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Yk12.8
YK-11 Research
Mostly mechanism / observational
5 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most YK-11 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2011–2023.
Based on 5 studies
Confidence
Low confidence
By outcome
Androgen-receptor activity
Mostly mechanism / observational5 studies
Muscle growth (claimed, in-vitro only)Muscle-growth and "myostatin inhibition" claims rest on cell-culture only; no human (or even live-animal efficacy) data, plus a rat neurotoxicity signal. · Not established (in-vitro only)
1Label accuracy of marketed SARM productsObservational2017
In plain English: Products marketed as selective androgen receptor modulators and sold via the internet frequently did not contain the labeled compound, contained substances not listed on the label, or differed substantially in the amount of the compound from the label claim.
Van Wagoner, Eichner, Bhasin, Deuster, Eichner · JAMA (2017)
Mandatory counter-evidence on the grey-market reality — analyzed internet-sold 'SARM' products using WADA-approved methods
Most products were mislabeled: wrong compound, undisclosed substances, or amounts differing substantially from the label
Several contained unapproved drugs or no active SARM at all
In plain English: The administration of YK11 resulted in alterations in the endogenous antioxidant system, promoting increased oxidative stress and proteotoxic effects, impairing all mitochondrial function markers in the hippocampus.
Dahleh, Bortolotto, Guerra, Boeira, Prigol · The Journal of steroid biochemistry and molecular biology (2023)
The ONLY in-vivo study — a harm signal, not a benefit: YK11 (0.35 g/kg) caused oxidative stress and mitochondrial dysfunction in the rat hippocampus over a 5-week protocol
Exercise alone was neuroprotective; YK11's neurochemical impairments were not reversed by co-administered exercise
No efficacy (muscle/strength) endpoint was demonstrated in this living-animal study
In plain English: YK11 treatment of C2C12 cells, but not DHT, induced the expression of follistatin (Fst), and the YK11-mediated myogenic differentiation was reversed by anti-Fst antibody. These results suggest that the induction of Fst is important for the anabolic effect of YK11.
In plain English: YK11 activates AR without causing N/C interaction, which may in turn be responsible for the partially agonistic nature of YK11; our results suggest that YK11 might act as a selective androgen receptor modulator (SARM).
In plain English: YK11-treated cells increased osteoblast specific differentiation markers, such as osteoprotegerin and osteocalcin... YK11 has osteogenic activity as well as androgen.