YK-11

YK-11, also written YK11 or YK 11, is a synthetic steroid: (17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester. Researchers at Toho University in Japan reported in 2011 that it is a partial agonist of the androgen receptor that might act as a selective androgen receptor modulator, or SARM (Kanno et al., 2011). In 2013 the same group reported that it raised expression of follistatin, a myostatin-binding protein, in C2C12 mouse myoblasts (Kanno et al., 2013).

The literature is small, almost all cell, rodent and anti-doping work, with no clinical trials.

PubChem also files separate stereoisomer records under the same CAS number, including a mixture of diastereomers (CID 72163177); YK-11 was first described in 2011 as a steroidal partial agonist of the androgen receptor (Kanno et al., 2011).

Published work on YK-11 falls into five areas. Each summary below states the model used. The record is small, fewer than 20 PubMed entries, and all data on its effects come from cell culture or rodents.

Androgen receptor pharmacology

In HEK293 cells engineered to express the androgen receptor, YK-11 activated an androgen response element reporter, but its maximal activity was only 10 to 20 percent of that of dihydrotestosterone (DHT), and at 5 and 10 micromolar it reduced DHT-driven activity. It moved the receptor into the nucleus without inducing the interaction between the receptor's N- and C-terminal domains that DHT produces.

In MDA-MB-453 breast cancer cells it induced some androgen target genes, such as FKBP51, as strongly as DHT, but not others, such as SARG (Kanno et al., 2011). A 2022 follow-up linked this gene selectivity to differences in DNA binding and cofactor recruitment (Kanno et al., 2022). A 2026 docking study predicted strong binding to the glucocorticoid and progesterone receptors as well, and cautioned that docking energies do not predict tissue selectivity (Mihalev et al., 2026). Models: human cell lines and computer docking.

Muscle cells, follistatin and myostatin

In C2C12 mouse myoblasts, YK-11 and DHT both increased myosin heavy chain, a marker of differentiation, and at 500 nM YK-11 raised the myogenic factors Myf5 and myogenin more than DHT did. YK-11, but not DHT, induced follistatin mRNA. An androgen receptor antagonist or receptor knockdown reduced that induction, and a neutralizing anti-follistatin antibody reversed the YK-11-driven myogenic differentiation (Kanno et al., 2013).

Follistatin matters because it blocks myostatin from binding its receptor, activin type IIB, and mice engineered to overexpress follistatin in muscle grow much larger muscles (Lee and McPherron, 2001). The C2C12 study measured follistatin, not myostatin itself. Model: mouse myoblast cell line.

Bone cells and bone repair

In MC3T3-E1 mouse osteoblast cells, YK-11 and DHT increased proliferation and mineralization, and YK-11 raised the differentiation markers osteoprotegerin and osteocalcin. An androgen receptor antagonist attenuated these effects. YK-11 also increased Akt phosphorylation, which the authors read as non-genomic androgen receptor signaling (Yatsu et al., 2018).

In bone marrow mesenchymal stem cells, 0.25 to 4 micromolar YK-11 increased osteogenic differentiation, and a hydrogel carrying YK-11 increased repair of cranial bone defects in rats. Androgen receptor inhibition suppressed both effects, and the authors pointed to BMP2/Smad signaling (Wang et al., 2025). Models: mouse osteoblast cell line, mesenchymal stem cells and rats.

Rodent studies of sepsis and the brain

In mice inoculated with gram-negative bacteria, myostatin and follistatin protein both rose in muscle. The authors called YK-11 a myostatin inhibitor and reported that it lowered pro-inflammatory cytokines and organ damage markers and reduced sepsis mortality (Lee et al., 2021). A Brazilian group gave male Wistar rats YK-11 over five weeks, alone or with swimming exercise.

In the hippocampus, the group reported oxidative stress and impaired mitochondrial function markers (Dahleh et al., 2023). A second paper reported higher IL-1β and IL-6, lower IL-10, reduced BDNF/TrkB/CREB signaling, activation of apoptotic proteins and impaired aversive memory consolidation (Dahleh et al., 2024). Exercise offset some of these changes, but not all. Models: mice and rats.

Metabolism and anti-doping detection

Under electrospray ionization, YK-11 readily loses methanol and other fragments in the ion source (Thevis et al., 2017). An excretion study with deuterium-labeled YK-11 found no intact compound in urine but 14 metabolites, with glucuronide and sulfate forms detectable for more than 48 hours.

In two Thoroughbred horses, parent YK-11 and seven phase I metabolites appeared in plasma (Harding et al., 2023), and the UCLA Olympic Analytical Laboratory has reported YK-11 in a doping control sample (Sobolevsky et al., 2024). Models: reference material, urine and plasma samples, and horses.