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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: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.