From a University web site, see half-life at end
Methyltestosterone (Danocrine)
This information is from Clinical Pharmacology 1.9
Description: Methyltestosterone was developed synthetically in the search for an androgen that could be given orally, without loss of bioavailability. Mehyltestosterone is structurally similar to testosterone, except it is methylated at 17 position, which is associated with less hepatic metabolism following oral administration when compared to testosterone. Methyltestosterone is used in the management of congenital or acquired hypogonadism. Methyltestosterone may be considered appropriate therapy for pathological, delayed puberty, and it is effective as palliative treatment for carcinoma of the breast in postmenopausal women, acting as an antiestrogen. Anabolic steroids have been the subject of drug misuse and abuse, often producing adverse effects such as changes in libido, hepatotoxicity, increased risk of cardiovascular disease, and antisocial behavior. Some of the masculinizing effects in women can be irreversible. Methyltestosterone was first approved as a topical ointment (which has been withdrawn from the market) by the FDA in 1939. Oral forms became available beginning in 1940.
Mechanism of Action: The function of androgens in male development begins in the fetus, is crucial during puberty, and continues to play an important role in the adult male. Women also secrete small amounts of androgen from the ovaries. The secretion of androgens from the adrenal cortex is insufficient to maintain male sexuality.
Normally, endogenous androgens stimulate RNA polymerase, increasing protein production. These proteins are responsible for normal male sexual development, including the growth and maturation of the prostate, seminal vesicle, penis, and scrotum. During puberty, androgens cause a sudden increase in growth and development of muscle, with a redistribution of body fat. Changes associated with endogenous androgens also take place in the larynx and vocal cords, deepening the voice. Puberty is completed with beard development and growth of body hair. Fusion of the epiphyses and termination of growth is governed by the androgens, as is the maintenance of spermatogenesis. Androgens have a high lipid solubility, enabling them to rapidly enter cells of target tissues. Increased androgen plasma levels suppress gonadotropin-releasing hormone, reducing endogenous testosterone, luteinizing hormone, and follicle-stimulating hormone through a negative-feedback mechanism. Exogenous replacement therapy stimulates the above process when endogenous supply is inadequate.
Pharmacokinetics: Methyltestosterone is administered orally or via the buccal cavity. After administration via the buccal cavity, first-pass hepatic metabolism is bypassed. Bioavailability is roughly 50% after oral administration. Peak serum concentrations are achieved about 2 hours after tablet administration. Methyltestosterone has an elimination half-life of 2.5-3.5 hours, somewhat longer than that of testosterone. Excretion of glucuronide and sulfate conjugates is primarily renal; there is little excretion of unchanged drug. Small amounts are eliminated in the feces.