Abstract
SAR on HTS hits 1 and 2 led to the potent, Notch-1-sparing GSI 9, which lowered brain Abeta in Tg2576 mice at 100 mg/kg po. Converting the metabolically labile methyl groups in 9 to trifluoromethyl groups afforded the more stable analogue 10, which had improved in vivo potency. Further side chain modification afforded the potent Notch-1-sparing GSI begacestat (5), which was selected for development for the treatment of Alzheimer's disease.
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / enzymology
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Amyloid Precursor Protein Secretases / antagonists & inhibitors*
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Amyloid Precursor Protein Secretases / metabolism
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Amyloid beta-Peptides / metabolism
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Animals
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Crystallography, X-Ray
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Drug Discovery*
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Enzyme Inhibitors / chemical synthesis
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Enzyme Inhibitors / chemistry
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Enzyme Inhibitors / pharmacology*
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Mice
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Mice, Transgenic
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Models, Molecular
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Molecular Conformation
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Receptor, Notch1 / metabolism*
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Stereoisomerism
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Structure-Activity Relationship
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Sulfonamides / chemical synthesis
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Sulfonamides / chemistry
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Sulfonamides / pharmacology*
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Thiophenes / chemical synthesis
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Thiophenes / chemistry
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Thiophenes / pharmacology*
Substances
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Amyloid beta-Peptides
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Enzyme Inhibitors
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Receptor, Notch1
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Sulfonamides
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Thiophenes
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begacestat
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Amyloid Precursor Protein Secretases