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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:AKT1_MOUSE
Synonyms:
AKT1 kinase
C-AKT
PKB
Protein kinase B
RAC-alpha serine/threonine-protein kinase
RAC-PK-alpha
Thymoma viral proto-oncogene
EC-Numbers:2.7.11.1
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

References:

17204906
Long-term inhibition of Rho-kinase ameliorates hypoxia-induced pulmonary hypertension in mice.. Kohtaro Abe; Shunsuke Tawara; Keiji Oi; Takatoshi Hizume; Toyokazu Uwatoku; Yoshihiro Fukumoto; Kozo Kaibuchi; Hiroaki Shimokawa (2006) Journal of cardiovascular pharmacology display abstract
Pulmonary hypertension (PH) is a fatal disease characterized by endothelial dysfunction, hypercontraction and proliferation of vascular smooth muscle cells, and migration of inflammatory cells for which no satisfactory treatment has yet been developed. It has been recently demonstrated that Rho-kinase, an effector of the small GTPase Rho, is involved in the pathogenesis of arteriosclerosis and that long-term inhibition of Rho-kinase markedly ameliorates monocrotaline-induced PH in rats. However, it remains to be examined whether direct inhibition of Rho-kinase also ameliorates PH with a different etiology and whether endothelial nitric oxide synthase (eNOS) is involved in the beneficial effects of Rho-kinase inhibition. This study was designed to address those 2 important issues in a hypoxia-induced PH model using wild-type (WT) and eNOS-deficient (eNOS) mice. Long-term blockade of Rho-kinase with fasudil (100 mg/kg/d) for 3 weeks markedly improved PH and right ventricular hypertrophy in WT mice with a lesser but significant inhibition noted in eNOS mice. Fasudil upregulated eNOS with increased Akt phosphorylation in WT but not in eNOS mice. These results suggest that long-term inhibition of Rho-kinase also ameliorates hypoxia-induced PH in mice, for which eNOS activation may partially be involved.
18369695
Antiangiogenic properties of fasudil, a potent Rho-Kinase inhibitor.. Yasuaki Hata; Muneki Miura; Shintaro Nakao; Shuhei Kawahara; Takeshi Kita; Tatsuro Ishibashi (2008) Japanese journal of ophthalmology display abstract
PURPOSE: Vascular endothelial growth factor (VEGF) plays a pivotal role in pathological angiogenesis. In this study, we addressed the therapeutic potential of fasudil, a potent Rho-kinase inhibitor, for VEGF-elicited angiogenesis and also for the intracellular signalings induced by VEGF. METHODS: In vitro, the inhibitory effects of fasudil on the VEGF-dependent VEGF receptor 2 (VEFGR2 or KDR), extracellular signal-related kinase (ERK) 1/2, Akt and myosin light chain (MLC) phosphorylation, as well as on the migration and proliferation of bovine retinal microvascular endothelial cells (BRECs) were analyzed with Western blotting, [3H]-thymidine uptake, and modified Boyden chamber assay. VEGF-elicited in vivo angiogenesis was analyzed with a mouse corneal micropocket assay coembedded with or without fasudil. RESULTS: VEGF caused enhanced MLC phosphorylation of BRECs, which was almost completely attenuated by 10microM fasudil. VEGF-dependent phosphorylation of ERK1/2 and Akt were also partially but significantly attenuated by treatment with fasudil without affecting VEGFR2 (KDR) phosphorylation. Moreover, both VEGF-induced [3H]-thymidine uptake and the migration of BRECs were significantly inhibited in the presence of fasudil. Finally, VEGF-elicited angiogenesis in the corneal micropocket assay was potently attenuated by coembedding with fasudil (P < 0.01). CONCLUSIONS: These findings indicate that fasudil might have a therapeutic potential for ocular angiogenic diseases. The antiangiogenic effect of fasudil appears to be mediated through the blockade not only of Rho-kinase signaling but also of ERK and Akt signaling.