YK-11
Myostatin Inhibitor & SARM Hybrid | Experimental
Community Research
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YK-11 is a steroidal compound that occupies a unique position among selective androgen receptor modulators (SARMs) due to its dual mechanism of action: it functions as both a partial agonist of the androgen receptor and an inhibitor of myostatin through upregulation of follistatin. First described by Kanno et al. in 2011, YK-11 was identified in cell-based assays as a compound that selectively activates androgen-responsive gene transcription while simultaneously inducing follistatin expression, a glycoprotein that binds and neutralizes myostatin, a negative regulator of muscle growth. Unlike all other commercially known SARMs, YK-11 possesses a steroidal backbone structurally related to dihydrotestosterone (DHT), making its classification as a traditional SARM debatable. It is more accurately described as a steroidal SARM hybrid with myostatin-inhibiting properties. The research base for YK-11 is extremely limited. All published data comes from in vitro (cell culture) studies only. There are no animal studies, no pharmacokinetic studies, and no human clinical trials. As a result, virtually everything reported about YK-11's effects in living organisms, its half-life, optimal dosing, and side effect profile, is derived from structural analogy to related compounds, theoretical pharmacology, and anecdotal user reports. YK-11 is not approved for any medical use and is classified as an investigational research chemical.
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.
Molecular Data
Research Indications
YK-11's dual mechanism of AR agonism and myostatin inhibition theoretically positions it as a potent anabolic compound for increasing lean muscle mass. Cell culture data supports increased anabolic signaling and follistatin expression. However, there is no in vivo or clinical evidence confirming these effects in animals or humans. All efficacy reports are anecdotal.
Users anecdotally report significant strength gains during YK-11 cycles, consistent with the compound's theoretical mechanism of action. The combination of AR-mediated protein synthesis and myostatin inhibition could theoretically support enhanced force production. No controlled studies exist to verify these claims.
The most distinctive proposed benefit of YK-11 is its ability to upregulate follistatin and thereby inhibit myostatin-mediated limitations on muscle growth. In cell culture, YK-11 induced greater follistatin expression than DHT. If this translates to in vivo activity, it could allow muscle growth beyond normal physiological limits. This remains entirely unproven outside of cell-based assays.
Follistatin has been shown in other research contexts to positively influence bone mineral density and bone formation. If YK-11's follistatin-inducing effects translate in vivo, there could be secondary benefits for bone density. This is entirely speculative and unsupported by any direct YK-11 bone data.
Dosing Protocols
YK-11 is administered exclusively via the oral route. It is available as a liquid solution (typically in PEG-400 or similar carrier) or in capsule form from research chemical suppliers. Due to its 17-alpha alkylated steroidal structure, it has sufficient oral bioavailability to be effective when taken by mouth. The estimated half-life of 6-10 hours (based on structural analogy rather than pharmacokinetic studies) necessitates twice-daily dosing to maintain more stable plasma concentrations throughout the day.
| Goal | Dose | Frequency | Route |
|---|---|---|---|
| Research Dose - Conservative | 5 mg/day (2.5 mg AM + 2.5 mg PM) | Twice daily (split AM/PM) | Oral (liquid or capsule) |
| Research Dose - Moderate | 10 mg/day (5 mg AM + 5 mg PM) | Twice daily (split AM/PM) | Oral (liquid or capsule) |
| Research Dose - Upper Range | 15 mg/day (7.5 mg AM + 7.5 mg PM) | Twice daily (split AM/PM) | Oral (liquid or capsule) |
Interactions
What to Expect
Side Effects & Safety
Common Side Effects
- Liver stress and enzyme elevation (ALT, AST) due to 17-alpha alkylated steroidal structure
- Testosterone suppression (dose- and duration-dependent, expected in all users)
- Joint dryness and discomfort (related to reduced estrogenic activity and potential drying effect)
- Hair shedding (consistent with androgenic activity from the DHT-derived structure; may or may not be reversible)
- Lipid disruption (HDL suppression, LDL elevation)
- Reduced libido and mood changes secondary to hormonal suppression
- Mild headaches, particularly during the first week
Stop Signs - Discontinue if:
- Jaundice (yellowing of skin or eyes) indicating significant liver injury
- Dark-colored urine (potential sign of liver damage)
- Severe or persistent abdominal pain, nausea, or vomiting
- Severe lethargy unresponsive to rest (may indicate profound suppression or liver stress)
- Chest pain, tightness, or palpitations
- Signs of allergic reaction: rash, swelling, difficulty breathing
Contraindications
- Pre-existing liver disease or elevated liver enzymes at baseline (17-alpha alkylated compounds are contraindicated in hepatic impairment)
- Hormone-sensitive cancers (prostate cancer or other androgen-responsive malignancies)
- Pregnancy or potential pregnancy (teratogenic risk from androgen receptor agonism and hormonal disruption)
- Breastfeeding
- Age under 25 (incomplete endocrine system maturation and higher risk of lasting HPG axis disruption)
- Concurrent use of other hepatotoxic compounds or medications (oral steroids, certain NSAIDs, statins, etc.)
- Known cardiovascular disease (insufficient safety data)
Quality Checklist
Good Signs
- Third-party lab tested with certificate of analysis (COA) showing purity above 98%
- Clearly labeled with compound name, concentration, batch number, and expiration date
- Solution is clear and free of particulate matter or discoloration
- Supplier provides HPLC or mass spectrometry verification of identity and purity
- Sold as a research chemical with appropriate disclaimers
Warning Signs
- No third-party testing or certificate of analysis available
- Sold in pre-made capsules without verifiable dosing accuracy
- Marketed with explicit muscle-building or performance enhancement claims
- Concentration claims that vary between batches
- Unusually low pricing compared to established research chemical suppliers
Bad Signs
- Cloudy, discolored, or precipitated solution indicating degradation or contamination
- No labeling, incorrect labeling, or missing batch/lot information
- Supplier has no verifiable reputation, reviews, or testing history
- Product tested by independent labs showing underdosed, mislabeled, or contaminated contents
- Contains unlisted active ingredients or adulterants
- Sold by a source that also sells controlled substances
References
- Selective Androgen Receptor Modulator, YK11, Regulates Myogenic Differentiation of C2C12 Myoblasts by Follistatin ExpressionKanno, Y., Hikosaka, R., Zhang, S.Y., et al.Biological and Pharmaceutical Bulletin (2011)
First published study on YK-11. Demonstrated that YK-11 induces myogenic differentiation of C2C12 myoblast cells through androgen receptor-dependent follistatin expression. YK-11-treated cells showed greater follistatin induction than DHT-treated cells, suggesting a unique dual mechanism of anabolic action.
- YK11 Effect on Myostatin and Follistatin Expression: A Novel Mechanism for a Selective Androgen Receptor ModulatorKanno, Y., Ota, R., Someya, K., et al.Biological and Pharmaceutical Bulletin (2013)
Follow-up study confirming that YK-11 increases follistatin expression in C2C12 cells in a dose-dependent manner and that this effect is mediated through the androgen receptor. Provided additional evidence for YK-11's role as a myostatin inhibitor acting via follistatin upregulation.
- Selective Androgen Receptor Modulators: Current Knowledge and Clinical ApplicationsNarayanan, R., Coss, C.C., Dalton, J.T.Sexual Medicine Reviews (2018)
Comprehensive review of SARM pharmacology and clinical development. Discusses the broader SARM class including tissue selectivity mechanisms, preclinical and clinical data, and regulatory status. Provides context for understanding YK-11 within the wider landscape of investigational androgen receptor modulators.
- Drug-Induced Liver Injury Associated with the Use of Selective Androgen Receptor ModulatorsFlores, J.E., Chitturi, S., Walker, N.I.Hepatology Communications (2020)
Case series documenting clinically significant drug-induced liver injury in individuals using SARMs. Relevant to YK-11 given its 17-alpha alkylated structure, which poses a higher theoretical hepatotoxicity risk than nonsteroidal SARMs. Highlights the importance of liver function monitoring during any SARM use.
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Disclaimer
This information is for educational and research purposes only. Consult a healthcare professional before use.