RESEARCH MONOGRAPH · KDC-MN-390

Stanozolol

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 2 min read

Our opinion on this compound

61/100

The Ben Johnson AAS; potent SHBG-displacer with a brutal hepatic and lipid profile

Stanozolol is famous for the wrong reason: the 1988 Seoul Olympics, Ben Johnson, the 100m gold stripped. The pharmacology is more interesting than the scandal. It's a 17-alpha-alkylated heterocyclic AAS with a pyrazole fused to the A-ring of the dihydrotestosterone skeleton, which makes it non-aromatizable and conformationally locked in a way that distinguishes it from most of the class.

The receptor pharmacology is unusual. Stanozolol has only moderate AR binding affinity but quite high SHBG binding affinity, which means it displaces endogenous testosterone from SHBG and elevates free T transiently. The myotrophic-to-androgenic ratio (caveat: from rat assays) is high. Clinically it was used historically for hereditary angioedema (which is its only US-approved indication, via stimulation of C1 esterase inhibitor levels) and for aplastic anemia in some contexts.

What we like for research is the unusual SHBG pharmacology, which makes it a useful tool compound for SHBG-displacement experiments without the aromatization confound.

What we dont like is everything else about its clinical profile. The lipid changes are dramatic and class-leading-bad: profound HDL suppression, LDL elevation, often in single-digit weeks. The hepatic profile is also worse than oxandrolone, with consistent transaminase elevations and a real cholestatic signal at higher doses. The cosmetic uses (the 'hardening' effect in athletic and bodybuilding contexts) trade those metabolic costs for real but cosmetic body composition effects.

The C1 esterase inhibitor mechanism in hereditary angioedema is genuinely interesting and underexplored. Stanozolol upregulates hepatic synthesis of C1-INH along with several other complement and acute-phase proteins, and the prophylactic efficacy in HAE was good before the modern bradykinin-pathway-targeted drugs (icatibant, lanadelumab) became standard. There's a small remaining niche of patients in resource-limited settings who still use it for HAE.

Sourcing is regulated, Schedule III in the US. Pharmaceutical reference standards are available, HPLC purity reliable. Stanozolol is poorly water-soluble (heterocyclic, lipophilic) so suspension formulations have historically had bioavailability issues that researchers should be aware of.

Evidence: 70
Mechanism: 78
Reliability: 75
Safety: 40
Sourcing: 55
Value: 50
Signal: 65
Staying power: 55

Plain-language summary Intrigue 48 / 100

Stanozolol (Winstrol) is a 17-alpha-alkylated synthetic anabolic steroid developed by Sterling-Winthrop in 1962, distinguished by a pyrazole ring fused to the steroid A-ring. The fusion shifts the anabolic-to-androgenic ratio higher than testosterone and supports oral activity. FDA-approved historically for hereditary angioedema (largely replaced now by C1-inhibitor and icatibant) and a few other niche uses. Its place in popular memory belongs to Ben Johnson, whose 1988 Seoul Olympic 100m gold medal was stripped after a positive stanozolol test. Hepatotoxicity is the main limiting concern, the standard cost of 17-alpha-alkylation. Schedule III. Used in research as a reference oral AAS. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

17-alpha-alkylated heterocyclic AAS

A pyrazol-fused 17-alpha-alkylated AAS; the steroid involved in the Ben Johnson 1988 Olympic doping case; clinically used historically for hereditary angioedema.

Abstract

Stanozolol (17-beta-hydroxy-17-alpha-methyl-5-alpha-androstano[3,2-c]pyrazole; CAS 10418-03-8; molecular formula C21H32N2O; molecular weight 328.49) is a pyrazol-fused 17-alpha-alkylated synthetic AAS developed by Sterling-Winthrop in 1962 and approved by the FDA (Winstrol) for hereditary angioedema and other indications. The pyrazole fusion at the A-ring increases the anabolic-to-androgenic ratio relative to testosterone and supports oral activity. Plasma half-life is approximately 9 hours (oral). Schedule III. The compound's place in popular culture is dominated by the Ben Johnson case at the 1988 Seoul Olympics, where his 100m gold medal was stripped after positive testing for stanozolol. The clinical use in hereditary angioedema (rare, often replaced by C1-INH or icatibant in modern practice) demonstrates the compound's effect on hepatic protein synthesis. Hepatotoxicity is the principal limitation. Used as a reference oral AAS in research.

Mechanism of action

Pyrazol-fused 17-alpha-alkylated AAS; AR agonism with elevated anabolic-to-androgenic ratio. Oral activity via 17-alpha-alkylation; hepatotoxic at high doses.

Reported research dose ranges

Reported research dose ranges vary across the published literature.

References

Mosby's Drug Reference. Stanozolol. 2018.
Cicardi M, et al. Hereditary angioedema treatment with stanozolol. J Allergy Clin Immunol 1991.
Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol 2008.

Read the full monograph

Available as a research-use-only PDF download.

KDC-MN-390

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

Download PDF →

FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

Kodiac sells research compounds for investigative use only.

Stanozolol

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

Quick actions

Categories

Help and policies

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

Adjacent monographs