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Fluoxymesterone structure.svg
Trade namesAndroxy, Halotestin, Ora-Testryl, Ultandren, others
Other namesFluoxymestrone; Androfluorene; NSC-12165
  • (8S,9R,10S,11S,13S,14S,17S)-9-fluoro-11,17-dihydroxy-10,13,17-trimethyl-1,2,6,7,8,11,12,14,15,16-decahydrocyclopenta[a]phenanthren-3-one
Clinical data
Drug classAndrogen; Anabolic steroid
Main usesLow testosterone, delayed puberty, breast cancer[1]
Side effectsFemales: Acne, hair growth, voice changes, aggressiveness[1][2]
Males: Breast enlargement, increased erections[1][2]
  • X
Routes of
By mouth[2]
External links
Legal status
BioavailabilityBy mouth: 80%[3]
MetabolismLiver (6β-hydroxylation, 5α- and 5β-reduction, 3α- and 3β-keto-oxidation, 11β-hydroxy-oxidation)[4]
Metabolites• 5α-Dihydrofluoxymesterone[4]
Elimination half-life9.2 hours[5][6]
ExcretionUrine (<5% unchanged)[3][4]
Chemical and physical data
Molar mass336.447 g·mol−1
3D model (JSmol)
  • O=C4\C=C3/[C@]([C@@]2(F)[C@@H](O)C[C@]1([C@@H](CC[C@@]1(O)C)[C@@H]2CC3)C)(C)CC4
  • InChI=1S/C20H29FO3/c1-17-8-6-13(22)10-12(17)4-5-15-14-7-9-19(3,24)18(14,2)11-16(23)20(15,17)21/h10,14-16,23-24H,4-9,11H2,1-3H3/t14-,15-,16-,17-,18-,19-,20-/m0/s1 checkY

Fluoxymesterone, sold under the brand names Androxy among others, is a medication used to treat low testosterone in men, delayed puberty in boys, and breast cancer in women.[1] It is taken by mouth.[1]

Common side effects in females include acne, increased hair growth, voice changes, and increased aggressiveness while common side effects in males include breast enlargement and increased erections.[1][2] Other side effects may include liver damage, heart failure, high blood calcium, and priapism.[1] Use during pregnancy may harm the baby.[1] It is a manufactured androgen and anabolic steroid.[1]

Fluoxymesterone was approved for medical use in the United States in 1956.[1] In the United States 100 tablets of 10 mg costs about 415 USD as of 2021.[7] In has also been used to improve physique and performance.[1] The medication is a controlled substance in many countries such that non-medical use is generally illicit.[2]

Medical uses

Fluoxymesterone is or has been used in the treatment of hypogonadism, delayed puberty, and anemia in males and the treatment of breast cancer in women.[2][8] It is specifically approved in one or more countries for the treatment of hypogonadism in men, delayed puberty in boys, and breast cancer in women.[9] Current prescribing guidelines in the United States list only the treatment of androgen deficiency in males and breast cancer in females as indications.[2]

Fluoxymesterone is less effective in inducing masculinization than testosterone, but is useful for maintaining established masculinization in adults.[10]


Fluoxymesterone is available in the form of 2, 5, and 10 mg oral tablets.[11]

Androgen replacement therapy formulations and dosages used in men
Route Medication Major brand names Form Dosage
Oral Testosteronea Tablet 400–800 mg/day (in divided doses)
Testosterone undecanoate Andriol, Jatenzo Capsule 40–80 mg/2–4x day (with meals)
Methyltestosteroneb Android, Metandren, Testred Tablet 10–50 mg/day
Fluoxymesteroneb Halotestin, Ora-Testryl, Ultandren Tablet 5–20 mg/day
Metandienoneb Dianabol Tablet 5–15 mg/day
Mesteroloneb Proviron Tablet 25–150 mg/day
Buccal Testosterone Striant Tablet 30 mg 2x/day
Methyltestosteroneb Metandren, Oreton Methyl Tablet 5–25 mg/day
Sublingual Testosteroneb Testoral Tablet 5–10 mg 1–4x/day
Methyltestosteroneb Metandren, Oreton Methyl Tablet 10–30 mg/day
Intranasal Testosterone Natesto Nasal spray 11 mg 3x/day
Transdermal Testosterone AndroGel, Testim, TestoGel Gel 25–125 mg/day
Androderm, AndroPatch, TestoPatch Non-scrotal patch 2.5–15 mg/day
Testoderm Scrotal patch 4–6 mg/day
Axiron Axillary solution 30–120 mg/day
Androstanolone (DHT) Andractim Gel 100–250 mg/day
Rectal Testosterone Rektandron, Testosteronb Suppository 40 mg 2–3x/day
Injection (IM or SC) Testosterone Andronaq, Sterotate, Virosterone Aqueous suspension 10–50 mg 2–3x/week
Testosterone propionateb Testoviron Oil solution 10–50 mg 2–3x/week
Testosterone enanthate Delatestryl Oil solution 50–250 mg 1x/1–4 weeks
Xyosted Auto-injector 50–100 mg 1x/week
Testosterone cypionate Depo-Testosterone Oil solution 50–250 mg 1x/1–4 weeks
Testosterone isobutyrate Agovirin Depot Aqueous suspension 50–100 mg 1x/1–2 weeks
Testosterone phenylacetateb Perandren, Androject Oil solution 50–200 mg 1x/3–5 weeks
Mixed testosterone esters Sustanon 100, Sustanon 250 Oil solution 50–250 mg 1x/2–4 weeks
Testosterone undecanoate Aveed, Nebido Oil solution 750–1,000 mg 1x/10–14 weeks
Testosterone buciclatea Aqueous suspension 600–1,000 mg 1x/12–20 weeks
Implant Testosterone Testopel Pellet 150–1,200 mg/3–6 months
Notes: Men produce about 3 to 11 mg testosterone per day (mean 7 mg/day in young men). Footnotes: a = Never marketed. b = No longer used and/or no longer marketed. Sources: See template.
Androgen replacement therapy formulations and dosages used in women
Route Medication Major brand names Form Dosage
Oral Testosterone undecanoate Andriol, Jatenzo Capsule 40–80 mg 1x/1–2 days
Methyltestosterone Metandren, Estratest Tablet 0.5–10 mg/day
Fluoxymesterone Halotestin Tablet 1–2.5 mg 1x/1–2 days
Normethandronea Ginecoside Tablet 5 mg/day
Tibolone Livial Tablet 1.25–2.5 mg/day
Prasterone (DHEA)b Tablet 10–100 mg/day
Sublingual Methyltestosterone Metandren Tablet 0.25 mg/day
Transdermal Testosterone Intrinsa Patch 150–300 μg/day
AndroGel Gel, cream 1–10 mg/day
Vaginal Prasterone (DHEA) Intrarosa Insert 6.5 mg/day
Injection Testosterone propionatea Testoviron Oil solution 25 mg 1x/1–2 weeks
Testosterone enanthate Delatestryl, Primodian Depot Oil solution 25–100 mg 1x/4–6 weeks
Testosterone cypionate Depo-Testosterone, Depo-Testadiol Oil solution 25–100 mg 1x/4–6 weeks
Testosterone isobutyratea Femandren M, Folivirin Aqueous suspension 25–50 mg 1x/4–6 weeks
Mixed testosterone esters Climacterona Oil solution 150 mg 1x/4–8 weeks
Omnadren, Sustanon Oil solution 50–100 mg 1x/4–6 weeks
Nandrolone decanoate Deca-Durabolin Oil solution 25–50 mg 1x/6–12 weeks
Prasterone enanthatea Gynodian Depot Oil solution 200 mg 1x/4–6 weeks
Implant Testosterone Testopel Pellet 50–100 mg 1x/3–6 months
Notes: Premenopausal women produce about 230 ± 70 μg testosterone per day (6.4 ± 2.0 mg testosterone per 4 weeks), with a range of 130 to 330 μg per day (3.6–9.2 mg per 4 weeks). Footnotes: a = Mostly discontinued or unavailable. b = Over-the-counter. Sources: See template.
Androgen/anabolic steroid dosages for breast cancer
Route Medication Form Dosage
Oral Methyltestosterone Tablet 30–200 mg/day
Fluoxymesterone Tablet 10–40 mg 3x/day
Calusterone Tablet 40–80 mg 4x/day
Normethandrone Tablet 40 mg/day
Buccal Methyltestosterone Tablet 25–100 mg/day
Injection (IM or SC) Testosterone propionate Oil solution 50–100 mg 3x/week
Testosterone enanthate Oil solution 200–400 mg 1x/2–4 weeks
Testosterone cypionate Oil solution 200–400 mg 1x/2–4 weeks
Mixed testosterone esters Oil solution 250 mg 1x/week
Methandriol Aqueous suspension 100 mg 3x/week
Androstanolone (DHT) Aqueous suspension 300 mg 3x/week
Drostanolone propionate Oil solution 100 mg 1–3x/week
Metenolone enanthate Oil solution 400 mg 3x/week
Nandrolone decanoate Oil solution 50–100 mg 1x/1–3 weeks
Nandrolone phenylpropionate Oil solution 50–100 mg/week
Note: Dosages are not necessarily equivalent. Sources: See template.

Side effects

Side effects that have been associated with fluoxymesterone include acne, edema, seborrhea/seborrheic dermatitis, alopecia, hirsutism, voice deepening, virilization in general, flushing, gynecomastia, breast pain, menstrual disturbances, hypogonadism, testicular atrophy, clitoral enlargement, penile enlargement, priapism, increased aggressiveness, prostate enlargement, cardiovascular toxicity, and hepatotoxicity, among others.[2][12]


It has strong androgenic effects and moderate anabolic effects, which make it useful for producing masculinization.[2][13]


Androgenic vs. anabolic activity
of androgens/anabolic steroids
Medication Ratioa
Testosterone ~1:1
Androstanolone (DHT) ~1:1
Methyltestosterone ~1:1
Methandriol ~1:1
Fluoxymesterone 1:1–1:15
Metandienone 1:1–1:8
Drostanolone 1:3–1:4
Metenolone 1:2–1:30
Oxymetholone 1:2–1:9
Oxandrolone 1:3–1:13
Stanozolol 1:1–1:30
Nandrolone 1:3–1:16
Ethylestrenol 1:2–1:19
Norethandrolone 1:1–1:20
Notes: In rodents. Footnotes: a = Ratio of androgenic to anabolic activity. Sources: See template.

As an AAS, fluoxymesterone is an agonist of the androgen receptor (AR), similarly to androgens like testosterone and DHT.[2][14] It is a substrate for 5α-reductase like testosterone, and so is potentiated in so-called "androgenic" tissues like the skin, hair follicles, and prostate gland via transformation into 5α-dihydrofluoxymesterone.[2][14][4] As such, fluoxymesterone has a relatively poor ratio of anabolic to androgenic activity similarly to testosterone and methyltestosterone.[2][14] However, fluoxymesterone is nonetheless proportionally less androgenic and more anabolic than methyltestosterone and testosterone.[13]

Fluoxymesterone has been reported to be non-aromatizable due to steric hindrance by its C11β hydroxyl group,[15] and hence is not considered to have a propensity for producing estrogenic effects such as gynecomastia or fluid retention.[2][16] However, paradoxically, a case report of severe fluoxymesterone-induced gynecomastia exists, and gynecomastia associated with fluoxymesterone has also been reported in other publications, although this may not be due to estrogenic activity.[17] Fluoxymesterone is thought to possess little or no progestogenic activity.[2][14]

Because of the presence of its 17α-methyl group, the metabolism of fluoxymesterone is impeded, resulting in it being orally active, although also hepatotoxic.[2][14]

11β-HSD inhibition

Fluoxymesterone has been found to act as a potent inhibitor of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) (IC50 = 60–630 nM), with a potency comparable to that of the 11β-HSD2 inhibitor glycyrrhetinic acid.[18][19] This action of fluoxymesterone is unique among AAS and is likely related to its 11β-hydroxyl group.[18] 11β-HSD2 is responsible for the inactivation of the glucocorticoids cortisol and corticosterone (into cortisone and 11-dehydrocorticosterone, respectively).[18][19] Inhibition of 11β-HSD2 by fluoxymesterone may result in mineralocorticoid receptor overactivation and associated side effects such as hypertension and fluid retention, and has been hypothesized to be involved in the cardiovascular and other adverse effects of fluoxymesterone.[18][19]

Glucocorticoid activity

Unlike other AAS, fluoxymesterone has structural features in common with corticosteroids, including its C9α fluoro and C11β hydroxyl groups.[20] In relation to this, it has weak (micromolar) but potentially clinically significant affinity for the glucocorticoid receptor.[21]


Fluoxymesterone has approximately 80% oral bioavailability, unlike testosterone, as the C17α methyl group of fluoxymesterone inhibits first-pass metabolism.[3][2] It has very low affinity for human serum sex hormone-binding globulin (SHBG), less than 5% of that of testosterone and less than 1% of that of DHT.[22] The drug is metabolized in the liver, mainly by 6β-hydroxylation, 5α- and 5β-reduction, 3α- and 3β-keto-oxidation, and 11β-hydroxy-oxidation.[4] Its known active metabolites include 5α-dihydrofluoxymesterone and 11-oxofluoxymesterone.[4][18][23][13] Fluoxymesterone has an elimination half-life of approximately 9.2 hours, which is long relative to that of testosterone.[5] It is eliminated in the urine, with less than 5% excreted unchanged.[3][4]


Fluoxymesterone, also known as 9α-fluoro-11β-hydroxy-17α-methyltestosterone or as 9α-fluoro-17α-methylandrost-4-en-11β,17β-diol-3-one, is a synthetic androstane steroid and a 17α-alkylated derivative of testosterone (androst-4-en-17β-ol-3-one).[24][25] It is specifically the derivative of testosterone with a fluorine atom at the C9α position, a hydroxyl group at the C11β position, and a methyl group at the C17α position.[24][25] Chemically it is known as 9α-Fluoro-11β-hydroxy-17α-methyltestosterone; 9α-Fluoro-17α-methylandrost-4-en-11β,17β-diol-3-one.


Step one: The first step in the synthesis of fluoxymesterone is the microbiological oxidation of commercially available androstenedione (1.11) by Actinomyces; this introduces a hydroxyl group to the 11α-position (1.12), which is then oxidised to a ketone using Jones' reagent, yielding the 3,11,17-triketone, adrenosterone (1.13). Pyrrolidine then reacts to form an enamine (1.14) by reaction with the 3α-keto group, protecting it from alkylation in a subsequent step. The regioselectivity of pyrrolidine for reaction at the 3α-position occurs inherently in the structure of adrenosterone, due to the position of the sterically bulky methyl groups. In subsequent steps, alkylation of the 17-keto group (1.14) using Grignard reagent, addition of hydride at the 11-position (1.15) and regeneration of the protected 3-keto group yields the starting material (1.16) for the final steps of the fluoxymesterone synthesis. This involves more standard synthetic transformations.

Scheme showing the full synthesis of fluoxymesterone from andrestenedione

Step two: The 11α-hydroxyl of the starting material (1.16) is sulfonylated by p-toluenesulfonyl chloride; addition of trimethylamine (base) deprotonates the 11α-carbon, yielding an (E2) elimination of tosylate (pka - 5) to give olefin (1.17). Stereospecificity of reaction between olefin and hypobromous acid (HOBr) in base, N-bromosuccinimide (NBS), is determined by the formation of a bromonium intermediate; the electrophilic bromonium cation approaches the ring's less sterically hindered α-face and is attacked by the π-electron density of the alkene. The hydroxide ion then attacks from above the ring (β-face) at the 11-carbon, resulting in a structure (1.18) by the stereospecific addition of hydroxyl and bromine across the double bond. Addition of sodium hydroxide results in deprotonation of the 11α-hydroxyl, and the subsequent structure undergoes an intramolecular SN2 epoxy ring formation. The epoxy ring of the β-epoxide (1.19) is protonated to give an oxironium ion intermediate. In a concerted process, fluoride attacks the ring's α-face from below, as one of the two oxygen-carbon bonds is broken on the opposite face; hence regenerating the 11α-hydroxyl trans to the fluorine substituent. The resulting structure (1.20) is the androgenic steroid, fluoxymesterone.

Detection in body fluids

Detection of halotestin and other such illegal anabolic steroids in sports is achieved by GS-MS identification of urinary excreted anabolic steroids and their metabolites. In a test for halotestin, a dry residue obtained from a urine sample is dissolved in dimethylformamide and a sulfur trioxide-pyridine complex and is heated with 1% potassium carbonate solution. Halotestin and many of its metabolites contain two polar hydroxyl groups, leading to intermolecular hydrogen bonding that increases their boiling point and reduces volatility. In order to attain a gaseous sample for GC-MS, the products of hydrolysis are extracted, dissolved in methanol and derivatised to form volatile trimethylsilyl (TMS) esters by adding N-methyl-N-trimethylsilyl-trifluoroacetamide (MSTFA) and trimethylsilylimidazole (TMSImi).[26]


Fluoxymesterone was first described in 1956 and was introduced for medical use in the United States in 1957.[2][27] Over time the use of fluoxymesterone has become increasingly controversial and limited.[2]

Society and culture

Generic names

Fluoxymesterone is the generic name of the drug and its INN, USP, BAN, DCIT, and JAN, while fluoxymestérone is its DCF.[24][25][28][29]

Brand names

Brand names of fluoxymesterone include Android-F, Androxy, Halotestin, Ora-Testryl, and Ultandren among others.[24][25][28][29]


United States

Fluoxymesterone is one of the few AAS that remains available for medical use in the United States.[30] The others (as of November 2017) are testosterone, testosterone cypionate, testosterone enanthate, testosterone undecanoate, methyltestosterone, oxandrolone, and oxymetholone.[30]

Other countries

Availability of fluoxymesterone aside from the United States remains scarce, but it is marketed in some other countries such as Mexico, Moldova, and Taiwan.[2][29]

Legal status

Fluoxymesterone, along with other AAS, is a schedule III controlled substance in the United States under the Controlled Substances Act.[31]

Non-medical uses

Fluoxymesterone is used for physique- and performance-enhancing purposes by competitive athletes, bodybuilders, and powerlifters.[2]


  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 "Fluoxymesterone Monograph for Professionals". Drugs.com. Archived from the original on 20 November 2021. Retrieved 14 December 2021.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 William Llewellyn (2011). Anabolics. Molecular Nutrition Llc. pp. 500–508. ISBN 978-0-9828280-1-4. Archived from the original on 2021-02-15. Retrieved 2021-09-17.
  3. 3.0 3.1 3.2 3.3 Thomas L. Lemke; David A. Williams (24 January 2012). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 1360–. ISBN 978-1-60913-345-0.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Kammerer RC, Merdink JL, Jagels M, Catlin DH, Hui KK (1990). "Testing for fluoxymesterone (Halotestin) administration to man: identification of urinary metabolites by gas chromatography-mass spectrometry". J. Steroid Biochem. 36 (6): 659–66. doi:10.1016/0022-4731(90)90185-u. PMID 2214783.
  5. 5.0 5.1 Seth Roberts (2009). Anabolic Pharmacology.
  6. Thomas L. Lemke; David A. Williams (2008). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 1279–. ISBN 978-0-7817-6879-5. Archived from the original on 2017-09-08. Retrieved 2021-09-17.
  7. "Androxy Prices, Coupons & Patient Assistance Programs". Drugs.com. Retrieved 14 December 2021.
  8. Susan M. Ford; Sally S. Roach (7 October 2013). Roach's Introductory Clinical Pharmacology. Lippincott Williams & Wilkins. pp. 502–. ISBN 978-1-4698-3214-2.
  9. "Fluoxymesterone - AdisInsight". Archived from the original on 2021-02-15. Retrieved 2021-09-17.
  10. John A. Thomas; Edward J. Keenan (6 December 2012). Principles of Endocrine Pharmacology. Springer Science & Business Media. pp. 125–. ISBN 978-1-4684-5036-1. Archived from the original on 2 January 2020. Retrieved 17 September 2021.
  11. Jacques Lorrain (1994). Comprehensive Management of Menopause. Springer Science & Business Media. pp. 301–. ISBN 978-0-387-97972-4. Archived from the original on 2021-10-31. Retrieved 2021-09-17.
  12. Jerome Z. Litt; Neil Shear (17 December 2014). Litt's Drug Eruptions and Reactions Manual, 19th Edition. CRC Press. pp. 177–. ISBN 978-1-84214-599-9.
  13. 13.0 13.1 13.2 Charles D. Kochakian (6 December 2012). Anabolic-Androgenic Steroids. Springer Science & Business Media. pp. 370, 374, 401, 454, 504–506. ISBN 978-3-642-66353-6. Archived from the original on 9 September 2019. Retrieved 17 September 2021.
  14. 14.0 14.1 14.2 14.3 14.4 Kicman, A T (2008). "Pharmacology of anabolic steroids". British Journal of Pharmacology. 154 (3): 502–521. doi:10.1038/bjp.2008.165. PMC 2439524. PMID 18500378.
  15. Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR (2008). "Dimethandrolone (7alpha,11beta-dimethyl-19-nortestosterone) and 11beta-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase". J. Steroid Biochem. Mol. Biol. 110 (3–5): 214–22. doi:10.1016/j.jsbmb.2007.11.009. PMC 2575079. PMID 18555683.
  16. Norman T. Adler; Donald Pfaff; Robert W. Goy (6 December 2012). Reproduction. Springer Science & Business Media. pp. 630–. ISBN 978-1-4684-4832-0.
  17. Lo TE, Andal ZC, Lantion-Ang FL (2015). "Fluoxymesterone-induced gynaecomastia in a patient with childhood aplastic anaemia". BMJ Case Rep. 2015: bcr2014207474. doi:10.1136/bcr-2014-207474. PMC 4434366. PMID 25948845.
  18. 18.0 18.1 18.2 18.3 18.4 Fürstenberger C, Vuorinen A, Da Cunha T, Kratschmar DV, Saugy M, Schuster D, Odermatt A (2012). "The anabolic androgenic steroid fluoxymesterone inhibits 11β-hydroxysteroid dehydrogenase 2-dependent glucocorticoid inactivation". Toxicol. Sci. 126 (2): 353–61. doi:10.1093/toxsci/kfs022. PMID 22273746.
  19. 19.0 19.1 19.2 Joseph JF, Parr MK (2015). "Synthetic androgens as designer supplements". Curr Neuropharmacol. 13 (1): 89–100. doi:10.2174/1570159X13666141210224756. PMC 4462045. PMID 26074745.
  20. Kirschbaum J (27 October 1978). Profiles of Drug Substances, Excipients and Related Methodology. Academic Press. pp. 253–. ISBN 978-0-08-086102-9.
  21. Mayer M, Rosen F (1975). "Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol". Am. J. Physiol. 229 (5): 1381–6. doi:10.1152/ajplegacy.1975.229.5.1381. PMID 173192.
  22. Saartok T, Dahlberg E, Gustafsson JA (1984). "Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin". Endocrinology. 114 (6): 2100–6. doi:10.1210/endo-114-6-2100. PMID 6539197.
  23. Gordan, G. S. (1976). "Cancer in Man". In Kochakian, Charles D. (ed.). Anabolic-Androgenic Steroids. pp. 499–513. doi:10.1007/978-3-642-66353-6_16. ISBN 978-3-642-66355-0.
  24. 24.0 24.1 24.2 24.3 J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 568–. ISBN 978-1-4757-2085-3.
  25. 25.0 25.1 25.2 25.3 Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. p. 461. ISBN 978-3-88763-075-1.
  26. Schänzer, Willi; Opfermann, Georg; Donike, Manfred (1992-11-01). "17-Epimerization of 17α-methyl anabolic steroids in humans: metabolism and synthesis of 17α-hydroxy-17β-methyl steroids". Steroids. 57 (11): 537–550. doi:10.1016/0039-128X(92)90023-3. PMID 1448813. S2CID 54380880.
  27. William Andrew Publishing (22 October 2013). Pharmaceutical Manufacturing Encyclopedia, 3rd Edition. Elsevier. pp. 1676–. ISBN 978-0-8155-1856-3. Archived from the original on 31 October 2021. Retrieved 17 September 2021.
  28. 28.0 28.1 I.K. Morton; Judith M. Hall (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 123–. ISBN 978-94-011-4439-1. Archived from the original on 1 August 2020. Retrieved 17 September 2021.
  29. 29.0 29.1 29.2 "Fluoxymesterone: Indications, Side Effects, Warnings". Archived from the original on 2017-11-11. Retrieved 2021-09-17.
  30. 30.0 30.1 "Drugs@FDA: FDA Approved Drug Products". United States Food and Drug Administration. Archived from the original on 16 November 2016. Retrieved 17 December 2016.
  31. Steven B. Karch (21 December 2006). Drug Abuse Handbook, Second Edition. CRC Press. pp. 30–. ISBN 978-1-4200-0346-8. Archived from the original on 14 April 2019. Retrieved 17 September 2021.

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