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Halotestin

Fluoxymesterone

Halotestin (fluoxymesterone) is a synthetic, orally active 17-alpha-methylated (17aa) anabolic-androgenic steroid, historically used in medicine for advanced/metastatic breast cancer (as an androgenic adjunct to tamoxifen), androgen-deficiency states, and delayed growth/puberty, and non-medically for strength and aggression with little muscle-mass gain. It is a strongly androgenic, non-aromatizable androgen. The main risks are those of the oral 17aa class: hepatotoxicity (cholestatic jaundice, and with the wider class peliosis hepatis and hepatic tumors), marked adverse shifts in blood lipids (large HDL-cholesterol reduction) that raise cardiovascular/atherosclerotic risk, suppression of the hypothalamic-pituitary-gonadal (HPTA) axis, virilization (especially serious and often irreversible in women), and neuropsychiatric effects such as aggression and mood disturbance. Much of the specific human safety data for fluoxymesterone is old and sparse; a substantial part of the risk profile is extrapolated from the broader anabolic-androgenic steroid literature. This is educational information only, not medical advice — these substances carry serious risks; consult a qualified physician and obtain regular bloodwork. 21+ only.

Clinical readoutAAS · oral-17aa
Hepatic strainHigh
CardiovascularModerate
HPTA suppressionHigh
Half-life
2 h
Route
Oral
Evidence
C
Active
Short-acting
2 h4 h6 h8 h10 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ A small human crossover bioavailability study (n=6) found a harmonic mean elimination half-life of approximately 2 hours after a single 10 mg oral or buccal dose; high-quality primary human pharmacokinetic data are otherwise limited, so this single-dose figure should be treated as approximate and may not reflect kinetics with the repeated dosing used clinically.
Pharmacology

Mechanism of action

Fluoxymesterone is a halogenated (9-fluoro), 11-beta-hydroxy, 17-alpha-methyl derivative of testosterone that binds and activates the androgen receptor, driving androgen-responsive gene transcription in muscle, bone, skin, the reproductive tract, and the central nervous system. The 17-alpha-methyl group makes it resistant to first-pass hepatic degradation (permitting oral activity) but is also the structural feature responsible for the 17aa class's characteristic hepatotoxicity. It is not appreciably converted to estrogen (non-aromatizable), so its actions are predominantly androgenic. Like other androgens it exerts negative feedback on the hypothalamus and pituitary, lowering LH and (to a lesser degree with androgen alone) FSH, and thereby suppressing endogenous testosterone production.
Kinetics

Pharmacokinetics

Half-life

A small human crossover bioavailability study (n=6) found a harmonic mean elimination half-life of approximately 2 hours after a single 10 mg oral or buccal dose; high-quality primary human pharmacokinetic data are otherwise limited, so this single-dose figure should be treated as approximate and may not reflect kinetics with the repeated dosing used clinically.

Active duration

Short-acting; clinical trials dosed it twice daily (e.g., 10 mg orally twice per day), consistent with a need for repeated daily dosing to maintain effect.

Route

Oral (17-alpha-methylated, making it orally bioavailable and resistant to first-pass hepatic breakdown).

Metabolism & clearance

Hepatic metabolism with renal excretion of metabolites; the 17aa structure slows hepatic clearance and burdens the liver. PK is presented for washout/monitoring reasoning and clinician discussion only, not for evading drug testing.

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

Reported effects

Physiological & performance effects

  • Androgenic effects: increased libido, acne, increased body/facial hair, and in the historical clinical setting palliation of some hormone-responsive breast cancers when added to tamoxifen
  • Strongly androgenic with relatively modest anabolic/muscle-mass effect compared with its androgenic potency
  • Used historically to promote growth in gonadal dysgenesis/delayed puberty and to treat androgen deficiency
  • Non-medically reported for increases in strength, aggression, and a 'harder' physique rather than large weight gain
  • Virilization (voice deepening, hirsutism, clitoromegaly, menstrual disruption) in women — an intended pharmacologic effect in some historical uses but an adverse effect otherwise
Safety

Adverse effects by system

Cardiovascular

Adverse lipid changes are a central concern: 17aa androgens as a class markedly lower HDL ('vessel-protective') cholesterol and can raise blood pressure, promoting atherosclerosis; the class is also associated with left ventricular hypertrophy, endothelial dysfunction, prothrombotic changes, and case reports of myocardial infarction and sudden cardiac death. Compound-specific fluoxymesterone cardiovascular trial data are limited; most evidence is class-level.

Hepatic

Hepatotoxic. In a randomized breast-cancer trial fluoxymesterone caused significantly more hepatotoxicity than a comparator steroid. The oral 17aa class characteristically causes cholestatic liver injury (jaundice, pruritus, bland canalicular cholestasis) and, more rarely, peliosis hepatis and hepatic tumors.

Endocrine / HPTA

Suppresses the HPTA axis: as an androgen it lowers serum LH and endogenous testosterone (and contributes to FSH suppression), producing hypogonadotropic hypogonadism; recovery after stopping can be prolonged and is variable.

Reproductive

In men: suppressed spermatogenesis/oligospermia, testicular atrophy, and reduced fertility from HPTA suppression. In women: virilization (hirsutism, voice deepening, clitoromegaly, menstrual irregularity), which may be irreversible.

Neuropsychiatric

Neuropsychiatric effects reported for the androgen class include increased aggression/hostility and mood disturbances (depression, hypomania/mania, irritability); a withdrawal syndrome with anxiety and depression can follow cessation of chronic use.

Renal

No large fluoxymesterone-specific renal dataset. In the broader AAS-induced liver-injury literature, cholestatic AAS injury was accompanied by acute kidney injury (cholemic nephropathy) in a substantial minority of cases; renal function should be monitored.

Hematologic

The androgen class stimulates erythropoiesis and can cause polycythemia (raised hematocrit), increasing thrombotic risk; increased platelet count has been observed in AAS users. Fluoxymesterone-specific hematologic data are limited.

Dermatologic

Androgenic skin effects: acne vulgaris, oily skin, increased body/facial hair; scalp hair loss in predisposed individuals.

Recovery

HPTA suppression & recovery

Suppression: Significant — as an androgen fluoxymesterone suppresses LH and endogenous testosterone, and the AAS class produces hypogonadotropic hypogonadism.

Endogenous hormone production is suppressed during use and recovery of the HPT axis after stopping is variable and can take months; individual outcomes differ. Any recovery approach should be directed by an endocrinologist. Only single-SERM approaches are within scope here; dual-SERM protocols are not described. Do not self-manage recovery.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function tests (ALT, AST, ALP, GGT, total/direct bilirubin)Fasting lipid panel (total, LDL, and especially HDL cholesterol, triglycerides)Complete blood count including hematocrit/hemoglobin (polycythemia)Total testosterone, LH, FSH (HPTA status)Renal function (creatinine, eGFR)Blood pressurePSA and prostate assessment in older men

Cadence: Obtain a baseline before any use, then periodically during use (e.g., roughly every 4-8 weeks while exposed, sooner if symptomatic), and again after cessation to assess recovery — all under a clinician's direction.

Warning signs — seek care
  • Jaundice (yellow skin/eyes), dark urine, pale stools, or pruritus (itching)
  • Right-upper-quadrant abdominal pain, nausea, or unexplained fatigue
  • Chest pain, breathlessness, palpitations, or signs of stroke/clot (leg swelling, sudden severe headache, one-sided weakness)
  • Markedly elevated blood pressure
  • Ruddy/flushed complexion, headaches, or visual changes suggesting a high hematocrit
  • New or worsening depression, aggression, or mood instability
  • In women: voice deepening, abnormal hair growth, clitoral enlargement, or menstrual changes (may be irreversible — stop and seek care)
Do not use if

Contraindications

  • Known or suspected prostate or male breast carcinoma
  • Pregnancy and breastfeeding (virilization/teratogenic risk to a female fetus)
  • Pre-existing liver disease, cholestasis, or hepatic tumors
  • Significant cardiovascular disease, uncontrolled hypertension, or an adverse lipid profile
  • Polycythemia or other conditions worsened by a rising hematocrit
  • Nephrotic syndrome/significant renal impairment
  • Women (particularly of reproductive age) given the high and often irreversible virilization risk
  • Concurrent hepatotoxic drugs or heavy alcohol use
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 educational information only and not medical advice; these substances carry serious risks — involve a qualified physician and obtain regular bloodwork. 21+ only.
  • Because fluoxymesterone is an oral 17aa steroid, hepatotoxicity is a leading concern: stop and seek medical care promptly if jaundice, dark urine, pale stools, itching, or right-upper-quadrant pain develop.
  • Establish baseline labs (liver panel, lipids/HDL, CBC/hematocrit, testosterone/LH/FSH, renal function, blood pressure) before any use and monitor periodically with a clinician; do not rely on 'feeling fine'.
  • Avoid combining with other hepatotoxic agents, other 17aa oral steroids, or heavy alcohol, which compounds liver risk. Absence of interaction data is not evidence of safety.
  • Women face a high risk of virilization that may be permanent (voice deepening, clitoromegaly, hair growth); early signs warrant stopping and medical review.
  • Watch for a rising hematocrit (polycythemia) and adverse lipid/blood-pressure changes that raise clot and cardiovascular risk; seek urgent care for chest pain, breathlessness, or stroke-like symptoms.
  • HPTA suppression and recovery are variable and should be managed by an endocrinologist; only single-SERM approaches are within scope, and self-directed recovery protocols are discouraged.
  • If neuropsychiatric changes (aggression, depression, mood instability) emerge during use or a depressive withdrawal syndrome after stopping, seek professional help.
  • Seek care rather than continuing: worsening labs or any warning sign is a reason to stop and consult a clinician, not to adjust dose.
Evidence

Citations (16)

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

  1. 01

    Fluoxymesterone is an oral androgen used clinically in advanced/metastatic breast cancer as an adjunct to tamoxifen, dosed 10 mg orally twice daily.

    RCTCombination hormonal therapy with tamoxifen plus fluoxymesterone versus tamoxifen alone in postmenopausal women with metastatic breast cancer. An updated analysis.PMID 1991261 ↗

  2. 02

    In a randomized trial fluoxymesterone caused significantly more hepatotoxicity than the comparator steroid mepitiostane, establishing a direct hepatotoxicity signal.

    RCT2alpha,3alpha-epithio-5alpha-androstan-17beta-yl 1-methoxycyclopentyl ether (mepitiostane) in the treatment of advanced breast cancer (Japanese Cooperative Group of Hormonal Treatment for Breast Cancer).PMID 343913 ↗

  3. 03

    Addition of fluoxymesterone to tamoxifen produced more virilization in women in a randomized adjuvant breast-cancer trial.

    RCTRandomized trial of tamoxifen alone or combined with fluoxymesterone as adjuvant therapy in postmenopausal women with resected ER-positive breast cancer (NCCTG 89-30-52).PMID 16538529 ↗

  4. 04

    Toxicity was more pronounced when fluoxymesterone was added to tamoxifen and was attributable to fluoxymesterone in a randomized trial in elderly women.

    RCTCombined endocrine treatment of elderly postmenopausal patients with metastatic breast cancer: randomized trial of tamoxifen vs. tamoxifen+aminoglutethimide+hydrocortisone and tamoxifen+fluoxymesterone in women above 65.PMID 10942095 ↗

  5. 05

    Fluoxymesterone was used as the androgenic (halotestin) component of a combination chemotherapy regimen (VATH) for metastatic breast cancer, dosed alongside cytotoxics.

    RCTCombination chemotherapy for metastatic or recurrent carcinoma of the breast: randomized phase III trial comparing CAF vs. VATH vs. VATH alternating with CMFVP (CALGB 8281).PMID 7751891 ↗

  6. 06

    In a small crossover bioavailability study (n=6), the harmonic mean elimination half-life of fluoxymesterone was approximately 2 hours after a single 10 mg oral or buccal dose.

    CohortPMID 4009439 ↗

  7. 07

    Fluoxymesterone (10-20 mg/day) affects gonadotropin regulation in adult men and is not appreciably converted to estrogen (non-aromatizable); androgen combined with estrogen suppressed LH.

    CohortEffect of chronic administration of estrogen, androgen, or both on serum levels of gonadotropins in adult men.PMID 122441 ↗

  8. 08

    Oral fluoxymesterone suppresses luteinizing hormone and endogenous testosterone, demonstrating HPTA/negative-feedback suppression by this non-aromatizable androgen.

    Case reportAndrogen receptor abnormalities in identical twins with oligospermia. Clinical and biochemical studies.PMID 6439037 ↗

  9. 09

    Fluoxymesterone suppressed serum LH and testosterone comparably to maximal normal male responses, confirming HPTA suppression.

    Case reportPrecocious puberty and hypothalamic hamartoma.PMID 7243449 ↗

  10. 10

    Fluoxymesterone suppresses endogenous androgen (and estrogen) production in normal men.

    Case seriesSuppression of androgen and oestrogen production in normal men.PMID 5068111 ↗

  11. 11

    The anabolic-androgenic steroid class markedly lowers HDL cholesterol and is associated with hypertension, left ventricular hypertrophy, prothrombotic changes, endothelial dysfunction, myocardial infarction, and sudden cardiac death.

    Review[Cardiovascular side effects of anabolic-androgenic steroids].PMID 17036188 ↗

  12. 12

    AAS use is associated with reduced HDL, elevated blood pressure, HPTA suppression (persisting months after withdrawal), acne, increased body hair, aggression/mood disturbance, and disturbed endogenous testosterone/gonadotropin production.

    ReviewEffects of androgenic-anabolic steroids in athletes.PMID 15248788 ↗

  13. 13

    Androgen/anabolic steroid abuse causes hypogonadotropic hypogonadism and infertility, very low HDL, polycythemia, and psychiatric, cardiovascular and hepatic complications, with a withdrawal syndrome of anxiety/depression; recovery management is an endocrinology concern.

    ReviewDoping with testosterone and androgenic/anabolic steroids: Impact on health, screening tools and medical care.PMID 36990315 ↗

  14. 14

    AAS users show lower HDL cholesterol, higher platelet count, suppressed FSH, and reduced flow-mediated (endothelial) dilation, consistent with increased cardiovascular risk.

    CohortIncreased atherothrombotic markers and endothelial dysfunction in steroid users.PMID 22345686 ↗

  15. 15

    Oral 17aa anabolic-androgenic steroids cause cholestatic drug-induced liver injury (jaundice, pruritus, bland canalicular cholestasis), frequently accompanied by acute kidney injury.

    Case seriesAndrogenic anabolic steroid-induced liver injury: two case reports assessed by updated RUCAM and a comprehensive review.PMID 33214235 ↗

  16. 16

    Fluoxymesterone alters hepatic drug-metabolizing enzyme activity in animal (rat) liver, supporting a hepatic burden mechanism (preclinical).

    PreclinicalEffect of training and anabolic-androgenic steroids on drug metabolism in rat liver.PMID 8350704 ↗

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