Abstract
The formation of a reactive intermediate was found to be responsible for CYP3A4 metabolism-dependent inhibition (MDI) observed with (S)-N-[1-(3-morpholin-4-ylphenyl)ethyl]-3-phenyl-acrylamide (1). Structure-3A4 MDI relationship studies culminated in the discovery of a difluoro analogue, (S)-N-[1-(4-fluoro-3-morpholin-4-ylphenyl)ethyl]-3-(4-fluoro-phenyl)acrylamide (2), as an orally bioavailable KCNQ2 opener free of CYP3A4 MDI.
MeSH terms
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Administration, Oral
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Animals
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Biological Availability
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Cell Line
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Cinnamates / chemical synthesis*
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Cinnamates / metabolism
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Cinnamates / pharmacology
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Cytochrome P-450 CYP3A
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Cytochrome P-450 Enzyme Inhibitors*
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Disease Models, Animal
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Fluorine / chemistry*
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Injections, Intravenous
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Ion Channel Gating
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KCNQ2 Potassium Channel
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Male
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Membrane Potentials
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Migraine Disorders / drug therapy
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Migraine Disorders / physiopathology
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Morpholines / chemical synthesis*
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Morpholines / metabolism
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Morpholines / pharmacology
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Parietal Lobe / drug effects
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Parietal Lobe / physiopathology
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Patch-Clamp Techniques
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Potassium Channels / drug effects*
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Potassium Channels / physiology
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Potassium Channels, Voltage-Gated
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Rats
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Rats, Sprague-Dawley
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Stereoisomerism
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Structure-Activity Relationship
Substances
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Cinnamates
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Cytochrome P-450 Enzyme Inhibitors
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KCNQ2 Potassium Channel
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Kcnq2 protein, rat
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Morpholines
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N-(1-(4-fluoro-3-morpholin-4-ylphenyl)ethyl)-3-(4-fluorophenyl)acrylamide
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Potassium Channels
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Potassium Channels, Voltage-Gated
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Fluorine
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CYP3A protein, human
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Cytochrome P-450 CYP3A
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CYP3A4 protein, human