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    Glimepiride (Glimperide; HOE-490)
    Glimepiride (Glimperide; HOE-490)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1673
    CAS #: 93479-97-1Purity ≥98%

    Description: Glimepiride (Glimperide; HOE-490), a third generation and medium-to-long acting sulfonylurea compound, is a potent Kir6.2/SUR inhibitor with IC50 of 3.0 nM, 5.4 nM, and 7.3 nM for SUR1, SUR2A and SUR2B, it is used in the treatment of type 2 diabetes mellitus. The mechanism of action of Glimepiride is to increase the release of insulin from pancreatic beta cells. In addition, glimepiride increases the activity of intracellular insulin receptors. Glimepiride increases osteoblast proliferation and differentiation, which is thought to be related to its ability to activate the PI3K and Akt pathway. 

    References: Br J Pharmacol. 2001;133(1):193-9; Horm Metab Res. 1996;28(9):469-87; Indian J Exp Biol. 2009;47(10):804-10.

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    Molecular Weight (MW)490.62
    CAS No.93479-97-1
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 11 mg/mL (22.4 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: 4-ethyl-3-methyl-N-[2-[4-[(4-methylcyclohexyl)carbamoylsulfamoyl]phenyl]ethyl]-5-oxo-2H-pyrrole-1-carboxamide


    InChi Code: InChI=1S/C24H34N4O5S/c1-4-21-17(3)15-28(22(21)29)24(31)25-14-13-18-7-11-20(12-8-18)34(32,33)27-23(30)26-19-9-5-16(2)6-10-19/h7-8,11-12,16,19H,4-6,9-10,13-15H2,1-3H3,(H,25,31)(H2,26,27,30)

    SMILES Code: CCC1=C(CN(C1=O)C(=O)NCCC2=CC=C(C=C2)S(=O)(=O)NC(=O)NC3CCC(CC3)C)C


    HOE-490; HOE 490; HOE-490; Glimepiride; Amaryl; Amarel; Glimepirida; Glimepiridum; Hoechst brand of glimepiride; Roname

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    In Vitro

    In vitro activity: Glimepiride inhibits Kir6.2/SUR currents by interaction with two sites: a low-affinity site on Kir6.2 (IC(50)= approximately 400 mM) and a high-affinity site on SUR (IC(50)=3.0 nM for SUR1, 5.4 nM for SUR2A and 7.3 nM for SUR2B). Glimepiride exhibits a higher potency compared to Glibenclamide with respect to stimulation of glucose transport, glucose transporter isoform 4 (GLUT4) translocation and lipid and glycogen synthesis in normal and insulin-resistant adipocytes and in muscle cells, as well as of the potential underlying signalling processes examined at the molecular level. Glimepiride associates in a time- and concentration dependent non-saturable manner with detergent-insoluble complexes of the plasma membrane which may correspond to caveolae. Glimepiride blocks pinacidil-activated whole-cell K(ATP) currents of cardiac myocytes with an IC(50) of 6.8 nM, comparable to the potency of Glibenclamide in these cells. Glimepiride blocks K(ATP) channels formed by co-expression of Kir6.2/SUR2A subunits in HEK 293 cells in outside-out excised patches with a similar IC(50) of 6.2 nM.

    Cell Assay: When cultured cells in the presence of a physiological insulin dose and glimepiride (10 μM), 2-deoxyglucose uptake was increased to 186% of control. Glimepiride also increased 2-deoxyglucose uptake in the absence of insulin. At the same time, glimepiride increased the expression of both GLUT1 and GLUT4 to 164% and 148% of control, respectively. These results suggested glimepiride increased cardiac glucose uptake in an insulin-independent pathway.

    In VivoGlimepiride prevents the NA-STZ induced increased frequency of micronucleus (MN) in polychromatic and normochromatic erythrocytes. Glimepiride also decreases the sperm shape abnormality and enhances the sperm count besides improving the antioxidant status in the diabetic rats. Glimepiride inhibits the NA-STZ mediated changes in the MN frequency and sperm abnormality and enhanced the antioxidant defense. In diabetic-prone (DP) BB rats, Glimepiride (200 mg/kg/day) reduced the incidence of diabetes by 23% compared with the control group. In the hyperinsulinemic hyperglycemic KK-Ay mice, glimepiride reduced blood glucose by 40%, HBA1c by 33% and plasma insulin by 50%. In the absence of insulin, glimepiride caused glucose transport up to 60% and 35% of the maximum insulin response in the rat diaphragm and in 3T3 adipocytes, respectively.
    Animal modelRats
    Formulation & Dosage200 mg/kg

    Br J Pharmacol. 2001 May;133(1):193-9; Horm Metab Res. 1996 Sep;28(9):469-87; Indian J Exp Biol. 2009 Oct;47(10):804-10.

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


    Inhibition of KATP currents by glimepiride. Br J Pharmacol. 2001 May;133(1):193-9.


    Block of Kir6.2ΔC36 currents by glimepiride. Br J Pharmacol. 2001 May;133(1):193-9.


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