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.
Fluoxymesterone is 17α-alkylated for oral bioavailability — a structural feature directly responsible for the most severe hepatotoxic class of AAS. Cholestatic injury, peliosis hepatis, and hepatic adenoma are all class-documented. Cycle length must be capped (typically < 6-8 weeks); LFTs (ALT, AST, GGT, bilirubin) baseline + every 2 weeks on cycle. Stop immediately on ALT/AST > 3× ULN or symptomatic jaundice.
Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-PERMANENT — risk:benefit fails for the canonical archetype.
Fluoxymesterone
17α-methylated halogenated testosterone derivative — Upjohn-era oral AAS, used historically for combat-sport pre-fight aggression and…
Aliases (5)
Overview
What is Fluoxymesterone?
Fluoxymesterone (Halotestin) is a 17-alpha-alkylated synthetic androgen / anabolic steroid. Originally FDA-approved for hypogonadism, breast cancer, and delayed puberty; now rarely prescribed and primarily used in performance contexts.
Key Benefits
High androgenic potency for strength, aggression, and pre-competition cutting. Minimal aromatization and water retention. Used in powerlifting and bodybuilding briefly before competition. Significant hepatotoxicity limits use.
Mechanism of Action
Binds androgen receptors with high affinity. The 17-alpha-methyl group resists hepatic first-pass metabolism, allowing oral activity but causing hepatotoxicity. Does not aromatize to estrogen due to 11-beta-hydroxyl group.
▸ Cycle structure & PCT AAS oral
Ramp dose over week 1, hold steady through cycle weeks. Track baseline labs (TT/FT/E2/SHBG/HCT/lipids/LFTs) at week 0; recheck at week 4 and end-of-cycle.
On the last dose, the ester clears over its half-life window (enanthate = est. 7 days). PCT begins after the active compound has cleared.
Standard PCT is enclomiphene 12.5-25 mg/day or clomid 50/50/25/25 over 4 weeks (or nolvadex 20/20/10/10). HCG bridge optional during cycle to preserve testicular volume + faster restart. Bloodwork at PCT week 4 + 8 to confirm HPG axis recovery (LH, FSH, TT back to baseline).
Research Protocols
Disclaimer: These are commonly discussed research protocols and not medical advice.
Peptide Interactions
hepatotoxicity additive, often catastrophic.
hepatic stress additive — but a user in this archetype is zero-alcohol so n/a.
hepatic + renal stress additive.
insomnia + aggression amplified.
Quality Indicators
Pharmacy-dispensed, intact packaging
Prescription tablets in original sealed packaging from a licensed pharmacy.
Generic vs branded
Generics are usually fine but bioavailability can vary slightly; track if you switch.
Unbranded blister or counterfeit risk
Counterfeit pharmaceuticals are a known issue; verify pharmacy and lot if buying internationally.
What to Expect
- Onset~1-2 hr oral
- Peakeffects: 2-4 hr (halflife ~9.5 hr)
Side Effects & Safety
- Common (>10% users):
- HDL crash (often >40% reduction) and LDL/ApoB elevation
- Acne (severe, often back/shoulder)
- Aggression / irritability / short fuse
- Insomnia
- Headache
- Elevated liver enzymes (ALT/AST/GGT) within first 2-4 weeks
- HPG suppression (LH/FSH crash → low natural T)
- Water retention (modest, less than aromatizing AAS)
- Less common (1-10%):
- Cholestatic jaundice (yellowing, dark urine, pale stool, pruritus)
- Hypertension
- Hematocrit/erythrocytosis elevation
- Accelerated androgenic alopecia in genetically predisposed
- Prostate symptoms (urinary changes)
- Gynecomastia rare (no aromatization) but possible via prolactin pathway
- Rare-serious (<1% but worth knowing):
- Peliosis hepatis — blood-filled cystic lesions in the liver that can rupture catastrophically. 17α-AAS (halo, methyltest, stanozolol) are the primary pharmacologic causes. May persist after cessation.
- Hepatocellular adenoma / hepatocellular carcinoma — documented with prolonged use of 17α-AAS; halo is among the highest-risk in the class.
- Cardiovascular events — MI, stroke, cardiomyopathy; HDL crash + hypertension + erythrocytosis stack to elevate risk acutely on-cycle.
- Severe psychiatric reactions — manic episodes, violent behavior, psychotic features in vulnerable users.
- Specific watch periods: Liver enzymes within first 2 weeks; lipids within 3-4 weeks; any RUQ pain, jaundice, or unexplained fatigue is an emergency stop.
How was your experience with this compound?
Anonymous · one vote per session · results below at 5+ votes.
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