In addition, MGA was marketed for veterinary use in dogs in 1969 in the United Kingdom and in 1974 in the United States.Progesterone was first found to be effective in the treatment of endometrial hyperplasia in 1951, and progestins were first found to be effective in the treatment of endometrial cancer in 1959. MGA was reported to be effective in the treatment of endometrial hyperplasia in the mid-1960s. It first started to be studied as a treatment for endometrial cancer in 1967, with findings published in 1973. MGA was reportedly introduced for the treatment of endometrial cancer in the United States in 1971. Progesterone was studied in the treatment of breast cancer in 1951 and 1952, but with relatively modest results. MGA was first studied in the treatment of breast cancer in 1967, and was one of the first progestins to be evaluated for the treatment of this disease. A second study was conducted in 1974. A "breakthrough" and surge of interest in progestins for breast cancer occurred in 1978 when a study using a massive dosage of medroxyprogesterone acetate to treat breast cancer was published. A third study of MGA for breast cancer was published in 1980, and this was followed by additional studies in the 1980s and beyond. MGA was approved for the treatment of breast cancer in the United States by at least 1983.Progestogens, including progesterone and ethisterone, were studied in the treatment prostate cancer in 1949. MGA was first studied in the treatment of prostate cancer in 1970.
In spite of these results, however, this combination has been very rarely used to treat prostate cancer in the United States.The antigonadotropic as well as anticorticotropic effects of MGA may be involved in its effectiveness in the treatment of postmenopausal breast cancer via substantially decreasing gonadal and adrenal production of sex steroids and by extension circulating levels of estrogens, by about 80%. Androgenic and antiandrogenic activity
MGA is a weak partial agonist of the androgen receptor (AR). It has been reported to bind to this receptor with 5% of the affinity of the anabolic steroid metribolone. Despite its weak intrinsic activity at the AR, at clinical doses in humans, MGA appears to behave, for all intents and purposes, purely as an antiandrogen. This is based on the fact that no virilizing side effects have been observed with the use of MGA in patients of either sex at dosages up to as high as 1,600 mg per day, the highest that has been assessed. Furthermore, MGA produces detectable androgenic effects in animals only at a dose that is the equivalent of approximately 200 times that typically used for the treatment of prostate cancer in men. However, the medication does have moderate androgenic effects on serum lipids in humans, causing a significant reduction of HDL and LDL cholesterol levels and no change in triglyceride levels at a dosage of only 5 mg/day. Conversely, MGA does not decrease SHBG levels.