Mesterolone is used in the treatment of androgen deficiency in male hypogonadism, anemia, and to support male fertility among other indications. It has also been used to treat delayed puberty in boys. Because it lacks estrogenic effects, mesterolone may be indicated for treating cases of androgen deficiency in which breast tenderness or gynecomastia is also present. The drug is described as a relatively weak androgen with partial activity and is rarely used for the purpose of androgen replacement therapy, but is still widely used in medicine. Mesterolone is used in androgen replacement therapy at a dosage of 50 to 100 mg 2 to 3 times per day.
Non-medical uses
Mesterolone has been used for physique- and performance-enhancing purposes by competitive athletes, bodybuilders, and powerlifters.
Side effects
s of mesterolone include virilization among others.
Pharmacology
Pharmacodynamics
Like other AAS, mesterolone is an agonist of the androgen receptor. It is not a substrate for 5α-reductase, as it is already 5α-reduced, and hence is not potentiated in so-called "androgenic" tissues such as the skin, hair follicles, and prostate gland. Mesterolone is described as a very poor anabolic agent due to inactivation by 3α-hydroxysteroid dehydrogenase in skeletal muscletissue, similarly to DHT and mestanolone. In contrast, testosterone is a very poor substrate for 3α-HSD, and so is not similarly inactivated in skeletal muscle. Because of its lack of potentiation by 5α-reductase in "androgenic" tissues and its inactivation by 3α-HSD in skeletal muscle, mesterolone is relatively low in both its androgenic potency and its anabolic potency. However, it does still show a greater ratio of anabolic activity to androgenic activity relative to testosterone. Mesterolone is not a substrate for aromatase, and so cannot be converted into an estrogen. As such, it has no propensity for producing estrogenic side effects such as gynecomastia and fluid retention. It also has no progestogenic activity. Because mesterolone is not 17α-alkylated, it has little or no potential for hepatotoxicity. However, its risk of deleterious effects on the cardiovascular system is comparable to that of several other oral AAS.
Pharmacokinetics
The C1α methyl group of mesterolone inhibits its hepatic metabolism and thereby confers significant oral activity, although its oral bioavailability is still much lower than that of 17α-alkylated AAS. In any case, mesterolone is one of the few non-17α-alkylated AAS that is active with oral ingestion. Uniquely among AAS, mesterolone has very high affinity for human serum sex hormone-binding globulin, about 440% that of DHT in one study and 82% of that of DHT in another study. As a result, it may displace endogenous testosterone from SHBG and thereby increase free testosterone concentrations, which may in part be involved in its effects.
Mesterolone was developed in the 1960s and was first described by 1966. It was introduced for medical use by Schering under the brand name Proviron by 1967. The well-established brand name Proviron had previously been used by Schering for testosterone propionate starting in 1936. Following the introduction of mesterolone as Proviron, Schering continued to market testosterone propionate under the brand name Testoviron. A number of sources incorrectly state that mesterolone was synthesized or introduced for medical use in 1934.
Society and culture
Generic names
Mesterolone is the generic name of the drug and its,,, and, while mestérolone is its.
Brand names
Mesterolone is marketed mainly under the brand name Proviron.
In one small scale clinical trial of depressed patients, an improvement of symptoms which included anxiety, lack of drive and desire was observed. In patients with dysthymia, unipolar, and bipolar depression significant improvement was observed. In this series of studies, mesterolone lead to a significant decrease in luteinizing hormone and testosterone levels. In another study, 100 mg mesterolone cipionate was administered twice monthly. With regards to plasma testosterone levels, there was no difference between the treated versus untreated group, and baseline luteinizing hormone levels were minimally affected.