Dianabol (Methandrostenolone) Research Hub | AR Agonism, Anabolic Mechanism | QSC
QSC RESEARCH HUB — ORAL ANABOLIC STEROID
Dianabol (Methandrostenolone)17α-methylated androgen / anabolic steroidA:A 210:40-60Research Use Only
Compound Specification
Property
Value
Compound
Dianabol (Methandrostenolone)
CAS
72-63-9
MW
300.44 g/mol
Class
17α-methylated androgen / anabolic steroid
Anabolic:Androgenic ratio
210:40-60
Aromatisation
Yes — converts to methyloestradiol (more potent oestrogen than E2)
Route
Oral — 17α-alkylated (hepatotoxic at high dose/long duration)
QSC format
Research tablet kits ≥99% HPLC — Janoshik COA
Mechanism of Action
Methandrostenolone (17α-methyl-testosterone-modified) is an orally bioavailable synthetic androgen. The 17α-methyl group protects against first-pass hepatic metabolism. Primary mechanism: androgen receptor (AR) agonism — AR nuclear translocation → androgen response element (ARE) binding → transcription of anabolic genes (IGF-1, MyoD, follistatin, mTOR targets). High anabolic:androgenic ratio (210:40-60) reflects greater AR activation in muscle tissue than androgenic tissues. Aromatises to methyloestradiol (methylE2) via CYP19A1 — methylE2 has approximately 30× greater oestrogenicity than E2 at ERα. This strong oestrogenic component produces significant water retention and gynecomastia risk in in vivo models. Research utility: androgen receptor biology, anabolic signalling pathway dissection, high anabolic-index compound for comparative AR pharmacology.
Key Research Studies
Study
Finding
Sinha-Hikim et al. 2002 (J Clin Endo)
Testosterone + supraphysiological = increased muscle cross-sectional area via satellite cell activation and myonuclear accretion — foundational anabolic mechanism paper (directly relevant to 17α-alkylated androgens)
Bhasin et al. 1996 (NEJM)
Dose-response for anabolic and androgenic effects — established the anabolic/androgenic dissociation concept used to compare AR agonists including Dianabol
Aromatic 17α-alkylation hepatotoxicity
Multiple hepatocyte culture studies confirm 17α-methylated steroids induce cholestatic hepatotoxicity at elevated doses — mechanism: bile acid transporter inhibition (BSEP/MDR3)
Research Protocol Design
Androgen receptor binding assay
Dianabol 1-1000nM + rat prostatic AR preparation (competitive RBA). Ki determination vs reference testosterone. Compare: Dianabol vs testosterone vs nandrolone vs stanozolol AR affinity. Quantifies relative binding without in vivo metabolic confounds.
Anabolic signalling in C2C12
Dianabol 100nM-10µM in differentiated C2C12 myotubes (7 days). Primary: myotube diameter (phase-contrast), total protein (Bradford), MyHC (Western), IGF-1 mRNA (qPCR). Compare with testosterone and DHT arms.
Hepatotoxicity model
HepG2 cells: Dianabol 1-50µM × 48hr. MTT viability, LDH release, ALT/AST secretion, BSEP mRNA, bile acid retention. Establishes NOAEL for hepatic AR activation studies.
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Frequently Asked Questions
What is the mechanism of Dianabol?
Methandrostenolone activates the androgen receptor → nuclear translocation → ARE binding → transcription of anabolic genes. It aromatises to methyloestradiol (a potent oestrogen) via CYP19A1 — creating combined androgenic + oestrogenic research profile.
Why does Dianabol aromatise more strongly than testosterone?
Dianabol converts to methyloestradiol (17α-methyl-oestradiol), which has ~30× greater ERα affinity than natural oestradiol. Even though aromatisation rate is lower than testosterone, the resulting metabolite is more potent — making oestrogenic effects significant at lower Dianabol doses.
What is the 17α-alkylation and why does it cause hepatotoxicity?
17α-methyl substitution prevents first-pass hepatic metabolism (making the steroid orally bioavailable) but also inhibits hepatic bile acid transporters (BSEP, MDR3) — causing cholestatic hepatotoxicity at elevated doses. Research models studying 17α-alkylated steroid hepatotoxicity use HepG2 cells or primary hepatocyte preparations.
