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CP 91149

Known as: CP-91149 
National Institutes of Health

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Papers overview

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2011
2011
Contributions of hepatic gluconeogenesis suppression and compensative glycogenolysis on the glucose-lowering effect of CS-917, a fructose 1,6-bisphosphatase inhibitor, in non-obese type 2 diabetes…
Contributions of gluconeogenesis suppression in liver, kidney, and intestine as major gluconeogenic organs to the glucose… 
2004
2004
Regulation of glycogen metabolism in cultured human muscles by the glycogen phosphorylase inhibitor CP-91149.
Pharmacological inhibition of liver GP (glycogen phosphorylase), which is currently being studied as a treatment for Type II (non… 
2004
2004
Activation of Glycogen Phosphorylase with 5-Aminoimidazole-4-Carboxamide Riboside (AICAR)
The experimental evaluation of the contribution of glycogen phosphorylase (GP) to biochemical pathways is limited to methods that… 
Highly Cited
2003
Highly Cited
2003
Inactivation of phosphorylase is a major component of the mechanism by which insulin stimulates hepatic glycogen synthesis.
Multiple signalling pathways are involved in the mechanism by which insulin stimulates hepatic glycogen synthesis. In this study… 
Highly Cited
2002
Highly Cited
2002
Diverse effects of two allosteric inhibitors on the phosphorylation state of glycogen phosphorylase in hepatocytes.
Two distinct allosteric inhibitors of glycogen phosphorylase, 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) and CP-91149 (an indole-2… 
Highly Cited
2001
Highly Cited
2001
Hepatic Glycogen Synthesis Is Highly Sensitive to Phosphorylase Activity
We used metabolic control analysis to determine the flux control coefficient of phosphorylase on glycogen synthesis in… 
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