Testosterone

Testosterone is the primary male sex hormone and androgen in males.[1] In humans, testosterone plays a key role in the development of male reproductive tissues such as testicles and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair. It is associated with increased aggression, sex drive, dominance, courtship display, and a wide range of behavioral characteristics.[2] In addition, testosterone in both sexes is involved in health and well-being, where it has a significant effect on overall mood, cognition, social and sexual behavior, metabolism and energy output, the cardiovascular system, and in the prevention of osteoporosis.[3][4] Insufficient levels of testosterone in men may lead to abnormalities including frailty, accumulation of adipose fat tissue within the body, anxiety and depression, sexual performance issues, and bone loss.

Excessive levels of testosterone in men may be associated with hyperandrogenism, higher risk of heart failure, increased mortality in men with prostate cancer,[5] and male pattern baldness.

Testosterone is a steroid hormone from the androstane class containing a ketone and a hydroxyl group at positions three and seventeen respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[6] It exerts its action through binding to and activation of the androgen receptor.[6] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about seven to eight times as great as in adult females.[7] As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men.[8][9] Females are also more sensitive to the hormone.[10] In addition to its role as a natural hormone, testosterone is used as a medication to treat hypogonadism and breast cancer.[11] Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.[12] The World Anti-Doping Agency lists it as S1 Anabolic agent substance "prohibited at all times".[13]

Regarding aggression, testosterone does not create aggression in an individual, but amplifies aggressive behaviors and responses that are already learned by the individual, increasing sensitivity to social triggers rather than inventing violence.[14]

## Contents

* 1 Biological effects
* 1.1 Effects on physiological development
* 1.1.1 Before birth
* 1.1.2 Early infancy
* 1.1.3 Before puberty
* 1.1.4 Pubertal
* 1.1.5 Adult
* 1.2 Health effects
* 1.2.1 Immune system and inflammation
* 1.2.2 Medical use
* 1.3 Behavioural correlations
* 1.3.1 Sexual arousal
* 1.3.2 Mammalian studies
* 1.3.3 Males
* 1.3.4 Females
* 1.3.5 Romantic relationships
* 1.3.6 Fatherhood
* 1.3.7 Motivation
* 1.3.8 Aggression and criminality
* 1.3.9 Fairness
* 2 Biological activity
* 2.1 Free testosterone
* 2.2 Steroid hormone activity
* 2.3 Neurosteroid activity
* 3 Biochemistry
* 3.1 Biosynthesis
* 3.1.1 Regulation
* 3.2 Distribution
* 3.3 Metabolism
* 3.4 Levels
* 4 Measurement
* 5 Distribution
* 6 History and production
* 7 Other species
* 8 See also
* 9 References
* 10 Further reading

## Biological effects

### Effects on physiological development

In general, androgens such as testosterone promote protein synthesis and thus growth of tissues with androgen receptors.[15] Testosterone can be described as having anabolic and androgenic (virilising) effects, though these categorical descriptions are somewhat arbitrary, as there is a great deal of mutual overlap between them.[16] The relative potency of these effects can depend on various factors and is a topic of ongoing research.[17][18] Testosterone can either directly exert effects on target tissues or be metabolized by 5α-reductase into dihydrotestosterone (DHT) or aromatized to estradiol (E2).[17] Both testosterone and DHT bind to an androgen receptor; however, DHT has a stronger binding affinity than testosterone and may have more androgenic effect in certain tissues at lower levels.[17]

* Anabolic effects include growth of muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation.
* Androgenic effects include maturation of the sex organs, particularly the penis, and the formation of the scrotum in the fetus, and after birth (usually at puberty) a deepening of the voice, growth of facial hair (such as the beard) and axillary (underarm) hair. Many of these fall into the category of male secondary sex characteristics.

Testosterone effects can also be classified by the age of usual occurrence. For postnatal effects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.[19]

#### Before birth

Effects before birth are divided into two categories, classified in relation to the stages of development.

During the second trimester, androgen level is associated with sex formation.[20] Specifically, testosterone, along with anti-Müllerian hormone (AMH) promote growth of the Wolffian duct and degeneration of the Müllerian duct respectively.[21] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult's own levels. Prenatal androgens apparently influence interests and engagement in gendered activities and have moderate effects on spatial abilities.[22] Among women with congenital adrenal hyperplasia, a male-typical play in childhood correlated with reduced satisfaction with the female gender and reduced heterosexual interest in adulthood.[23]

#### Early infancy

Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age.[24][25] The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body.[26] The male brain is masculinized by the aromatization of testosterone into estradiol,[27] which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.[28]

#### Before puberty

Before puberty, effects of rising androgen levels occur in both boys and girls. These include adult-type body odor, increased oiliness of skin and hair, acne, pubarche (appearance of pubic hair), axillary hair (armpit hair), growth spurt, accelerated bone maturation, and facial hair.[29]

#### Pubertal

Pubertal effects begin to occur when androgen has been higher than normal adult female levels for months or years. In males, these are usual late pubertal effects, and occur in women after prolonged periods of heightened levels of free testosterone in the blood. The effects include:[29][30]

* Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement occurs.
* Growth of jaw, brow, chin, and nose and remodeling of facial bone contours, in conjunction with human growth hormone occurs.[31]
* Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women.
* Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple.
* Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases.
* Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.

#### Adult

Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute hypothalamic–pituitary–adrenal axis (HPA axis) response under dominance challenge.[32] Androgens including testosterone enhance muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[33][34]

Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels might decrease in the later decades of adult life.[35]

The brain is also affected by this sexual differentiation;[20] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital disorders of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[36]

There are some differences between a male and female brain that may be due to different testosterone levels, one of them being size: the male human brain is, on average, larger.[37]

### Health effects

Testosterone does not appear to increase the risk of developing prostate cancer. In people who have undergone testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate of spread of an existing prostate cancer.[38][39][40]

Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[41][42] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and improved glycemic control.[43]

High androgen levels are associated with menstrual cycle irregularities in both clinical populations and healthy women. [44] There also can be effects in unusual hair growth, acne, weight gain, infertility, and sometimes even scalp hair loss. These effects are seen largely in women with polycystic ovary syndrome (PCOS). For women with PCOS, hormones like birth control pills can be used to help lessen the effects of this increased level of testosterone.[45]

Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer's type,[46][47][48][49] a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[50] where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.

#### Immune system and inflammation

Testosterone deficiency is associated with an increased risk of metabolic syndrome, cardiovascular disease and mortality, which are also sequelae of chronic inflammation.[51] Testosterone plasma concentration inversely correlates to multiple biomarkers of inflammation including CRP, interleukin 1 beta, interleukin 6, TNF alpha and endotoxin concentration, as well as leukocyte count.[51] As demonstrated by a meta-analysis, substitution therapy with testosterone results in a significant reduction of inflammatory markers.[51] These effects are mediated by different mechanisms with synergistic action.[51] In androgen-deficient men with concomitant autoimmune thyroiditis, substitution therapy with testosterone leads to a decrease in thyroid autoantibody titres and an increase in thyroid's secretory capacity (SPINA-GT).[52]

#### Medical use

Main article: Chemistry:Testosterone (medication)

Testosterone is used as a medication for the treatment of male hypogonadism, gender dysphoria, and certain types of breast cancer.[11][53] This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[54] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[55]

Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[56] It is available as a generic medication.[11] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[11]

Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[11] Serious side effects may include liver toxicity, heart disease (though a randomized trial found no evidence of major adverse cardiac events compared to placebo in men with low testosterone[57]), and behavioral changes.[11] Women and children who are exposed may develop virilization.[11] It is recommended that individuals with prostate cancer not use the medication.[11] It can cause harm if used during pregnancy or breastfeeding.[11]

2020 guidelines from the American College of Physicians support the discussion of testosterone treatment in adult men with age-related low levels of testosterone who have sexual dysfunction. They recommend yearly evaluation regarding possible improvement and, if none, to discontinue testosterone; physicians should consider intramuscular treatments, rather than transdermal treatments, due to costs and since the effectiveness and harm of either method is similar. Testosterone treatment for reasons other than possible improvement of sexual dysfunction may not be recommended.[58][59] Current clinical guidelines recommend comprehensive baseline evaluation including complete blood count, lipid panel, prostate-specific antigen, and cardiovascular risk assessment before initiating testosterone replacement therapy.[60] Regular monitoring during treatment typically includes hematocrit levels every 3-6 months to prevent polycythemia, along with PSA monitoring in men over 40.[61][62]

### Behavioural correlations

#### Sexual arousal

Testosterone levels follow a circadian rhythm that peaks early each day, regardless of sexual activity.[63]

In women, correlations may exist between positive orgasm experience and testosterone levels. Studies have shown small or inconsistent correlations between testosterone levels and male orgasm experience, as well as sexual assertiveness in both sexes.[64][65]

Sexual arousal and masturbation in women produce small increases in testosterone concentrations.[66] The plasma levels of various steroids significantly increase after masturbation in men and the testosterone levels correlate to those levels.[67]

#### Mammalian studies

Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone. When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviours (copulation, partner preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may provide a model for studying clinical populations among humans with sexual arousal deficits such as hypoactive sexual desire disorder.[68]

Every mammalian species examined demonstrated a marked increase in a male's testosterone level upon encountering a novel female. The reflexive testosterone increases in male mice is related to the male's initial level of sexual arousal.[69]

In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[70] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).[70]

In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[71] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.

#### Males

In men, higher levels of testosterone are associated with periods of sexual activity.[72][73]

Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films.[74] Men who watch sexually explicit films also report increased motivation and competitiveness, and decreased exhaustion.[75] A link has also been found between relaxation following sexual arousal and testosterone levels.[76]

#### Females

Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[77] Women's level of testosterone is higher when measured pre-intercourse vs. pre-cuddling, as well as post-intercourse vs. post-cuddling.[78] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[79]

Testosterone may prove to be an effective treatment in female sexual arousal disorders,[80] and is available as a dermal patch. There is no FDA-approved androgen preparation for the treatment of androgen insufficiency; however, it has been used as an off-label use to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[80]

#### Romantic relationships

Falling in love has been linked with decreases in men's testosterone levels while mixed changes are reported for women's testosterone levels.[81][82] There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.[82] However, the testosterone changes observed do not seem to be maintained as relationships develop over time.[81][82]

Men who produce less testosterone are more likely to be in a relationship[83] or married,[84] and men who produce more testosterone are more likely to divorce.[84] Marriage or commitment could cause a decrease in testosterone levels.[85] Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts.[86] Married men who engage in bond-maintenance activities such as spending the day with their spouse or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities is more relevant to changes in testosterone levels.[87]

Men who produce more testosterone are more likely to engage in extramarital sex.[84] Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.[83] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[88]

#### Fatherhood

Fatherhood decreases testosterone levels in men, suggesting that the emotions and behaviour tied to paternal care decrease testosterone levels. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the two parents to raise multiple children simultaneously. This increases the reproductive fitness of the parents because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[89] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals.[90]

While the extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels as well as temporary fluctuations.[91] For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant.[92]

#### Motivation

Testosterone levels play a major role in risk-taking during financial decisions.[93][94] Higher testosterone levels in men reduce the risk of becoming or staying unemployed.[95] Research has also found that heightened levels of testosterone and cortisol are associated with an increased risk of impulsive and violent criminal behavior.[96] On the other hand, elevated testosterone in men may increase their generosity, primarily to attract a potential mate.[97][98]

#### Aggression and criminality

Most studies support a link between adult criminality and testosterone.[99][100][101][102] Nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have found testosterone to be associated with behaviors or personality traits linked with antisocial behavior[103] and alcoholism. Many studies[which?] have been undertaken on the relationship between more general aggressive behavior, and feelings, and testosterone. About half of studies have found a relationship and about half, no relationship.[104] Studies have found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.[105]

There are two theories on the role of testosterone in aggression and competition.[106] The first is the challenge hypothesis which states that testosterone would increase during puberty, thus facilitating reproductive and competitive behavior which would include aggression.[106] It is therefore the challenge of competition among males that facilitates aggression and violence.[106] Studies conducted have found direct correlation between testosterone and dominance, especially among the most violent criminals in prison who had the highest testosterone.[106] The same research found fathers (outside competitive environments) had the lowest testosterone levels compared to other males.[106]

The second theory is similar and known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[107][108] Testosterone and other androgens have evolved to motivate men to pursue competition, even when doing so leads to risk. By doing so, individuals with masculinized brains are better able to survive and copulate with as many mates as possible.[107] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[109] Studies have found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression.[110][111][112][113][114]

The rise in testosterone during competition predicted aggression in males, but not in females.[115] In one experiment, subjects who interacted with handguns showed higher testosterone levels and aggression than those who interacted with toys.[116] One study proposed that natural selection may have caused men to be more sensitive to situations in which their status is challenged, and that testosterone is the key factor that causes these situations to spark into aggression.[117] Structural brain characteristics associated with testosterone levels have also been found to predict individuals' levels of aggression.[118]

The Annals of the New York Academy of Sciences has found that the use of anabolic steroids (which increases testosterone) among teenagers is correlated with increased likelihood of using violence.[119] One study found that administering testosterone increased verbal aggression in some participants.[120]

A few studies indicate that the testosterone derivative estradiol might play an important role in male aggression.[104][121][122][123] Estradiol is known to correlate with aggression in male mice.[124] Moreover, the conversion of testosterone to estradiol regulates male aggression in sparrows during breeding season.[125] Rats who were given anabolic steroids that increase testosterone were also more physically aggressive to provocation as a result of "threat sensitivity".[126]

The relationship between testosterone and aggression may also function indirectly, as it has been proposed that testosterone does not amplify tendencies towards aggression, but rather amplifies whatever tendencies will allow an individual to maintain social status when challenged. In most animals, aggression is the means of maintaining social status. However, humans have multiple ways of obtaining status. This could explain why some studies find a link between testosterone and pro-social behaviour, if pro-social behaviour is rewarded with social status. Thus the link between testosterone and aggression and violence is due to these being rewarded with social status.[127] The relationship may also be one of a "permissive effect" whereby testosterone does elevate aggression levels, but only in the sense of allowing average aggression levels to be maintained; chemically or physically castrating the individual will reduce aggression levels (though not eliminate them) but the individual only needs a small-level of pre-castration testosterone to have aggression levels to return to normal, which they will remain at even if additional testosterone is added. Testosterone may also simply exaggerate or amplify existing aggression; for example, chimpanzees who receive testosterone increases become more aggressive to chimps lower than them in the social hierarchy, but will still be submissive to chimps higher than them. Testosterone thus does not make the chimpanzee indiscriminately aggressive, but instead amplifies his pre-existing aggression towards lower-ranked chimps.[128]

In humans, testosterone appears more to promote status-seeking and social dominance than simply increasing physical aggression. When controlling for the effects of belief in having received testosterone, women who have received testosterone make fairer offers than women who have not received testosterone.[129]

Robert Sapolsky explains by citing different studies that, testosterone does not "invent" aggression. Instead, it acts as an amplifier, increasing the "volume" of an individual's sensitivity to social triggers for aggression that they have already learned. Aggression can persist even after testosterone is removed (for example, by castration) if someone has prior experience with aggressive behavior, showing hormones are not the sole cause. Studies in animals show testosterone reinforces existing social hierarchies rather than overturning them, making individuals more aggressive only toward those already below them, but not challenging those who are above them in hierarchy. According to the Challenge Hypothesis, testosterone mainly motivates behavior that helps maintain status when it is threatened. In humans, this can lead to pro-social outcomes—such as generosity, honesty, or cooperation—when those traits bring respect and help them maintain their status in society (as status in human society does not come only through aggression, but through other means too), meaning testosterone’s effects depend heavily on social context. Ultimately societal norms, not testosterone itself, determine whether aggression or cooperation is rewarded.[14]

#### Fairness

Testosterone might encourage fair behavior. For one study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[130][131][132] However men with high testosterone were significantly 27% less generous in an ultimatum game.[133] This additional information could suggest, contrarily, that testosterone may encourage greed or selfishness. Fairer offers from test subjects with higher testosterone in the original study increase the likeliness of the offer being accepted by the negotiating partner, therefore decreasing the probability of both participants leaving without any money.

## Biological activity

### Free testosterone

Lipophilic hormones (soluble in lipids but not in water), such as steroid hormones, including testosterone, are transported in water-based blood plasma through specific and non-specific proteins. Specific proteins include sex hormone-binding globulin (SHBG), which binds testosterone, dihydrotestosterone, estradiol, and other sex steroids. Non-specific binding proteins include albumin. The part of the total hormone concentration that is not bound to its respective specific carrier protein is the free part. As a result, testosterone which is not bound to SHBG is called free testosterone. Only the free amount of testosterone can bind to an androgenic receptor, which means it has biological activity.[134] While a significant portion of testosterone is bound to SHBG, a small fraction of testosterone (1%-2%)[135] is bound to albumin and the binding of testosterone to albumin is weak and can be reversed easily;[136][137] as such, both albumin-bound and unbound testosterone are considered to be bioavailable testosterone.[136][137] This binding plays an important role in regulating the transport, tissue delivery, bioactivity, and metabolism of testosterone.[137][136] At the tissue level, testosterone dissociates from albumin and quickly diffuses into the tissues. The percentage of testosterone bound to SHBG is lower in men than in women. Both the free fraction and the one bound to albumin are available at the tissue level (their sum constitutes the bioavailable testosterone), while SHBG effectively and irreversibly inhibits the action of testosterone.[135] The relationship between sex steroids and SHBG in physiological and pathological conditions is complex, as various factors may influence the levels of plasma SHBG, affecting bioavailability of testosterone.[138][139][140]

### Steroid hormone activity

The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as dihydrotestosterone), and by conversion to estradiol and activation of certain estrogen receptors.[141][142] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[143][144][145]

Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (5α-DHT) by the cytoplasmic enzyme 5α-reductase. 5α-DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[146] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.

Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account for a share of biological differences between males and females.

The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[147] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[148]

### Neurosteroid activity

Testosterone, via its active metabolite 3α-androstanediol, is a potent positive allosteric modulator of the GABAA receptor.[149]

Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor (NGF), with high affinity (around 5 nM).[150][151][152] In contrast to testosterone, DHEA and DHEA sulfate have been found to act as high-affinity agonists of these receptors.[150][151][152]

Testosterone is an antagonist of the sigma-1 receptor (Ki = 1,014 or 201 nM).[153] However, the concentrations of testosterone required for binding the receptor are far above even total circulating concentrations of testosterone in adult males (which range between 10 and 35 nM).[154]

## Biochemistry

Figure 1: Human steroidogenesis, showing testosterone near bottom[27]

### Biosynthesis

Like other steroid hormones, testosterone is derived from cholesterol (Figure 1).[155] The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[156] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.

The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[157] In the testes, testosterone is produced by the Leydig cells.[158] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).

v * d * e Production rates, secretion rates, clearance rates, and blood levels of major sex hormones  Sex  | Sex hormone  | Reproductive
phase  | Blood
production rate  | Gonadal
secretion rate  | Metabolic
clearance rate  | Reference range (serum levels)

|
|
|
|
|
|

SI units  | Non-SI units
Men  | Androstenedione |

| 2.8 mg/day  | 1.6 mg/day  | 2200 L/day  | 2.8–7.3 nmol/L  | 80–210 ng/dL
Testosterone |

| 6.5 mg/day  | 6.2 mg/day  | 950 L/day  | 6.9–34.7 nmol/L  | 200–1000 ng/dL
Estrone |

| 150 μg/day  | 110 μg/day  | 2050 L/day  | 37–250 pmol/L  | 10–70 pg/mL
Estradiol |

| 60 μg/day  | 50 μg/day  | 1600 L/day  | <37–210 pmol/L  | 10–57 pg/mL
Estrone sulfate |

| 80 μg/day  | Insignificant  | 167 L/day  | 600–2500 pmol/L  | 200–900 pg/mL
Women  | Androstenedione |

| 3.2 mg/day  | 2.8 mg/day  | 2000 L/day  | 3.1–12.2 nmol/L  | 89–350 ng/dL
Testosterone |

| 190 μg/day  | 60 μg/day  | 500 L/day  | 0.7–2.8 nmol/L  | 20–81 ng/dL
Estrone | Follicular phase  | 110 μg/day  | 80 μg/day  | 2200 L/day  | 110–400 pmol/L  | 30–110 pg/mL
Luteal phase  | 260 μg/day  | 150 μg/day  | 2200 L/day  | 310–660 pmol/L  | 80–180 pg/mL
Postmenopause  | 40 μg/day  | Insignificant  | 1610 L/day  | 22–230 pmol/L  | 6–60 pg/mL
Estradiol | Follicular phase  | 90 μg/day  | 80 μg/day  | 1200 L/day  | <37–360 pmol/L  | 10–98 pg/mL
Luteal phase  | 250 μg/day  | 240 μg/day  | 1200 L/day  | 699–1250 pmol/L  | 190–341 pg/mL
Postmenopause  | 6 μg/day  | Insignificant  | 910 L/day  | <37–140 pmol/L  | 10–38 pg/mL
Estrone sulfate | Follicular phase  | 100 μg/day  | Insignificant  | 146 L/day  | 700–3600 pmol/L  | 250–1300 pg/mL
Luteal phase  | 180 μg/day  | Insignificant  | 146 L/day  | 1100–7300 pmol/L  | 400–2600 pg/mL
Progesterone | Follicular phase  | 2 mg/day  | 1.7 mg/day  | 2100 L/day  | 0.3–3 nmol/L  | 0.1–0.9 ng/mL
Luteal phase  | 25 mg/day  | 24 mg/day  | 2100 L/day  | 19–45 nmol/L  | 6–14 ng/mL

Notes and sources

Notes: "The concentration of a steroid in the circulation is determined by the rate at which it is secreted from glands, the rate of metabolism of precursor or prehormones into the steroid, and the rate at which it is extracted by tissues and metabolized. The secretion rate of a steroid refers to the total secretion of the compound from a gland per unit time. Secretion rates have been assessed by sampling the venous effluent from a gland over time and subtracting out the arterial and peripheral venous hormone concentration. The metabolic clearance rate of a steroid is defined as the volume of blood that has been completely cleared of the hormone per unit time. The production rate of a steroid hormone refers to entry into the blood of the compound from all possible sources, including secretion from glands and conversion of prohormones into the steroid of interest. At steady state, the amount of hormone entering the blood from all sources will be equal to the rate at which it is being cleared (metabolic clearance rate) multiplied by blood concentration (production rate = metabolic clearance rate × concentration). If there is little contribution of prohormone metabolism to the circulating pool of steroid, then the production rate will approximate the secretion rate." Sources: See template.

#### Regulation

Figure 2. Hypothalamic–pituitary–testicular axis

In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.[159]

The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (Figure 2).[160] When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These latter two hormones stimulate the testis to synthesize testosterone. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.

Factors affecting testosterone levels may include:

* Age: Testosterone levels gradually reduce as men age.[161][162] This effect is sometimes referred to as andropause or late-onset hypogonadism.[163]
* Exercise: Resistance training increases testosterone levels acutely,[164] however, in older men, that increase can be avoided by protein ingestion.[165] Endurance training in men may lead to lower testosterone levels.[166]
* Nutrients: Vitamin A deficiency may lead to sub-optimal plasma testosterone levels.[167] The secosteroid vitamin D in levels of 400–1000 IU/d (10–25 μg/d) raises testosterone levels.[168] Zinc deficiency lowers testosterone levels[169] but over-supplementation has no effect on serum testosterone.[170] There is limited evidence that low-fat diets may reduce total and free testosterone levels in men.[171]
* Weight loss: Reduction in weight may result in an increase in testosterone levels. Fat cells synthesize the enzyme aromatase, which converts testosterone, the male sex hormone, into estradiol, the female sex hormone.[172] However no clear association between body mass index and testosterone levels has been found.[173]
* Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[174]
* Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[175]
* Foods: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[176][177][178] Licorice can decrease the production of testosterone and this effect is greater in females.[179]

### Distribution

The plasma protein binding of testosterone is 98.0 to 98.5%, with 1.5 to 2.0% free or unbound.[180] It is bound 65% to sex hormone-binding globulin (SHBG) and 33% bound weakly to albumin.[181]

Template:Plasma protein binding of testosterone and dihydrotestosterone

### Metabolism

Template:Testosterone metabolism mini

Both testosterone and 5α-DHT are metabolized mainly in the liver.[182][183] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[182] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[182][183][184] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[182][183] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[182][183][184] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[183]

In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[182][183] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[182][183] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[182][183] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[185][186] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[184]

In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6.[187] 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[187] The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism.[187] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[187][188] Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[187]

Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[183] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[2][183][189][190] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[191] skin, hair follicles, and brain[192] and aromatase is highly expressed in adipose tissue, bone, and the brain.[193][194] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[184] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[195] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[196]

### Levels

Total levels of testosterone in the body have been reported as 264 to 916 ng/dL (nanograms per deciliter) in non-obese European and American men age 19 to 39 years,[197] while mean testosterone levels in adult men have been reported as 630 ng/dL.[198] Although commonly used as a reference range,[199] some physicians have disputed the use of this range to determine hypogonadism.[200][201] Several professional medical groups have recommended that 350 ng/dL generally be considered the minimum normal level,[202] which is consistent with previous findings.[203][non-primary source needed] Levels of testosterone in men decline with age.[197] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[204][205] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[204][205]

Template:Testosterone levels in males and females

Total testosterone levels in males throughout life  Life stage | Tanner stage | Age range | Mean age | Levels range | Mean levels

|
|
|
|
|

Child | Stage I | <10 years | – | <30 ng/dL | 5.8 ng/dL
Puberty | Stage II | 10–14 years | 12 years | <167 ng/dL | 40 ng/dL
Stage III | 12–16 years | 13–14 years | 21–719 ng/dL | 190 ng/dL
Stage IV | 13–17 years | 14–15 years | 25–912 ng/dL | 370 ng/dL
Stage V | 13–17 years | 15 years | 110–975 ng/dL | 550 ng/dL
Adult | – | ≥18 years | – | 250–1,100 ng/dL | 630 ng/dL
Sources: [206][207][198][208][209]

Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left

## Measurement

In measurements of testosterone in blood samples, different assay techniques can yield different results.[210][211] Immunofluorescence assays exhibit considerable variability in quantifying testosterone concentrations in blood samples due to the cross-reaction of structurally similar steroids, leading to overestimating the results. In contrast, the liquid chromatography/tandem mass spectrometry method is more desirable: it offers superior specificity and precision, making it a more suitable choice for this application.[212]

Testosterone's bioavailable concentration is commonly determined using the Vermeulen calculation or more precisely using the modified Vermeulen method,[213][214] which considers the dimeric form of sex hormone-binding globulin.[215]

Both methods use chemical equilibrium to derive the concentration of bioavailable testosterone: in circulation, testosterone has two major binding partners, albumin (weakly bound) and sex hormone-binding globulin (strongly bound). These methods are described in detail in the accompanying figure.

* Dimeric sex hormone-binding globulin with its testosterone ligands

* Two methods for determining the concentration of bioavailable testosterone

## Distribution

Testosterone has been detected at variably higher and lower levels among men of various nations and from various backgrounds, explanations for the causes of this have been relatively diverse.[216][217]

## History and production

Nobel Prize winner, Leopold Ružička of Ciba, a pharmaceutical industry giant that synthesized testosterone

A testicular action was linked to circulating blood fractions – now understood to be a family of androgenic hormones – in the early work on castration and testicular transplantation in fowl by Arnold Adolph Berthold (1803–1861).[218] Research on the action of testosterone received a brief boost in 1889, when the Harvard professor Charles-Édouard Brown-Séquard (1817–1894), then in Paris, self-injected subcutaneously a "rejuvenating elixir" consisting of an extract of dog and guinea pig testicle. He reported in The Lancet that his vigor and feeling of well-being were markedly restored but the effects were transient,[219] and Brown-Séquard's hopes for the compound were dashed. Suffering the ridicule of his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings.

In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles – the Chicago stockyards – and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, re-masculinized them.[220] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but the isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants – Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba – began full-scale steroid research and development programs in the 1930s.

The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[221] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[222][223]

The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[224] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[225] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[223][226] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.

The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group[227] was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry",[228] and work during this period progressed quickly.[229]

Like other androsteroids, testosterone is manufactured industrially from microbial fermentation of plant cholesterol (e.g., from soybean oil). In the early 2000s, the steroid market weighed around one million tonnes and was worth $10 billion, making it the 2nd largest biopharmaceutical market behind antibiotics.[230]

## Other species

Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in gnathostomes (jawed vertebrates).[231] Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but instead use androstenedione as a male sex hormone.[232] Fish make a slightly different form called 11-ketotestosterone.[233] Its counterpart in insects is ecdysone.[234] The presence of these ubiquitous steroids in a wide range of animals suggest that sex hormones have an ancient evolutionary history.[235]

## See also

* List of androgens/anabolic steroids
* List of human hormones

## References

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71. ↑ "Role of testosterone secretion and penile reflexes in sexual behavior and sperm competition in male rats: a theoretical contribution". Physiology & Behavior 31 (6): 823–27. Dec 1983. doi:10.1016/0031-9384(83)90279-2. PMID 6665072.
72. ↑ "Orgasmic frequency and plasma testosterone levels in normal human males". Archives of Sexual Behavior 5 (2): 125–32. Mar 1976. doi:10.1007/BF01541869. PMID 1275688.
73. ↑ "Behavioral and hormonal responses of men to brief interactions with women". Evolution and Human Behavior 24 (6): 365–75. 2003. doi:10.1016/S1090-5138(03)00053-9. Bibcode: 2003EHumB..24..365R.
74. ↑ "Psychosexual stimulation and plasma testosterone in man". Archives of Sexual Behavior 3 (6): 577–84. Nov 1974. doi:10.1007/BF01541140. PMID 4429441.
75. ↑ "Changes in saliva testosterone after psychological stimulation in men". Psychoneuroendocrinology 10 (1): 77–81. 1985. doi:10.1016/0306-4530(85)90041-1. PMID 4001279.
76. ↑ "Endocrine, psychological and genital response to sexual arousal in men". Psychoneuroendocrinology 12 (2): 149–58. 1987. doi:10.1016/0306-4530(87)90045-X. PMID 3602262.
77. ↑ "Role of androgens in female genital sexual arousal: receptor expression, structure, and function". Fertility and Sterility 77 (Suppl 4): S11–8. Apr 2002. doi:10.1016/s0015-0282(02)02978-3. PMID 12007897.
78. ↑ "Associations between testosterone secretion and sexual activity in women". Hormones and Behavior 51 (4): 477–82. Apr 2007. doi:10.1016/j.yhbeh.2007.01.003. PMID 17320881.
79. ↑ "Time course of effects of testosterone administration on sexual arousal in women". Archives of General Psychiatry 57 (2): 149–53; discussion 155–6. Feb 2000. doi:10.1001/archpsyc.57.2.149. PMID 10665617.
80. ↑ 80.0 80.1 "Testosterone therapy in women: a review". International Journal of Impotence Research 17 (5): 399–408. 2005. doi:10.1038/sj.ijir.3901334. PMID 15889125.
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83. ↑ 83.0 83.1 "Relationship status and testosterone in North American heterosexual and non-heterosexual men and women: cross-sectional and longitudinal data". Psychoneuroendocrinology 31 (6): 715–23. July 2006. doi:10.1016/j.psyneuen.2006.01.008. PMID 16621328.
84. ↑ 84.0 84.1 84.2 "Testosterone and Men's Marriages". Social Forces 72 (2): 463–77. 1993. doi:10.1093/sf/72.2.463.
85. ↑ "Marriage, Divorce, and Male Testosterone". Social Forces 77 (1): 315–30. 1998. doi:10.1093/sf/77.1.315.
86. ↑ "Human male pair bonding and testosterone". Human Nature 15 (2): 119–31. Jun 2004. doi:10.1007/s12110-004-1016-6. PMID 26190409.
87. ↑ "Social variables predict between-subject but not day-to-day variation in the testosterone of US men". Psychoneuroendocrinology 29 (9): 1153–62. Oct 2004. doi:10.1016/j.psyneuen.2004.01.008. PMID 15219639.
88. ↑ "Testosterone levels in women and men who are single, in long-distance relationships, or same-city relationships". Hormones and Behavior 51 (2): 286–91. Feb 2007. doi:10.1016/j.yhbeh.2006.11.005. PMID 17196592.
89. ↑ "Male Life History, Reproductive Effort, and the Evolution of the Genus Homo". Current Anthropology 53 (S6): S424–S435. December 2012. doi:10.1086/667538.
90. ↑ "When mothers need others: The impact of hominin life history evolution on cooperative breeding". Journal of Human Evolution 84: 16–24. July 2015. doi:10.1016/j.jhevol.2015.01.009. PMID 25843884. Bibcode: 2015JHumE..84...16K.
91. ↑ "Applying socioendocrinology to evolutionary models: fatherhood and physiology". Evolutionary Anthropology 23 (4): 146–60. 2014-07-08. doi:10.1002/evan.21412. PMID 25116846.
92. ↑ "Parenting Skills Influenced by Testosterone Levels, Empathy". 2015-10-30. https://psychcentral.com/news/2015/10/30/parenting-skills-influenced-by-testosterone-levels-empathy/94175.html.
93. ↑ "Gender differences in financial risk aversion and career choices are affected by testosterone". Proceedings of the National Academy of Sciences of the United States of America 106 (36): 15268–15273. September 2009. doi:10.1073/pnas.0907352106. PMID 19706398. Bibcode: 2009PNAS..10615268S.
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95. ↑ "In and out of unemployment-Labour market transitions and the role of testosterone". Economics and Human Biology 46. August 2022. doi:10.1016/j.ehb.2022.101123. PMID 35338911.
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97. ↑ "Study shows that testosterone levels can have an impact on generosity". https://medicalxpress.com/news/2021-03-testosterone-impact-generosity.amp.
98. ↑ "Testosterone causes both prosocial and antisocial status-enhancing behaviors in human males". Proceedings of the National Academy of Sciences of the United States of America 113 (41): 11633–11638. October 2016. doi:10.1073/pnas.1608085113. PMID 27671627. Bibcode: 2016PNAS..11311633D.
99. ↑ "Testosterone, cortisol, and criminal behavior in men and women". Hormones and Behavior 146. November 2022. doi:10.1016/j.yhbeh.2022.105260. PMID 36122515.
100. ↑ "Salivary testosterone and cortisol among late adolescent male offenders". Journal of Abnormal Child Psychology 19 (4): 469–78. August 1991. doi:10.1007/BF00919089. PMID 1757712.
101. ↑ "Sex, violence, and hormones: Why young men are horny and violent". Psychology Today. 15 July 2009. https://www.psychologytoday.com/us/blog/the-human-beast/200907/sex-violence-and-hormones.
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103. ↑ "Testosterone, cortisol, and psychopathic traits in men and women". Physiology & Behavior 129: 230–6. April 2014. doi:10.1016/j.physbeh.2014.02.057. PMID 24631306.
104. ↑ 104.0 104.1 Handbook of crime correlates. San Diego: Academic Press. 2009. pp. 208–10. ISBN 978-0-12-373612-3. https://archive.org/details/handbookcrimecor00elli.
105. ↑ "Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus". Physiology & Behavior 60 (1): 25–9. July 1996. doi:10.1016/0031-9384(95)02246-5. PMID 8804638.
106. ↑ 106.0 106.1 106.2 106.3 106.4 "Testosterone and human aggression: an evaluation of the challenge hypothesis". Neuroscience and Biobehavioral Reviews 30 (3): 319–345. 2006. doi:10.1016/j.neubiorev.2004.12.007. PMID 16483890. Bibcode: 2006NBRev..30..319A. http://www.homepage.psy.utexas.edu/homepage/faculty/josephs/pdf_documents/Arch_Chall_NBR.pdf.
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109. ↑ "The second-to-fourth digit ratio correlates with aggressive behavior in professional soccer players". Molecular Medicine Reports 7 (6): 1733–1738. Jun 2013. doi:10.3892/mmr.2013.1426. PMID 23588344.
110. ↑ "Finger length ratio (2D:4D) correlates with physical aggression in men but not in women". Biological Psychology 68 (3): 215–222. Mar 2005. doi:10.1016/j.biopsycho.2004.05.001. PMID 15620791.
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111. ↑ "Digit length ratios predict reactive aggression in women, but not in men". Hormones and Behavior 46 (5): 558–564. Dec 2004. doi:10.1016/j.yhbeh.2004.06.004. PMID 15555497.
112. ↑ "Association between a marker for prenatal testosterone exposure and externalizing behavior problems in children". Development and Psychopathology 24 (3): 771–782. August 2012. doi:10.1017/S0954579412000363. PMID 22781854.
113. ↑ "Digit ratio (2D:4D), aggression, and dominance in the Hadza and the Datoga of Tanzania". American Journal of Human Biology 27 (5): 620–627. 2015-10-01. doi:10.1002/ajhb.22718. PMID 25824265.
114. ↑ "Second to fourth digit ratio confirms aggressive tendencies in patients with boxers fractures". Injury 44 (11): 1636–1639. Nov 2013. doi:10.1016/j.injury.2013.07.018. PMID 23972912.
115. ↑ "Social neuroendocrinology of human aggression: examining the role of competition-induced testosterone dynamics". Neuroscience 286: 171–186. Feb 2015. doi:10.1016/j.neuroscience.2014.11.029. PMID 25463514. http://carrelab.nipissingu.ca/wp-content/uploads/sites/32/2014/10/Carre-Olmstead-2015.pdf. Retrieved December 30, 2015.
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118. ↑ "A testosterone-related structural brain phenotype predicts aggressive behavior from childhood to adulthood". Psychoneuroendocrinology 63: 109–118. Jan 2016. doi:10.1016/j.psyneuen.2015.09.021. PMID 26431805.
119. ↑ "Anabolic androgenic steroids and aggression: studies using animal models". Annals of the New York Academy of Sciences 1036 (1): 399–415. Dec 2004. doi:10.1196/annals.1330.024. PMID 15817752. Bibcode: 2004NYASA1036..399M.
120. ↑ "Testosterone, 5 alpha-dihydrotestosterone and cortisol in men with and without alcohol-related aggression". Journal of Studies on Alcohol 63 (5): 518–26. Sep 2002. doi:10.15288/jsa.2002.63.518. PMID 12380846.
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125. ↑ "Acute and chronic effects of an aromatase inhibitor on territorial aggression in breeding and nonbreeding male song sparrows". Journal of Comparative Physiology A 186 (7–8): 759–69. 2000. doi:10.1007/s003590000129. PMID 11016791.
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127. ↑ "Doubled-Edged Swords in the Biology of Conflict". Frontiers in Psychology 9. 2018. doi:10.3389/fpsyg.2018.02625. PMID 30619017.
128. ↑ The trouble with testosterone.. New York: Simon and Schuster. 1998. pp. 153–55. ISBN 978-0-684-83891-5.
129. ↑ "The role of testosterone in social interaction". Trends in Cognitive Sciences 15 (6): 263–71. June 2011. doi:10.1016/j.tics.2011.04.008. PMID 21616702. http://www.zora.uzh.ch/id/eprint/58008/1/Testosterone_social_interaction_revision_(12_Apr_11).pdf. Retrieved December 22, 2020.
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139. ↑ "Sex Hormone-Binding Globulin (SHBG) as an Early Biomarker and Therapeutic Target in Polycystic Ovary Syndrome". Int J Mol Sci 21 (21): 8191. November 2020. doi:10.3390/ijms21218191. PMID 33139661.
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145. ↑ "Targeting membrane androgen receptors in tumors". Expert Opin. Ther. Targets 17 (8): 951–63. 2013. doi:10.1517/14728222.2013.806491. PMID 23746222.
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156. ↑ "Expression of bovine 17 alpha-hydroxylase cytochrome P-450 cDNA in nonsteroidogenic (COS 1) cells". Science 234 (4781): 1258–61. Dec 1986. doi:10.1126/science.3535074. PMID 3535074. Bibcode: 1986Sci...234.1258Z.
157. ↑ "Androgen action on human skin – from basic research to clinical significance". Experimental Dermatology 13 (Suppl 4): 5–10. 2004. doi:10.1111/j.1600-0625.2004.00255.x. PMID 15507105.
158. ↑ "Androgens". Clinics in Endocrinology and Metabolism 4 (3): 503–20. Nov 1975. doi:10.1016/S0300-595X(75)80045-4. PMID 58744.
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160. ↑ "Developments in the control of testicular function". Baillière's Clinical Endocrinology and Metabolism 6 (2): 451–83. Apr 1992. doi:10.1016/S0950-351X(05)80158-2. PMID 1377467.
161. ↑ "Introduction". Testosterone and Aging: Clinical Research Directions.. National Academies Press (US). January 1, 2004. doi:10.17226/10852. ISBN 978-0-309-09063-6. https://www.ncbi.nlm.nih.gov/books/NBK216164/. Retrieved September 26, 2016.
162. ↑ "Late-onset hypogonadism: current concepts and controversies of pathogenesis, diagnosis and treatment". Asian Journal of Andrology 16 (2): 192–202. 2014. doi:10.4103/1008-682X.122336. PMID 24407185.
163. ↑ "Andropause--lessons from the European Male Ageing Study". Annales d'Endocrinologie 75 (2): 128–31. 2014. doi:10.1016/j.ando.2014.03.005. PMID 24793989.
164. ↑ "Testosterone physiology in resistance exercise and training: the up-stream regulatory elements". Sports Medicine 40 (12): 1037–53. 2010. doi:10.2165/11536910-000000000-00000. PMID 21058750.
165. ↑ "Androgen receptors and testosterone in men—effects of protein ingestion, resistance exercise and fiber type". The Journal of Steroid Biochemistry and Molecular Biology 110 (1–2): 130–37. May 2008. doi:10.1016/j.jsbmb.2008.03.030. PMID 18455389.
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171. ↑ "Low-fat diets and testosterone in men: Systematic review and meta-analysis of intervention studies". The Journal of Steroid Biochemistry and Molecular Biology 210. June 2021. doi:10.1016/j.jsbmb.2021.105878. PMID 33741447.
172. ↑ "Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men". Reproductive Health 8 (1). 2011. doi:10.1186/1742-4755-8-24. PMID 21849026.
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188. ↑ (in de) Steroidhormone: Biosynthese, Stoffwechsel, Wirkung. Springer-Verlag. 1977. p. 349. ISBN 978-0-387-08012-3.
189. ↑ "Role of 5 alpha-reductase in health and disease". Baillière's Clinical Endocrinology and Metabolism 8 (2): 405–31. Apr 1994. doi:10.1016/S0950-351X(05)80259-9. PMID 8092979.
190. ↑ "The essential role of the aromatase/p450arom". Seminars in Reproductive Medicine 20 (3): 277–84. August 2002. doi:10.1055/s-2002-35374. PMID 12428207.
191. ↑ Arthur's Veterinary Reproduction and Obstetrics. Elsevier Health Sciences UK. 23 April 2009. pp. 695–. ISBN 978-0-7020-3990-4. https://books.google.com/books?id=W5TdAwAAQBAJ&pg=PA695.
192. ↑ Testosterone: Action, Deficiency, Substitution. Cambridge University Press. 1 April 2004. pp. 626–. ISBN 978-1-139-45221-2. https://books.google.com/books?id=ZiZ7MWDqo5oC&pg=PA626.
193. ↑ Estrogens, Estrogen Receptor and Breast Cancer. IOS Press. 2000. pp. 25–. ISBN 978-0-9673355-4-4. https://books.google.com/books?id=v7ai5Mz9TZQC&pg=PA25.
194. ↑ Hormones. Academic Press. 30 July 2014. pp. 261–. ISBN 978-0-08-091906-5. https://books.google.com/books?id=_renonjXq68C&pg=PA261.
195. ↑ 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.
196. ↑ "Different patterns of metabolism determine the relative anabolic activity of 19-norandrogens". J. Steroid Biochem. Mol. Biol. 53 (1–6): 253–7. 1995. doi:10.1016/0960-0760(95)00056-6. PMID 7626464.
197. ↑ 197.0 197.1 "Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe". The Journal of Clinical Endocrinology and Metabolism 102 (4): 1161–1173. April 2017. doi:10.1210/jc.2016-2935. PMID 28324103.
198. ↑ 198.0 198.1 Pediatric Endocrinology E-Book. Elsevier Health Sciences. 10 April 2014. pp. 488–. ISBN 978-1-4557-5973-6. https://books.google.com/books?id=GgXnAgAAQBAJ&pg=PA488. Retrieved March 25, 2018.
199. ↑ "Testosterone, total". https://www.labcorp.com/tests/004226/testosterone-total.
200. ↑ "Andrology: Testosterone reference ranges and diagnosis of testosterone deficiency". Nature Reviews. Urology 14 (5): 263–264. May 2017. doi:10.1038/nrurol.2017.35. PMID 28266512.
201. ↑ "Commentary: Who is a candidate for testosterone therapy? A synthesis of international expert opinions". The Journal of Sexual Medicine 11 (7): 1636–1645. July 2014. doi:10.1111/jsm.12546. PMID 24797325.
202. ↑ "ISA, ISSAM, EAU, EAA and ASA recommendations: investigation, treatment and monitoring of late-onset hypogonadism in males". International Journal of Impotence Research 21 (1): 1–8. 16 October 208. doi:10.1038/ijir.2008.41. PMID 18923415. https://biblio.ugent.be/publication/631584/file/741306.
203. ↑ "Reference ranges for testosterone in men generated using liquid chromatography tandem mass spectrometry in a community-based sample of healthy nonobese young men in the Framingham Heart Study and applied to three geographically distinct cohorts". The Journal of Clinical Endocrinology and Metabolism 96 (8): 2430–2439. August 2011. doi:10.1210/jc.2010-3012. PMID 21697255.
204. ↑ 204.0 204.1 Evidence-Based Endocrinology. Lippincott Williams & Wilkins. 26 September 2012. pp. 217–. ISBN 978-1-4511-7146-4. https://books.google.com/books?id=s06wXkPAnfcC&pg=PA217. Retrieved May 19, 2018.
205. ↑ 205.0 205.1 "Utilization of commercial laboratory results in management of hyperandrogenism in women". Endocrine Practice 4 (1): 1–10. 1998. doi:10.4158/EP.4.1.1. PMID 15251757.
206. ↑ Berman's Pediatric Decision Making. Elsevier Health Sciences. 1 January 2011. pp. 160–. ISBN 978-0-323-05405-8. https://books.google.com/books?id=NPhnHrDQ1_kC&pg=PA160. Retrieved March 25, 2018.
207. ↑ Pediatric Endocrinology: A Clinical Handbook. Springer. 25 April 2016. pp. 191–. ISBN 978-3-319-18371-8. https://books.google.com/books?id=akMWDAAAQBAJ&pg=PA191. Retrieved March 25, 2018.
208. ↑ Mosby's Diagnostic and Laboratory Test Reference – E-Book. Elsevier Health Sciences. 19 September 2014. pp. 879–. ISBN 978-0-323-22592-2. https://books.google.com/books?id=J7eXBAAAQBAJ&pg=PA879. Retrieved March 25, 2018.
209. ↑ The Harriet Lane Handbook E-Book. Elsevier Health Sciences. 1 May 2014. pp. 240–. ISBN 978-0-323-11246-8. https://books.google.com/books?id=6cSLAwAAQBAJ&pg=PA240. Retrieved March 25, 2018.
210. ↑ "Challenges in Testosterone Measurement, Data Interpretation, and Methodological Appraisal of Interventional Trials | the Journal of Sexual Medicine | Oxford Academic". The Journal of Sexual Medicine 13 (7): 1029–1046. July 2016. doi:10.1016/j.jsxm.2016.04.068. PMID 27209182.
211. ↑ "Testosterone concentrations, using different assays, in different types of ovarian insufficiency: A systematic review and meta-analysis | Human Reproduction Update | Oxford Academic". Human Reproduction Update 18 (4): 405–419. July 2012. doi:10.1093/humupd/dms013. PMID 22525963. https://academic.oup.com/humupd/article/18/4/405/665632. Retrieved February 20, 2024.
212. ↑ "[A promising approach for therapy control in congenital adrenal hyperplasia. Problems of Endocrinology"] (in Russian). Probl Endokrinol (Mosk) 69 (6): 102–108. January 2024. doi:10.14341/probl13328. PMID 38311999.
213. ↑ "Calculation of bioavailable and free testosterone in men: a comparison of 5 published algorithms". Clinical Chemistry 52 (9): 1777–84. September 2006. doi:10.1373/clinchem.2005.063354. PMID 16793931.
214. ↑ "Impact of recent biochemical findings on the determination of free and bioavailable testosterone: evaluation and proposal for clinical use". LaboratoriumsMedizin 30 (6): 492–505. 1 January 2006. doi:10.1515/JLM.2006.050.
215. ↑ "RCSB PDB - 1D2S". Crystal Structure of the N-Terminal Laminin G-Like Domain of SHBG in Complex with Dihydrotestosterone. https://www.rcsb.org/3d-view/1D2S/1. Retrieved February 19, 2019.
216. ↑ "Low Testosterone in Adolescents & Young Adults". Frontiers in Endocrinology 10. 2020-01-10. doi:10.3389/fendo.2019.00916. PMID 32063884.
217. ↑ "Physiology, Testosterone". StatPearls. Treasure Island (FL): StatPearls Publishing. 2024. https://www.ncbi.nlm.nih.gov/books/NBK526128/. Retrieved 2024-03-03.
218. ↑ "Transplantation der Hoden" (in de). Arch. Anat. Physiol. Wiss. 16: 42–46. 1849.
219. ↑ "The effects produced on man by subcutaneous injections of liquid obtained from the testicles of animals". Lancet 2 (3438): 105–107. 1889. doi:10.1016/S0140-6736(00)64118-1. https://zenodo.org/record/1428532. Retrieved September 16, 2019.
220. ↑ "The testicular hormone". J. Biol. Chem. 84 (2): 495–500. November 1929. doi:10.1016/S0021-9258(18)77008-7.
221. ↑ "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" (in de). Hoppe-Seyler's Z Physiol Chem 233 (5–6): 281–83. May 1935. doi:10.1515/bchm2.1935.233.5-6.281.
222. ↑ "Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin" (in de). Hoppe-Seyler's Z Physiol Chem 237 (2): 89–97. 1935. doi:10.1515/bchm2.1935.237.1-3.89.
223. ↑ 223.0 223.1 "A brief history of testosterone". The Journal of Urology 165 (2): 371–73. Feb 2001. doi:10.1097/00005392-200102000-00004. PMID 11176375.
224. ↑ "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]" (in de). Chemische Berichte 68 (9): 1859–62. 1935. doi:10.1002/cber.19350680937.
225. ↑ "Uber die kristallinische Herstellung des Testikelhormons, Testosteron (Androsten-3-ol-17-ol) [The crystalline production of the testicle hormone, testosterone (Androsten-3-ol-17-ol)]" (in de). Helvetica Chimica Acta 18: 1264–75. 1935. doi:10.1002/hlca.193501801176.
226. ↑ "The history of synthetic testosterone". Scientific American 272 (2): 76–81. Feb 1995. doi:10.1038/scientificamerican0295-76. PMID 7817189. Bibcode: 1995SciAm.272b..76H.
227. ↑ "A comparative study of the metabolic effects of testosterone propionate in normal men and women and in eunuchoidism". Endocrinology 26 (1): 26–45. February 1940. doi:10.1210/Endo-26-1-26.
228. ↑ "The steroid story of Jenapharm: from the late 1940s to the early 1970s". Steroids 64 (7): 439–45. July 1999. doi:10.1016/S0039-128X(99)00003-3. PMID 10443899.
229. ↑ The Male Hormone. New York: Harcourt, Brace. 1945. https://archive.org/details/malehormone00dekr.
230. ↑ Batth, Rituraj; Nicolle, Clément; Cuciurean, Ilenuta Simina; Simonsen, Henrik Toft (2020-09-03). "Biosynthesis and Industrial Production of Androsteroids". Plants 9 (9): 1144. doi:10.3390/plants9091144. ISSN 2223-7747. PMID 32899410. Bibcode: 2020Plnts...9.1144B.
231. ↑ "Vertebrate sex steroid receptors: evolution, ligands, and neurodistribution". Annals of the New York Academy of Sciences 1163 (1): 154–68. 2009. doi:10.1111/j.1749-6632.2009.04460.x. PMID 19456336. Bibcode: 2009NYASA1163..154G.
232. ↑ "Sex steroids and their receptors in lampreys". Steroids 73 (1): 1–12. 2008. doi:10.1016/j.steroids.2007.08.011. PMID 17931674.
233. ↑ An introduction to behavioral endocrinology. Sunderland, Mass: Sinauer Associates. 2005. p. 143. ISBN 978-0-87893-617-5.
234. ↑ "Ecdysteroids: the overlooked sex steroids of insects? Males: the black box". Insect Science 13 (5): 325–338. October 2006. doi:10.1111/j.1744-7917.2006.00101.x. Bibcode: 2006InsSc..13..325D.
235. ↑ "Estrogens in insects". Cellular and Molecular Life Sciences 40 (9): 942–44. September 1984. doi:10.1007/BF01946450. Bibcode: 1984Expea..40..942M.

## Further reading

* "On the effects of testosterone on brain behavioral functions". Frontiers in Neuroscience 9: 12. February 2015. doi:10.3389/fnins.2015.00012. PMID 25741229.
* "Sperm, testosterone, masculinities and fatherhood". Nevada Law Journal 13 (2): 8. 2013. http://scholars.law.unlv.edu/nlj/vol13/iss2/8. Retrieved December 10, 2017.
* "Molecular Biology of Androgen Action: Perspectives on Neuroprotective and Neurotherapeutic Effects.". Molecular Mechanisms of Hormone Actions on Behavior. Elsevier Inc.. 2010. pp. 1219–1246. doi:10.1016/B978-008088783-8.00036-X. ISBN 978-0-12-374939-0. https://books.google.com/books?id=Y8jxd5vu6N8C&pg=PA127.

* v
* t
* e

Testosterone

Topics|

* Testosterone (as a hormone)
* Testosterone (as a medication)
* Pharmacodynamics of testosterone
* Pharmacokinetics of testosterone
* Androgen (as a hormone)
* Androgen/anabolic steroid (as a medication)
* Androgen replacement therapy
* Transgender hormone therapy (female-to-male)

Esters|

* Androgen ester
* Testosterone ester
* Testosterone buciclate
* Testosterone caproate
* Testosterone cypionate
* Testosterone decanoate
* Testosterone enanthate
* Testosterone isobutyrate
* Testosterone isocaproate
* Testosterone phenylpropionate
* Testosterone propionate
* Testosterone undecanoate
* Mixed testosterone esters

Related|

* Dihydrotestosterone (DHT; androstanolone)
* Methyltestosterone
* Nandrolone (19-nortestosterone)
* Dehydroepiandrosterone (DHEA; prasterone)
* Estradiol

* v
* t
* e

Hormones

Endocrine
glands|

| Hypothalamic-
pituitary|

| Hypothalamus|

* GnRH
* TRH
* Dopamine
* CRH
* GHRH
* Somatostatin (GHIH)
* MCH

|

Posterior pituitary|

* Oxytocin
* Vasopressin

Anterior pituitary|

* FSH
* LH
* TSH
* Prolactin
* POMC
* CLIP
* ACTH
* MSH
* Endorphins
* Lipotropin
* GH

Adrenal axis|

* Adrenal cortex
* Aldosterone
* Cortisol
* Cortisone
* DHEA
* DHEA-S
* Androstenedione
* Adrenal medulla
* Epinephrine
* Norepinephrine

Thyroid|

* Thyroid hormones
* T3
* T4
* Calcitonin
* Thyroid axis

Parathyroid|

* PTH

Gonadal axis|

| Testis|

* Testosterone
* AMH
* Inhibin

|

Ovary|

* Estradiol
* Progesterone
* Activin
* Inhibin
* Relaxin
* GnSAF

Placenta|

* hCG
* HPL
* Estrogen
* Progesterone

Pancreas|

* Glucagon
* Insulin
* Amylin
* Somatostatin
* Pancreatic polypeptide

Pineal gland|

* Melatonin
* N,N-Dimethyltryptamine
* 5-Methoxy-N,N-dimethyltryptamine

Other|

| Thymus|

* Thymosins
* Thymosin α1
* Beta thymosins
* Thymopoietin
* Thymulin

|

Digestive system|

| Stomach|

* Gastrin
* Ghrelin

|

Duodenum|

* CCK
* Incretins
* GIP
* GLP-1
* Secretin
* Motilin
* VIP

Ileum|

* Enteroglucagon
* Peptide YY

Liver/other|

* Insulin-like growth factor
* IGF-1
* IGF-2

Adipose tissue|

* Leptin
* Adiponectin
* Resistin

Skeleton|

* Osteocalcin

Kidney|

* Renin
* EPO
* Calcitriol
* Prostaglandin

Heart|

* Natriuretic peptide
* ANP
* BNP

* v
* t
* e

Endogenous steroids

Precursors|

* Cholesterol
* 22R-Hydroxycholesterol
* 20α,22R-Dihydroxycholesterol
* Pregnenolone
* 11β-Hydroxypregnenolone
* 17α-Hydroxypregnenolone
* 21-Hydroxypregnenolone
* 17α,21-Dihydroxypregnenolone
* 11β,17α,21-Trihydroxypregnenolone

Corticosteroids|

| Glucocorticoids|

* 3α,5α-Tetrahydrocorticosterone
* 5α-Dihydrocorticosterone
* 11-Deoxycorticosterone
* 11-Deoxycortisol
* 11-Ketoprogesterone
* 21-Deoxycortisol
* 21-Deoxycortisone
* Corticosterone
* Cortisol
* Cortisone
* 17α-Hydroxypregnenolone
* 17α-Hydroxyprogesterone
* Pregnenolone
* Progesterone

* Metabolites: 5α-Dihydrocortisol
* 3α,5α-Tetrahydrocortisol

|

Mineralocorticoids|

* 5α-Dihydroaldosterone
* 11-Dehydrocorticosterone (11-oxocorticosterone, 17-deoxycortisone)
* 11-Deoxycortisol
* 11-Deoxycorticosterone
* 11β-Hydroxyprogesterone (21-deoxycorticosterone)
* 18-Hydroxy-11-deoxycorticosterone
* 18-Hydroxycorticosterone
* 18-Hydroxyprogesterone
* Aldosterone
* Corticosterone
* Cortisol

Sex steroids|

| Androgens|

* 11-Ketodihydrotestosterone
* 11-Ketotestosterone
* 7β-Hydroxyepiandrosterone
* 11β-Hydroxyandrostenedione
* Adrenosterone (11-ketoandrostenedione)
* Androstenediol
* Androstenedione
* Androsterone
* Dehydroandrosterone
* DHEA
* DHEA sulfate
* Dihydrotestosterone
* Epiandrosterone
* Epitestosterone
* 16α-Hydroxyandrostenedione
* 16α-Hydroxy-DHEA
* 16α-Hydroxy-DHEA sulfate
* Testosterone

* Metabolites: 3α-Androstanediol
* 3α-Androstanediol glucuronide
* 3β-Androstanediol
* 5β-Dihydrotestosterone
* 3α-Etiocholanediol
* 3β-Etiocholanediol
* Androstanetriols
* Androstenediol sulfate
* Androsterone glucuronide
* Androsterone sulfate
* Dihydrotestosterone glucuronide
* Dihydrotestosterone sulfate
* Etiocholanedione
* Etiocholanolone
* Etiocholanolone glucuronide
* Epietiocholanolone
* Testosterone glucuronide
* Testosterone sulfate

|

Estrogens|

* Estranes: Estetrol
* Estradiol
* Estrone
* Estriol
* 17α-Estradiol
* 16β-Epiestriol (16β-hydroxyestradiol)
* 17α-Epiestriol (16α-hydroxy-17α-estradiol)
* 16β,17α-Epiestriol (16β-hydroxy-17α-estradiol)
* 2-Hydroxyestradiol
* 2-Hydroxyestriol
* 2-Hydroxyestrone
* 4-Hydroxyestradiol
* 4-Hydroxyestriol
* 4-Hydroxyestrone
* 4-Methoxyestradiol
* 16α-Hydroxyestrone

* Others: 27-Hydroxycholesterol
* 3α-Androstanediol
* 3β-Androstanediol
* 4-Androstenedione
* 5-Androstenediol
* DHEA
* DHEA sulfate
* 7-Keto-DHEA
* 7α-Hydroxy-DHEA
* 16α-Hydroxy-DHEA

* Metabolites: 2-Methoxyestradiol
* 2-Methoxyestrone
* 4-Methoxyestrone
* Estradiol glucuronide
* Estradiol 3-glucuronide
* Estradiol sulfate
* Estradiol 17β-sulfate
* Estrone glucuronide
* Estrone sulfate
* Estriol glucuronide
* Estriol sulfate
* Lipoidal estradiol (e.g., estradiol stearate, estradiol palmitate)

Progestogens|

* Progesterone
* 16α-Hydroxyprogesterone
* 17α-Hydroxyprogesterone
* 20α-Dihydroprogesterone
* 20β-Dihydroprogesterone
* 5α-Dihydroprogesterone
* 11-Deoxycorticosterone
* 5α-DHDOC

* Metabolites: Allopregnanediol
* Pregnanediol
* Pregnanediol glucuronide
* Pregnanetriol

Neurosteroids|

* Cholestanes: 24S-Hydroxycholesterol
* Cholesterol

* Pregnanes: 3α-Dihydroprogesterone
* 3β-Dihydroprogesterone
* 5α-Dihydrocorticosterone
* 5α-Dihydroprogesterone
* 5β-Dihydroprogesterone
* Allopregnanolone
* Corticosterone
* DHC
* DHDOC
* 11-Deoxycorticosterone
* Epipregnanolone
* Isopregnanolone
* Pregnanolone
* Pregnenolone
* Pregnenolone sulfate
* Progesterone
* THB
* THDOC

* Androstanes: 3α-Androstanediol
* 3α-Androstenol
* 7-Keto-DHEA
* 7α-Hydroxy-DHEA
* 7β-Hydroxy-DHEA
* 7α-Hydroxyepiandrosterone
* 7β-Hydroxyepiandrosterone
* Androsterone
* DHEA
* DHEA sulfate
* Etiocholanolone

* Pheromones: 3α-Androstenol
* 3β-Androstenol
* Androstadienol
* Androstadienone
* Androstenone
* Androsterone
* Estratetraenol

Others|

* Vitamin D: 7-Dehydrocholesterol
* Calcidiol/Calcifediol
* Calcitriol
* Cholecalciferol

* Others: 7α-Hydroxycholesterol
* 11α-Hydroxyprogesterone
* 11β-Hydroxyprogesterone
* Cholesterol sulfate

{{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

Biological activity

* 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

* v
* t
* e

Estrogen receptor modulators

ER|

| Agonists|

* Steroidal: 2-Hydroxyestradiol
* 2-Hydroxyestrone
* 3-Methyl-19-methyleneandrosta-3,5-dien-17β-ol
* 3α-Androstanediol
* 3α,5α-Dihydrolevonorgestrel
* 3β,5α-Dihydrolevonorgestrel
* 3α-Hydroxytibolone
* 3β-Hydroxytibolone
* 3β-Androstanediol
* 4-Androstenediol
* 4-Androstenedione
* 4-Hydroxyestradiol
* 4-Hydroxyestrone
* 4-Methoxyestradiol
* 4-Methoxyestrone
* 5-Androstenediol
* 7-Oxo-DHEA
* 7α-Hydroxy-DHEA
* 7α-Methylestradiol
* 7β-Hydroxyepiandrosterone
* 8,9-Dehydroestradiol
* 8,9-Dehydroestrone
* 8β-VE2
* 10β,17β-Dihydroxyestra-1,4-dien-3-one (DHED)
* 16α-Fluoroestradiol
* 16α-Hydroxy-DHEA
* 16α-Hydroxyestrone
* 16α-Iodoestradiol
* 16α-LE2
* 16β,17α-Epiestriol (16β-hydroxy-17α-estradiol)
* 17α-Estradiol (alfatradiol)
* 17α-Dihydroequilenin
* 17α-Dihydroequilin
* 17α-Epiestriol (16α-hydroxy-17α-estradiol)
* 17β-Dihydroequilenin
* 17β-Dihydroequilin
* Abiraterone
* Abiraterone acetate
* Alestramustine
* Almestrone
* Anabolic steroids (e.g., testosterone and esters, methyltestosterone, metandienone (methandrostenolone), nandrolone and esters, many others; via estrogenic metabolites)
* Atrimustine
* Bolandiol
* Bolandiol dipropionate
* Butolame
* Clomestrone
* Cloxestradiol
* Cloxestradiol acetate
* Conjugated estriol
* Conjugated estrogens
* Cyclodiol
* Cyclotriol
* DHEA
* DHEA-S
* Epiestriol (16β-epiestriol, 16β-hydroxy-17β-estradiol)
* Epimestrol
* Equilenin
* Equilin
* ERA-63 (ORG-37663)
* Esterified estrogens
* Estetrol
* Estradiol
* Estradiol esters
* Lipoidal estradiol
* Polyestradiol phosphate
* Estramustine
* Estramustine phosphate
* Estrapronicate
* Estrazinol
* Estriol
* Estriol esters
* Polyestriol phosphate
* Estrofurate
* Estromustine
* Estrone
* Estrone esters
* Estrone methyl ether
* Estropipate
* Etamestrol (eptamestrol)
* Ethinylestradiol
* Ethinylestradiol 3-benzoate
* Ethinylestradiol sulfonate
* Ethinylestriol
* Ethylestradiol
* Etynodiol
* Etynodiol diacetate
* Hexolame
* Hippulin
* Hydroxyestrone diacetate
* Lynestrenol
* Lynestrenol phenylpropionate
* Mestranol
* Methylestradiol
* Moxestrol
* Mytatrienediol
* Nilestriol
* Norethisterone
* Noretynodrel
* Orestrate
* Pentolame
* Prodiame
* Prolame
* Promestriene
* RU-16117
* Quinestradol
* Quinestrol
* Tibolone

* Nonsteroidal: (R,R)-THC
* (S,S)-THC
* 2,8-DHHHC
* β-LGND1
* β-LGND2 (GTx-878)
* AC-186
* Allenestrol
* Allenolic acid
* Benzestrol
* Bifluranol
* Bisdehydrodoisynolic acid
* Carbestrol
* D-15414
* DCW234
* Diarylpropionitrile
* Dienestrol
* Dienestrol diacetate
* Diethylstilbestrol
* Diethylstilbestrol esters
* Dimestrol (dianisylhexene)
* Doisynoestrol (fenocycline)
* Doisynolic acid
* Efavirenz
* ERB-196 (WAY-202196)
* Erteberel (SERBA-1, LY-500307)
* Estrobin (DBE)
* Fenestrel
* FERb 033
* Fosfestrol (diethylstilbestrol diphosphate)
* Furostilbestrol (diethylstilbestrol difuroate)
* GTx-758
* Hexestrol
* Hexestrol esters
* ICI-85966 (Stilbostat)
* Mestilbol
* Methallenestril
* Methestrol
* Methestrol dipropionate
* Paroxypropione
* Pentafluranol
* Phenestrol
* Prinaberel (ERB-041, WAY-202041)
* Propylpyrazoletriol
* Quadrosilan
* SC-4289
* SERBA-2
* SKF-82,958
* Terfluranol
* Triphenylbromoethylene
* Triphenylchloroethylene
* Triphenyliodoethylene
* Triphenylmethylethylene (triphenylpropene)
* WAY-166818
* WAY-169916
* WAY-200070
* WAY-204688 (SIM-688)
* WAY-214156

* Unknown/unsorted: ERB-26
* ERA-45
* ERB-79
* ZK-283197

* Xenoestrogens: Anise-related (e.g., anethole, anol, dianethole, dianol, photoanethole)
* Chalconoids (e.g., isoliquiritigenin, phloretin, phlorizin (phloridzin), wedelolactone)
* Coumestans (e.g., coumestrol, psoralidin)
* Flavonoids (incl. 7,8-DHF, 8-prenylnaringenin, apigenin, baicalein, baicalin, biochanin A, calycosin, catechin, daidzein, daidzin, ECG, EGCG, [[Chemistry:Epicateepicatechin, Chemistry:Equol|equol]], formononetin, glabrene, glabridin, Genistein|genistein]], genistin, glycitein, kaempferol, Chemistry:Liquiritigenin

|

Mixed
(SERMs)|

* 2-Phenylbenzofuran
* 2-Phenylbenzothiophene
* 4'-Hydroxynorendoxifen
* 27-Hydroxycholesterol
* Acefluranol
* Acolbifene
* Afimoxifene
* Anordiol
* Anordrin
* Arzoxifene
* Bazedoxifene
* Brilanestrant
* Broparestrol
* Chlorotrianisene
* Clomifene
* Clomifenoxide
* Cyclofenil
* D-15413
* Droloxifene
* Elacestrant
* Enclomifene
* Endoxifen
* Etacstil (GW-5638, DPC-974)
* Ethamoxytriphetol (MER-25)
* Femarelle
* Fispemifene
* GW-7604
* ICI-55548
* Idoxifene
* Lasofoxifene
* Levormeloxifene
* LN-1643
* LN-2299
* LY-117018
* Menerba
* Miproxifene
* Miproxifene phosphate
* Nafoxidine
* Nitromifene
* NNC 45-0095
* NNC 45-0320
* NNC 45-0781
* NNC 45-1506
* Ormeloxifene
* Ospemifene
* Panomifene
* Pipendoxifene
* Promensil
* Raloxifene
* Rimostil (P-081)
* Spironolactone
* SS1010
* Tamoxifen
* TAS-108 (SR-16234)
* Toremifene
* Trioxifene
* TZE-5323
* Y-134
* Zindoxifene
* Zuclomifene

Antagonists|

* (R,R)-THC
* 7β-Hydroxy-DHEA
* Chloroindazole
* Cytestrol acetate
* EM-800
* Epitiostanol
* ERA-90
* ERB-88
* Fulvestrant (ICI-182780)
* Glyceollins (I, II, III, IV)
* ICI-164384
* Mepitiostane
* Methylepitiostanol
* Methylpiperidinopyrazole
* MIBE
* Oxabicycloheptene sulfonate
* Phenytoin
* PHTPP
* Prochloraz
* RU-58668
* SS1020
* TAS-108 (SR-16234)
* ZB716
* ZK-164015
* ZK-191703

* Coregulator-binding modulators: ERX-11

GPER|

| Agonists|

* 2-Methoxyestradiol
* 7β-Hydroxyepiandrosterone
* Afimoxifene (4-hydroxytamoxifen)
* Atrazine
* Bisphenol A
* Daidzein
* DDT (p,p'-DDT, o',p'-DDE)
* Equol
* Estradiol
* Ethinylestradiol
* Fulvestrant (ICI-182780)
* G-1
* Genistein
* GPER-L1
* GPER-L2
* Hydroxytyrosol
* Kepone
* Niacin
* Nicotinamide
* Nonylphenol
* Oleuropein
* PCBs (2,2',5'-PCB-4-OH)
* Propylpyrazoletriol
* Quercetin
* Raloxifene
* Resveratrol
* Tamoxifen
* Tectoridin
* Zearalanone
* Zearalenol
* Zearalenone
* Zeranol (zearalanol))

|

Antagonists|

* CCL18
* Estriol
* G-15
* G-36
* MIBE

See also
Receptor/signaling modulators
Estrogens and antiestrogens
Androgen receptor modulators
Progesterone receptor modulators
List of estrogens

* v
* t
* e

GABAA receptor positive modulators

Alcohols|

* Brometone
* Butanol
* Chloralodol
* Chlorobutanol (cloretone)
* Ethanol (alcohol) (alcoholic drink)
* Ethchlorvynol
* Isobutanol
* Isopropanol
* Menthol
* Methanol
* Methylpentynol
* Pentanol
* Petrichloral
* Propanol
* tert-Butanol (2M2P)
* tert-Pentanol (2M2B)
* Tribromoethanol
* Trichloroethanol
* Triclofos
* Trifluoroethanol

Barbiturates|

* (-)-DMBB
* Allobarbital
* Alphenal
* Amobarbital
* Aprobarbital
* Barbexaclone
* Barbital
* Benzobarbital
* Benzylbutylbarbiturate
* Brallobarbital
* Brophebarbital
* Butabarbital/Secbutabarbital
* Butalbital
* Buthalital
* Butobarbital
* Butallylonal
* Carbubarb
* Crotylbarbital
* Cyclobarbital
* Cyclopentobarbital
* Difebarbamate
* Enallylpropymal
* Ethallobarbital
* Eterobarb
* Febarbamate
* Heptabarb
* Heptobarbital
* Hexethal
* Hexobarbital
* Metharbital
* Methitural
* Methohexital
* Methylphenobarbital
* Narcobarbital
* Nealbarbital
* Pentobarbital
* Phenallymal
* Phenobarbital
* Phetharbital
* Primidone
* Probarbital
* Propallylonal
* Propylbarbital
* Proxibarbital
* Reposal
* Secobarbital
* Sigmodal
* Spirobarbital
* Talbutal
* Tetrabamate
* Tetrabarbital
* Thialbarbital
* Thiamylal
* Thiobarbital
* Thiobutabarbital
* Thiopental
* Thiotetrabarbital
* Valofane
* Vinbarbital
* Vinylbital

Benzodiazepines|

* 2-Oxoquazepam
* 3-Hydroxyphenazepam
* Adinazolam
* Alprazolam
* Arfendazam
* Avizafone
* Bentazepam
* Bretazenil
* Bromazepam
* Brotizolam
* Camazepam
* Carburazepam
* Chlordiazepoxide
* Ciclotizolam
* Cinazepam
* Cinolazepam
* Clazolam
* Climazolam
* Clobazam
* Clonazepam
* Clonazolam
* Cloniprazepam
* Clorazepate
* Clotiazepam
* Cloxazolam
* CP-1414S
* Cyprazepam
* Delorazepam
* Demoxepam
* Diazepam
* Diclazepam
* Doxefazepam
* Elfazepam
* Estazolam
* Ethyl carfluzepate
* Ethyl dirazepate
* Ethyl loflazepate
* Etizolam
* EVT-201
* FG-8205
* Fletazepam
* Flubromazepam
* Flubromazolam
* Fludiazepam
* Flunitrazepam
* Flunitrazolam
* Flurazepam
* Flutazolam
* Flutemazepam
* Flutoprazepam
* Fosazepam
* Gidazepam
* Halazepam
* Haloxazolam
* Iclazepam
* Imidazenil
* Irazepine
* Ketazolam
* Lofendazam
* Lopirazepam
* Loprazolam
* Lorazepam
* Lormetazepam
* Meclonazepam
* Medazepam
* Menitrazepam
* Metaclazepam
* Mexazolam
* Midazolam
* Motrazepam
* N-Desalkylflurazepam
* Nifoxipam
* Nimetazepam
* Nitrazepam
* Nitrazepate
* Nitrazolam
* Nordazepam
* Nortetrazepam
* Oxazepam
* Oxazolam
* Phenazepam
* Pinazepam
* Pivoxazepam
* Prazepam
* Premazepam
* Proflazepam
* Pyrazolam
* QH-II-66
* Quazepam
* Reclazepam
* Remimazolam
* Rilmazafone
* Ripazepam
* Ro48-6791
* Ro48-8684
* SH-053-R-CH3-2′F
* Sulazepam
* Temazepam
* Tetrazepam
* Tolufazepam
* Triazolam
* Triflubazam
* Triflunordazepam (Ro5-2904)
* Tuclazepam
* Uldazepam
* Zapizolam
* Zolazepam
* Zomebazam

Carbamates|

* Carisbamate
* Carisoprodol
* Clocental
* Cyclarbamate
* Difebarbamate
* Emylcamate
* Ethinamate
* Febarbamate
* Felbamate
* Hexapropymate
* Lorbamate
* Mebutamate
* Meprobamate
* Nisobamate
* Pentabamate
* Phenprobamate
* Procymate
* Styramate
* Tetrabamate
* Tybamate

Flavonoids|

* 6-Methylapigenin
* Ampelopsin (dihydromyricetin)
* Apigenin
* Baicalein
* Baicalin
* Catechin
* EGC
* EGCG
* Hispidulin
* Linarin
* Luteolin
* Rc-OMe
* Skullcap constituents (e.g., baicalin)
* Wogonin

Imidazoles|

* Etomidate
* Metomidate
* Propoxate

Kava constituents|

* 10-Methoxyyangonin
* 11-Methoxyyangonin
* 11-Hydroxyyangonin
* Desmethoxyyangonin
* 11-Methoxy-12-hydroxydehydrokavain
* 7,8-Dihydroyangonin
* Kavain
* 5-Hydroxykavain
* 5,6-Dihydroyangonin
* 7,8-Dihydrokavain
* 5,6,7,8-Tetrahydroyangonin
* 5,6-Dehydromethysticin
* Methysticin
* 7,8-Dihydromethysticin
* Yangonin

Monoureides|

* Acecarbromal
* Apronal (apronalide)
* Bromisoval
* Carbromal
* Capuride
* Ectylurea

Neuroactive steroids|

* Acebrochol
* Allopregnanolone (brexanolone)
* Alfadolone
* Alfaxalone
* 3α-Androstanediol
* Androstenol
* Androsterone
* Certain anabolic-androgenic steroids
* Cholesterol
* DHDOC
* 3α-DHP
* 5α-DHP
* 5β-DHP
* DHT
* Etiocholanolone
* Ganaxolone
* Hydroxydione
* Minaxolone
* ORG-20599
* ORG-21465
* P1-185
* Pregnanolone (eltanolone)
* Progesterone
* Renanolone
* SAGE-105
* SAGE-324
* SAGE-516
* SAGE-689
* SAGE-872
* Testosterone
* THDOC
* Zuranolone

Nonbenzodiazepines|

* Cyclopyrrolones: Eszopiclone
* Pagoclone
* Pazinaclone
* Suproclone
* Suriclone
* Zopiclone

* Imidazopyridines: Alpidem
* DS-1
* Necopidem
* Saripidem
* Zolpidem

* Pyrazolopyrimidines: Divaplon
* Fasiplon
* Indiplon
* Lorediplon
* Ocinaplon
* Panadiplon
* Taniplon
* Zaleplon

* Others: Adipiplon
* CGS-8216
* CGS-9896
* CGS-13767
* CGS-20625
* CL-218,872
* CP-615,003
* CTP-354
* ELB-139
* GBLD-345
* Imepitoin
* JM-1232
* L-838,417
* Lirequinil (Ro41-3696)
* NS-2664
* NS-2710
* NS-11394
* Pipequaline
* ROD-188
* RWJ-51204
* SB-205,384
* SX-3228
* TGSC01AA
* TP-003
* TPA-023
* TP-13
* U-89843A
* U-90042
* Viqualine
* Y-23684

Phenols|

* Fospropofol
* Propofol
* Thymol

Piperidinediones|

* Glutethimide
* Methyprylon
* Piperidione
* Pyrithyldione

Pyrazolopyridines|

* Cartazolate
* Etazolate
* ICI-190,622
* Tracazolate

Quinazolinones|

* Afloqualone
* Cloroqualone
* Diproqualone
* Etaqualone
* Mebroqualone
* Mecloqualone
* Methaqualone
* Methylmethaqualone
* Nitromethaqualone
* SL-164

Volatiles/gases|

* Acetone
* Acetophenone
* Acetylglycinamide chloral hydrate
* Aliflurane
* Benzene
* Butane
* Butylene
* Centalun
* Chloral
* Chloral betaine
* Chloral hydrate
* Chloroform
* Cryofluorane
* Desflurane
* Dichloralphenazone
* Dichloromethane
* Diethyl ether
* Enflurane
* Ethyl chloride
* Ethylene
* Fluroxene
* Gasoline
* Halopropane
* Halothane
* Isoflurane
* Kerosine
* Methoxyflurane
* Methoxypropane
* Nitric oxide
* Nitrogen
* Nitrous oxide
* Norflurane
* Paraldehyde
* Propane
* Propylene
* Roflurane
* Sevoflurane
* Synthane
* Teflurane
* Toluene
* Trichloroethane (methyl chloroform)
* Trichloroethylene
* Vinyl ether

Others/unsorted|

* 3-Hydroxybutanal
* α-EMTBL
* AA-29504
* Avermectins (e.g., ivermectin)
* Bromide compounds (e.g., lithium bromide, potassium bromide, sodium bromide)
* Carbamazepine
* Chloralose
* Chlormezanone
* Clomethiazole
* DEABL
* Dihydroergolines (e.g., dihydroergocryptine, dihydroergosine, dihydroergotamine, ergoloid (dihydroergotoxine))
* DS2
* Efavirenz
* Etazepine
* Etifoxine
* Fenamates (e.g., flufenamic acid, mefenamic acid, niflumic acid, tolfenamic acid)
* Fluoxetine
* Flupirtine
* Hopantenic acid
* Lanthanum
* Lavender oil
* Lignans (e.g., 4-O-methylhonokiol, honokiol, magnolol, obovatol)
* Loreclezole
* Menthyl isovalerate (validolum)
* Monastrol
* Niacin
* Nicotinamide (niacinamide)
* Org 25,435
* Phenytoin
* Propanidid
* Retigabine (ezogabine)
* Safranal
* Seproxetine
* Stiripentol
* Sulfonylalkanes (e.g., sulfonmethane (sulfonal), tetronal, trional)
* Terpenoids (e.g., borneol)
* Topiramate
* Valerian constituents (e.g., isovaleric acid, isovaleramide, valerenic acid, valerenol)

* Unsorted benzodiazepine site positive modulators: α-Pinene
* MRK-409 (MK-0343)
* TCS-1105
* TCS-1205

See also: Receptor/signaling modulators • GABA receptor modulators • GABA metabolism/transport modulators

* v
* t
* e

Growth factor receptor modulators

Angiopoietin|

* Agonists: Angiopoietin 1
* Angiopoietin 4

* Antagonists: Angiopoietin 2
* Angiopoietin 3

* Kinase inhibitors: Altiratinib
* CE-245677
* Rebastinib

* Antibodies: Evinacumab (against angiopoietin 3)
* Nesvacumab (against angiopoietin 2)

CNTF|

* Agonists: Axokine
* CNTF
* Dapiclermin

EGF (ErbB)|

| EGF
(ErbB1/HER1)|

* Agonists: Amphiregulin
* Betacellulin
* EGF (urogastrone)
* Epigen
* Epiregulin
* Heparin-binding EGF-like growth factor (HB-EGF)
* Murodermin
* Nepidermin
* Transforming growth factor alpha (TGFα)

* Kinase inhibitors: Afatinib
* AG-490
* Agerafenib
* Brigatinib
* Canertinib
* Dacomitinib
* Erlotinib
* Gefitinib
* Grandinin
* Icotinib
* Lapatinib
* Neratinib
* Osimertinib
* Vandetanib
* WHI-P 154

* Antibodies: Cetuximab
* Depatuxizumab
* Depatuxizumab mafodotin
* Futuximab
* Imgatuzumab
* Matuzumab
* Necitumumab
* Nimotuzumab
* Panitumumab
* Zalutumumab

|

ErbB2/HER2|

* Agonists: Unknown/none

* Antibodies: Ertumaxomab
* Pertuzumab
* Trastuzumab
* Trastuzumab duocarmazine
* Trastuzumab emtansine

* Kinase inhibitors: Afatinib
* AG-490
* Lapatinib
* Mubritinib
* Neratinib

ErbB3/HER3|

* Agonists: Neuregulins (heregulins) (1, 2, 6 (neuroglycan C))

* Antibodies: Duligotumab
* Patritumab
* Seribantumab

ErbB4/HER4|

* Agonists: Betacellulin
* Epigen
* Heparin-binding EGF-like growth factor (HB-EGF)
* Neuregulins (heregulins) (1, 2, 3, 4, 5 (tomoregulin, TMEFF))

FGF|

| FGFR1|

* Agonists: Ersofermin
* FGF (1, 2 (bFGF), 3, 4, 5, 6, 8, 10 (KGF2), 20)
* Repifermin
* Trafermin
* Velafermin

|

FGFR2|

* Agonists: Ersofermin
* FGF (1, 2 (bFGF), 3, 4, 5, 6, 7 (KGF), 8, 9, 10 (KGF2), 17, 18, 22)
* Palifermin
* Repifermin
* Sprifermin
* Trafermin

* Antibodies: Aprutumab
* Aprutumab ixadotin

FGFR3|

* Agonists: Ersofermin
* FGF (1, 2 (bFGF), 4, 8, 9, 18, 23)
* Sprifermin
* Trafermin

* Antibodies: Burosumab (against FGF23)

FGFR4|

* Agonists: Ersofermin
* FGF (1, 2 (bFGF), 4, 6, 8, 9, 19)
* Trafermin

Unsorted|

* Agonists: FGF15/19

HGF (c-Met)|

* Agonists: Hepatocyte growth factor

* Potentiators: Dihexa (PNB-0408)

* Kinase inhibitors: Altiratinib
* AM7
* AMG-458
* Amuvatinib
* BMS-777607
* Cabozantinib
* Crizotinib
* Foretinib
* Golvatinib
* INCB28060
* JNJ-38877605
* K252a
* MK-2461
* PF-04217903
* PF-2341066
* PHA-665752
* SU-11274
* Tivantinib
* Volitinib

* Antibodies: Emibetuzumab
* Ficlatuzumab
* Flanvotumab
* Onartuzumab
* Rilotumumab
* Telisotuzumab
* Telisotuzumab vedotin

IGF|

| IGF-1|

* Agonists: des(1-3)IGF-1
* Insulin-like growth factor-1 (somatomedin C)
* IGF-1 LR3
* Insulin-like growth factor-2 (somatomedin A)
* Insulin
* Mecasermin
* Mecasermin rinfabate

* Kinase inhibitors: BMS-754807
* Linsitinib
* NVP-ADW742
* NVP-AEW541
* OSl-906

* Antibodies: AVE-1642
* Cixutumumab
* Dalotuzumab
* Figitumumab
* Ganitumab
* Robatumumab
* R1507
* Teprotumumab
* Xentuzumab (against IGF-1 and IGF-2)

|

IGF-2|

* Agonists: Insulin-like growth factor-2 (somatomedin A)

* Antibodies: Dusigitumab
* Xentuzumab (against IGF-1 and IGF-2)

Others|

* Binding proteins: IGFBP (1, 2, 3, 4, 5, 6, 7)

* Cleavage products/derivatives with unknown target: Glypromate (GPE, (1-3)IGF-1)
* Trofinetide

LNGF (p75NTR)|

* Agonists: BDNF
* BNN-20
* BNN-27
* Cenegermin
* DHEA
* DHEA-S
* NGF
* NT-3
* NT-4

* Antagonists: ALE-0540
* Dexamethasone
* EVT-901 (SAR-127963)
* Testosterone

* Antibodies: Against NGF: ABT-110 (PG110)
* ASP-6294
* Fasinumab
* Frunevetmab
* Fulranumab
* MEDI-578
* Ranevetmab
* Tanezumab

* Aptamers: Against NGF: RBM-004

* Decoy receptors: LEVI-04 (p75NTR-Fc)

PDGF|

* Agonists: Becaplermin
* Platelet-derived growth factor (A, B, C, D)

* Kinase inhibitors: Agerafenib
* Axitinib
* Crenolanib
* Imatinib
* Lenvatinib
* Masitinib
* Motesanib
* Nintedanib
* Pazopanib
* Radotinib
* Quizartinib
* Sunitinib
* Sorafenib
* Toceranib

* Antibodies: Olaratumab
* Ramucirumab
* Tovetumab

RET (GFL)|

| GFRα1|

* Agonists: Glial cell line-derived neurotrophic factor (GDNF)
* Liatermin

* Kinase inhibitors: Vandetanib

|

GFRα2|

* Agonists: Neurturin (NRTN)

* Kinase inhibitors: Vandetanib

GFRα3|

* Agonists: Artemin (ARTN)

* Kinase inhibitors: Vandetanib

GFRα4|

* Agonists: Persephin (PSPN)

* Kinase inhibitors: Vandetanib

Unsorted|

* Kinase inhibitors: Agerafenib

SCF (c-Kit)|

* Agonists: Ancestim
* Stem cell factor

* Kinase inhibitors: Agerafenib
* Axitinib
* Dasatinib
* Imatinib
* Masitinib
* Nilotinib
* Pazopanib
* Quizartinib
* Sorafenib
* Sunitinib
* Toceranib

TGFβ|

* See here instead.

Trk|

| TrkA|

* Agonists: Amitriptyline
* BNN-20
* BNN-27
* Cenegermin
* DHEA
* DHEA-S
* Gambogic amide
* NGF
* Tavilermide

* Antagonists: ALE-0540
* Dexamethasone
* FX007
* Testosterone

* Negative allosteric modulators: VM-902A

* Kinase inhibitors: Altiratinib
* AZD-6918
* CE-245677
* CH-7057288
* DS-6051
* Entrectinib
* GZ-389988
* K252a
* Larotrectinib
* Lestaurtinib
* Milciclib
* ONO-4474
* ONO-5390556
* PLX-7486
* Rebastinib
* SNA-120 (pegylated K252a))

* Antibodies: Against TrkA: GBR-900; Against NGF: ABT-110 (PG110)
* ASP-6294
* Fasinumab
* Frunevetmab
* Fulranumab
* MEDI-578
* Ranevetmab
* Tanezumab

* Aptamers: Against NGF: RBM-004

* Decoy receptors: ReN-1820 (TrkAd5)

|

TrkB|

* Agonists: 3,7-DHF
* 3,7,8,2'-THF
* 4'-DMA-7,8-DHF
* 7,3'-DHF
* 7,8-DHF
* 7,8,2'-THF
* 7,8,3'-THF
* Amitriptyline
* BDNF
* BNN-20
* Deoxygedunin
* Deprenyl
* Diosmetin
* DMAQ-B1
* HIOC
* LM22A-4
* N-Acetylserotonin
* NT-3
* NT-4
* Norwogonin (5,7,8-THF)
* R7
* R13
* TDP6

* Antagonists: ANA-12
* Cyclotraxin B
* Gossypetin (3,5,7,8,3',4'-HHF)

* Ligands: DHEA

* Kinase inhibitors: Altiratinib
* AZD-6918
* CE-245677
* CH-7057288
* DS-6051
* Entrectinib
* GZ-389988
* K252a
* Larotrectinib
* Lestaurtinib
* ONO-4474
* ONO-5390556
* PLX-7486

TrkC|

* Agonists: BNN-20
* DHEA
* NT-3

* Kinase inhibitors: Altiratinib
* AZD-6918
* CE-245677
* CH-7057288
* DS-6051
* Entrectinib
* GZ-389988
* K252a
* Larotrectinib
* Lestaurtinib
* ONO-4474
* ONO-5390556
* PLX-7486

VEGF|

* Agonists: Placental growth factor (PGF)
* Telbermin
* VEGF (A, B, C, D (FIGF))

* Allosteric modulators: Cyclotraxin B

* Kinase inhibitors: Agerafenib
* Altiratinib
* Axitinib
* Cabozantinib
* Cediranib
* Lapatinib
* Lenvatinib
* Motesanib
* Nintedanib
* Pazopanib
* Pegaptanib
* Rebastinib
* Regorafenib
* Semaxanib
* Sorafenib
* Sunitinib
* Toceranib
* Tivozanib
* Vandetanib
* WHI-P 154

* Antibodies: Alacizumab pegol
* Bevacizumab
* Icrucumab
* Ramucirumab
* Ranibizumab

* Decoy receptors: Aflibercept

Others|

* Additional growth factors: Adrenomedullin
* Colony-stimulating factors (see here instead)
* Connective tissue growth factor (CTGF)
* Ephrins (A1, A2, A3, A4, A5, B1, B2, B3)
* Erythropoietin (see here instead)
* Glucose-6-phosphate isomerase (GPI; PGI, PHI, AMF)
* Glia maturation factor (GMF)
* Hepatoma-derived growth factor (HDGF)
* Interleukins/T-cell growth factors (see here instead)
* Leukemia inhibitory factor (LIF)
* Macrophage-stimulating protein (MSP; HLP, HGFLP)
* Midkine (NEGF2)
* Migration-stimulating factor (MSF; PRG4)
* Oncomodulin
* Pituitary adenylate cyclase-activating peptide (PACAP)
* Pleiotrophin
* Renalase
* Thrombopoietin (see here instead)
* Wnt signaling proteins

* Additional growth factor receptor modulators: Cerebrolysin (neurotrophin mixture)

See also
Receptor/signaling modulators
Signaling peptide/protein receptor modulators
Cytokine receptor modulators

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

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*[SI]: Système International
*[v]: View this template
*[t]: Discuss this template
*[e]: Edit this template
*[AAS]: anabolic–androgenic steroid
*[AR]: Androgen receptor
*[SARMs]: Selective androgen receptor modulator
*[GPRC6A]: G protein-coupled receptor family C group 6 member A
*[ER]: Estrogen receptor
*[SERMs]: Selective estrogen receptor modulators
*[GPER]: G protein-coupled estrogen receptor
*[GABAA]: γ-Aminobutyric acid A