynecomastia).[66][251][252][254] 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.[252][253][255][256][254] Dimethandrolone undecanoate (developmental code name CDB-4521), an orally active dual AAS and progestogen, is under investigation as a potential male contraceptive and as the first male birth control pill.[257][258]

### 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.[259][260][261][262][263]

### Miscellaneous

Antiandrogens might be effective and useful in the treatment of obsessive–compulsive disorder (OCD).[264]

## See also

* Androgen insensitivity syndrome
* Antiandrogens in the environment
* Androgen replacement therapy

## References

1. ↑ "Antiandrogens. Mechanisms and paradoxical effects". Ann. Endocrinol. (Paris) 50 (3): 50(3):189–99. 1989. PMID 2530930.
2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 "Sex Hormones (Male): Analogs and Antagonists". Encyclopedia of Molecular Cell Biology and Molecular Medicine. Wiley-VCH Verlag GmbH & Co. KGaA. 2006. doi:10.1002/3527600906.mcb.200500066. ISBN 3-527-60090-6.
3. ↑ Using Medical Terminology: A Practical Approach. Lippincott Williams & Wilkins. 2006. pp. 977–. ISBN 978-0-7817-4868-1. https://archive.org/details/usingmedicalterm0000nath.
4. ↑ 4.0 4.1 4.2 4.3 4.4 "Anti-androgen hormonal therapy for cancer and other diseases". Eur. J. Pharmacol. 866. January 2020. doi:10.1016/j.ejphar.2019.172783. PMID 31712062.
5. ↑ "Antiandrogen treatments in locally advanced prostate cancer: are they all the same?". J Cancer Res Clin Oncol 1 (Suppl 1): S17-26. 2006. doi:10.1007/s00432-006-0133-5. PMID 16845534.
6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 "Androgen deprivation therapy for prostate cancer chemoprevention: current status and future directions for agent development". Urology 58 (2 Suppl 1): 83–90. 2001. doi:10.1016/s0090-4295(01)01247-x. PMID 11502457. "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); [...]".
7. ↑ 7.0 7.1 7.2 "Steroidal Antiandrogens". Hormone Therapy in Breast and Prostate Cancer. Humana Press. 2009. pp. 325–346. doi:10.1007/978-1-59259-152-7_15. ISBN 978-1-60761-471-5. https://archive.org/details/hormonetherapybr00crai.
8. ↑ 8.0 8.1 8.2 "Nonsteroidal Antiandrogens". Hormone Therapy in Breast and Prostate Cancer. Humana Press. 2009. pp. 347–368. doi:10.1007/978-1-59259-152-7_16. ISBN 978-1-60761-471-5. https://archive.org/details/hormonetherapybr00crai.
9. ↑ 9.0 9.1 9.2 9.3 "Antiandrogens: clinical applications". The Journal of Steroid Biochemistry and Molecular Biology 37 (3): 349–362. November 1990. doi:10.1016/0960-0760(90)90484-3. PMID 2147859.
10. ↑ "Priapism: pathogenesis, epidemiology, and management". The Journal of Sexual Medicine 7 (1 Pt 2): 476–500. January 2010. doi:10.1111/j.1743-6109.2009.01625.x. PMID 20092449.
11. ↑ Disorders of Hemoglobin: Genetics, Pathophysiology, and Clinical Management. Cambridge University Press. 17 August 2009. pp. 476–. ISBN 978-1-139-48080-2. https://books.google.com/books?id=5UcgAwAAQBAJ&pg=PA476.
12. ↑ 12.0 12.1 12.2 "Dermatology of androgen-related disorders". Clinics in Dermatology 24 (4): 289–298. 2006. doi:10.1016/j.clindermatol.2006.04.004. PMID 16828411.
13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 "Treatment of hyperandrogenism in women". Gynecological Endocrinology 10 (sup3): 1–44. 2009. doi:10.3109/09513599609045658. ISSN 0951-3590.
14. ↑ 14.0 14.1 14.2 14.3 "Care of transsexual persons". N. Engl. J. Med. 364 (26): 2559–60; author reply 2560. 2011. doi:10.1056/NEJMc1104884. PMID 21714669.
15. ↑ 15.0 15.1 "Psychological and medical care of gender nonconforming youth". Pediatrics 134 (6): 1184–92. 2014. doi:10.1542/peds.2014-0772. PMID 25404716. http://pediatrics.aappublications.org/content/pediatrics/134/6/1184.full.pdf. Retrieved 2018-05-14.
16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 16.7 "Therapeutic Rationales, Progresses, Failures, and Future Directions for Advanced Prostate Cancer". Int. J. Biol. Sci. 12 (4): 409–26. 2016. doi:10.7150/ijbs.14090. PMID 27019626.
17. ↑ 17.0 17.1 "Targeting continued androgen receptor signaling in prostate cancer". Clin. Cancer Res. 17 (12): 3876–83. 2011. doi:10.1158/1078-0432.CCR-10-2815. PMID 21680543.
18. ↑ "Luteinising hormone-releasing hormone antagonists in prostate cancer therapy". Expert Opin Emerg Drugs 12 (2): 285–99. 2007. doi:10.1517/14728214.12.2.285. PMID 17604502.
19. ↑ 19.0 19.1 "Combined androgen blockade for prostate cancer: review of efficacy, safety, and cost-effectiveness". Cancer Science 102 (1): 51–6. Jan 2011. doi:10.1111/j.1349-7006.2010.01774.x. PMID 21091846.
20. ↑ "Novel drugs targeting the androgen receptor pathway in prostate cancer". Cancer Metastasis Rev. 33 (2–3): 567–79. 2014. doi:10.1007/s10555-013-9472-2. PMID 24390422.
21. ↑ 21.0 21.1 21.2 21.3 "Nonsteroidal antiandrogens: a therapeutic option for patients with advanced prostate cancer who wish to retain sexual interest and function". BJU Int. 87 (1): 47–56. 2001. doi:10.1046/j.1464-410x.2001.00988.x. PMID 11121992.
22. ↑ "Antiandrogen monotherapy: a new form of treatment for patients with prostate cancer". Urology 58 (2 Suppl 1): 16–23. August 2001. doi:10.1016/s0090-4295(01)01237-7. PMID 11502439.
23. ↑ "Hormonal therapy: historical perspective to future directions". Urology 61 (2 Suppl 1): 3–7. 2003. doi:10.1016/s0090-4295(02)02393-2. PMID 12667881.
24. ↑ 24.0 24.1 Smith and Williams' Introduction to the Principles of Drug Design and Action, Fourth Edition. CRC Press. 10 October 2005. pp. 489–. ISBN 978-0-203-30415-0. https://books.google.com/books?id=P2W6B9FQRKsC&pg=PA489.
25. ↑ Cancer Chemotherapy and Biotherapy: Principles and Practice. Lippincott Williams & Wilkins. 8 November 2010. pp. 679–680. ISBN 978-1-60547-431-1. https://books.google.com/books?id=WL4arNFsQa8C&pg=PA680. Retrieved 27 December 2016. "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."
26. ↑ "Management of advanced prostate cancer". Revista da Associação Médica Brasileira 54 (2): 178–82. 2008. doi:10.1590/S0104-42302008000200025. PMID 18506331. http://www.scielo.br/pdf/ramb/v54n2/a25v54n2.pdf. Retrieved 2016-12-27.
27. ↑ Bicalutamide BPCA Drug Use Review in the Pediatric Population, U.S. Department of Health and Human Service, 10 March 2010, https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/PediatricAdvisoryCommittee/UCM214400.pdf, retrieved 20 July 2016
28. ↑ Prostate Cancer. Demos Medical Publishing. 2011. pp. 81–. ISBN 978-1-935281-91-7. https://books.google.com/books?id=WJkjgbRJe3EC&pg=PT81.
29. ↑ Controversies in the Treatment of Prostate Cancer. Karger Medical and Scientific Publishers. 1 January 2008. pp. 41–42. ISBN 978-3-8055-8524-8. https://books.google.com/books?id=4J4OCRyHWRYC&pg=PA41. Retrieved 27 December 2016.
30. ↑ Prostate Cancer. Demos Medical Publishing. 20 December 2011. pp. 505–. ISBN 978-1-935281-91-7. https://books.google.com/books?id=WJkjgbRJe3EC&pg=PA505.
31. ↑ 31.00 31.01 31.02 31.03 31.04 31.05 31.06 31.07 31.08 31.09 Drug Management of Prostate Cancer. Springer Science & Business Media. 14 September 2010. pp. 71–72, 75, 91–96. ISBN 978-1-60327-829-4. https://books.google.com/books?id=4KDrjeWA5-UC&pg=PA93.
32. ↑ 32.0 32.1 "Chemoprevention of prostate cancer". Acta Oncol 50 (Suppl 1): 127–36. 2011. doi:10.3109/0284186X.2010.527367. PMID 21604953.
33. ↑ "Spironolactone use and risk of incident cancers: a retrospective, matched cohort study". Br J Clin Pharmacol 83 (3): 653–663. 2016. doi:10.1111/bcp.13152. PMID 27735065.
34. ↑ "Endocrine treatment of transsexual persons: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 94 (9): 3132–54. 2009. doi:10.1210/jc.2009-0345. PMID 19509099.
35. ↑ "Prostate cancer incidence in orchidectomised male-to-female transsexual persons treated with oestrogens". Andrologia 46 (10): 1156–60. 2014. doi:10.1111/and.12208. PMID 24329588.
36. ↑ "Metastatic prostate cancer in transsexual diagnosed after three decades of estrogen therapy". Can Urol Assoc J 7 (7–8): E544–6. 2013. doi:10.5489/cuaj.175. PMID 24032068.
37. ↑ 37.0 37.1 "5alpha-Reductase inhibitor treatment of prostatic diseases: background and practical implications". Prostate Cancer Prostatic Dis. 12 (2): 130–6. 2009. doi:10.1038/pcan.2008.56. PMID 19030020.
38. ↑ "Evidence-based meta-analysis of pharmacotherapy for benign prostatic hypertrophy". Int. J. Urol. 9 (11): 607–12. 2002. doi:10.1046/j.1442-2042.2002.00539.x. PMID 12534901.
39. ↑ International Symposium on the Treatment of Carcinoma of the Prostate, Berlin, November 13 to 15, 1969: Life Science Monographs. Elsevier. 22 October 2013. pp. 165–. ISBN 978-1-4831-8711-2. https://books.google.com/books?id=8RjLBAAAQBAJ&pg=PA165.
40. ↑ 40.0 40.1 40.2 Male Alopecia: Guide to Successful Management. Springer Science & Business Media. 13 February 2014. pp. 91–93. ISBN 978-3-319-03233-7. https://books.google.com/books?id=0ue5BAAAQBAJ&pg=PA93.
41. ↑ 41.0 41.1 41.2 Dermatology. Gulf Professional Publishing. 2003. pp. 1072–. ISBN 978-99976-38-99-1. https://books.google.com/books?id=f2IwYiyh3YUC&pg=PT1072.
42. ↑ 42.0 42.1 "The Effect of Drugs on Hair". Pharmacology of the Skin II. Handbook of Experimental Pharmacology. 87 / 2. Springer. 1989. pp. 495–508. doi:10.1007/978-3-642-74054-1_37. ISBN 978-3-642-74056-5.
43. ↑ 43.0 43.1 "Androgenetic alopecia and its treatment. A historical overview". Hair Transplantation (Third ed.). Taylor & Francis. 1 February 1995. pp. 1–33. ISBN 978-0-8247-9363-0. https://books.google.com/books?id=_KxsAAAAMAAJ.
44. ↑ 44.0 44.1 Chapter 18. Chemical Control of Androgen Action. Annual Reports in Medicinal Chemistry. 21. Academic Press. 1986. pp. 179–188. doi:10.1016/S0065-7743(08)61128-8. ISBN 978-0-12-040521-3.
45. ↑ 45.0 45.1 "Cyproteronacetate in the management of severe acne in males". Archives of Dermatological Research 271 (2): 183–187. 1981. doi:10.1007/BF00412545. ISSN 0340-3696.
46. ↑ "Potential side effects of androgen deprivation treatment in sex offenders". The Journal of the American Academy of Psychiatry and the Law 37 (1): 53–58. 2009. PMID 19297634.
47. ↑ "Medical Management Options for Hair Loss". Aesthetic Medicine. Springer. 2012. pp. 529–535. doi:10.1007/978-3-642-20113-4_41. ISBN 978-3-642-20112-7.
48. ↑ 48.0 48.1 "Pharmacology of Cyproterone Acetate — A Short Review". Antiandrogens in Prostate Cancer. 1996. pp. 31–44. doi:10.1007/978-3-642-45745-6_3. ISBN 978-3-642-45747-0.
49. ↑ "Dermatologic therapy: December, 1982, through November, 1983". Journal of the American Academy of Dermatology 11 (1): 25–52. July 1984. doi:10.1016/S0190-9622(84)80163-2. PMID 6376557.
50. ↑ ACNE and ROSACEA. Springer Science & Business Media. 6 December 2012. pp. 687–. ISBN 978-3-642-59715-2. https://books.google.com/books?id=0cD-CAAAQBAJ&pg=PA687.
51. ↑ Koda-Kimble and Young's Applied Therapeutics: The Clinical Use of Drugs. Lippincott Williams & Wilkins. 1 February 2012. pp. 952–. ISBN 978-1-60913-713-7. https://books.google.com/books?id=qcVpuHngXK0C&pg=PA952.
52. ↑ "Isotretinoin. A review of its pharmacological properties and therapeutic efficacy in acne and other skin disorders". Drugs 28 (1): 6–37. July 1984. doi:10.2165/00003495-198428010-00002. PMID 6235105.
53. ↑ "Response of male acne to antiandrogen therapy with cyproterone acetate". Dermatologica 173 (3): 139–142. 1986. doi:10.1159/000249236. PMID 2945742.
54. ↑ 54.0 54.1 "The efficacy of Topical Clascoterone versus systematic spironolactone for treatment of acne vulgaris: A systematic review and network meta-analysis". PLOS ONE 19 (5). 2024. doi:10.1371/journal.pone.0298155. PMID 38814916. Bibcode: 2024PLoSO..1998155B.
55. ↑ "What's new in the management of acne vulgaris". Cutis 104 (1): 48–52. July 2019. PMID 31487336. https://www.mdedge.com/dermatology/article/204308/acne/whats-new-management-acne-vulgaris. Retrieved 2020-03-30.
56. ↑ "The use of hormonal agents in the treatment of acne". Seminars in Cutaneous Medicine and Surgery 35 (2): 68–73. June 2016. doi:10.12788/j.sder.2016.027. PMID 27416311.
57. ↑ "Cassiopea Receives FDA Approval for Winlevi® (clascoterone cream 1%), First-in-Class Topical Acne Treatment Targeting the Androgen Receptor - Cassiopea". 2020-08-28. 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/.
58. ↑ "Drugs@FDA: FDA-Approved Drugs" (in en). https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=213433.
59. ↑ Human Reproductive Biology. Academic Press. 28 September 2013. pp. 77–. ISBN 978-0-12-382185-0. https://books.google.com/books?id=M4kEdSnS-pkC&pg=PA77.
60. ↑ 60.0 60.1 "The neurobiology, neuropharmacology, and pharmacological treatment of the paraphilias and compulsive sexual behaviour". Can J Psychiatry 46 (1): 26–34. 2001. doi:10.1177/070674370104600104. PMID 11221487.
61. ↑ 61.0 61.1 "Drug treatment of paraphilic and nonparaphilic sexual disorders". Clin Ther 31 (1): 1–31. 2009. doi:10.1016/j.clinthera.2009.01.009. PMID 19243704.
62. ↑ Handbook of Sexual Assault: Issues, Theories, and Treatment of the Offender. Springer Science & Business Media. 21 November 2013. pp. 297–. ISBN 978-1-4899-0915-2. https://books.google.com/books?id=lkf2BwAAQBAJ&pg=PA297.
63. ↑ 63.0 63.1 Eating, Sleeping, and Sex. Psychology Press. 1989. pp. 209–. ISBN 978-0-8058-0280-1. https://books.google.com/books?id=bf-dRU-Ie9EC&pg=PA209.
64. ↑ Sexual Offending: Predisposing Antecedents, Assessments and Management. Springer. 7 December 2015. pp. 759–. ISBN 978-1-4939-2416-5. https://books.google.com/books?id=NhEpCwAAQBAJ&pg=PA759.
65. ↑ 65.0 65.1 65.2 65.3 "Update on the etiology, diagnosis and therapeutic management of sexual precocity". Arq Bras Endocrinol Metabol 52 (1): 18–31. February 2008. doi:10.1590/S0004-27302008000100005. PMID 18345393.
66. ↑ 66.0 66.1 66.2 66.3 66.4 "Androgen antagonists in androgen target tissues". Pharmacol. Ther. 24 (3): 367–400. 1984. doi:10.1016/0163-7258(84)90010-x. PMID 6205409.
67. ↑ "Clinical applications of antiandrogens". J. Steroid Biochem. 31 (4B): 719–29. October 1988. doi:10.1016/0022-4731(88)90023-4. PMID 2462132.
68. ↑ 68.0 68.1 "Clinical applications of LHRH analogues". Baillière's Clin. Endocrinol. Metab. 1 (1): 43–70. February 1987. doi:10.1016/S0950-351X(87)80052-6. PMID 3109366.
69. ↑ "Experience with cyproterone acetate in the treatment of precocious puberty". J. Pediatr. Endocrinol. Metab. 13 (Suppl 1): 805–10. July 2000. doi:10.1515/jpem.2000.13.s1.805. PMID 10969925.
70. ↑ "Cyproterone acetate in the treatment of sexual disorders: pharmacological base and clinical experience". Exp. Clin. Endocrinol. 98 (2): 71–80. 1991. doi:10.1055/s-0029-1211103. PMID 1838080.
71. ↑ 71.0 71.1 "Gonadotropin-independent precocious puberty". Endocrinol. Metab. Clin. North Am. 20 (1): 191–210. March 1991. doi:10.1016/s0889-8529(18)30288-3. PMID 1903104.
72. ↑ 72.0 72.1 "Testotoxicosis: current viewpoint". Pediatr Endocrinol Rev 3 (2): 77–86. December 2005. PMID 16361981.
73. ↑ "Medical management of ischemic stuttering priapism: a contemporary review of the literature". Asian Journal of Andrology 14 (1): 156–63. 2012. doi:10.1038/aja.2011.114. PMID 22057380.
74. ↑ "Priapism: pathogenesis, epidemiology, and management". The Journal of Sexual Medicine 7 (1 Pt 2): 476–500. 2010. doi:10.1111/j.1743-6109.2009.01625.x. PMID 20092449.
75. ↑ "The pharmacological management of intermittent priapismic states". BJU International 102 (11): 1515–21. 2008. doi:10.1111/j.1464-410X.2008.07951.x. PMID 18793304.
76. ↑ "Antiandrogens in the treatment of priapism". Urology 59 (1): 138. 2002. doi:10.1016/S0090-4295(01)01492-3. PMID 11796309.
77. ↑ "Insights of priapism mechanism and rationale treatment for recurrent priapism". Asian Journal of Andrology 10 (1): 88–101. 2008. doi:10.1111/j.1745-7262.2008.00314.x. PMID 18087648.
78. ↑ Textbook of Cosmetic Dermatology. CRC Press. 1 October 1998. pp. 388–. ISBN 978-1-85317-478-0. https://books.google.com/books?id=yIVfq5Lpl2EC&pg=PA388.
79. ↑ Evidence Based Dermatology. PMPH-USA. 2011. pp. 526–. ISBN 978-1-60795-039-4. https://books.google.com/books?id=V2L1MAoGHVkC&pg=PA526.
80. ↑ Evidence-Based Dermatology. John Wiley & Sons. 22 January 2009. pp. 529–. ISBN 978-1-4443-0017-8. https://books.google.com/books?id=SbsQij5xkfYC&pg=PA529. Retrieved 27 December 2016.
81. ↑ 81.0 81.1 "Update on idiopathic hirsutism: diagnosis and treatment". Acta Clin Belg 68 (4): 268–74. 2013. doi:10.2143/ACB.3267. PMID 24455796.
82. ↑ 82.0 82.1 Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. 2001. pp. 1004, 1196. ISBN 978-0-7817-1750-2. https://books.google.com/books?id=FVfzRvaucq8C&pg=PA1004.
83. ↑ 83.0 83.1 83.2 Evidence-Based Endocrinology. Lippincott Williams & Wilkins. 2012. pp. 199–. ISBN 978-1-4511-1091-3. https://books.google.com/books?id=TrLaw_CX1i8C&pg=PA199.
84. ↑ "Gender-Affirming Hormone Therapy for Transgender Females". Clin Obstet Gynecol 61 (4): 705–721. December 2018. doi:10.1097/GRF.0000000000000396. PMID 30256230.
85. ↑ 85.0 85.1 85.2 85.3 85.4 85.5 85.6 85.7 "Androgen receptor antagonists (antiandrogens): structure-activity relationships". Current Medicinal Chemistry 7 (2): 211–247. February 2000. doi:10.2174/0929867003375371. PMID 10637363.
86. ↑ 86.0 86.1 86.2 86.3 "Androgen Receptor Antagonists". Drug Management of Prostate Cancer. Springer. 2010. pp. 71–81. doi:10.1007/978-1-60327-829-4_6. ISBN 978-1-60327-831-7.
87. ↑ "Do progestins contribute to (anti-)androgenic activities in aquatic environments?". Environmental Pollution 242 (Pt A): 417–425. November 2018. doi:10.1016/j.envpol.2018.06.104. PMID 29990947. Bibcode: 2018EPoll.242..417S.
88. ↑ "Progestogens with antiandrogenic properties". Drugs 63 (5): 463–492. 2003. doi:10.2165/00003495-200363050-00003. PMID 12600226.
89. ↑ "Androgens and antiandrogens". Annals of the New York Academy of Sciences 997 (1): 292–306. November 2003. doi:10.1196/annals.1290.033. PMID 14644837. Bibcode: 2003NYASA.997..292S.
90. ↑ 90.0 90.1 90.2 90.3 90.4 90.5 Yen and Jaffe's Reproductive Endocrinology. Elsevier Health Sciences. 13 September 2013. pp. 90–. ISBN 978-1-4557-2758-2. https://books.google.com/books?id=KZ95AAAAQBAJ&pg=PA90.
91. ↑ "An overview on 5alpha-reductase inhibitors". Steroids 75 (2): 109–53. 2010. doi:10.1016/j.steroids.2009.10.005. PMID 19879888.
92. ↑ 92.0 92.1 92.2 The Molecular Basis of Cancer. Springer Science & Business Media. 6 December 2012. pp. 232–. ISBN 978-1-4684-7313-1. https://books.google.com/books?id=Bva8BAAAQBAJ&pg=PA232.
93. ↑ 93.0 93.1 93.2 93.3 93.4 93.5 Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. 24 January 2012. pp. 228–231, 1371–1372. ISBN 978-1-60913-345-0. https://books.google.com/books?id=Sd6ot9ul-bUC&pg=PA1372.
94. ↑ 94.0 94.1 94.2 "Pharmacodynamics of oestrogens and progestogens". Cephalalgia: An International Journal of Headache 20 (3): 200–7. April 2000. doi:10.1046/j.1468-2982.2000.00042.x. PMID 10997774.
95. ↑ Chronic Pelvic Pain. Cambridge University Press. 11 December 2014. pp. 55–. ISBN 978-1-316-21414-5. https://books.google.com/books?id=ON-VBQAAQBAJ&pg=PA55.
96. ↑ 96.0 96.1 Practical Clinical Oncology. Cambridge University Press. 19 November 2015. pp. 37–. ISBN 978-1-107-68362-4. https://books.google.com/books?id=wm_OCgAAQBAJ&pg=PA37.
97. ↑ 97.0 97.1 Molecular Therapies of Cancer. Springer. 22 July 2015. pp. 314, 316. ISBN 978-3-319-13278-5. https://books.google.com/books?id=dhs_CgAAQBAJ&pg=PA316.
98. ↑ "Clinical pharmacokinetics of the antiandrogens and their efficacy in prostate cancer". Clin Pharmacokinet 34 (5): 405–17. May 1998. doi:10.2165/00003088-199834050-00005. PMID 9592622.
99. ↑ 99.0 99.1 Endocrine Toxicology, Second Edition. CRC Press. 12 March 1997. pp. 152–. ISBN 978-1-4398-1048-4. https://books.google.com/books?id=URc5JMoNirgC&pg=PA152. Retrieved 27 December 2016.
100. ↑ "The role of antiandrogen monotherapy in the treatment of prostate cancer". BJU Int. 91 (5): 455–61. 2003. doi:10.1046/j.1464-410x.2003.04026.x. PMID 12603397.
101. ↑ Cancer Chemotherapy in Clinical Practice. Springer Science & Business Media. 26 May 2012. pp. 97–. ISBN 978-0-85729-727-3. https://books.google.com/books?id=K41Lf91GULcC&pg=PA97.
102. ↑ 102.0 102.1 102.2 "Side effects of androgen deprivation therapy: monitoring and minimizing toxicity". Urology 61 (2 Suppl 1): 32–8. 2003. doi:10.1016/S0090-4295(02)02397-X. PMID 12667885.
103. ↑ "Management of gynaecomastia in patients with prostate cancer: a systematic review". Lancet Oncol. 6 (12): 972–9. December 2005. doi:10.1016/S1470-2045(05)70464-2. PMID 16321765.
104. ↑ Hair Disorders: Current Concepts in Pathophysiology, Diagnosis and Management, An Issue of Dermatologic Clinics. Elsevier Health Sciences. 12 November 2012. pp. 187–. ISBN 978-1-4557-7169-1. https://books.google.com/books?id=9rLeICotHEoC&pg=PT187.
105. ↑ Polycystic Ovarian Disease. Springer Science & Business Media. 6 December 2012. pp. 282–. ISBN 978-1-4613-8289-8. https://books.google.com/books?id=siSSBgAAQBAJ&pg=PT282.
106. ↑ "Hormonal therapy for acne: why not as first line therapy? facts and controversies". Clin. Dermatol. 28 (1): 17–23. 2010. doi:10.1016/j.clindermatol.2009.03.006. PMID 20082945.
107. ↑ "The cardiometabolic effect of current management of polycystic ovary syndrome: strategies of prevention and treatment". Gynecol Endocrinol 34 (2): 87–91. February 2018. doi:10.1080/09513590.2017.1381681. PMID 28944709.
108. ↑ "Short term effects of spironolactone on blood lipid profile: a 3-month study on a cohort of young women with hirsutism". Br J Clin Pharmacol 68 (4): 634–7. October 2009. doi:10.1111/j.1365-2125.2009.03483.x. PMID 19843067.
109. ↑ "Pharmacological Approaches to Controlling Cardiometabolic Risk in Women with PCOS". Int J Mol Sci 21 (24): 9554. December 2020. doi:10.3390/ijms21249554. PMID 33334002.
110. ↑ "Combined Oral Contraception and Bicalutamide in Polycystic Ovary Syndrome and Severe Hirsutism: A Double-Blind Randomized Controlled Trial". J. Clin. Endocrinol. Metab. 103 (3): 824–838. March 2018. doi:10.1210/jc.2017-01186. PMID 29211888.
111. ↑ Coleman, E. et al. (19 August 2022). "Standards of Care for the Health of Transgender and Gender Diverse People, Version 8". International Journal of Transgender Health 23 (Suppl 1): S1–S259. doi:10.1080/26895269.2022.2100644. ISSN 2689-5269. PMID 36238954.
112. ↑ "Sex, plasma lipoproteins, and atherosclerosis: prevailing assumptions and outstanding questions". American Heart Journal 114 (6): 1467–1503. December 1987. doi:10.1016/0002-8703(87)90552-7. PMID 3318361.
113. ↑ "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". Circulation 139 (25): e1082–e1143. June 2019. doi:10.1161/CIR.0000000000000625. PMID 30586774.
114. ↑ 114.0 114.1 "Hepatotoxicity induced by antiandrogens: a review of the literature". Urol. Int. 73 (4): 289–95. 2004. doi:10.1159/000081585. PMID 15604569.
115. ↑ "Enzalutamide: a review of its use in chemotherapy-naïve metastatic castration-resistant prostate cancer". Drugs & Aging 32 (3): 243–9. March 2015. doi:10.1007/s40266-015-0248-y. PMID 25711765.
116. ↑ 116.0 116.1 Primary Care for Women. Lippincott Williams & Wilkins. 2004. pp. 277–. ISBN 978-0-7817-3790-6. https://books.google.com/books?id=PiiD0iUNhlIC&pg=PA277.
117. ↑ Human sexuality in a world of diversity. Pearson Allyn and Bacon. 2005. p. 313. ISBN 978-0-205-40615-9. https://books.google.com/books?id=HahZAAAAYAAJ. Retrieved 2016-12-27.
118. ↑ 118.0 118.1 118.2 118.3 118.4 "Comparison of the antiandrogenic/androgenic activities of flutamide, cyproterone acetate and megestrol acetate". Molecular and Cellular Endocrinology 42 (3): 283–8. October 1985. doi:10.1016/0303-7207(85)90059-0. PMID 3930312.
119. ↑ "Androgenic activity of synthetic progestins and spironolactone in androgen-sensitive mouse mammary carcinoma (Shionogi) cells in culture". Journal of Steroid Biochemistry 31 (5): 845–52. 1988. doi:10.1016/0022-4731(88)90295-6. PMID 2462135.
120. ↑ "Spironolactone, a possible selective androgen receptor modulator, should be used with caution in patients with metastatic carcinoma of the prostate". BMJ Case Rep 2012: bcr1120115238. 2012. doi:10.1136/bcr.11.2011.5238. PMID 22665559.
121. ↑ "Case Report: Spironolactone Withdrawal Associated With a Dramatic Response in a Patient With Metastatic Castrate-Resistant Prostate Cancer". Clin Genitourin Cancer 15 (1): e95–e97. 2016. doi:10.1016/j.clgc.2016.08.006. PMID 27641657.
122. ↑ Hormonal Steroids: Proceedings of the Sixth International Congress on Hormonal Steroids. Elsevier Science. 22 October 2013. pp. 391–. ISBN 978-1-4831-9067-9. https://books.google.com/books?id=1VMJAwAAQBAJ&pg=PA391.
123. ↑ 123.0 123.1 "Maximum androgen blockade in advanced prostate cancer: a meta-analysis of published randomized controlled trials using nonsteroidal antiandrogens". Urology 49 (1): 71–8. 1997. doi:10.1016/S0090-4295(96)00325-1. PMID 9000189. "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.".
124. ↑ 124.0 124.1 124.2 "Androgen receptor antagonists (antiandrogens): structure-activity relationships". Current Medicinal Chemistry 7 (2): 211–47. February 2000. doi:10.2174/0929867003375371. PMID 10637363.
125. ↑ 125.0 125.1 125.2 125.3 "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". J. Steroid Biochem. 33 (2): 251–5. August 1989. doi:10.1016/0022-4731(89)90301-4. PMID 2788775.
126. ↑ 126.0 126.1 "Comparison of the Hershberger assay and androgen receptor binding assay of twelve chemicals". Toxicology 195 (2–3): 177–86. 2004. doi:10.1016/j.tox.2003.09.012. PMID 14751673. Bibcode: 2004Toxgy.195..177Y.
127. ↑ The Anticancer Drugs. Oxford University Press. 1994. pp. 220–. ISBN 978-0-19-506739-2. https://books.google.com/books?id=nPR1L4K5HuEC&pg=PA220. "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"
128. ↑ "Molecular cell biology of androgen receptor signalling". Int. J. Biochem. Cell Biol. 42 (6): 813–27. 2010. doi:10.1016/j.biocel.2009.11.013. PMID 19931639.
129. ↑ "G protein-coupled receptors: extranuclear mediators for the non-genomic actions of steroids". Int J Mol Sci 15 (9): 15412–25. 2014. doi:10.3390/ijms150915412. PMID 25257522.
130. ↑ "Targeting membrane androgen receptors in tumors". Expert Opin. Ther. Targets 17 (8): 951–63. 2013. doi:10.1517/14728222.2013.806491. PMID 23746222.
131. ↑ 131.0 131.1 Pediatric Endocrinology: Mechanisms, Manifestations, and Management. Lippincott Williams & Wilkins. 2004. pp. 248–. ISBN 978-0-7817-4059-3. https://books.google.com/books?id=9gvBlktAT6YC&pg=PA248.
132. ↑ 132.0 132.1 Neonatology: A Practical Approach to Neonatal Diseases. Springer Science & Business Media. 28 January 2012. pp. 1012–. ISBN 978-88-470-1405-3. https://books.google.com/books?id=n_L2XpJbhLoC&pg=PA1012.
133. ↑ Brain Storm. Harvard University Press. 7 January 2011. pp. 82–. ISBN 978-0-674-05879-8. https://books.google.com/books?id=2V9UuOWMXOMC&pg=PA82.
134. ↑ Gender Development. Psychology Press. 13 May 2013. pp. 115–. ISBN 978-1-135-07932-1. https://books.google.com/books?id=PQ3Ylt6KnA4C&pg=PT115.
135. ↑ Hormonal Therapy for Male Sexual Dysfunction. John Wiley & Sons. 30 January 2012. pp. 6–. ISBN 978-0-470-65760-7. https://books.google.com/books?id=o_A9DnMVi3cC&pg=PA6.
136. ↑ 136.0 136.1 136.2 136.3 136.4 "Androgen receptor targeted therapies in castration-resistant prostate cancer: Bench to clinic". International Journal of Urology 23 (8): 654–665. August 2016. doi:10.1111/iju.13137. PMID 27302572.
137. ↑ "EPI-001, A Compound Active against Castration-Resistant Prostate Cancer, Targets Transactivation Unit 5 of the Androgen Receptor". ACS Chemical Biology 11 (9): 2499–2505. September 2016. doi:10.1021/acschembio.6b00182. PMID 27356095.
138. ↑ "Recent advances in allosteric androgen receptor inhibitors for the potential treatment of castration-resistant prostate cancer". Pharmaceutical Patent Analyst 4 (5): 387–402. 2015. doi:10.4155/ppa.15.20. PMID 26389532.
139. ↑ 139.0 139.1 "Induced protein degradation: an emerging drug discovery paradigm". Nature Reviews. Drug Discovery 16 (2): 101–114. February 2017. doi:10.1038/nrd.2016.211. PMID 27885283. Bibcode: 2017NRvDD..16..101L.
140. ↑ 140.0 140.1 "New therapeutic approach to suppress castration-resistant prostate cancer using ASC-J9 via targeting androgen receptor in selective prostate cells". The American Journal of Pathology 182 (2): 460–473. February 2013. doi:10.1016/j.ajpath.2012.10.029. PMID 23219429.
141. ↑ "ASCJ 9". AdisInsight. Springer Nature Switzerland AG. http://adisinsight.springer.com/drugs/800028542.
142. ↑ "Ketoconazole high dose in management of hormonally pretreated patients with progressive metastatic prostate cancer. Dutch South-Eastern Urological Cooperative Group". Urology 33 (5): 411–5. May 1989. doi:10.1016/0090-4295(89)90037-X. PMID 2652864.
143. ↑ 143.0 143.1 Contemporary Issues in Prostate Cancer: A Nursing Perspective. Jones & Bartlett Learning. 2006. pp. 275–. ISBN 978-0-7637-3075-8. https://books.google.com/books?id=dZe4ZSVDdBsC&pg=PA275.
144. ↑ "The hunt for a selective 17,20 lyase inhibitor; learning lessons from nature". J. Steroid Biochem. Mol. Biol. 163: 136–46. 2016. doi:10.1016/j.jsbmb.2016.04.021. PMID 27154414.
145. ↑ "Steroid 5alpha-reductase inhibitors". Mini-Reviews in Medicinal Chemistry 3 (3): 225–37. May 2003. doi:10.2174/1389557033488196. PMID 12570838.
146. ↑ Handbook of Drug Interactions: A Clinical and Forensic Guide. Springer Science & Business Media. 18 September 2011. pp. 656–. ISBN 978-1-61779-222-9. https://books.google.com/books?id=NhBJ6kg_uP0C&pg=PA656.
147. ↑ 147.0 147.1 147.2 Medical Biochemistry. Academic Press. 2002. pp. 787–. ISBN 978-0-12-095440-7. https://books.google.com/books?id=b7Dc9bOs9uAC&pg=PA787.
148. ↑ "Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review". J Clin Aesthet Dermatol 9 (7): 56–62. 2016. PMID 27672412.
149. ↑ "Pharmacokinetics and testosterone suppression of a single dose of polyestradiol phosphate (Estradurin) in prostatic cancer patients". Prostate 28 (5): 307–10. 1996. doi:10.1002/(SICI)1097-0045(199605)28:5<307::AID-PROS6>3.0.CO;2-8. PMID 8610057.
150. ↑ "Tolerability of Antiandrogens in the Treatment of Prostate Cancer". UroOncology 4 (1): 5–13. 2015. doi:10.1080/1561095042000191655. ISSN 1561-0950.
151. ↑ Urotext (1 January 2001). Urotext-Luts: Urology. Urotext. pp. 71–. ISBN 978-1-903737-03-3. https://books.google.com/books?id=6zjtA37qDsMC&pg=PA71. Retrieved 2016-12-27.
152. ↑ "The physiological action of progesterone and the pharmacological effects of progestogens--a short review". Postgraduate Medical Journal 54 (Suppl 2): 11–24. 1978. PMID 368741.
153. ↑ "Treatment of advanced prostatic cancer with parenteral cyproterone acetate: a phase III randomised trial". Br J Urol 52 (3): 208–15. 1980. doi:10.1111/j.1464-410x.1980.tb02961.x. PMID 7000222.
154. ↑ Campbell-Walsh Urology: Expert Consult Premium Edition: Enhanced Online Features and Print, 4-Volume Set. Elsevier Health Sciences. 25 August 2011. pp. 2938–. ISBN 978-1-4160-6911-9. https://books.google.com/books?id=fu3BBwAAQBAJ&pg=PA2938. Retrieved 27 December 2016.
155. ↑ "Effects of norgestrel and ethinyloestradiol ingestion on serum levels of sex hormones and gonadotrophins in men". Clinical Endocrinology 11 (5): 497–504. 1979. doi:10.1111/j.1365-2265.1979.tb03102.x. PMID 519881.
156. ↑ "Parenteral oestrogen in the treatment of prostate cancer: a systematic review". Br. J. Cancer 98 (4): 697–707. 2008. doi:10.1038/sj.bjc.6604230. PMID 18268497.
157. ↑ "Anti-prostatic activity of bifluranol, a fluorinated bibenzyl". Br. J. Pharmacol. 71 (1): 11–6. 1980. doi:10.1111/j.1476-5381.1980.tb10903.x. PMID 6258683.
158. ↑ "On gestagen treatment of advanced prostatic carcinoma". Scand. J. Urol. Nephrol. 12 (2): 119–21. 1978. doi:10.3109/00365597809179977. PMID 694436.
159. ↑ Forensic Management of Sexual Offenders. Springer Science & Business Media. 31 July 2000. pp. 219–. ISBN 978-0-306-46278-8. https://books.google.com/books?id=-50Of8_n_TAC&pg=PA219.
160. ↑ "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". Acta Endocrinol Suppl (Copenh) 229: 53–66. 1979. doi:10.1530/acta.0.092s053. PMID 294107.
161. ↑ 161.0 161.1 Testosterone: Action, Deficiency, Substitution. Cambridge University Press. 26 July 2012. pp. 62–. ISBN 978-1-107-01290-5. https://books.google.com/books?id=MkrAPaQ4wJkC&pg=PA62.
162. ↑ 162.0 162.1 162.2 IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; World Health Organization; International Agency for Research on Cancer (2007). Combined Estrogen-progestogen Contraceptives and Combined Estrogen-progestogen Menopausal Therapy. World Health Organization. pp. 157–. ISBN 978-92-832-1291-1. https://books.google.com/books?id=aGDU5xibtNgC&pg=PA157.
163. ↑ "Preclinical characterization of a novel diphenyl benzamide selective ERα agonist for hormone therapy in prostate cancer". Endocrinology 153 (3): 1070–81. 2012. doi:10.1210/en.2011-1608. PMID 22294742.
164. ↑ 164.0 164.1 Adolescent Gynecology (pb). Orient Blackswan. 1 January 2000. pp. 121–. ISBN 978-81-250-1793-6. https://books.google.com/books?id=B8hcC17D154C&pg=PA121.
165. ↑ Contraception: Science and Practice. Elsevier Science. 22 October 2013. pp. 26–. ISBN 978-1-4831-6366-6. https://books.google.com/books?id=Ug3-BAAAQBAJ&pg=PA26.
166. ↑ 166.0 166.1 "Estrogens and Antiestrogens in the Male". Estrogens and Antiestrogens II. Handbook of Experimental Pharmacology. 135 / 2. Berlin, Heidelberg: Springer Berlin Heidelberg. 1999. pp. 505–571. doi:10.1007/978-3-642-60107-1_25. ISBN 978-3-642-64261-6.
167. ↑ 167.0 167.1 Adrenal Disorders. Springer Science & Business Media. 20 April 2001. pp. 84–. ISBN 978-1-59259-101-5. https://books.google.com/books?id=XB73BwAAQBAJ&pg=PA84.
168. ↑ 168.0 168.1 168.2 "Effects of gonadal androgens and oestrogens on adrenal androgen levels". Clin. Endocrinol. (Oxf) 43 (4): 415–21. October 1995. doi:10.1111/j.1365-2265.1995.tb02611.x. PMID 7586614.
169. ↑ "Orchidectomy or oestrogen treatment in prostatic cancer: effects on serum levels of adrenal androgens and related steroids". Int. J. Androl. 10 (4): 581–7. August 1987. doi:10.1111/j.1365-2605.1987.tb00357.x. PMID 2958420.
170. ↑ 170.0 170.1 170.2 "Androgens during different modes of endocrine treatment of prostatic cancer". Urol. Res. 17 (2): 95–8. 1989. doi:10.1007/BF00262027. PMID 2734983.
171. ↑ 171.0 171.1 171.2 "Estrogens in the treatment of prostate cancer". J. Urol. 154 (6): 1991–8. December 1995. doi:10.1016/S0022-5347(01)66670-9. PMID 7500443.
172. ↑ "Estrogen therapy and liver function--metabolic effects of oral and parenteral administration". Prostate 14 (4): 389–95. 1989. doi:10.1002/pros.2990140410. PMID 2664738.
173. ↑ 173.0 173.1 Williams Textbook of Endocrinology E-Book. Elsevier Health Sciences. 12 May 2011. pp. 753–. ISBN 978-1-4377-3600-7. https://books.google.com/books?id=nbg1QOAObicC&pg=PA753.
174. ↑ 174.0 174.1 Robbins & Cotran Pathologic Basis of Disease E-Book. Elsevier Health Sciences. 10 June 2009. pp. 1154–. ISBN 978-1-4377-2015-0. https://books.google.com/books?id=_1Zmvm4JVNcC&pg=PA1154.
175. ↑ 175.0 175.1 "Is There a Role for Antiandrogen Therapy for Hidradenitis Suppurativa? A Systematic Review of Published Data". American Journal of Clinical Dermatology 20 (4): 503–513. August 2019. doi:10.1007/s40257-019-00442-w. PMID 31073704.
176. ↑ "Effect of metformin on clinical, metabolic and endocrine outcomes in women with polycystic ovary syndrome: a meta-analysis of randomized controlled trials". Current Medical Research and Opinion 33 (9): 1545–1557. September 2017. doi:10.1080/03007995.2017.1279597. PMID 28058854.
177. ↑ "The Effect of Metformin on Polycystic Ovary Syndrome in Overweight Women: A Systematic Review and Meta-Analysis of Randomized Controlled Trials". International Journal of Endocrinology 2020. 2020. doi:10.1155/2020/5150684. PMID 33014044.
178. ↑ 178.0 178.1 Embryonic Mortality in Farm Animals. Springer Science & Business Media. 6 December 2012. pp. 172–. ISBN 978-94-009-5038-2. https://books.google.com/books?id=QKFyBgAAQBAJ&pg=PA172.
179. ↑ 179.0 179.1 Biotechnology in Animal Health and Production. New India Publishing. 2010. pp. 77–. ISBN 978-93-80235-35-6. https://books.google.com/books?id=e9yFom2LWTcC&pg=PA77.
180. ↑ Clinical Gynecologic Endocrinology and Infertility. Lippincott Williams & Wilkins. 28 March 2012. pp. 750–751, 963. ISBN 978-1-4511-4847-3. https://books.google.com/books?id=KZLubBxJEwEC&pg=PA750.
181. ↑ Clinical Urologic Endocrinology: Principles for Men's Health. Springer Science & Business Media. 17 October 2012. pp. 7–. ISBN 978-1-4471-4404-5. https://books.google.com/books?id=osURyQf4-2EC&pg=PR7.
182. ↑ Advances in Drug Research. Academic Press. 12 August 1997. pp. 34–. ISBN 978-0-08-052628-7. https://books.google.com/books?id=f1aKl17UpxkC&pg=PA34.
183. ↑ Aging and Heart Failure: Mechanisms and Management. Springer Science & Business Media. 19 February 2014. pp. 175–. ISBN 978-1-4939-0268-2. https://books.google.com/books?id=0e23BAAAQBAJ&pg=PA175. Retrieved 27 December 2016.
184. ↑ The Practice of Murl=https://books.google.com/books?id=Qmt1_DQkCpEC&pg=PA34. Academic Press. 2 May 2011. pp. 34–. ISBN 978-0-08-056877-5.
185. ↑ Androgen Excess Disorders in Women. Springer Science & Business Media. 8 November 2007. pp. 382–. ISBN 978-1-59745-179-6. https://books.google.com/books?id=Ch-BsGAOtucC&pg=PA382.
186. ↑ Female Contraception: Update and Trends. Springer Science & Business Media. 6 December 2012. pp. 136–. ISBN 978-3-642-73790-9. https://books.google.com/books?id=LtT6CAAAQBAJ&pg=PA136.
187. ↑ Hair Research: Status and Future Aspects; Proceedings of the First International Congress on Hair Research, Hamburg, March 13th–16, 1979. Springer Science & Business Media. 6 December 2012. pp. 587–. ISBN 978-3-642-81650-5. https://books.google.com/books?id=4gBJCAAAQBAJ&pg=PT587.
188. ↑ Sexual Chemistry: A History of the Contraceptive Pill. Yale University Press. 2010. pp. 76–78. ISBN 978-0-300-16791-7. https://books.google.com/books?id=_i-s4biQs7MC&pg=PA76.
189. ↑ Ovarian Function and its Disorders: Diagnosis and Therapy. Springer Science & Business Media. 6 December 2012. pp. 112–. ISBN 978-94-009-8195-9. https://books.google.com/books?id=7IrpCAAAQBAJ&pg=PA112.
190. ↑ Vitamins and Hormones. Academic Press. 18 May 1976. pp. 682–. ISBN 978-0-08-086630-7. https://books.google.com/books?id=5ZbLRONHoDoC&pg=PA682.
191. ↑ Tumours in Urology. Springer Science & Business Media. 6 December 2012. pp. 233–. ISBN 978-1-4471-2086-5. https://books.google.com/books?id=k28yBwAAQBAJ&pg=PT233.
192. ↑ Nuclear Receptors as Drug Targets. John Wiley & Sons. 8 September 2008. pp. 255–. ISBN 978-3-527-62330-3. https://books.google.com/books?id=iATfLbPgRugC&pg=PA255.
193. ↑ Cellular Mechanisms Modulating Gonadal Action. University Park Press. 1 January 1976. p. 239. ISBN 978-0-8391-0776-7. https://books.google.com/books?id=2eNqAAAAMAAJ.
194. ↑ "Developments in nonsteroidal antiandrogens targeting the androgen receptor". ChemMedChem 5 (10): 1651–1661. October 2010. doi:10.1002/cmdc.201000259. PMID 20853390.
195. ↑ "Androgen binding in rat uterus cytosol. Study of the specificity". Journal of Steroid Biochemistry 7 (5): 335–343. May 1976. doi:10.1016/0022-4731(76)90092-3. PMID 180344.
196. ↑ Annual Reports in Medicinal Chemistry. Academic Press. 16 September 1986. pp. 182–. ISBN 978-0-08-058365-5. https://books.google.com/books?id=qsFCGskRHZQC&pg=PA182.
197. ↑ "Endocrine profile of a nonsteroidal antiandrogen N-(3,5-dimethyl-4-isoxazolylmethyl)phthalimide (DIMP)". Acta Endocrinologica 72 (3): 604–614. March 1973. doi:10.1530/acta.0.0720604. PMID 4739363.
198. ↑ 198.0 198.1 198.2 Bioorganic and Medicinal Chemistry of Fluorine. John Wiley & Sons. 2 June 2008. pp. 327–. ISBN 978-0-470-28187-1. https://books.google.com/books?id=QMVSvZ-R7I0C&pg=PA327. Retrieved 27 December 2016.
199. ↑ "Enzalutamide, a second generation androgen receptor antagonist: development and clinical applications in prostate cancer". Current Oncology Reports 15 (2): 69–75. April 2013. doi:10.1007/s11912-013-0293-9. PMID 23341368.
200. ↑ 200.0 200.1 "Development of a second-generation antiandrogen for treatment of advanced prostate cancer". Science 324 (5928): 787–790. May 2009. doi:10.1126/science.1168175. PMID 19359544. Bibcode: 2009Sci...324..787T.
201. ↑ "FDA approves new treatment for a certain type of prostate cancer using novel clinical trial endpoint". 24 March 2020. https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm596768.htm.
202. ↑ Drug Discovery: A History. John Wiley & Sons. 23 June 2005. pp. 367–. ISBN 978-0-471-89979-2. https://books.google.com/books?id=Cb6BOkj9fK4C&pg=PA367.
203. ↑ Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. Lippincott Williams & Wilkins. 2008. pp. 624–. ISBN 978-0-7817-8355-2. https://books.google.com/books?id=az8uSDkB0mgC&pg=PA624. Retrieved 2016-12-27.
204. ↑ Prostate Cancer. Demos Medical Publishing. 20 December 2011. pp. 518–. ISBN 978-1-935281-91-7. https://books.google.com/books?id=WJkjgbRJe3EC&pg=PA518.
205. ↑ Challenges in Prostate Cancer. John Wiley & Sons. 15 April 2008. pp. 138–. ISBN 978-1-4051-7177-9. https://books.google.com/books?id=E3VNhLkqPmUC&pg=PA138.
206. ↑ Polycystic Ovary Syndrome. Anshan. 2007. pp. 184–. ISBN 978-1-904798-74-3. https://books.google.com/books?id=HX0JxcrWJvAC&pg=PA184.
207. ↑ Frontiers in Medicinal Chemistry. Bentham Science Publishers. 2010. pp. 329–. ISBN 978-1-60805-208-0. https://books.google.com/books?id=b7hCWvdP5OYC&pg=PA329.
208. ↑ 208.0 208.1 "Elagolix - Abbvie/Neurocrine Biosciences". AdisInsight. Springer Nature Switzerland AG. https://adisinsight.springer.com/drugs/800020238.
209. ↑ "Androgen Receptor Targeted Treatments of Prostate Cancer: 35 Years of Progress with Antiandrogens". J. Urol. 200 (5): 956–966. November 2018. doi:10.1016/j.juro.2018.04.083. PMID 29730201.
210. ↑ 210.0 210.1 210.2 "30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor antagonists: 60 years of research and development". J. Endocrinol. 234 (1): T125–T140. July 2017. doi:10.1530/JOE-16-0600. PMID 28634268.
211. ↑ "Treatment of androgen excess in females: yesterday, today and tomorrow". Gynecol. Endocrinol. 11 (6): 411–33. December 1997. doi:10.3109/09513599709152569. PMID 9476091.
212. ↑ "Spironolactone and gynaecomastia". The Lancet 280 (7261): 886. 1962. doi:10.1016/S0140-6736(62)90668-2. ISSN 0140-6736.
213. ↑ 213.0 213.1 "Antiandrogens and the skin". Int. J. Dermatol. 17 (3): 167–79. April 1978. doi:10.1111/j.1365-4362.1978.tb06057.x. PMID 148431.
214. ↑ "Effect of an antiandrogen, 17-alpha-methyl-B-nortestosterone, on acne and hirsutism". J. Clin. Endocrinol. Metab. 26 (12): 1394–8. December 1966. doi:10.1210/jcem-26-12-1394. PMID 4225258.
215. ↑ "Intrauterine Antimaskuline Beeinflussung von Rattenfeten Durch ein Stark Gestagen Wirksames Steroid" (in de). Acta Endocrinologica 44 (3): 380–388. November 1963. doi:10.1530/acta.0.0440380. PMID 14071315.
216. ↑ "The World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the biological treatment of paraphilias". World J. Biol. Psychiatry 11 (4): 604–55. June 2010. doi:10.3109/15622971003671628. PMID 20459370.
217. ↑ "Behandlung des Hirsutismus mit Cyproteronacetat" (in de). Deutsche Medizinische Wochenschrift 94 (16): 829–34. April 1969. doi:10.1055/s-0028-1111126. ISSN 0012-0472. PMID 4304873.
218. ↑ "Anti-androgenic activity of spironolactone". Steroids 14 (4): 449–50. 1969. doi:10.1016/s0039-128x(69)80007-3. PMID 5344274.
219. ↑ "A biological profile of a nonsteroidal antiandrogen, SCH 13521 (4'-nitro-3'trifluoromethylisobutyranilide)". Endocrinology 91 (2): 427–37. August 1972. doi:10.1210/endo-91-2-427. PMID 4264731.
220. ↑ "Effects of a novel nonsteroidal antiandrogen on canine prostatic hyperplasia". Invest Urol 10 (2): 123–30. September 1972. PMID 4116667.
221. ↑ "The antiandrogen cyproterone acetate: discovery, chemistry, basic pharmacology, clinical use and tool in basic research". Exp. Clin. Endocrinol. 102 (1): 1–32. 1994. doi:10.1055/s-0029-1211261. PMID 8005205.
222. ↑ "Action of a non-steroid anti-androgen, RU 23908, in peripheral and central tissues". J. Steroid Biochem. 11 (1A): 93–9. 1979. doi:10.1016/0022-4731(79)90281-4. PMID 385986.
223. ↑ "Spironolactone therapy for hirsutism in a hyperandrogenic woman". Ann. Intern. Med. 89 (5 Pt 1): 643–4. 1978. doi:10.7326/0003-4819-89-5-643. PMID 717935.
224. ↑ "Combined androgen blockade: an update". Urol. Clin. North Am. 33 (2): 161–6, v–vi. May 2006. doi:10.1016/j.ucl.2005.12.001. PMID 16631454.
225. ↑ "New hormonal therapy in prostatic carcinoma: combined treatment with an LHRH agonist and an antiandrogen". Clin Invest Med 5 (4): 267–75. 1982. PMID 6819101.
226. ↑ Pharmaceutical Substances: Syntheses, Patents and Applications of the most relevant APIs (5th ed.). Thieme. 2009. pp. 153–154. ISBN 978-3-13-179275-4. https://books.google.com/books?id=4lCGAwAAQBAJ&pg=PA153.
227. ↑ William Andrew Publishing (22 October 2013). Pharmaceutical Manufacturing Encyclopedia, 3rd Edition. Elsevier. pp. 1695–. ISBN 978-0-8155-1856-3. https://books.google.com/books?id=_J2ti4EkYpkC&pg=PA1695. Retrieved 2 January 2019.
228. ↑ 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. Incorporated Council of Law Reporting for Ireland. 1990. pp. 501–502. https://books.google.com/books?id=FQhMAQAAIAAJ. Retrieved 2019-01-02.
229. ↑ Sex and Gender Differences in Pharmacology. Springer Science & Business Media. 2 October 2012. pp. 575–. ISBN 978-3-642-30725-6. https://books.google.com/books?id=J3VxihGDh9wC&pg=PA575.
230. ↑ "Abiraterone: A story of scientific innovation and commercial partnership - the Institute of Cancer Research, London". https://www.icr.ac.uk/news-features/latest-features/abiraterone-a-story-of-scientific-innovation-and-commercial-partnership.
231. ↑ "Nilutamide". AdisInsight. Springer Nature Switzerland AG. http://adisinsight.springer.com/drugs/800004379.
232. ↑ 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 [1]
233. ↑ "Espacenet - Original document". https://worldwide.espacenet.com/publicationDetails/originalDocument?FT=D&date=20071108&DB=EPODOC&locale=en_EP&CC=WO&NR=2007126765A2&KC=A2&ND=6.
234. ↑ "Abiraterone acetate - Johnson & Johnson". AdisInsight. Springer Nature Switzerland AG. https://adisinsight.springer.com/drugs/800005133.
235. ↑ "Enzalutamide - Astellas Pharma/Medivation". AdisInsight. Springer Nature Switzerland AG. https://adisinsight.springer.com/drugs/800026688.
236. ↑ "Apalutamide - Janssen Research and Development". AdisInsight. Springer Nature Switzerland AG. http://adisinsight.springer.com/drugs/800032695.
237. ↑ "Relugolix - Myovant/Takeda". AdisInsight. Springer Nature Switzerland AG. https://adisinsight.springer.com/drugs/800028257.
238. ↑ "Darolutamide - Bayer HealthCare/Orion". 21 January 2025. https://adisinsight.springer.com/drugs/800033671.
239. ↑ 239.0 239.1 "Pharmacology and potential use of cyproterone acetate". Hormone and Metabolic Research 9 (1): 1–13. January 1977. doi:10.1055/s-0028-1093574. PMID 66176.
240. ↑ 240.0 240.1 "Biological Activity of Antiandrogens". British Journal of Dermatology 82 (s6): 3. 1970. doi:10.1111/j.1365-2133.1970.tb07998.x. ISSN 0007-0963.
241. ↑ 241.0 241.1 "Clinical Uses of Antiandrogens". Androgens II and Antiandrogens / Androgene II und Antiandrogene. Springer. 1974. pp. 485–542. doi:10.1007/978-3-642-80859-3_7. ISBN 978-3-642-80861-6.
242. ↑ Comprehensive Textbook of Genitourinary Oncology. Lippincott Williams & Wilkins. 2006. pp. 316–. ISBN 978-0-7817-4984-8. https://books.google.com/books?id=WIsiGZnZ_mgC&pg=PA316.
243. ↑ 243.0 243.1 243.2 Textbook of Therapeutics: Drug and Disease Management. Lippincott Williams & Wilkins. 2006. pp. 211–. ISBN 978-0-7817-5734-8. https://books.google.com/books?id=aVmRWrknaWgC&pg=PA211.
244. ↑ Diagnosis and Management of Polycystic Ovary Syndrome. Springer Science & Business Media. 27 February 2009. pp. 235–. ISBN 978-0-387-09718-3. https://books.google.com/books?id=fgMYVxmPDnMC&pg=PA235. Retrieved 30 December 2016.
245. ↑ "Clascoterone - Cosmo Pharmaceuticals". 12 February 2025. https://adisinsight.springer.com/drugs/800026561.
246. ↑ "Clascoterone: First Approval". Drugs 80 (16): 1745–1750. November 2020. doi:10.1007/s40265-020-01417-6. PMID 33030710.
247. ↑ "The influence of pharmaceutical compounds on male fertility". Andrologia 8 (3): 203–35. 1976. doi:10.1111/j.1439-0272.1976.tb02137.x. PMID 793446.
248. ↑ "Target sites for suppressing fertility in the male". Adv Sex Horm Res 2: 263–87. 1976. PMID 797248.
249. ↑ "Endogenous antispermatogenic agents: prospects for male contraception". Annu. Rev. Pharmacol. Toxicol. 18: 167–87. 1978. doi:10.1146/annurev.pa.18.040178.001123. PMID 206192.
250. ↑ "A review of the current status in male contraceptive studies". East Afr Med J 60 (4): 203–11. April 1983. PMID 6354690.
251. ↑ 251.0 251.1 Ernst Jucker, ed (1989). "Emerging concepts towards the development of contraceptive agents". Progress in Drug Research. Progress in Drug Research. Fortschritte der Arzneimittelforschung. Progres des Recherches Pharmaceutiques. 33. Birkhäuser. pp. 267–315. doi:10.1007/978-3-0348-9146-2_9. ISBN 978-3-0348-9925-3.
252. ↑ 252.0 252.1 252.2 "Male contraception: current status and future prospects". Clin. Endocrinol. (Oxf) 29 (4): 443–65. October 1988. doi:10.1111/j.1365-2265.1988.tb02894.x. PMID 3075164.
253. ↑ 253.0 253.1 "Use of progestins in male contraception". Steroids 68 (10–13): 965–72. November 2003. doi:10.1016/s0039-128x(03)00135-1. PMID 14667989.
254. ↑ 254.0 254.1 "Clinical trials in male hormonal contraception". Contraception 82 (5): 457–70. 2010. doi:10.1016/j.contraception.2010.03.020. PMID 20933120. http://www.kup.at/kup/pdf/10172.pdf. Retrieved 2019-07-08.
255. ↑ "Male contraception: expanding reproductive choice". Indian J. Exp. Biol. 43 (11): 1032–41. November 2005. PMID 16313066.
256. ↑ "The current state of male hormonal contraception". Pharmacol. Ther. 163: 109–17. July 2016. doi:10.1016/j.pharmthera.2016.03.012. PMID 27016468.
257. ↑ "Dimethandrolone undecanoate: a new potent orally active androgen with progestational activity". Endocrinology 147 (6): 3016–26. June 2006. doi:10.1210/en.2005-1524. PMID 16497801.
258. ↑ "Comparison of the single dose pharmacokinetics, pharmacodynamics, and safety of two novel oral formulations of dimethandrolone undecanoate (DMAU): a potential oral, male contraceptive". Andrology 5 (2): 278–285. March 2017. doi:10.1111/andr.12303. PMID 27907978.
259. ↑ "Revising the role of the androgen receptor in breast cancer". J. Mol. Endocrinol. 52 (3): R257–65. June 2014. doi:10.1530/JME-14-0030. PMID 24740738.
260. ↑ "Targeting the androgen receptor in triple-negative breast cancer". Curr Probl Cancer 40 (2–4): 141–150. 2016. doi:10.1016/j.currproblcancer.2016.09.004. PMID 27816190.
261. ↑ "Complete Response of Metastatic Androgen Receptor-Positive Breast Cancer to Bicalutamide: Case Report and Review of the Literature". J. Clin. Oncol. 34 (4): e21–4. February 2016. doi:10.1200/JCO.2013.49.8899. PMID 24888812.
262. ↑ "[Androgen receptors in breast cancer: Expression, value and therapeutic prospects]" (in fr). Bull Cancer 104 (4): 363–369. April 2017. doi:10.1016/j.bulcan.2017.01.005. PMID 28216075.
263. ↑ "Androgen receptor in triple negative breast cancer: A potential target for the targetless subtype". Cancer Treat. Rev. 68: 102–110. June 2018. doi:10.1016/j.ctrv.2018.06.005. PMID 29940524.
264. ↑ "Anti-androgen drugs in the treatment of obsessive-compulsive disorder: a systematic review". Curr Med Chem 27 (40): 6825–6836. December 2019. doi:10.2174/0929867326666191209142209. PMID 31814547.

## Further reading

* "Antiandrogens". Androgens II and Antiandrogens / Androgene II und Antiandrogene. Springer. 1974. pp. 235–484. doi:10.1007/978-3-642-80859-3_6. ISBN 978-3-642-80861-6.
* "Clinical Uses of Antiandrogens". Androgens II and Antiandrogens / Androgene II und Antiandrogene. Springer. 1974. pp. 485–542. doi:10.1007/978-3-642-80859-3_7. ISBN 978-3-642-80861-6.

{{Navbox

| name = Androgens and antiandrogens
| title = Androgens and antiandrogens
| state = collapsed
| listclass = hlist
| groupstyle = text-align:center;

| group1 = Androgens
(incl. AAS)

| list1 =

AR agonists|

* Testosterone derivatives: Androstenediol dipropionate
* Boldenone undecylenate
* Clostebol
* Clostebol acetate
* Clostebol caproate
* Clostebol propionate
* Cloxotestosterone acetate
* Prasterone (dehydroepiandrosterone, DHEA)
* Prasterone enanthate (DHEA enanthate)
* Prasterone sulfate (DHEA sulfate)
* Quinbolone
* Testosterone#
* Testosterone esters (e.g., testosterone cypionate, testosterone enanthate]], testosterone propionate]], testosterone undecanoate]], testosterone ester mixture]]s (Deposterona, Omnadren, Sustanon, Testoviron Depot))

* Dihydrotestosterone derivatives: Androstanolone (stanolone, dihydrotestosterone, DHT)
* Androstanolone esters
* Bolazine capronate
* Drostanolone propionate (dromostanolone propionate)
* Epitiostanol
* Mepitiostane
* Mesterolone
* Metenolone acetate (methenolone acetate)
* Metenolone enanthate (methenolone enanthate)
* Stenbolone acetate

* 19-Nortestosterone derivatives: Bolandiol dipropionate
* Nandrolone esters (e.g., nandrolone decanoate, nandrolone phenylpropionate)
* Norclostebol
* Norclostebol acetate
* Oxabolone cipionate (oxabolone cypionate)
* Trenbolone acetate
* Trenbolone hexahydrobenzylcarbonate (trenbolone cyclohexylmethylcarbonate)

* 17α-Alkylated testosterone derivatives: Bolasterone
* Calusterone
* Chlorodehydromethyltestosterone (CDMT)
* Fluoxymesterone
* Formebolone
* Metandienone (methandienone, methandrostenolone)
* Methandriol (methylandrostenediol)
* Methandriol bisenanthoyl acetate
* Methandriol dipropionate
* Methandriol propionate
* Methyltestosterone
* Methyltestosterone 3-hexyl ether
* Oxymesterone
* Penmesterol
* Tiomesterone (thiomesterone)

* 17α-Alkylated dihydrotestosterone derivatives: Androisoxazole
* Furazabol
* Mebolazine (dimethazine)
* Mestanolone
* Oxandrolone
* Oxymetholone
* Stanozolol

* 17α-Alkylated 19-nortestosterone derivatives: Ethylestrenol
* Mibolerone
* Norethandrolone
* Normethandrone (methylestrenolone, normethisterone)
* Propetandrol (propethandrol)

* 17α-Vinyltestosterone derivatives: Norvinisterone (vinylnortestosterone)

* 17α-Ethynyltestosterone derivatives: Danazol
* Gestrinone
* Progestins (e.g., ethisterone (ethynyltestosterone), levonorgestrel, norgestrel, norethisterone (norethindrone), [[Chemistry:Lynestrlynestrenol, Norgestrienone|norgestrienone]])
* Tibolone

* Progesterone derivatives: Medroxyprogesterone acetate

|

Progonadotropins|

* Antiestrogens (e.g., tamoxifen, Chemistry:Clomifene

| group2 = Antiandrogens
| list2 = {{Navbox|child
| groupstyle = text-align:center;
| groupwidth = 9em;

| group1 = AR antagonists
| list1 =

* Steroidal: Abiraterone acetate
* Canrenone
* Chlormadinone acetate
* Cyproterone acetate
* Delmadinone acetate
* Dienogest
* Drospirenone
* Medrogestone
* Megestrol acetate
* Nomegestrol acetate
* Osaterone acetate
* Oxendolone
* Potassium canrenoate
* Spironolactone

* Nonsteroidal: Apalutamide
* Bicalutamide
* Cimetidine
* Darolutamide
* Enzalutamide
* Flutamide
* Ketoconazole
* Nilutamide
* Seviteronel†
* Topilutamide (fluridil)

| group2 = Steroidogenesis
inhibitors

| list2 =

5α-Reductase|

* Alfatradiol
* Dutasteride
* Epristeride
* Finasteride
* Saw palmetto extract

|

Others|

* Abiraterone acetate
* Aminoglutethimide
* Bifluranol
* Cyproterone acetate
* Flutamide
* Ketoconazole
* Nilutamide
* Seviteronel†
* Spironolactone

| group3 = Antigonadotropins
| list3 =

* D2 receptor antagonists (prolactin releasers) (e.g., domperidone, metoclopramide, risperidone, haloperidol, chlorpromazine, sulpiride)
* Estrogens (e.g., bifluranol, [[diethylstilbestrol, estradiol, estradiol esters, ethinylestradiol, ethinylestradiol sulfonate, paroxypropione)
* GnRH agonists (e.g., leuprorelin)
* GnRH antagonists (e.g., cetrorelix)
* Progestogens (incl., chlormadinone acetate, [[cyproterone acetate, hydroxyprogesterone caproate, gestonorone caproate, [[Chemistry:Medroxyprogesterone medroxyprogesterone acetate, Chemistry:Megestrol acetate|megestrol acetate]])

| group4 = Others
| list4 =

* Androstenedione immunogens: Androvax (androstenedione albumin)
* Ovandrotone albumin (Fecundin)

| liststyle = background:#DDDDFF;

| list3 =

* #WHO-EM
* ‡Withdrawn from market
* Clinical trials:
* †Phase III
* §Never to phase III

See also
Androgen receptor modulators
Estrogens and antiestrogens
Progestogens and antiprogestogens
List of androgens/anabolic steroids

* v
* t
* e

Androgen receptor modulators

AR|

| Agonists|

* Testosterone derivatives: 4-Androstenediol
* 4-Dehydroepiandrosterone (4-DHEA)
* 4-Hydroxytestosterone
* 4,17α-Dimethyltestosterone
* 5-Androstenedione
* 11-Ketotestosterone
* 11β-Hydroxyandrostenedione
* Adrenosterone (11-ketoandrostenedione, 11-oxoandrostenedione)
* Androstenediol (5-androstenediol)
* Androstenediol 3β-acetate
* Androstenediol 17β-acetate
* Androstenediol diacetate
* Androstenediol dipropionate
* Androstenedione (4-androstenedione)
* Atamestane
* Boldenone
* Boldenone undecylenate
* Boldione (1,4-androstadienedione)
* Clostebol
* Clostebol acetate
* Clostebol caproate
* Clostebol propionate
* Cloxotestosterone
* Cloxotestosterone acetate
* Dehydroandrosterone
* DHEA (androstenolone, prasterone; 5-DHEA)
* DHEA enanthate (prasterone enanthate)
* DHEA sulfate
* Exemestane
* Formestane
* Plomestane
* Quinbolone
* Silandrone
* Testosterone# (+dutasteride)
* Testosterone esters
* Polytestosterone phloretin phosphate

* Dihydrotestosterone derivatives: 1-Androstenediol
* 1-Androstenedione
* 1-Androsterone (1-andro, 1-DHEA)
* 1-Testosterone
* 3α-Androstanediol
* 5α-Androst-2-en-17-one
* 7β-Hydroxyepiandrosterone
* 11-Ketodihydrotestosterone
* Androsterone
* Bolazine
* Bolazine capronate
* Dihydroethisterone
* Dihydroethyltestosterone
* Dihydrofluoxymesterone
* Dihydromethylandrostenediol
* Dihydrotestosterone (DHT) (androstanolone, stanolone)
* Dihydrotestosterone esters
* Drostanolone
* Drostanolone propionate
* Epiandrosterone
* Epitiostanol
* Mepitiostane
* Mesabolone
* Mesterolone
* Mesterolone cipionate
* Methyldiazinol
* Nisterime
* Nisterime acetate
* Prostanozol
* Stenbolone
* Stenbolone acetate
* Testifenon (testiphenon, testiphenone)

* 19-Nortestosterone derivatives: 7α-Methyl-19-norandrostenedione (MENT dione, trestione)
* 11β-Methyl-19-nortestosterone
* 11β-Methyl-19-nortestosterone dodecylcarbonate
* 19-Nor-5-androstenediol
* 19-Nor-5-androstenedione
* 19-Nordehydroepiandrosterone
* Bolandiol
* Bolandiol dipropionate
* Bolandione (19-nor-4-androstenedione)
* Bolmantalate (nandrolone adamantoate)
* Dienedione
* Dienolone
* Dimethandrolone
* Dimethandrolone buciclate
* Dimethandrolone dodecylcarbonate
* Dimethandrolone undecanoate
* LS-1727 (nandrolone 17β-N-(2-chloroethyl)-N-nitrosocarbamate)
* Methoxydienone (methoxygonadiene)
* Nandrolone
* Nandrolone esters
* Norclostebol
* Norclostebol acetate
* Normethandrone (methylestrenolone, normethisterone)
* Oxabolone
* Oxabolone cipionate (oxabolone cypionate)
* Trenbolone
* Trenbolone acetate
* Trenbolone enanthate
* Trenbolone hexahydrobenzylcarbonate
* Trenbolone undecanoate
* Trendione
* Trestolone (MENT)
* Trestolone acetate
* Trestolone enanthate

* Dihydrotestosterone and 19-nortestosterone derivatives: 5α-Dihydrolevonorgestrel
* 5α-Dihydronandrolone
* 5α-Dihydronorethandrolone
* 5α-Dihydronorethisterone
* 5α-Dihydronormethandrone
* 5α-Dihydrotrestolone
* 19-Norandrosterone

* 17α-Alkylated testosterone derivatives: Bolasterone
* Calusterone
* Chlorodehydromethylandrostenediol (CDMA)
* Chlorodehydromethyltestosterone (CDMT)
* Chloromethylandrostenediol (CMA)
* Enestebol
* Ethyltestosterone
* Fluoxymesterone
* Formebolone
* Hydroxystenozole
* Metandienone (methandrostenolone)
* Methandriol (methylandrostenediol)
* Methandriol bisenanthoyl acetate
* Methandriol diacetate
* Methandriol dipropionate
* Methandriol propionate
* Methylclostebol (chloromethyltestosterone)
* Methyltestosterone (+esterified estrogens)
* Methyltestosterone 3-hexyl ether
* Oxymesterone
* Penmesterol
* Tiomesterone

* 17α-Alkylated dihydrotestosterone derivatives: Androisoxazole
* Desoxymethyltestosterone
* Furazabol
* Mebolazine (dimethazine)
* Mestanolone
* Metenolone
* Metenolone acetate
* Metenolone enanthate
* Methasterone
* Methyl-1-testosterone
* Methylepitiostanol
* Methylstenbolone
* Oxandrolone
* Oxymetholone
* Stanozolol

* 17α-Alkylated 19-nortestosterone derivatives: Bolenol
* Dimethyldienolone
* Dimethyltrienolone
* Ethyldienolone
* Ethylestrenol
* Methyldienolone
* Methylhydroxynandrolone (MOHN, MHN)
* Metribolone
* Mibolerone
* Norboletone
* Norethandrolone
* Propetandrol
* RU-2309
* Tetrahydrogestrinone

* 17α-Vinyltestosterone derivatives: Norvinisterone (vinylnortestosterone)
* Vinyltestosterone

* 17α-Ethynyltestosterone derivatives: Δ4-Tibolone
* Danazol
* Desogestrel
* Ethisterone (ethynyltestosterone)
* Etonogestrel
* Etynodiol
* Etynodiol diacetate
* Gestodene
* Gestrinone
* Levonorgestrel
* Levonorgestrel esters (e.g., levonorgestrel butanoate)
* Lynestrenol
* Lynestrenol phenylpropionate
* Norethisterone
* Norethisterone esters (e.g., norethisterone acetate, norethisterone enanthate)
* Norgestrel
* Norgestrienone
* Quingestanol
* Quingestanol acetate
* Tibolone

* Progesterone derivatives: Medroxyprogesterone acetate
* Megestrol acetate

* Others/unsorted: 3-Keto-5α-abiraterone
* 5α-Androstane
* Alternariol
* Cl-4AS-1
* Drupanol
* ZM-182345

|

Mixed
(SARMs)|

* Nonsteroidal: 198RL26
* ACP-105
* AC-262536
* Acetothiolutamide
* Andarine (acetamidoxolutamide, androxolutamide, GTx-007, S-4)
* BMS-564929
* DTIB
* Enobosarm (ostarine, MK-2866, GTx-024, S-22)
* FTBU-1
* GSK-4336A
* GSK-8698
* LG-121071 (LGD-121071)
* LGD-2226
* LGD-2941 (LGD-122941)
* LGD-3303
* LGD-4033
* JNJ-26146900
* JNJ-28330835
* JNJ-37654032
* ORM-11984
* R-1
* RAD140
* RU-59063
* S-1
* S-23
* S-40503
* S-101479
* Triclosan

* Steroidal: EM-9017
* MK-0773
* TFM-4AS-1
* YK-11

Antagonists|

* Steroidal: 7α-Thioprogesterone
* 7α-Thiospironolactone
* 7α-Thiomethylspironolactone
* 11α-Hydroxyprogesterone
* 15β-Hydroxycyproterone acetate
* Abiraterone
* Abiraterone acetate
* Allyltestosterone
* Benorterone
* BOMT
* Canrenoic acid
* Canrenone
* Chlormadinone acetate
* Clascoterone
* Clometerone
* Cyproheptadine
* Cyproterone
* Cyproterone acetate
* Delanterone
* Delmadinone acetate
* Dicirenone
* Dienogest
* Drospirenone
* DU-41165
* Edogestrone
* EM-4350
* EM-5854
* EM-5855
* EM-6537
* Epitestosterone
* Galeterone
* Guggulsterone
* Medrogestone
* Megestrol acetate
* Mespirenone
* Metogest
* Mexrenone
* Mifepristone
* Nomegestrol acetate
* Nordinone
* Osaterone
* Osaterone acetate
* Oxendolone
* Potassium canrenoate
* Promegestone
* Prorenone
* Rosterolone
* RU-15328
* SC-5233 (spirolactone)
* Spironolactone
* Spirorenone
* Spiroxasone
* Topterone
* Trimegestone
* Trimethyltrienolone (R-2956)
* Zanoterone

* Nonsteroidal: 5N-Bicalutamide
* AA560
* Antarlides
* Arabilin
* Apalutamide
* Atraric acid
* AZD-3514
* Bakuchiol
* BAY-1024767
* Bicalutamide
* Bisphenols (e.g., BADGE, BFDGE, bisphenol A, bisphenol F, bisphenol S)
* BMS-501949
* BMS-570511
* BMS-641988
* CH5137291
* Cimetidine
* Cioteronel
* Cyanonilutamide
* Darolutamide
* DDT (via metabolite p,p’-DDE)
* Dieldrin
* DIMP
* Endosulfan
* Enzalutamide
* EPI-001
* Fenarimol
* Flutamide
* Hydroxyflutamide
* Inocoterone
* Inocoterone acetate
* Ketoconazole
* Ketodarolutamide
* Lavender oil
* LG-105
* LG-120907
* LGD-1331
* Linuron
* Methiocarb
* N-Butylbenzenesulfonamide
* N-Desmethylapalutamide
* N-Desmethylenzalutamide
* Nilutamide
* ONC1-13B
* Pentomone
* PF-998425
* Phenothrin
* Prochloraz
* Procymidone
* Proxalutamide
* Ralaniten (EPI-002)
* Ralaniten acetate (EPI-506)
* RD-162
* Ro 2-7239
* Ro 5-2537
* RU-22930
* RU-56187
* RU-57073
* RU-58642
* RU-58841
* Seviteronel
* Thalidomide
* Topilutamide (fluridil)
* Valproic acid
* Vinclozolin
* YM-580
* YM-92088
* YM-175735

GPRC6A|

| Agonists|

* Cations (incl. aluminum, calcium, Gadolinium

|

See also
Receptor/signaling modulators
Androgens and antiandrogens
Estrogen receptor modulators
Progesterone receptor modulators
List of androgens/anabolic steroids

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Original source: https://en.wikipedia.org/wiki/Antiandrogen. Read more

|

Retrieved from "https://handwiki.org/wiki/index.php?title=Biology:Antiandrogen&oldid=4518506"
*[Hits]: Google Search hits (February 2018)
*[IM]: Intramuscular injection
*[SC]: Subcutaneous injection
*[AR]: Androgen receptor
*[PR]: Progesterone receptor
*[ER]: Estrogen receptor
*[GR]: Glucocorticoid receptor
*[MR]: Mineralocorticoid receptor
*[s.c.]: subcutaneous injection
*[AAS]: anabolic–androgenic steroid
*[v]: View this template
*[t]: Discuss this template
*[e]: Edit this template
*[SARMs]: Selective androgen receptor modulator
*[GPRC6A]: G protein-coupled receptor family C group 6 member A