Furazabol (Miotolan)
A Japanese DHT-derived oral steroid (Miotolan) bearing a furazan (oxadiazole) ring fused to the A-ring, structurally akin to stanozolol. Studied and used partly for its reputed cholesterol-lowering effect, it is a non-aromatising, 17-alpha-methylated oral with the usual hepatic and lipid liabilities.
01 Overview
Furazabol is a dihydrotestosterone derivative with a furazan (1,2,5-oxadiazole) ring fused to the A-ring and a 17-alpha-methyl group for oral activity, making it a close structural relative of stanozolol (which carries a pyrazole ring instead). It was developed and marketed in Japan as Miotolan.
Unusually, part of its historical interest was a claimed lipid-lowering / anti-atherosclerotic action, and it was investigated in that context. As a non-aromatising 17-alpha-alkylated oral it produces dry, non-estrogenic effects but shares stanozolol-like drawbacks: hepatotoxicity and adverse effects on cholesterol (lowering HDL, raising LDL) despite the historical lipid narrative. Human data are limited and mostly older Japanese literature; it survives largely as a grey-market and doping-control curiosity.
02 Mechanism
Androgen receptor agonist derived from DHT; does not aromatise. The furazan-fused A-ring blocks estrogenic conversion and the 17-alpha-methyl group gives oral bioavailability, with attendant hepatic strain.
03 Dosing
| Tier | Dose | Route | Notes |
|---|---|---|---|
| Anecdotal | 10–30 mg/day | Oral | No reliable controlled dosing data. |
Ester comparison
| Ester | Half-life | Injection freq. | Testosterone by mass |
|---|
04 Effects
| Effect | Magnitude | Evidence | |
|---|---|---|---|
| Lean, dry gainsNon-estrogenic lean-mass and strength support, stanozolol-like. | Anecdotal | ||
| Claimed lipid-lowering actionHistorically investigated for cholesterol lowering; net lipid effect is debated. | Observational |
05 Side effects
| Effect | Severity | Frequency | Evidence | Countermeasures |
|---|---|---|---|---|
| Adverse lipid changesLike stanozolol, oral non-aromatising androgens tend to lower HDL and raise LDL despite the historical lipid claim. | Moderate | Class effect | Observational | |
| HepatotoxicityLiver enzyme elevation expected from 17-alpha-methylation. | Moderate | Class effect of 17aa orals | Anecdotal | |
| HPTA suppressionSuppression of endogenous testosterone. | Moderate | Expected | Anecdotal |