GlibornurideGlibornuride
MedChemExpress (MCE)
HY-17451
26944-48-9
98.92%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Room temperature in continental US
may vary elsewhere.
Glibornuride is a blocker of ATP-sensitive K+ channels (KATP channel) with a pKi of 5.75. Antidiabetic agent.
Administration of Glibornuride (5 mg/kg
gavage, daily for 28 days) for 28 days causes an increase in body weights in the diabetic groups in Swiss albino rats[2]. Treatment with Glibornuride for 28 days decreases the serum uric acid levels in diabetic rats[2]. Administration of Glibornuride for 28 days, insignificantly increases the liver lipid peroxidation levels in diabetic rats[2].
pKi: 5.75 (KATP channel)[1] In Vivo Administration of Glibornuride (5 mg/kg
gavage, daily for 28 days) for 28 days causes an increase in body weights in the diabetic groups in Swiss albino rats[2]. Treatment with Glibornuride for 28 days decreases the serum uric acid levels in diabetic rats[2]. Administration of Glibornuride for 28 days, insignificantly increases the liver lipid peroxidation levels in diabetic rats[2]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: 6-6.5-month-old male Swiss Albino rats, weighing 150-200 g[2]
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[1]. Löffler C, et al. Pharmacological characterization of the sulphonylurea receptor in rat isolated aorta. Br J Pharmacol. 1997 Feb
120(3):476-80. [Content Brief]
[2]. Ozsoy-Sacan O, et al. Effects of parsley (Petroselinum crispum) extract versus Glibornuride on the liver of streptozotocin-induced diabetic rats. J Ethnopharmacol. 2006 Mar 8
104(1-2):175-81. [Content Brief]