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Drug-Target Interaction

Drug

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PubChem ID:163751
Structure:
Synonyms:
105628-07-7
133337-43-6
1H-1,4-Diazepine, hexahydro-1-(5-isoquinolinylsulfonyl)-,
1H-1,4-Diazepine, hexahydro-1-(5-isoquinolinylsulfonyl)-, monohydrochloride
AT 877 hydrochloride
AT-877
C14H17N3O2S.HCl
D01840
Eril
Fasdil
fasudil
Fasudil hydrochloride
Fasudil hydrochloride (JAN)
HA 1077 hydrochloride
HA-1077
HA-1077 DIHYDROCHLORIDE
Hexahydro-1-(5-isoquinolinylsulfonyl)-1H-1,4-diazepine monohydrochloride
LS-60222
MLS000069344
NCGC00180915-01
SMR000058993
ATC-Codes:

Target

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Uniprot ID:DUOX1_RAT
Synonyms:
Dual oxidase 1
EC-Numbers:1.11.1.-
1.6.3.1
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

17511984
The Rho-kinase inhibitor, fasudil, attenuates diabetic nephropathy in streptozotocin-induced diabetic rats.. Atsushi Gojo; Kazunori Utsunomiya; Kanta Taniguchi; Tamotsu Yokota; Shoh Ishizawa; Yasushi Kanazawa; Hideaki Kurata; Naoko Tajima (2007) European journal of pharmacology display abstract
This study aimed to investigate the effect of the Rho-kinase inhibitor fasudil on the development of diabetic nephropathy and clarify a contribution of the Rho/Rho-kinase pathway to the pathogenesis of diabetic nephropathy. Diabetes was induced in male Sprague-Dawley rats with an intraperitoneal injection of streptozotocin. Animals were then divided into the following 4 groups; normal control rats, diabetic rats, diabetic rats administered fasudil orally and diabetic rats administered fluvastatin (3-hydroxy-methylglutaryl coenzyme A reductase inhibitor, statin) orally. After 1 month of treatment, neither fasudil nor statin had any influence on blood glucose or blood pressure in diabetic rats. While urinary excretion of albumin and 8-hydroxydeoxyguanosine (8-OHdG) was increased in diabetic rats, both of these increases were abolished by fasudil and statin. Rho activity was enhanced in the renal cortex of diabetic rats compared to normal controls, and this enhancement was abolished by statin treatment. Expression of transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF) mRNA was up-regulated in the renal cortex of diabetic rats, and this was abolished by fasudil as well as statin. Expression of NOX4 mRNA (catalytic subunit of NAD(P)H oxidase) was up-regulated in the renal cortex of diabetic rats, an effect which was also abolished by fasudil as well as statin. The present study demonstrates that the Rho/Rho-kinase pathway is involved in up-regulation of TGF-beta, CTGF and NAD(P)H oxidase in diabetic kidney. We conclude that suppression of the Rho/Rho-kinase pathway could be a new strategy for the treatment of diabetic nephropathy.