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Drug-Target Interaction

Drug

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PubChem ID:7454
Structure:
Synonyms:
.alpha.,p-Dibromoacetophenone
.alpha.-p-Dibromoacetophenone
2,4 -Dibromoacetophenone
2,4'-dibromo acetophenone
2,4'-Dibromo-acetophenone
2,4'-Dibromoacetophenone
2,4-dibromoacetophenone
2-Bromo-1-(4-bromo-phenyl)-ethanone
2-bromo-1-(4-bromophenyl)ethan-1-one
2-bromo-1-(4-bromophenyl)ethanone
4'-Bromophenacyl bromide
4-07-00-00652 (Beilstein Handbook Reference)
4-BPB
4-Bromo(bromoacetyl)benzene
4-Bromophenacyl bromide
99-73-0
a,p-dibromoacetophenone
A5501
AC1L1OSP
AC1Q27E1
Acetophenone, 2,4'-dibromo-
AG-I-02352
AI3-52310
AIDS-026799
AIDS026799
AKOS000210402
alpha,4'-Dibromoacetophenone
alpha,4-Dibromoacetophenone
alpha,p-Dibromoacetophenone
alpha-4-Dibromoacetophenone
alpha-para-dibromoacetophenone
ARONIS007671
BRN 0607604
Bromomethyl 4-bromophenyl ketone
Bromomethyl p-bromophenyl ketone
bromophenacyl bromide
bromophenacylbromide
C006821
C8H6Br2O
CCRIS 3623
CHEMBL142826
D0164
D38308_ALDRICH
dibromoacetophenone-2,4
EINECS 202-783-6
Ethanone, 2-bromo-1-(4-bromophenyl)-
F1723-0259
FS000052
GSK-3beta Inhibitor VII
Halomethyl Phenyl Ketone deriv. 24
HSCI1_000166
IN1317
LS-13457
MolPort-000-153-851
NSC 6224
NSC6224
p-.alpha.-Dibromoacetophenone
p-Bromophenacyl bromide
p-Bromophenacyl-8
P-DIBROMOACETOPHENONE
Parabromophenacyl bromide
PBPAB
pbpb
S01-0145
ST001361
STL069069
Tau Protein Kinase I Inhibitor
TL8006077
TOS-BB-1138
TPK I Inhibitor
WLN: E1VR DE
ZINC00028146

Target

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Uniprot ID:Q62710_RAT
Synonyms:
Nitric oxide synthase
EC-Numbers:-
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

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

References:

15777770
Xanthine oxidase, nitric oxide synthase and phospholipase A(2) produce reactive oxygen species via mitochondria.. Basavaraju G Sanganahalli; Preeti G Joshi; Nanda B Joshi (2005) Brain research display abstract
The formation of reactive oxygen species (ROS) has been suggested to be associated with excitotoxicity but the involvement of cytoplasmic enzymes in ROS formation is not clearly known. In the present study, we examined the role of xanthine oxidase (XO), nitric oxide synthase (NOS) and phospholipase A(2) (PLA(2)) in glutamate-induced oxidative stress in rat cortical slices. Glutamate-induced ROS formation and mitochondrial depolarization were measured in rat cortical slices in presence of allopurinol, L-NAME and 4-bromophenacylbromide, the specific inhibitors of XO, NOS and PLA(2), respectively. Upon stimulation of slices with glutamate, a significant increase in ROS formation and mitochondrial depolarization was observed. However, pretreatment of slices with allopurinol, L-NAME and 4-bromophenacylbromide inhibited the glutamate-induced ROS formation and mitochondrial depolarization. The glutamate-induced ROS formation was dependent on the concentration of these inhibitors and also on the duration of the treatment. Allopurinol was found to be less effective as compared to L-NAME and 4-bromophenacylbromide. The combined treatment of slices with these enzyme inhibitors showed further inhibition in ROS formation and mitochondrial depolarization. The inhibition in ROS formation as well as mitochondrial depolarization by allopurinol, L-NAME and 4-bromophenacylbromide clearly suggests that the activation of XO, NOS and PLA(2) by calcium during glutamate receptor stimulation may release some chemicals which depolarize mitochondria resulting in ROS formation.