History

Methasterone was synthesized by Syntex in the mid-1950s (around 1956; the synthesis was detailed in a 1959 publication) during anabolic and anti-tumor screening, where it was characterized as a potent orally active anabolic agent with comparatively weak androgenic activity — but it was never commercialized as a medicine. Its non-17α-alkylated parent, drostanolone (as drostanolone propionate), was marketed by Syntex as Masteron, whereas methasterone itself was not. It re-emerged in 2005 as a "designer steroid," sold openly as an over-the-counter "dietary supplement" / pro-hormone (notably as Superdrol) through roughly the latter half of the 2000s before being placed under federal control.

Methasterone — better known by the designer-supplement name Superdrol, and chemically as methyldrostanolone — is a synthetic anabolic-androgenic steroid (AAS), not a peptide. It is an oral 17α-alkylated derivative of dihydrotestosterone that was made by Syntex in the 1950s but never approved as a medicine; it later surfaced as an over-the-counter “supplement” in the mid-2000s before being scheduled. Its claimed muscle-building effects have never been tested in controlled human trials, while the strongest human evidence about it concerns serious harm: severe cholestatic liver injury in previously healthy young men.

What it is

Methasterone is a synthetic, orally active anabolic-androgenic steroid (CAS 3381-88-2). Chemically it is a derivative of dihydrotestosterone (DHT) — 2α,17α-dimethyl-17β-hydroxy-5α-androstan-3-one — meaning, relative to testosterone, it has no Δ4 (C4–C5) double bond (a 5α-reduced, DHT-type A-ring), a 2α-methyl group, and a 17α-methyl group. In practical terms it is drostanolone with an added 17α-methyl group. The 2α-methyl raises anabolic potency and resistance to 3α-HSD metabolism, while the 17α-alkylation lets it survive first-pass hepatic metabolism, making it orally bioavailable; it is an oral 17α-alkylated steroid, not an injectable ester.

Mechanistically, like other AAS it acts as an androgen receptor (AR) agonist, driving AR-mediated transcription that increases muscle protein synthesis and lean mass. As a 5α-reduced DHT derivative it is not a substrate for aromatase, so it cannot convert directly to estradiol; the original Syntex work described it as strongly anabolic with comparatively weaker androgenic activity. Aromatase-independence does not, however, prevent gynecomastia in real-world use (see Safety).

The claims

Methasterone has no approved medical indication anywhere; historically it drew only laboratory interest in anabolic and anti-tumor screening. In athletic and bodybuilding circles it is used illicitly or off-label for lean mass gain, strength, and “recomposition,” typically in a cutting or lean-bulk context, and is valued because it is oral and does not aromatize.

What the evidence actually shows

There are no controlled human efficacy trials of methasterone. Because it was never a clinical drug, claims of lean-mass and strength gains rest on historical animal and in-vitro anabolic-screening data from the Syntex era plus anecdote, not randomized human studies. Evidence for its claimed performance and physique effects is therefore very low / essentially uncontrolled.

The only robust human clinical literature concerns harm — specifically a consistent, well-documented pattern of severe cholestatic liver injury in previously healthy young men using Superdrol/methasteron:

Shah et al., 2008 — a case series of 5 patients with methasteron-associated cholestatic liver injury; jaundice appeared roughly 2 weeks after stopping, bilirubin peaked over the following 2–3 weeks, and all 5 ultimately resolved (about 12 weeks) with no residual hepatic dysfunction and without transplant.
Kafrouni, Anders & Verma, 2007 — 2 young men with significant cholestatic injury from anabolic-steroid–containing dietary supplements; both recovered without transplant.
Jasiurkowski et al., 2006 — Superdrol-induced cholestatic jaundice plus IgA nephropathy, a notable case linking the agent to kidney involvement as well.
Nasr & Ahmad, 2009 — severe cholestasis with renal failure attributed to Superdrol/methasteron, with a literature review.

The NIH LiverTox monograph on Androgenic Steroids discusses Superdrol/methasteron among C17-alkylated androgens causing “bland cholestasis,” and catalogs the broader 17α-alkylated liver-injury spectrum: transient transaminase elevation, bland cholestasis, peliosis hepatis (blood-filled hepatic sinusoids/cysts), and hepatic tumors (adenoma/HCC, typically after years of use).

Legal and regulatory status

In the United States, methasterone is a Schedule III controlled substance. Anabolic steroids are Schedule III under the Anabolic Steroid Control Act (within the Controlled Substances Act). Methasterone specifically was scheduled by a DEA Final Rule published July 30, 2012 (effective August 29, 2012) — classified, alongside prostanozol, as a Schedule III anabolic steroid. It was subsequently named among the substances addressed by the Designer Anabolic Steroid Control Act of 2014 (DASCA, signed December 18, 2014), which expanded the statutory definition of “anabolic steroid” and named specific substances; DEA’s implementing rule followed (published August 1, 2023, revising the regulatory list to include all variations of the chemical names of methasterone and prostanozol). The net effect is that methasterone is federally controlled (Schedule III) and can no longer be legally sold as a supplement.

In sport, methasterone (methyldrostanolone) is prohibited at all times (in- and out-of-competition) under WADA Class S1 – Anabolic Agents, specifically S1.1 Anabolic Androgenic Steroids, where it appears as a named example AAS. The 2026 Prohibited List, in force as of 1 January 2026, also clarifies that esters and substances of similar chemical structure or biological effect are likewise prohibited. (For context: clenbuterol is classified under S1.2 “Other Anabolic Agents,” also banned at all times; that subclass does not apply to methasterone, which is an actual steroid and therefore falls under S1.1.)

Safety

Methasterone carries the full risk profile of an oral 17α-alkylated androgen, and its signature documented harm in humans is liver injury.

Hepatotoxicity (signature risk): As a 17α-alkylated oral steroid, methasterone is markedly hepatotoxic. The documented human pattern is cholestatic jaundice — fatigue, pruritus, dark urine, marked hyperbilirubinemia (case bilirubin reported well above 40 mg/dL), often with only modest ALT/ALP rise — appearing during or 1–2 months after use, sometimes worsening after cessation before resolving over weeks to months. The class also carries risk of peliosis hepatis and hepatic tumors with prolonged exposure.
Renal: Documented acute kidney injury / renal failure and IgA nephropathy in case reports, sometimes accompanying the cholestasis.
Cardiovascular / lipids: Like other oral 17α-alkylated AAS, it is expected to cause adverse lipid shifts (sharply lowered HDL, raised LDL) and is associated with the general AAS cardiovascular risk profile (hypertension, cardiac/LV remodeling, dyslipidemia-driven atherosclerotic risk). Compound-specific human cardiovascular trials do not exist; this is class-level evidence.
HPTA suppression / fertility: Suppresses the hypothalamic-pituitary-testicular axis, lowering endogenous testosterone and LH/FSH and causing testicular atrophy, impaired spermatogenesis, and potential infertility, which may be prolonged after discontinuation.
Gynecomastia: Can occur despite the non-aromatizing chemistry, via suppression of endogenous testosterone and a disrupted androgen-to-estrogen balance.
Virilization (women): Androgenic effects including voice deepening, hirsutism, menstrual disruption, and clitoral enlargement, some of which are irreversible.
Hematologic: AAS class effect of raised hematocrit/erythrocytosis, increasing thrombotic risk.
Other AAS class effects: Acne, hair loss/androgenic alopecia, and mood/aggression changes; adolescent use risks premature epiphyseal closure.

A note on evidence grade: the efficacy claims (lean mass and strength) are not supported by controlled human trials — they derive from historical animal anabolic screening and anecdote (very low confidence). The strongest, well-replicated human evidence concerns harm, particularly cholestatic hepatotoxicity. No doses, cycles, stacks, or PCT protocols are included here by design.

Bottom line

Methasterone (Superdrol) is a synthetic oral anabolic-androgenic steroid — a 17α-methylated version of drostanolone — that was synthesized in the 1950s, never approved as a medicine, and briefly sold as a “supplement” before being scheduled. Its muscle-building claims have never been tested in controlled human trials; the only robust human evidence about it documents serious harm, most notably severe cholestatic liver injury in otherwise healthy young men, with additional renal, cardiovascular, hormonal, and other AAS risks. It is a federally controlled Schedule III substance and is banned at all times in sport. It is an anabolic steroid, not a peptide.

Evidence grade: Animal only.