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MID-1

  Cat. No.:  DC11162   Featured
Chemical Structure
312608-54-1
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More than 5000 active chemicals with high quality for research!
Field of application
MID-1 (ChemBridge5655896) is a specific small molecule MG53-IRS-1 interaction disruptor (MID), but not MG53-FAK and-Cav-3 interaction; increases the IRS-1 protein level in C2C12 myotubes, abrogates MG53-induced IRS-1 ubiquitination and degradation; potent
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 312608-54-1
Chemical Name: 4-Ethoxy-N-(5-nitrothiazol-2-yl)benzamide
Synonyms: ChemBridge5655896;MID 1;MID1
SMILES: O=C(NC1=NC=C([N+]([O-])=O)S1)C2=CC=C(OCC)C=C2
Formula: C12H11N3O4S
M.Wt: 293.3
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Publication: 1. Lee H, et al. J Biol Chem. 2016 Dec 23;291(52):26627-26635.
Description: MID-1 is an inhibitor 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[1].
In Vivo: MID-1 does not have good pharmacokinetics in vivo[1].
In Vitro: MID-1 (5 μM; 24 h) increases the IRS-1 expression level in skeletal muscle by disrupting the MG53-IRS-1 interaction[1]. MID-1 (10 μM; 12 h) reduces the luciferase activity in HEK 293 cell line expressing NLUC-IRS-1 and CLUC-C14A[1]. MID-1 (1-20 μM; 12 h) disrupts the MG53-IRS-1 interaction but not MG53-FAK interaction in HEK 293 cells[1]. MID-1 (0.1-10 μM; 4-24 h) abolishes MG53-induced IRS-1 ubiquitination and degradation in HEK 293 cells[1]. MID-1 (5-10 μM; 24 h) increases insulin signaling and insulin-elicited glucose uptake in C2C12 myotubes[1]. MID-1 (5-10 μM; 24 h) enhances skeletal myogenesis[1]. Western Blot Analysis[1] Cell Line: C2C12 myotubes Concentration: 5 μM Incubation Time: 24 h Result: Increased the IRS-1 protein level.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
2018-0101
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