No — 2α-methylation prevents CYP19A1 substrate recognition
Route
Oral — 17α-alkylated (hepatotoxic at high dose/long duration)
QSC format
Research tablet kits ≥99% HPLC — Janoshik COA
Mechanism of Action
Methasterone (2α,17α-dimethyl-5α-androstan-3-one-17β-ol) is a DHT derivative with modifications at two positions — 17α-methyl (oral bioavailability) and 2α-methyl (increased AR affinity and reduced androgenic metabolic conversion). The 2α-methyl group is the key pharmacological differentiator: it dramatically increases AR binding affinity compared to DHT itself while simultaneously preventing 3α-hydroxysteroid dehydrogenase (3α-HSD) reduction to a less potent metabolite — a metabolic fate that limits DHT activity in many tissues. Result: methasterone is a highly potent, non-aromatisable AR agonist with an anabolic:androgenic ratio of approximately 400:20. Research value: highly potent AR agonism model for in vitro binding and transcriptional activation studies. Also of interest for hepatotoxicity research — 17α-methylation plus high potency creates significant hepatotoxic potential that models severe 17α-alkylated steroid hepatotoxicity.
Key Research Studies
Study
Finding
Fragkaki et al. 2009 (Steroids)
Methasterone metabolism characterisation — urinary metabolite profiling relevant to research on steroid phase I/II metabolism
Adverse event reports (case series)
Multiple clinical case reports of severe hepatotoxicity with methasterone use — liver failure, peliosis hepatis, cholestatic jaundice. Most potent hepatotoxin in the oral androgen class
AR binding studies (Handelsman 2006)
Methasterone/methyl-DHT class ranked for AR affinity — among highest AR affinity synthetic androgens tested
Research Protocol Design
Potent AR agonism reference compound
Methasterone 1-100nM in AR binding assay (competitive RBA vs [3H]-DHT). Reporter gene (ARE-luc in AR-transfected 293T). Establishes relative potency: methasterone vs testosterone vs DHT vs oxandrolone. Reference point for high-affinity AR pharmacology.
17α-alkylated steroid hepatotoxicity model
HepG2 or HepaRG cells: methasterone 1-25µM × 24-72hr. MTT viability, LDH, ALT secretion, CYP3A4 activity, BSEP/MDR3 expression, mitochondrial membrane potential (JC-1). As most potent hepatotoxic oral androgen, methasterone establishes the upper bound for hepatotoxicity mechanistic studies.
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Frequently Asked Questions
What makes Superdrol (methasterone) different from other oral steroids?
The 2α-methyl + 17α-methyl dual modification confers extremely high AR affinity (preventing 3α-HSD metabolic inactivation) and oral bioavailability. The result is the highest AR potency-to-androgenic ratio in the oral steroid class — and correspondingly the most severe hepatotoxicity profile.
Why is methasterone useful for hepatotoxicity research?
Methasterone is the most potent 17α-alkylated steroid hepatotoxin in the research catalog — making it the upper-range reference for studying BSEP/MDR3 bile transporter inhibition, cholestatic mechanisms, and CYP3A4 effects of 17α-alkylated steroids. Its hepatotoxic ceiling defines the maximum hepatotoxic potential of this compound class.
Does Superdrol aromatise?
No — the 2α-methyl group prevents CYP19A1 from recognising methasterone as a substrate. This makes methasterone a non-oestrogenic potent AR agonist — useful for studying high-potency AR effects without oestrogen confounds.
