Primobolan (Methenolone)
Methenolone, 1-methyl-DHT-derivative "mild" AAS in two ester formats: oral acetate (short, low bioavailability) and injectable enanthate (Bayer Primobolan Depot, prescription in Germany + Spain). Classic cutting steroid.
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WHAT IS PRIMOBOLAN (METHENOLONE)?
Detailed overview
Primobolan (Methenolone) is a 1-methyl-dihydrotestosterone derivative synthesized by Schering AG in 1962. Two marketed forms: the acetate ester (Primobolan, oral tablet, originally 5 mg) and the enanthate ester (Primobolan Depot, IM oil 100 mg/ml). Original FDA approval (1962) was for anemia, osteoporosis and severe debilitating illness recovery; withdrawn from the US market by 1965, but Bayer still manufactures Primobolan Depot as a prescription in Germany and Spain (anemia, premature infant catabolic states). Anabolic:androgenic ratio 88:44, indicating moderate anabolic and low androgenic profile. NOT 17α-alkylated, so hepatotoxicity is minimal. Does NOT aromatize. AR affinity is low (~28% vs testosterone in vitro), BUT in muscle tissue indirectly raises free-T levels via SHBG suppression. Oral acetate bioavailability is only ~6% (rapid hepatic metabolism of the 17β-OH-acetate ester), so extremely high doses (50-100 mg/day) are needed to match injectable 100 mg/week enanthate effect. WADA-banned year-round.
Mechanism
AR agonist, 1-methyl-DHT, NOT aromatized
Anabolic:Androgenic
88:44
Half-life
4-6 h (Ac oral), 5-7 d (Enan IM)
Onset
1-2 h (Ac oral), 48-72 h (Enan IM)
Legal status
Bayer Primobolan Depot DE/ES Rx, USA: discontinued
Data console
Lab data
Safety
Side effects, stop signs, contraindications
Side effects · 7
- Androgenic skin and hair effects: methenolone is a DHT structural analog, so it can accelerate hair loss in those genetically prone to androgenetic alopecia, plus acne and oily skin (5-alpha-reductase inhibitors like finasteride do NOT protect, as the molecule is already 5-alpha-reduced).
- Virilization in women: although methenolone has one of the lowest androgenic potentials among AAS, the risk is NOT zero, higher doses can cause voice deepening, hirsutism, clitoral enlargement and menstrual disruption, some of which is irreversible. Any virilization sign warrants immediate cessation.
- Adverse lipid profile: HDL cholesterol falls and LDL may rise (roughly 15-25% HDL drop expected during a cycle). The effect can be more sustained with injectable enanthate due to longer cumulative exposure than with the short-half-life oral acetate.
- HPTA suppression and impaired fertility: methenolone suppresses the hypothalamic-pituitary axis, lowering LH/FSH and thereby endogenous testosterone production and spermatogenesis. Though milder than with testosterone-based steroids, post-cycle therapy (e.g. clomiphene + tamoxifen) is advised in men for recovery.
- Oral acetate form: hepatotoxicity is low (NOT 17-alpha-alkylated), but because of the very low oral bioavailability (~6%) the high daily dose required (50-100 mg) can cause mild liver enzyme elevation (ALT/AST), so liver panel monitoring is warranted.
- Injectable enanthate form: the oily IM injection can cause local reactions, post-injection pain (PIP), redness, swelling, and with non-sterile technique a risk of abscess or infection.
- Prostate stimulation: as a DHT analog, methenolone can stimulate androgen-dependent prostate tissue, potentially worsening prostate enlargement (BPH symptoms) in older men; PSA monitoring is advised above age 30-40.
Contraindications · 7
- Pregnancy and breastfeeding: methenolone's androgenic action is teratogenic and can virilize a female fetus, absolutely contraindicated during pregnancy and lactation.
- Prostate or breast carcinoma (in men): in androgen-dependent tumors AAS can promote tumor growth, so known or suspected prostate or male breast cancer is a contraindication.
- Family history of androgenetic alopecia: as a DHT structural analog it accelerates genetically determined hair loss, which cannot be prevented even by a 5-alpha-reductase inhibitor.
- Cardiovascular disease or dyslipidemia: due to the HDL-lowering, LDL-raising effect, it should be avoided with pre-existing heart disease, high LDL or uncontrolled hypertension.
- Significant liver dysfunction (especially the oral acetate form): with pre-existing elevated ALT/AST or active liver disease the high-dose oral form should be avoided; concurrent alcohol and paracetamol increase the burden.
- Concurrent coumarin-type anticoagulants (e.g. warfarin): AAS can potentiate the anticoagulant effect and bleeding risk, requiring close INR monitoring and dose adjustment.
- Competitive sport under WADA testing: methenolone is banned year-round (S1.1), and the injectable enanthate's metabolites are detectable in urine for up to 4-6 months, contraindicated for tested athletes.
Related Performance Compounds
Same therapeutic category
Studies
Related research and clinical findings
Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement
Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S.
Effects of androgenic-anabolic steroids in athletes
Hartgens F, Kuipers H.
Metabolism of anabolic androgenic steroids
Schänzer W.
Anabolic-androgenic steroid dependence: an emerging disorder
Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr.
Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline
Bhasin S, Brito JP, Cunningham GR et al.
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The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.