Abstract
A series of inhibitors of Autotaxin (ATX) has been developed using the binding mode of known inhibitor, PF-8380, as a template. Replacement of the benzoxazolone with a triazole zinc-binding motif reduced crystallinity and improved solubility relative to PF-8380. Modification of the linker region removed hERG activity and led to compound 12 - a selective, high affinity, orally-bioavailable inhibitor of ATX. Compound 12 concentration-dependently inhibits autotaxin and formation of LPA in vivo, as shown in pharmacokinetic-pharmacodynamic experiments.
Keywords:
Autotaxin inhibition; Idiopathic pulmonary fibrosis; PK/PD; Solubility; hERG inhibition.
Copyright © 2018 Elsevier Ltd. All rights reserved.
MeSH terms
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Administration, Oral
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Animals
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Benzoxazoles / pharmacology
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Drug Design*
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Drug Stability
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Humans
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Male
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Microsomes / metabolism
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Phosphodiesterase Inhibitors / administration & dosage
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Phosphodiesterase Inhibitors / chemical synthesis
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Phosphodiesterase Inhibitors / pharmacokinetics
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Phosphodiesterase Inhibitors / pharmacology*
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Phosphoric Diester Hydrolases / metabolism*
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Piperazines / pharmacology
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Rats, Sprague-Dawley
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Solubility
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Triazoles / administration & dosage
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Triazoles / chemical synthesis
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Triazoles / pharmacokinetics
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Triazoles / pharmacology*
Substances
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6-(3-(piperazin-1-yl)propanoyl)benzo(d)oxazol-2(3H)-one
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Benzoxazoles
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Phosphodiesterase Inhibitors
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Piperazines
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Triazoles
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Phosphoric Diester Hydrolases
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alkylglycerophosphoethanolamine phosphodiesterase