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Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

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Winstrol

Extensively Studied

Stanozolol — synthetic 17α-alkylated DHT-derivative AAS with a fused pyrazole ring; oral or aqueous-suspension injectable; the "Ben Johnson 1988 Seoul" steroid

Aliases (12)
stanozolol · Stanozolol · Winny · Winstrol Depot · Stromba · Stanazol · oral stanozolol · Stanabol · Strombafort · Menabol · 17α-methyl-2'H-androst-2-eno[3 · 2-c]pyrazol-17β-ol
TYPICAL DOSE
Oral: 30-50mg/day; Injectable: 50mg EOD; HAE cl…
Oral 2-3× daily; Injectable EOD-daily
ROUTE
Oral tablet OR intramuscular aqueous suspension
Oral OR aqueous IM
CYCLE
6-8 weeks on (oral); 8-10 weeks on (depot)
6-8 weeks max (hepatotoxicity)
STORAGE
Room temp; original container; protect from light
Room temperature

Overview

What is Winstrol?

Stanozolol (Winstrol) is a synthetic anabolic-androgenic steroid derived from dihydrotestosterone, with a fused pyrazole ring on the A-ring and 17α-methyl group enabling oral bioavailability. Originally FDA-approved in 1962 for hereditary angioedema (HAE) prophylaxis (NDA withdrawn 2010 by Sanofi). DEA Schedule III. WADA S1.1 prohibited at all times. The compound that ended Ben Johnson's 100m gold at the 1988 Seoul Olympics — culturally synonymous with sports doping.

Key Benefits

Lean, dry, hard physique without water retention; strength + power gains useful for weight-class sports; SHBG suppression sharply elevates free testosterone; non-aromatizing so no gyno or estrogen-related water retention; available in both oral and injectable forms.

Mechanism of Action

17α-methylated tablet absorbed orally; first-pass intact through liver; ~9-hour half-life requiring multiple daily doses. Maximum hepatotoxicity profile of any common AAS due to oral 17α-aa exposure across all gut-blood-liver passes. Free fraction rises rapidly via SHBG crash.

Pharmacokinetics

—·—
PeakHalf-life
Approximate curve — visual aid only, not data-precise PK

Research Indications

Most Effective

What stanozolol is, structurally

Stanozolol is 17α-methyl-2'H-androst-2-eno[3,2-c]pyrazol-17β-ol — a synthetic anabolic-androgenic steroid derived from 5α-dihydrotestoste…

Effective

Receptor + signaling

Stanozolol is a direct AR agonist with binding affinity approximately 22% of DHT — modest in absolute terms, but the high anabolic-to-and…

Investigational

Why SHBG crash dominates the systemic profile

The single most distinctive pharmacological feature of stanozolol is its dramatic suppression of sex hormone-binding globulin (SHBG): - S…

Investigational

Hepatotoxicity — among the worst in the AAS class

17α-alkylation forces the parent molecule to traverse the liver intact, producing dose-dependent cholestatic injury. Stanozolol's hepatot…

Investigational

Atherogenic dyslipidemia — among the worst in the AAS class

Stanozolol has one of the most severe lipid profiles of any AAS: - Thompson et al. 1989 JAMA (PMID 2915439): Direct comparison of stanozo…

Investigational

Tendon, ligament, and cartilage signals — the signature combat-athlete concern

This is the section that determines the verdict for the user: - Karpakka et al. 1992 (PMID 1636855, AJSM): Rat skeletal muscle + Achilles…

Peptide Interactions

Testosterone esters (cypionate, enanthate):
Synergistic

Standard "test base" — prevents total HPG crash, preserves libido during cycle. Common protocol: test enanthate 300-400 mg/week × 12 weeks + Winstrol 30-50 m…

[anavar / oxandrolone](anavar.md):
Synergistic

Both DHT-derivative orals, both 17α-alkylated — stacking compounds hepatotoxicity dramatically. Sometimes used in contest prep ("oral stacking") but widely c…

[primobolan](primobolan.md):
Synergistic

DHT-derivative injectable (methenolone enanthate) often paired with Winstrol for cutting; primobolan adds anabolic without compounding hepatotoxicity (it's a…

[masteron-enanthate](masteron-enanthate.md):
Synergistic

Another DHT-derivative; similar hardening + anti-estrogen profile. Common contest-prep stack with Winstrol — compounds DHT-class side effects (joint dryness,…

Trenbolone:
Synergistic

Synergistic for aggressive cutting; compounds cardiovascular + neurologic + lipid risks dramatically.

Clenbuterol / T3:
Synergistic

Common cutting stack additions; compound cardiovascular load.

GH / IGF-1:
Synergistic

Adds anabolic synergy + theoretical tendon support (collagen synthesis); compounds insulin resistance + cancer-pathway concerns.

Other 17α-alkylated orals (methyltestosterone, fluoxymesterone, oxandrolone, dianabol, anadrol):
Avoid

Compounds hepatotoxicity dramatically; Winstrol is at the high end of C17-aa hepatotoxicity already.

[anastrozole](anastrozole.md) / aromatase inhibitors:
Avoid

Stanozolol is non-aromatizing — adding an AI on top crashes E2 below normal range, producing severe joint pain (already a Winstrol problem), low libido, lipi…

Hepatotoxic medications (acetaminophen chronic, methotrexate, isoniazid, alcohol):
Avoid

Additive liver burden. Real-world collision for athletes using NSAIDs/acetaminophen for training pain.

Statins:
Avoid

Pharmacologically logical for crashing HDL/LDL but adds hepatic burden on top of an already-hepatotoxic 17α-aa drug. The appropriate move is to discontinue t…

Warfarin / DOACs:
Avoid

Stanozolol potentiates warfarin significantly; per prescribing information, dose reduction with frequent INR monitoring required.

Quality Indicators

✓

Pharmaceutical-grade tablet, sealed pharmacy packaging

Genuine pharmaceutical Winstrol (now rare in US; available abroad as Stromba, Stanazol, Menabol). Sealed, lot-numbered, intact blister packaging from licensed pharmacy.

✓

Injectable: milky-white aqueous suspension, particles re-suspend with vigorous shake

Injectable stanozolol is a water-based suspension of micronized particles — appears milky-white. Particles settle quickly; need to shake vial vigorously immediately before drawing. Clear or slightly opalescent solution suggests counterfeit (oil-based product mislabeled, or solvent-based knockoff).

!

Generic / international pharmacy variation

Bioequivalence between brands varies modestly. Common generics: Stanabol, Stanazol, Strombafort, Stromba, Menabol. Track lot if switching between sources.

!

Injectable: PIP (post-injection pain) + cough is normal but harsh

Aqueous suspension Winstrol famously causes injection-site pain, redness, and a transient 'Winstrol cough' (vasovagal/PE-mimicking) if particle hits venule. Painful enough that many users prefer oral despite hepatotoxicity tradeoff.

✗

Crystalline residue, brown/yellow discoloration, or oil base on supposed injectable

Genuine injectable Winstrol is white aqueous suspension. Discolored, oil-based, or crystalline product is counterfeit. Counterfeit is endemic in the Winstrol UGL market — frequently substituted with cheaper oral powder dissolved in oil.

✗

Underground lab (UGL) tablets without batch testing

UGL Winstrol tablets are commonly underdosed, contaminated with fillers, or substituted with cheaper compounds (often dianabol or methyltestosterone). Third-party batch testing strongly recommended; many users in tested sports have failed for other compounds in 'pure' Winstrol product.

What to Expect

  • Day 1-3
    Subjective drive shift; libido often spikes early as free T rises (SHBG crash). Strength noticeable in gym within 3-5 sessions.
  • Week 1-2
    Aesthetic shift begins — drier appearance, vascularity increasing, "harder" muscle quality. Strength climbing. Joint stiffness emerging in some users (espec…
  • Week 2-4
    Peak aesthetic phase — dry, hard, vascular look maximally expressed. Power output up. Lipid changes well-established on bloodwork; HDL crash measurable. Joi…
  • Week 4-6
    Side-effect curve climbs. Libido may swing from initial spike to depression (HPG suppression catching up). ALT/AST starting to rise meaningfully on oral use…
  • Week 6-8
    Cycle exit window. Hepatotoxicity risk rises with continued use; most users plan to stop here.

Side Effects & Safety 15

Side Effects

  1. 1HDL crash + LDL elevation — universal on bloodwork; HDL drops 30-50% within weeks, often acutely within 3-7 days per Haffner timeline
  2. 2ALT/AST elevation — dose-dependent transaminitis, typically reversible on cessation; meaningful elevation common at 4-6 weeks of oral cycle
  3. 3HPG suppression — measurable LH/FSH suppression and endogenous testosterone reduction; recovery typically 4-12 weeks post-cycle without PCT
  4. 4Joint pain / "dry joints" — universal complaint; loaded movement uncomfortable; pre-existing joint issues exacerbated
  5. 5SHBG crash — 50-70% reduction within days; sharp free-T spike (subjective drive/aggression); rebound on cessation
  6. 6Acne — mild-to-moderate, especially shoulders/back (DHT-derivative signaling)
  7. 7Hair shedding in genetically predisposed users — DHT-class signaling at scalp follicles
  8. 8Injection site pain (Winstrol Depot) — notorious; many users prefer oral despite hepatotoxicity tradeoff
  9. 9Cholestatic jaundice — yellowing of skin/sclera, dark urine, pruritus; may persist weeks post-cessation per Petrolini phenotype data
  10. 10Mood changes — irritability, occasional aggression; less than testosterone or trenbolone but reported
  11. 11Hypertension — modest BP elevation, dose-dependent
  12. 12Erythrocytosis — mild hematocrit increase; less than testosterone esters
  13. 13Sleep disturbance in some users
  14. 14"Winstrol cough" — transient post-injection cough/chest tightness from particle entry into small venule; resolves in seconds; alarming if first-time experience
  15. 15Virilization in women — clitoral hypertrophy, voice deepening (often irreversible), hirsutism, menstrual disruption — rises sharply above 10 mg/day

When to Stop

  • Acute liver failure — Rui 2017 (PMID 28856252), Patel 2023 (PMID 37948000); fatal cases documented
  • Hepatocellular adenoma — Cerullo 2025 (PMID 40909442); chronic-exposure benign hepatic neoplasm
  • Peliosis hepatis — cystic blood-filled hepatic lesions; potentially life-threatening (hepatic hemorrhage); documented across 17α-aa class
  • Hepatocellular carcinoma — extremely rare, documented with long-term high-dose 17α-aa exposure
  • Tendon rupture — Kanayama 2015 baseline 22% in long-term users; risk concentrated in upper-body explosive tendons (pec, biceps long head, quadriceps tendon) and Achilles
  • Severe atherogenic dyslipidemia leading to accelerated CVD — particularly with cumulative multi-cycle use over years
  • Cardiomyopathy — Baggish et al. (Circulation 2017) — cardiac MRI evidence of LV hypertrophy + diastolic dysfunction in long-term AAS users; cumulative-exposure-dependent
  • Severe HPG suppression with prolonged hypogonadism post-cycle — secondary hypogonadism failing to recover, requiring TRT salvage; risk rises with cycle length
  • Mood crash / post-cycle depression — well-documented bodybuilding-community phenomenon; persistent anhedonia / low mood for weeks-to-months post-cycle in susceptible users
  • Counterfeit / contaminated product effects — UGL Winstrol is endemically counterfeit (often substituted with cheaper compounds); multiple WADA failures by athletes who claimed "I was on Winstrol" but tested for other AAS
  • Day 3-7: SHBG nadir + HDL crash should be measurable; if HDL drops >50% at week 1 bloodwork, this is a particularly bad responder
  • Week 4 of any cycle: ALT/AST + lipid panel — flag if ALT >3× ULN, HDL drops >50%, or any cholestatic symptom (jaundice, pruritus, dark urine)
  • Week 6-8: Hepatotoxicity escalation window; cholestasis can present 7-9 weeks per Petrolini phenotype
  • End of cycle: Full HPG panel (T, LH, FSH, E2) to confirm degree of suppression
  • Week 4-8 post-cycle: HPG recovery check; if still suppressed, formal PCT or endocrinology consult
  • Multi-cycle users (years): Periodic echocardiogram, lipid trend tracking, liver imaging at any symptom or persistent transaminase elevation
  • New tendon pain or pop during loaded movement — STOP IMMEDIATELY for combat athletes; this is the highest-relevance early warning

References

Stanozolol — Wikipedia

en.wikipedia.org

structural / pharmacokinetic / historical context

View Study

Small M et al. 1984 — Alteration of hormone levels in normal males given the anabolic steroid stanozolol (Clin Endocrinol)

pubmed.ncbi.nlm.nih.gov · 1984

PMID 6430603, 55% T reduction + SHBG crash

View Study

Sinnecker GH et al. 1989 — SHBG response to stanozolol (Acta Endocrinol)

pubmed.ncbi.nlm.nih.gov · 1989

PMID 2723028, basis of androgen-sensitivity test

View Study

Thompson PD et al. 1989 — Contrasting effects of testosterone and stanozolol on serum lipoprotein levels (JAMA)

pubmed.ncbi.nlm.nih.gov · 1989

PMID 2915439, head-to-head HDL crash comparison

View Study

Haffner SM et al. 1983 — Studies on metabolic mechanism of reduced HDL during anabolic steroid therapy (Metabolism)

pubmed.ncbi.nlm.nih.gov · 1983

PMID 6413814, HTGL upregulation mechanism

View Study
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