Stanozolol, first sold as Winstrol, is an oral anabolic-androgenic steroid built on a dihydrotestosterone (DHT)-type skeleton with a pyrazole ring fused to its A-ring. The FDA approved Winstrol tablets in 1962. Its last US labeled use was to prevent attacks of hereditary angioedema (HAE), a rare inherited disorder of swelling.

Outside medicine it is one of the best-known doping steroids, and it has produced many positive doping tests. In the US the brand was discontinued, and FDA withdrew approval of the application in 2010 at the manufacturer’s request because the product was no longer marketed. An injectable suspension also exists; see Winstrol Depot.

This page summarizes what the former FDA label, clinical studies and regulators report. It is for education only and is not medical advice.

Property	Detail
Drug class	17α-methylated anabolic-androgenic steroid (DHT derivative with a fused pyrazole ring)
Brand / approval	Winstrol tablets, NDA 012885; approved January 9, 1962; discontinued
Route	Oral tablet (an injectable suspension exists for veterinary use)
Former strength	2 mg tablet
Former labeled dose (HAE)	2 mg three times a day, tapered to 2 mg/day or 2 mg every other day
Half-life	No human half-life published in a source we could verify
Formula	C₂₁H₃₂N₂O, 328.5 g/mol
US status	Approval withdrawn 2010 (no longer marketed); Schedule III controlled substance
WADA status	Prohibited at all times (S1.1 anabolic androgenic steroids), non-Specified

What it is

The label gives the chemical name as 17-methyl-2’H-5α-androst-2-eno[3,2-c]pyrazol-17β-ol (Winstrol label). PubChem lists the formula as C₂₁H₃₂N₂O and the molecular weight as 328.5 g/mol (PubChem). Two structural features define it:

Feature	What it does
Pyrazole ring fused to the A-ring (positions 2 and 3)	Replaces the usual 3-keto group of testosterone and DHT. This makes stanozolol structurally unusual among steroids.
17α-methyl group	Slows breakdown in the liver so the drug works by mouth. The label ties this group to cholestatic hepatitis and jaundice “at relatively low doses.”

Because the skeleton is 5α-reduced (DHT-type) and the A-ring is replaced by a pyrazole, stanozolol is not expected to convert to estradiol the way testosterone does.

The label notes that “complete dissociation of anabolic and androgenic effects has not been achieved.” In other words, it is still an androgen, and it can masculinize women. Like other androgens it suppresses the pituitary signals (LH and FSH) that drive the testes.

About anabolic:androgenic ratios. Websites often quote stanozolol figures such as “320:30.” A 1981 clinical paper described it as having a “30:1” ratio but did not report the assay behind the number (Sheffer et al., JACI 1981). We could not trace either figure to an original assay. In the same HAE studies, women on low daily doses still developed hirsutism, menstrual changes and virilization.

How it works in the body

There is little published human pharmacokinetic data. We could not find a peer-reviewed human study reporting a plasma half-life, so we do not give one.

What is known comes mostly from doping-control research:

Extensive metabolism. After a single 20 mg oral dose in humans, twelve urinary metabolites, including unchanged stanozolol, were identified. Most were excreted as conjugates (bound to glucuronic acid or similar groups) (Massé et al., J Chromatogr 1989). Hydroxylated forms such as 3’-hydroxystanozolol and 16-hydroxystanozolol were among the most abundant.
Long detection window. A long-term metabolite, 17-epistanozolol-N-glucuronide, was detected up to 28 days after administration (Schänzer et al., Drug Test Anal 2013). This reflects how long metabolites remain in urine, not how long the drug acts.
Strong effect on SHBG. Sex hormone-binding globulin (SHBG) is the protein that carries testosterone in blood. In 25 control subjects, stanozolol at 0.2 mg/kg/day for 3 days lowered SHBG to a mean of 51.6% of its starting value (Sinnecker and Köhler, JCEM 1989). The response was blunted or absent in people with androgen insensitivity, so the test was proposed as a diagnostic tool.

Former approved medical use

The last US label approved Winstrol for one use: prophylaxis “to decrease the frequency and severity of attacks” of hereditary angioedema (Winstrol label). HAE is caused by a deficient or nonfunctional C1 esterase inhibitor (C1-INH). The label states the drug raised C1-INH and C4 levels and that it does not stop an attack that is already under way.

Labeled dosing step	Detail
Starting dose	2 mg three times a day
Taper	Reduce at 1–3 month intervals after a good response
Maintenance	2 mg/day; some patients 2 mg every other day
Children	Long-term prophylaxis generally not recommended

The label advised placing patients on the lowest effective dose because many adverse reactions are dose-related.

FDA approved the original application on January 9, 1962 (Drugs@FDA). Lundbeck, the last holder, told FDA the product was no longer marketed, and FDA withdrew approval effective August 20, 2010 (Federal Register 2010). The notice cites discontinuation of marketing, not a safety finding.

In HAE care today, androgens have been pushed aside by newer prophylactic drugs. A 2025 expert consensus noted that guidelines are now shifting danazol, a related attenuated androgen, to a second-line option (Dias de Castro et al., Clin Transl Allergy 2025).

Federal regulations still list stanozolol 2 mg tablets (dogs and cats) and a 50 mg/mL injectable suspension (dogs, cats and horses) as approved veterinary drugs, restricted to use by or on the order of a veterinarian (21 CFR 520.2150; 21 CFR 522.2150).

What the research shows

Nearly all human data are from small trials from the 1980s and 1990s. We found no randomized trial measuring muscle mass or strength gains from stanozolol in healthy people.

Hereditary angioedema

A Harvard group treated 27 patients (12 men, 15 women) for 2 years to find the lowest dose that controlled attacks (Sheffer et al., JACI 1981). All reached a minimal effective dose of 0.5–2 mg/day.

Daily maintenance dose	Attack frequency
2 mg	1 per 14.6 weeks
1 mg	1 per 7.2 weeks
0.5 mg	1 per 8.2 weeks

Side effects on maintenance included menstrual changes and virilization in 4 women and raised creatine kinase in 5 men. C1-INH and C4 rose but stayed below the normal range. The authors judged 4 mg/day unjustified for long-term use because it caused more side effects without better control.

A decade later, 37 patients had been treated (Sheffer et al., JACI 1987):

18 had adverse reactions while the minimal dose was being found, most often abnormal liver tests, then hirsutism and menstrual irregularities;
every reaction subsided after a dose reduction;
by 1986, 3 patients were on daily doses, 18 on alternate-day doses and 16 on no maintenance therapy.

The same center later followed 21 patients treated for 20–40 years (Sloane et al., JACI 2007). Ten of 21 had treatment-related symptoms, including hirsutism, weight gain, menstrual irregularities or postmenopausal bleeding, acne and mood changes. There were no persistent liver enzyme abnormalities. Five had reduced HDL and 2 had raised triglycerides.

Blood lipids

Stanozolol’s effect on cholesterol is one of its best-documented effects. In a crossover trial, 11 male weightlifters took oral stanozolol 6 mg/day or intramuscular testosterone enanthate 200 mg/week, each for 6 weeks (Thompson et al., JAMA 1989):

Measure	Stanozolol 6 mg/day	Testosterone enanthate 200 mg/week
HDL cholesterol	−33%	−9%
HDL2 subfraction	−71%	Fall was in HDL3 instead
Apolipoprotein A-I	−40%	−8%
LDL cholesterol	+29%	−16%
Hepatic lipase activity	+123%	+25% (not significant)

Weight gain was similar with both drugs, while testosterone suppressed the pituitary gonadotropins more. The authors concluded that the lipid effects of oral 17α-alkylated steroids differ from those of injected testosterone.

The effect was even larger in 10 postmenopausal women treated for osteoporosis for 6 weeks (Taggart et al., Metabolism 1982). HDL fell by 53% (−32.5 mg/dL), LDL rose by 21% (+30.9 mg/dL), and the LDL/HDL ratio rose from 2.5 to 6.8. All changes reversed within 5 weeks of stopping.

Postmenopausal osteoporosis

A 29-month double-blind trial compared stanozolol with placebo in 46 postmenopausal women with osteoporosis, 23 per group (Chesnut et al., Metabolism 1983):

total body calcium, a measure of total bone mass, rose by 4.4% on stanozolol and was unchanged on placebo;
regional bone mass, measured by single-photon absorptiometry, showed no difference between groups;
there were no new spinal fractures on stanozolol vs 3 on placebo, too few to draw conclusions;
76% of treated women developed raised SGOT (a liver enzyme) or other side effects.

Stanozolol was never approved for osteoporosis in the US.

Fibrinolysis and vascular conditions

Stanozolol increases fibrinolysis, the body’s system for dissolving blood clots. In 16 healthy adults given 5 mg twice daily, it raised tissue plasminogen activator activity and plasminogen, lowered fibrinogen, and raised protein C and antithrombin III (Kluft et al., Thromb Haemost 1984). HDL fell in the same volunteers.

This led to trials in conditions thought to involve fibrin deposits. In lipodermatosclerosis (hardening of the skin and fat of the lower leg in venous disease), 60 patients were randomized to stanozolol 5 mg twice daily or placebo for 6 months, both with compression stockings (McMullin et al., Aust N Z J Surg 1991):

Group	Reduction in affected area (95% CI)
Stanozolol + stockings	28% (5.3–46%)
Placebo + stockings	14% (−2.6 to 31%)

Side effects were significantly more common on stanozolol, and skin oxygen levels did not change.

Side effects and risks

Labeled warnings

The Winstrol label carried capitalized warnings, shared with other anabolic steroids (Winstrol label):

Peliosis hepatis: blood-filled cysts in the liver, sometimes found only when life-threatening liver failure or abdominal bleeding develops.
Liver tumors: usually benign, but fatal malignant tumors have been reported. They may be silent until they bleed.
Blood lipid changes: decreased HDL and sometimes increased LDL, which “may be very marked.”

The label also stated that anabolic steroids “have not been shown to enhance athletic ability.”

Liver

Cholestasis (blocked bile flow, causing jaundice and itching) is the classic liver injury from 17α-alkylated steroids. The label lists cholestatic jaundice “with, rarely, hepatic necrosis and death,” and advises periodic liver tests.

At therapeutic doses, a randomized, double-blind trial in 44 patients with lipodermatosclerosis and venous ulcers gave stanozolol 2 mg twice daily or placebo for up to 6 months (Carson et al., Int J Low Extrem Wounds 2015). Liver enzymes (AST, ALT) rose significantly in about 30% of treated patients. The rises caused no symptoms and returned to baseline after stopping.

Severe cases occur at higher, non-medical doses. A 19-year-old who injected 50 mg every other day for 2 months developed intrahepatic cholestasis with a peak bilirubin of 56.6 mg/dL, and his liver tests took 5 months to normalize (Stępień et al., Clin Exp Hepatol 2015).

Cholesterol and cardiovascular risk

HDL reductions of 33–53% in the trials above are large. In the lipodermatosclerosis trial, 91% of patients on just 4 mg/day had a significant fall in HDL (Carson et al. 2015). In the studies that followed patients after stopping, the lipid changes reversed. We found no trial measuring heart attacks or strokes on stanozolol.

Virilization and hormonal effects

Even at 0.5–2 mg/day for HAE, women developed hirsutism, menstrual irregularities and, in some cases, virilization (Sheffer et al. 1981; Sloane et al. 2007). The label warns that some virilizing changes in women, such as voice deepening, can be irreversible even after prompt discontinuation. In men, the label lists testicular atrophy, low sperm count (oligospermia) and impotence.

Interactions

The label lists these interactions:

Anticoagulants: anabolic steroids increase sensitivity, so the anticoagulant dose may need to be lowered.
Insulin and oral diabetes drugs: doses may need adjustment.
Corticosteroids or ACTH: may add to fluid retention.
Thyroid tests: lower thyroxine-binding globulin reduces total T4, while free thyroid hormone stays normal.

Who should not use it

The label contraindicated Winstrol in:

men with breast cancer or known or suspected prostate cancer;
women with breast cancer and high blood calcium;
nephrosis or the nephrotic phase of nephritis;
women who are or may become pregnant (Pregnancy Category X).

In children, anabolic steroids can close the growth plates early and reduce adult height.

Legal status and use outside medicine

United States: stanozolol is a Schedule III anabolic steroid, listed by name in 21 CFR 1308.13(f) (eCFR). No human stanozolol product is FDA-approved today.
Sport: the WADA 2026 Prohibited List names stanozolol under S1.1 anabolic androgenic steroids. It is prohibited in and out of competition and is a non-Specified Substance (WADA 2026 List).
Detection: newer methods targeting glucuronide metabolites found 85 adverse analytical findings in 659 routine doping samples over six months; 72 of them would have been missed by older methods (Schänzer et al. 2013).

Product bought outside a pharmacy is not regulated for dose, purity or identity.

Key takeaways

An oral DHT derivative with a pyrazole ring. The 17α-methyl group makes it work by mouth and ties it to the class’s liver risks.
Approved only for hereditary angioedema in the US. Labeled doses ranged from 2 mg every other day to 6 mg/day, and the brand was discontinued, with approval withdrawn in 2010.
Marked effects on cholesterol. At 6 mg/day it cut HDL by a third and raised LDL by 29% in six weeks, far more than injected testosterone at 200 mg/week.
Liver effects are dose-related. Transient enzyme rises occurred in about 30% of patients at 4 mg/day, and severe cholestasis is reported with non-medical doses.
Not free of androgenic effects. Women developed hirsutism and menstrual changes even at 0.5–2 mg/day, and the popular ratio figures cannot be traced to a primary assay.
Little human pharmacokinetic data. No verifiable human half-life is published, but metabolites can be detected in urine for weeks.

Sources

Winstrol (stanozolol tablets) prescribing information, NDA 012885. RxList.
Food and Drug Administration. Drugs@FDA: Winstrol, NDA 012885. FDA.
Food and Drug Administration. Novartis Pharmaceuticals Corp. et al.; Withdrawal of approval of 27 new drug applications and 58 abbreviated new drug applications. Federal Register. July 21, 2010;75:42455 (FR Doc 2010-17785). govinfo.
National Center for Biotechnology Information. Stanozolol, PubChem CID 25249. PubChem.
Massé R, Ayotte C, Bi HG, et al. Studies on anabolic steroids. III. Detection and characterization of stanozolol urinary metabolites in humans by gas chromatography-mass spectrometry. J Chromatogr. 1989;497:17–37. PubMed.
Schänzer W, Guddat S, Thomas A, et al. Expanding analytical possibilities concerning the detection of stanozolol misuse by means of high resolution/high accuracy mass spectrometric detection of stanozolol glucuronides in human sports drug testing. Drug Test Anal. 2013;5(11-12):810–818. PubMed.
Sinnecker G, Köhler S. Sex hormone-binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test. J Clin Endocrinol Metab. 1989;68(6):1195–1200. PubMed.
Sheffer AL, Fearon DT, Austen KF. Clinical and biochemical effects of stanozolol therapy for hereditary angioedema. J Allergy Clin Immunol. 1981;68(3):181–187. PubMed.
Sheffer AL, Fearon DT, Austen KF. Hereditary angioedema: a decade of management with stanozolol. J Allergy Clin Immunol. 1987;80(6):855–860. PubMed.
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Dias de Castro E, Cardoso LM, Jácome de Castro J, et al. Delphi consensus on attenuated androgen use for long-term prophylaxis in hereditary angioedema: AURA project. Clin Transl Allergy. 2025;15(11):e70116. PubMed.
Thompson PD, Cullinane EM, Sady SP, et al. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA. 1989;261(8):1165–1168. PubMed.
Taggart HM, Applebaum-Bowden D, Haffner S, et al. Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis. Metabolism. 1982;31(11):1147–1152. PubMed.
Chesnut CH 3rd, Ivey JL, Gruber HE, et al. Stanozolol in postmenopausal osteoporosis: therapeutic efficacy and possible mechanisms of action. Metabolism. 1983;32(6):571–580. PubMed.
Kluft C, Preston FE, Malia RG, et al. Stanozolol-induced changes in fibrinolysis and coagulation in healthy adults. Thromb Haemost. 1984;51(2):157–164. PubMed.
McMullin GM, Watkin GT, Coleridge Smith PD, et al. Efficacy of fibrinolytic enhancement with stanozolol in the treatment of venous insufficiency. Aust N Z J Surg. 1991;61(4):306–309. PubMed.
Carson P, Hong CJ, Otero-Vinas M, et al. Liver enzymes and lipid levels in patients with lipodermatosclerosis and venous ulcers treated with a prototypic anabolic steroid (stanozolol): a prospective, randomized, double-blinded, placebo-controlled trial. Int J Low Extrem Wounds. 2015;14(1):11–18. PubMed.
Stępień PM, Reczko K, Wieczorek A, et al. Severe intrahepatic cholestasis and liver failure after stanozolol usage - case report and review of the literature. Clin Exp Hepatol. 2015;1(1):30–33. PubMed.
Drug Enforcement Administration. Schedule III, 21 CFR 1308.13(f). eCFR.
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World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA.

Winstrol (Stanozolol)