We use essential cookies (authentication, your saved goals/stack) by default. With your permission we'll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Prescription medication — not a dietary supplement
Fluoxymesterone (Halotestin)is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most Fluoxymesterone (Halotestin) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 1974–2016.
Based on 6 studies · 1 RCT
Confidence
LowBy outcome
Fluoxymesterone (Halotestin) has an evidence score of 3.4/10 — emerging evidence based on 6 indexed studies. A 17α-methylated ORAL anabolic-androgenic steroid (brand Halotestin) and a DEA Schedule III controlled substance. Unlike purely veterinary or research steroids, fluoxymesterone DOES have real — if narrow and now largely historical — human prescription indications: androgen replacement in hypogonadal men, delayed puberty in boys, and palliative treatment of androgen-responsive metastatic breast cancer in women, with older use in hereditary angioedema. So there IS some genuine human clinical literature, including a randomized breast-cancer trial and case series. But it is notoriously HEPATOTOXIC: because it is 17α-alkylated, it causes cholestatic jaundice, peliosis hepatis (blood-filled liver cavities, sometimes fatal), and is linked to hepatic adenoma/carcinoma. It is strongly androgenic and virilizing, suppresses the hypothalamic-pituitary-testicular axis, and severely worsens lipids. Illicit bodybuilding use is for pre-contest strength and aggression. This is NOT a dietary supplement and NOT a longevity or performance drug this library endorses — informational, harm-reduction entry only, gated out of recommendations. The score sits low: real but narrow legacy indications cannot offset heavy hepatotoxicity and the absence of any healthy-population benefit. Representative study: PMID 3284975.
Yohimbine
Mostly mechanism / observationalThe purified alkaloid (not crude yohimbe bark) — an alpha-2 adrenoceptor antagonist with modest evidence for erectile dysfunction and fasted fat loss, but real anxiety and cardiovascular risks and notoriously mislabeled supplement potency.
Ephedrine
Mostly mechanism / observationalLast reviewed June 2026 · evidence from 6 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Fluoxymesterone (Halotestin) — a 17α-methylated ORAL anabolic-androgenic steroid; DEA Schedule III controlled substance with narrow, now largely historical human prescription indications and a notorious hepatotoxic profile
A 17α-methylated ORAL anabolic-androgenic steroid (brand Halotestin) and a DEA Schedule III controlled substance. Unlike purely veterinary or research steroids, fluoxymesterone DOES have real — if narrow and now largely historical — human prescription indications: androgen replacement in hypogonadal men, delayed puberty in boys, and palliative treatment of androgen-responsive metastatic breast cancer in women, with older use in hereditary angioedema. So there IS some genuine human clinical literature, including a randomized breast-cancer trial and case series. But it is notoriously HEPATOTOXIC: because it is 17α-alkylated, it causes cholestatic jaundice, peliosis hepatis (blood-filled liver cavities, sometimes fatal), and is linked to hepatic adenoma/carcinoma. It is strongly androgenic and virilizing, suppresses the hypothalamic-pituitary-testicular axis, and severely worsens lipids. Illicit bodybuilding use is for pre-contest strength and aggression. This is NOT a dietary supplement and NOT a longevity or performance drug this library endorses — informational, harm-reduction entry only, gated out of recommendations. The score sits low: real but narrow legacy indications cannot offset heavy hepatotoxicity and the absence of any healthy-population benefit.
Fluoxymesterone (Halotestin) is a 17α-methylated ORAL anabolic-androgenic steroid and a DEA Schedule III controlled substance. Unlike purely veterinary steroids it DOES have real — if narrow and now largely historical — human indications (androgen replacement in hypogonadal men, delayed puberty, palliative androgen-responsive metastatic breast cancer, older use in hereditary angioedema), so a small genuine human literature exists: a randomized breast-cancer trial (Ingle 1988), a 103-patient cohort (Kono 2016), open-label HAE prophylaxis (Davis 1974), and a prospective men's-health study (Van Thiel 1983). But that is exactly where the score is capped: even in oncology the randomized evidence showed only a modest, non-significant, survival-neutral benefit at the cost of greater androgenic toxicity, and there is no demonstrated benefit in healthy people. Against that sits a heavy harm profile dominated by HEPATOTOXICITY — as a 17α-alkylated oral steroid it shares the class hepatotoxicity that Welder 1995 demonstrated directly for tested 17α-alkylated AAS, and clinically it is linked to cholestatic jaundice, peliosis hepatis (fatal in 3/12 cases; Nadell 1977) and hepatic adenoma/carcinoma — plus strong virilization, HPTA suppression, impaired fertility and severely worsened lipids. The score sits slightly above pure-veterinary steroids because narrow human indications and a real human literature exist, but hepatotoxicity and the absence of any healthy-population benefit keep it low.
Fluoxymesterone is a synthetic anabolic-androgenic steroid (AAS) — 9-fluoro-11β-hydroxy-17α-methyltestosterone — sold for decades under the brand Halotestin.
It is orally active precisely because it is 17α-alkylated (a methyl group at the 17α position resists first-pass hepatic breakdown), and that same modification is what makes the entire 17α-alkylated class hepatotoxic.
Unlike several of the other steroids in this collection (e.g. boldenone, trenbolone) that have NO human approval, fluoxymesterone is genuinely different: it has real, if narrow and now largely historical, human prescription indications.
It has been used for androgen-replacement therapy in hypogonadal men, to treat delayed puberty in adolescent boys, and — most distinctively — as a palliative androgen for androgen-responsive metastatic breast cancer in postmenopausal women, with older use as long-term prophylaxis in hereditary angioedema.
So there IS a body of real human clinical literature here, and it is reflected honestly in the studies below: a randomized clinical trial of tamoxifen with or without fluoxymesterone in metastatic breast cancer (Ingle 1988), a 103-patient cohort of fluoxymesterone in heavily pretreated hormone-receptor-positive metastatic breast cancer (Kono 2016), open-label long-term androgen prophylaxis in hereditary angioedema (Davis 1974), and a prospective study using it for sexual dysfunction in abstinent alcoholic men (Van Thiel 1983).
What that human and laboratory literature also establishes — and what keeps the score low — is harm. Fluoxymesterone is one of the most hepatotoxic AAS in routine use.
As a 17α-alkylated oral steroid it is directly toxic to hepatocytes; a primary rat-hepatocyte study found the tested 17α-alkylated steroids (methyltestosterone, oxymetholone and stanozolol) directly toxic to hepatocytes while non-alkylated androgens were not — fluoxymesterone was in the dosed panel but was not among the compounds that reached significant toxicity in that assay, and as a 17α-alkylated steroid it is expected to share the class hepatotoxicity the study demonstrated (Welder 1995), and a clinicopathologic series documented peliosis hepatis — blood-filled hepatic cavities, fatal in three of twelve cases — in patients on high-dose oral oxymetholone or fluoxymesterone (Nadell 1977).
The class is associated with cholestatic jaundice and with hepatic adenoma and hepatocellular carcinoma on prolonged use.
On top of the liver risk, it is strongly androgenic (virilization in women — deepened voice, hirsutism, clitoral enlargement, often irreversible; acne and aggression in men), it suppresses the hypothalamic-pituitary-testicular axis (lowered LH, FSH and endogenous testosterone with impaired fertility), and as an oral 17α-alkylated androgen it severely suppresses HDL cholesterol and worsens the lipid profile — a recognised cardiovascular concern.
Even in its legitimate oncology niche, the randomized evidence was unflattering: adding fluoxymesterone to tamoxifen produced only a modest, non-significant gain in response and progression that did not translate into a survival benefit, at the cost of greater androgenic toxicity, which is why the combination was not recommended for routine use (Ingle 1988) — and the drug has since been largely superseded.
The score therefore reflects the reality squarely: a controlled-substance oral AAS with real but narrow and now mostly historical human indications, a small genuine human literature, but a heavy hepatotoxic and virilizing profile, HPTA suppression and adverse lipids, and no demonstrated benefit in healthy people for body composition, performance or longevity.
It is not a dietary supplement, not an anti-aging drug, and this library endorses no performance or longevity use; any current legitimate use is a supervised medical decision, and illicit pre-contest bodybuilding use is unmonitored and risky.
Fluoxymesterone is a 9-fluoro-11β-hydroxy-17α-methyl testosterone derivative that binds and activates the androgen receptor, driving anabolic (protein-building) and virilizing signalling. This is the basis of both its legitimate medical uses (androgen replacement, palliative androgen therapy in breast cancer) and its illicit use for pre-contest strength and aggression. It does not appreciably aromatize, so its effects are predominantly androgenic rather than estrogenic.
The 17α-methyl group makes fluoxymesterone orally active by resisting first-pass hepatic metabolism — but that same modification makes the 17α-alkylated class directly toxic to hepatocytes. This drives cholestatic jaundice, peliosis hepatis (blood-filled liver cavities), and an elevated risk of hepatic adenoma and hepatocellular carcinoma with prolonged use. It is the dominant safety signal for this compound.
As an exogenous androgen, fluoxymesterone suppresses the hypothalamic-pituitary-testicular axis (lowering LH, FSH and endogenous testosterone, impairing fertility). As an oral 17α-alkylated androgen it also markedly suppresses HDL cholesterol and shifts the lipid profile adversely — a recognised cardiovascular concern shared across this steroid class.
How Fluoxymesterone (Halotestin) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
There is no dose this library recommends for healthy people. Fluoxymesterone (Halotestin) is a DEA Schedule III controlled prescription steroid; any legitimate use is a supervised medical decision for a narrow, now largely historical indication. For context only, historical prescribing ranged from roughly 5–20 mg/day orally for androgen replacement or delayed puberty, and palliative breast-cancer regimens used on the order of 10–30 mg/day in divided doses — figures provided for context, not as a recommendation. Illicit pre-contest bodybuilding 'Halo' dosing (commonly tens of mg/day) is unstudied for benefit in healthy people, unmonitored, hepatotoxic, and used without liver-function, lipid or hormonal-axis monitoring.
Take with food
| Form | Type |
|---|---|
| 💊Oral fluoxymesterone tablets (Halotestin) — for supervised medical use in narrow, largely historical indications only; no performance or longevity form is endorsed | Recommended |
There is no legitimate over-the-counter or supplement form. It is a Schedule III controlled prescription steroid; non-prescription material ('Halo') is illegal to possess without authorization and frequently counterfeit.
Minimum: 4 weeks
Optimal: 8 weeks
Cycling: Not required
Note: No healthy-population timing is endorsed. Fluoxymesterone is a hepatotoxic, virilizing, controlled-substance oral steroid; any legitimate use is a supervised medical decision. This library does not schedule its use for performance or longevity.
Dose-response data unavailable. The current published research for Fluoxymesterone (Halotestin) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
Fluoxymesterone has genuine human evidence as a palliative androgen in androgen-responsive metastatic breast cancer: a 103-patient cohort of heavily pretreated hormone-receptor-positive disease showed a clinical-benefit rate of about 43%, and a randomized trial added it to tamoxifen. But the randomized benefit was modest, non-significant and survival-neutral, came with greater androgenic toxicity, and the drug has since been largely superseded.
As an oral androgen, fluoxymesterone has historically been prescribed for androgen replacement in hypogonadal men and for delayed puberty in boys, and was used for sexual dysfunction in abstinent alcoholic men — a real but now largely historical indication, since most androgen replacement has moved to testosterone esters/gels with a safer hepatic profile.
Fluoxymesterone is notoriously hepatotoxic. As a 17α-alkylated oral steroid it is directly toxic to hepatocytes and is linked to cholestatic jaundice, peliosis hepatis (blood-filled hepatic cavities, sometimes fatal), and hepatic adenoma/hepatocellular carcinoma on prolonged use. Liver injury can be clinically silent until advanced.
Strongly androgenic: in women it causes deepened voice, hirsutism, acne and clitoral enlargement that are frequently irreversible; in men, acne, oily skin, increased aggression and androgenetic effects. This androgenic toxicity was a key reason its breast-cancer combination was not adopted for routine use.
As an exogenous androgen, fluoxymesterone suppresses the hypothalamic-pituitary-testicular axis — lowering LH, FSH and endogenous testosterone and impairing fertility. Recovery after non-medical use is variable and, without monitoring, unpredictable.
As an oral 17α-alkylated androgen, fluoxymesterone severely suppresses HDL cholesterol and shifts the lipid profile adversely. AAS as a class lower HDL and are linked to cardiovascular harm at supraphysiologic doses — a risk that compounds the hepatic one.
Illicit bodybuilding use is for short-run strength and 'aggression' in the run-up to competition, exploiting the strong androgenic effect without water retention. This is unstudied for benefit in healthy people, unmonitored, and comes bundled with the hepatotoxic, virilizing and lipid harms above.
Avoid — a hepatotoxic, virilizing controlled-substance oral steroid with no healthy-population evidence of benefit and a documented harm profile (liver, lipids, fertility, virilization). Not a supplement, and illegal without a prescription.
Avoid — fluoxymesterone is directly hepatotoxic and can precipitate cholestasis, peliosis hepatis and liver failure.
Avoid — strongly androgenic; virilizing effects (voice, hair, clitoral enlargement) are frequently permanent.
Avoid — suppresses the gonadal axis and impairs fertility; non-medical use risks unmonitored, variable recovery.
Avoid entirely — strongly androgenic with fetal-virilization risk.
17α-alkylated anabolic steroids markedly potentiate warfarin and raise bleeding risk; fluoxymesterone can require substantial anticoagulant dose reductions and close INR monitoring if ever co-administered.
Fluoxymesterone is itself directly hepatotoxic as a 17α-alkylated oral steroid; combining it with other hepatotoxic agents or alcohol compounds the risk of cholestatic jaundice, peliosis hepatis and liver injury.
Tip: As a 17α-alkylated oral steroid, fluoxymesterone is directly toxic to hepatocytes and is linked to cholestatic jaundice, peliosis hepatis (blood-filled liver cavities, sometimes fatal) and hepatic adenoma/hepatocellular carcinoma. Liver injury can be silent; in legitimate use it demands liver-function monitoring, and there is no safe self-monitoring framework for non-medical use.
Tip: Strongly androgenic: deepened voice, hirsutism, acne and clitoral enlargement that are frequently irreversible. Avoid entirely outside a supervised palliative-oncology decision.
Tip: As an exogenous androgen it lowers LH, FSH and endogenous testosterone and impairs fertility; recovery after non-medical use is variable and unmonitored.
Tip: Oral 17α-alkylated androgens severely suppress HDL and shift lipids adversely; report chest pain, breathlessness or palpitations and monitor lipids in any legitimate use.
The commonly studied dose of Fluoxymesterone (Halotestin) is There is no dose this library recommends for healthy people. Fluoxymesterone (Halotestin) is a DEA Schedule III controlled prescription steroid; any legitimate use is a supervised medical decision for a narrow, now largely historical indication. For context only, historical prescribing ranged from roughly 5–20 mg/day orally for androgen replacement or delayed puberty, and palliative breast-cancer regimens used on the order of 10–30 mg/day in divided doses — figures provided for context, not as a recommendation. Illicit pre-contest bodybuilding 'Halo' dosing (commonly tens of mg/day) is unstudied for benefit in healthy people, unmonitored, hepatotoxic, and used without liver-function, lipid or hormonal-axis monitoring.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Fluoxymesterone (Halotestin) is with meals. Take it with food. Historical oral fluoxymesterone was typically taken in divided daily doses, often with food to reduce gastrointestinal upset.
Fluoxymesterone (Halotestin) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are hepatotoxicity (cholestasis, peliosis hepatis, tumors), virilization (women), HPTA suppression & impaired fertility. Use caution if any of these apply to you: Any non-medical use — a DEA Schedule III controlled prescription steroid; possession or use without a prescription is illegal, and it is NOT a dietary supplement; Pre-existing liver disease — fluoxymesterone is notoriously hepatotoxic (cholestasis, peliosis hepatis, hepatic tumors) and should never be added to a compromised liver; Anyone seeking it for body composition, performance or anti-aging — there is no healthy-population evidence of benefit and a heavy hepatotoxic/virilizing harm profile.
A sympathomimetic stimulant — the 'E' in the ECA (ephedrine/caffeine/aspirin) fat-loss stack. Ephedrine plus caffeine genuinely produces MODEST fat loss in 6-month RCTs (~0.9 kg/month more than placebo, ~3 kg over a controlled diet trial). But that is the whole upside: ephedra alkaloids were BANNED from US dietary supplements in 2004 after the FDA tied them to cardiovascular and psychiatric harms and deaths (the JAMA meta-analysis found a 2.2–3.6× increase in psychiatric/autonomic/GI symptoms and palpitations). Pharmaceutical ephedrine survives only as a restricted behind-the-counter decongestant/vasopressor. NOT a dietary supplement, NOT a longevity drug — a gated harm-reduction entry.
Androgens can alter glucose handling and insulin sensitivity; diabetic medication may need adjustment under supervision.
Stacking androgenic agents compounds HPTA suppression, the adverse lipid shift and androgenic toxicity, and adds hepatotoxic load when other 17α-alkylated orals are combined; the combined harm is additive and uncharacterised in non-medical use.
Tip: Androgenic skin effects and mood/aggression changes are common; they typically ease on discontinuation but reflect the strong androgenicity that also drives the more serious harms.
Tip: Androgen-driven sodium and fluid retention can occur, of concern in those with cardiac or renal compromise; requires supervision.