YK‑11 (Myostatin Inhibitor SARM)
Synthetic steroidal-like SARM, the ONLY compound with a dual mechanism: AR agonist + myostatin pathway inhibitor (follistatin upregulation, Kanno 2013 PMID 23291286). UGL marketed for 'natural-cap breaking' – BUT hepatotoxicity signals + 17α-steroid-like profile. WADA-banned.
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WHAT IS YK-11 (MYOSTATIN INHIBITOR SARM)?
Detailed overview
YK-11 (chemically close to a 17α-(methoxycarbonyl)-5α-androst-(17,3:17,1)-bis-pyranone-like steroid scaffold, NOT a classic non-steroidal SARM!) is a synthetic steroid-derivative-based selective androgen receptor modulator developed by Kanno and colleagues in 2011 (Kanno 2011 PMID 21893547). It is unique among SARMs for two reasons: (1) structurally steroid-like (NOT an aryl-propionamide like RAD/LGD/Ostarine), a 5α-androstane scaffold with 17α-methoxycarbonyl substitution; (2) dual mechanism: AR agonist (in vitro AR-binding ~50% of testosterone) + myostatin pathway inhibitor via follistatin upregulation (Kanno 2013 PMID 23291286) in C2C12 myoblast cells – blocks the natural-cap-like myostatin-mediated muscle mass limitation. No clinical trial as of 2024 (Phase 0 in vitro + rat bioassay only). On the bodybuilding market UGL marketed for 'natural-cap breaking' (myostatin mechanism hype) – BUT Yatsu 2018 PMID 30005896 in vitro re-testing called the scalability of the follistatin effect in vivo in humans into question. Hepatotoxicity risk: due to the 17α-steroid-like scaffold a profile similar to 17α-alkylated steroids is expected (Solomon 2019 PMID 31077635 SARM-DILI review – 2 documented YK-associated hepatocellular injury cases). WADA-banned year-round (S1.2 – other anabolic agents). Does NOT aromatize (Δ4,9-triene structural block).
Mechanism
Steroidal SARM (5α-androstane scaffold) + myostatin pathway inhibitor (follistatin upregulation)
Clinical precedent
Phase 0 in vitro only (Kanno 2011/2013, Yatsu 2018). No Phase I/II/III in humans.
Anabolic activity
AR binding ~50% testosterone (in vitro) + myostatin block dual effect
Half-life
~6-10 h (oral, estimated)
Legal status
Never an Rx. UGL 'research chemical'. WADA-banned S1.2.
Data console
Lab data
Safety
Side effects, stop signs, contraindications
Side effects · 7
- Hepatotoxicity (liver injury): the 17alpha-methoxycarbonyl steroidal scaffold gives a profile similar to 17alpha-alkylated oral AAS, with ALT/AST elevation and documented SARM-associated drug-induced liver injury (DILI) cases.
- HPTA suppression: suppression of endogenous testosterone production (reduced LH/FSH), which can cause lowered libido, fatigue and post-cycle hypogonadism, requiring PCT.
- Adverse lipid profile: marked drop in HDL (good cholesterol), typical of oral androgenic compounds, increasing cardiovascular risk.
- Androgenic side effects: per anecdotal reports, acne, increased oiliness and possible hair loss in androgen-sensitive individuals (due to AR-agonist activity).
- Neuropsychiatric effects: anecdotal user reports of aggression, irritability, insomnia and libido fluctuations.
- No water retention / dry effect: it does not aromatize (Delta-4,9-triene configuration), so there is no estrogen-mediated water retention, though the dryness may anecdotally cause joint discomfort.
- Adulteration / contamination risk: on the gray market it is often substituted with or contaminated by methylstenbolone (a cheaper 17alpha-methyl prohormone), causing different and unpredictable toxicity. An HPLC-tested source is mandatory.
Contraindications · 7
- Pregnancy, breastfeeding and women in general: due to AR-agonist activity, risk of potentially irreversible virilization (voice deepening, hirsutism) and fetal harm; strongly contraindicated in women of childbearing age.
- Pre-existing liver dysfunction or elevated ALT/AST: absolute contraindication given the steroidal hepatotoxicity, when baseline liver values are raised.
- Concurrent alcohol use or other hepatotoxic agents: risk of cumulative liver injury; alcohol and other liver-burdening drugs should be avoided during the cycle.
- Stacking with other SARMs or 17alpha-alkylated oral AAS: not advised due to cumulative hepatotoxicity and lipid toxicity.
- Planned fatherhood / fertility concerns: HPTA suppression can temporarily impair spermatogenesis, with full recovery taking up to 3-6 months.
- Competitive athletes: banned year-round by WADA (S1.2, other anabolic agents), detectable in urine for 3-5 weeks; will cause an anti-doping violation.
- Pre-existing cardiovascular disease or dyslipidemia: the marked HDL drop can further worsen the lipid profile and raise cardiovascular risk.
Related Performance Compounds
Same therapeutic category
Studies
Related research and clinical findings
Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression.
Kanno Y, Ota R, Someya K, Bochimoto H, Kondo S, Inouye Y
Pharmacokinetics and pharmacodynamics of LGD-3303 [9-chloro-2-ethyl-1-methyl-3-(2,2,2-trifluoroethyl)-3H-pyrrolo-[3,2-f]quinolin-7(6H)-one], an orally available nonsteroidal-selective androgen receptor modulator.
Vajda EG, López FJ, Rix P, Hermann R, Allan G
LGD-4033 and a Case of Drug-Induced Liver Injury: Exploring the Clinical Implications of Off-Label Selective Androgen Receptor Modulator Use in Healthy Adults.
Labban H, Kwait B, Paracha A, Khan A, Singh M, Lopez R
Selective androgen receptor modulator use and related adverse events including drug-induced liver injury: Analysis of suspected cases.
Leciejewska N, Jędrejko K, Gómez-Renaud VM, Manríquez-Núñez J, Muszyńska B, Pokrywka A
Myostatin: A Skeletal Muscle Chalone.
Lee SJ
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The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.