Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of AC-262536 and YK-11 — mechanism, side effects, legal status, and pricing.
AC-262536 is a non-peptide nonsteroidal selective androgen receptor modulator (SARM) with an azabicyclooctane naphthalene-carbonitrile structure. It acts as a partial AR agonist, showing tissue-selective anabolic effects in preclinical models. No human trials have been conducted, and it is not FDA-approved. SARMs are prohibited in athletic competition under WADA category S1.2.
YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM) — a 19-nor DHT-derived analog with a spiro-dioxolane modification at C-17, structurally distinct from non-steroidal SARMs. It is not FDA-approved for any human use and is prohibited in competitive sport; anti-doping laboratories actively screen for YK-11 metabolites. No human safety, tolerability, or efficacy trials exist; the only published human study administered deuterated YK-11 solely to identify urinary metabolites for doping-control method development.
AC-262536
YK-11
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
AC-262536
YK-11
COA corpus from Disclosed Labs — independently tested batches only.
AC-262536
No COA data yet.
Submit testing data →YK-11
3
COAs
99.2%
Avg purity
2
Labs
No human data exist. All pharmacology derives from a single 2008 preclinical publication. In castrated male rats dosed chronically for two weeks, AC-262536 significantly increased levator ani muscle growth and suppressed elevated luteinizing hormone, while producing only weak effects on prostate and seminal vesicle weight compared to testosterone. The compound has also been included in validated analytical panels for SARM residue surveillance in bovine muscle tissue, reflecting its presence in food-safety monitoring rather than therapeutic development.
No human safety, tolerability, or efficacy trials exist for YK-11. The only published human study administered six-fold deuterated YK-11 to volunteers solely to identify urinary metabolites for anti-doping method development; no intact parent compound was recovered in urine, and 14 metabolites (unconjugated, glucuronidated, sulfated) were characterized. In vitro (mouse C2C12 myoblasts), YK-11 (1–500 nM) increased myosin heavy chain and myogenic regulatory factor expression more strongly than equimolar DHT and uniquely induced follistatin, a pathway necessary for its pro-differentiation effect. In vivo (mouse model of gram-negative bacterial sepsis), YK-11 reduced circulating pro-inflammatory cytokines and organ-damage markers, decreased sepsis mortality, and was associated with protection against sepsis-induced muscle wasting.
AC-262536 and YK-11 are both in the Performance category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing