LibraryCompound reference · v1.0

Trestolone

Last reviewed May 2026

Educational reference only. Informational material drawn from peer-reviewed literature. Not medical advice and not a recommendation to use, dose, or modify any therapy. Decisions about hormone therapy should be made with a qualified healthcare provider.

Overview

Overview

Trestolone, more commonly known by the research designation MENT (7α-methyl-19-nortestosterone), is an investigational synthetic anabolic-androgenic steroid with a distinctive development history. Unlike most AAS in non-medical use (which were developed as therapeutic agents, used for decades, and eventually fell out of pharmaceutical favor), trestolone was developed beginning in the 1960s by the Population Council in New York with the specific intent of becoming a male hormonal contraceptive and treatment for male hypogonadism. It progressed through several phases of human clinical trials but was never brought to market by any pharmaceutical company.

The compound's intended clinical purpose was unique: to simultaneously suppress spermatogenesis (the contraceptive effect, achieved through HPG axis suppression) while replacing the androgenic effects of suppressed endogenous testosterone (preventing hypogonadism symptoms during contraceptive use). MENT was selected for this purpose because it has approximately 10× the potency of testosterone on a milligram-for-milligram basis, allowing effective doses to be delivered through long-acting subdermal implants no larger than a matchstick.

The parent trestolone molecule itself has a circulating half-life of only a few hours. The acetate ester is rapidly cleaved, making injectable trestolone acetate effectively short-acting despite the ester. This unusual pharmacokinetic profile is part of why subdermal implants were the formulation developed for clinical trials rather than injectable products.

Forms

Available forms & half-lives

FormApproximate half-life
Acetate (injectable)~12 hours (very short)
Enanthate (injectable, unregulated)~7–10 days (estimated; not formally characterized)
Subdermal implant (acetate)~12 months sustained release

What it does

Main effects

  • Approximately 10× the androgen-receptor potency of testosterone PMID: 8146434PMID: 8489761, one of the most potent AAS at the AR ever characterized
  • No 5α-reduction to a more potent metabolite: delivers full AR activity in all tissues, with substantially reduced prostatic effects compared to testosterone (the original clinical-development rationale)
  • Strong HPG axis suppression with androgen replacement, the unique pharmacology that made trestolone attractive as a male hormonal contraceptive: suppresses spermatogenesis while replacing the androgenic effects of suppressed endogenous testosterone
  • Strong anabolic effects on muscle and bone documented in Population Council Phase II trials
  • Aromatization to a non-standard estrogen (7α-methyl-estradiol): does aromatize, but to a metabolite distinct from estradiol with its own pharmacology
  • Progestogenic activity: like other 19-nor compounds (nandrolone, trenbolone), binds the progesterone receptor in addition to the AR

What to watch for

Common side effects

  • Profound HPG axis suppression: the intended pharmacological effect in contraceptive context; severe and clinically meaningful adverse effect outside that context
  • Erythrocytosis: documented in Phase II clinical trials PMID: 14602755; expected to be more pronounced at the higher doses used in non-medical contexts
  • HDL reduction and LDL elevation: expected based on 19-nor compound pharmacology
  • Gynecomastia and other estrogenic effects: reported in trial participants; mediated by 7α-methyl-estradiol and may be underestimated by standard estradiol assays
  • Potential prolactin elevation and progestogenic effects: inferred from related 19-nor compounds (nandrolone, trenbolone); less well-characterized for trestolone specifically
  • Severe acne and androgenic skin effects in genetically predisposed users: the high AR potency drives this even without 5α-reduction
  • Scalp hair loss in genetically predisposed users: different mechanism than testosterone-mediated loss (not DHT-driven), but similar outcome; 5α-reductase inhibitors do not protect
  • Inconvenient pharmacokinetics: acetate ester effective half-life ~12 hours, which produces significant peak-to-trough variation; underground enanthate has uncharacterized PK
  • Underground-only supply: no legitimate pharmaceutical source; all product is unregulated with the standard purity/sterility/dose-accuracy concerns

Key facts

Key facts worth knowing

  • Trestolone is structurally a hybrid: it is 19-nortestosterone (nandrolone) with a 7α-methyl group added. This combination produces a compound with both androgenic and progestogenic activity.
  • Trestolone cannot be 5α-reduced to a more potent metabolite. This is the basis of its selective tissue effect profile: it has strong effects on muscle, bone, and HPG axis suppression while having substantially reduced effects on the prostate compared to testosterone. PMID: 8146434
  • Trestolone does aromatize to estrogen: like nandrolone, the parent 19-nor structure permits aromatization. The estrogen produced is not estradiol but rather 7α-methyl-estradiol, a unique estrogen with its own pharmacology.
  • The most rigorous human clinical data on trestolone comes from the Population Council Phase II contraceptive trials in the early 2000s, which used subdermal implants delivering approximately 400-1600 μg/day for up to 12 months. These trials demonstrated dose-dependent spermatogenesis suppression and characterized side effects in a controlled clinical setting. PMID: 14602755
  • The compound has been investigated as part of the NES/T (Nestorone/Testosterone) combination contraceptive gel, currently in late-stage clinical trials, though that formulation uses testosterone rather than trestolone.
  • There is no legitimate pharmaceutical source for trestolone.

Legal status

Legal status

Schedule III controlled substance in the United States (DEA) by inclusion in the anabolic-androgenic steroid class. No FDA approval for any indication. WADA-prohibited at all times in competitive sport.