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Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.
Primobolan (Methenolone)
DHT-derived AAS — 1-methyl-5α-dihydrotestosterone — available as injectable enanthate (long ester) and oral acetate (short, non-17α-alkylated, low oral bioavailability).
Aliases (15)
Overview
What is Primobolan (Methenolone)?
Primobolan is the trade name (Schering, then Bayer) for methenolone — a 1-methylated 5α-dihydrotestosterone derivative anabolic-androgenic steroid. Available as injectable methenolone enanthate (long ester, ~10.5-day half-life, IM-only) and oral methenolone acetate (short half-life, NOT 17α-alkylated, oral bioavailability roughly 6-8% — among the lowest of any oral AAS). Originally developed by Squibb (1960) and licensed to Schering in 1962 for clinical anemia and pediatric growth-failure indications. Schedule III in the US and WADA S1.1a-prohibited at all times. Schering withdrew the product from most markets by the early 2000s; legitimate pharma supply now restricted to Spain and Turkey (Bayer-Schering Primobolan Depot ampules) — and those ampules are themselves the most-counterfeited AAS presentation on the global black market.
Key Benefits
Lean-mass retention during caloric deficit (cutting / pre-contest cycles), no aromatization (no estradiol-driven water retention or gynecomastia), low DHT-pathway side-effect intensity per mg, modest hepatotoxicity (acetate is 1-methylated, not 17α-alkylated, so liver burden is far lower than oral testosterone, oxandrolone, or anadrol), one of the lowest-virilization AAS for female users (anabolic:androgenic ratio ~88:44 on classic rat assays), and SHBG preservation that helps maintain endogenous androgen tone during cycling.
Mechanism of Action
Methenolone acetate — oral bioavailability is poor (~6-8% per most pharmacokinetic estimates), substantially below 17α-alkylated orals (40-60%). The 1-methyl group at C1 partially protects from first-pass hepatic metabolism without imposing the c17 alkylation hepatotoxicity. Practical effect: oral acetate requires 2-3x daily dosing at 50-100 mg/day to deliver bioactive doses comparable to ~75-150 mg/week of injectable enanthate. The trade-off is convenience (no needles) at a cost (poor bioavailability, more API per dose, higher per-mg cost).
Pharmacokinetics
Peptide Interactions
Standard "TRT base" companion to any AAS cycle including methenolone. Without testosterone base at 200-300 mg/week, methenolone-only cycles deliver paradoxic…
Both mild AAS, both low aromatization. Stack creates a "lean-mass-only" pre-contest profile. Hepatotoxicity stacking concern exists because oxandrolone is 17…
Both DHT-derivatives, both non-aromatizing. Functional duplication risk — both compounds drive similar AR signaling profile. Stacked in pre-contest for addit…
"Quality lean" stacking partner — both mild AAS, both non-alkylated (boldenone is testosterone-derivative with 1-double bond, not DHT-derivative), both relat…
Maintains testicular volume / responsiveness; eases PCT.
Trenbolone's CNS / cardiovascular / lipid disturbance + HPTA-crushing effects are independent of and additive to methenolone's profile. Common in advanced bo…
methenolone acetate is itself oral but 1-methylated, not 17αα — adding multiple 17αα compounds escalates hepatotoxicity even though methenolone itself doesn'…
AAS-class effect potentiates warfarin via albumin displacement and clotting-factor synthesis modulation. Methenolone label historically carried this warning.
AAS-class glucose tolerance shift; diabetic users may need dose adjustment.
Quality Indicators
Verified third-party lab analysis (HPLC + GC-MS)
Real methenolone enanthate or acetate confirmed by independent mass-spec analysis matching reference spectra. Given >50% counterfeit rate per published seizure analyses, third-party verification is the single most important quality gate for this compound.
Pharma-grade Bayer/Schering ampules with intact tax stamps
Historic 1 mL/100 mg Schering Primobolan Depot ampules from Spain or Turkey (still manufactured there as of mid-2020s) are the legacy 'gold standard.' Authentic ampules carry batch-specific holograms, intact pharmacy stamps, and verifiable serial numbers — though Schering-branded ampules are themselves the most-counterfeited steroid presentation on the market.
Underground lab (UGL) product without published COA
The vast majority of 'primobolan' on the underground market is UGL-produced. Without batch-specific Certificate of Analysis from an independent lab (Janoshik, AnabolicLab, SIMEC), the identity and concentration claims are unverifiable. Some UGLs deliberately substitute boldenone or testosterone because methenolone API costs ~5-10× more per gram.
Suspiciously cheap product
Real methenolone enanthate retails (UGL) at $90-150 per 10 mL/100 mg vial — substantially more than testosterone, nandrolone, or boldenone. Anything priced at testosterone-tier ($40-60 per vial) is statistically far more likely to be a substituted compound than a 'great deal.' This is the single most reliable counterfeit signal.
Cloudy oil, particulates, or inconsistent color
Pharmaceutical-grade injectable oil should be clear (light yellow to pale amber for sesame/cottonseed/grapeseed bases); cloudiness, sedimentation, or color inconsistency between vials suggests sterility failure, undissolved hormone, or a dosed solvent. Discard.
What to Expect
- OnsetSlow. Long ester (enanthate) requires 2-3 weeks of twice-weekly injection to reach steady-state. Subjective effects emerge week 3-5 — modest improvement in …
- Peakeffect: Weeks 6-10. Lean-mass gain modest — typically 5-12 lb across a 12-week cycle even at 600 mg/week, vs 15-25 lb on equivalent test+tren stack. Strength…
- Off-cycleHPG recovery typically 4-12 weeks for first or second cycle users with proper PCT (tamoxifen / clomiphene 4 weeks). Longer with stacked or extended-duration…
Side Effects & Safety
Common (>10%): Mild oily skin, minor acne (face, back), modest hematocrit elevation, modest LDL rise / HDL drop, injection-site mild soreness (oil-based IM).
Less common (1-10%): Increased aggression / mood shift (less than testosterone or trenbolone), libido changes (paradoxically can decrease in methenolone-only cycles due to lack of aromatization → low estradiol), mild hair-loss acceleration in genetically susceptible users, transient liver-enzyme elevation (oral acetate, mild — substantially less than 17αα orals).
Rare-serious (<1%): Peliosis hepatis (vascular hepatic complication, more associated with 17αα orals but methenolone acetate fatal case documented — Solans-Domenech 1993, PMID 8334198), prolonged hypogonadism after withdrawal (Rasmussen 2016), polycythemia requiring phlebotomy (less likely than with boldenone or testosterone), severe lipid disturbance, blood pressure elevation.
Theoretical concerns / class-wide:
- Cardiovascular long-term risk. AAS-class effect — Pope HG Jr et al. 2014 (Endocrine Reviews 35:341) and Kanayama / Pope long-term cohort work documents accelerated cardiomyopathy, atherosclerosis, and dysrhythmia in chronic AAS users. Methenolone is on the milder end of this profile but not exempt.
- HPG-axis permanent shutdown. Real risk in young / chronic users. Methenolone's "milder suppression" claim is dose-dependent — at clinical doses suppression is modest, at physique doses it's substantial.
- Female virilization permanence. Voice changes and clitoral enlargement often do not reverse on discontinuation. STOP IMMEDIATELY at first virilization sign.
- Counterfeit substitution. The most-likely "side effect" the average user actually encounters is "this isn't methenolone." Substituted compound (testosterone, nandrolone, boldenone) carries its OWN side-effect profile — typically MORE side effects than expected because user dosed for "mild methenolone" but actually injected a stronger AAS.
Specific watch periods: Week 3-4 lab check (hematocrit, lipids, LFTs, total T trend if monitoring suppression); week 6-8 mid-cycle check; post-cycle week 4 (HPG recovery onset); post-cycle week 12 (full HPG recovery should be present in healthy first-cycle users).
WADA / commission detection windows: Methenolone enanthate detectable in urine ~5-10 weeks post-cycle for routine GC-MS; >30 days for long-term sulfate metabolites via current LC-HRMS / GC-HRMS methods (Albertsdóttir 2020, PMID 32386339). Acetate slightly shorter (4-6 weeks routine, 20-30 days for long-term metabolites). For tested MMA: assume methenolone is detectable for at minimum 6 weeks post-cycle and likely much longer with current testing technology.
References
DEA Diversion Control: Anabolic Steroids
Schedule III status, federal law context
View StudyWADA 2026 Prohibited List
S1.1a banned at all times, detection-window context
View StudyWikipedia: Metenolone enanthate
general background, history, Schering 1962 licensing
View StudyPubChem CID 248271 — Methenolone Enanthate
ester form molecular reference
View StudyAllen DM et al. 1968 — Anabolic Androgenic Steroids in the Treatment of Acquired Aplastic Anemia (Blood 34:283)
foundational clinical evidence
View StudyHast R et al. 1978 — Treatment of refractory anemias with methenolone (PMID 367090)
19-patient series
View StudyAmmus SS 1981 — Pathophysiology of aplastic anemia and treatment with methenolone enanthate (PMID 7467606)
mechanism review
View StudySchmidt-Gayk H et al. 1975 — Methenolone enanthate effect on albumin pool in liver cirrhosis (PMID 1224752)
historic hepatic-use reference
View StudySolans-Domenech M et al. 1993 — Fatal outcome after metenolone acetate in severe aplastic anemia (PMID 8334198)
rare-serious adverse outcome
View StudySchänzer W, Geyer H, Donike M 1990 — Identification of new urinary metabolites of methenolone (PMID 2242348)
metabolite mapping for doping detection
View StudySaudan C et al. 2015 — Sulfo-conjugated vs gluco-conjugated metabolites for methenolone misuse detection (PMID 26259657)
extended-detection-window WADA work
View StudyAlbertsdóttir AD et al. 2020 — Long-term urinary metabolites of metenolone via GC-MS focus on non-hydrolysed sulfates (PMID 32386339)
current state of doping detection
View StudyMagnolato A et al. 2017 — GC-MS quantitative analysis of black-market AAS seized by Brazilian Federal Police (PMID 28432962)
counterfeit prevalence empirical data
View StudyCoopman V et al. 2022 — Fake AAS on the black market: systematic review and meta-analysis (PMC9288681)
42% counterfeit, 67.5% under-dosed
View StudyMusshoff F, Daldrup T — Black Market in Anabolic Steroids
European seizure analysis
View StudyBond P et al. 2022 — AAS-induced liver injury: An update (PMC9331524)
non-17αα agents substantially safer
View StudyLiverTox: Androgenic Steroids (NCBI Bookshelf NBK548931)
NIH-curated drug-induced liver injury reference
View StudyPope HG Jr et al. 2014 — Adverse Health Consequences of Performance-Enhancing Drugs (Endocrine Reviews 35:341)
AAS adverse effects review
View StudyRasmussen JJ et al. 2016 — Former AAS users with persistent hypogonadism (J Clin Endocrinol Metab 101:1396)
long-term HPG dysfunction
View StudySaartok T, Dahlberg E, Gustafsson JA 1984 — Relative AAS binding affinity to AR and SHBG (PMID 6539197)
methenolone AR-binding and SHBG-binding data
View StudyVanberg P, Atar D 2010 — AAS abuse and the cardiovascular system (Handbook of Experimental Pharmacology)
CV mechanism review
View StudyHartgens F, Kuipers H 2004 — Effects of AAS in athletes (Sports Medicine)
class-wide physiology + side-effect review
View StudyHow was your experience with this compound?
Anonymous · one vote per session · results below at 5+ votes.
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