Skip to product information
A transparent glass vial filled with clear liquid, labeled ‘YK-11 70 mg/mL – Batch No.002 – 17-07-2025,’ sealed with a gray rubber stopper and matte aluminum cap, set against a soft beige background
1/2
Injectable YK-11 700mg vial

Injectable YK-11 700mg vial

€90,00 EUR
Taxes included.

                                        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

  • AR partial agonist (steroidal): Binds AR, drives a ligand-specific co-activator profile; less classical AR transactivation than DHT.

  • Follistatin transcription: AR-dependent induction of FST, which binds and neutralizes myostatin/activin A, relieving SMAD2/3 repression.

  • 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

  • Route: Marketed only as research-use oral material; no clinical PK.

  • Half-life/bioavailability: Unknown in humans; steroidal scaffold suggests hepatic metabolism and high protein binding.

  • Metabolites/detection: Urinary metabolites are characterized for anti-doping assays.

  • 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

  • Human safety: Unknown—no clinical datasets.

  • Endocrine: As an AR-active steroidal agent, expect HPG-axis suppression (↓ LH/FSH/testosterone) with recovery taking weeks–months after cessation.

  • Lipids: SARM-class pattern of HDL-C ↓ (± LDL/TG ↑) is plausible—no formal YK-11 data.

  • Hepatic: Case reports of hepatotoxicity exist with unregulated “SARM” products; risk for YK-11 is undetermined but credible given class/steroidal chemistry.

  • Dermatologic/androgenic: Acne, oily skin, hair shedding possible.

  • Musculoskeletal (theoretical): Rapid strength gains under myostatin restraint could outpace tendon/ECM adaptation, raising injury risk.

  • Neuropsych: Stimulatory/irritability/insomnia are anecdotal in uncontrolled settings.

  • 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

  • Approvals: None (not a medicine).

  • Sport: Banned at all times (WADA S1, other anabolic agents; and as a non-approved substance).

  • Market: Appears on research-chemical sites; purity/adulteration problems are frequent.

8. Future Directions

  • First-in-human PK/PD with GMP material (exposure, metabolites, dose–response).

  • Mechanistic biomarkers: Circulating myostatin, follistatin, SMAD2/3 phosphorylation, IGF-1, and DXA/MRI muscle CSA; strength/function endpoints (1RM, stair-climb power).

  • Safety program: Liver, lipids, endocrine recovery, ECG, and tendon injury surveillance.

  • Comparative trials: YK-11 vs non-steroidal SARMs to test added value of myostatin-axis engagement.

  • Medicinal chemistry: Separate AR and myostatin activities to improve benefit–risk; explore tissue-targeteddelivery.

Selected References

  • Kanno Y. et al. Androgen-receptor–dependent induction of follistatin and suppression of myostatin signaling.Biochem Biophys Res Commun; J Steroid Biochem Mol Biol.

  • Myogenesis & hypertrophy: Skeletal Muscle; Molecular Endocrinology — AR-linked myogenic differentiation and mTOR activation paradigms.

  • Bone/osteoblast AR signaling: Bone; Journal of Bone and Mineral Research.

  • Catabolic gene control (MAFbx/MuRF1): AJP-Endocrinology; FASEB Journal.

  • Anti-doping analytics: Drug Testing & Analysis — YK-11 metabolite identification and detection windows.

  • ECM/tendon considerations under myostatin modulation: Matrix Biology; Journal of Orthopaedic Research.