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.
Fluoxymesterone
Emerging17α-methylated halogenated testosterone derivative — Upjohn-era oral AAS, used historically for combat-sport pre-fight aggression and… | AAS · Oral
Aliases (5)
▸ 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).
▸ Overview TL;DR
17α-methylated halogenated testosterone derivative — Upjohn-era oral AAS, used historically for combat-sport pre-fight aggression and strength surges in the final week of a cut. Severe hepatotoxicity (cholestasis, peliosis hepatis, adenoma risk) plus a uniquely aggression-promoting androgenic profile. Permanently skip — actively conflicts with brain-as-#1 priority and offers nothing modafinil/bromantane/standard anabolics don't do safer.
▸ Mechanism of action
Fluoxymesterone is testosterone with three structural changes:
- 9α-fluorine — halogenation that blocks 11β-hydroxysteroid dehydrogenase metabolism and dramatically increases AR binding affinity per molecule
- 11β-hydroxyl group — further locks in resistance to enzymatic deactivation
- 17α-methyl group — the survival mechanism for oral bioavailability (prevents first-pass hepatic deactivation), but is the structural feature responsible for the severe hepatotoxicity shared by all 17α-alkylated steroids (methyltest, oxandrolone, stanozolol, methandrostenolone, etc.)
The androgenic:anabolic ratio is roughly 1900:850 on the classic Vida scale (vs testosterone at 100:100), meaning per unit of muscle-protein synthesis it's substantially more androgenic than test — this maps clinically to its aggression-promoting reputation. It does not aromatize to estradiol (no E2 conversion pathway from the 9α-fluoro/11β-OH structure), so estrogenic side effects are absent, but DHT-pathway sides (acne, hair loss in genetically predisposed, prostate effects) are exaggerated. Strongly suppressive of HPG axis (LH/FSH crash) at any meaningful dose.
The "aggression" effect is partially androgenic (AR-mediated CNS effects on amygdala/hypothalamus) and partially the lack of estrogenic counterbalance — most aromatizing AAS soften the behavioral edge via E2; halo doesn't.
▸ Pharmacokinetics No data
▸Research protocols1 protocols
| Goal | Dose | Frequency | Solo | Cycle |
|---|---|---|---|---|
| No microdose / cycled protocol that is meaningfully safer | — | — | — | — |
Auto-extracted from dosing notes. For full context including caveats and Dylan-specific protocols, see the Dosing protocols section.
▸Quality indicators4 checks
▸ What to expect From notes
- 1Onset~1-2 hr oral
- 2Peakeffects: 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.
▸Interactions4 compounds
- Other 17α-alkylated orals (methyltestosterone, oxandrolone, stanozolol, methandrostenolone):Avoidhepatotoxicity additive, often catastrophic.
- Alcohol:Avoidhepatic stress additive — but Dylan is zero-alcohol so n/a.
- NSAIDs (chronic):Avoidhepatic + renal stress additive.
- Other CNS stimulants at high dose (modafinil, amphetamines):Avoidinsomnia + aggression amplified.