YK-11

YK-11 (CAS 1370003-76-1; molecular formula C₂₅H₃₄O₆; molar mass 430.5 g/mol) is a synthetic steroidal compound first characterized by Kanno et al. in 2011 as a partial agonist of the androgen receptor (AR). Unlike full AR agonists such as dihydrotestosterone (DHT), YK-11 does not induce the N-terminal domain/activation function 1 (NTD/AF1) and ligand-binding domain/activation function 2 (LBD/AF2) interaction that is required for complete receptor transactivation. This gene-selective partial activation is the basis for its classification as a SARM.

A second, mechanistically distinct pathway was described by Kanno et al. in 2013. In C2C12 mouse myoblast cultures, YK-11 treatment — but not equimolar DHT — induced robust expression of follistatin (Fst), a glycoprotein that binds and neutralizes myostatin. Myostatin (GDF-8) is a TGF-beta family member that functions as a negative regulator of skeletal muscle mass. When researchers applied an anti-follistatin antibody to the cultures, the YK-11-mediated enhancement of myogenic differentiation was abolished, demonstrating that follistatin induction is the principal driver of its anabolic effects in that model rather than AR activation alone.

A third pathway was identified in a 2025 rat model study (Wang et al.), in which YK-11 promoted osteogenic differentiation of bone marrow stromal cells (BMSCs) via the BMP2/Smad signaling axis; blocking the AR eliminated this effect, confirming receptor dependence for the osseous arm of activity.

• AR partial agonism: selective gene activation without full NTD-LBD interaction • Follistatin induction: indirectly suppresses myostatin, relieving a brake on myofibrillar growth • BMP2/Smad activation: promotes osteoblastic differentiation in preclinical bone models

All efficacy evidence for YK-11 derives from in vitro cell culture experiments and small-animal models. No human clinical trials have been registered or published as of mid-2026.

The foundational in vitro work consists of two papers by Kanno and colleagues published in Biological and Pharmaceutical Bulletin. The 2011 study (PMID 21372378) established that YK-11 is a partial AR agonist in cell-based reporter assays and exhibits anabolic activity in C2C12 myoblasts exceeding that of DHT at equivalent concentrations. The 2013 study (PMID 23995658) demonstrated in the same myoblast model that YK-11 upregulates the myogenic regulatory factors MyoD, Myf5, and myogenin more strongly than DHT, and that this enhancement is follistatin-dependent.

A 2021 mouse study (Lee et al., PMID 33588136; Biochemical and Biophysical Research Communications, DOI 10.1016/j.bbrc.2021.01.030) used a gram-negative bacterial sepsis model in rodents. Myostatin protein levels were elevated in septic animals; treatment with YK-11 reduced circulating pro-inflammatory cytokines and markers of organ damage and was associated with a lower mortality rate. The authors proposed that myostatin inhibition by YK-11 may mitigate sepsis-associated muscle wasting and systemic inflammation. Exact animal numbers were not reported in the abstract.

A 2025 study (Wang et al., PMID 39660819; Journal of Molecular Endocrinology, DOI 10.1530/JME-24-0073) examined YK-11 in rat BMSC cultures and a cranial bone defect model. Concentrations of 0.25–4 µM promoted osteogenic differentiation in a dose-dependent manner, and local application of 0.5–1 mg/mL improved healing of surgically created skull defects in vivo, with effects linked to the BMP2/Smad pathway.

On the analytical side, Piper et al. (2018, PMID 30379415, Drug Testing and Analysis) characterized 14 deuterated urinary metabolites following administration of deuterium-labeled YK-11, with glucuronidated and sulfated conjugates detectable for more than 48 hours. Sobolevsky et al. (2024, PMID 37946705, Drug Testing and Analysis) reported the first confirmed detection of YK-11 in a real doping control sample at the UCLA Olympic Analytical Laboratory, documenting its actual use by a competitive athlete.

In summary, the evidence base is entirely preclinical and analytical. No randomized trials, observational cohort studies, or controlled case series in humans exist.

Typical dosage: Research protocols (varies).

No clinically established dosing regimen exists for YK-11. The compound has never been studied in human pharmacokinetic, pharmacodynamic, or efficacy trials, and regulatory agencies including Health Canada have stated it is not authorized for any therapeutic use.

Reported protocols in unregulated community and bodybuilding contexts — derived entirely from self-reported anecdotal accounts on forums and supplement-oriented websites, not from controlled studies — describe the following patterns:

• Beginners: 5 mg orally per day, often taken as a single morning dose, for 4–6 weeks • Intermediate to advanced users: 10–15 mg per day, sometimes divided into two doses approximately 12 hours apart to attempt to maintain more stable plasma levels given the compound's estimated short half-life • Cycle length: most anecdotal reports describe cycles of 4–8 weeks, after which a post-cycle therapy (PCT) protocol with a selective estrogen receptor modulator (e.g., clomiphene or tamoxifen) is often described, reflecting user awareness of hypothalamic-pituitary-gonadal axis suppression

Doses above 15 mg/day appear rarely in community reports, and several users who have described higher doses also report more pronounced androgenic and hepatic side effects.

The compound is sold as a liquid or powder "for research use only" and product purity is unverified, introducing further uncertainty about actual dosing.

This information is provided for educational and harm-reduction reference only. It does not constitute medical advice, and no dose of YK-11 has been validated for safety or efficacy in humans. Consult a qualified healthcare provider before considering any use of unapproved compounds.

No compound-specific stability data has been identified for this peptide. The general lyophilized-peptide handling framework applies — see Storage & handling for temperature, reconstitution diluent, and beyond-use dating principles.

All combination practices described below are anecdotal; no controlled or observational research exists on YK-11 in multi-compound regimens.

In bodybuilding communities, YK-11 is most frequently reported to be stacked with other SARMs or growth-promoting agents on the basis of perceived complementary mechanisms. Common anecdotal pairings include:

• YK-11 with RAD-140 (testolone): users cite dual AR modulation with the aim of compounding anabolic signaling; this combination is reported to produce pronounced androgenic side effects including marked testosterone suppression • YK-11 with MK-677 (ibutamoren, a ghrelin mimetic): the rationale is that MK-677 raises growth hormone and IGF-1 levels, which users expect to amplify myostatin inhibition downstream; the combination is anecdotal only • YK-11 with LGD-4033 (ligandrol): positioned as a bulking stack; no pharmacological interaction data exist

The mechanistic argument for combining YK-11 with a non-steroidal SARM or a GH secretagogue is plausible in very general terms (independent signaling pathways), but the absence of any human pharmacology data means that synergy, additive toxicity, and drug-drug interactions are entirely unknown. Community reports of increased liver enzyme elevations and more severe hypothalamic-pituitary-gonadal suppression with multi-compound stacks containing YK-11 are consistent with what would be expected from combining androgenic agents, though these remain unverified anecdotes.

YK-11 is not currently FDA-approved for any indication. It is generally classified as a research compound. Regulatory status varies by country.

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Reported side effects: Limited human studies

No formal human safety studies for YK-11 have been published. The following is derived from structural reasoning, animal model data, analytical chemistry findings, and anecdotal community reports; the overall safety profile in humans is unknown.

Potential hepatotoxicity: YK-11 is a 17-alpha-alkylated steroidal structure, a chemical feature associated with first-pass hepatic stress in the oral anabolic steroid class. No liver biopsy case reports attributable specifically to YK-11 have been published in peer-reviewed literature, but the structural concern is well-grounded. Anecdotal reports of elevated liver enzymes (AST, ALT) circulate in bodybuilding communities, particularly at doses above 10 mg/day or when combined with other hepatically metabolized compounds.

Hypothalamic-pituitary-gonadal (HPG) axis suppression: as a partial AR agonist with demonstrable anabolic potency, YK-11 is expected to suppress endogenous testosterone via negative feedback. Community reports describe reduced libido, testicular atrophy, and mood disturbances during and after cycles.

Androgenic effects: despite SARM labeling, YK-11's steroidal backbone carries inherent androgenic activity. Anecdotal reports include accelerated androgenic alopecia in genetically susceptible individuals, acne, and increased aggression.

Other anecdotally reported effects: joint pain and tendon discomfort, fatigue, and headaches.

Regulatory context: Health Canada (2022) classified YK-11-containing supplements as unauthorized and warned of risks including cardiac events, stroke, and liver damage. The World Anti-Doping Agency lists YK-11 explicitly as a prohibited anabolic agent (S1 class) for all athletes subject to the World Anti-Doping Code; its presence in a doping control sample has been confirmed in a peer-reviewed publication (Sobolevsky et al., 2024).

Contraindications (by structural analogy): hormone-sensitive cancers, active hepatic disease, cardiovascular disease, pregnancy, and use by minors. Long-term effects are entirely unknown.