Trestolone acetate is the acetate ester of trestolone, a synthetic steroid better known in the research literature as MENT (7α-methyl-19-nortestosterone). Trestolone is nandrolone with one extra methyl group. The Population Council developed it as a long-acting androgen for male contraception and for treating low testosterone (Nieschlag et al., Contraception 2013). The acetate form was used in the subdermal implants tested in men.
The single most important fact: MENT never received approval as a medicine anywhere (Piper et al., Drug Test Anal 2026). All published human data come from a handful of small early-phase studies, each reporting on fewer than 50 men, mostly using implants. No human trial has measured muscle mass or strength. Outside research, trestolone acetate is sold online, sometimes labeled as a nutritional supplement.
This page summarizes what the clinical studies, animal research and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Synthetic anabolic-androgenic steroid; 7α-methylated nandrolone (19-nortestosterone) derivative |
| Chemistry | 17β-acetate ester of trestolone; C₂₁H₃₀O₃, 330.5 g/mol; trestolone is ≈87% of the weight |
| Approval | Never approved as a medicine in any country |
| Forms studied in men | Subdermal implants of MENT acetate (≈115 mg each); single or daily IM injections of micronized MENT (not the acetate); a transdermal MENT gel (phase 1) |
| Half-life | Acetate is hydrolyzed rapidly to MENT; MENT’s terminal half-life was ≈40 min after an IV dose in men. No human half-life has been published for oil-based acetate injections |
| Key mechanism facts | Binds the androgen receptor strongly; cannot be 5α-reduced; does not bind SHBG; can be aromatized to an estrogen (7α-methylestradiol) |
| US status | Not FDA-approved; not named in the DEA Schedule III anabolic steroid list |
| WADA status | Named in class S1.1 (anabolic androgenic steroids); prohibited at all times |
What it is
Trestolone (MENT) is 17β-hydroxy-7α-methylestr-4-en-3-one: nandrolone with a methyl group added at the 7α position. Trestolone weighs 288.4 g/mol and trestolone acetate 330.5 g/mol (PubChem). So about 87% of a given weight of the acetate is trestolone itself.
Unlike oral steroids such as methyltestosterone, trestolone is not 17α-alkylated. Its extra methyl group sits on the B-ring instead, at carbon 7.
The library has separate pages for the other forms sold under this name. This page covers the acetate:
| Form | What it is | Human data |
|---|---|---|
| Trestolone acetate (this page) | 17β-acetate ester; a short ester that is cleaved quickly in the body | Implant trials in healthy and hypogonadal men |
| Trestolone base | Unesterified MENT | IV and IM pharmacokinetic studies; transdermal gel trial |
| Trestolone enanthate | Longer enanthate ester | No human studies found on PubMed |
Researchers chose the acetate for implants because its diffusion characteristics suited slow release from a polymer rod. Once released, the acetate is quickly hydrolyzed, and MENT is the active hormone in the blood (Anderson et al., JCEM 1999). In monkeys given equal molar amounts by continuous infusion, MENT and MENT acetate produced the same blood MENT levels (11.3 vs 13.1 nmol/L). Incubating the acetate with blood also released MENT (Kumar et al., J Androl 1997).
MENT was studied in cancer research as early as the 1960s (Piper et al., Drug Test Anal 2026). In studies published from 1992 onward, the Population Council developed it systematically for male contraception and hypogonadism (Nieschlag et al., Contraception 2013). The only MENT trial registered on ClinicalTrials.gov is a Population Council phase 1 study of a MENT gel in 68 men. It was completed in 2014 with no results posted (ClinicalTrials.gov NCT00812630).
Why the 7α-methyl group matters
Testosterone is converted in the prostate by 5α-reductase to dihydrotestosterone (DHT), which amplifies its effect there. MENT cannot be 5α-reduced, so its effect is not amplified in the prostate. In castrated rats given a 5α-reductase inhibitor, testosterone lost activity on the prostate but MENT acetate did not (Kumar et al., Endocrinology 1992).
Animal studies compared MENT with testosterone across tissues:
| Model | Measure | MENT relative to testosterone |
|---|---|---|
| Castrated rats (MENT acetate) | Levator ani/bulbocavernosus muscle weight | ≈10× more potent |
| Castrated rats | Prostate and seminal vesicle weight | ≈4× more potent |
| Castrated rats | Suppression of gonadotropins (LH, FSH) | ≈12× more potent |
| Castrated monkeys | Dose for complete LH suppression | 0.3 mg/day vs 3.0 mg/day (10×) |
| Castrated monkeys | Support of body weight | 10× more potent |
| Castrated monkeys | Dose to maintain prostate volume | 0.1–0.2 mg/day vs 0.3 mg/day (≈2×) |
Sources: rats from Kumar et al., Endocrinology 1992; monkeys (6 per group, 20 weeks) from Cummings et al., JCEM 1998.
Other properties seen in laboratory and animal studies:
- Aromatization. Human placental aromatase converted MENT to 7α-methylestradiol in vitro, and the product bound estrogen receptors (LaMorte et al., J Steroid Biochem Mol Biol 1994).
- Progestational activity. In immature rabbits, MENT’s progestational activity and its binding to the progesterone receptor were comparable to progesterone’s (Beri et al., J Steroid Biochem Mol Biol 1998).
- Weak direct estrogen binding. MENT bound the estrogen receptor about 3,500 times less strongly than estradiol in the same study.
About anabolic:androgenic ratios and the “SARM” label. Online sources quote large anabolic:androgenic ratios for trestolone. The traceable primary data are the rat and monkey comparisons above, which show muscle and LH effects exceeding prostate effects by about 2.5-fold in rats and 5-fold in monkeys. No human ratio has been measured. Trestolone is also sometimes called a selective androgen receptor modulator (SARM), including in one case report. It is a steroid, and WADA lists it among anabolic androgenic steroids, not SARMs.
Pharmacokinetics
No pharmacokinetic study has been published for trestolone acetate injected in oil, the form sold outside research. Human data come from IV and IM doses of MENT itself and from acetate implants:
| Study | Dose and form | Key findings |
|---|---|---|
| Kumar et al., J Androl 1997 | Single IV bolus, 500 µg MENT, normal men | Peak at 3 min; undetectable by 180 min; terminal half-life 40 min; clearance 2,360 L/day |
| Suvisaari et al., Hum Reprod 1997 | Single IM 2, 4 or 8 mg micronized MENT in water, 18 men | Peak 1–2 h after injection; doubling the dose raised peak levels by 60%; clearance 1,790 L/day |
| Noé et al., Hum Reprod 1999 | 1, 2 or 4 MENT acetate implants for 28 days, 45 men | Steady MENT levels of 0.7, 1.2 and 2.0 nmol/L; ≈500 µg/day released per implant |
| Anderson et al., JCEM 1999 | 2 implants of 115 mg MENT acetate for 6 weeks, 20 hypogonadal men | Stable MENT of 1.4 nmol/L at 3 weeks and 1.3 nmol/L at 6 weeks |
MENT clears much faster than testosterone. One reason is that, unlike testosterone, it does not bind sex hormone-binding globulin (SHBG), the carrier protein that holds testosterone in the blood (Kumar et al., J Androl 1997). Fast clearance fits the development program’s reliance on continuous-release implants rather than periodic injections.
In human liver preparations in vitro, MENT was metabolized by CYP3A4, 17β-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase (Prasad et al., Steroids 2009).
A 2026 anti-doping study gave single 30 mg oral doses of MENT acetate to volunteers (Piper et al., Drug Test Anal 2026):
- 50 candidate urinary metabolites were found.
- Unchanged MENT was detectable in urine for 23–43 h.
- Two newly identified metabolites extended detection to 3–4 days.
- The authors noted that, according to WADA testing reports, no doping sample had been reported positive for MENT since 2003, possibly because older target metabolites were hard to tell apart from natural steroids.
Regulatory status
- Approval. No MENT or MENT acetate product has been approved for medical use (Piper et al., Drug Test Anal 2026). There is no prescribing label, so there are no official indications, doses or contraindications.
- United States. Trestolone is not among the anabolic steroids named in Schedule III (21 CFR 1308.13). It is also not an approved drug, so products sold for human use are unapproved.
- Sport. The WADA 2026 Prohibited List names “Trestolone (7α-Methyl-19-nortestosterone, MENT)” under S1.1. It is prohibited in and out of competition and is a non-specified substance. Esters such as the acetate are covered.
- Market. MENT acetate is sold by online distributors, including as a “nutritional supplement” (Piper et al., Drug Test Anal 2026). These products are not regulated for identity, dose or sterility.
What the research shows
Suppression of LH, FSH and testosterone
MENT strongly suppresses the pituitary hormones LH and FSH, which drive the testes to make testosterone and sperm. Two studies in healthy men measured this:
| Study | Regimen | Testosterone | LH | FSH |
|---|---|---|---|---|
| Suvisaari et al., Hum Reprod 1997 (24 men) | 4 mg MENT IM daily for 6 days (highest dose) | −74% | −70% | −57% |
| Noé et al., Hum Reprod 1999 (45 men) | 2 or 4 MENT acetate implants for 28 days | −93% | −97% | −95% |
In the implant study, DHT also fell by 80%: the men’s own testosterone, the source of DHT, was suppressed, and MENT is not converted to DHT. Suppression reversed completely after the implants were removed.
Male contraception
The largest trial randomized 35 healthy men to 1, 2 or 4 MENT acetate implants. Treatment lasted 6 months, extended at two clinics to 9 months (2 implants) or 12 months (4 implants) (von Eckardstein et al., JCEM 2003):
| Implants | Men | Result |
|---|---|---|
| 1 | 12 | None reached oligozoospermia (under 3 million sperm/mL) |
| 2 | 11 | 4 oligozoospermic, 2 of whom became azoospermic (no sperm) |
| 4 | 12 | 8 azoospermic, 1 oligozoospermic, 2 did not respond |
A later trial randomized 29 healthy men to 2 etonogestrel (progestin) implants plus either 2 MENT implants or 600 mg testosterone pellets every 12 weeks, for up to 48 weeks (Walton et al., J Androl 2007):
- At 12 weeks, sperm counts fell below 1 million/mL in 8 of 10 men on MENT and 13 of 16 on testosterone.
- Suppression was not maintained on MENT because release from the implants declined. Six men noted loss of libido.
- All 14 men who completed 48 weeks of testosterone became azoospermic.
A 2021 NIH review still listed MENT among single-agent male contraceptives under evaluation (Long et al., JCEM 2021), but no product has reached the market.
Androgen replacement in hypogonadal men
In a crossover trial, 20 hypogonadal men in Edinburgh and Hong Kong received 2 MENT acetate implants (115 mg each) for 6 weeks and testosterone enanthate 200 mg IM twice, 3 weeks apart (Anderson et al., JCEM 1999). Both treatments increased sexual interest and activity and spontaneous erections, and the differences between them were minor. In the Edinburgh group, both also improved mood.
A 24-week trial randomized 16 hypogonadal men to 1 or 2 implants, each releasing ≈400 µg/day (Anderson et al., JCEM 2003):
| Outcome | 1 implant | 2 implants |
|---|---|---|
| Hemoglobin and hematocrit | Maintained | Maintained |
| Prostate volume | Fell | Small, non-significant fall |
| PSA | Fell significantly | Fell significantly |
| Lumbar spine bone density | Decreased | Decreased |
| Sexual behavior and erections | Declined | Maintained |
The authors concluded that one implant gave less than physiological replacement. Two implants maintained most androgen-dependent functions except bone. The lower PSA and prostate volume were the first human evidence of the prostate-sparing effect seen in animals.
Muscle, strength and body composition
No human trial has reported muscle mass or strength outcomes for MENT or its acetate. The claims of high anabolic potency rest on muscle weights in castrated rats and body weight in castrated monkeys (see the table above). These animal results cannot be translated into expected effects or doses in people.
Side effects and risks
There is no approved label, so there is no boxed warning or official list of adverse effects. What follows is what the small human studies and animal toxicology reported.
Shutdown of natural testosterone and fertility
Suppression of LH, FSH and testosterone is the intended effect in contraception trials, and it was dose-dependent in every study above. In the MENT arm of the etonogestrel trial, the men’s own testosterone fell to about 2 nmol/L (≈58 ng/dL) (Walton et al., J Androl 2007). At higher implant doses, sperm production stopped in most men. In these supervised trials, hormone suppression reversed after implant removal.
Low libido and bone loss when exposure is too low
Because MENT cannot form DHT and suppresses the body’s own testosterone, falling MENT levels leave little androgen in circulation. In trials, this showed up as:
- loss of libido in 6 men as implant release declined (Walton et al., J Androl 2007);
- declining sexual function on one implant, and lower lumbar spine bone density on both doses over 24 weeks (Anderson et al., JCEM 2003).
In the shorter etonogestrel trial, bone mass did not change in the MENT group.
Blood counts, lipids and liver
In the contraceptive implant trial, red cell count, hematocrit (the share of blood made up of red cells) and hemoglobin rose and SHBG fell. These changes were reversible. Lipid changes were moderate and transient, and liver enzymes showed small changes (von Eckardstein et al., JCEM 2003). In the etonogestrel trial, hemoglobin rose and HDL cholesterol fell with both MENT and testosterone (Walton et al., J Androl 2007).
Animal data on the liver come from rabbits given oral MENT at 10 mg/kg/day for 14 days (Hild et al., J Androl 2010):
- liver enzymes rose and liver clearance of a test dye slowed;
- the effects were smaller than with 17α-methyltestosterone at the same dose;
- all measures returned to baseline 2 weeks after stopping;
- 1 mg/kg/day caused no effect.
The “not 17α-alkylated, so liver safe” idea is therefore not fully supported, at least at high oral doses in rabbits. No human data exist for long-term or high-dose use.
Estrogenic and progestational effects
MENT can be aromatized to 7α-methylestradiol in lab studies and has progesterone-like activity in rabbits (see above). The human trials used low, steady implant doses, so they say little about estrogen- or progestin-related effects at other doses.
Anesthesia: a reported sugammadex interaction
A 2023 case report described a 60-year-old man who was self-injecting testosterone and trestolone acetate for bodybuilding and underwent kidney surgery (Farkas et al., Anaesth Rep 2023):
- After 200 mg of sugammadex, his muscle function recovered only partway in 15 minutes (train-of-four ratio from 33% to 52%).
- Reversal was completed with neostigmine.
The authors suggested the steroids might bind sugammadex, the drug that reverses the muscle relaxant rocuronium, but called the explanation speculative.
Product quality
Trestolone acetate bought online is not a pharmaceutical product. Its identity, dose and sterility are not regulated, and no published studies have tested the contents of these products.
Key takeaways
- An unapproved research steroid. Trestolone acetate is the acetate ester of MENT, a 7α-methyl nandrolone derivative developed for male contraception and hormone replacement. It was never approved as a medicine.
- Very fast clearance. The acetate is cleaved quickly, and MENT itself had a ≈40-minute half-life after IV dosing, partly because it does not bind SHBG. No half-life has been published for oil-based acetate injections.
- Potent in animals, untested for muscle in people. MENT was about 10 times as potent as testosterone on muscle in rats and body weight in monkeys, but only 2–4 times on the prostate. No human trial has measured muscle or strength.
- Strong suppression. Implants cut testosterone by 93% and LH by 97% in healthy men, and higher doses stopped sperm production in most men.
- Cannot form DHT, but can be aromatized in lab studies. Lower PSA and prostate volume in hypogonadal men fit the “prostate-sparing” idea. Loss of libido and bone density occurred when MENT exposure was too low.
- Banned in sport. WADA names trestolone in S1.1, prohibited at all times.
Sources
- Nieschlag E, Kumar N, Sitruk-Ware R. 7α-methyl-19-nortestosterone (MENTR): the population council’s contribution to research on male contraception and treatment of hypogonadism. Contraception. 2013;87(3):288–295. PubMed.
- Piper T, Fusshöller G, Thevis M. Investigations into the human metabolism of trestolone (7α-methyl-19-nortestosterone). Drug Test Anal. 2026;18(3):341–353. PubMed.
- National Center for Biotechnology Information. Trestolone acetate, PubChem CID 10246085; trestolone, PubChem CID 9838899. PubChem.
- Population Council. A two-part trial assessing the effects of 7α-methyl-19-nortestosterone (MENT) on blood pressure in normal men. NCT00812630. ClinicalTrials.gov.
- Kumar N, Didolkar AK, Monder C, Bardin CW, Sundaram K. The biological activity of 7 alpha-methyl-19-nortestosterone is not amplified in male reproductive tract as is that of testosterone. Endocrinology. 1992;130(6):3677–3683. PubMed.
- Cummings DE, Kumar N, Bardin CW, Sundaram K, Bremner WJ. Prostate-sparing effects in primates of the potent androgen 7alpha-methyl-19-nortestosterone: a potential alternative to testosterone for androgen replacement and male contraception. J Clin Endocrinol Metab. 1998;83(12):4212–4219. PubMed.
- LaMorte A, Kumar N, Bardin CW, Sundaram K. Aromatization of 7 alpha-methyl-19-nortestosterone by human placental microsomes in vitro. J Steroid Biochem Mol Biol. 1994;48(2-3):297–304. PubMed.
- Beri R, Kumar N, Savage T, Benalcazar L, Sundaram K. Estrogenic and progestational activity of 7alpha-methyl-19-nortestosterone, a synthetic androgen. J Steroid Biochem Mol Biol. 1998;67(3):275–283. PubMed.
- Kumar N, Suvisaari J, Tsong YY, et al. Pharmacokinetics of 7 alpha-methyl-19-nortestosterone in men and cynomolgus monkeys. J Androl. 1997;18(4):352–358. PubMed.
- Suvisaari J, Sundaram K, Noé G, et al. Pharmacokinetics and pharmacodynamics of 7alpha-methyl-19-nortestosterone after intramuscular administration in healthy men. Hum Reprod. 1997;12(5):967–973. PubMed.
- Noé G, Suvisaari J, Martin C, et al. Gonadotrophin and testosterone suppression by 7alpha-methyl-19-nortestosterone acetate administered by subdermal implant to healthy men. Hum Reprod. 1999;14(9):2200–2206. PubMed.
- Anderson RA, Martin CW, Kung AW, et al. 7Alpha-methyl-19-nortestosterone maintains sexual behavior and mood in hypogonadal men. J Clin Endocrinol Metab. 1999;84(10):3556–3562. PubMed.
- Anderson RA, Wallace AM, Sattar N, Kumar N, Sundaram K. Evidence for tissue selectivity of the synthetic androgen 7 alpha-methyl-19-nortestosterone in hypogonadal men. J Clin Endocrinol Metab. 2003;88(6):2784–2793. PubMed.
- von Eckardstein S, Noe G, Brache V, et al. A clinical trial of 7 alpha-methyl-19-nortestosterone implants for possible use as a long-acting contraceptive for men. J Clin Endocrinol Metab. 2003;88(11):5232–5239. PubMed.
- Walton MJ, Kumar N, Baird DT, Ludlow H, Anderson RA. 7alpha-methyl-19-nortestosterone (MENT) vs testosterone in combination with etonogestrel implants for spermatogenic suppression in healthy men. J Androl. 2007;28(5):679–688. PubMed.
- Prasad PV, Arumugam R, Willman M, Ge RS, Sitruk-Ware R, Kumar N. Distribution, metabolism and excretion of a synthetic androgen 7alpha-methyl-19-nortestosterone, a potential male-contraceptive. Steroids. 2009;74(1):121–131. PubMed.
- Hild SA, Attardi BJ, Koduri S, Till BA, Reel JR. Effects of synthetic androgens on liver function using the rabbit as a model. J Androl. 2010;31(5):472–481. PubMed.
- Farkas K, Aeberhard AC, Schiffer E, Brull SJ, Czarnetzki C, Maillard J. Potential interaction between exogenous anabolic steroids and sugammadex: failed reversal of rocuronium in a patient taking testosterone and trestolone acetate. Anaesth Rep. 2023;11(2):e12262. PubMed.
- Long JE, Lee MS, Blithe DL. Update on novel hormonal and nonhormonal male contraceptive development. J Clin Endocrinol Metab. 2021;106(6):e2381–e2392. PubMed.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.
- Code of Federal Regulations. Schedule III, 21 CFR 1308.13. 21 CFR 1308.13.