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Drug-Target Interaction

Drug

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PubChem ID:1701
Structure:
Synonyms:
34284-75-8
35452-30-3
4-(2-Aminoethyl)benzenesulfonyl fluoride
4-(2-Aminoethyl)benzenesulfonyl fluoride hydrochloride
4-(2-Aminoethyl)benzenesulfonylfluoride
4-beta-Aminoethylbenzolsulfofluoride
AC1L1C1L
AC1Q4OX1
AEBSF
AES
AIDS-122624
AIDS122624
AR-1F5821
Benzenesulfonyl fluoride, 4-(2-aminoethyl)-
C002010
C8H10FNO2S
CCG-204227
CHEBI:40582
CHEMBL1096339
DB07347
Lopac-A-8456
Lopac0_000132
LS-174460
NCGC00015097-01
NCGC00015097-02
NCGC00015097-03
NCGC00162071-01
Pefabloc
[4-(2-Aminoethyl)-benzenesulphonyl fluoride]

Target

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Uniprot ID:NOS3_HUMAN
Synonyms:
cNOS
Constitutive NOS
EC-NOS
Endothelial NOS
eNOS
Nitric oxide synthase, endothelial
NOS type III
NOSIII
EC-Numbers:1.14.13.39
Organism:Homo sapiens
Human
PDB IDs:1M9J 1M9K 1M9M 1M9Q 1M9R 3EAH 3NOS
Structure:
3NOS

Binding Affinities:

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

References:

15740722
Antioxidants inhibit human endothelial cell functions through down-regulation of endothelial nitric oxide synthase activity.. Christos Polytarchou; Evangelia Papadimitriou (2005) European journal of pharmacology display abstract
We have recently shown that superoxide and hydrogen peroxide are putative inducers of angiogenesis in vivo, possibly through up regulation of inducible nitric oxide synthase (NOS) and increased production of endogenous nitric oxide (NO). The aim of the present work was to elucidate the implication of reactive oxygen species in endothelial cell functions, using cultures of human umbilical vein endothelial cells (HUVEC). Superoxide dismutase (SOD), tempol (membrane permeable SOD mimetic) and the NADPH oxidase inhibitors, 4-(2-aminoethyl)-benzenesulfonyl fluoride and apocynin, but not allopurinol, inhibited HUVEC proliferation and migration, as well as activity of endothelial NOS (eNOS). Catalase and the intracellular hydrogen peroxide scavenger sodium pyruvate decreased, while hydrogen peroxide increased HUVEC proliferation, migration and activity of eNOS. Dexamethasone induced the proliferation and migration of HUVEC and activated eNOS. Nomega-nitro-L-arginine methyl ester (L-NAME), but not Nomega-nitro-D-arginine methyl ester, decreased endothelial cell functions and reversed the effects of dexamethasone and hydrogen peroxide. N5-(1-iminoethyl)-L-ornithine dihydrochloride, but not the inducible NOS specific inhibitor N-[[3-(aminomethyl)phenyl]methyl]-ethanimidamide dihydrochloride also decreased endothelial cell functions, similarly to L-NAME. The guanylate cyclase inhibitor 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one inhibited HUVEC proliferation in a concentration-dependent manner and completely reversed hydrogen peroxide-induced proliferation, migration and cGMP accumulation. In conclusion, superoxide and hydrogen peroxide seem to play a significant role in promoting endothelial cell proliferation and migration, possibly through regulation of eNOS activity.