product name Gliquidone
Description: Gliquidone is an ATP-sensitive K+ channel antagonist with IC50 of 27.2 NM. It is a sulfonylurea class anti-diabetic drug that is used in the treatment of diabetes mellitus type 2. In patients with type 2 diabetes mellitus, gliquidone reduced the mean plasma glucose levels by 15% and increased insulin levels by 40%. In Caucasian patients with new-onset diabetes mellitus (NODM) after kidney transplantation, gliquidone reduced fasting blood glucose (FBG) from 154 mg/dl to 120 mg/dl.
References: Fundam Clin Pharmacol. 1991;5(2):107-15; Arzneimittelforschung. 1997 Mar;47(3):247-52.
527.63
Formula
C27H33N3O6S
CAS No.
33342-05-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 105 mg/mL (199.0 mM)
Water: <1 mg/mL
Ethanol: 6 mg/mL (11.4 mM)
Solubility (In vivo)
2% DMSO+Corn oil: 5mg/mL
Synonyms
Glurenorm
other peoduct :
| In Vitro |
In vitro activity: Gliquidone is an ATP-sensitive K+ channel antagonist. In mice, gliquidone (10 or 40 μg) antagonized morphine (20 mg/kg) induced hypermotility in a dose-dependent way. These results suggested that ATP-sensitive K+ channels played an important role in morphine-induced hypermotility. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Gliquidone (0.1–1.0 μg per mouse i.c.v.) prevents antinociception produced by amitriptyline and clomipramine in a dose-dependent manner in male swiss albino mice. Gliquidone (0.06–16 μg per mouse, i.c.v.) antagonizes the antinociception induced by buprenorphine, morphine and methadone. Gliquidone (6 μg per mouse, i.c.v.) prevents the antinociception induced by clonidine (0.125 mg/kg, s.c.) and guanabenz (0.30 mg/kg, s.c.), while a lower dose of gliquidone (3 μg per mouse, i.c.v.) is ineffective. Glurenorm (10 mg/kg) given to the diabetic rats produces significant reductions in blood glucose, nonenzymatic glycosylation, and total protein in the lenses, and significantly increases in glutathione levels in the lenses. |
| Animal model | |
| Formulation & Dosage | |
| References | Fundam Clin Pharmacol. 1991;5(2):107-15; Neuropharmacology. 2001;40(1):75-84; Br J Pharmacol. 1995 Mar;114(6):1296-302. |
