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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.
Superdrol
Methasterone / Methyldrostanolone (M-Drol, Mdrol, 2a,17a-dimethyl-5a-androstan-17b-ol-3-one) — designer oral 17α-alkylated DHT-derivative AAS; sold as 'supplement' 2005-2012; explicitly scheduled by Designer Anabolic Steroid Control Act 2014.
Aliases (11)
Overview
What is Superdrol?
Superdrol (methasterone, methyldrostanolone, 2α,17α-dimethyl-5α-androstan-17β-ol-3-one) is a synthetic 17α-alkylated DHT-derivative anabolic-androgenic steroid — structurally a methylated drostanolone analog. First synthesized in 1956 (Vida 1969 reference compound), it was never approved by the FDA for any medical indication. It was sold legally in the United States as a 'dietary supplement' from 2005 to 2012 — initially by Anabolic Extreme as 'Superdrol' (10 mg caps, 2005-2007), then by ProMera Health as 'Methyl Masterdrol' (2008-2012) — exploiting a loophole in the 2004 Anabolic Steroid Control Act. The Designer Anabolic Steroid Control Act of 2014 (DASCA, H.R. 4771, Public Law 113-260) explicitly added methasterone to Schedule III of the Controlled Substances Act, closing the gray zone. WADA-banned (S1.1.a). LiverTox classifies methasterone with Likelihood A for clinically apparent liver injury; multiple peer-reviewed case reports document severe cholestatic hepatitis (Singh 2009, Schwartz 2008, El Sherrif 2014, Nasr 2009, Jasiurkowski 2006), with at least one published case requiring liver transplant evaluation. Among the 3-5 most hepatotoxic oral AAS ever marketed.
Key Benefits
Rapid dry/hard strength + lean mass gain (8-15 lb scale gain in 4 weeks) without water retention or estrogenic side effects (because 2α-methyl-DHT-derivative skeleton is non-aromatizing). Reputation as 'oral trenbolone' or 'oral masteron' for the dry, vascular look. The cosmetic appeal that drove its 2005-2012 supplement-era popularity — and its 2014 federal scheduling.
Mechanism of Action
Direct androgen receptor (AR) agonist with very high anabolic potency (~400% of testosterone in animal A:A assays) and moderate androgenic potency (~20% of testosterone). The 17α-methyl group enables oral bioavailability; the 2α-methyl group shifts the steroid skeleton further from native testosterone, blocking aromatization and 5α-reductase metabolism. Profound HPG-axis suppression at any therapeutic dose. No estrogen pathway activation (non-aromatizing, no ER binding).
Pharmacokinetics
Peptide Interactions
Standard kickstart pair. Superdrol weeks 1-3 (rapid early gains, dry profile), Test-E 400-500 mg/week weeks 1-12 (sustained anabolic). The synergy is real (m…
Maintains testicular volume / Leydig responsiveness during cycle; eases PCT.
Most-cited liver-protection adjunct. Mechanism: improves bile flow, displaces hydrophobic bile acids, reduces cholestatic stress — directly relevant to Super…
Glutathione precursor; supports phase-II hepatic detoxification. Same caveat as TUDCA — risk-narrowing, not risk-eliminating. Best paired with TUDCA + milk t…
Older harm-reduction standard. Weaker evidence than TUDCA/NAC for Superdrol-specific protection. Doesn't hurt; modest additive benefit.
([oxandrolone](oxandrolone.md), stanozolol, methyltestosterone, [oxymetholone (Anadrol)](anadrol.md), [methandienone (Dianabol)](dianabol.md), fluoxymesteron…
Dramatically additive hepatic load. Multiple Superdrol DILI case reports involved concurrent alcohol use as accelerator.
at chronic dose. Even therapeutic-dose acetaminophen meaningfully adds to hepatic burden when combined with Superdrol.
Compounding lipid disruption + hepatic load. Superdrol crashes HDL on its own; statins compound the hepatic risk without addressing the underlying cause.
AAS class effect — potentiates anticoagulant action and raises bleeding risk.
Compounding hepatic + renal load. Relevant for combat athletes who use chronic NSAIDs for joint/training pain.
Compounding BP/CV strain. The 2008-2012 ER cluster of CV events in young bodybuilders involved Superdrol + DMAA-era preworkout combinations.
Quality Indicators
No legitimate pharmacy source — never FDA-approved
Methasterone never received FDA approval for any indication. There is no 'pharmacy-grade Superdrol.' From 2005-2012 it was sold as Anabolic Extreme Superdrol then ProMera Health Methyl Masterdrol via supplement retailers (gray-zone exploitation of pre-DSHEA loopholes). The Designer Anabolic Steroid Control Act of 2014 (DASCA) explicitly added methasterone to Schedule III, eliminating any remaining gray zone. Anything sold as 'Superdrol' or 'methasterone' in 2026 is underground-lab (UGL) product — there is no 'good source' verification path.
Historical supplement-era branding (Anabolic Extreme, ProMera Health)
Original Anabolic Extreme Superdrol bottles (2005-2007) had reasonably consistent dosing per third-party assays of the era; ProMera Health Methyl Masterdrol (2008-2012) had higher variability. Any old-stock retail product is now 12-20+ years past expiration — not a viable source path.
UGL tablets without third-party HPLC
Common UGL issues with Superdrol clones: under-dosed (cost-cutting), over-dosed (tablet inconsistency), or substituted (sometimes contains a different methylated steroid altogether — methylstenbolone, dimethazine, M1T, halodrol). Without third-party HPLC, you don't know what you took. Independent labs (Janoshik, AnaboLab) recommended for any UGL Superdrol product.
Generic 'designer prohormone' rebrands post-2014
Post-DASCA 2014, supplement retailers sometimes rebrand methasterone or methasterone-analogs (methylstenbolone, dimethazine) under non-Superdrol names ('Mass Drol', 'M-Sten', 'Brutal 4ce') to skirt naming bans. These are explicitly Schedule III under DASCA's 'substantially similar' clause and carry the same hepatic risk profile. Felony possession in US.
Online 'old stock' Superdrol from non-US sites
Counterfeit or expired product is the dominant pattern. Schedule III importation is a federal felony. Even verified-old-stock product would now be 12+ years past manufacture, with unknown stability.
What to Expect
- Day 3-7Strength surge, increased aggression / "on edge" feeling, scale weight up 2-5 lb (primarily glycogen — no water retention because non-aromatizing). Subjecti…
- Week 1-2Continued strength gains, dry/lean look intensifying. ALT/AST detectably elevated by day 10. HDL crashing rapidly. BP elevation 10-20 mmHg above baseline co…
- Week 2-4Plateau onset. LFTs often peak in this window — ALT 3-5× ULN typical, sometimes much higher. Cholestatic injury onset most commonly presents weeks 2-6 — pru…
- Week 4-6(if continued — strongly inadvisable): Diminishing returns vs. sharply accelerating side-effect curve. Most published case reports of severe DILI involved us…
Side Effects & Safety
The dominant concern is hepatotoxicity — arguably worst-in-class among oral AAS. Everything else is secondary.
Common (>10%):
- ALT / AST elevation (often 3-5x ULN even on a 4-week cycle)
- HDL crash 60-80% (more severe than most 17αAAs)
- LDL elevation 40-60%
- Blood pressure elevation (systolic +10-20 mmHg typical)
- Acne (chest, back, shoulders)
- Hair shedding (DHT-pathway, irreversible if androgenic alopecia is genetic)
- HPG-axis suppression
- Sleep disruption
- Mood lability / aggression / "on edge" feeling
- Increased appetite (some users; less consistent than other AAS)
- Joint dryness / aches (no estrogenic lubrication; common subjective complaint)
Less common (1-10%):
- Bilirubin elevation (early cholestasis signal — this is the critical biomarker)
- GGT elevation (cholestatic pattern)
- Alkaline phosphatase elevation (cholestatic pattern)
- Polycythemia (hematocrit >52%)
- Erectile dysfunction (post-cycle, during HPG recovery)
- Insulin resistance / dysglycemia
- Severe fatigue, weight loss (early DILI signs)
Rare-serious — but case-report-documented in this compound (estimated >1% in users at standard doses past 4 weeks; far higher than typical AAS DILI rates):
- Cholestatic jaundice (typically 2-6 weeks in; can present up to 8 weeks post-cessation)
- Acute renal failure (concurrent with hepatic injury — see Nasr 2009, El Sherrif 2014)
- Liver transplant evaluation (at least one published case)
- Hepatic adenoma (rare; class effect of all 17αAAs)
- Peliosis hepatis (rare)
- Acute hepatic failure (case reports cluster here, more severe per mg than other 17αAAs)
- Thromboembolic events (DVT, PE, stroke) from polycythemia + lipid + BP triple-hit
- Persistent secondary hypogonadism (HPG axis fails to recover even at 12+ months)
Watch periods:
- Week 1-2: ALT/AST should be checked. Even 2× ULN at week 2 is a stop-discussion threshold for Superdrol given the case-report literature. Most other AAS allow more permissive ALT/AST elevation; Superdrol does not.
- Week 2-4: Bilirubin, GGT, alkaline phosphatase — early cholestasis signals. Bilirubin >2× ULN with rising GGT/AlkPhos is an unambiguous stop sign.
- Anytime: jaundice, dark urine + light stool, pruritus without rash, RUQ pain, severe fatigue, unexplained weight loss → STOP IMMEDIATELY, present to ED if jaundice present.
- BP at home weekly; sustained >150/95 → stop.
- Post-cessation week 2, 4, 6, 8: Continue LFT monitoring — cholestatic injury can present or worsen up to 8 weeks after stopping. This is unique among oral AAS.
Drug-induced liver injury (DILI) onset: Typical onset 2-6 weeks into chronic dosing — earlier than other 17αAAs. The 4-week supplement-bottle recommendation puts users squarely in the high-risk window. Cholestasis can present at end-of-cycle or up to 4-8 weeks after cessation.
References
Singh V et al. 2009 — A case of bodybuilder with severe cholestatic jaundice (Superdrol)
foundational case report, 28yo bodybuilder, severe cholestatic jaundice after 4 weeks Superdrol
View StudySchwartz JM et al. 2008 — Methylated steroid Superdrol causing severe cholestatic hepatitis (Am J Med, PMID 18391541)
17yo with cholestatic hepatitis from OTC Superdrol; major driver of public-health concern
View StudyEl Sherrif Y, Potts JR, et al. 2013 — Hepatotoxicity from AAS marketed as dietary supplements: contribution from ATP8B1/ABCB11 mutations? (Liver Int)
case series of four bodybuilders with Superdrol-induced severe cholestatic injury; BSEP/MRP2 transporter polymorphism susceptibility
View StudyNasr J, Ahmad J 2009 — Severe cholestasis and renal failure from Superdrol (methasterone) (Dig Dis Sci)
case report + literature review; cholestatic injury with concurrent acute kidney injury
View StudyJasiurkowski B et al. 2006 — Cholestatic jaundice and IgA nephropathy induced by OTC muscle building agent superdrol (Am J Gastroenterol)
earliest peer-reviewed Superdrol DILI case
View StudyMethasterone — LiverTox NCBI Bookshelf NBK548194
dedicated LiverTox entry on methasterone hepatotoxicity; Likelihood A; cholestatic injury pattern
View StudyAnabolic Steroids — LiverTox NCBI Bookshelf NBK548931
class entry on AAS hepatotoxicity; methasterone listed among most hepatotoxic
View StudyAnabolic androgenic steroid-induced liver injury: An update — Niedfeldt 2022 / PMC9331524
modern review including designer-steroid era
View StudyAnabolic Steroid-Induced Cholestatic Liver Injury — PMC9426951
bland cholestasis mechanism review; BSEP/MRP2 transporter inhibition mechanism
View StudyDesigner Anabolic Steroid Control Act of 2014 (DASCA) — H.R. 4771, Public Law 113-260
explicit federal scheduling of methasterone and 27 other designer steroids; closed the post-2004 gray-zone loophole
View StudyAnabolic Steroid Control Act of 2004 — Public Law 108-358
precursor 2004 Act with DEA emergency-scheduling authority
View StudyNorth Carolina cluster investigation — Public Health Reports 2013
Superdrol-related hepatic injury cluster; legislative driver for DASCA
View StudyDEA Final Rule — Schedule III placement of designer steroids (2014, post-DASCA)
DEA enforcement action
View StudyDILIN prospective study — Hepatology, PMID 26346203
drug-induced liver injury network cohort context for designer steroid DILI
View StudyMethasterone — DrugBank DB16763
pharmacology, mechanism, structural details
View StudyMethasterone — Wikipedia
general background, history (Vida 1969 first synthesis, Anabolic Extreme 2005, ProMera Health, DASCA 2014)
View StudyWADA 2026 Prohibited List — S1.1.a Exogenous AAS
methasterone prohibited
View StudyPope HG Jr et al. 2014 — Adverse Health Consequences of Performance-Enhancing Drugs (Endocrine Reviews)
AAS adverse-effects class review including designer steroid era
View StudyRasmussen JJ et al. 2016 — Former AAS users with persistent hypogonadism (J Clin Endocrinol Metab)
long-term HPG dysfunction
View StudyVanberg P, Atar D 2010 — AAS abuse and the cardiovascular system
CV mechanism review across class
View StudyImpact of AAS Abuse on the Cardiovascular System — MDPI IJMS 2025
2025 mechanistic synthesis
View StudyHepatotoxicity associated with illicit use of AAS in doping — European Review
doping-context review including designer steroids
View StudyLatest research
- reviewImpact of AAS Abuse on the Cardiovascular System — Molecular Mechanisms and Clinical Implications (MDPI IJMS 2025)Recent mechanistic synthesis of AAS-induced cardiovascular molecular pathways including oxidative stress, lipid disruption, hypertrophic signaling — applicable across class including methasterone.
- reviewAnabolic androgenic steroid-induced liver injury — An update (Niedfeldt, World J Hepatol)Modern review confirming AAS hepatotoxicity profile (cholestasis, peliosis hepatis, hepatic adenoma/HCC) is a structural class effect of 17α-alkylated orals; methasterone explicitly discussed as one of the worst designer-steroid era examples.
- case-seriesHepatotoxicity from anabolic androgenic steroids marketed as dietary supplements — contribution from ATP8B1/ABCB11 mutations? (El Sherrif et al., Liver Int)Four bodybuilders with severe cholestatic injury after Superdrol; explored BSEP/MRP2 transporter polymorphism as susceptibility factor; one progressed to renal failure.
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