D tier · weak
Trestolone has one published, properly conducted human clinical trial of 35 men and a Population Council development programme behind it, which is more than most compounds in this set, but it was never marketed, development appears to have stalled after 2013, and the human dataset remains a single small contraceptive study.
trestolone
Trestolone is an experimental 19-nortestosterone derivative developed by the Population Council as a candidate male hormonal contraceptive and as a possible androgen replacement agent. A published clinical trial of MENT acetate implants in 35 men demonstrated dose-dependent suppression of spermatogenesis to azoospermia, but the compound was never approved or marketed anywhere and its development appears to have halted after 2013.
the explanation
Trestolone, or MENT, was designed as a male birth control implant by a reproductive health non-profit, and a small trial showed it could shut down sperm production. It was never approved, never sold as a medicine, and the research programme seems to have stopped over a decade ago.
regulatory status
Investigational; never approved or marketed in any jurisdiction
Trestolone is an experimental medication not approved for medical use anywhere. Development was led by the Population Council beginning around 1993, with no additional development apparently conducted since 2013. It is not listed individually by name in the DEA alphabetical controlled substances table, but falls within the statutory definition of an anabolic steroid at 21 CFR 1300.01 and is therefore captured as a Schedule III anabolic steroid in the US. Prohibited in sport.
how it works · proposed mechanism
Trestolone was engineered specifically to decouple gonadotropin suppression from prostatic androgen amplification.
7-alpha-methyl blocks 5-alpha-reduction
The 7-alpha-methyl group prevents conversion by 5-alpha-reductase, so the molecule is not amplified in prostate and skin the way testosterone is. This was the intended tissue-selectivity advantage in the Population Council's design rationale for hypogonadism therapy.
Potent gonadotropin suppression
Primate work reported trestolone to be roughly ten times as potent as testosterone at suppressing gonadotropin secretion. Suppressing LH and FSH is the intended contraceptive mechanism, since it withdraws the intratesticular androgen drive required for spermatogenesis.
Retained aromatisation
Trestolone is aromatised to a 7-alpha-methyl oestrogen, so oestrogen-dependent functions such as bone maintenance are preserved rather than lost. This distinguishes it from non-aromatisable androgens, and also means oestrogenic side effects remain possible.
what’s reported
evidence shape
5 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The one substantive human study was a 35-man contraceptive trial designed to measure sperm suppression, not muscle, strength, body composition or long-term safety. Its findings say a great deal about trestolone's ability to shut down the reproductive axis and essentially nothing about any other claimed effect.
key published findings
- Human trial (von Eckardstein 2003, JCEM): 35 normal male volunteers across three clinics were randomised to 1 implant (12 men), 2 implants (11 men) or 4 implants (12 men) of MENT acetate, each releasing approximately 400 micrograms per day initially, over 6 months extended to 9 or 12 months at two clinics.
- Human trial (von Eckardstein 2003, outcomes): no man in the 1-implant group became oligozoospermic; 4 in the 2-implant group became oligozoospermic of whom 2 reached azoospermia; 8 of 12 in the 4-implant group reached azoospermia, 1 was oligozoospermic and 2 were non-responders.
- Human trial (von Eckardstein 2003, safety): increases in erythrocyte count, haematocrit and haemoglobin were observed and were reversible; changes in lipid parameters were described as moderate and transient with minimal liver enzyme alteration.
- Preclinical/review (Nieschlag 2013, Contraception): the Population Council review documents the systematic development of MENT for male hypogonadism and contraception, and records that trestolone-induced infertility is quickly reversible on discontinuation.
- Chemistry (PubChem, verified): trestolone is C19H28O2, molar mass 288.4, CAS 3764-87-2; trestolone acetate is C21H30O3, molar mass 330.5.
limitations of the evidence
- A single small non-blinded implant trial of 35 men is the entire substantive human dataset, and it was designed around a contraceptive endpoint.
- Development appears to have stopped after 2013, so there is no modern safety programme, no regulatory dossier and no manufacturing standard.
- Reported side effects in the wider literature include sexual dysfunction and decreased bone mineral density, but these are not quantified in a form that supports a risk estimate.
documented safety signals
- Profound, dose-dependent suppression of spermatogenesis to azoospermia was the trial's primary observed effect; this is the intended contraceptive action, and while described as quickly reversible on discontinuation, 2 of 12 men in the highest-exposure group were non-responders, indicating variable and unpredictable individual response.
- Erythrocytosis: the trial recorded increases in erythrocyte count, haematocrit and haemoglobin, reversible on discontinuation but representing the same polycythaemia risk seen across androgens.
- Decreased bone mineral density and sexual dysfunction are reported in the secondary literature as trestolone side effects.
- Lipid changes were characterised as moderate and transient in the trial, but the trial was small, short and not powered for cardiovascular outcomes.
- Complete HPG-axis suppression by design, with the attendant risk of a prolonged hypogonadal recovery period after cessation; class data show 27.2% of former AAS users remain below the lower testosterone reference limit a mean 2.5 years after stopping (Rasmussen 2016).
- No approved product means no pharmacopoeial standard, no sterility assurance and no verified potency for any material circulating outside research settings.
- Because trestolone is aromatisable, oestrogenic adverse effects including gynaecomastia remain mechanistically possible.
- Class-level cardiovascular signals for anabolic androgenic steroids, including cardiomyopathy and accelerated atherosclerosis (Baggish 2017), have never been assessed for this compound because no long-term human exposure study exists.
- Injection-related infection risks apply to any non-clinical injectable use (Hope 2015: 42% injection-site inflammation, 6.8% abscess or open wound among 366 men injecting image- and performance-enhancing drugs).
identity
| full name | Trestolone acetate (7alpha-methyl-19-nortestosterone, MENT) |
| category | Anabolic & Androgenic |
| modality | steroid |
| formula | C19H28O2 |
| molar mass | 288.4 g/mol |
| cas | 3764-87-2 |
laboratory handling
| storage | No approved product and therefore no authoritative storage labelling. The clinical trial material was a subdermal implant, not an oil-based injectable, so no storage claim from the trial transfers to injectable preparations. |
| solubility | Practically insoluble in water. The acetate ester is lipophilic and oil-soluble; note that the only published human trial used subdermal silastic implants rather than an oil solution, so formulation data from that trial do not describe injectable preparations. |
| co-studied with | Reference note only, not guidance: because trestolone suppresses gonadotropins roughly ten times as potently as testosterone in primate work and was developed specifically as a contraceptive, its reproductive-axis effect is the dominant documented pharmacology and is not offset by co-administration of other androgens, which suppress the axis further rather than restoring it. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
5 citedPubChem, US National Library of Medicine · 2026 · official
US DEA Diversion Control Division · 2025 · official
Journal of Clinical Endocrinology & Metabolism · 2003 · randomized
Contraception · 2013 · reviews
Endocrine Reviews · 2014 · reviews
others in Anabolic & Androgenic