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    Repaglinide (AG-EE 623ZW)
    Repaglinide (AG-EE 623ZW)

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V1675
    CAS #: 135062-02-1Purity ≥98%

    Description: Repaglinide (also known as AG-EE 623 ZW) is a potent and short-acting potassium channel blocker, which lowers blood glucose by stimulating the release of insulin from the pancreas. Repaglinide is an antidiabetic drug in the class of medications known as meglitinides, and was invented in 1983. Repaglinide is an oral medication used for the treatment of type 2 diabetes mellitus. The mechanism of action of repaglinide involves promoting insulin release from β-islet cells of the pancreas. 

    ReferencesBr J Pharmacol. 2005 Feb;144(4):551-7; Eur J Pharmacol. 1997 Sep 24;335(2-3):227-34.

    Related CAS: 1217709-85-7 (Repaglinide D5); 874908-14-2 (3'-Hydroxy Repaglinide)

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    Molecular Weight (MW)452.59
    CAS No.135062-02-1
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 91 mg/mL (201.1 mM)
    Water: <1 mg/mL
    Ethanol: 91 mg/mL (201.1 mM)
    Other infoChemical Name: 2-ethoxy-4-[2-[[(1S)-3-methyl-1-(2-piperidin-1-ylphenyl)butyl]amino]-2-oxoethyl]benzoic acid


    InChi Code: InChI=1S/C27H36N2O4/c1-4-33-25-17-20(12-13-22(25)27(31)32)18-26(30)28-23(16-19(2)3)21-10-6-7-11-24(21)29-14-8-5-9-15-29/h6-7,10-13,17,19,23H,4-5,8-9,14-16,18H2,1-3H3,(H,28,30)(H,31,32)/t23-/m0/s1

    SMILES Code: O=C(O)C1=CC=C(CC(N[[email protected]](C2=CC=CC=C2N3CCCCC3)CC(C)C)=O)C=C1OCC

    SynonymsAG-EE-623 ZW; AG-EE 388 ZW; AG-EE388 ZW; AG-EE-388 ZW; AG-EE623 ZW, AG-EE-623 ZW, Prandin, GlucoNorm, Surepost, NovoNorm

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    In Vitro

    In vitro activity: Repaglinide is found to bind with low affinity (K(D)=59 nM) to SUR1 alone, but with high affinity (increased approximately 150-fold) when SUR1 is co-expressed with Kir6.2. Repaglinide binds with low affinity (K(D)=51 nM) to SUR1 co-expressed with Kir6.2DeltaN14. Repaglinide lowers the plasma glucose concentration in the control rat, whilst failing to affect significantly the plasma insulin concentration or insulin/glucose ratio. Repaglinide administration affects neither plasma glucose nor insulin concentration, restores a normal value for the otherwise abnormally high basal insulin output, increases the 16.7 mM/2.8 mM ratio for insulin release, and again augmented protein biosynthesis at both low and high hexose concentrations in Goto-Kakizaki (GK) rats. Repaglinide is found to bind to NCS proteins, but not to CaM or S100 proteins, in a Ca2+-dependent manner. Repaglinide antagonizes the inhibitory action of recoverin in a rhodopsin kinase assay with IC50 values of 400 mM. Repaglinide tightly binds to the visinin-like domain of CCaMK and PpCaMK in a Ca2+-dependent manner and antagonizes the regulatory function of the domain with IC50 values of 55 and 4 mM for CCaMK and PpCaMK respectively.

    In VivoRepaglinide provokes a greater and more rapid increase in plasma insulin concentration and an earlier fall in glycemia than those observed after administration of the hypoglycemic sulfonylureas in both fed and starved normal rats.
    Animal modelRats
    Formulation & DosageN/A

    Br J Pharmacol. 2005 Feb;144(4):551-7; Eur J Pharmacol. 1997 Sep 24;335(2-3):227-34.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Inhibition of [3H]glibenclamide binding to SUR1 expressed alone (open circles) or co-expressed with Kir6.2 (filled circles) by repaglinide (a), glibenclamide (b), tolbutamide (c) and nateglinide (d). Br J Pharmacol. 2005 Feb;144(4):551-7.


    Saturation analysis of [3H]glibenclamide (a) and [3H]repaglinide (b) binding to SUR1 expressed alone (open circles) or co-expressed with Kir6.2 (filled circles). Inset: Scatchard analysis of data. Single representative experiments. Br J Pharmacol. 2005 Feb;144(4):551-7.


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