D tier · weak
Its US marketing authorisation for osteoporosis and aplastic anaemia was withdrawn in 1984 for insufficient data and the product left the US market entirely in 2010, leaving no approved indication — yet it holds the single best-quantified adverse-lipid dataset of any compound here, meaning the strongest evidence attached to it documents harm.
stanozolol
Stanozolol is a pyrazole-fused DHT derivative whose US marketing authority was withdrawn in 1984 on grounds of insufficient efficacy data and which left the US market in 2010. It is the compound in this group with the most precisely characterised adverse lipid profile, with a controlled crossover trial documenting a 33% fall in HDL cholesterol and a 71% fall in the HDL2 subfraction.
the explanation
Stanozolol, known as Winstrol, was pulled from US pharmacy shelves after regulators decided the evidence it worked was not good enough. The best study of it measured harm rather than benefit, showing it cut protective HDL cholesterol by a third and raised LDL by nearly a third in six weeks.
regulatory status
US Schedule III controlled substance; UK Class C (Misuse of Drugs Act). NO approved US medical indication; discontinued.
Stanozolol is Schedule III under the US Controlled Substances Act, having been scheduled by the Anabolic Steroids Control Act of 1990, and is Class C under the UK Misuse of Drugs Act. In April 1984 the FDA announced the data were insufficient and withdrew marketing authority for stanozolol for senile and postmenopausal osteoporosis and for raising haemoglobin in aplastic anaemia; a hereditary angioedema indication was also historically pursued. Lundbeck withdrew stanozolol from the US market in 2010 and no company has since marketed it as a pharmaceutical in the US, so it retains NO approved US medical indication. Veterinary formulations have been used in animals, and it is prohibited at all times in sport under the WADA List.
how it works · proposed mechanism
Stanozolol is a non-aromatisable androgen receptor agonist whose A-ring pyrazole and 17α-methyl substitutions define both its oral activity and its lipid toxicity.
Pyrazole A-ring fusion
Fusion of a pyrazole heterocycle to the A-ring of dihydrotestosterone blocks aromatisation entirely, so stanozolol produces no oestrogenic metabolites. It also binds sex hormone-binding globulin weakly, increasing the free fraction of circulating androgen.
Hepatic triglyceride lipase induction
Oral 17α-alkylated androgens strongly induce hepatic triglyceride lipase, which accelerates catabolism of HDL2 particles. Thompson et al. showed the enzyme rise precedes the fall in HDL2 cholesterol, establishing a mechanistic sequence rather than mere association.
Fibrinolytic and connective tissue effects
Stanozolol has documented effects on fibrinolysis, which underpinned its historical investigation in hereditary angioedema and vascular disorders. Effects on collagen turnover form the mechanistic rationale for concern about tendon integrity, though direct quantitative human tendon data for stanozolol specifically remain limited.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The best-controlled human trial of stanozolol was designed to measure cardiovascular risk markers, and it found severe adverse changes within six weeks — a 33% HDL reduction and a 40% fall in apolipoprotein A-I. The tendon concern that circulates widely is mechanistically plausible and supported at class level by case series and reviews, but direct quantitative human evidence naming stanozolol specifically is thinner than commonly asserted, and this index grades it accordingly.
key published findings
- Human randomized crossover trial (Thompson et al., JAMA 1989, 11 male weightlifters, 6 weeks): oral stanozolol reduced HDL cholesterol by 33% versus only 9% for intramuscular testosterone enanthate.
- Human crossover trial (same): the HDL2 subfraction fell 71% and apolipoprotein A-I fell 40% on stanozolol, versus an 8% apoA-I fall on testosterone.
- Human crossover trial (same): LDL cholesterol INCREASED 29% on stanozolol while DECREASING 16% on testosterone, demonstrating that route and 17α-alkylation, not androgen exposure alone, drive the atherogenic shift.
- Human mechanistic study: the rise in hepatic triglyceride lipase precedes the fall in HDL2 cholesterol during anabolic steroid therapy, establishing the enzymatic sequence underlying the dyslipoproteinaemia.
- Human case series (J Surg Case Rep 2024, 26 men with acute pectoralis major tendon rupture): MRI showed superior tendinopathy in 57.1% and total tendinopathy in 35.7%, with degenerative histological changes in 66.7% of fragments, supporting pre-existing tendon degeneration in weightlifters — a class-level, not stanozolol-specific, finding.
limitations of the evidence
- The pivotal lipid trial enrolled only 11 subjects over 6 weeks, so while the effect sizes are large and internally consistent, precision and long-term extrapolation are limited.
- Direct quantitative human evidence linking stanozolol specifically to tendon rupture is limited; the available support is class-level, drawn from case series, narrative reviews and animal work rather than controlled human biomechanical studies.
- No modern efficacy trials exist for any indication, since marketing authority was withdrawn in 1984 and the product left the US market in 2010.
documented safety signals
- ADVERSE LIPID EFFECTS — MOST SEVERE IN CLASS: Thompson et al. (JAMA 1989) documented a 33% fall in HDL cholesterol, a 71% fall in the HDL2 subfraction, a 40% fall in apolipoprotein A-I and a 29% RISE in LDL cholesterol over six weeks — a profoundly atherogenic shift produced within a single short exposure period.
- HEPATOTOXICITY — NAMED AGENT: NIH LiverTox names stanozolol explicitly among agents in which dose-related acute cholestasis occurs in approximately 1% of treated patients, with onset typically 1-4 months and delayed presentation documented to 6-24 months.
- PELIOSIS HEPATIS: blood-filled hepatic sinusoidal cysts documented after 2-27 months of androgen therapy, capable of asymptomatic progression to fatal hepatic rupture and haemorrhage.
- HEPATIC ADENOMA AND HEPATOCELLULAR CARCINOMA: associated with long-term androgen use, typically after 5-15 years but documented within 2 years in some cases.
- CARDIOMYOPATHY AND ATHEROSCLEROSIS: Baggish et al. (Circulation 2017, n=140) found LVEF 52±11% in AAS users versus 63±8% in non-users (p<0.001), impaired diastolic relaxation (9.3±2.4 vs 11.1±2.0 cm/s, p<0.001), and coronary plaque burden scaling with lifetime dose (0.60 SD units per 10 years, p=0.008) — a signal directly amplified by stanozolol's HDL suppression.
- TENDON AND CONNECTIVE TISSUE: reviews and case series associate anabolic steroid use with impaired collagen quality and elevated tendon rupture risk at the triceps, pectoralis major and quadriceps; a 2024 case series of 26 men with acute pectoralis major rupture found degenerative histological change in 66.7% of tendon fragments. Direct stanozolol-specific quantitative human data are limited.
- HPG AXIS SUPPRESSION: suppression of GnRH and pituitary LH/FSH producing testicular atrophy, impaired spermatogenesis and suppressed endogenous testosterone, with recovery that may be prolonged or incomplete.
- VIRILISATION IN WOMEN: hirsutism, voice deepening, male-pattern baldness, clitoral enlargement and menstrual disruption; voice change and clitoromegaly are frequently irreversible.
- GROWTH-PLATE EFFECTS IN ADOLESCENTS: androgen-driven acceleration of epiphyseal maturation risks premature growth-plate fusion and permanent loss of adult height.
- REGULATORY EFFICACY FAILURE: the FDA withdrew marketing authority in April 1984 specifically because the efficacy data were judged insufficient for osteoporosis and for raising haemoglobin in aplastic anaemia.
- UNREGULATED SUPPLY: with no US pharmaceutical supply since 2010, circulating material is of unverified identity, purity and dose.
identity
| full name | Stanozolol (17α-methyl-5α-androstano[3,2-c]pyrazol-17β-ol) |
| category | Anabolic & Androgenic |
| modality | steroid |
| formula | C21H32N2O |
| molar mass | 328.5 g/mol |
| cas | 10418-03-8 |
| half-life | ~9 h (oral) |
laboratory handling
| storage | Reference material is typically stored as a dry solid at controlled room temperature protected from light; analytical standards are commonly held at −20 °C, sealed and desiccated. |
| solubility | Practically insoluble in water; soluble in ethanol, methanol, chloroform and DMSO; the pyrazole nitrogen confers weak basicity permitting salt formation. White crystalline solid. |
| co-studied with | This index does not describe combination use. Stanozolol's HDL suppression is additive with that of other oral 17α-alkylated androgens, and combined exposure features prominently in the case literature on cholestatic hepatic injury. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
6 citedLiverTox: Clinical and Research Information on Drug-Induced Liver Injury, NIDDK/NIH (NBK548931) · 2020 · official
JAMA (PMID 2915439) · 1989 · randomized
Metabolism (PMID 3657514) · 1987 · observational
Circulation · 2017 · observational
Cureus (PMID 41185795, doi 10.7759/cureus.93649) · 2025 · reviews
Journal of Surgical Case Reports (PMID 38524673, doi 10.1093/jscr/rjae126) · 2024 · observational
others in Anabolic & Androgenic