Stanozolol
Stanozolol, 17-alpha-alkylated anabolic androgen
Written by Aaron CuhaReviewed Sep 2026
Also known as: Winstrol, Winny, Stanazol
Best known from the 1988 Olympics, and its only real medical record is long-term use in hereditary angioedema, a rare disease where androgens work through a mechanism unrelated to muscle.
Overview
Stanozolol is the compound most people can name and least people understand, because its medical use has nothing to do with what it is famous for.
In hereditary angioedema, a rare genetic disorder causing episodes of severe swelling, androgens have been used for decades because they raise hepatic production of C1 esterase inhibitor, the protein patients lack. That is a liver effect, unrelated to muscle, and it is the basis of the one long-term human safety dataset that exists for this drug.
That dataset is genuinely useful because it follows patients on continuous therapy over years, which almost no anabolic steroid literature does. It also documents the cost of that exposure.
Outside that indication the human evidence is thin, and modern hereditary angioedema treatment has targeted options that largely displaced androgens.
Mechanism of action
A synthetic derivative of dihydrotestosterone with a pyrazole ring fused to the A ring and a 17-alpha methyl group. The 17-alpha alkylation permits oral dosing and carries the liver risk characteristic of that structure. It binds the androgen receptor and does not aromatise. Its hereditary angioedema effect works through a different route entirely: androgens increase hepatic synthesis of C1 esterase inhibitor, the complement regulator that is deficient or dysfunctional in that disease, which reduces attack frequency without addressing the genetic defect.
Human evidence
One genuine medical indication with long-term safety follow-up, in a rare disease, through a mechanism unrelated to muscle. Essentially nothing for the use it is famous for.
- Used for decades in hereditary angioedema prophylaxis, where androgens raise hepatic C1 esterase inhibitor production.
- A long-term safety study followed patients on continuous therapy, which is rare in this class.
- The mechanism in that disease is hepatic protein synthesis, not anabolism, so the evidence does not transfer to muscle claims.
- It is a 17-alpha-alkylated oral compound, the structural class associated with liver strain and pronounced adverse lipid changes.
- No randomised trial supports its use for athletic performance or body composition in healthy people.
- Modern hereditary angioedema treatment has targeted options that have largely displaced androgens.
What this does not tell you: The evidence base is one rare disease and one mechanism that has nothing to do with why people take it. The long-term safety data describes supervised patients on a medical indication with monitoring, not unsupervised use at higher doses. Its reputation for producing lean gains without water retention comes from user report and mechanism rather than from any trial.
Reading the research record
Stanozolol is a useful page because it shows how a drug can be simultaneously famous, medically real, and unsupported for the thing it is famous for.
Its genuine medical record is in hereditary angioedema, working through hepatic protein synthesis rather than muscle. That is not a technicality: it means the long-term safety data, which is the most valuable thing about this compound's literature, was generated in patients being treated for something else entirely.
The honest summary is that this is an oral 17-alpha-alkylated androgen with a documented capacity to strain the liver and move lipids in the wrong direction, a real indication in a rare disease that modern medicine has largely moved past, and no trial evidence for performance or body composition in healthy people.
The harms of this class are well characterised and are not exotic. Suppression of the body's own testosterone production through negative feedback, with reduced sperm production that is usually but not always reversible. Adverse lipid changes, typically a fall in HDL cholesterol and a rise in LDL, which is more pronounced with oral 17-alpha-alkylated compounds. Liver strain, again concentrated in the oral alkylated compounds, which is the specific reason those exist as a separate risk category. Raised haematocrit. In women, virilising effects including voice deepening and hair growth that are partly irreversible, which is why dosing in women is a different problem rather than a smaller version of the same one. Cardiac effects at supraphysiological doses are documented and are not the same question as replacement-dose testosterone, which has its own large safety trial.
The evidence, charted
Fig. 1 · evidence composition
1of 1 citation (100%) is in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Every citation here was published in 2007.
Too few distinct publication years on this page to plot as a timeline. The newest citation on file is from 2007, more than five years ago; the published record may have gone quiet.
Fig. 3 · legal status at a glance
US
Not approved
UK
Approved
AU
Approved
CA
Approved
Approved in 3 of 4, prescription route in 0, not approved in 1. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Key studies & citations
- Human2007
Hereditary angioedema: safety of long-term stanozolol therapy
The long-term human safety dataset for this drug, following patients on continuous androgen therapy for hereditary angioedema over years. Valuable because almost no anabolic steroid has long-term monitored human follow-up, and it documents the cost of that exposure rather than only the benefit.
Journal of Allergy and Clinical Immunology
Frequently asked questions
What is stanozolol actually approved for?
It held an approval for preventing attacks in hereditary angioedema, a rare genetic disorder, where androgens raise the liver's production of the protein patients are missing. That is a liver effect with nothing to do with muscle, and it has since been discontinued in the United States while targeted treatments displaced androgens for that disease.
Is there evidence it builds lean muscle without water retention?
No trial supports it. That reputation comes from user report and from the fact that it does not aromatise to oestradiol, so it produces less fluid retention than testosterone. Not aromatising also removes oestradiol's contributions to bone, mood and libido, which is rarely mentioned alongside it.
Why is the liver risk emphasised for this one?
Because it is 17-alpha-alkylated, the structural modification that lets an androgen survive first-pass metabolism and be taken orally. That same modification is responsible for the liver strain and the sharp adverse lipid changes seen across this subgroup, which is why orals are treated as a separate risk category rather than as a convenient format.