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Drug-Target Interaction

Drug

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PubChem ID:3547
Structure:
Synonyms:
(5-ISOQUINOLINESULFONYL)HOMOPIPERAZINE
1-(5-Isoquinolinesulfonyl)homopiperazine
1-(5-Isoquinolinesulphonyl)homopiperazine
1-(5-Isoquinolinylsulfonyl)homopiperazine
1-(5-Isoquinolylsulfonyl)-1,4-diazaperhydroepine
103745-39-7
105628-07-7
105628-07-7(HYDROCHLORIDE)
1H-1,4-Diazepine, hexahydro-1-(5-isoquinolinylsulfonyl)-
1H-1,4-Diazepine, hexahydro-1-(5-isoquinolinylsulfonyl)- (9CI)
1q8w
2esm
2gni
5-(1,4-DIAZEPAN-1-SULFONYL)ISOQUINOLINE
5-(1,4-diazepan-1-ylsulfonyl)isoquinoline
5-(1,4-diazepane-1-sulfonyl)isoquinoline
AC1L1G6K
AC1Q6UWJ
AC1Q6VJ2
AIDS-108016
AIDS108016
AR-1A6371
AT 877
AT-877
AT877
Bio2_000386
Bio2_000866
BiomolKI2_000046
BiomolKI_000038
BRD-K76617868-001-02-2
BRD-K76617868-001-03-0
BRD-K76617868-300-03-6
BRD-K76617868-300-04-4
BSPBio_001111
C14H17N3O2S
CCG-100642
CHEMBL38380
D07941
DB08162
Eril
Fasudil
Fasudil (HA-1077)
Fasudil (INN)
Fasudil hydrochloride
Fasudil [INN]
Fasudilum
Fasudilum [INN-Latin]
FH
HA 1077
HA-1077
HA1077
Hexahydro-1-(5-isoquinolinylsulfonyl)-1H-1,4-diazepine
Hexahydro-1-(5-isoquinolylsulfonyl)-1H-1,4-diazepine
HMS1362G13
HMS1792G13
HMS1990G13
HMS2089F13
HMS3264M10
I06-1557
IDI1_002141
KBio2_000451
KBio2_003019
KBio2_005587
KBio3_000841
KBio3_000842
KBioGR_000451
KBioSS_000451
Kinome_3390
Kinome_3391
KST-1A0465
LS-60220
M77
NCGC00018100-01
NCGC00018100-02
NCGC00018100-03
NCGC00018100-04
NCGC00018100-05
NCGC00018100-06
NCGC00018100-07
NCGC00024299-02
NCGC00024299-04
NCGC00024299-05
SMP2_000083
ST51053125
Tocris-0541
UNII-Q0CH43PGXS
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.