KDC-MN-390 – Kodiac biolabs

Plain-language summaryIntrigue 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 Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

37/100

A historically significant reference AAS with mature mechanism and declining research relevance

Look, stanozolol is not a mystery. It’s been around since 1962, it made Ben Johnson the most famous disqualified sprinter in history, and the mechanism is what you’d expect: androgen receptor agonism via a pyrazol-fused 17-alpha-alkylated backbone that shifts the anabolic-to-androgenic ratio favorably relative to testosterone. Sterling-Winthrop knew what they were doing structurally. But knowing what something does and finding it interesting in 2026 are different things.

The mechanism story starts and ends with AR binding. The pyrazole fusion at the A-ring is chemically clever for its era, and the oral bioavailability is real. What isn’t real anymore is the clinical urgency. The hereditary angioedema indication that got Winstrol its FDA approval has been largely displaced by C1-inhibitor concentrates and icatibant. Those agents are cleaner, better-tolerated, and don’t carry the hepatotoxicity liability that 17-alpha-alkylated steroids all share to varying degrees. The indication that justified the compound’s existence in the clinic is essentially a historical artifact at this point.

What we’re left with is a Schedule III reference compound. That’s not nothing. If you’re running AAS pharmacology studies, SHBG displacement work, or comparative androgen receptor affinity panels, stanozolol occupies a specific and well-characterized position in the reference set. The literature is extensive enough that you can contextualize your findings against a real body of evidence. That’s the bench value argument, and it’s legitimate but limited. Newer AAS analogs with more interesting selectivity profiles have appeared in the literature if your goal is genuinely advancing the mechanistic frontier.

The evidence quality is actually respectable for what it is. FDA approval, multi-decade use, clear pharmacokinetics, well-characterized toxicity. But high evidence quality on a mature well-understood compound is almost a negative signal for research interest. It means the question has already been answered. There’s no ambiguity left to resolve with stanozolol that hasn’t already been resolved, which is why the novelty score sits at the floor and drags the overall down hard.

Honestly, if you’re building a research program around androgen biology in 2026, the interesting questions are in selective androgen receptor modulators, tissue-selective AAS fragments, or non-steroidal AR modulators. Stanozolol tells you where that field came from, not where it’s going. We think it earns its place in the library as a reference compound, but we’d be doing investigators a disservice if we scored it as if it were an active frontier.

Novelty: 18
Mechanism promise: 22
In-category differentiation: 35
Evidence quality: 60
Translational signal: 55
Research bench value: 48

Rationale Stanozolol scores low on novelty and mechanism because it’s a 1962 oral AAS with well-understood AR agonism and an indication space that modern therapy has largely superseded; evidence quality and translational signal are genuine given FDA approval and decades of clinical use, but those points are offset by near-zero novelty and limited differentiation from a saturated class. Schedule III cap (75) does not bind; the raw weighted score of 37 reflects the compound’s historical-reference-only status.

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.

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The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

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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.

Tag: KDC-MN-390

Stanozolol

Abstract

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