DMAU is an experimental medication and is not currently approved for medical use.[5] It is under development for use as a potential male hormonal contraceptive, specifically as a birth control pill for men.[2][3][4] The medication has been found to profoundly and rapidly reversibly suppress testiculartestosteroneproduction in men when taken by mouth once per day for a month.[5][10] The circulating levels of testosterone achieved with oral DMAU were equivalent to those seen on average with surgical castration (13.4 ng/dL for DMAU, 15 ng/dL for castration).[10][11] Following discontinuation of DMAU, testosterone levels began to recover within days and reached normal levels within a month.[10][12] Testicular testosterone production is essential for spermatogenesis and fertility in men.[13] Suppression of spermatogenesis and the actual contraceptive effects of DMAU in men have not yet been clinically assessed, but future studies are being planned to confirm the contraceptive effectiveness of the medication.[5][10] In addition to male contraception, there has also been interest in the potential use of DMAU in androgen replacement therapy for low testosterone levels in men.[14][2][15]
Unlike testosterone but similarly to 17α-alkyated AAS like methyltestosterone (17α-methyltestosterone), DMAU has been found to produce some effects indicative of potential liver toxicity when it was administered orally to animals.[21] However, the effects were significantly less than those of methyltestosterone.[21] Both DMAU and trestolone (7α-methyl-19-nortestosterone) showed potential signs of liver toxicity whereas 11β-methyl-19-nortestosterone 17β-dodecylcarbonate showed few to no such effects, suggesting that the C7α methyl group of DMAU and trestolone could be an important contributing factor to their liver toxicity potential.[21] In any case, however, in a clinical study, DMAU was found to be safe in terms of liver and kidney function when administered to men for a month.[5]
A pharmacokinetic study of DMAU in men found that only 2 to 3% of the drug was hydrolyzed into dimethandrolone when it was administered orally in the form of powder in capsules.[3] In contrast, hydrolysis of testosterone undecanoate into testosterone is rapid and appears to be complete.[3] The difference in conversion efficiency with DMAU relative to testosterone undecanoate is attributed to steric hindrance in DMAU caused by its additional C7α and C11β methyl groups.[3] Although the hydrolysis of DMAU into dimethandrolone was very limited, it was still sufficient to produce dose-dependent biological effects at the dosages assessed, including reversible suppression of luteinizing hormone and testosterone levels.[3] A subsequent pharmacokinetic study found that the conversion of DMAU into dimethandrolone was improved when the drug was delivered orally in castor oil/benzyl benzoate or a self-emulsifying drug delivery system contained in capsules as opposed to powder in capsules.[22]
^ abcUS 20030069215, Blye R, Kim H, "Methods of making and using 7a, 11b-dimethyl-17b-hydroxy-4-estren-3-one 17b-trans-4-n-butylcyclohexane carboxylate and 7a, 11b-dimethyl-17b-hydroxyestr-4-en-3-one 17-undecanoate.", assigned to US Department of Health and Human Services.
^Hurmuz P, Akyol F (1 August 2017). "The Role of Hormal Treatments in Prostate Cancer". In Hurmuz P, Akyol F, Gultekin M, Yazici G, Sari SY, Ozyigit G (eds.). Principles and Practice of Urooncology: Radiotherapy, Surgery and Systemic Therapy. Springer. pp. 334–. ISBN978-3-319-56114-1. The castrate level was defined as testosterone being less than 50 ng/dL (1.7 nmol/L), many years ago. However contemporary laboratory testing methods showed that the mean value after surgical castration is 15 ng/dL [1]. Thus, recently the level is defined as being less than 20 ng/dL (1 nmol/L).
^ abcCorona G, Rastrelli G, Vignozzi L, Maggi M (June 2012). "Emerging medication for the treatment of male hypogonadism". Expert Opinion on Emerging Drugs. 17 (2): 239–259. doi:10.1517/14728214.2012.683411. PMID22612692. S2CID22068249. However, also lumbar spine bone mineral density decreased in both groups, most probably because of insufficient MENT aromatization [104], limiting its potential for hormonal substitution in hypogonadal men.
^Wibowo E, Schellhammer P, Wassersug RJ (January 2011). "Role of estrogen in normal male function: clinical implications for patients with prostate cancer on androgen deprivation therapy". The Journal of Urology. 185 (1): 17–23. doi:10.1016/j.juro.2010.08.094. PMID21074215.
^Wibowo E, Wassersug RJ (September 2013). "The effect of estrogen on the sexual interest of castrated males: Implications to prostate cancer patients on androgen-deprivation therapy". Critical Reviews in Oncology/Hematology. 87 (3): 224–238. doi:10.1016/j.critrevonc.2013.01.006. PMID23484454.
^Nieschlag E, Kumar N, Sitruk-Ware R (March 2013). "7α-methyl-19-nortestosterone (MENTR): the population council's contribution to research on male contraception and treatment of hypogonadism". Contraception. 87 (3): 288–295. doi:10.1016/j.contraception.2012.08.036. PMID23063338.
^US 7820642, Blye RP, Kim HK, "Nandrolone 17β-carbonates.", issued 26 October 2010, assigned to US Department of Health and Human Services.
^US 5952319, Cook CE, Kepler JA, Lee YW, Wani MC, "Androgenic steroid compounds and a method of making and using the same", issued 14 September 1999, assigned to Research Triangle Institute.