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Msd3.0
Methasterone (Superdrol) Research
Mostly mechanism / observationalLimited safety
6 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most Methasterone (Superdrol) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2006–2020.
Based on 6 studies
Confidence
Low
By outcome
Safety profile
Mostly mechanism / observational6 studies
Cholestatic liver injury
Mostly mechanism / observational4 studies
Renal injury
Mostly mechanism / observational3 studies
Androgenic anabolism (unverified)
Mostly mechanism / observational3 studies
Older research base
Newest study from 2020
200620132020
1Case Study2008
Methasteron use can result in severe hepatotoxicity. Liver failure can worsen after initial presentation, especially within 2 weeks.
Shah NL, Zacharias I, Khettry U, Afdhal N, Gordon FD. · Clinical gastroenterology and hepatology (2008)
Clinicopathologic case series of five men who developed cholestatic liver injury after using methasteron (Superdrol), with clinical course, laboratory data and liver histopathology
All presented with cholestatic hepatitis (jaundice, pruritus, marked hyperbilirubinemia); biopsies showed bland intrahepatic/canalicular cholestasis characteristic of 17α-alkylated AAS
Critically, liver failure could WORSEN after presentation — especially within the first two weeks after stopping the drug — a dangerous, counterintuitive course
Severe cholestasis and renal failure associated with the use of the designer steroid Superdrol (methasteron).
Nasr J, Ahmad J. · Digestive diseases and sciences (2009)
Case report with literature review of a patient who developed severe cholestasis AND renal failure after using the designer steroid Superdrol (methasteron)
Captures the liver-plus-kidney pattern — severe cholestatic injury accompanied by renal dysfunction (bile-cast nephropathy can follow severe cholestasis)
Reviews the emerging literature on Superdrol/methasteron hepatotoxicity, reinforcing the 17α-alkylated-AAS cholestasis signal
Liver biopsies showed 'bland' canalicular cholestasis ... a high proportion of patients developed associated kidney injury, and peak bilirubin levels were very high.
Abeles RD, Foxton M, Khan S, Goldin R, Smith B, Thursz MR, Verma S. · BMJ open gastroenterology (2020)
Two RUCAM-scored cases of anabolic-androgenic-steroid-induced liver injury plus a comprehensive literature review of AAS hepatotoxicity, the class to which methasterone belongs
Liver biopsies showed the bland canalicular cholestasis characteristic of 17α-alkylated AAS, with very high peak bilirubin
A high proportion of patients developed associated kidney injury — reinforcing the liver-plus-kidney pattern seen with Superdrol/methasteron
Cholestatic jaundice and IgA nephropathy induced by OTC muscle building agent superdrol.
Jasiurkowski B, Raj J, Wisinger D, Carlson R, Zou L, Nadir A. · The American journal of gastroenterology (2006)
Case report of a young man who developed cholestatic jaundice together with IgA nephropathy after using the over-the-counter 'muscle building' agent superdrol (methasterone)
Documents combined hepatic and renal injury from an illicitly-marketed OTC 'prohormone' supplement — hepatic cholestasis plus renal disease
Authors emphasize that misleading supplement labeling creates false confidence in safety, with no clinical evidence of utility or safety
Several metabolites, including a 3-keto reduced metabolite and numerous hydroxylated metabolites, were identified for methasterone in the chimeric mouse model with humanized liver.
Lootens L, Meuleman P, Leroux-Roels G, Van Eenoo P. · The Journal of steroid biochemistry and molecular biology (2011)
Characterized the metabolism of methasterone (and the designer steroids promagnon and methylclostebol) using uPA+/+-SCID chimeric mice with a humanized liver, for anti-doping detection purposes
Identified methasterone's phase I metabolites (3-keto-reduced and hydroxylated species) relevant to forensic urine detection of its illicit use
Part of the dominant non-clinical literature — characterizing the drug for DETECTION, not demonstrating any human benefit
Common 3alpha-hydroxy (major) and 3beta-hydroxy reduced metabolites were identified for drostanolone and 17-methyldrostanolone using cryopreserved human hepatocytes.
Identified the metabolites of 17-methyldrostanolone (methasterone/methyldrostanolone) and drostanolone produced by cryopreserved human hepatocytes, an in-vitro hepatic system
Characterized the 3α- and 3β-reduced (hydroxylated) metabolites used to detect methyldrostanolone in anti-doping testing
Confirms that methasterone is hepatically metabolized and tracked as a designer-steroid doping agent — detection science, not human benefit