Abstract
Rho kinase is an important target implicated in a variety of cardiovascular diseases. Herein, we report the optimisation of the fragment derived ATP-competitive ROCK inhibitors 1 and 2 into lead compound 14A. The initial goal of improving ROCK-I potency relative to 1, whilst maintaining a good PK profile, was achieved through removal of the aminoisoquinoline basic centre. Lead 14A was equipotent against both ROCK-I and ROCK-II, showed good in vivo efficacy in the spontaneous hypertensive rat model, and was further optimised to demonstrate the scope for improving selectivity over PKA versus hydroxy Fasudil 3.
Copyright © 2010 Elsevier Ltd. All rights reserved.
MeSH terms
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / therapeutic use
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Amines / chemical synthesis
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Amines / chemistry*
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Amines / therapeutic use
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Animals
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Disease Models, Animal
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Hypertension / drug therapy
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Isoquinolines / chemistry*
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Models, Chemical
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Models, Molecular
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Piperidines / chemical synthesis
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Piperidines / chemistry*
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Piperidines / therapeutic use
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Protein Kinase Inhibitors / chemical synthesis
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Protein Kinase Inhibitors / chemistry*
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Protein Kinase Inhibitors / therapeutic use
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Quinolones / chemical synthesis
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Quinolones / chemistry*
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Quinolones / therapeutic use
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Rats
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Structure-Activity Relationship
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rho-Associated Kinases / antagonists & inhibitors*
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rho-Associated Kinases / metabolism
Substances
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Amines
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Isoquinolines
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Piperidines
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Protein Kinase Inhibitors
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Quinolones
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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rho-Associated Kinases
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isoquinoline
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fasudil