YK-11

Overview

YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM) — a 19-nor DHT-derived analog with a spiro-dioxolane modification at C-17, structurally distinct from non-steroidal SARMs. It is not FDA-approved for any human use and is prohibited in competitive sport; anti-doping laboratories actively screen for YK-11 metabolites. No human safety, tolerability, or efficacy trials exist; the only published human study administered deuterated YK-11 solely to identify urinary metabolites for doping-control method development.

Mechanism of Action

YK-11 acts as a partial androgen receptor (AR) agonist in mouse C2C12 myoblasts, activating AR without inducing the classical N/C-terminal interaction that full agonists like DHT produce. Distinct from DHT, YK-11 induces expression of follistatin, an endogenous myostatin antagonist; this follistatin induction is AR-dependent (blocked by AR antagonist flutamide and by AR knockdown) and is required for YK-11's enhancement of myogenic differentiation. Myostatin inhibition is therefore indirect — via AR-driven follistatin upregulation — rather than direct binding or antagonism of myostatin.

Research Summary

No human safety, tolerability, or efficacy trials exist for YK-11. The only published human study administered six-fold deuterated YK-11 to volunteers solely to identify urinary metabolites for anti-doping method development; no intact parent compound was recovered in urine, and 14 metabolites (unconjugated, glucuronidated, sulfated) were characterized. In vitro (mouse C2C12 myoblasts), YK-11 (1–500 nM) increased myosin heavy chain and myogenic regulatory factor expression more strongly than equimolar DHT and uniquely induced follistatin, a pathway necessary for its pro-differentiation effect. In vivo (mouse model of gram-negative bacterial sepsis), YK-11 reduced circulating pro-inflammatory cytokines and organ-damage markers, decreased sepsis mortality, and was associated with protection against sepsis-induced muscle wasting.

Vendors selling YK-11

Scored vendors carrying YK-11, ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Reported Side Effects

• No human safety or adverse-event data exist
• Prohibited in competitive sport; actively screened in anti-doping testing
• Class-level concerns (hepatic strain, HPG-axis suppression) are biologically plausible but not directly demonstrated for YK-11
• Not FDA-approved; not a legal dietary supplement ingredient in the US
• Widely sold by online vendors as 'research chemical, not for human consumption' — no evidence of identity, purity, or safety

Compare YK-11 with Others

Research References

• YK-11, PubChem Compound Summary for CID 119058028.
• Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression. 2013. PMID 23995658.
• Myostatin inhibitor YK11 as a preventative health supplement for bacterial sepsis. 2021. PMID 33588136.
• Studies on the in vivo metabolism of the SARM YK11: Identification and characterization of metabolites potentially useful for doping controls. 2018. PMID 30379415.

Frequently asked questions

Has YK-11 been independently lab-tested?

Disclosed Labs has collected 3 Certificates of Analysis (COA) for YK-11 from 2 independent testing labs. 1 vendor has submitted material for testing. Products average 99.2% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/yk-11/testing.

What is the average purity of YK-11 on the market?

Based on 3 COAs analyzed by Disclosed Labs, YK-11 products average 99.2% (±0.4%) tested purity. Individual vendor results vary; see per-vendor COA data at https://www.disclosedlabs.com/peptides/yk-11/coas.

Where can researchers source YK-11?

1 vendor with Disclosed Labs trust grades currently list YK-11, including Kimera Chems. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/yk-11.

How does YK-11 work?

YK-11 acts as a partial androgen receptor (AR) agonist in mouse C2C12 myoblasts, activating AR without inducing the classical N/C-terminal interaction that full agonists like DHT produce. Distinct from DHT, YK-11 induces expression of follistatin, an endogenous myostatin antagonist; this follistatin induction is AR-dependent (blocked by AR antagonist flutamide and by AR knockdown) and is required for YK-11's enhancement of myogenic differentiation. Myostatin inhibition is therefore indirect — via AR-driven follistatin upregulation — rather than direct binding or antagonism of myostatin.

What does the research say about YK-11?

No human safety, tolerability, or efficacy trials exist for YK-11. The only published human study administered six-fold deuterated YK-11 to volunteers solely to identify urinary metabolites for anti-doping method development; no intact parent compound was recovered in urine, and 14 metabolites (unconjugated, glucuronidated, sulfated) were characterized. In vitro (mouse C2C12 myoblasts), YK-11 (1–500 nM) increased myosin heavy chain and myogenic regulatory factor expression more strongly than equimolar DHT and uniquely induced follistatin, a pathway necessary for its pro-differentiation effect. In vivo (mouse model of gram-negative bacterial sepsis), YK-11 reduced circulating pro-inflammatory cytokines and organ-damage markers, decreased sepsis mortality, and was associated with protection against sepsis-induced muscle wasting.