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Drug-Target Interaction

Drug

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PubChem ID:2214
Structure:
Synonyms:
1-(4-hydroxy-3-methoxyphenyl)-ethanone
1-(4-hydroxy-3-methoxyphenyl)ethan-1-one
1-(4-Hydroxy-3-methoxyphenyl)ethanone
3-Methoxy-4-hydroxyacetophenone
3-Metoksy-4-hydroksyacetofenon
3-Metoksy-4-hydroksyacetofenon [Polish]
4'-Hydroxy-3'-methoxyacetophenone
4-08-00-01814 (Beilstein Handbook Reference)
4-Acetyl-2-methoxyphenol
4-Hydroxy-3-methoxyacetophenone
4-Hydroxy-3-methoxyphenyl methyl ketone
498-02-2
A10809_ALDRICH
AA-504/20839006
AB1003774
AC-11656
AC1L1D6F
AC1Q46A5
AC1Q7AD6
Acetoguaiacon
Acetoguaiacone
Acetophenone, 4'-hydroxy-3'-methoxy-
ACETOPHENONE,4-HYDROXY,3-METHOXY ACETOVANILLON
ACETOPHENONE,4-HYDROXY,3-METHOXY ACETOVANILLON
Acetovanillon
Acetovanillone
Acetovanilone
Acetovanyllon
AI3-15892
AKOS000120562
Apocynin
Apocynine
AR-1H7512
BB_NC-2250
bmse000584
bmse010031
BRN 0637373
C056165
C11380
C9H10O3
CCRIS 7285
CHEBI:2781
CHEMBL346919
EINECS 207-854-5
Ethanone, 1-(4-hydroxy-3-methoxyphenyl)-
H0261
I01-7005
LS-13569
MLS001304972
MolPort-000-000-274
NCGC00247065-01
nchembio.83-comp20
NSC 209524
NSC209524
NSC2146
SBB008060
SMR000752909
W508454_ALDRICH
WLN: 1VR DQ CO1
ZINC00162515

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.