Home Compounds Body Composition YK-11
Body Composition Research Emerging

YK-11

Steroidal SARM with unique dual mechanism: androgen receptor partial agonist AND myostatin inhibitor via follistatin induction. Studied for exceptional anabolic potential with potentially lower androgenic side effects than testosterone. Research compound only.

SARMmyostatinfollistatinandrogen receptoranabolicbody compositionresearch
Half-life
6–10 hours estimated from steroidal pharmacology
SKUs
1
Evidence
Emerging

YK11 is a synthetic compound that is often described as a SARM (selective androgen receptor modulator), but its actual pharmacology is more complex — research suggests it may function primarily as a myostatin inhibitor through a mechanism distinct from classic SARMs. It has been studied for muscle growth in cell culture and animal research, but has not been tested in human clinical trials. It is not FDA-approved and its safety profile in humans is unknown.

Myostatin Inhibition Research
YK11 has been shown in cell culture studies to inhibit myostatin — the protein that limits how large muscles can grow. Unlike myostatin antibodies or follistatin-based approaches that block myostatin externally, YK11 appears to work inside muscle cells by reducing follistatin-related gene expression inhibition, effectively telling cells to produce more follistatin, which then neutralizes myostatin locally.
Androgen Receptor Research
YK11 does bind to the androgen receptor, which classifies it structurally as a SARM. Cell studies show it activates androgen receptor signaling in muscle and bone, similar to testosterone, but with a distinct downstream signaling profile. This dual mechanism — AR activation plus myostatin inhibition — is what distinguishes it from standard SARMs.
Bone Research
Cell culture studies have examined YK11 effects on bone cells, showing it may activate pathways involved in bone mineral density and bone formation through androgen receptor activation.
  • Cell culture studies show myostatin inhibition and androgen receptor activation.
  • Greater muscle cell growth observed in vitro compared to DHT (a potent androgen) at equivalent concentrations.
  • Bone cell studies suggest potential bone-forming activity.
  • No animal studies with comprehensive safety and efficacy data published.
  • No human clinical trials — safety and efficacy in people are entirely unknown.

YK11's research base is almost entirely cell culture studies — the lowest level of evidence in the research hierarchy. There are essentially no published animal studies with proper safety or efficacy evaluation, and zero human clinical trials. The extraordinary lack of in vivo data means there is no pharmacokinetic data, no dose-response data in living organisms, and no toxicology data of any kind from controlled studies. Claims about YK11's effects in humans are entirely speculative. This is among the least evidence-supported compounds in the broader SARM and muscle research space.

Testosterone and other androgens signal through the androgen receptor inside muscle and bone cells, activating genes that promote growth and maintenance. YK11 activates the androgen receptor similarly, but with a subtly different signaling signature — it recruits slightly different cofactor proteins to the receptor, which may change which genes get activated. Separately, YK11 appears to promote the expression of follistatin inside muscle cells. Follistatin neutralizes myostatin — the natural growth-limiting signal for muscle. By increasing follistatin, YK11 may effectively release the brake on muscle growth from inside the cell, rather than blocking myostatin externally as drugs like ACE-031 attempt to do. Whether either of these effects is meaningful in a living organism at safe doses has not been tested.

YK11 has no published human clinical trial data and no comprehensive animal safety studies. As a compound that activates the androgen receptor, it would be expected to carry risks similar to other androgenic compounds — including effects on natural testosterone production suppression, potential liver effects, and cardiovascular considerations. The actual risk profile is unknown because it has never been properly evaluated. It is not FDA-approved and is not legal to sell as a supplement or drug. Research use carries the highest level of uncertainty of any compound in this category.

Emerging

This compound is in early-stage research. Evidence is limited to small studies or in vitro data.

Published Research Ranges
No established human research doses; animal and in vitro studies only; case reports of 5–10mg/day in experimental contexts
Research Context Only: These are ranges reported in published scientific studies for educational reference. They are not dosing recommendations. This is not medical advice. Always consult a qualified healthcare professional.

Sources listed here are from the platform research library. All links open the original publication. No citations are generated by AI.

YK11 Induces Myogenic Differentiation and Activates the Androgen Receptor
Biological & Pharmaceutical Bulletin • 2011  • DOI: 10.1248/bpb.34.318
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YK11 Inhibits Myostatin by Promoting Follistatin Expression in Differentiated Myotubes
Biological & Pharmaceutical Bulletin • 2013  • DOI: 10.1248/bpb.b12-01016
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The Potential of SARMs and Antimyostatin Agents in Addressing Lean Body Mass Loss From GLP-1 Agonists: A Literature Review
 • 2025  • DOI: 10.1111/1753-0407.70119
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Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression
 • 2025  • DOI: 10.34133/research.0977
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Systematic Review of Safety of Selective Androgen Receptor Modulators in Healthy Adults: Implications for Recreational Users
 • 2023  • DOI: 10.3390/jox13020017
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Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF
 • 2023  • DOI: 10.3389/fcvm.2023.1149065
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Selective androgen receptor modulators: the future of androgen therapy?
 • 2020  • DOI: 10.21037/tau.2019.11.02
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A SARM a Day Keeps the Weakness Away: A Computational Approach for Selective Androgen Receptor Modulators (SARMs) and Their Interactions with Androgen Receptor and 5‑Alpha Reductase Proteins
 • 2025  • DOI: 10.1021/acsomega.5c02504
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World Congress on Osteoporosis, Osteoarthritis and Musculoskeletal Diseases (WCO-IOF-ESCEO 2025)
 • 2025  • DOI: 10.1007/s40520-025-03119-z
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Myostatin antisense administration prevents sepsis-induced muscle atrophy and weakness in male mice
 • 2025  • DOI: 10.14814/phy2.70566
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YK11 promotes osteogenic differentiation of BMSCs and repair of bone defects
 • 2025  • DOI: 10.1530/jme-24-0073
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Social Interest Data as a Proxy for Off-Label Performance-Enhancing Drug Use: Implications and Clinical Considerations
 • 2024  • DOI: 10.7759/cureus.52011
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YK11 induces oxidative stress and mitochondrial dysfunction in hippocampus: The interplay between a selective androgen receptor modulator (SARM) and exercise
 • 2023  • DOI: 10.1016/j.jsbmb.2023.106364
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Ostarine-Induced Myogenic Differentiation in C2C12, L6, and Rat Muscles
 • 2022  • DOI: 10.3390/ijms23084404
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Differential DNA-binding and cofactor recruitment are possible determinants of the synthetic steroid YK11-dependent gene expression by androgen receptor in breast cancer MDA-MB 453 cells
 • 2022  • DOI: 10.1016/j.yexcr.2022.113333
View Source
Selective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1 Cells
 • 2018  • DOI: 10.1248/bpb.b17-00748
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Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression
 • 2013  • DOI: 10.1248/bpb.b13-00231
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(17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester (YK11) is a partial agonist of the androgen receptor
 • 2011  • DOI: 10.1248/bpb.34.318
View Source
From gains to gaps? How Selective Androgen Receptor Modulator (SARM) YK11 impact hippocampal function: In silico, in vivo, and ex vivo perspectives
 • 2024  • DOI: 10.1016/j.cbi.2024.110971
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Studies on the in vivo metabolism of the SARM YK11: Identification and characterization of metabolites potentially useful for doping controls
 • 2018  • DOI: 10.1002/dta.2527
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Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases
 • 2024  • DOI: 10.1038/s41392-024-01756-w
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Sarcopenia and Cardiovascular Diseases
 • 2023  • DOI: 10.1161/circulationaha.123.064071
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Molecular Mechanisms of Inflammation in Sarcopenia: Diagnosis and Therapeutic Update
 • 2022  • DOI: 10.3390/cells11152359
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Medicinal Use of Testosterone and Related Steroids Revisited
 • 2021  • DOI: 10.3390/molecules26041032
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Cancer Cachexia: Definition, Staging, and Emerging Treatments
 • 2020  • DOI: 10.2147/cmar.s261585
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Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments
 • 2020  • DOI: 10.3389/fendo.2020.00568
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Mechanisms Underlying Metabolic Syndrome-Related Sarcopenia and Possible Therapeutic Measures
 • 2019  • DOI: 10.3390/ijms20030647
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PGC-1α as a Pivotal Factor in Lipid and Metabolic Regulation
 • 2018  • DOI: 10.3390/ijms19113447
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Circulating Testosterone as the Hormonal Basis of Sex Differences in Athletic Performance
 • 2018  • DOI: 10.1210/er.2018-00020
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Sarcopenia: assessment of disease burden and strategies to improve outcomes
 • 2018  • DOI: 10.2147/cia.s149232
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Safety, pharmacokinetics and pharmacological effects of the selective androgen receptor modulator, GSK2881078, in healthy men and postmenopausal women
 • 2017  • DOI: 10.1111/bcp.13316
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Effects of enobosarm on muscle wasting and physical function in patients with cancer: a double-blind, randomised controlled phase 2 trial
 • 2013  • DOI: 10.1016/s1470-2045(13)70055-x
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The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men
 • 2013  • DOI: 10.1093/gerona/gls078
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Pharmacological management of cachexia in adult cancer patients: a systematic review of clinical trials
 • 2018  • DOI: 10.1186/s12885-018-5080-4
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Cellular zinc metabolism and zinc signaling: from biological functions to diseases and therapeutic targets
 • 2024  • DOI: 10.1038/s41392-023-01679-y
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Sarcopenia in chronic kidney disease: from bench to bedside
 • 2023  • DOI: 10.3904/kjim.2022.338
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Understanding Cancer Cachexia and Its Implications in Upper Gastrointestinal Cancers
 • 2022  • DOI: 10.1007/s11864-022-01028-1
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Metastasis-Initiating Cells and Ecosystems
 • 2021  • DOI: 10.1158/2159-8290.cd-21-0010
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Cancer Cachexia: Its Mechanism and Clinical Significance
 • 2021  • DOI: 10.3390/ijms22168491
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Cancer-Mediated Muscle Cachexia: Etiology and Clinical Management
 • 2021  • DOI: 10.1016/j.tem.2021.03.007
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Targeting autophagy to overcome drug resistance: further developments
 • 2020  • DOI: 10.1186/s13045-020-01000-2
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Muscle Wasting and Sarcopenia in Heart Failure-The Current State of Science
 • 2020  • DOI: 10.3390/ijms21186549
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Pancreatic Cancer and Cachexia-Metabolic Mechanisms and Novel Insights
 • 2020  • DOI: 10.3390/nu12061543
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TFEB dysregulation as a driver of autophagy dysfunction in neurodegenerative disease: Molecular mechanisms, cellular processes, and emerging therapeutic opportunities
 • 2019  • DOI: 10.1016/j.nbd.2018.05.012
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Selective Androgen Receptor Modulators: Current Knowledge and Clinical Applications
 • 2019  • DOI: 10.1016/j.sxmr.2018.09.006
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New insights into the pathogenesis and treatment of sarcopenia in chronic heart failure
 • 2019  • DOI: 10.7150/thno.33000
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Functions of autophagy in the tumor microenvironment and cancer metastasis
 • 2018  • DOI: 10.1111/febs.14388
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Development of selective androgen receptor modulators (SARMs)
 • 2018  • DOI: 10.1016/j.mce.2017.06.013
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Contribution of STAT3 to Inflammatory and Fibrotic Diseases and Prospects for its Targeting for Treatment
 • 2018  • DOI: 10.3390/ijms19082299
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Innate Immunity in the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome and Its Implications for Therapy
 • 2018  • DOI: 10.3389/fimmu.2018.00595
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Deterioration of Limb Muscle Function during Acute Exacerbation of Chronic Obstructive Pulmonary Disease
 • 2018  • DOI: 10.1164/rccm.201703-0615ci
View Source
Skeletal muscle aging: influence of oxidative stress and physical exercise
 • 2017  • DOI: 10.18632/oncotarget.14670
View Source
Cancer-induced muscle wasting: latest findings in prevention and treatment
 • 2017  • DOI: 10.1177/1758834017698643
View Source
Research priorities in cancer cachexia: The University of Rochester Cancer Center NCI Community Oncology Research Program Research Base Symposium on Cancer Cachexia and Sarcopenia
 • 2017  • DOI: 10.1097/spc.0000000000000301
View Source
Study Design and Rationale for the Phase 3 Clinical Development Program of Enobosarm, a Selective Androgen Receptor Modulator, for the Prevention and Treatment of Muscle Wasting in Cancer Patients (POWER Trials)
 • 2016  • DOI: 10.1007/s11912-016-0522-0
View Source
Anamorelin hydrochloride for the treatment of cancer-anorexia-cachexia in NSCLC
 • 2015  • DOI: 10.1517/14656566.2015.1041500
View Source
Interaction between Muscle and Bone
 • 2014  • DOI: 10.11005/jbm.2014.21.1.29
View Source
Sarcopenia and Androgens: A Link between Pathology and Treatment
 • 2014  • DOI: 10.3389/fendo.2014.00217
View Source
Androgen effects on skeletal muscle: implications for the development and management of frailty
 • 2014  • DOI: 10.4103/1008-682x.122581
View Source
Glucocorticoid-induced skeletal muscle atrophy
 • 2013  • DOI: 10.1016/j.biocel.2013.05.036
View Source

60 sources · Platform research library · Not generated by AI

YK11

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Research Education Only: This profile is for educational purposes only. All information is sourced from published scientific literature. This is not medical advice. Not for human consumption. Consult qualified medical professionals for any health decisions.