Oxymetholone is a synthetic derivative of DHT that is commonly known by the trade name Anadrol. Anadrol is considered to be a very potent and toxic oral steroid. This is due to the fact that oxymetholone has a long half-life, about 8 hours, and several active metabolites1,2. Oxymetholone, as a DHT derivative, is incapable of being converted to estrogenic metabolites. Additionally, since oxymetholone is already 5-alpha reduced, it is not acted upon by 5-alpha reductase but likely inhibits the action of this enzyme.
Oxymetholone was originally produced by Syntex in the US under the trade name Anadrol, by which it is commonly known. Oxymetholone has the reputation of being very potent causing drastic size and strength gains. It is also well known for its propensity for causing side effects including edema, gynecomastia, balding, acne, increased aggressiveness and liver toxicity3. The average anabolic to androgenic ratio reported in the medical literature is 5.8. Oxymetholone does not bind strongly to the androgen receptor but it has been shown to activate the androgen receptor4,5. This steroid does not bind to SHBG and has a long half-life in the body of about 8 hours2. Oxymetholone is metabolized in the body, in part, to 17-alpha-methyl DHT (17AMDHT)1. 17AMDHT does bind as strongly to the AR and SHBG as DHT with slight affinity for the PR1,6.
Oxymetholone is considered to be exceptional at raising red blood cell levels. The fact is, all androgens cause this effect to some degree and oxymetholone is actually not the most potent at producing this effect7,8. The strong binding of 17AMDHT to SHBG displaces testosterone and estrogen into the free circulation. This free estrogen can lead to gynecomastia. Although oxymetholone has a reputation for dramatic size and strength gains, it is also well known that these gains tend to disappear once treatment is ended. This is due to the fact that only a portion of the gains made while using oxymetholone are attributable to actual muscle growth. This is likely due to a large degree of water retention brought on through inhibition of 11-beta hydroxylase which would also explain the bloating and elevated blood pressure that most people report while using this drug. Oxymetholone is well known for its propensity for raising liver enzymes and with long-term treatment, causing liver damage. This is due to the C-17 alkylation that makes oral administration possible and the relatively large amount of drug that one must ingest to reach therapeutic levels.
Much has been made of the fact that anadrol seems to cause gynecomastia. Oxymetholone cannot be converted to estrogen so many theories have been put forth to explain this effect. Some have theorized that oxymetholone binds directly to the estrogen receptor but there is no scientific evidence to support this theory. Others have blamed this effect on progestational activity of oxymetholone. Oxymetholone has been shown in the literature to have anti-progestational effects9. As explained earlier, antagonism of the progesterone receptor upregulates the estrogen receptor. This, coupled with the displacement of estrogen from SHBG is the likely culprit in oxymetholone induced gyno. Mifepristone, a progesterone receptor antagonist has also been shown to induce gynecomastia when taken chronically. Like methandrostenolone, oxymetholone elicits an increase in CBG which is contrary to most other AAS. Oxymetholone, unlike methandrostenolone, actually causes a slight decrease in non-plasma bound cortisol10. Oxymetholone decreases TBG pretty strongly resulting in increased T3 uptake10.
1. Schanzer W: Metabolism of anabolic androgenic steroids. Clin Chem. Jul;42(7):1001-20, 1996
2. Cardoso CR, Marques MA, Caminha RC, Maioli MC, Aquino Neto FR: Validation of the determination of oxymetholone in human plasma analysis using gas chromatography-mass spectrometry. Application to pharmacokinetic studies. J Chromatogr B Analyt Technol Biomed Life Sci. Jul 25;775(1):1-8, 2002
3. Pavlatos AM, Fultz O, Monberg MJ, Vootkur A, Pharmd: Review of oxymetholone: a 17alpha-alkylated anabolic-androgenic steroid. Clin Ther. Jun;23(6):789-801; discussion 771, 2001
4. Saartok T, Dahlberg E, Gustafsson JA: 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. Jun;114(6):2100-6, 1984
5. Feldkoren BI, Andersson S. Anabolic-androgenic steroid interaction with rat androgen receptor in vivo and in vitro: a comparative study. J Steroid Biochem Mol Biol. 94(5):481-7, 2005
6. Ojasoo T, Delettre J, Mornon JP, Turpin-VanDycke C, Raynaud JP: Towards the mapping of the progesterone and androgen receptors. J Steroid Biochem. 27(1-3):255-69, 1987
7. Gorshein D, Murphy S, Gardner FH. Comparative study on the erythropoietic effects of androgens and their mode of action. J Appl Physiol. 35(3):276-8, 1973
8. Allen DM, Fine MH, Necheles TF, Dameshek W. Oxymetholone therapy in aplastic anemia. Blood. 32(1):83-9, 1968
9. Chatterton RT. Inhibition of progestational activity for fertility regulation. Res Front Fertil Regul. 1(3):1-14, 1981
10. Barbosa J, Seal US, Doe RP: Effects of anabolic steroids on hormone-binding proteins, serum cortisol and serum nonprotein-bound cortisol. J Clin Endocrinol Metab. Feb;32(2):232-40, 1971
Adapted with permission from Seth Robert’s Anabolic Pharmacology, all rights reserved.