Injectable YK-11 700mg vial
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Reconstitution and bench supplies researchers pair with Injectable YK-11 700mg vial
NOT FOR HUMAN CONSUMPTION
YK-11 is a steroidal selective androgen-receptor modulator (SARM) first described in academic screens of AR-active compounds. Unlike many non-steroidal SARMs, YK-11 behaves as a partial AR agonist that strongly up-regulates follistatin (FST), thereby antagonizing myostatin/activin-A (ActRIIB–SMAD2/3) signaling, a pathway that restrains skeletal-muscle growth. The compound has no approved medical use, no published human PK, and remains a research chemical. It is prohibited in sport as an anabolic agent.
Additional Benefits of YK-11 Now Under Investigation
| Benefit | Key take-aways |
|---|---|
| 1 Myostatin–follistatin axis modulation | YK-11 increases follistatin expression via AR-dependent transcription, neutralizing myostatin/activin and de-repressing hypertrophy programs. <br/><em>Biochem Biophys Res Commun; J Steroid Biochem Mol Biol</em> |
| 2 Myogenic differentiation & hypertrophy (cells) | In C2C12 myoblasts, YK-11 accelerates myotube formation, enlarges myotube diameter, and up-regulates MyoD/Myogenin. <br/><em>Skeletal Muscle; Molecular Endocrinology</em> |
| 3 mTOR anabolism / anti-catabolic shift | Downstream of myostatin blockade: ↑ mTOR/S6K, ↓ FoxO → ↓ MAFbx/MuRF1, favoring net protein synthesis. <br/><em>AJP-Endocrinology; FASEB J</em> |
| 4 Osteoblast signaling (in vitro) | Steroidal AR agonism promotes osteoblast differentiation (↑ RUNX2/OSX) and mineralization markers in cell systems, preclinical only. <br/><em>Bone; JBMR</em> |
| 5 Satellite-cell milieu (hypothesis) | Follistatin up-shift may support Pax7⁺ satellite-cell activation and repair kinetics; direct in-vivo evidence for YK-11 is limited. <br/><em>Development; Stem Cell Reports</em> |
| 6 Fat-mass reduction (indirect) | Anabolism and myostatin restraint shift partitioning toward lean mass with secondary fat-mass signals in models; no robust in-vivo YK-11 body-comp data. <br/><em>Metabolism; Obesity</em> |
| 7 Tendon/connective-tissue remodeling (theory) | Myostatin blockade can modify ECM/collagen programs; clinical implications for tendon stiffness/fragility remain theoretical. <br/><em>J Orthop Res; Matrix Biology</em> |
| 8 Rehab synergy | Conceptually additive with resistance training/nutrition due to AR + myostatin pathways; data for YK-11 specifically are absent in humans. <br/><em>Sports Med; J Physiol</em> |
| 9 Doping-control relevance | Anti-doping labs report YK-11 metabolites enabling multi-week detection; positives tied to “SARM” products. <br/><em>Drug Testing & Analysis</em> |
2. Molecular Mechanism of Action
2.1 Receptor Pharmacodynamics
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AR partial agonist (steroidal): Binds AR, drives a ligand-specific co-activator profile; less classical AR transactivation than DHT.
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Follistatin transcription: AR-dependent induction of FST, which binds and neutralizes myostatin/activin A, relieving SMAD2/3 repression.
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Functional result: Dual pathway, AR anabolism plus myostatin-pathway disinhibition.
2.2 Down-stream Biology
| Pathway | Functional outcome | Context |
|---|---|---|
| AR → FST↑ → ActRIIB/SMAD2/3↓ | Myostatin blockade; hypertrophy programs released | Skeletal muscle |
| mTOR/S6K/4E-BP1 | ↑ Protein synthesis, myofiber hypertrophy | Muscle |
| FoxO → MAFbx/MuRF1↓ | ↓ Proteolysis (anti-catabolic) | Catabolic stress |
| RUNX2/OSX (AR-osteoblast) | ↑ Osteoblastogenesis, mineralization markers | Bone |
3. Pharmacokinetics
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Route: Marketed only as research-use oral material; no clinical PK.
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Half-life/bioavailability: Unknown in humans; steroidal scaffold suggests hepatic metabolism and high protein binding.
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Metabolites/detection: Urinary metabolites are characterized for anti-doping assays.
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Implication: Retail dosing claims are unsupported by peer-reviewed PK.
4. Pre-clinical and Translational Evidence
4.1 Cell systems
Original reports show AR-dependent FST up-regulation, myotube hypertrophy, and SMAD2/3 repression in myogenic cells.
4.2 Animal data
Scarce publicly available in-vivo YK-11 datasets; most supportive evidence for myostatin blockade outcomes comes from other FST/ActRIIB interventions, not YK-11 itself.
4.3 Human data
None from controlled trials. Real-world “supplement” reports are anecdotal and confounded by adulteration/co-ingestants.
Evidence quality note: YK-11’s efficacy/safety profile is based primarily on in-vitro biology and class inferences. Robust animal and human studies are lacking.
5. Emerging Clinical Interests
| Field | Rationale | Current status |
|---|---|---|
| Sarcopenia/frailty | AR anabolism + myostatin restraint | Concept only |
| Cachexia | Anti-catabolic + FST up-shift | Preclinical rationale |
| Muscular dystrophies | Myostatin pathway relevance | Theoretical/indirect |
| Osteopenia | AR-osteoblast signals | In-vitro rationale |
| Rehabilitation | Potential to speed lean-mass regain | Hypothesis only |
6. Safety and Tolerability
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Human safety: Unknown, no clinical datasets.
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Endocrine: As an AR-active steroidal agent, expect HPG-axis suppression (↓ LH/FSH/testosterone) with recovery taking weeks–months after cessation.
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Lipids: SARM-class pattern of HDL-C ↓ (± LDL/TG ↑) is plausible, no formal YK-11 data.
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Hepatic: Case reports of hepatotoxicity exist with unregulated “SARM” products; risk for YK-11 is undetermined but credible given class/steroidal chemistry.
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Dermatologic/androgenic: Acne, oily skin, hair shedding possible.
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Musculoskeletal (theoretical): Rapid strength gains under myostatin restraint could outpace tendon/ECM adaptation, raising injury risk.
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Neuropsych: Stimulatory/irritability/insomnia are anecdotal in uncontrolled settings.
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Drug interactions: Unknown; presume hepatic enzyme interactions are possible. Contraindicated in pregnancy.
Comparative safety matrix
| Concern | YK-11 | LGD-4033 | Enobosarm (MK-2866) |
|---|---|---|---|
| Mechanism | Steroidal AR partial agonist + FST↑ | Non-steroidal AR agonist | Non-steroidal AR agonist |
| Human trials | None | Small RCT (21 d) | Multiple Phase 2 |
| HPG suppression | Likely strong | Moderate | Moderate |
| Lipid effects | Unknown (likely adverse) | HDL ↓ common | HDL ↓ common |
| Myostatin pathway | Direct via FST | No | No |
7. Regulatory Landscape
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Approvals: None (not a medicine).
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Sport: Banned at all times (WADA S1, other anabolic agents; and as a non-approved substance).
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Market: Appears on research-chemical sites; purity/adulteration problems are frequent.
8. Future Directions
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First-in-human PK/PD with GMP material (exposure, metabolites, dose–response).
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Mechanistic biomarkers: Circulating myostatin, follistatin, SMAD2/3 phosphorylation, IGF-1, and DXA/MRI muscle CSA; strength/function endpoints (1RM, stair-climb power).
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Safety program: Liver, lipids, endocrine recovery, ECG, and tendon injury surveillance.
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Comparative trials: YK-11 vs non-steroidal SARMs to test added value of myostatin-axis engagement.
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Medicinal chemistry: Separate AR and myostatin activities to improve benefit–risk; explore tissue-targeteddelivery.
Selected References
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Kanno Y. et al. Androgen-receptor–dependent induction of follistatin and suppression of myostatin signaling.Biochem Biophys Res Commun; J Steroid Biochem Mol Biol.
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Myogenesis & hypertrophy: Skeletal Muscle; Molecular Endocrinology, AR-linked myogenic differentiation and mTOR activation paradigms.
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Bone/osteoblast AR signaling: Bone; Journal of Bone and Mineral Research.
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Catabolic gene control (MAFbx/MuRF1): AJP-Endocrinology; FASEB Journal.
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Anti-doping analytics: Drug Testing & Analysis, YK-11 metabolite identification and detection windows.
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ECM/tendon considerations under myostatin modulation: Matrix Biology; Journal of Orthopaedic Research.
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