MID-1 is a disruptor of MG53-IRS-1 (Mitsugumin 53-insulin receptor substrate-1) interaction. MID-1 disrupts molecular association of MG53 with IRS-1 and abolishes MG53-induced IRS-1 ubiquitination and degradation in skeletal muscle, leading to elevated IRS-1 expression level and increased insulin signaling and glucose uptake. In Vitro MID-1 (5 μM; 24 h) increases the IRS-1 expression level in skeletal muscle by disrupting the MG53-IRS-1 interaction. MID-1 (10 μM; 12 h) reduces the luciferase activity in HEK 293 cell line expressing NLUC-IRS-1 and CLUC-C14A. MID-1 (1-20 μM; 12 h) disrupts the MG53-IRS-1 interaction but not MG53-FAK interaction in HEK 293 cells. MID-1 (0.1-10 μM; 4-24 h) abolishes MG53-induced IRS-1 ubiquitination and degradation in HEK 293 cells. MID-1 (5-10 μM; 24 h) increases insulin signaling and insulin-elicited glucose uptake in C2C12 myotubes. MID-1 (5-10 μM; 24 h) enhances skeletal myogenesis. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: C2C12 myotubes Concentration: 5 μM Incubation Time: 24 h Result: Increased the IRS-1 protein level. In Vivo MID-1 does not have good pharmacokinetics in vivo . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid