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|Class||Route of administration||Availability||Notes|
|Spironolactone||Steroidal antiandrogen||Oral||Readily available||Most common antiandrogen in the US.|
|Cyproterone acetate||Steroidal antiandrogen||Oral, intramuscular injection||Readily available||Not approved by the FDA in the US. Common outside of the US.|
|Bicalutamide||Nonsteroidal antiandrogen||Oral||Readily available||Not frequently prescribed to trans people.|
|Enzalutamide||Nonsteroidal antiandrogen||Oral||Available||No instances of it being prescribed to trans people in medical literature.|
|Darolutamide||Nonsteroidal antiandrogen||Oral||Phase III trials|
|Leuprorelin||GnRH agonist||Injection, implant||Available||Frequently used to block puberty.|
|Finasteride||5α-reductase inhibitor||Oral||Readily available||Often prescribed for hair loss.|
|Dutasteride||5α-reductase inhibitor||Oral||Readily available||Sometimes prescribed for hair loss.|
|Estradiol||Antigonadotropin||Oral, sublingual, injection, implant, transdermal, others||Readily available|
Mechanism of action
Spironolactone has two primary factors that contribute to its antiandrogenic activity:
- Androgen receptor partial agonism: Spironolactone binds to the androgen receptor and causes it to express much more weakly than if an androgen such as testosterone or DHT had bound to it.
- 17α-hydroxylase and 17,20-lyase inhibition: These two enzymes are key in the steroidogenesis of androgens (and estrogens and some glucocorticoids).
Cyproterone acetate has two primary factors that contribute to its antiandrogenic activity:
- Androgen receptor partial agonism: Cyproterone acetate binds to the androgen receptor and causes it to express much more weakly than if an androgen such as testosterone or DHT had bound to it.
- Progestogenic activity: Cyproterone acetate acts as a progestogen, inducing negative feedback on the HPG axis. In people with testes, this results in lower testosterone levels. In people with ovaries, this results in lower estrogen levels.
Leuprorelin is a GnRH agonist. It induces strong positive feedback on the HPG axis, which causes an increase in LH, FSH, testosterone (in males), and estrogen (in females) levels. After some time, the body downregulates the GnRH receptor, causing LH, FSH, endogenous testosterone (in males), and endogenous estrogen (in females) levels to drop.
Note that finasteride does not prevent testosterone from binding to the androgen receptor, so finasteride alone is insufficient to prevent masculinization.
Note that dutasteride does not prevent testosterone from binding to the androgen receptor, so dutasteride alone is insufficient to prevent masculinization.