Abstract
Using structure-based drug design, we identified a novel series of 5,6-dihydroimidazolo[1,5-f]pteridine PLK1 inhibitors. Rational improvements to compounds of this class resulted in single-digit nanomolar enzyme and cellular activity against PLK1, and oral bioavailability. Compound 1 exhibits >7 fold induction of phosphorylated Histone H3 and is efficacious in an in vivo HT-29 tumor xenograft model.
Keywords:
Antitumor activity; Multidrug resistance; PLK1 inhibitor; Structure-based drug design.
Copyright © 2016 Elsevier Ltd. All rights reserved.
MeSH terms
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Animals
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Cell Cycle Proteins / antagonists & inhibitors*
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Drug Design*
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Enzyme Activation / drug effects
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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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Female
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HT29 Cells
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Heterografts
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Humans
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Imidazoles / chemical synthesis*
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Imidazoles / chemistry
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Imidazoles / pharmacology
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Mice
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Molecular Structure
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Polo-Like Kinase 1
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Protein Serine-Threonine Kinases / antagonists & inhibitors*
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Proto-Oncogene Proteins / antagonists & inhibitors*
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Pteridines / chemical synthesis*
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Pteridines / chemistry
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Pteridines / pharmacology
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Structure-Activity Relationship
Substances
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Cell Cycle Proteins
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Enzyme Inhibitors
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Imidazoles
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Proto-Oncogene Proteins
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Pteridines
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imidazolone
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Protein Serine-Threonine Kinases