189224-48-4
Chemical Structure
KU14R
- CAS No.: 189224-48-4
- Formula:C13H14N2O
- Molecular Weight:214.26
IUPAC Name: 2-(2-ethyl-2,3-dihydrobenzofuran-2-yl)-1H-imidazole
InChIKey: JCWVNNMJXQJVNC-UHFFFAOYSA-N
SMILES: CCC1(C2=NC=CN2)OC3=CC=CC=C3C1
Biological Activity:
KU14R, an imidazole analog of efaroxan, is a putative imidazoline I3 receptor antagonist and reversible KATP channel inhibitor. KU14R inhibits KATP channel activity in mouse pancreatic β cells with an IC50 of 31.9 μmol/L, and also suppresses Kir6.2 ΔC26 channel activity. KU14R exerts model-dependent antagonistic effects on imidazoline-sensitive insulin secretion. KU14R can be used in the research of diabetes-related diseases[1][2][3][4][5].
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KU14R | 98.91% | KU14R, an imidazole analog of efaroxan, is a putative imidazoline I3 receptor antagonist and reversible KATP channel inhibitor. KU14R inhibits KATP channel activity in mouse pancreatic β cells with an IC50 of 31.9 μmol/L, and also suppresses Kir6.2 ΔC26 channel activity. KU14R exerts model-dependent antagonistic effects on imidazoline-sensitive insulin secretion. KU14R can be used in the research of diabetes-related diseases. |
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References
- [1]. Bleck C, et al. Essential role of the imidazoline moiety in the insulinotropic effect but not the KATP channel-blocking effect of imidazolines; a comparison of the effects of efaroxan and its imidazole analogue, KU14R. Diabetologia. 2005;48:2567-2575.
- [2]. Mayer G, et al. Effects of the imidazoline ligands efaroxan and KU14R on blood glucose homeostasis in the mouse. European journal of pharmacology. 2002 Nov 01;454(1):95-102. [Content Brief]
- [3]. Lin MH, et al. Investigation of morin-induced insulin secretion in cultured pancreatic cells. Clin Exp Pharmacol Physiol. 2017; 44: 1254-1262.
- [4]. Chan SL, et al. Characterization of a KATP channel-independent pathway involved in potentiation of insulin secretion by efaroxan. Diabetes. 2001 Feb;50(2):340-7.
- [5]. Chan SL, et al. Evidence that the ability of imidazoline compounds to stimulate insulin secretion is not due to interaction with sigma receptors. European journal of pharmacology. 1997 Apr 04;323(2-3):241-4.
