YK-11 is a synthetic steroidal compound that acts as a partial agonist of the androgen receptor. It was reported in the early 2010s by a Japanese university group (Kanno, Inouye and colleagues), and is usually grouped with the selective androgen receptor modulators (SARMs) even though most SARMs are nonsteroidal.
Researchers became interested in YK-11 for two reasons: it appeared to activate the androgen receptor in an unusual, gene-selective way, and in mouse muscle cells it raised expression of follistatin, a protein that binds myostatin. Its published literature is very small, it has never been developed as a drug, and it sits in the same regulatory and safety picture as other SARMs. This overview covers that context first, then the chemistry and the handful of cell studies behind the compound’s reputation.
At a glance
- Class: Synthetic steroidal SARM; partial androgen receptor agonist
- Origin: Kanno, Inouye and colleagues, Japan; first reports in the early 2010s
- Structure: C25H34O6; MW 430.5 g/mol; CAS 1370003-76-1
- Main research areas: Androgen receptor mechanism, myoblast differentiation and follistatin, osteoblast cell models, metabolism and anti-doping detection
- Regulatory status: Not approved by the FDA; never clinically developed; prohibited under WADA S1.2
Regulatory status and safety signals
YK-11 is not approved by the FDA for any use, and unlike several nonsteroidal SARMs, it has never entered registered clinical trials. There are no controlled human safety or pharmacokinetic data for it.
The FDA has addressed SARMs as a group. In 2017 the agency issued a public warning about body-building products containing SARMs, citing serious safety concerns including liver toxicity and a potential for increased risk of heart attack and stroke, and it has sent warning letters to companies selling SARMs as dietary supplements. The agency’s position is that SARMs are unapproved drugs, not lawful dietary supplement ingredients.
The medical literature now includes case reports and case series of drug-induced liver injury in people who took products sold as SARMs (Flores et al., 2020). Because YK-11 is a steroid rather than a nonsteroidal SARM, its liver and endocrine risk cannot be inferred from the clinical data on compounds such as enobosarm; for YK-11 there are simply no controlled data. Product quality adds a further problem: a 2017 analysis published in JAMA found that many products sold online as SARMs did not contain what their labels stated.
As an anabolic agent acting at the androgen receptor, YK-11 falls under section S1.2 (other anabolic agents) of the World Anti-Doping Agency’s Prohibited List, which is in force at all times.
Structure and origin
YK-11 keeps a four-ring steroid skeleton with a 3-keto A-ring, but in place of the simple 17β-hydroxyl group of testosterone or DHT it carries a heavily modified D-ring region: an oxygen-bridged ring fused at C17 and a methyl ester side chain. That region makes the molecule chemically less stable than a typical steroid, a point that matters for both storage and analysis.
The compound was designed as part of a search for steroidal ligands that would activate the androgen receptor without producing the full conformational change triggered by DHT. The original reports framed it as a gene-selective agonist: a ligand that switches on some androgen-responsive genes but not others.
Mechanism: what the research shows
When a full agonist such as DHT binds the androgen receptor, the receptor’s N-terminal domain folds back onto its ligand-binding domain. This N/C interaction stabilizes the active receptor and helps recruit coactivators. In transfected cell reporter assays, the Inouye group’s original reports described YK-11 as activating androgen receptor-driven transcription without inducing the N/C interaction, which is the basis for calling it a partial, gene-selective agonist.
In the group’s 2013 muscle cell study, the androgen receptor antagonist flutamide blocked the effects of YK-11, indicating that its activity in that system runs through the receptor rather than an unrelated target (Kanno et al., 2013). A later report from the same group extended the work to MC3T3-E1 mouse pre-osteoblast cells, again using androgen receptor-dependent readouts.
Key areas of study
Myoblast differentiation in C2C12 cells
The best-known YK-11 study used C2C12 mouse myoblasts, a standard model for muscle cell differentiation. YK-11 increased expression of the myogenic regulatory factors MyoD, Myf5 and myogenin, and induced differentiation more strongly than DHT under the same conditions (Kanno et al., 2013). These are cell-culture readouts of gene expression and differentiation markers.
Follistatin as a downstream mediator
In the same study, YK-11 raised follistatin expression in C2C12 cells, while DHT did not. Adding an antibody that neutralized follistatin reduced the YK-11-induced differentiation, suggesting that follistatin, and by extension reduced myostatin signaling, contributed to the effect in this model (Kanno et al., 2013). This finding is the source of much of the later interest in the compound, but it rests on one cell line in one laboratory.
Liver safety in the SARM case literature
Clinical case reports of liver injury after SARM-labeled products have made hepatotoxicity a research question for the whole category (Flores et al., 2020). Published cases often involve multi-ingredient or mislabeled products, so they rarely isolate a single compound. For YK-11 specifically, no mechanistic liver toxicology has been published.
Metabolism and detection
Because the modified D-ring region is labile, YK-11 is extensively broken down in biological samples. Anti-doping laboratories have therefore studied its metabolites to find markers that can be detected after the parent compound has disappeared, using mass spectrometry. This analytical work is one of the more active parts of the YK-11 literature.
What the evidence does not show
Almost everything known about YK-11’s biology comes from a few cell-culture papers from one research group. There are no published controlled animal studies establishing its pharmacokinetics, tissue selectivity, or long-term toxicology, and no human studies of any kind. The follistatin finding has not been widely replicated, and C2C12 differentiation in a dish is not a measure of muscle in an organism. The compound’s instability raises the question of how much of any in vivo effect would come from YK-11 itself rather than its breakdown products. The “myostatin inhibitor” label sometimes attached to YK-11 overstates the data: the evidence is increased follistatin expression in one cell line.
Handling and storage in the lab
YK-11 capsules should be kept sealed at room temperature (20–25°C), away from heat, moisture and light. Given the compound’s chemical lability, keep the pouch closed between uses to limit exposure to humidity.
Sourcing and documentation
Rogue Compounds has YK-11 made in small batches. Every batch is tested by an independent U.S. lab and the batch COA is on the product page and in the COA Library.
References
- Kanno Y, et al. Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression. Biol Pharm Bull. 2013;36(9):1460-1465. PMID 23995658
- Flores JE, Chitturi S, Walker S. Drug-induced liver injury by selective androgenic receptor modulators. Hepatol Commun. 2020;4(3). PMID 32140660
Research use only. Rogue Compounds products are sold strictly for laboratory research. They are not for human or veterinary use, and nothing in this article is medical advice. The studies cited here describe published research, not this product or any use of it.