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Testosterone
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This article is about testosterone as a hormone. For its use as a medication, see Testosterone (medication). For other uses, see Testosterone (disambiguation).
Testosterone
Names
IUPAC name
(8R,9S,10R,13S,14S,17S)-17-hydroxy-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17- dodecahydrocyclopenta[a]phenanthren-3-one
Other names
Androst-4-en-17β-ol-3-one
Identifiers
CAS Number
58-22-0 Y
3D model (JSmol)
Interactive image
ChEBI
CHEBI:17347 Y
ChemSpider
5791 Y
DrugBank
DB00624 Y
ECHA InfoCard 100.000.336
KEGG
D00075 Y
PubChem CID
6013
UNII
3XMK78S47O Y
InChI[show]
InChI=1S/C19H28O2/c1-18-9-7-13(20)11-12(18)3-4-14-15-5-6-17(21)19(15,2)10-8-16(14)18/h11,14-17,21H,3-10H2,1-2H3/t14-,15-,16-,17-,18-,19-/m0/s1 Y
Key: MUMGGOZAMZWBJJ-DYKIIFRCSA-N Y
SMILES[show]
O=C4\C=C2/[C@]([C@H]1CC[C@@]3([C@@H](O)CC[C@H]3[C@@H]1CC2)C)(C)CC4
Properties
Chemical formula
C19H28O2
Molar mass 288.42 g/mol
Melting point 155
Pharmacology
ATC code
G03BA03 (WHO)
License data
EU EMA: by INN
Routes of
administration
Transdermal (gel, cream, solution, patch), by mouth (as testosterone undecanoate), in the cheek, intranasal (gel), intramuscular injection (as esters), subcutaneous pellets
Pharmacokinetics:
Bioavailability
Oral: very low (due to extensive first pass metabolism)
Protein binding
97.0–99.5% (to SHBG and albumin)[1]
Metabolism
Liver (mainly reduction and conjugation)
Biological half-life
2–4 hours[citation needed]
Excretion
Urine (90%), feces (6%)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Y verify (what is Y N ?)
Infobox references
Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.[2] In addition, testosterone is involved in health and well-being,[3] and the prevention of osteoporosis.[4] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] 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 7 to 8 times as great as in adult females.[6] As the metabolic consumption of testosterone in males is greater, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]
In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men and breast cancer in women.[10] 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. For more information on testosterone as a medication, see the testosterone (medication) article.
Contents
[hide]
1 Physiological effects
1.1 Before birth
1.2 Early infancy
1.3 Before puberty
1.4 Pubertal
1.5 Adult
1.5.1 Biological function
1.5.2 Health risks
1.5.3 Sexual arousal
1.5.3.1 Mammalian studies
1.5.3.2 Males
1.5.3.3 Females
1.5.4 Romantic relationships
1.5.5 Fatherhood
1.5.6 Motivation
1.5.7 Aggression and criminality
1.6 Brain
2 Biochemistry
2.1 Biosynthesis
2.2 Regulation
2.3 Distribution
2.4 Metabolism
3 Mechanism of action
3.1 Steroid hormone activity
3.2 Neurosteroid activity
4 Medical use
5 Other animals
6 History
7 See also
8 References
9 Further reading
Physiological effects[edit]
In general, androgens such as testosterone promote protein synthesis and thus growth of tissues with androgen receptors.[11] Testosterone can be described as having virilising and anabolic effects (though these categorical descriptions are somewhat arbitrary, as there is a great deal of mutual overlap between them).[12]
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.
Before birth[edit]
Effects before birth are divided into two categories, classified in relation to the stages of development.
The first period occurs between 4 and 6 weeks of the gestation. Examples include genital virilisation such as midline fusion, phallic urethra, scrotal thinning and rugation, and phallic enlargement; although the role of testosterone is far smaller than that of dihydrotestosterone. There is also development of the prostate gland and seminal vesicles.
During the second trimester, androgen level is associated with gender formation.[13] 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. A mother's testosterone level during pregnancy is correlated with her daughter's sex-typical behavior as an adult, and the correlation is even stronger than with the daughter's own adult testosterone level.[14]
Early infancy[edit]
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 4–6 months of age.[15][16] The function of this rise in humans is unknown. It has been speculated that "brain masculinization" is occurring since no significant changes have been identified in other parts of the body.[17] The male brain is masculinized by the aromatization of testosterone into estrogen, 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.[18]
Before puberty[edit]
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.[19]
Pubertal[edit]
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:[19][20]
Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement. Growth of jaw, brow, chin, nose, and remodeling of facial bone contours, in conjunction with human growth hormone.[21] 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[edit]
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.[22]
Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left.
Biological function[edit]
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (Hypothalamic–pituitary–adrenal axis) response under dominance challenge.[23] Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[24][25]
Health risks[edit]
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.[26][27][28]
Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] 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 glycemic control.[31]
High androgen levels are associated with menstrual cycle irregularities in both clinical populations and healthy women.[32]
Sexual arousal[edit]
See also: Hormones and sexual arousal
When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's)[citation needed]
Testosterone levels follow a nyctohemeral rhythm that peaks early each day, regardless of sexual activity.[33]
There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation was a key perception of the experience. There is no correlation between testosterone and men's perceptions of their orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either sex.[34]
Sexual arousal and masturbation in women produce small increases in testosterone concentrations.[35] The plasma levels of various steroids significantly increase after masturbation in men and the testosterone levels correlate to those levels.[36]
Mammalian studies[edit]
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 behaviors (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 suffering from sexual arousal deficits such as hypoactive sexual desire disorder.[37]
In 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.[38]
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.[39] 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.).[39]
Sperm competition theory: Testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] 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[edit]
In men, higher levels of testosterone are associated with periods of sexual activity.[41] Testosterone also increased in heterosexual men after having had a brief conversation with a woman. The increase in testosterone levels was associated with the degree that the women thought the men were trying to impress them.[42]
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.[43] Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion.[44] A link has also been found between relaxation following sexual arousal and testosterone levels.[45]
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[46] This may be linked to the ovulatory shift hypothesis,[47] where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.
Men with lower thresholds for sexual arousal have a greater likelihood to attend to sexual information and that testosterone may work by enhancing their attention to the relevant stimuli.[48]
Females[edit]
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[49] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[50] 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.[51]
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[52]
Testosterone may prove to be an effective treatment in female sexual arousal disorders,[53] 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 off-label 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.[53]
Romantic relationships[edit]
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.[54] However, it is suggested that after the "honeymoon phase" ends—about one to three years into a relationship—this change in testosterone levels is no longer apparent.[54] Men who produce less testosterone are more likely to be in a relationship[55] and/or married,[56] and men who produce more testosterone are more likely to divorce;[56] however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels.[57] 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.[58] Married men who engage in bond-maintenance activities such as spending the day with their spouse/and 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 are more relevant to changes in testosterone levels.[59]
Men who produce more testosterone are more likely to engage in extramarital sex.[56] Testosterone levels do not rely on physical presence of a partner for men engaging in relationships (same-city vs. long-distance), men have similar testosterone levels across the board.[55] 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.[60]
Fatherhood[edit]
Fatherhood also decreases testosterone levels in men, suggesting that the resulting emotional and behavioral changes promote paternal care.[61] The way testosterone levels change when a child is in distress is indicative of fathering styles. If the levels reduce, then there is more empathy by the father than in fathers whose levels go up.[62]
Motivation[edit]
Testosterone levels play a major role in risk-taking during financial decisions.[63][64] Even in an intellectual activity such as a chess tournament or a final examination, prior testosterone levels can accurately predict which individuals will be motivated to do their best.[65][66]
Aggression and criminality [edit]
See also: Aggression § Testosterone, and Biosocial criminology
Most studies support a link between adult criminality and testosterone, although the relationship is modest if examined separately for each sex. Nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done on the relationship between more general aggressive behavior/feelings and testosterone. About half the studies have found a relationship and about half no relationship.[67]
Testosterone is only one of many factors that influence aggression and the effects of previous experience and environmental stimuli have been found to correlate more strongly. A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression.[67][68][69][70] Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.[71]
The sexual hormone can encourage fair behavior. For the 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.[72][73][74] However men with high testosterone were significantly 27% less generous in an ultimatum game while men with the lowest testosterone were 560% more generous.[75] The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence.[76] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.[77]
Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.[78] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.[78] Thus it is the challenge of competition among males of the species that facilitates aggression and violence.[78] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.[78] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[78]
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[79][80] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[79] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. 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.[81] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[82][83][84][85][86]
The rise in testosterone levels during competition predicted aggression in males but not in females.[87] Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression.[88] Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations.[89] Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and to physical violence.[90] Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli.[91] Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.[92]
Estradiol is known to correlate with aggression in male mice.[93] Moreover, the conversion of testosterone to estradiol regulates male aggression in sparrows during breeding season.[94] Rats who were given anabolic steroids that increase testosterone were also more physical aggressive to provocation as a result of "threat sensitivity".[95]
Brain[edit]
The brain is also affected by this sexual differentiation;[13] 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 diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[96]
There are some differences between a male and female brain (possibly the result of different testosterone levels), one of them being size: the male human brain is, on average, larger.[97] Men were found to have a total myelinated fiber length of 176,000 km at the age of 20, whereas in women the total length was 149,000 km (approx. 15% less).[98]
No immediate short term effects on mood or behavior were found from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men.[99] A correlation between testosterone and risk tolerance in career choice exists among women.[63][100]
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,[101][102][103][104] 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,[105] where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.
Biochemistry[edit]
Human steroidogenesis, showing testosterone near bottom.[106]
Biosynthesis[edit]
Like other steroid hormones, testosterone is derived from cholesterol (see figure).[107] 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.[108] 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.[109] In the testes, testosterone is produced by the Leydig cells.[110] 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).
Regulation[edit]
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.[111]
The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (see figure to the right).[112] 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.[113][114] This effect is sometimes referred to as andropause or late-onset hypogonadism.[115]
Exercise: Resistance training increases testosterone levels,[116] however, in older men, that increase can be avoided by protein ingestion.[117] Endurance training in men may lead to lower testosterone levels.[118]
Nutrients: Vitamin A deficiency may lead to sub-optimal plasma testosterone levels.[119] The secosteroid vitamin D in levels of 400–1000 IU/d (10–25 µg/d) raises testosterone levels.[120] Zinc deficiency lowers testosterone levels[121] but over-supplementation has no effect on serum testosterone.[122]
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.[123] However no clear association between body mass index and testosterone levels has been found.[124]
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[125] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[126] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[127][128][129] Licorice can decrease the production of testosterone and this effect is greater in females.[130]
Distribution[edit]
In plasma, 98% of testosterone is bound to protein, with 65% bound to sex hormone-binding globulin (SHBG) and 33% bound weakly to albumin.[131] Plasma testosterone level in the body (free or bound): 10.4–24.3 nmol/L in adult men.[citation needed] In women: 30–70 ng/dL.
Metabolism[edit]
Both testosterone and 5α-DHT are metabolized mainly in the liver.[1][132] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[1] 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.[1][132][133] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[1][132] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[1][132][133] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[132]
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.[1][132] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α,5α-androstanediol and 3α,5β-androstanediol, respectively.[1][132] Subsequently, 3α,5α-androstanediol and 3α,5β-androstanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][132] 3β,5α-Androstanediol and 3β,5β-androstanediol 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.[134][135] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[133]
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.[136] 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[136] 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.[136] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[136][137] Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[136]
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.[132] 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][132][138][139] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[140] skin, hair follicles, and brain[141] and aromatase is highly expressed in adipose tissue, bone, and the brain.[142][143] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[133] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[144] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[145]
Mechanism of action[edit]
Steroid hormone activity[edit]
The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[146][147] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[148][149][150]
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 (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[151] 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).[152] 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.[153]
Neurosteroid activity[edit]
Testosterone, via its active metabolite 3α-androstanediol, is a potent positive allosteric modulator of the GABAA receptor.[154]
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).[155][156][157] In contrast to testosterone, DHEA and DHEA sulfate have been found to act as high-affinity agonists of these receptors.[155][156][157]
Testosterone is an antagonist of the sigma σ1 receptor (Ki = 1,014 or 201 nM).[158] 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).[159]
Medical use[edit]
Main article: Testosterone (medication)
Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer,[10] and gender dysphoria in transgender men. 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.[160] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[161]
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.[162] It is available as a generic medication.[10] The price depends on the form of testosterone used.[163] 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.[10]
Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[10] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[10] Women and children who are exposed may develop virilization.[10] It is recommended that individuals with prostate cancer not use the medication.[10] It can cause harm if used during pregnancy or breastfeeding.[10]
Other animals[edit]
Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in gnathostomes (jawed vertebrates).[164] Agnathans (jawless vertebrates) such as lampreys don't produce testosterone but instead use androstenedione as a male sex hormone.[165] Fish make a slightly different form called 11-ketotestosterone.[166] Its counterpart in insects is ecdysone.[167] The presence of these ubiquitous steroids in a wide range of animals suggest that sex hormones have an ancient evolutionary history.[168]
History[edit]
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).[169] 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,[170] 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, remasculinized them.[171] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but 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 (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
Nobel Prize winner, Leopold Ruzicka of Ciba, a pharmaceutical industry giant that synthesized testosterone.
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)".[172] 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.[173][174]
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[175] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[176] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[174][177] 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[178] 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",[179] and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[180]
See also[edit]
Chemistry portal
Molecular and cellular biology portal
Pharmacy and Pharmacology portal
List of androgens/anabolic steroids
References[edit]
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Further reading[edit]
Fargo KN, Pak TR, Foecking EM, Jones KJ (2010). "Molecular Biology of Androgen Action: Perspectives on Neuroprotective and Neurotherapeutic Effects.". In Pfaff DW, Etgen AM. Molecular Mechanisms of Hormone Actions on Behavior. Elsevier Inc. pp. 1219–1246. doi:10.1016/B978-008088783-8.00036-X. ISBN 978-0-12-374939-0.
Dowd, Nancy E. (2013). "Sperm, testosterone, masculinities and fatherhood". Nevada Law Journal, special issue: Men, Masculinities, and Law: A Symposium on Multidimensional Masculinities Theory. William S. Boyd School of Law. 13 (2): 8.
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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
3α,5β-Androstanediol
3β,5β-Androstanediol
5β-Androstanedione
5β-Dihydrotestosterone
Androstanetriols
Androstenediol sulfate
Androsterone glucuronide
Androsterone sulfate
Dihydrotestosterone glucuronide
Dihydrotestosterone sulfate
Etiocholanolone
Etiocholanolone glucuronide
Epietiocholanolone
Testosterone glucuronide
Testosterone sulfate
Estrogens
Estranes: Estetrol
Estradiol
Estrone
Estriol
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 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
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
[show]
v
t
e
Androgens and antiandrogens
Androgens
(incl. AAS)
AR agonists
Testosterone derivatives: Androstenediol dipropionate
Boldenone undecylenate
Clostebol
Clostebol acetate
Clostebol caproate
Clostebol propionate
Cloxotestosterone acetate
Dehydroepiandrosterone (DHEA) (androstenolone, prasterone)
DHEA enanthate (prasterone enanthate)
Quinbolone
Testosterone#
Testosterone esters (e.g., testosterone cypionate, testosterone enanthate, testosterone propionate, testosterone undecanoate, testosterone ester mixtures (Deposterona, Omnadren, Sustanon, Testoviron Depot))
Dihydrotestosterone derivatives: Bolazine capronate
Dihydrotestosterone (DHT) (androstanolone, stanolone)
Dihydrotestosterone esters
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 (+esterified estrogens)
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), lynestrenol, norgestrienone)
Tibolone
Progesterone derivatives: Medroxyprogesterone acetate
Progonadotropins
Antiestrogens (e.g., tamoxifen, clomifene)
GnRH agonists (e.g., GnRH (gonadorelin), leuprorelin)
Gonadotropins (e.g., LH, hCG)
Antiandrogens
AR antagonists
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)
Steroidogenesis
inhibitors
5α-Reductase
Alfatradiol
Dutasteride (+tamsulosin)
Epristeride
Finasteride
Saw palmetto extract
Others
Abiraterone acetate
Aminoglutethimide
Bifluranol
Cyproterone acetate
Flutamide
Ketoconazole
Nilutamide
Seviteronel†
Spironolactone
Antigonadotropins
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, medroxyprogesterone acetate, megestrol acetate)
Others
Androstenedione immunogens: Androvax (androstenedione albumin)
Ovandrotone albumin (Fecundin)
#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
[show]
Biological activity
[show]
v
t
e
Androgen receptor modulators
AR
Agonists
Testosterone derivatives: 4-Androstenediol
4-Dehydroepiandrosterone (4-DHEA)
4-Hydroxytestosterone
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
Dihydrofluoxymesterone
Dihydrotestosterone (DHT) (androstanolone, stanolone)
Dihydrotestosterone esters
Drostanolone
Drostanolone propionate
Epiandrosterone
Epitiostanol
Mepitiostane
Mesabolone
Mesterolone
Mesterolone cipionate
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
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
Trestolone (MENT)
Trestolone acetate
Dihydrotestosterone and 19-nortestosterone derivatives: 5α-Dihydronandrolone
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
Dimethyltrienolone (7α-methylmetribolone, 7α,17α-dimethyltrenbolone)
Ethyldienolone
Ethylestrenol
Methyldienolone
Methylhydroxynandrolone (MOHN, MHN)
Metribolone
Mibolerone
Norboletone
Norethandrolone
Propetandrol
Tetrahydrogestrinone
17α-Vinyltestosterone derivatives: Norvinisterone (vinylnortestosterone)
Vinyltestosterone
17α-Ethynyltestosterone derivatives: Δ4-Tibolone
Danazol
Desogestrel
Ethisterone (ethynyltestosterone)
Etonogestrel
Etynodiol
Etynodiol diacetate
Gestodene
Gestrinone
Levonorgestrel
Levonorgestrel butanoate
Lynestrenol
Norethisterone
Norethisterone acetate
Norethisterone acetate oxime
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: MK-0773
TFM-4AS-1
YK-11
Antagonists
Steroidal: 7α-Thioprogesterone
7α-Thiospironolactone
7α-Thiomethylspironolactone
9,11-Dehydrocortexolone 17α-butyrate (CB-03-04)
11α-Hydroxyprogesterone
15β-Hydroxycyproterone acetate
Abiraterone
Abiraterone acetate
Allyltestosterone
Benorterone
BOMT
Canrenoic acid
Canrenone
Chlormadinone acetate
Clometerone
Cortexolone 17α-propionate (CB-03-01)
Cyproterone
Cyproterone acetate
Delanterone
Delmadinone acetate
Dicirenone
Dienogest
Drospirenone
Edogestrone
Epitestosterone
Galeterone
Guggulsterone
Medrogestone
Megestrol acetate
Mespirenone
Metogest
Mexrenone
Mifepristone
Nomegestrol acetate
Nordinone
Osaterone
Osaterone acetate
Oxendolone
Potassium canrenoate
Prorenone
Rosterolone
SC-5233 (spirolactone)
Spironolactone
Spirorenone
Spiroxasone
Topterone
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-641988
Cimetidine
Cioteronel
Darolutamide
DDT (via metabolite p,p’-DDE)
Dieldrin
DIMP
Endosulfan
Enzalutamide
EPI-001
Fenarimol
Flutamide
Hydroxyflutamide
Inocoterone
Inocoterone acetate
Ketoconazole
Lavender oil
LG-105
LG-120907
Linuron
Methiocarb
N-Butylbenzenesulfonamide
N-Desmethylenzalutamide
Nilutamide
ONC1-13B
ORM-15341
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, magnesium, strontium, zinc)
Dehydroandrosterone
Dihydrotestosterone
Estradiol
L-α-Amino acids (incl. L-arginine, L-lysine, L-ornithine)
Osteocalcin
SHBG
Testosterone
See also
Receptor/signaling modulators
Androgens and antiandrogens
Estrogen receptor modulators
Progesterone receptor modulators
List of androgens/anabolic steroids
[show]
v
t
e
Estrogen receptor modulators
ER
Agonists
Steroidal: 2-Hydroxyestradiol
2-Hydroxyestrone
3-Methyl-19-methyleneandrosta-3,5-dien-17β-ol
3α-Androstanediol
3β-Androstanediol
4-Androstenediol
4-Androstenedione
4-Hydroxyestradiol
4-Hydroxyestrone
4-Methoxyestradiol
4-Methoxyestrone
5-Androstenediol
7-Oxo-DHEA
7α-Hydroxy-DHEA
7β-Hydroxyepiandrosterone
8,9-Dehydroestradiol
8,9-Dehydroestrone
8β-VE2
10β,17β-Dihydroxyestra-1,4-dien-3-one (DHED)
16α-Hydroxy-DHEA
16α-Hydroxyestrone
16α-Iodo-E2
16α-LE2
16β,17α-Epiestriol (16β-hydroxy-17α-estradiol)
17α-Dihydroequilenin
17α-Dihydroequilin
17α-Epiestriol (16α-hydroxy-17α-estradiol)
17β-Dihydroequilenin
17β-Dihydroequilin
Abiraterone
Abiraterone acetate
17α-Estradiol (alfatradiol)
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 estrogens
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
Estrofurate
Estromustine
Estrone
Estrone esters
Estropipate
Etamestrol (eptamestrol)
Ethinylestradiol
Ethinylestradiol sulfonate
Ethinylestriol
Etynodiol diacetate
Hexolame
Hippulin
Hydroxyestrone diacetate
Mestranol
Methylestradiol
Moxestrol
Mytatrienediol
Nilestriol
Noretynodrel
Orestrate
Pentolame
Prodiame
Prolame
Promestriene
Quinestradol
Quinestrol
Nonsteroidal: (R,R)-THC
(S,S)-THC
2,8-DHHHC
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-200070
WAY-214156
Unknown/unsorted: ERB-26
ERA-45
ERB-79
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, epicatechin, equol, formononetin, glabrene, glabridin, genistein, genistin, glycitein, kaempferol, liquiritigenin, mirificin, myricetin, naringenin, penduletin, pinocembrin, prunetin, puerarin, quercetin, tectoridin, tectorigenin)
Lavender oil
Lignans (e.g., enterodiol, enterolactone, nyasol (cis-hinokiresinol))
Metalloestrogens (e.g., cadmium)
Pesticides (e.g., alternariol, dieldrin, endosulfan, fenarimol, methiocarb, methoxychlor, triclocarban, triclosan)
Phytosteroids (e.g., digitoxin (digitalis), diosgenin, guggulsterone)
Phytosterols (e.g., β-sitosterol, campesterol, stigmasterol)
Resorcylic acid lactones (e.g., zearalanone, α-zearalenol, β-zearalenol, zearalenone, zeranol (α-zearalanol), taleranol (teranol, β-zearalanol))
Steroid-like (e.g., deoxymiroestrol, miroestrol)
Stilbenoids (e.g., resveratrol)
Synthetic xenoestrogens (e.g., alkylphenols, bisphenols (e.g., BPA, BPF, BPS), DDT, parabens, PBBs, PHBA, phthalates, PCBs)
Others (e.g., agnuside, rotundifuran)
Mixed
(SERMs)
2-Phenylbenzofuran
2-Phenylbenzothiophene
4'-Hydroxynorendoxifen
27-Hydroxycholesterol
Acefluranol
Acolbifene
Afimoxifene
Anordiol
Anordrin
Arzoxifene
Bazedoxifene
Brilanestrant
Broparestrol
Elacestrant
Chlorotrianisene
Clomifene
Clomifenoxide
Cyclofenil
D-15413
Droloxifene
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
Ormeloxifene
Ospemifene
Panomifene
Pipendoxifene
Raloxifene
Spironolactone
SS1010
Tamoxifen
TAS-108 (SR-16234)
Tibolone
Toremifene
Trioxifene
TZE-5323
Y-134
Zindoxifene
Zuclomifene
Antagonists
(R,R)-THC
7β-Hydroxy-DHEA
Chloroindazole
Cytestrol acetate
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
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
[show]
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-217
SAGE-324
SAGE-516
SAGE-689
SAGE-872
Testosterone
THDOC
Nonbenzodiazepines
β-Carbolines: Abecarnil
Gedocarnil
Harmane
SL-651,498
ZK-93423
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
[show]
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
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
Retrieved from "https://en.wikipedia.org/w/index.php?title=Testosterone&oldid=818406881"
Categories:
Androgens and anabolic steroids
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Hormones of the testis
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Neuroendocrinology
Human hormones
Sex hormones
Testosterone
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Testosterone (disambiguation)

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The chemical structure of testosterone.

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ECHA InfoCard

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