YK-11 10mg is a research compound oral tablet formulation supplied in a 50 tablet pack. Manufactured for consistent potency, stability, and laboratory applications.
Format50 Tablets
Concentration10mg
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YK-11 occupies an unusual position within the SARM research category, it is structurally a steroidal compound derived from DHT, technically classifying it as a synthetic steroid rather than a true non steroidal SARM like LGD-4033 or S23, yet it produces a SARM like partial androgen receptor agonist activity profile that has led to its common grouping alongside the SARM compound class in research literature. F40 Biotech’s formulation delivers 10mg per tablet in a 50 count format, consistent with the concentration most commonly referenced in preclinical YK-11 research.
YK-11’s most distinctive and research relevant characteristic is its documented activity as a myostatin inhibitor, a mechanism entirely separate from its androgen receptor binding activity and unique among CSD’s SARM range. Myostatin is a TGF-β superfamily member that functions as the primary negative regulator of skeletal muscle growth, similarly to the mechanism through which Follistatin 344 antagonizes myostatin signaling. YK-11 has been documented in preclinical research to increase follistatin expression while directly suppressing myostatin gene expression in muscle satellite cells, producing a dual mechanism where androgen receptor partial agonism and myostatin pathway suppression operate simultaneously through structurally and functionally independent pathways within the same compound.
This dual mechanism distinguishes YK-11’s research profile fundamentally from every other compound in CSD’s SARM range. LGD-4033 and S23 operate purely through androgen receptor binding selectivity without myostatin pathway involvement. YK-11’s myostatin suppression activity creates a direct mechanistic parallel to Follistatin 344’s research applications — both compounds are studied for their influence on the myostatin mediated brake on muscle growth, though through entirely different molecular approaches: Follistatin 344 sequesters myostatin directly as a binding protein, while YK-11 appears to suppress myostatin gene expression at the transcriptional level while simultaneously activating androgen receptor signaling through its steroidal DHT derived structure.
F40 Biotech formulations are stocked by Canada Steroid Depot following the same rigorous third party lab verification process applied to every product in our range. Each batch is tested for concentration accuracy and purity before being made available, with COA documentation available on request. CSD’s sourcing standards apply uniformly across all manufacturers we carry, and F40 Biotech’s YK-11 meets those standards consistently. All orders ship discreetly across Canada in plain, unmarked packaging with no identifying information on the exterior.
Store in a cool, dry place away from direct light and heat. Intended for research purposes only.
Commonly researched alongside Follistatin 344 in comparative myostatin pathway and muscle growth regulation studies. Browse CSD’s full SARM and peptide range for complete sourcing.
YK-11 is a synthetic steroidal compound with a dual mechanism that sets it apart from all other SARMs, it acts as both a partial androgen receptor agonist and a myostatin inhibitor. Myostatin (GDF-8) is a protein that limits muscle growth by inhibiting satellite cell proliferation and muscle fiber hypertrophy, suppressing myostatin removes the natural ceiling on muscle development. YK-11 is the only research compound that simultaneously activates androgen receptors in muscle and bone tissue while inhibiting myostatin; a combination that theoretically produces greater anabolic potential than androgen receptor activation alone. It is studied for lean mass accretion, strength enhancement, and bone density improvement, and is considered one of the most potent compounds in the SARM research catalogue.
Myostatin acts as a brake on muscle growth; limiting satellite cell activation, protein synthesis, and muscle fiber size through SMAD2/3 signaling pathway activation. By inhibiting myostatin, YK-11 removes this natural growth limitation, allowing muscle tissue to respond more aggressively to androgen receptor stimulation and mechanical loading than would be possible with androgen receptor activation alone. Research in myoblast cell cultures demonstrates that YK-11 increases follistatin expression; the primary endogenous myostatin antagonist at concentrations achievable with standard research doses. This dual androgen receptor agonism and myostatin inhibition makes YK-11 one of the most theoretically compelling anabolic research compounds available.
YK-11 has a half-life of approximately 6–10 hours, administered twice daily in research protocols for stable plasma levels. Morning and evening administration splitting the daily dose into two equal doses is the most common research schedule. Common research doses range from 10–20mg daily, a single 10mg tablet twice daily delivers 20mg total. The 50 tablet pack at 10mg provides 500mg total; sufficient for 25 days of research at 20mg daily (two tablets) or 50 days at 10mg daily. Research cycle duration typically ranges from 6–8 weeks for YK-11 protocols.
Yes! YK-11 produces meaningful HPG axis suppression through androgen receptor activation, though the degree of suppression is debated in the research literature due to limited human clinical data. Given its steroidal structure and potent androgen receptor activity, YK-11 is generally treated similarly to more suppressive SARMs such as LGD-4033 in terms of PCT requirements. A SERM based PCT protocol; Nolvadex 20 40mg daily for 4 weeks is commonly researched following YK-11 cycles. Blood work before and after the research cycle is strongly recommended to assess individual suppression response and guide PCT decisions.
Yes! This batch has been independently HPLC tested by an accredited third party laboratory confirming concentration accuracy at 10mg per tablet and compound identity as YK-11. A certificate of analysis is available.
