Injectables

Trestolone Enanthate

Updated · 22 sources · Editorial policy

Trestolone enanthate is trestolone (7α-methyl-19-nortestosterone, often called MENT) with a seven-carbon enanthate (heptanoate) ester attached. Trestolone itself is a synthetic androgen related to nandrolone. The Population Council studied it from the 1990s onward as a possible testosterone substitute for male hormonal contraception and for treating low testosterone (hypogonadism) (Nieschlag et al., Contraception 2013).

The single most important fact about this form: no published human or animal study of trestolone enanthate exists. Every clinical study of trestolone used either the unesterified steroid or trestolone acetate, mostly in slow-release implants. The enanthate is sold outside medicine, and its dose, kinetics and safety have never been characterized. It has never been approved as a medicine anywhere we could verify.

This page summarizes what the clinical and laboratory research on the parent steroid reports, and what is and is not known about the enanthate ester. It is for education only and is not medical advice.

Property Detail
Drug class Synthetic anabolic-androgenic steroid (19-nortestosterone derivative); not 17α-alkylated
Chemical name 7α-methyl-3-oxoestr-4-en-17β-yl heptanoate; C₂₆H₄₀O₃, 400.6 g/mol (CAS 81005-56-3)
Approval status Never approved; no trestolone product in FDA’s drug approval database
Route No studied route for this ester; trials of other forms used subdermal implants and IM injection
Studied doses None for the enanthate. Human trials used trestolone acetate implants or injected unesterified trestolone
Half-life Not measured for the enanthate. Unesterified trestolone: terminal half-life ≈ 40 minutes after IV dosing in men
Trestolone content ≈ 72% of the ester’s weight (100 mg ester ≈ 72 mg trestolone)
Key mechanism fact Not converted by 5α-reductase; is converted by aromatase to an estrogen; does not bind SHBG
US schedule Not named in the DEA’s Schedule III list of anabolic steroids
WADA Prohibited at all times (S1.1, named, including esters)

What it is

Trestolone is 19-nortestosterone (nandrolone) with a methyl group added at the 7α position. Its formula is C₁₉H₂₈O₂ and its molecular weight is 288.4 g/mol (PubChem CID 9838899). The enanthate ester is attached at the 17β-hydroxyl group, raising the molecular weight to 400.6 g/mol (PubChem CID 101235236). The ester therefore makes up about 28% of the weight, so a labeled “100 mg” of trestolone enanthate contains about 72 mg of trestolone.

Like other steroid esters, the enanthate is a prodrug: it has to be cleaved off before the steroid can act. In the clinical program, researchers chose the acetate ester for implants and showed that it is rapidly hydrolyzed to free trestolone in the blood (Kumar et al., J Androl 1997; Anderson et al., JCEM 1999). Organon chemists later synthesized a series of trestolone esters and measured how quickly human liver enzymes split them, as a way to choose esters for different formulations (Bursi et al., Steroids 2003). That was a laboratory study; no ester other than the acetate went into published human trials.

The library has separate pages for the other forms:

Form What it is Where it was studied
Trestolone acetate (MENT) Short ester Subdermal implants in the human trials below
Trestolone base Unesterified steroid Single IV and short-course IM injections in men
Trestolone enanthate (this page) Long ester, same ester as testosterone enanthate No published studies

Why the 7α-methyl group matters

Testosterone is converted in the prostate and other tissues to dihydrotestosterone (DHT) by the enzyme 5α-reductase, which amplifies its effect there. The 7α-methyl group blocks this step. Laboratory and animal studies built the case for trestolone on this point:

  • Receptor binding (in cell culture). Trestolone bound the androgen receptor with higher affinity than testosterone and was the most potent androgen tested in a reporter-gene assay, ahead of DHT, nandrolone and testosterone (Kumar et al., J Steroid Biochem Mol Biol 1999).
  • In castrated rats, trestolone acetate was about 4 times as potent as testosterone on prostate and seminal vesicle weight, about 10 times as potent on the levator ani muscle, and about 12 times as potent at suppressing gonadotropins. A 5α-reductase inhibitor blunted testosterone’s prostate effect but did not change trestolone’s (Kumar et al., Endocrinology 1992).
  • In castrated monkeys, trestolone was 10 times as potent as testosterone for LH suppression and body weight but only about twice as potent for prostate growth (Cummings et al., JCEM 1998).

These are animal results. They suggested a wider gap between muscle and prostate effects than testosterone has, but they were never confirmed as a muscle-building advantage in people.

Estrogen and progesterone activity

Trestolone is not “non-aromatizing.” Incubated with human aromatase from placental tissue, it was converted to 7α-methylestradiol, an estrogen (LaMorte et al., J Steroid Biochem Mol Biol 1994). In rabbits, its progestational activity was comparable to progesterone, and it bound the progesterone receptor with similar affinity (Beri et al., J Steroid Biochem Mol Biol 1998).

About “10 times stronger than testosterone.” This figure is often quoted for trestolone. It comes from animal bioassays (the rat and monkey studies above) and from 1960s anabolic testing (Piper et al., Drug Test Anal 2026). It describes milligram-for-milligram potency of the parent steroid in animals. It is not a measured human effect, and it says nothing specific about the enanthate ester.

Pharmacokinetics

Nothing has been published on how trestolone enanthate is absorbed or how long it lasts. What is known concerns the parent steroid:

Measure (unesterified trestolone, healthy men) Result Source
Terminal half-life after a 500 µg IV dose ≈ 40 minutes; undetectable by 180 minutes Kumar et al. 1997
Metabolic clearance rate 2,360 L/day (IV); 1,790 L/day (IM) Kumar et al. 1997; Suvisaari et al. 1997
Time to peak after 2–8 mg IM in aqueous suspension ≈ 1–2 hours Suvisaari et al. 1997
Binding to SHBG (sex hormone-binding globulin) None detected Kumar et al. 1997

The researchers attributed trestolone’s clearance being much faster than testosterone’s partly to its lack of SHBG binding. This short half-life is why the clinical program used continuous-release implants.

An oil-based enanthate depot would be expected to release trestolone over days rather than hours, as enanthate esters do for other steroids. That is an inference from chemistry, not a measurement. Any specific half-life quoted for trestolone enanthate has no published source we could find.

In human liver tissue preparations, trestolone was metabolized by CYP3A4, 17β-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase (Prasad et al., Steroids 2009).

What the research shows

All human data below come from trestolone acetate implants or injected unesterified trestolone. They show what the active steroid does in men at those exposures, not what the enanthate does.

Suppression of the body’s own testosterone

Trestolone strongly suppresses LH and FSH, the pituitary hormones that drive the testes:

Study Design Main hormonal result
Suvisaari et al., Hum Reprod 1997 24 healthy men; 6 daily IM injections of 1, 2 or 4 mg At 4 mg: testosterone −74%, LH −70%, FSH −57%
Noé et al., Hum Reprod 1999 45 healthy men; 1, 2 or 4 acetate implants for 28 days With 2 or 4 implants: testosterone −93%, DHT −80%, LH −97%, FSH −95%; fully reversed after removal

Serum trestolone levels rose with the number of implants: 0.7, 1.2 and 2.0 nmol/L with 1, 2 and 4 implants in the Noé trial, with each implant releasing about 500 µg per day.

Male contraception

Because it shuts down LH and FSH, trestolone was tested as a contraceptive. In a randomized trial of 35 men given 1, 2 or 4 acetate implants for 6–12 months (von Eckardstein et al., JCEM 2003):

Implants Men Result on sperm count
1 12 None reached oligozoospermia (under 3 million/mL)
2 11 4 became oligozoospermic, 2 of them azoospermic (no sperm)
4 12 8 azoospermic, 1 oligozoospermic, 2 non-responders

A later Edinburgh trial combined two trestolone implants with the progestin etonogestrel in 29 men, against testosterone pellets (Walton et al., J Androl 2007). Sperm fell below 1 million/mL by 12 weeks in 8 of 10 men on trestolone. Suppression was then lost as release from the implants declined, and 6 men in the trestolone group reported loss of libido. A 2012 Cochrane review concluded that no male hormonal contraceptive was ready for clinical use (Grimes et al., Cochrane 2012).

Androgen replacement in hypogonadal men

  • Sexual function and mood. In a crossover trial of 20 hypogonadal men, two 115 mg acetate implants for 6 weeks were compared with two 200 mg injections of testosterone enanthate. Both improved sexual interest, activity, spontaneous erections and mood, with only minor differences (Anderson et al., JCEM 1999).
  • Tissue selectivity. In 16 hypogonadal men treated for 24 weeks, one implant gave below-normal replacement and sexual function declined. Two implants maintained most androgen-dependent functions, and PSA fell in both groups. However, lumbar spine bone density fell in both groups, which the authors saw as consistent with the importance of adequate estrogen activity in replacement therapy (Anderson et al., JCEM 2003).

No controlled trial has measured muscle mass or strength gains from trestolone in people, in any form.

Side effects and risks

What the implant trials reported

The human trials were small and used modest, steady exposures. Within those limits they reported:

Liver (animal data)

Trestolone is not 17α-alkylated, but it was not free of liver effects in animals. In male rabbits given 10 mg/kg/day by mouth for 14 days, trestolone raised liver enzymes and impaired dye clearance (a liver function test), though less than methyltestosterone did. The no-effect dose was 1 mg/kg/day, and values returned to baseline 2 weeks after dosing stopped (Hild et al., J Androl 2010). How this translates to people is unknown.

Fertility and hormonal shutdown

Trestolone is a stronger suppressor of LH, FSH and natural testosterone than testosterone itself, milligram for milligram. In the implant trials, suppression and sperm effects reversed after removal. Recovery after use of an uncharacterized long-acting ester, at unknown doses, has not been studied.

Unknowns specific to the enanthate

  • Dose and exposure. With no pharmacokinetic study, there is no evidence-based way to relate a given amount of the enanthate to the trestolone levels seen in the trials.
  • Product quality. Trestolone enanthate exists only as an unregulated product, so identity, dose and sterility are not assured.
  • Long-term safety. The longest human exposure in the trials cited here was about 12 months, using implants.
  • United States. Trestolone has never been approved as a drug, and no trestolone product is listed in Drugs@FDA. Trestolone is not among the anabolic steroids named in the DEA’s Schedule III list (21 CFR 1308.13).
  • Sport. The WADA 2026 Prohibited List names trestolone (7α-methyl-19-nortestosterone, MENT) under S1.1 anabolic androgenic steroids, together with their esters. It is prohibited at all times and is a non-Specified Substance.
  • Detection. A 2026 anti-doping study noted that no doping sample had been reported positive for trestolone in two decades, even though it is readily available online, and attributed this partly to analytical difficulties. Using deuterium-labeled trestolone acetate, the researchers found 50 candidate metabolites; two newly identified ones detected a single 30 mg oral dose of trestolone acetate for up to 4 days (Piper et al., Drug Test Anal 2026).

Key takeaways

  • An unstudied ester of a studied steroid. Trestolone itself was tested in men as an implant; the enanthate ester has no published human or animal data at all.
  • About 72% trestolone by weight. The enanthate ester accounts for the rest and only controls the release rate.
  • The half-life is unknown. Unesterified trestolone clears in about 40 minutes after IV dosing; no study has measured how long the enanthate lasts.
  • Potent, but the potency figures are from animals. Rat and monkey studies found about 10 times testosterone’s effect on muscle and gonadotropin suppression, with relatively less prostate stimulation.
  • Strongly suppressive and not estrogen-free. In men it cut LH, FSH and testosterone by over 90%; it aromatizes to an estrogen, and spine bone density still fell in hypogonadal men on implants.
  • Unapproved and banned in sport. No country approval was found, and WADA lists trestolone and its esters by name.

Sources

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  8. Cummings DE, Kumar N, Bardin CW, et al. 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.
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  14. Walton MJ, Kumar N, Baird DT, et al. 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.
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  21. Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
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