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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:Q62710_RAT
Synonyms:
Nitric oxide synthase
EC-Numbers:-
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

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

References:

11553365
Involvement of Rho-kinase in vascular remodeling caused by long-term inhibition of nitric oxide synthesis in rats.. I Ikegaki; T Hattori; T Yamaguchi; Y Sasaki; S I Satoh; T Asano; H Shimokawa (2001) European journal of pharmacology display abstract
Long-term inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine methyl ester (L-NAME) induces coronary vascular remodeling in rats. To determine the pathogenic mechanism involved in vascular remodeling, we examined the effects of fasudil, a Rho-kinase inhibitor, on vascular lesion formation. In rats treated with L-NAME at 10 mg/kg/day, vascular remodeling was evident in both large and small coronary arteries at the fourth week. Fasudil (3 mg/kg, p.o., twice daily) markedly prevented the development of vascular remodeling in small coronary arteries. Coronary flow was measured in Langendorff perfused isolated heart preparations. Long-term treatment with L-NAME caused a significant decrease in coronary flow, which was significantly inhibited by fasudil. Fasudil suppressed the structural and functional changes in coronary arteries by chronic blockade of NO synthesis. Thus, the Rho-kinase pathway may be substantially involved in the pathogenesis of vascular remodeling in this rat model.