Yk-11 (15 Mg),60 Capsules Per Bottle

$100.00

YK11 is a partial agonist of androgen receptor, with osteogenic activity.

YK11 is a partial agonist of androgen receptor, and induces myogenic differentiation of C2C12 Cells at 500 nM via Fst mRNA upregulation by AR. YK11 enhances Myf5 and myogenin mRNA expression, but requires high concentrations (YK11, 100 nM or 500 nM)[1]. YK11 (0.5 µM) increases the cell growth of osteoblastic MC3T3-E1 cells, and enhances ALP activity via AR. YK11 also elevates osteoprotegerin mRNA expression (0.5 µM) and dose-dependently increases osteocalcin mRNA expression (0.1-1.0 µM). In addition, YK11 enhances phosphorylation of Akt protein via rapid non-genomic signaling[2].

[1]. Kanno Y, et al. Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression. Biol Pharm Bull. 2013;36(9):1460-5. [2]. Yatsu T, et al. Selective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1

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The selective androgen receptor (AR) modulator YK11 promotes the anabolism of muscle cells and osteoblastic precursor cells. However, its effects on bone marrow-derived mesenchymal stem cells (BMSCs) and the repair of cranial bone defects are unknown. Here, the effects of different concentrations of YK11 on the osteogenic differentiation of BMSCs were determined. Subsequently, the AR was inhibited to investigate whether the effect of YK11 on the osteogenic differentiation of BMSCs was affected. A model of cranial defects was constructed to investigate the effects of the YK11-equipped hydrogel on cranial defect repair as well as the effects of YK11 on cranial defect repair after inhibiting the AR. Finally, the possible pathway of YK11 regulating the osteogenic differentiation of BMSCs was explored. Our results show 2 μM YK11 promoted the proliferation of BMSCs. A dose of 0.25–4 μM YK11 could promote osteogenesis of BMSCs, and the promoting effect was gradually enhanced with increasing concentration. In vivo, 0.5 and 1 mg/mL YK11 could promote the repair of cranial bone defects. After inhibiting the AR, the effects of YK11 on promoting both the osteogenic differentiation of BMSCs and repair of cranial defects were suppressed. YK11 may regulate the osteogenic differentiation of BMSCs through the BMP2 (bone morphogenetic protein 2)/Smad signaling pathway. In conclusion, YK11 promoted the osteogenic differentiation of BMSCs by activation on the AR. Meanwhile, YK11 promoted the repair of cranial bone defects in rats in vivo. The BMP2/Smad signaling pathway may be involved in the regulation of the osteogenic differentiation of BMSCs by YK11.