Abstract
Inhibition of acetyl-CoA carboxylases has the potential for modulating long chain fatty acid biosynthesis and mitochondrial fatty acid oxidation. Hybridization of weak inhibitors of ACC2 provided a novel, moderately potent but lipophilic series. Optimization led to compounds 33 and 37, which exhibit potent inhibition of human ACC2, 10-fold selectivity over inhibition of human ACC1, good physical and in vitro ADME properties and good bioavailability. X-ray crystallography has shown this series binding in the CT-domain of ACC2 and revealed two key hydrogen bonding interactions. Both 33 and 37 lower levels of hepatic malonyl-CoA in vivo in obese Zucker rats.
Copyright © 2011 Elsevier Ltd. All rights reserved.
MeSH terms
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Acetyl-CoA Carboxylase / antagonists & inhibitors*
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Acetyl-CoA Carboxylase / metabolism
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Animals
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Crystallography, X-Ray
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Diabetes Mellitus, Type 2 / drug therapy*
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Diabetes Mellitus, Type 2 / enzymology
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Drug Design
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Enzyme Inhibitors / chemistry*
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Enzyme Inhibitors / pharmacokinetics
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Enzyme Inhibitors / pharmacology*
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Enzyme Inhibitors / therapeutic use
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Fatty Acids / metabolism
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Humans
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Liver / drug effects
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Liver / enzymology
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Male
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Malonyl Coenzyme A / metabolism
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Mice
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Mice, Inbred C57BL
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Models, Molecular
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Obesity / drug therapy*
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Obesity / enzymology
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Rats
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Rats, Zucker
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Small Molecule Libraries / chemistry*
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Small Molecule Libraries / pharmacokinetics
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Small Molecule Libraries / pharmacology*
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Small Molecule Libraries / therapeutic use
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Structure-Activity Relationship
Substances
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Enzyme Inhibitors
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Fatty Acids
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Small Molecule Libraries
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Malonyl Coenzyme A
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Acetyl-CoA Carboxylase