This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.
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.
Anadrol
Oxymetholone (Anadrol-50, A50, A-Bombs, Anapolon) — oral 17α-alkylated DHT-derivative AAS; FDA-approved for anemias of bone-marrow failure; among the most hepatotoxic AAS in clinical use.
Aliases (8)
Overview
What is Anadrol?
Anadrol (oxymetholone) is a synthetic 17α-alkylated DHT-derivative anabolic-androgenic steroid (AAS), FDA-approved (Anadrol-50, Alaven Pharmaceutical) for anemias caused by deficient red cell production — acquired and congenital aplastic anemia, myelofibrosis, and hypoplastic anemias due to myelotoxic drugs. Schedule III in the US under the Anabolic Steroids Control Act; WADA-banned S1.1a. Famous in bodybuilding culture for producing the fastest oral mass + strength curve of any AAS — and the most severe hepatotoxicity, with ALT >5× ULN documented in 27-35% of subjects on 100-150 mg/day in the Hengge/Schroeder 2003 Phase 3 trial.
Key Benefits
Rapid mass + strength gains (15-25 lb scale gain in 4-6 weeks; 5-10 lb true LBM after water sheds). Pronounced glycogen storage and 'fullness.' Strong erythropoietic effect (FDA-approved indication) — directly stimulates EPO production. Aggressive appetite increase. Mood elevation / drive in many users. Effective for severe medical wasting (AIDS-cachexia, aplastic anemia, Fanconi anemia) under specialist supervision.
Mechanism of Action
Direct androgen receptor (AR) agonist (anabolic:androgenic ratio ~320:45). The 17α-methyl group enables oral bioavailability but obligates first-pass hepatic burden — cholestasis, peliosis hepatis, hepatic adenoma, hepatocellular carcinoma at chronic high-dose use. The 2-hydroxymethylene A-ring substitution blocks aromatase yet oxymetholone produces estrogenic side effects (gynecomastia, water retention) via direct estrogen receptor binding (Pavlatos 2001) — exact mechanism still debated, may include weak progesterone receptor or mineralocorticoid activity. Profound HPG-axis suppression at any therapeutic dose. Stimulates erythropoietin (FDA-approved mechanism).
Pharmacokinetics
Research Indications
Structure
Oxymetholone is 17β-hydroxy-2-(hydroxymethylene)-17-methyl-5α-androstan-3-one — a synthetic anabolic-androgenic steroid derived from dihy…
Receptor activity
Oxymetholone is a direct androgen receptor (AR) agonist, with binding affinity at peripheral AR (skeletal muscle, bone). The published an…
The "non-aromatizing yet estrogenic" paradox
This is the mechanistic detail that defines Anadrol's clinical and bodybuilding profile. Most aromatizable AAS (testosterone, methyltesto…
HPG suppression
Oxymetholone produces rapid and complete HPG-axis suppression at any therapeutic dose: - AR activation at hypothalamic neurons → suppress…
Pharmacokinetics
- Oral bioavailability: Near-complete; the 17α-methyl modification protects from first-pass deactivation - Half-life: ~9 hours (allows on…
Peptide Interactions
(300-500 mg/week, "TRT base") — Standard bodybuilding pairing. The injectable T provides foundational androgen (preventing complete HPG-driven androgen crash…
(250-500 IU 2× weekly during cycle) — Maintains testicular volume / Leydig responsiveness; eases PCT.
TUDCA 500-1000 mg/day, NAC 1.2-2.4 g/day, milk thistle 600 mg silymarin extract/day, choline 500 mg/day. Mandatory if running Anadrol despite recommendation.…
Tamoxifen 10-20 mg/day OR raloxifene 60 mg/day — Required for Anadrol-driven gyno control because AIs don't work (Anadrol doesn't aromatize but binds ER dire…
(oxandrolone, stanozolol, methandrostenolone, methyltestosterone, fluoxymesterone, danazol) — Additive hepatotoxicity. Stacking two oral 17αAA is one of the …
(anastrozole, letrozole) — Mechanically ineffective for Anadrol gyno (because Anadrol doesn't aromatize); may crash systemic E2 from background T conversion,…
Dramatically additive hepatic load. Avoid entirely during cycle.
Additive hepatotoxicity. Use ibuprofen for acute pain control if absolutely necessary, but minimize.
Additive lipid disruption + hepatic load. Notable because the lipid crash from Anadrol may prompt a statin script in poorly-counseled users — that compounds …
Renal + hepatic compounding; additive BP load; relevant for combat athletes who often use chronic NSAIDs for joint/training pain.
Additive hepatic load.
Not directly relevant to user but worth noting for partnered scenarios.
Quality Indicators
Pharmacy-dispensed in original sealed packaging
Anadrol-50 (Alaven Pharmaceutical) prescription tablets in original sealed packaging from a licensed US pharmacy. Verify NDC and lot number.
International generic with verifiable manufacturer
Generics from established international manufacturers (Anapolon by Galenika; Plenastril historically) acceptable if manufacturer + lot + COA verifiable. Quality risk significantly higher than US Rx pharmacy.
Generic vs branded
Generic Anadrol from international pharmacy is generally fine if manufacturer is established, but bioavailability and dosing accuracy can vary. Track LFTs more frequently if switching products.
Underground lab (UGL) product without third-party testing
Common UGL issues: under-dosed (cost-cutting), substituted (dianabol or methyl-1-testosterone instead), or contaminated. Lab testing services (Janoshik, AnaboLab) recommended for any UGL product before use.
Counterfeit pharmaceutical packaging
Counterfeit Anadrol is a known issue in international markets. Verify pharmacy, NDC, and lot number against manufacturer database.
What to Expect
- Week 1Tolerability and dose-response.
- Week 2-4Early effect window.
- Week 4-8Peak benefit assessment.
- Week 8+Cycle decision point.
Side Effects & Safety 18
Side Effects
- 1Markedly elevated ALT/AST — most consistent finding. Hengge/Schroeder 2003: 27-35% of subjects developed ALT >5× ULN within 16 weeks at 100-150 mg/day. Lower at 50 mg/day but still typically 2-3× ULN within 4-6 weeks.
- 2Elevated GGT and alkaline phosphatase — cholestatic pattern.
- 3HDL crash — often 50-80% reduction within 6-8 weeks; among the most adverse of any AAS on lipid markers.
- 4LDL elevation — additive CV risk.
- 5Substantial water retention — 5-10+ lb fluid weight in week 1 alone; visibly puffy face/abdomen; not controlled by AIs (because not aromatization-mediated).
- 6Hypertension — combined fluid retention + direct vascular effects. BP elevation 10-30 mmHg systolic common.
- 7Gynecomastia — uncontrollable by AIs; requires SERM (tamoxifen 10-20 mg/day or raloxifene 60 mg/day). Can become irreversible if untreated past nodule formation.
- 8HPG axis suppression — testicular atrophy, ↓endogenous T, ↓libido on/post cycle.
- 9Acne, oily skin, accelerated androgenic alopecia — direct AR effects. Anadrol is among the worst AAS for acne.
- 10Mood changes, irritability, aggression, sleep disruption — Anadrol has a particularly notable mood/aggression profile in user reports.
- 11Increased hematocrit / polycythemia — direct EPO stimulation. Hematocrit can exceed 54% within 6-8 weeks at 100 mg/day. Stop-rule at HCT >54%.
- 12Increased appetite ("Anadrol hunger") — pronounced; useful for bulking, contributing to weight gain efficacy.
- 13Cholestatic jaundice — yellowing of skin/sclera, dark urine, pruritus, RUQ discomfort. Onset typically 4-8 weeks at 100 mg/day. Reversible with discontinuation in most cases; can require hospitalization.
- 14Erectile dysfunction during cycle — paradoxical at supraphysiologic dose due to HPG suppression + estrogenic side effects overriding direct androgen drive.
- 15Voice changes in females (irreversible vocal cord thickening). Anadrol is severely virilizing for women.
- 16Prostate hypertrophy / accelerated BPH in older males.
- 17Insomnia, night sweats — partly from BP/HCT elevation, partly from mood/cortisol effects.
- 18Marked aggression / "roid rage" — Anadrol has a reputation in bodybuilding culture for the most pronounced aggression effect of any oral AAS.
When to Stop
- Peliosis hepatis — blood-filled cystic spaces in liver parenchyma. Multiple historical case reports specifically linked to oxymetholone (PMIDs 433907, 666906, 4132832, 577673). Can rupture → fatal hemorrhage. Often asymptomatic until advanced. Detected on imaging (US, MRI).
- Hepatic adenoma → hepatocellular carcinoma — chronic high-dose use. Specifically documented in Fanconi-anemia patients (PMID 168333: 6-year-old developed HCC 2 months after starting oxymetholone) and chronic AAS users. Anadrol is among the most-associated agents.
- Stroke, MI, sudden cardiac death — via combined hypertension + adverse lipid + polycythemia + LV hypertrophy effects. Acute risk meaningful for combat-sport athletes who already train near cardiovascular ceiling.
- Thromboembolic events (DVT, PE) — driven by polycythemia + altered coagulation balance.
- Psychiatric — mania, psychosis, suicidality (rare but documented in AAS literature; oxymetholone has notable mood-effect signal).
- Sleep apnea exacerbation — soft tissue effects + polycythemia.
- Baseline (before starting): Full LFT panel, lipid panel, CBC w/ HCT, total + free testosterone, SHBG, estradiol (sensitive assay), LH, FSH, prolactin, BP, ECG, abdominal US for liver/biliary architecture. Hepatitis B/C serology.
- Week 2: full LFT — stop drug if ALT/AST >3× ULN. Symptom check (jaundice, RUQ pain, pruritus, dark urine).
- Week 4: full LFT, lipid panel, CBC — monitor cholestatic markers, HDL nadir, HCT trajectory, BP. Tactile chest/breast exam for early gynecomastia.
- Week 6: full LFT, lipid, hormonal panel, BP, gyno check.
- HCT >54% = stop drug, consider therapeutic phlebotomy.
- Months 3-12 post-cycle: peliosis hepatis / adenoma surveillance — abdominal imaging for chronic users.
- Indefinite: hormonal recovery monitoring — total + free T, LH, FSH at 4 weeks post, 12 weeks post, and 24 weeks post. PCT decision based on trajectory.
References
Hengge UR et al. 2003 — Double-blind, randomized, placebo-controlled phase III trial of oxymetholone for the treatment of HIV wasting (AIDS)
landmark Phase 3 RCT establishing efficacy + 27-35% ALT >5× ULN safety signal
View StudySchroeder ET et al. 2003 — Oxymetholone for the treatment of HIV-wasting: a double-blind, randomized, placebo-controlled phase III trial in eugonadal men and women (companion analysis)
eugonadal subgroup confirming additive anabolic effect on top of normal endogenous T
View StudyHengge UR et al. 1996 — Oxymetholone promotes weight gain in patients with advanced human immunodeficiency virus (HIV-1) infection (British Journal of Nutrition)
pilot study foundation for the Phase 3 trial
View StudyPavlatos AM et al. 2001 — Review of oxymetholone: a 17α-alkylated anabolic-androgenic steroid (Clinical Therapeutics)
reference review; articulates the non-aromatizing-yet-estrogenic paradox and proposes direct ER activation
View StudyZhang QS et al. 2014 — Oxymetholone therapy of Fanconi anemia suppresses osteopontin transcription and induces hematopoietic stem cell cycling (Stem Cell Reports)
extends FDA-approved Fanconi indication mechanistic understanding
View StudyWang J et al. 2022 — Efficacy of Oxymetholone in Severe and Nonsevere Acquired Aplastic Anemia: A Propensity Score Matching Analysis
modern cohort confirming continued role in aplastic anemia
View StudyBacigalupo A et al. 1993 — Treatment of aplastic anaemia (AA) with antilymphocyte globulin (ALG) and methylprednisolone (MPred) with or without androgens: a randomized trial from the EBMT SAA working party (Br J Haematol)
134-patient randomized trial; 56% vs 40% response with androgen
View StudyAnadrol-50 (oxymetholone) FDA label, Alaven Pharmaceutical
current US label, indications, dosing
View StudyAnabolic Steroids — LiverTox NCBI Bookshelf NBK548931
class entry on AAS hepatotoxicity; oxymetholone Likelihood A
View StudyAnabolic androgenic steroid-induced liver injury: An update — PMC9331524
modern review of AAS-induced DILI
View StudyPeliosis hepatis case reports — PMID 433907 (oxymetholone, "clinically benign")
early case series
View StudyPeliosis hepatis case reports — PMID 666906 (oxymetholone, JAMA 1978)
landmark JAMA case report
View StudyPeliosis hepatis — PMID 577673 (12 cases, oral androgen therapy)
multi-case series
View StudyHepatic adenoma in Fanconi anemia treated with oxymetholone — PMID 168333
pediatric Fanconi case
View StudySaberi MR et al. 2009 — Oxymetholone ameliorates insulin sensitivity in maintenance hemodialysis patients
secondary metabolic finding
View StudyPope HG Jr et al. 2014 — Adverse Health Consequences of Performance-Enhancing Drugs (Endocrine Reviews)
class review of AAS adverse effects
View StudyKanayama G, Pope HG Jr — Long-term cardiovascular consequences of AAS (Am J Cardiol)
cardiomyopathy literature
View StudyRasmussen JJ et al. 2016 — Former AAS users with persistent hypogonadism (J Clin Endocrinol Metab)
long-term HPG dysfunction
View StudyVanberg P, Atar D 2010 — Androgenic anabolic steroid abuse and the cardiovascular system (Handbook of Experimental Pharmacology)
CV mechanism review
View StudyDEA Diversion Control: Anabolic Steroids
Schedule III status, federal regulation
View StudyOxymetholone — 15th Report on Carcinogens, NCBI Bookshelf NBK590816
formal carcinogenic classification context
View StudyLatest research
- cohortEfficacy of Oxymetholone in Severe and Nonsevere Acquired Aplastic Anemia: A Propensity Score Matching AnalysisModern cohort confirming the FDA-approved aplastic anemia indication. Response rates ~50-70% in patients ineligible for IST or HSCT. Reaffirms oxymetholone as a continuing hematology tool despite the broader AAS regulatory winter.
- mechanismOxymetholone therapy of Fanconi anemia suppresses osteopontin transcription and induces hematopoietic stem cell cyclingAged Fancd2-/- mouse model; oxymetholone improved hematological parameters; RNA-Seq implicated osteopontin downregulation as a key mechanism of action — extends the FDA-approved Fanconi indication mechanistic understanding beyond simple erythropoietin upregulation.
- rctOxymetholone for the treatment of HIV-wasting: a double-blind, randomized, placebo-controlled phase III trial in eugonadal men and women (Schroeder et al.)Companion publication; eugonadal subgroup analysis. Confirmed efficacy in subjects with normal endogenous testosterone — Anadrol's anabolic effect is additive to baseline T, not just a deficiency-replacement effect. Liver-toxicity findings paralleled main trial.
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