Skip to content
StackItSmart
CCase reports / series
HepatotoxicHigh riskCardiotoxicNeuropsychiatric

Winstrol

Stanozolol · Winny

Winstrol (stanozolol) is a synthetic, DHT-derived, 17-alpha-alkylated (17aa) oral anabolic-androgenic steroid, also available as an aqueous injectable suspension. It has legitimate medical history in hereditary angioedema prophylaxis, some anemias, and adjunctive cancer/wasting therapy, but is widely misused non-medically for physique and performance. Lead dangers: because it is 17aa, it is directly hepatotoxic and is a documented cause of a distinctive cholestatic drug-induced liver injury (marked jaundice, pruritus, high bilirubin) with rare fatal cases; it produces severe adverse shifts in blood lipids (sharp HDL fall, LDL rise); it suppresses the hypothalamic-pituitary-testicular axis and spermatogenesis; and in women it causes virilization that can be irreversible. Most stanozolol-specific human evidence comes from small studies and case reports/series, so certainty is limited. Anyone using or considering it should not do so without physician oversight and regular bloodwork, and should stop and seek urgent care at the first sign of jaundice or dark urine.

Clinical readoutAAS · oral-17aa
Hepatic strainHigh
CardiovascularVery high
HPTA suppressionVery high
Half-life
9 h
Route
Oral 17-alpha-alkylated…
Evidence
C
Active
Approximately once-dail…
9 h18 h27 h36 h45 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Rigorous human pharmacokinetic data are sparse. Oral stanozolol is commonly described as having a plasma half-life on the order of several hours (roughly ~9 hours cited historically), while the aqueous injectable depot form persists longer; controlled PK characterization in humans is limited, and the best-quantified data are from animal (equine intramuscular) studies.
Pharmacology

Mechanism of action

Stanozolol is a synthetic derivative of dihydrotestosterone bearing a pyrazole ring fused to the steroid A-ring and a 17-alpha-methyl (alkyl) group. It acts as an androgen-receptor agonist, promoting nitrogen retention and anabolic (protein-synthesis) effects in muscle. The 17-alpha-alkylation resists first-pass hepatic degradation to allow oral activity, but this same modification is responsible for its cholestatic hepatotoxicity. It is not a substrate for aromatase, so it does not convert to estrogen. Its oral route drives strong first-pass hepatic effects on lipoprotein metabolism (a large increase in hepatic triglyceride lipase activity and reductions in HDL and apolipoprotein A-I). It also modulates the fibrinolytic/haemostatic system (e.g., lowering plasminogen activator inhibitor-1) and increases hepatic synthesis of C1-esterase inhibitor, the basis of its use in hereditary angioedema.
Kinetics

Pharmacokinetics

Half-life

Rigorous human pharmacokinetic data are sparse. Oral stanozolol is commonly described as having a plasma half-life on the order of several hours (roughly ~9 hours cited historically), while the aqueous injectable depot form persists longer; controlled PK characterization in humans is limited, and the best-quantified data are from animal (equine intramuscular) studies.

Active duration

Approximately once-daily oral dosing was used in clinical/therapeutic settings, consistent with a short-to-intermediate active duration for the oral form; the injectable suspension is longer-acting. Precise human active-duration data are limited.

Route

Oral 17-alpha-alkylated tablets, and an aqueous injectable (intramuscular) suspension.

Metabolism & clearance

Extensively hepatically metabolized (hydroxylation, e.g., to 3'-hydroxystanozolol, and conjugation), with urinary and biliary/fecal excretion of metabolites. Reported here for washout/monitoring context, not for detection avoidance; because clearance is hepatic, impaired liver function can prolong exposure.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Androgen-receptor-mediated anabolic effect promoting nitrogen retention and lean-mass gain (demonstrated as weight gain in a human crossover study)
  • Non-aromatizing, so it does not raise estrogen levels directly
  • Lowers HDL cholesterol and apolipoprotein A-I and raises LDL cholesterol via first-pass hepatic effects
  • Historically used medically as long-term prophylaxis for hereditary angioedema (increases C1-esterase inhibitor)
  • Stimulates haematopoiesis and has been used adjunctively in some anemias and hematologic conditions
  • Modulates fibrinolysis (lowers plasminogen activator inhibitor-1)
  • Suppresses pituitary gonadotropins (LH/FSH) and endogenous testosterone
Safety

Adverse effects by system

Cardiovascular

Marked adverse lipid changes: in a human crossover study, oral stanozolol reduced HDL cholesterol ~33% and the HDL2 subfraction ~71%, lowered apolipoprotein A-I ~40%, raised LDL cholesterol ~29%, and increased hepatic triglyceride lipase activity ~123%. AAS users show impaired endothelium-independent vasoreactivity, and long-term AAS use (class-level cohort data) is associated with reduced left-ventricular systolic and diastolic function and greater coronary atherosclerotic plaque burden. Overall cardiovascular impact is strongly adverse.

Hepatic

As a 17-alpha-alkylated oral steroid, stanozolol causes a characteristic cholestatic drug-induced liver injury: marked elevation of bilirubin with only mild transaminase rise and near-normal GGT, presenting with jaundice and pruritus after a mean latency of ~55 days. Rare fatal outcomes with sub-massive hepatic necrosis and acute liver failure have been reported.

Endocrine / HPTA

Suppresses hypothalamic-pituitary-testicular axis output; stanozolol suppressed gonadotropins in a human study, and AAS as a class cause secondary hypogonadism with low LH/FSH and suppressed endogenous testosterone. Recovery is variable and can be prolonged.

Reproductive

Testicular atrophy, impaired spermatogenesis, oligo-/azoospermia and reduced fertility from HPTA suppression (class-level evidence in AAS-using men). In women, prolonged use causes virilization (deepening voice, clitoral enlargement, hirsutism) that may be irreversible. Contraindicated in pregnancy due to fetal virilization risk. Because stanozolol does not aromatize, estrogenic gynecomastia is not a typical direct effect.

Neuropsychiatric

AAS use is associated with aggression/violence, mood disturbance, dependence syndromes, and withdrawal symptoms; a subset report severe aggressiveness and, rarely, suicide attempts during withdrawal. Stanozolol-specific controlled psychiatric data are limited, so this reflects class-level human evidence.

Renal

No evidence of a primary direct nephrotoxic syndrome specific to stanozolol at typical exposure, but two secondary renal harms are documented in AAS users: acute bile-cast nephropathy (cholemic nephrosis) in the setting of severe AAS-induced cholestasis, and focal segmental glomerulosclerosis with heavy proteinuria and renal insufficiency after long-term AAS abuse (partially reversible on cessation).

Hematologic

Androgens including stanozolol alter haemostasis, lowering plasminogen activator inhibitor-1 and enhancing fibrinolysis; above an individual threshold, net effects on platelets and vasomotion may become prothrombotic, and AAS misuse has been associated with thromboembolic events. Androgens also stimulate erythropoiesis and can raise hematocrit (erythrocytosis). Direct high-quality stanozolol-specific hematologic outcome data are limited.

Dermatologic

Androgenic skin effects including acne and androgenic alopecia; in women, hirsutism and other virilizing skin/appendage changes were observed with prolonged stanozolol therapy. Stanozolol-specific dermatologic data are limited.

Recovery

HPTA suppression & recovery

Suppression: Moderate to marked suppression of the hypothalamic-pituitary-testicular axis (secondary hypogonadism with suppressed LH/FSH and endogenous testosterone).

Recovery of endogenous testosterone and spermatogenesis after stopping is variable and can be prolonged. Management of suppressed axis and any consideration of pharmacologic restart therapy (which in the literature may involve a single selective estrogen receptor modulator, hCG, or other agents) must be individualized and directed by an endocrinologist or reproductive specialist with appropriate lab monitoring; this monograph does not endorse self-directed recovery protocols. Do not attempt multi-agent self-management.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver panel: ALT, AST, alkaline phosphatase, total and direct bilirubin, GGTFasting lipid panel (HDL, LDL, triglycerides, apolipoprotein A-I where available)Complete blood count with hematocrit/hemoglobin (erythrocytosis)Renal function: serum creatinine and urinalysis for proteinuriaReproductive/endocrine: total testosterone, LH, FSHPSA (age-appropriate men)Coagulation/INR if on anticoagulants

Cadence: Baseline before any use, then periodically during use (e.g., roughly every 4-12 weeks) and again after cessation to confirm recovery; more frequently if symptoms or abnormal results appear. All monitoring should be done with a clinician, not self-interpreted.

Warning signs — seek care
  • Jaundice (yellow skin/eyes), dark urine, pale stools, or generalized itching
  • Right-upper-quadrant abdominal pain, nausea, or unexplained fatigue/malaise
  • Swelling/edema or reduced urine output
  • Chest pain, shortness of breath, or signs of clot/stroke
  • New or worsening aggression, mood disturbance, or suicidal thoughts
  • In women: voice deepening, facial/body hair growth, clitoral enlargement (seek care early, as some changes are irreversible)
Do not use if

Contraindications

  • Pregnancy and breastfeeding (risk of fetal/infant virilization; androgens are teratogenic)
  • Pre-existing liver disease, cholestasis, or abnormal liver function
  • Known or suspected prostate or male breast carcinoma
  • Significant dyslipidemia or established cardiovascular disease
  • Nephrotic syndrome or significant renal impairment/proteinuria
  • Hypercalcemia (including malignancy-associated)
  • Concurrent use of other hepatotoxins or heavy alcohol use
  • Concurrent anticoagulant therapy without close monitoring (androgens can potentiate anticoagulant effect)
  • Women seeking to avoid irreversible virilization
Combinations

Interaction profile

  • MajorWith another anabolic steroid: Additive cardiovascular strain
  • MajorWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith growth hormone: Additive cardiovascular strain
  • MajorWith another 17α-alkylated oral: Additive liver strain
  • MajorWith a liver-signal SARM: Additive liver strain
  • MajorWith another anabolic steroid: Blood / clotting
  • MajorWith a clot-promoting SERM: Blood / clotting
  • ModerateWith an aromatase inhibitor: Hormonal
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Stop the drug immediately and seek urgent medical care at the first sign of jaundice, dark urine, pale stools, itching, or right-upper-quadrant pain; these signal cholestatic liver injury.
  • 17-alpha-alkylated oral steroids like stanozolol are particularly hepatotoxic; avoid combining with alcohol, acetaminophen, or other liver-stressing drugs.
  • Obtain baseline bloodwork (liver panel, lipids, CBC/hematocrit, renal function, testosterone/LH/FSH) and repeat periodically with a clinician; do not rely on how you feel.
  • Because stanozolol sharply lowers HDL and raises LDL, cardiovascular risk rises even in young users; discuss lipid and cardiac monitoring with a clinician.
  • Women should be aware that virilizing effects (voice deepening, clitoral enlargement, hirsutism) can be permanent; seek care early if they begin.
  • Do not use in pregnancy or when trying to conceive; androgens can virilize a fetus and impair male fertility.
  • For a suppressed hormonal axis or fertility concerns after stopping, consult an endocrinologist or reproductive specialist rather than self-managing recovery.
  • Seek emergency care for chest pain, shortness of breath, or neurological symptoms, which may indicate a cardiovascular or thromboembolic event.
Evidence

Citations (17)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Stanozolol is a 17-alpha-alkylated oral AAS that causes a distinctive cholestatic drug-induced liver injury with marked bilirubin elevation, mild transaminase rise, near-normal GGT, jaundice and pruritus after ~55 day latency.

    Case seriesStanozolol-induced Liver Injury: A Distinctive Cholestatic Clinical and Biochemical Phenotype at Presentation.PMID 40040852 ↗

  2. 02

    Stanozolol overdose/misuse can cause fatal acute liver failure with sub-massive hepatic necrosis and cholestasis.

    Case reportFatal anabolic androgenic steroid overdose in an amateur bodybuilder: a clinical and autopsy reportPMID 37948000 ↗

  3. 03

    Oral stanozolol (6 mg/day) in male weightlifters reduced HDL cholesterol ~33%, HDL2 ~71%, apolipoprotein A-I ~40%, raised LDL ~29%, increased hepatic triglyceride lipase ~123%, and suppressed gonadotropins.

    RCTContrasting effects of testosterone and stanozolol on serum lipoprotein levels.PMID 2915439 ↗

  4. 04

    AAS-using bodybuilders show impaired (endothelium-independent) vasoreactivity that may improve after discontinuation.

    CohortImpaired vasoreactivity in bodybuilders using androgenic anabolic steroids.PMID 16796605 ↗

  5. 05

    Long-term AAS use is associated with reduced left-ventricular systolic and diastolic function and greater, dose-related coronary atherosclerotic plaque burden.

    CohortCardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid UsePMID 28533317 ↗

  6. 06

    Severe AAS-induced cholestasis can precipitate acute kidney injury via bile-cast nephropathy (cholemic nephrosis).

    Case reportAcute bile nephropathy secondary to anabolic steroids.PMID 26587777 ↗

  7. 07

    Long-term AAS abuse is associated with focal segmental glomerulosclerosis, heavy proteinuria and renal insufficiency, partially reversible on cessation.

    Case seriesDevelopment of focal segmental glomerulosclerosis after anabolic steroid abuse.PMID 19917783 ↗

  8. 08

    AAS use is associated with aggression/violence, mood disturbance, dependence, and withdrawal symptoms including rare suicide attempts.

    CohortPast anabolic-androgenic steroid use among men admitted for substance abuse treatment: an underrecognized problem?PMID 12633124 ↗

  9. 09

    AAS use causes secondary hypogonadism with suppressed spermatogenesis and impaired male fertility; recovery is variable and may involve specialist-directed pharmacologic strategies.

    ReviewAnabolic steroid misuse and male infertility: management and strategies to improve patient awareness.PMID 33973822 ↗

  10. 10

    AAS-induced hypogonadism/infertility recovery should be individualized and specialist-managed.

    ReviewManagement of Anabolic Steroid-Induced Infertility: Novel Strategies for Fertility Maintenance and Recovery.PMID 30929329 ↗

  11. 11

    Prolonged stanozolol therapy produces virilization in women.

    Case series[Trial of androgen therapy in the treatment of non-lymphoblastic acute leukemia. First results].PMID 1064847 ↗

  12. 12

    Androgens including stanozolol alter haemostasis (lower PAI-1, enhance fibrinolysis) with a possible prothrombotic threshold effect.

    ReviewEffects of androgens on haemostasis.PMID 8844628 ↗

  13. 13

    Stanozolol is used as a long-term prophylactic option in hereditary angioedema.

    Case reportHereditary Angioedema: A Gynecology and Obstetrics Perspective.PMID 34976488 ↗

  14. 14

    Stanozolol, combined with cyclosporine, has been used adjunctively in aplastic anemia and hypoplastic myelodysplastic syndrome, improving peripheral blood counts in a pediatric case series.

    Case seriesPMID 23791060 ↗

  15. 15

    Quantified pharmacokinetic characterization of stanozolol is available chiefly from animal (equine intramuscular) studies; robust human PK data are limited.

    PreclinicalPharmacokinetics of stanozolol in Thoroughbred horses following intramuscular administration.PMID 22489613 ↗

  16. 16

    Stanozolol induces hepatic oxidative stress in preclinical (rat) models, supporting a hepatotoxic mechanism.

    PreclinicalEffects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and HSP72 levels in rat liver.PMID 14698208 ↗

  17. 17

    Stanozolol promotes aortic lipid deposition and atherogenesis in a preclinical (LDLr-knockout mouse) model via inflammatory and oxidative pathways.

    PreclinicalStanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet.PMID 30295413 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice