Superdrol
Methasterone · Methyldrostanolone
Superdrol (methasterone / methyldrostanolone; 2alpha,17alpha-dimethyl-5alpha-androstan-17beta-ol-3-one) is an orally active, 17-alpha-alkylated anabolic-androgenic steroid (AAS), a methylated derivative of drostanolone. It was sold from the mid-2000s as an over-the-counter "prohormone"/muscle-building supplement, misrepresented as non-hormonal, before the US DEA classified it as a Schedule III anabolic steroid in 2012. It is used non-medically to increase muscle mass and strength. The main danger is severe, often cholestatic and prolonged, drug-induced liver injury: multiple published case reports and small case series describe deep jaundice, intense pruritus, and bilirubin that continues to rise for weeks after the drug is stopped, at doses within the range users report. Liver injury has been accompanied by acute kidney injury (including biopsy-proven IgA nephropathy), and there is at least one report of hepatitis-associated aplastic anemia. There are no randomized controlled trials and no formal human pharmacokinetic or safety studies of methasterone; the entire human evidence base is case reports and small case series, so certainty is low and the true frequency of harm is unknown. As a non-aromatizing 17-alkylated oral AAS it also predictably suppresses the hypothalamic-pituitary-testicular (HPTA) axis and is expected to worsen the lipid profile, though these specific effects are poorly quantified for methasterone itself. This monograph is deliberately risk-forward and is not a how-to guide: it exists to describe dangers and monitoring, not to direct use. Anyone using or considering it should involve a physician and get baseline and follow-up bloodwork.
Mechanism of action
Pharmacokinetics
Not formally characterized in humans. No published human pharmacokinetic study reports a validated plasma half-life; commonly cited short (single-digit hours) values are not backed by rigorous human PK data. Do not treat any half-life figure as reliable.
Not established in controlled human studies. Because it is a non-esterified oral 17-alkylated steroid, biological androgenic activity is presumed short (dosed one or more times daily in reported use), but this is inference, not measured data.
Oral (17-alpha-methylation confers oral bioavailability). Reported/marketed only as an oral tablet or capsule.
Hepatic metabolism dominates: extensive phase I hydroxylation and 3-keto reduction with phase II glucuronidation and sulfation, characterized in human hepatocytes, human urine, and chimeric (humanized-liver) mouse models. Parent drug and metabolites are excreted in urine; some metabolites remain detectable in urine for up to ~10 days. Note: metabolism/washout information here is for clinical monitoring and understanding persistence of effect, not for evading drug testing.
For monitoring and washout planning, not drug-test evasion.
Physiological & performance effects
- Increases skeletal-muscle mass and body weight and strength when used with resistance training (reported user-level effect; consistent with androgen-receptor agonism, no controlled efficacy trials exist)
- Non-aromatizing: does not convert to estrogen, so estrogenic effects such as gynecomastia are not expected from the parent compound
- Androgenic effects typical of DHT-derived steroids (e.g., acne, potential accelerated male-pattern hair loss, virilization in females)
- Note: benefits are unquantified in any controlled human study; the compound was marketed with false claims of being non-hormonal and harmless
Adverse effects by system
No methasterone-specific human cardiovascular outcome or lipid data exist. As a 17-alpha-alkylated non-aromatizing oral AAS it belongs to a class strongly associated with adverse lipid changes (reduced HDL-C, raised LDL-C) and cardiovascular risk; this is a class-based expectation extrapolated from other oral AAS, not directly measured for methasterone. Treat cardiovascular risk as plausible and monitor, but recognize the direct evidence gap.
The dominant and best-documented harm. Multiple case reports and a 5-patient case series describe severe cholestatic drug-induced liver injury: profound jaundice, pruritus, and markedly elevated bilirubin that can keep rising for up to ~2 weeks after stopping the drug, with a predominantly cholestatic (bland canalicular cholestasis on biopsy) pattern and comparatively modest transaminase elevation. A larger AAS-DILI review found methyldrostanolone (methasterone) the single most commonly implicated agent, with RUCAM causality mostly 'possible' to 'probable'. Recovery over weeks-to-months is typical with supportive care, but the course can worsen before it improves.
No methasterone-specific human endocrine data, but as an exogenous androgen it is expected to suppress the hypothalamic-pituitary-testicular axis (reduced LH/FSH and endogenous testosterone). Magnitude and recovery time are not quantified for this compound. See hptaSuppression.
No methasterone-specific human fertility data. HPTA suppression from exogenous androgens is expected to reduce spermatogenesis and cause testicular atrophy; virilization is expected in females. These are extrapolations from androgen class effects, not measured for methasterone.
No methasterone-specific human psychiatric data. Mood disturbance, irritability, and aggression are reported broadly with AAS use as a class, but no primary methasterone-specific evidence supports or quantifies this; stated here as an evidence gap rather than an established methasterone effect.
Acute kidney injury is reported in association with methasterone-related liver injury. One biopsy-proven case of IgA nephropathy with cholestatic jaundice attributed to Superdrol, one case of cholestasis with renal failure, and in an AAS-DILI series 43% of patients developed kidney injury (often as cholemic nephropathy/bile-cast injury accompanying severe cholestasis). Renal injury is generally reversible with recovery of liver function and supportive care in reported cases.
One published case links methasterone to transient cholestatic hepatitis followed by severe hepatitis-associated aplastic anemia in a young man. This is a single case report (rare, causality not proven) but is a serious hematologic signal warranting a CBC if a user develops hepatitis. Broader AAS classes can raise hematocrit, but that specific effect is not documented for methasterone.
No dedicated methasterone studies; androgenic dermatologic effects (acne, oily skin, potential acceleration of male-pattern hair loss) are expected for a DHT-derived androgen but are not documented in the primary methasterone case literature. Reported as class-based expectation with a direct evidence gap.
HPTA suppression & recovery
Suppression: Expected to be significant (suppression of LH/FSH and endogenous testosterone) as with any exogenous androgen, but not quantified for methasterone in any human study.
No methasterone-specific recovery data exist. Timeframe and completeness of HPTA recovery are unknown for this compound. Any post-cycle management, including whether and how a single selective estrogen receptor modulator might be used, must be individualized and directed by an endocrinologist or qualified physician with laboratory monitoring; this monograph does not recommend any specific recovery protocol and never endorses multi-drug SERM regimens. Persistent fatigue, low libido, or symptoms of hypogonadism after stopping warrant endocrinology referral and testing rather than self-treatment.
Monitoring
Cadence: Obtain baseline labs before any use; if used, recheck liver and renal panels early (e.g., within the first few weeks) and promptly at any symptom. Because bilirubin can keep rising for ~2 weeks after cessation, continue monitoring after stopping until values clearly trend down. Any abnormality warrants immediate clinician involvement rather than a fixed schedule.
- Jaundice (yellow eyes/skin) or dark urine
- Intense generalized itching (pruritus)
- Right-upper-quadrant or abdominal pain, nausea, poor appetite
- Pale/clay-colored stools
- Reduced urine output, swelling, or other signs of kidney injury
- Unusual bruising, bleeding, pallor, or fatigue (possible marrow/hematologic problem)
- Any of these: stop the compound immediately and seek urgent medical care
Contraindications
- Any pre-existing liver disease or abnormal baseline liver function
- Pre-existing kidney disease or reduced renal function
- Pregnancy and breastfeeding (androgen exposure; virilization risk to a female fetus)
- Female use generally (virilization risk) and adolescents/anyone not skeletally/endocrinologically mature
- Pre-existing cardiovascular disease or dyslipidemia (class-based adverse lipid expectation)
- Concurrent hepatotoxic drugs, other 17-alpha-alkylated oral steroids, or heavy alcohol use
- History of hormone-sensitive cancer or unexplained cytopenias
- Note: this is not a medically approved drug for muscle building; there is no clinical indication for such use
Interaction profile
- MajorWith another anabolic steroid: Additive cardiovascular strain
- MajorWith a thermogenic stimulant: Additive cardiovascular strain
- ModerateWith thyroid hormone: Additive cardiovascular strain
- ModerateWith growth hormone: Additive cardiovascular strain
- MajorWith another 17α-alkylated oral: Additive liver strain
- MajorWith a liver-signal SARM: Additive liver strain
- MajorWith another anabolic steroid: Blood / clotting
- MajorWith a clot-promoting SERM: Blood / clotting
- ModerateWith an aromatase inhibitor: Hormonal
- ModerateWith an anabolic steroid: Hormonal
- ContraindicatedWith DNP: Additive cardiovascular strain
Check a specific combination in the interaction checker.
Reducing harm & when to stop
- Methasterone can cause severe, prolonged cholestatic liver injury and kidney injury even at commonly reported doses; there is no known 'safe' dose and no controlled human safety data.
- Get baseline bloodwork (liver panel, renal function, lipids, CBC) with a physician before any use, and repeat during and after use.
- Bilirubin/jaundice can worsen for up to ~2 weeks after stopping, so stopping does not mean the danger has passed; keep monitoring until labs clearly improve.
- Stop immediately and seek urgent medical care for jaundice, dark urine, intense itching, abdominal pain, pale stools, reduced urination/swelling, or unusual bruising/bleeding/pallor.
- Avoid combining with alcohol, other 17-alpha-alkylated oral steroids, or other hepatotoxic drugs.
- Do not use with any pre-existing liver, kidney, or cardiovascular disease, or if pregnant/breastfeeding; not appropriate for female or adolescent use given virilization risk.
- Any concerns about hormonal recovery after use should be handled by an endocrinologist with lab testing rather than self-managed; this monograph does not provide a recovery protocol.
- This information is for risk reduction and clinical safety, not to optimize, dose, or stack the compound.
Citations (11)
Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.
- 01
Methasterone (2alpha,17alpha-dimethyl-5alpha-androstan-17beta-ol-3-one) and prostanozol were classified by the US DEA as Schedule III anabolic steroids under the Controlled Substances Act (2012).
GuidelineClassification of two steroids, prostanozol and methasterone, as Schedule III anabolic steroids under the Controlled Substance Act. Final rule.PMID 22844688 ↗
- 02
Methasterone is the 17-alpha-methylated derivative of drostanolone; its structure and human/hepatocyte phase I metabolism (3-keto reduction, hydroxylation) were characterized, confirming hepatic biotransformation.
PreclinicalIdentification of drostanolone and 17-methyldrostanolone metabolites produced by cryopreserved human hepatocytes.PMID 19056412 ↗
- 03
Methasterone (superdrol) undergoes extensive hepatic phase I and phase II (glucuronide/sulfate) metabolism, studied in humanized (chimeric) mouse and human models.
PreclinicalMetabolic studies with promagnon, methylclostebol and methasterone in the uPA+/+-SCID chimeric mice.PMID 21762781 ↗
- 04
Methasterone metabolites are excreted in human urine and some remain detectable for up to ~10 days, indicating persistence of metabolites after dosing.
PreclinicalNew Potential Biomarker for Methasterone Misuse in Human Urine by Liquid Chromatography Quadrupole Time of Flight Mass Spectrometry.PMID 27669235 ↗
- 05
Several anabolic steroids including methasterone competitively inhibit human AKR1D1 (a bile-acid synthesis enzyme whose loss of function causes hepatic cholestasis), providing a mechanistic basis for cholestatic hepatotoxicity.
PreclinicalAssessment of the inhibitory potential of anabolic steroids towards human AKR1D1 by computational methods and in vitro evaluation.PMID 37451653 ↗
- 06
Methasterone use causes severe cholestatic drug-induced liver injury: 5 previously healthy patients developed jaundice about 2 weeks after discontinuation, with bilirubin peaking weeks later and resolution over ~12 weeks.
Case seriesMethasteron-associated cholestatic liver injury: clinicopathologic findings in 5 casesPMID 18187367 ↗
- 07
Superdrol/methasterone caused cholestatic jaundice together with biopsy-proven IgA nephropathy in a previously healthy man, showing combined hepatic and renal injury.
Case reportCholestatic jaundice and IgA nephropathy induced by OTC muscle building agent superdrol.PMID 16952289 ↗
- 08
The methasteron-containing supplement Superdrol caused severe cholestasis accompanied by acute renal failure.
Case reportSevere cholestasis and renal failure associated with the use of the designer steroid Superdrol (methasteron): a case report and literature review.PMID 18720005 ↗
- 09
A methasteron-containing performance-enhancing supplement caused severe hepatotoxicity.
Case reportSevere hepatotoxicity caused by a methasteron-containing performance-enhancing supplement.PMID 18813027 ↗
- 10
In an AAS drug-induced liver injury review (2 new cases plus 50 from the literature, graded by updated RUCAM), methyldrostanolone (methasterone) was the most commonly implicated agent; presentation was cholestatic (bland canalicular cholestasis), 43% developed kidney injury, and no deaths/transplants occurred.
Case seriesAndrogenic anabolic steroid-induced liver injury: two case reports assessed for causality by the updated Roussel Uclaf Causality Assessment Method (RUCAM) score and a comprehensive review of the literature.DOI 10.1136/bmjgast-2020-000549 ↗
- 11
Methasterone was linked to transient cholestatic hepatitis followed by severe hepatitis-associated aplastic anemia in a young man.
Case reportHepatitis associated aplastic anemia: case report and discussion.PMID 25314890 ↗
Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice