Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of ACP-105 and YK-11 — mechanism, side effects, legal status, and pricing.
ACP-105 is a non-peptide nonsteroidal selective androgen receptor modulator (SARM) of the azabicyclooctane chemotype, structurally related to AC-262536 and RAD140. It acts as a partial agonist at the androgen receptor with tissue-selective anabolic effects demonstrated in preclinical models. ACP-105 is not an approved drug in any jurisdiction and has never entered human clinical trials. SARMs as a class are prohibited at all times under WADA Prohibited List S1.2 'Other Anabolic Agents'; ACP-105 falls under this class-wide ban and has been the subject of equine anti-doping metabolite-detection research.
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.
ACP-105
YK-11
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
ACP-105
YK-11
COA corpus from Disclosed Labs — independently tested batches only.
ACP-105
2
COAs
99.3%
Avg purity
1
Labs
YK-11
3
COAs
99.2%
Avg purity
2
Labs
No human data exist for ACP-105. In castrated male rats, 2-week oral dosing improved anabolic parameters consistent with tissue-selective partial AR agonism, suppressed the LH surge, and produced levator ani muscle anabolic effects. In female mice (whole-body irradiated and sham-irradiated), ACP-105 preserved rotorod sensorimotor performance impaired by radiation and enhanced cued fear conditioning while reducing MAP-2 immunoreactivity in sensorimotor cortex. In male gonadectomized 3xTg-AD Alzheimer's-model mice, ACP-105 alone reduced anxiety-like behavior; combined with the ER-beta agonist AC-186, it improved cognition (Morris water maze), increased amyloid-beta-degrading enzymes (neprilysin, IDE), and decreased brain amyloid-beta versus vehicle. Equine in vitro liver microsome studies identified twelve Phase I metabolites for doping-control detection purposes.
Key references
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.
ACP-105 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
Key references