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BHuman cohort / observational
High riskHepatotoxic

Anadrol

Oxymetholone · A50

Anadrol (oxymetholone, "A50") is a synthetic, orally active 17-alpha-alkylated anabolic-androgenic steroid derived from dihydrotestosterone. Medically it was developed to treat anemias of marrow failure and, in trials, HIV-associated wasting; in human RCTs at 50-150 mg/day it reliably raises hemoglobin/hematocrit, lean body mass and weight. The main danger is dose-dependent hepatotoxicity: in placebo-controlled trials 25-43% of patients on 100-150 mg/day had ALT/AST rise to more than five times baseline, and long-term use is linked in case reports to cholestasis, peliosis hepatis, hepatic adenoma and hepatocellular carcinoma. It also sharply lowers HDL cholesterol, suppresses the HPTA, causes fluid retention and (from marrow stimulation) erythrocytosis. No trial has ever studied the supraphysiologic doses used in bodybuilding, and there are no long-term cardiovascular-outcome or mortality data. This is a high-risk hepatotoxic oral AAS; anyone using it needs a clinician and regular bloodwork.

Clinical readoutAAS · oral-17aa
Hepatic strainHigh
CardiovascularHigh
HPTA suppressionHigh
Half-life
8.5 h
Route
Oral
Evidence
B
Active
Short
8.5 h17 h25.5 h34 h42.5 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Human pharmacokinetic data are limited; the terminal half-life is commonly cited at roughly 8-9 hours, consistent with the twice- to three-times-daily dosing used in trials. Treat as approximate.
Pharmacology

Mechanism of action

Oxymetholone is a 17-alpha-alkylated, 2-hydroxymethylene derivative of dihydrotestosterone that binds and activates the androgen receptor, driving anabolic gene transcription (increased protein synthesis, lean mass) and erythropoiesis (increased erythropoietin sensitivity/red-cell production). The 17-alpha-alkyl group blocks first-pass hepatic degradation to allow oral activity but is also the structural basis of its hepatotoxicity. It is not a substrate for aromatase, yet it produces clinically estrogenic effects (fluid retention, gynecomastia) through a still-incompletely-defined mechanism thought to involve direct estrogen-receptor activity. Mechanistic/pharmacologic description; not all mechanistic detail is supported by dedicated human studies.
Kinetics

Pharmacokinetics

Half-life

Human pharmacokinetic data are limited; the terminal half-life is commonly cited at roughly 8-9 hours, consistent with the twice- to three-times-daily dosing used in trials. Treat as approximate.

Active duration

Short; clinical trials dosed 2-3 times daily (e.g., 50 mg BID or TID), implying an effective duration of roughly 8-12 hours per dose.

Route

Oral (tablet), enabled by 17-alpha-alkylation which resists hepatic first-pass metabolism.

Metabolism & clearance

Hepatic metabolism with renal excretion of metabolites. The 17-alpha-alkyl structure prolongs hepatic exposure and underlies its liver toxicity. Washout/clearance framing is for monitoring and clinician planning only; no washout schedule circumvents the liver injury risk, which can persist or progress after stopping.

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

Reported effects

Physiological & performance effects

  • Increases hemoglobin and hematocrit; used clinically for anemias of marrow failure and enhances the erythropoietic response to recombinant erythropoietin in dialysis patients (Aramwit 2010 RCT; Cochrane 2014)
  • Increases body weight, lean body mass and body cell mass in HIV-associated wasting (Hengge 2003 RCTs; ~3-3.5 kg weight gain over 16 weeks vs ~1 kg placebo)
  • Increases lean body mass and maximal voluntary muscle strength and reduces trunk fat in older men over 12 weeks (Schroeder 2002 RCT)
  • Improves appetite, food intake and self-reported well-being in wasting patients (Hengge 2003)
  • Causes fluid retention/weight gain that is partly non-lean (estrogenic effect)
  • No trial has evaluated the high supraphysiologic doses used non-medically; reported benefits come from 50-150 mg/day therapeutic studies
Safety

Adverse effects by system

Cardiovascular

Marked, consistent reduction in HDL cholesterol: HDL fell 19-23 mg/dL in older men at 50-100 mg/day (Schroeder 2002) and by ~15.7 mg/dL in the Cochrane pooled analysis. This is an atherogenic lipid shift. No long-term cardiovascular-outcome, blood-pressure or mortality data exist for oxymetholone; cardiovascular risk is inferred from lipid changes, fluid retention and the broader AAS class.

Hepatic

The principal and best-documented toxicity. In placebo-controlled HIV-wasting trials, 25-43% of patients on 100-150 mg/day had ALT/AST/GGT rise to more than 5x baseline versus 0-8% on placebo (Hengge 2003); ALT rose a mean 72 U/L at 100 mg/day in older men (Schroeder 2002); liver-enzyme elevation was the main adverse event in dialysis patients (Aramwit 2010). Case reports document cholestatic jaundice, peliosis hepatis, hepatic adenoma and hepatocellular carcinoma with prolonged use (Kuhbock 1975; Kosaka 1996; Velazquez & Alter 2004).

Endocrine / HPTA

As an androgen it suppresses the hypothalamic-pituitary-gonadal axis; luteinizing hormone suppression was observed in the older-men RCT (Schroeder 2002). Expected consequences include reduced endogenous testosterone and impaired spermatogenesis. Long-term suppression and recovery kinetics after oxymetholone specifically have not been characterized.

Reproductive

Via HPTA/LH suppression, expected effects include decreased spermatogenesis, testicular atrophy and reduced fertility in men, and virilization in women; direct oxymetholone-specific fertility data are lacking. Contraindicated in pregnancy due to fetal virilization risk (androgen class effect).

Neuropsychiatric

No adequate oxymetholone-specific human data. Controlled trials in wasting and dialysis patients did not report increased neuropsychiatric events, but they were small and not designed to detect mood/behavioral effects; class-level AAS concerns (mood changes, aggression) cannot be excluded.

Renal

No direct nephrotoxicity has been demonstrated; in CKD/dialysis trials it did not lower BUN or creatinine (Cochrane 2014). Sodium and fluid retention with edema can occur and may burden patients with heart or kidney disease. No adequate human data show direct renal injury.

Hematologic

Stimulates erythropoiesis, raising hemoglobin and hematocrit (the therapeutic mechanism in anemia); this same effect can cause erythrocytosis/polycythemia and increased blood viscosity when used in people who are not anemic (Aramwit 2010; Cochrane 2014).

Dermatologic

Androgenic skin effects (acne, oily skin) and, in women, virilization (hirsutism, voice deepening) are expected class effects of a potent oral androgen; oxymetholone-specific controlled dermatologic data are limited and the wasting trials did not report excess dermatologic events over placebo.

Recovery

HPTA suppression & recovery

Suppression: Expected to be significant (potent oral androgen). LH suppression was observed in a controlled trial (Schroeder 2002), consistent with HPTA suppression; oxymetholone-specific severity and duration have not been formally characterized.

There are no adequate human data on the timing or completeness of HPTA recovery after oxymetholone specifically. Recovery of endogenous testosterone can be slow and is not guaranteed. Any post-use recovery or restart-of-function plan must be individualized and supervised by an endocrinologist with baseline and serial hormone testing. If any single-agent SERM (selective estrogen receptor modulator) approach is ever considered, that decision belongs to the treating endocrinologist — this monograph does not recommend a protocol, dose, or combination, and dual-SERM regimens are never advised. Do not self-manage suppression.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function tests (ALT, AST, GGT, bilirubin, alkaline phosphatase) at baseline and regularly during useComplete blood count with hematocrit/hemoglobin (to detect erythrocytosis/polycythemia)Fasting lipid panel including HDL and LDLTestosterone, LH and FSH (HPTA status), with endocrinology inputLiver imaging (ultrasound/CT) for anyone on prolonged androgen therapy, to screen for peliosis and hepatic tumorsBlood pressure and body weight (fluid retention)PSA in older men where prostate risk is relevant

Cadence: Baseline before use; liver enzymes and hematocrit checked early (e.g., within the first few weeks) and then at regular intervals (roughly every 4-12 weeks) during use; periodic liver imaging with prolonged/long-term exposure. Any use should be under a clinician who sets the schedule.

Warning signs — seek care
  • Jaundice (yellow skin/eyes), dark urine, pale stools
  • Right-upper-quadrant or abdominal pain, nausea, unexplained fatigue (possible hepatitis, peliosis, or tumor)
  • Sudden severe abdominal pain or signs of internal bleeding (peliosis hepatis can cause hepatic rupture/hemorrhage)
  • Rising ALT/AST above ~3-5x upper normal — stop and seek medical evaluation
  • Headache, flushing, visual changes or very high hematocrit (hyperviscosity/thrombosis risk)
  • Chest pain, shortness of breath, leg swelling, or rapid weight gain (fluid retention/cardiovascular)
  • In women: voice deepening, hirsutism, menstrual changes (virilization, may be irreversible)
Do not use if

Contraindications

  • Pre-existing liver disease, abnormal liver function, or hepatic tumors (drug is directly hepatotoxic and tumor-associated)
  • Pregnancy and breastfeeding (fetal virilization; androgen class contraindication)
  • Known or suspected prostate or male breast carcinoma (androgen-sensitive malignancy)
  • Polycythemia / elevated hematocrit or hyperviscosity states (further raises red-cell mass)
  • Significant dyslipidemia or established cardiovascular disease (marked HDL suppression, fluid retention)
  • Nephrotic states / conditions worsened by fluid and sodium retention, and edema-prone heart or kidney failure
  • Concomitant hepatotoxic or interacting drugs (e.g., cyclosporine, where hepatotoxicity was potentiated in a case report; also potentiates warfarin/anticoagulants)
  • Non-medical use in the absence of a diagnosed indication and clinician oversight
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

  • This is a hepatotoxic oral 17-alpha-alkylated steroid; do not use it without a diagnosed medical indication and a supervising clinician who orders and reviews bloodwork.
  • Get baseline labs (liver enzymes, CBC/hematocrit, lipids, testosterone/LH/FSH) before any use and repeat them on a clinician-set schedule; abnormal liver enzymes or rising hematocrit are reasons to stop.
  • Stop immediately and seek medical care for jaundice, dark urine, right-upper-quadrant or severe abdominal pain, unexplained fatigue, or signs of internal bleeding — these can signal serious liver injury, peliosis, or tumor.
  • Avoid combining with alcohol or other hepatotoxic/interacting drugs; oxymetholone hepatotoxicity was worsened by cyclosporine and it can potentiate anticoagulants like warfarin.
  • Because it raises hematocrit, watch for polycythemia/hyperviscosity (headache, flushing, thrombosis risk); do not use if you already have a high hematocrit.
  • Longer use raises tumor risk — periodic liver imaging is advised for anyone on prolonged androgen therapy.
  • HPTA suppression is expected; do not attempt to self-manage recovery. Discuss any endocrine/recovery plan with an endocrinologist. This monograph does not provide dosing to maximize effect, stacks, or restart protocols.
  • Women and anyone who could become pregnant should be aware of virilization risk (some effects, e.g., voice change, may be permanent) and fetal harm.
  • No safe supraphysiologic dose has been established; trial doses were 50-150 mg/day under medical supervision, always attached to the toxicities above.
Evidence

Citations (12)

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

  1. 01

    Oxymetholone increases body weight, lean body mass and body cell mass in HIV-associated wasting in a double-blind placebo-controlled RCT.

    RCTDouble-blind, randomized, placebo-controlled phase III trial of oxymetholone for the treatment of HIV wasting.PMID 12646793 ↗

  2. 02

    In the HIV-wasting RCT, 27-35% (double-blind phase) of patients on 100-150 mg/day had ALT rise to more than five times baseline versus none on placebo, identifying hepatotoxicity as the main adverse event.

    RCTDouble-blind, randomized, placebo-controlled phase III trial of oxymetholone for the treatment of HIV wasting.DOI 10.1097/00002030-200303280-00008 ↗

  3. 03

    Phase III placebo-controlled trial: 43% (TID) and 25% (BID) of oxymetholone patients versus 8% placebo had ALT/AST/GGT more than 5x baseline; other adverse events not increased over placebo.

    RCTOxymetholone for the treatment of HIV-wasting: a double-blind, randomized, placebo-controlled phase III trialPMID 12815555 ↗

  4. 04

    Oxymetholone promoted weight gain and improved Karnofsky performance status in advanced HIV cachexia (pilot randomized study).

    RCTOxymetholone promotes weight gain in patients with advanced human immunodeficiency virus (HIV-1) infection.PMID 8785183 ↗

  5. 05

    In older men, oxymetholone 50-100 mg/day increased lean body mass and maximal muscle strength and reduced trunk fat, but raised ALT (mean +72 U/L at 100 mg/day) and lowered HDL by 19-23 mg/dL, with LH suppression.

    RCTEffects of an oral androgen on muscle and metabolism in older, community-dwelling men.DOI 10.1152/ajpendo.00363.2002 ↗

  6. 06

    Oxymetholone plus erythropoietin significantly increased hematocrit, hemoglobin, lean body mass and albumin in dialysis (CAPD) patients; rise in liver enzymes was the main side effect.

    RCTThe efficacy of oxymetholone in combination with erythropoietin on hematologic parameters and muscle mass in CAPD patients.DOI 10.5414/cpp48803 ↗

  7. 07

    Meta-analysis: oxymetholone increases hemoglobin and hematocrit and ALT/AST and decreases HDL, but overall evidence is insufficient to confirm net benefit of androgens for CKD anemia.

    Meta-analysisAndrogens for the anaemia of chronic kidney disease in adults.DOI 10.1002/14651858.CD006881.pub2 ↗

  8. 08

    Oxymetholone hepatotoxicity was potentiated by concomitant cyclosporine in a bone marrow transplant patient.

    Case reportOxymetholone hepatotoxicity enhanced by concomitant use of cyclosporin A in a bone marrow transplant patient.PMID 7955931 ↗

  9. 09

    Long-term oxymetholone caused cholestatic jaundice and peliosis hepatis with fatal outcome in a patient with aplastic anemia.

    Case report[Peliosis hepatis, complicating treatment with anabolic steroids] (in German).PMID 810650 ↗

  10. 10

    Long-term oxymetholone therapy was associated with development of hepatocellular carcinoma.

    Case reportHepatocellular carcinoma associated with anabolic steroid therapy: report of a case and review of the Japanese literature.DOI 10.1007/BF02355039 ↗

  11. 11

    Review of androgen-associated liver tumors: oxymetholone and methyltestosterone were most associated with hepatocellular carcinoma; all patients on anabolic androgenic steroids are at risk of liver tumors regardless of underlying diagnosis.

    ReviewAndrogens and liver tumors: Fanconi's anemia and non-Fanconi's conditions.DOI 10.1002/ajh.20183 ↗

  12. 12

    Anabolic steroid therapy (oxymetholone) is considered a promoter of hepatocellular neoplasms in Fanconi anemia.

    Case reportHepatocellular carcinoma in an 11-year-old girl with Fanconi's anemia. Report of a case and review of the literature.PMID 3026193 ↗

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