Pharmacodynamics Like other AAS,<unk>  is an agonist of the androgen receptor, similar to androgens such as testosterone and DHT. The relative binding affinity of<unk>  for the androgen receptor is about 0.8% of that of metribolone. Activation of the androgen receptor stimulates protein synthesis, which increases muscle growth, lean body mass, and bone mineral density. Compared to testosterone and many other AAS,<unk>  is less androgenic relative to its strength as an anabolic.<unk>  has about 322 to 633% of the anabolic potency and 24% of the androgenic potency of methyltestosterone. Similarly,<unk>  has as much as 6 times the anabolic potency of testosterone and has significantly reduced androgenic potency in comparison. The reduced ratio of anabolic to androgenic activity of<unk>  often motivates its medical use in children and women because less androgenic effect implies less risk of virilization. The bodybuilding community also considers this fact when choosing between AAS. As<unk>  is already 5α-reduced, it is not a substrate for 5α-reductase, hence is not potentiated in androgenic tissues such as the skin, hair follicles, and prostate gland. This is involved in its reduced ratio of anabolic to androgenic activity. Due to the substitution of one of the carbon atoms with an<unk> ygen atom at the C2 position in the A ring,<unk>  is resistant to inactivation by 3α-hydroxysteroid dehydrogenase in skeletal muscle. This is in contrast to DHT, and is thought to underlie the preserved anabolic potency with<unk> . Because it is 5α-reduced,<unk>  is not a substrate for aromatase, hence cannot be aromatized into metabolites with estrogenic activity.<unk>  similarly possesses no progestogenic activity.<unk>  is, uniquely, far less hepatotoxic than other 17α-alkylated AAS, which may be due to differences in metabolism. Pharmacokinetics The oral bioavailability of<unk>  is 97%. Its plasma protein binding is 94 to 97%. The drug is metabolized primarily by the kidneys and to a lesser extent by the liver.<unk>  is the only AAS that is not primarily or extensively metabolized by the liver, and this is thought to be related to its diminished hepatotoxicity relative to other AAS. Its elimination half-life is reported as 9.4 to 10.4 hours, but is extended to 13.3 hours in the elderly. About 28% of an oral dose of<unk>  is eliminated unchanged in the urine and 3% is excreted in the feces.
Oxandrolone
Norethandrolone
Nandrolone
Gestrinone
Nandrolone propionate
Allenestrol
Mestanolone
Androstanolone