Trestolone, also known as 7α-methyl-19-nortestosterone (MENT), is an experimental androgen / anabolic steroid (AAS) and progestogen drug that has been under development for potential use as a form of hormonal contraception for men and androgen replacement therapy for low testosterone levels in men but has never been marketed for medical use. It is an implant that is inserted into the fat . Like trestolone acetate, an androgen ester, and a prodrug of trestolone, this drug can also be injected into the muscle.

Side effects of Trestolone include low estrogen levels and related symptoms such as decreased sexual function and decreased bone mineral density, among others. Trestolone is AAC, and, therefore, is an agonist of the androgen receptor, the biological target of androgens, such as testosterone. It is also a progestin or synthetic progestogen and therefore is an agonist of the progesterone receptor, a biological target of progestogens such as progesterone. Due to its androgenic and progestagenic activity, Trestolone has an antigonadotropicact. These effects lead to a reversible suppression of sperm production and are responsible for the contraceptive effects of Trestolone in men. The drug has a weak estrogenic activity.Source:

Trestolon was first described in 1963. It was not subsequently investigated until 1990. The development of Trestolone for potential clinical use began in 1993 and continued thereafter. No additional development appears to have been underway since 2013, the drug was developed by the Population Council, a non-profit, nongovernmental organization dedicated to reproductive health.

Mechanism of action

Sperm are produced in the testes of men in a process called spermatogenesis. To render a man infertile, hormone-based male contraception must stop spermatogenesis by interrupting the release of gonadotropins from the pituitary gland. Even at low concentrations, trestolone is a potent inhibitor of the release of gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH).

For spermatogenesis to occur in the testes, both FSH and testosterone must be present. By inhibiting the release of FSH, Trestolone creates an endocrine environment in which conditions for spermatogenesis are not ideal. Sperm production is further impaired by the suppression of LH, which in turn drastically reduces testosterone production.

Sufficient regular doses of Trestolone cause severe oligozoospermia or azoospermia and hence infertility in most men. It has been found that infertility caused by Trestolone is rapidly reversible after discontinuation. When LH release is suppressed, the amount of testosterone produced in the testes drops dramatically.

As a result of Trestolone’s ability to suppress gonadotropins, serum testosterone levels drop sharply in men who receive sufficient amounts of the drug. Testosterone is the main hormone responsible for maintaining secondary sex characteristics in men. Insufficient testosterone levels usually cause unwanted effects such as fatigue, loss of skeletal muscle mass, decreased libido, and weight gain. However, the androgenic and anabolic properties of Trestolone largely solve this problem. Essentially, Trestolone replaces testosterone as the main male hormone in the body.