Glycogen Phosphorylase Inhibitor

Product NameGlycogen Phosphorylase Inhibitor
CAS648926-15-2
MFC17H15ClF2N4O4
MW412.78
EINECS
MOL File648926-15-2.mol

Chemical Properties

Density	1.490±0.06 g/cm3(Predicted)
storage temp.	Store at -20°C
solubility	DMF:5.0(Max Conc. mg/mL);12.11(Max Conc. mM) DMSO:5.0(Max Conc. mg/mL);12.11(Max Conc. mM)
form	White powder solid.
pka	8.47±0.46(Predicted)
color	white
InChI	1S/C17H15ClF2N4O4/c1-21-16(26)22-8-3-4-14(28-2)13(5-8)23-17(27)24-15(25)9-6-11(19)12(20)7-10(9)18/h3-7H,1-2H3,(H2,21,22,26)(H2,23,24,25,27)
InChIKey	ROJNYKZWTOHRNU-UHFFFAOYSA-N
SMILES	Fc1c(cc(c(c1)Cl)C(=O)NC(=O)Nc2c(ccc(c2)NC(=O)NC)OC)F

Safety Information

WGK Germany	WGK 1
Storage Class	11 - Combustible Solids

Usage And Synthesis

Description

Glycogen phosphorylase in the liver, muscle, and brain initiate glycogenolysis by releasing glucose-1-phosphate from glycogen. Glycogen phosphorylase inhibitor is a cell-permeable acyl urea first identified as an inhibitor of human liver glycogen phosphorylase (IC₅₀ = 53 nM). It blocks glucagon-induced hepatic glycogenolysis in vivo. Glycogen phosphorylase inhibitor has been used to study glycogen utilization in human liver HepG2 cells, retinal explants, and human T lymphocyte Kit 225 cells.

Uses

Glycogen Phosphorylase Inhibitor is used in biological studies to evaluate glycogen utilization in human liver HepG2 cells.

in vivo

Glycogen phosphorylase-IN-1 (5 mg/kg, i.v., single dose) inhibits the glycogenolysis in hepatocytes, ameliorates the glucagon stimulated hyperglycemic in wistar rats^[1].

Animal Model:	Glucagon-stimulated hyperglycemic in wistar rats^[1]
Dosage:	5 mg/kg
Administration:	i.v., single dose
Result:	Reduced blood glucose.

References

[1] THOMAS KLABUNDE. Acyl Ureas as Human Liver Glycogen Phosphorylase Inhibitors for the Treatment of Type 2 Diabetes[J]. Journal of Medicinal Chemistry, 2005, 48 20: 6178-6193. DOI: 10.1021/jm049034y
[2] ALAN CHENG. A role for AGL ubiquitination in the glycogen storage disorders of Lafora and Cori’s disease.[J]. Genes & development, 2007, 21 19: 2399-2409. DOI: 10.1101/gad.1553207
[3] KONSTANTINOS PAPPELIS. The retinal ganglion cells in metabolic syndrome.[J]. Annals of translational medicine, 2024, 12 1: 2. DOI: 10.21037/atm-23-1796
[4] ONETSINE ARRIZABALAGA. Rac1 protein regulates glycogen phosphorylase activation and controls interleukin (IL)-2-dependent T cell proliferation.[J]. The Journal of Biological Chemistry, 2012: 11878-11890. DOI: 10.1074/jbc.m111.297804

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