C tier · mixed
Methenolone held genuine marketing authorisation for anaemia due to bone marrow failure and avoids 17alpha-alkylation, but the product has been almost entirely discontinued and the published human evidence base is sparse, dated, and dominated by secondary compendia rather than accessible primary trials.
methenolone acetate
Methenolone acetate is the oral 17beta-acetate ester of methenolone, a 1-methylated dihydrotestosterone derivative historically marketed as Primobolan for anaemia arising from bone marrow failure. Because it is esterified at C17beta rather than alkylated at C17alpha, it lacks the classical hepatotoxic signature of the alkylated orals, but it has been discontinued in most markets and reliable modern human pharmacokinetic data are difficult to locate.
the explanation
Methenolone acetate is the swallowable form of an old prescription steroid once used to treat certain anaemias. It is not built the way most steroid pills are, so it is easier on the liver, but it has largely disappeared from pharmacies.
regulatory status
US Schedule III controlled substance; approved medical indication historically held, now largely withdrawn
Methenolone is enumerated at 21 CFR 1308.13(f)(49) as 'methenolone (1-methyl-17beta-hydroxy-5alpha-androst-1-en-3-one)', which captures its esters. Introduced in West Germany in 1961 and the United States in 1962 and historically indicated for anaemia due to bone marrow failure, the drug has since been discontinued in most territories, with secondary drug directories reporting persisting medical availability only in a small number of markets such as Japan. No current US marketing authorisation exists. Anabolic steroids as a class are Class C under the UK Misuse of Drugs Act 1971, and methenolone is prohibited at all times in sport under WADA.
how it works · proposed mechanism
Methenolone acetate is a prodrug ester of a non-aromatisable, DHT-derived androgen receptor agonist.
17beta ester, not 17alpha alkyl
Oral activity relies on a C17beta acetate ester and A-ring methylation rather than a C17alpha methyl group. This spares the compound the specific structural feature that LiverTox identifies as the driver of cholestatic injury in oral androgens.
1-methyl delta-1 A-ring
The 1-methyl substituent on a delta-1 unsaturated A-ring stabilises the molecule against hepatic 3-keto reduction. It also underpins the compound's classically reported bias toward anabolic over androgenic activity in preclinical assays.
Non-aromatisable 5alpha steroid
With a saturated 5alpha configuration, methenolone is not an aromatase substrate and cannot form oestradiol. Consequently oestrogen-mediated effects on lipids, fluid balance and gonadotrophin feedback are absent.
what’s reported
evidence shape
4 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 reputation of methenolone as a 'mild' steroid rests largely on structural reasoning and older secondary compendia rather than on published human safety cohorts, and no accessible modern pharmacokinetic dataset defines its oral half-life or bioavailability. Because the licensed product has essentially vanished from legitimate supply, essentially all material in circulation is of unverified identity and purity.
key published findings
- Human regulatory history: methenolone acetate was introduced in West Germany in 1961 and the United States in 1962 with an indication in anaemia due to bone marrow failure, and has since been discontinued in most markets (secondary drug directories).
- Chemistry (PubChem): methenolone acetate is C22H32O3, molar mass 344.5 g/mol, CAS 434-05-9; the ester is hydrolysed to free methenolone, C20H30O2.
- Regulatory (21 CFR 1308.13(f)(49)): methenolone is listed as a Schedule III anabolic steroid under its parent chemical name, which by statute extends to its esters.
- Structure-toxicity (LiverTox review): C17alpha-alkylated androgens are identified as the most hepatotoxic subgroup, while non-alkylated and C17beta-esterified preparations are assigned lower hepatic risk — the category into which methenolone acetate falls.
- No accessible primary human study reporting oral bioavailability or elimination half-life for methenolone acetate was located; these parameters are recorded as null rather than estimated.
limitations of the evidence
- Oral bioavailability and elimination half-life could not be verified against any primary source and are reported as null.
- Most descriptive pharmacology for this compound circulates through secondary compendia and non-peer-reviewed handbooks rather than indexed primary literature.
- The claim of comparative mildness is inferred from structure and class-level hepatotoxicity data rather than from methenolone-specific human safety cohorts.
documented safety signals
- HPG-axis suppression: as with any exogenous androgen, suppression of LH and FSH leads to reduced endogenous testosterone, testicular atrophy and impaired spermatogenesis, with recovery time uncertain.
- Adverse lipid effects: androgens generally lower HDL cholesterol and raise LDL; being non-aromatisable, methenolone provides no oestrogen-mediated offset to this atherogenic shift.
- Hepatic risk is lower than for 17alpha-alkylated orals but not zero — androgens as a class are associated with peliosis hepatis and hepatic adenoma/carcinoma on prolonged high exposure (LiverTox).
- Virilisation in women: deepening voice, hirsutism, menstrual disturbance and clitoral enlargement, which may be irreversible; DHT-derived androgens are not attenuated by aromatisation.
- Androgenic effects: acne, seborrhoea, androgenic alopecia and, in susceptible men, prostatic hypertrophy.
- Premature epiphyseal closure and accelerated skeletal maturation with exposure before completion of growth.
- Polycythaemia and increased haematocrit are recognised androgen class effects, relevant given the historical use of this drug precisely to stimulate erythropoiesis in marrow failure.
- Because licensed supply is effectively absent, counterfeit and mislabelled material is a dominant practical hazard, with substitution by more hepatotoxic alkylated steroids documented across this market.
identity
| full name | Methenolone acetate / metenolone acetate (17beta-acetoxy-1-methyl-5alpha-androst-1-en-3-one) |
| category | Anabolic & Androgenic |
| modality | steroid |
| formula | C22H32O3 |
| molar mass | 344.5 g/mol |
| cas | 434-05-9 |
laboratory handling
| storage | Solid; store tightly closed, protected from light and moisture at controlled room temperature; analytical standards are typically stored refrigerated or frozen. As an ester, avoid humid conditions that promote hydrolysis. |
| solubility | Practically insoluble in water; soluble in ethanol, methanol and DMSO. The 17beta-acetate ester is more lipophilic than the parent alcohol. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
4 citedElectronic Code of Federal Regulations (DEA) · 2026 · official
PubChem, US National Library of Medicine · 2026 · official
NIDDK / NCBI Bookshelf · 2020 · review
British Journal of Pharmacology · 2008 · review
others in Anabolic & Androgenic