YK-11

Etki Mekanizması

YK-11 exerts its effects through two distinct but complementary pathways. First, it acts as a partial agonist of the androgen receptor (AR). In C2C12 myoblast cell culture studies, YK-11 induced androgen receptor-dependent gene transcription at levels comparable to DHT for certain target genes, but with partial rather than full agonist activity. This partial agonism may theoretically confer some degree of tissue selectivity, though this has never been demonstrated in vivo. Second, and more uniquely, YK-11 stimulates the expression of follistatin in muscle cells. Follistatin is an endogenous glycoprotein that binds and inhibits myostatin (GDF-8), a member of the TGF-beta superfamily that acts as a potent negative regulator of skeletal muscle mass. By increasing follistatin levels, YK-11 may effectively reduce myostatin signaling, thereby removing a biological brake on muscle hypertrophy. In the original Kanno et al. study, YK-11-treated C2C12 cells showed significantly greater follistatin expression than cells treated with DHT alone, and this effect was blocked by an androgen receptor antagonist, indicating the follistatin induction is AR-dependent. The 17-alpha alkylation of YK-11's steroidal structure provides oral bioavailability but also subjects it to hepatic first-pass metabolism, with the associated risk of liver stress characteristic of 17-alpha alkylated compounds. Due to the complete absence of in vivo pharmacokinetic data, the compound's actual bioavailability, distribution, metabolism, and elimination profile in living systems remain unknown.