Common medications in HRT

Authors: Zennith and Roo.
First posted: 2023-11-29

Hormone Replacement Therapy (HRT) is a major tool in the toolbox for gender affirming care. For most patients, whether they have goals in the direction of either feminization or masculinization, the medications in use are safe and effective.

There are many medications in use. There are different drugs, available in different dosages, and even available in different formats (like pills, versus skin patches, versus injections). In this page, we want to introduce you to medications being used for feminization, masculinization, and even non-binary treatments. 

While we cannot cover all the details, and we may make mistakes in our discussion below, we hope to uncover some of the mystique for you. This will help you be a more informed and active patient, working together with your medical professionals to make the best decisions for your care. Please remember, this page is for general educational purposes only. This page is not a recommendation to use, or not use, any medications discussed (or not discussed), and is not medical advice.

The ways the medications work are interesting as well. For a more conceptual discussion of how these medications work, our page Biological Concepts in HRT provides a good overview.

1 – Transfeminine medications

Feminizing therapies generally include an estrogen source, and for patients with testes, additionally tend to include an antiandrogen (testosterone/androgen lowering medication) (spironolactone in the US, cyproterone acetate in most of Europe, and Gonadotropin Releasing Hormone agonists in the UK). (Mamoojee et al., 2017, Angus et al, Clinical Endocrinology, 2021; Kuijpers et al., 2021, Coleman et al, Int J Transgend Health, 2022). 

The standard of care for feminizing therapy is that for most patients, estrogen combined with an antiandrogen is effective and has satisfactorily low risk (Coleman et al, Int J Transgend Health, 2022). However, there is relatively little comparative data between different antiandrogens. In addition, since combination therapies are common, it is often difficult to determine whether effects from a treatment (whether positive effects or side effects) are specifically due to the estrogen source, due to the antiandrogen, or due to a combined synergistic effect.

Main physical effects include “breast development (usually to Tanner stage 2 or 3), a redistribution of facial and body subcutaneous fat, reduction of muscle mass, reduction of body hair (and to a lesser extent, facial hair), change in sweat and odor patterns, and arrest and possible reversal of scalp hair loss” (Deutsch, UCSF, 2016-Fem). Feminizing therapy may also cause a wider range of emotions, as well as a potential change to libido (Deutsch, UCSF, 2020-Fem).

1.1 – Estrogens

Estradiol (E2) is a name used both for a naturally occurring estrogen hormone and a medication delivering the E2 hormone to the recipient. As a medication, it is considered to be “bioidentical” to endogenous estrogen in how it is processed by estrogen receptors. E2 can be administered by way of several different routes depending on the patient and physician. Generally speaking, the bioavailability and effectiveness of the estrogen produced will be higher in administration methods that have a shorter path to the bloodstream, such as with injections, subdermal implants, and patches. However, oral and topical applications are also available. (https://en.wikipedia.org/wiki/Estradiol_(medication))

Depending on where in the world you live, it may be more common to be prescribed a prodrug variant of E2 (i.e., estradiol valerate or cypionate) rather than in its more “pure” form. The downstream effects of taking one of the prodrug variants are typically identical to those one would experience on E2 alone (https://go.drugbank.com/drugs/DB13954). There exist some anecdotal claims that a prodrug variant may work more or less effectively than other options; for this reason, it is ideal to work with your physician to determine how you are responding to the medication you are prescribed.

Estradiol valerate (E2V) is a prodrug and ester of estradiol, in which estradiol is compounded with valeric acid. Since estradiol on its own has a relatively low bioavailability through some administration methods, creation of a prodrug like E2V aims to help improve the bioavailability of the estradiol, especially in oral and intramuscular injection methods. After it is administered, it typically results in the same downstream effects of endogenous estradiol or E2. (https://go.drugbank.com/drugs/DB13956) As mentioned above, anecdotal reports suggest that some individuals may experience slight differences in effectiveness across the different estrogen prodrugs, so it is ideal to work closely with your physician to determine what the best medication options are for you.

E2V in its oral form is more commonly seen in Europe. While oral E2V is available in the USA, it is not prescribed for the purposes of transgender HRT therein. As an intramuscular injection, however, it is available all around the world. (https://en.wikipedia.org/wiki/Estradiol_valerate#Availability)

Estradiol cypionate (EC) is a prodrug and ester of estradiol, in which estradiol is compounded with cypionic acid. Since estradiol on its own has a relatively low bioavailability through some administration methods, creation of a prodrug like EC aims to help improve the bioavailability of the estradiol, especially in oral and intramuscular injection methods. After it is administered, it typically results in the same downstream effects of endogenous estradiol or E2. (https://go.drugbank.com/drugs/DB13954) As mentioned above, anecdotal reports suggest that some individuals may experience slight differences in effectiveness across the different estrogen prodrugs, so it is ideal to work closely with your physician to determine what the best medication options for you.

EC is primarily available in the USA, with some limited availability in Southeast Asia and other parts of the world. (https://en.wikipedia.org/wiki/Estradiol_cypionate#Availability)

Conjugated estrogens (CEs) refers to an estrogen medication created with a mixture of estrogen salts which can be manufactured synthetically, or more historically with urine from pregnant horses. Its intended and observed effects are for the most part similar to that of endogenous estrogen or prodrugs of estradiol. In decades past, it has been one of the most commonly prescribed estrogen medications for the purposes of HRT. More recently however, CEs’ use in HRT has declined; CEs have a more pronounced effect on the liver and a comparatively higher risk of blood clots and cardiovascular issues compared to bioidentical estradiol and its prodrug variants.

CEs are widely available throughout the world. (https://en.wikipedia.org/wiki/Conjugated_estrogens)

Ethinylestradiol is a molecule similar to estradiol, modified to be far more stable. It is generally used in a contraceptive setting (Deutsch, UCSF, 2016-Fem). While it has a “better” ability to stay in the body’s circulation and affect estrogen receptors, it is associated with increased risks of blood clots, and its use is discouraged in the current standard of care for gender affirmation (Coleman et al, Int J Transgend Health, 2022).

Estriol is a weak estrogen generally used for menopausal hormone therapy, e.g. to help resolve hot flashes and vaginal inflammation (https://en.wikipedia.org/wiki/Estriol_(medication)), and is currently of lower interest for gender affirmation therapies.

1.2 – Antiandrogens

Medications that lower testosterone (and related androgens) are referred to as antiandrogens. Antiandrogens can work through a variety of ways, ranging from indirect to more direct. Antiandrogens that work indirectly might, for example, reduce the body’s signals that lead to the creation of testosterone. On the other hand, antiandrogens that work directly might either block the chemical reactions that create testosterone or dihydrotestosterone (DHT), or might block receptors to prevent them from detecting any testosterone or DHT present.

Spironolactone (Spiro) is used as an antiandrogen in gender affirmation contexts. Even though its strongest binding target is mineralocorticoid receptors, Spiro still has strong antagonistic binding affinity for the androgen receptor, and agonistic binding of the progesterone receptor (https://en.wikipedia.org/wiki/Pharmacodynamics_of_spironolactone; Gomez-Sanches, J Cardiovasc Pharmacol, 2016; Gabbard et al, Biomolecules, 2020). Spiro is the main antiandrogen prescribed for gender affirmation in the United States (Deutsch, UCSF, 2016-Fem).

Spironolactone, by itself, has uncertain effect on the production of testosterone when it is used at clinically relevant concentrations in humans (Aly, Transfem Science, 2018). When Spiro is combined with estrogen, suppression of circulating testosterone levels has been demonstrated, but the reduction might be due to action by estrogen (Aly, Transfem Science, 2018; Deutsch et al, Obstetrics & Gynecology, 2015; Leinung et al, Transgender Health, 2018; Angus et al, Clinical Endocrinology, 2021; Angus et al, Endocrine Connections, 2019). But again, it is important to keep in mind that Spiro is known to act as an androgen receptor antagonist, reducing actual androgen receptor activity even if testosterone is present. 

WPATH SOC-8 guidelines for transfeminine patients taking estrogen include a recommendation to combine treatment with an antiandrogen such as spironolactone (or alternately, cyproterone acetate, discussed later, or GnRH agonists) if they have testes (Coleman et al, Int J Transgend Health, 2022). More specifically, for Spiro, guidelines recommend dosages of 100 to 300 mg/day (Coleman et al, Int J Transgend Health, 2022). 

Spiro is, like other antiandrogens, used with the intention of promoting feminizing effects including reduction of body hair and acne; softening skin; redistributing fat to follow feminine patterns; and developing feminine sexual characteristics including possible breast growth while suppressing masculine ones (Coleman et al, Int J Transgend Health, 2022; Deutsch, UCSF, 2016-Fem). 

Some of the more common side effects include dehydration and frequent urination (Coleman et al, Int J Transgend Health, 2022), drowsiness or dizziness (NHS, retrieved 2023), and reduction in libido.

An uncommon but serious risk of combined estrogen and Spiro treatment is thromboembolic events/blood clots (Coleman et al, Int J Transgend Health, 2022).

Hyperkalemia – excess potassium in the blood, which can be dangerous – is also often named as a risk with Spiro use, but is interpreted as uncommon and manageable according to WPATH SOC-8 guidelines (Millington et al, J Endocr Soc, 2019; Coleman et al, Int J Transgend Health, 2022). Guidelines suggest that for “individuals receiving spironolactone, serum electrolytes, in particular potassium, and kidney function, in particular creatinine, should be monitored” (Coleman et al, Int J Transgend Health, 2022).

Cyproterone acetate (CyprAc) is an antiandrogen that mainly inhibits androgen signaling by activating the progesterone receptor. At higher doses, CyprAc additionally directly binds to and inhibits the androgen receptor (Angus et al, Clinical Endocrinology, 2021; Kuhl, Climacteric, 2005). CyprAc is not available in the United States, but is approved for use in other countries including in the European Union (Angus et al, Clinical Endocrinology, 2021).

When used for gender affirmation purposes, CyprAc, in combination with estrogen, has been demonstrated to reduce testosterone levels, approaching the female reference range (Fung R et al, Int J Transg, 2017; Angus et al, Endocrine Connections, 2019). In particular, CyprAc doses of as low as 10 mg per day have been demonstrated to be effective in combination therapy, and are recommended by WPATH SOC-8 (Coleman et al, Int J Transgend Health, 2022).

CyprAc is, like other antiandrogens, used with the intention of promoting feminizing effects including reduction of body hair and acne; softening skin; redistributing fat to follow feminine patterns; and developing feminine sexual characteristics including possible breast growth while suppressing masculine ones (Coleman et al, Int J Transgend Health, 2022; Deutsch, UCSF, 2016-Fem). Reduction in libido is a common side effect of cyproterone acetate. 

CyprAc, when combined with estrogen, might be associated with increased risks thromboembolic events/blood clots, but this largely seems to correlate with excessively CyprAc high dosage, or the use of estrogen sources that do not follow the best-practice of non-oral (e.g. transdermal) delivery of 17β-estradiol (Asscheman et al, Andrologica, 2014). 

Additionally, CyprAc increases the risk of developing meningioma (excessive growth of a membrane surrounding the nervous system, causing physical pressure on it). While the risk appears low in absolute terms within a time window of a few years (0.0207% per person per year over a study’s followup period) (Weill et al, BMJ, 2021), we have not seen any studies that track very long-term use (i.e. decades). It is hard to say whether extended use of low doses of CyprAc would, or would not, increase cumulative risk of meningiomas (Lee et al, Scientific Reports, 2022). Mechanistically, since CyprAc targets the progesterone and androgen receptors at different concentrations, dosage would necessarily have a profound effect on risks and side effects. 

Finally, liver damage has been identified as a risk of cyproterone acetate use, but this has largely been studied when using CyprAc at very high dosages (>= 200 mg/day), i.e. as a drug for prostate cancer (NIH, 2012; Savidou et al, World J Gastroenterol, 2006).

If you are in a country where doctors prescribe cyproterone acetate, and your doctor is considering prescribing it to you, remember to double check dosage with your doctor (Coleman et al, Int J Transgend Health, 2022), and ask your doctor about any special considerations, such as monitoring for side effects, and to get advice such as whether or not you should temporarily stop taking the medication around a surgery, or if you should stop taking it if you receive an orchiectomy (Asscheman et al, Andrologia, 2014).

GnRH modulators are another effective, and well-established, option for antiandrogen medication and are commonly used in the United Kingdom. We will expand discussion on them in a later version of this page.

Bicalutamide is an androgen receptor antagonist (Angus et al, Clinical Endocrinology, 2021). However, there is little data about its effectiveness or safety in gender affirmation procedures, and WPATH SOC-8 does not recommend its use (Coleman et al, Int J Transgend Health, 2022). Interest in bicalutamide is increasing for gender affirmation, but it is still early stage and less supported by evidence than the antiandrogens currently used as the standard of care (https://transfemscience.org/articles/bica-adoption/).

Finasteride and dutasteride are 5ɑ reductase inhibitors, generally taken orally (but finasteride is also available as a cream). They suppress enzymes that convert testosterone into a more active form, dihydrotestosterone. 

Generally speaking, finasteride and dutasteride are used in a dermatology context, e.g. attenuating male-pattern baldness. They are not as commonly used for gender affirming feminizing therapy (Coleman et al, Int J Transgend Health, 2022). In addition, inhibition of 5ɑ reductase has little effect on the other androgens, including testosterone, circulating in the body, implying a possible need for combination with a second antiandrogen anyway. Nevertheless, these may be useful for some patients; medical professionals can help you figure out if these drugs are appropriate for your goals.

1.3 – Progestogens or progestins

There are anecdotes of patients using progestins (synthetic progestogens) with aims of improving breast development, mood, and libido (Deutsch, UCSF, 2016-Fem). However, there is debate in the field as to whether progestins should actually be used, discussed in the WPATH SOC-8 guidelines. WPATH SOC-8 generally recommends against the use of progestins, except that they make a positive recommendation for using cyproterone acetate when it is used as an antiandrogen and combined with estrogen (Coleman et al, Int J Transgend Health, 2022). 

Scientific support of other progestins’ safety and effectiveness is sparse for feminizing HRT. Notably, scientific support in favor of cyproterone acetate tends to focus on its ability to reduce testosterone levels, whereas evidence of other potentially desirable outcomes of cyproterone acetate/progestin use (breast development, mood, libido) is hard to find. 

Other progestogens/progestins include progesterone (including micronized progesterone), dienogest, desogestrel, norethisterone, medroxyprogesterone acetate, and dydrogesterone. Detailed discussion is beyond the scope of this article.

2 – Transmasculine medications

Masculinizing therapies generally use a source of testosterone as a single-drug therapy (Coleman et al, Int J Transgend Health, 2022). 

Main physical effects include “the development of facial hair, virilizing changes in voice, a redistribution of facial and body subcutaneous fat, increased muscle mass, increased body hair, change in sweat and odor patterns” (Deutsch, UCSF, 2016-Masc). Testosterone may also cause emotional changes, potentially a narrower range of emotions, as well as a potential change to libido (Deutsch, UCSF, 2020-Masc). 

The standard of care for masculinizing therapy is that for most patients, testosterone therapy is effective and has satisfactorily low risk (Coleman et al, Int J Transgend Health, 2022). This is true whether or not they have a uterus. However, testosterone is available in multiple formats and dosages, and these details can have a big impact on the drug’s safety and effectiveness.

Occasionally, additional drugs are used to help individualize the treatment, but again, testosterone monotherapy is most common.

2.1 – Testosterone-based drugs

While several molecules can activate the Androgen Receptor, testosterone (and prodrugs that are metabolized into it) are the main ones in use for masculinizing HRT. Testosterone is sufficient to suppress estradiol levels (Chan et al, Endocr Pract, 2018), assuming the dosage is optimized for the patient. Antiestrogens are not needed to suppress estradiol, and are not included in the WPATH SOC-8 guidelines (Coleman et al, Int J Transgend Health, 2022).

2.1.1 – Effects, side effects, and risks

Testosterone alone is capable of inducing most of the changes associated with masculinizing HRT. Testosterone increases body hair growth, causes deepening of the voice, redistributes fat, and increases muscle mass. Testosterone therapy may also reduce anxiety and depression (Deutsch, UCSF, 2016-Masc). It also causes menstrual cycles to stop (Coleman et al, Int J Transgend Health, 2022).

Side effects can include oily skin and acne (which generally peaks at 6 months of treatment), and a large fraction of patients experience male-pattern hair loss (Wierckx, J Sex Med, 2014). There are potentially undesired mental or mood changes that might include increased aggression. Additionally, the decline in estradiol levels can cause vaginal atrophy (CDC, 2021).

Testosterone is associated with increased risks of polycythemia/increased hematocrit (too many red blood cells), heart attacks and stroke, increased blood pressure, increased “bad” and decreased “good” cholesterol, and sleep apnea (Coleman et al, Int J Transgend Health, 2022). These risks are generally low for gender affirmation in healthy patients as long as testosterone is not taken orally, but should be carefully discussed with your doctor.

Generally, the expression of sex hormones, whether androgens or estrogens, is important to preserve bone and cardiovascular health. Therefore, continued testosterone treatment is likely to be the default recommendation for doctors (perhaps at a lower dose) for AFAB patients who have been ovariectomized.

2.1.2 – Forms and dosages

WPATH SOC-8 guidelines recommend various forms of non-oral testosterone. The dosages they recommend are starting points, and should be titrated up or down according to patient needs (Coleman et al, Int J Transgend Health, 2022).

Testosterone levels should be monitored frequently, such as every 3 months at first, and 1-2 times per year after hormone levels have stabilized. This information might help optimize dosage and protect against risks and side effects.

Intramuscular injections of various testosterone derivatives/prodrugs provide a range of different injection intervals. Testosterone undecanoate can be taken every 12 weeks (with a 1,000 mg injection), or every 10 weeks (with a 750 mg injection). Or, testosterone enanthate or testosterone cypionate can be taken every 2 weeks (with a 100-200 mg injection), or every week with a 50-100 mg injection (Coleman et al, Int J Transgend Health, 2022).

Subcutaneous injections of testosterone are also possible for testosterone enanthate or testosterone cypionate, with weekly intervals of 50-100 mg (Coleman et al, Int J Transgend Health, 2022). This may be more comfortable for the patient than intramuscular injections, and reduce the chance of scarring from long-term use (Deutsch, UCSF, 2016-Masc).

Transdermal application of testosterone can use either gels applied daily (50-100 mg), or transdermal patches (2.5-7.5 mg/day) (Coleman et al, Int J Transgend Health, 2022).

2.2 – 5ɑ-reductase inhibitors

Finasteride and dutasteride are 5ɑ reductase inhibitors, reducing the production of the male-associated hormone DHT. They can be used to modulate a primarily testosterone-centric transmasculine therapy plan. For example, they could prevent or address male pattern baldness. At least for finasteride, WPATH SOC-8 mentions it may be considered to treat undesired hair loss on the head, though potentially at the expense of reduced development of male characteristics (less development of body hair or clitoral growth) (Coleman et al, Int J Transgend Health, 2022).  

Interestingly, for transmasculine individuals receiving testosterone (testosterone undecanoate injections) who have been ovariectomized, dutasteride has been used in a small research study to lower the concentration of DHT while leaving intact the concentration of testosterone (Meriggiola et al, J Sex Med, 2008). Combined testosterone and dutasteride reduced the growth of lean muscle mass, compared to testosterone alone.

2.3 – A note about other drug types

Aside from testosterone, few other drugs are mentioned in masculinizing HRT literature. We are providing this section about non-testosterone drugs for the sake of completeness.

While aromatase inhibitors (such as Anastrozole, Letrozole, or Exemestane) could theoretically increase the concentration of testosterone and reduce that of estrogens, there have not been many studies using aromatase inhibitors for gender affirmation, and the drugs may cause important risks such as osteoporosis (Eastell et al, J Clin Oncol, 2008). 

As well, it is theoretically possible to use drugs that block the Estrogen Receptors (ERɑ and ERβ). An example of this mechanism is Fulvestrant, used for managing advanced breast cancer. It can only be administered in a healthcare setting (Farooq and Patel, 2023).

Frankly, testosterone monotherapy is highly effective for masculinization purposes, so the consideration of other drugs is probably a low priority for patients with similar goals.

3 – Non-binary medications and regimes

Non-binary treatment regimens may be used for individuals aiming for a mixture or blend of masculine or feminine traits, or for an androgynous form. Unfortunately, non-binary HRT is less well-trodden. It may use different dosages than binary gender affirmation HRT, mixtures of feminizing and masculinizing therapies, and/or different drugs altogether (Hastings, UCSF, 2016; Xu J et al, Front Endocrinol, 2021).

Any treatments being pursued in this category may involve additional risks not seen in the usual feminizing or masculinizing gender affirming HRT approaches. Drug actions, risks, interactions, and so on are less well known by medical professionals, and only some doctors are knowledgeable enough to give informed opinions about non-binary medication plans.

Drug titration – i.e., using doses that are lower than traditionally feminizing or masculinizing therapies – is a common approach. However, titration may not accomplish all patient goals. In addition, applying testosterone for AFAB individuals, even at a low dose, has the potential to cause permanent or hard-to-reverse changes such as a deeper voice or inducing facial hair growth.

Mixtures of feminizing and masculinizing therapies are hypothetically possible. For example, finasteride or dutasteride (which reduce dihydrotestosterone (DHT) production) could be used by either AFAB and AMAB people for different purposes to modulate the response. Or, an antiandrogen alone, without estrogen, could be used by AMAB non-binary people, though potentially with new risks, such as increased risk of osteoporosis or lethargy. 

Interestingly, for transmasculine individuals receiving testosterone (testosterone undecanoate injections) who have been ovariectomized, dutasteride was used in a small research study to lower the concentration of DHT while leaving intact the concentration of testosterone (Meriggiola et al, J Sex Med, 2008). Combined testosterone and dutasteride reduced the growth of lean muscle mass, compared to testosterone alone. This might be useful to non-binary AFAB individuals.

Finally, we have found a brief implicit mention of simultaneously using both estrogen and testosterone HRT in non-binary people (Coleman et al, Int J Transgend Health, 2022, see statement 8.3).

“Hormone therapy is not required for any of these procedures, but hormone replacement therapy (either with estrogens, testosterone, or both) is advisable in those individuals undergoing a total gonadectomy to prevent adverse effects on their cardiovascular and musculoskeletal systems” (emphasis ours)

This makes us curious whether this might be an option for some patients, even outside the gonadectomy context. If we find more information, we’ll add it to this page.

Selective Estrogen Receptor Modulators (SERMs) are a class of drugs that includes Raloxifene, Bazedoxifene acetate, and Tamoxifen, and could be of interest for AMAB non-binary people (Xu J et al, Front Endocrinol, 2021). These are drugs that are used in treating either osteoporosis or breast cancer, mainly in women who are AFAB. They unfortunately have limited direct clinical evidence for use in non-binary people at this time. 

SERMs activate the Estrogen Receptor ɑ, and not ERβ. While the biology of estrogen receptors ERɑ and ERβ (and other receptors that are bound by estrogens) is complex, the theoretical result for non-binary individuals is that only some feminizing changes would take place. SERMs, especially Raloxifene, may cause skin to soften, and fat to be redistributed, without causing breast growth (Xu J et al, Front Endocrinol, 2021).

SERMs are associated with slightly increased risk of blood clots/venous thromboembolisms when used in AFAB women for osteoporosis (Hadji, Climacteric, 2012), though the overall risk still appears low in this context at least for Raloxifene (Martino et al, Curr Med Res Opin, 2005; Ettinger et al, JAMA, 1999). Changes in cholesterol levels are also possible (Hadji, Climacteric, 2012).

We have not seen discussion of the effect of SERMs on emotional state in non-binary people. Unlike the known effect of estrogens or testosterone on emotional state, SERMs are less characterized. Raloxifene may be able to cross the blood-brain barrier, implying it may be able to at least partially substitute for estrogens in the brain (Littleton-Kearney, CNS Drug Reviews, 2002). But, in a study in postmenopausal AFAB women, Raloxifene did not have any notable effects on measures of cognition or mood (Nickelsen, Clinical Trial, 1999). This means that, long-term, Raloxifene (and other SERMs) may have unknown effects on mental health if used for non-binary AMAB people.

We are not aware of any precedent for whether or not antiandrogens should be used at all, or if so, whether a specific antiandrogen should be used. Speaking highly speculatively, if an antiandrogen is needed, Cyproterone Acetate (CyprAc) might be a more appropriate choice than Spironolactone (Spiro). We reason that, since the evidence for CyprAc’s suppression of testosterone production is stronger than the evidence for Spiro, a SERM+CyprAc combination might be more effective than a SERM+Spiro combination. (Recall, as we discussed above, Spiro suppresses testosterone signaling, not testosterone production; the reduction in testosterone seen over time with estrogen + Spiro combinations might be primarily due to the estrogen).

Selective Androgen Receptor Modulators (SARMs) are a still-developing class of drugs that could hypothetically be used by, for example, AFAB non-binary people. Unfortunately, no drugs from this class are approved by the United States FDA for any indication (https://en.wikipedia.org/wiki/Selective_androgen_receptor_modulator). We intend to gather more information about SARMs in a future version of this page.

References

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