Fluoxymesterone, best known by the Upjohn brand name Halotestin, is an oral anabolic-androgenic steroid (AAS). Chemically it is methyltestosterone with two extra changes: a fluorine atom at carbon 9 and a hydroxyl group at carbon 11. The FDA approved Halotestin in 1956 for men with low testosterone, for delayed puberty and for palliation of advanced breast cancer in women.

Fluoxymesterone is no longer sold in the US. Pfizer/Pharmacia asked FDA to withdraw the Halotestin application in 2009, the last generic approval (Upsher-Smith) was withdrawn in 2022, and every fluoxymesterone listing in Drugs@FDA is marked discontinued. It remains a Schedule III controlled substance and is banned in sport at all times.

This page summarizes what the former FDA label, clinical trials and regulators report. It is for education only and is not medical advice.

Property	Detail
Drug class	17α-methylated anabolic-androgenic steroid (9α-fluoro, 11β-hydroxy derivative of methyltestosterone)
Brands	Halotestin (Upjohn, NDA 010611, approved October 15, 1956); Ora-Testryl (Squibb); Android-F; generics
Route	Oral tablet
Former strengths	2 mg, 5 mg and 10 mg
Former labeled dose	Men: 5–20 mg/day. Breast cancer: 10–40 mg/day in divided doses
Half-life	≈9.2 h (label); 2.0 h harmonic mean in a 6-person study
US status	All products discontinued; Halotestin approval withdrawn June 2009; Schedule III
WADA status	Prohibited at all times (S1.1 anabolic androgenic steroid, non-Specified)

What it is

The label gives the chemical name as 9-fluoro-11β,17β-dihydroxy-17-methylandrost-4-en-3-one: formula C₂₀H₂₉FO₃, molecular weight 336.45 g/mol (Halotestin label; PubChem). It is a white or nearly white, odorless powder that is practically insoluble in water.

Each structural change has a known or proposed role:

Change vs testosterone	What it does
17α-methyl group (shared with methyltestosterone)	Slows breakdown in the liver so the drug works by mouth. This group is tied to the liver toxicity of the whole oral-steroid class.
9α-fluoro and 11β-hydroxy groups	Make the molecule resemble cortisol around the C-ring. In enzyme studies fluoxymesterone binds 11β-HSD2, an enzyme that inactivates cortisol, in a way similar to cortisol itself (see Side effects).

Like other androgens, fluoxymesterone acts through the androgen receptor. The label notes that the class causes nitrogen, sodium and water retention, stimulates red blood cell production and suppresses the body’s own testosterone through feedback on the pituitary.

About anabolic:androgenic ratios. Websites often quote fixed potency ratios for fluoxymesterone. The only primary source we found is a 1963 animal bioassay paper (Arnold et al., J Endocrinol 1963), whose data we could not access, so we do not repeat the numbers. Animal ratios also do not predict human effects. We found no controlled human study of fluoxymesterone’s effect on muscle mass or strength in healthy people.

Pharmacokinetics

Human pharmacokinetic data are sparse. The two sources disagree on half-life:

Source	Design	Half-life	Other findings
Halotestin label	Not described	≈9.2 h	Label advises divided daily doses “because of its short action”
Capponi et al., J Pharm Sci 1985	6 volunteers, single 10 mg tablet, oral vs buccal crossover	2.0 h (harmonic mean)	Peak 40–150 ng/mL at 1–2 h; oral exposure ≈76–80% of buccal

In people, fluoxymesterone is metabolized mainly by 6β-hydroxylation, reduction of the A-ring and oxidation of the 11-hydroxyl group (Kammerer et al., J Steroid Biochem 1990). After a single 10 mg dose, the parent drug was undetectable in urine after 1 day, but two metabolites were still detectable for at least 5 days. Human 11β-HSD2 converts it to 11-oxofluoxymesterone (Fürstenberger et al., Toxicol Sci 2012).

Former medical use

The last Halotestin label (Pharmacia & Upjohn, 2002) listed these indications:

Men: replacement therapy for primary hypogonadism (testicular failure) and hypogonadotropic hypogonadism (pituitary or hypothalamic failure), congenital or acquired;
Boys: delayed puberty, once it is clearly established and not just a familial trait;
Women: palliation of androgen-responsive recurrent breast cancer in women 1–5 years past menopause, or with a tumor shown to be hormone-dependent.

Indication	Labeled daily dose
Male hypogonadism	5–20 mg, as one dose or divided into 3–4 doses
Delayed puberty	Low dose, titrated with bone-age X-rays, limited to 4–6 months
Inoperable breast cancer	10–40 mg, in divided doses; at least 1 month for subjective and 2–3 months for objective response

The label also states that the drug “has not been shown to be safe and effective for the enhancement of athletic performance.”

Regulatory status

FDA approval. Halotestin (NDA 010611) was approved on October 15, 1956 and later listed as discontinued (Drugs@FDA).
2009 withdrawal. FDA withdrew approval of the Halotestin application, effective June 18, 2009, after the holder reported the product was no longer marketed (74 FR 23407). This was a business withdrawal, not a safety action.
2022 withdrawal. Upsher-Smith’s fluoxymesterone 10 mg tablet (ANDA 088342) was withdrawn as of May 25, 2022, for the same reason (87 FR 24320). The other generic and branded entries in Drugs@FDA are all listed as discontinued.
Controlled substance. Fluoxymesterone is named in the US Schedule III list of anabolic steroids (21 CFR 1308.13).
Sport. It is listed by name under S1.1 anabolic androgenic steroids, prohibited in and out of competition (WADA 2026 Prohibited List).

What the research shows

Most controlled human data come from oncology. We found no controlled trials of fluoxymesterone for muscle, strength or athletic performance.

Metastatic breast cancer

Fluoxymesterone was used as an additive hormonal therapy in postmenopausal women with advanced breast cancer, alone or with tamoxifen.

Trial	Design and n	Arms	Main result
Westerberg, Cancer Treat Rep 1980	Open randomized crossover, 79 women, first-line	Tamoxifen vs fluoxymesterone first	Remission 30% vs 19%; longer time to treatment change (p = 0.003) and better survival (p = 0.05) with tamoxifen first
Tormey et al., Ann Intern Med 1983	Randomized, 108 women, mostly pretreated	Tamoxifen vs tamoxifen + fluoxymesterone 7 mg/m² twice daily	Remission 15% vs 38% (p = 0.016); time to treatment failure 64 vs 180 days (p = 0.01); median survival 330 vs 380 days
Ingle et al., Cancer 1991	Randomized, 238 women	Tamoxifen 10 mg twice daily ± fluoxymesterone 10 mg twice daily	Response 42% vs 54% (p = 0.07); median time to progression 6.5 vs 11.6 months (p = 0.03); survival similar
Rose et al., Breast Cancer Res Treat 2000	Randomized, 279 eligible women over 65	Tamoxifen vs tamoxifen + fluoxymesterone (third arm: tamoxifen + aminoglutethimide and hydrocortisone)	No significant difference in response (p = 0.30), time to treatment failure (9.2 vs 9.2 months) or survival (22.0 vs 21.1 months)

The pattern is consistent: adding fluoxymesterone sometimes raised response rates or delayed progression but did not clearly prolong survival, and every combination trial reported more androgenic side effects. In Ingle’s trial, a subgroup analysis of 97 women aged 65 or older with an estrogen receptor level of 10 fmol or more suggested better response, time to progression and survival, but the Danish trial in women over 65 did not confirm a benefit.

A later retrospective series looked at 103 women whose estrogen receptor-positive metastatic breast cancer had progressed on modern hormonal drugs (Kono et al., Breast Cancer Res Treat 2016). Of the 70 who did not stop early:

3% had a complete and 10% a partial response;
30% had stable disease for at least 6 months (clinical benefit rate 43%);
median progression-free survival was 3.9 months (95% CI 3.2–5.3).

Thirty-three women stopped before progression, 14 of them because of toxicity or adverse events. This was an uncontrolled study.

Early breast cancer (adjuvant)

The NCCTG 89-30-52 trial randomized 541 postmenopausal women with resected, estrogen receptor-positive breast cancer to tamoxifen 20 mg/day for 5 years, with or without fluoxymesterone 10 mg twice daily for the first year (Ingle et al., Breast Cancer Res Treat 2006). After a median 11.4 years of follow-up:

Outcome	Hazard ratio, tamoxifen + fluoxymesterone vs tamoxifen (95% CI)
Relapse or death	0.84 (0.64–1.10)
Death	0.89 (0.67–1.18)

Neither difference was significant, and women given fluoxymesterone had more virilization.

A randomized trial compared megestrol acetate 800 mg/day, dexamethasone 0.75 mg four times daily and fluoxymesterone 10 mg twice daily in patients with cancer anorexia/cachexia (Loprinzi et al., J Clin Oncol 1999). Fluoxymesterone produced significantly less appetite improvement than the other two drugs and had no toxicity advantage. The authors called it “an inferior choice” for this use.

Anemia

In a small randomized study, 29 patients with anemia from myelofibrosis or related bone marrow disorders received fluoxymesterone 30 mg/day plus transfusions, or transfusions alone (Brubaker et al., Arch Intern Med 1982). Among the 24 who could be evaluated:

4 of 14 (29%) on fluoxymesterone had a good hemoglobin response, all with myelofibrosis;
none of 10 on transfusions alone had a good response;
survival did not differ between arms.

Short stature and delayed puberty in boys

A prospective, non-randomized study treated 82 short boys with 2.5 mg/day fluoxymesterone for 6–60 months (Strickland, Pediatrics 1993). Growth velocity rose 1.7–2.5-fold during treatment, and final adult height exceeded pretreatment predictions by about 6 cm. The author reported no adverse androgenic effects at this low dose. This dose is half the lowest adult replacement dose on the label, and the label still requires bone-age X-rays every 6 months because androgens can close growth plates early.

Side effects and risks

Liver

The label warns that prolonged high-dose use of 17α-alkylated androgens has been linked to:

peliosis hepatis (blood-filled cysts in the liver);
hepatic adenomas and hepatocellular carcinoma;
cholestatic hepatitis and jaundice, which the label describes as reversible on stopping.

A pathology series described 12 patients with peliosis hepatis after high-dose oxymetholone or fluoxymesterone therapy; liver failure was the main cause of death in three (Nadell and Kosek, Arch Pathol Lab Med 1977). The label recommends periodic liver function tests. See also Anadrol (oxymetholone), the other drug in that series.

Testicular suppression

Nine healthy men took 10, 20 or 30 mg/day of fluoxymesterone for 12 weeks (Jones et al., JCEM 1977). Their testosterone fell within 24 hours and stayed profoundly suppressed throughout. Notably, LH and FSH did not change significantly, and sperm counts were lower at times but not consistently suppressed. The authors proposed a direct effect on the testes. The label adds that oligospermia (low sperm count) may occur with prolonged or high-dose use.

Cortisol metabolism and blood pressure (lab data)

In enzyme and human cell-line studies, fluoxymesterone was a potent inhibitor of human 11β-HSD2, with half-maximal inhibition at 60–100 nM in cell lysates and 160 nM in intact cells (Fürstenberger et al., Toxicol Sci 2012). This enzyme normally inactivates cortisol. The authors proposed that blocking it could let cortisol activate the mineralocorticoid receptor, leading to electrolyte disturbances and contributing to high blood pressure and cardiovascular disease.

This is an in-vitro finding. The authors also showed that the rat and mouse versions of the enzyme are much less affected, so rodent studies cannot test it. Whether it causes hypertension in people at clinical doses has not been studied. The label separately lists retention of sodium, chloride, water and potassium, and warns that edema can be serious in people with heart, kidney or liver disease.

Androgenic and other effects

The label lists:

Women: amenorrhea and other menstrual changes; virilization, including deepening of the voice and clitoral enlargement, which is usually not reversible. Breast cancer trials consistently reported more masculinizing effects when fluoxymesterone was added.
Men: gynecomastia, and too-frequent or prolonged erections (priapism), which the label calls a sign of excessive dosage.
Skin and hair: acne, oily skin, hirsutism and male-pattern hair loss.
Blood: polycythemia (too many red cells), and suppression of clotting factors II, V, VII and X.
Lipids and calcium: serum cholesterol may increase; hypercalcemia can occur in immobilized patients and women with breast cancer.
Nervous system: increased or decreased libido, headache, anxiety and depression.

The tablets contained tartrazine (FD&C Yellow No. 5), which can cause allergic-type reactions, more often in people with aspirin sensitivity.

Interactions

Warfarin and other oral anticoagulants: androgens increase their effect, and the anticoagulant dose may need reduction.
Diabetes medicines: androgens may lower blood glucose and insulin needs.
Thyroid tests: androgens lower thyroxine-binding globulin, so total T4 falls while free thyroid hormone is unchanged.

Who should not use it

The label contraindicated fluoxymesterone in:

men with breast cancer or known or suspected prostate cancer;
women who are or may be pregnant (Pregnancy Category X, because androgens can virilize a female fetus);
people with serious heart, liver or kidney disease;
anyone with known hypersensitivity to the drug.

It was not recommended during breastfeeding.

Detection in sport

Because the parent drug clears quickly but metabolites persist, anti-doping tests target metabolites. In the 1990 UCLA study, metabolites remained detectable for at least 5 days after one 10 mg dose (Kammerer et al., J Steroid Biochem 1990).

Key takeaways

A modified methyltestosterone. Fluoxymesterone adds 9α-fluoro and 11β-hydroxy groups to the methyltestosterone skeleton. The 17α-methyl group makes it oral and links it to the class’s liver risks.
Off the US market. Halotestin’s approval was withdrawn in 2009 and the last generic in 2022, both because they were no longer marketed. It is still Schedule III and WADA-prohibited.
Short-acting. The label gives a half-life of about 9 hours and one small study measured about 2 hours. The label advised divided daily doses for breast cancer for this reason.
Modest cancer benefit. Added to tamoxifen, it sometimes raised response rates in metastatic breast cancer but did not clearly improve survival, and it failed as an adjuvant and as an appetite stimulant.
No performance evidence. We found no controlled human trials of fluoxymesterone for muscle or strength; its reputation as a “strength” steroid is not backed by trial data.
Known risks. Peliosis hepatis and liver tumors with high-dose use, profound testosterone suppression, virilization in women and, in lab studies, blockade of the enzyme that inactivates cortisol.

Sources

Pharmacia and Upjohn Company. Halotestin (fluoxymesterone tablets, USP) prescribing information. May 2002. DailyMed.
Food and Drug Administration. Drugs@FDA: NDA 010611, Halotestin (fluoxymesterone). FDA.
National Center for Biotechnology Information. Fluoxymesterone, PubChem CID 6446. PubChem.
Food and Drug Administration. Novartis Pharmaceuticals Corp. et al.; withdrawal of approval of 92 new drug applications and 49 abbreviated new drug applications. Federal Register. May 19, 2009;74:23407 (FR Doc E9-11628). govinfo.
Food and Drug Administration. Baxter Healthcare Corporation, et al.; withdrawal of approval of 14 abbreviated new drug applications. Federal Register. April 25, 2022;87:24320 (FR Doc 2022-08744). govinfo.
Drug Enforcement Administration. Schedule III, 21 CFR 1308.13. eCFR.
World Anti-Doping Agency. The 2026 Prohibited List. WADA.
Capponi VJ, Cox SR, Harrington EL, et al. Liquid chromatographic assay for fluoxymesterone in human serum with application to a preliminary bioavailability study. J Pharm Sci. 1985;74(3):308–311. PubMed.
Kammerer RC, Merdink JL, Jagels M, et al. Testing for fluoxymesterone (Halotestin) administration to man: identification of urinary metabolites by gas chromatography-mass spectrometry. J Steroid Biochem. 1990;36(6):659–666. PubMed.
Fürstenberger C, Vuorinen A, Da Cunha T, et al. The anabolic androgenic steroid fluoxymesterone inhibits 11β-hydroxysteroid dehydrogenase 2-dependent glucocorticoid inactivation. Toxicol Sci. 2012;126(2):353–361. PubMed.
Westerberg H. Tamoxifen and fluoxymesterone in advanced breast cancer: a controlled clinical trial. Cancer Treat Rep. 1980;64(1):117–121. PubMed.
Tormey DC, Lippman ME, Edwards BK, Cassidy JG. Evaluation of tamoxifen doses with and without fluoxymesterone in advanced breast cancer. Ann Intern Med. 1983;98(2):139–144. PubMed.
Ingle JN, Twito DI, Schaid DJ, et al. Combination hormonal therapy with tamoxifen plus fluoxymesterone versus tamoxifen alone in postmenopausal women with metastatic breast cancer. An updated analysis. Cancer. 1991;67(4):886–891. PubMed.
Rose C, Kamby C, Mouridsen HT, et al. Combined endocrine treatment of elderly postmenopausal patients with metastatic breast cancer. A randomized trial of tamoxifen vs. tamoxifen + aminoglutethimide and hydrocortisone and tamoxifen + fluoxymesterone in women above 65 years of age. Breast Cancer Res Treat. 2000;61(2):103–110. PubMed.
Kono M, Fujii T, Lyons GR, et al. Impact of androgen receptor expression in fluoxymesterone-treated estrogen receptor-positive metastatic breast cancer refractory to contemporary hormonal therapy. Breast Cancer Res Treat. 2016;160(1):101–109. PubMed.
Ingle JN, Suman VJ, Mailliard JA, et al. Randomized trial of tamoxifen alone or combined with fluoxymesterone as adjuvant therapy in postmenopausal women with resected estrogen receptor positive breast cancer. North Central Cancer Treatment Group Trial 89-30-52. Breast Cancer Res Treat. 2006;98(2):217–222. PubMed.
Loprinzi CL, Kugler JW, Sloan JA, et al. Randomized comparison of megestrol acetate versus dexamethasone versus fluoxymesterone for the treatment of cancer anorexia/cachexia. J Clin Oncol. 1999;17(10):3299–3306. PubMed.
Brubaker LH, Brière J, Laszlo J, et al. Treatment of anemia in myeloproliferative disorders: a randomized study of fluoxymesterone v transfusions only. Arch Intern Med. 1982;142(8):1533–1537. PubMed.
Strickland AL. Long-term results of treatment with low-dose fluoxymesterone in constitutional delay of growth and puberty and in genetic short stature. Pediatrics. 1993;91(4):716–720. PubMed.
Nadell J, Kosek J. Peliosis hepatis. Twelve cases associated with oral androgen therapy. Arch Pathol Lab Med. 1977;101(8):405–410. PubMed.
Jones TM, Fang VS, Landau RL, Rosenfield RL. The effects of fluoxymesterone administration on testicular function. J Clin Endocrinol Metab. 1977;44(1):121–129. PubMed.
Arnold A, Potts GO, Beyler AL. The ratio of anabolic to androgenic activity of 7:17-dimethyltestosterone, oxymesterone, mestanolone and fluoxymesterone. J Endocrinol. 1963;28:87–92. PubMed.

Halotestin (Fluoxymesterone)