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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:DUOX2_HUMAN
Synonyms:
Dual oxidase 2
Large NOX 2
Long NOX 2
NADH/NADPH thyroid oxidase p138-tox
NADPH oxidase/peroxidase DUOX2
NADPH thyroid oxidase 2
p138 thyroid oxidase
Thyroid oxidase 2
EC-Numbers:1.11.1.-
1.6.3.1
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

9272382
Low-density lipoprotein stimulated peroxide production and endocytosis in cultured human endothelial cells: mechanisms of action.. J A Holland; J W Meyer; M E Schmitt; M D Sauro; D K Johnson; R W Abdul-Karim; V Patel; L M Ziegler; K J Schillinger; R F Small; L F Lemanski (1997) Endothelium : journal of endothelial cell research display abstract
The effects of arachidonic acid metabolism and NADPH oxidase inhibitor on the hydrogen peroxide (H2O2) generation and endocytotic activity of cultured human endothelial cells (EC) exposed to atherogenic low-density lipoprotein (LDL) levels have been investigated. EC were incubated with 240 mg/dl LDL cholesterol and cellular H2O2 production and endocytotic activity measured in the presence and absence of the arachidonic acid metabolism inhibitors, indomethacin, nordihydroguaiaretic acid, and SKF525A, and NADPH oxidase inhibitor, apocynin. All inhibitors, with the exception of indomethacin, markedly reduced high LDL-induced increases in EC H2O2 generation and endocytotic activity. EC exposed to exogenously applied arachidonic acid had cellular functional changes similar to those induced by high LDL concentrations. EC incubated with 1-25 uM arachidonic acid had increased H2O2 production and heightened endocytotic activity. Likewise, EC pre-loaded with [3H]arachidonic acid when exposed to increasing LDL levels (90-330 mg/dl cholesterol) had a dose-dependent rise in cytosolic [3H]arachidonic acid. The phospholipase A2 inhibitors, 4-bromophenacyl bromide and 7,7-dimethyleicosadienoic acid, markedly inhibited H2O2 production in EC exposed to 240 mg/dl LDL cholesterol. These findings suggest that arachidonic acid contributes mechanistically to high LDL-perturbed EC H2O2 generation and heightened endocytosis. Such cellular functional changes add to our understanding of endothelial perturbation, which has been hypothesized to be a major contributing factor in the pathogenesis of atherosclerosis.