Pharmacodynamics Like other AAS,<unk>  is an agonist of the androgen receptor (AR). It is not a substrate for 5α-reductase (as it is already 5α-reduced) and is a poor substrate for 3α-hydroxysteroid dehydrogenase (3α-HSD), and therefore shows a high ratio of anabolic to androgenic activity. As a DHT derivative,<unk>  is not a substrate for aromatase and hence cannot be aromatized into estrogenic metabolites. However, uniquely among DHT derivatives,<unk>  is nonetheless associated with relatively high estrogenicity, and is known to have the potential to produce estrogenic side effects such as gynecomastia (rarely) and water retention. It has been suggested that this may be due to direct binding to and activation of the estrogen receptor by<unk> .<unk>  does not possess any significant progestogenic activity. Pharmacokinetics There is limited information available on the pharmacokinetics of<unk> . It appears to be well-absorbed with oral administration.<unk>  has very low affinity for human serum sex hormone-binding globulin (SHBG), less than 5% of that of testosterone and less than 1% of that of DHT. The drug is metabolized in the liver by oxidation at the C2 position, reduction at the C3 position, hydroxylation at the C17 position, and conjugation. The C2 hydroxymethylene group of<unk>  can be cleaved to form mestanolone (17α-methyl-DHT), which may contribute to the effects of<unk> . The elimination half-life of<unk>  is unknown.<unk>  and its metabolites are eliminated in the urine.
Oxymetholone
Metenolone
Oxendolone
Trestolone
Fluocinonide
Methylstenbolone
Mometasone
Trenbolone acetate