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Drug-Target Interaction

Drug

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PubChem ID:3652
Structure:
Synonyms:
118-42-3
118-42-3 (FREE BASE)
2-((4-((7-Chloro-4-quinolyl)amino)pentyl)ethylamino)ethanol
2-(N-(4-(7-Chlor-4-chinolylamino)-4-methylbutyl)ethylamino)ethanol
2-[4-[(7-chloroquinolin-4-yl)amino]pentyl-ethylamino]ethanol
2-[{4-[(7-chloroquinolin-4-yl)amino]pentyl}(ethyl)amino]ethanol
5-22-10-00280 (Beilstein Handbook Reference)
7-Chloro-4-(4-(ethyl(2-hydroxyethyl)amino)-1-methylbutylamino)quinoline
7-Chloro-4-(4-(N-ethyl-N-beta-hydroxyethylamino)-1-methylbutylamino)quinol
7-Chloro-4-(4-(N-ethyl-N-beta-hydroxyethylamino)-1-methylbutylamino)quinoline
7-Chloro-4-(5-(N-ethyl-N-2-hydroxyethylamino)-2-pentyl)aminoquinoline
747-36-4
747-36-4 (MONOSULFATE SALT)
AIDS-001918
AIDS001918
BRN 0253894
C07043
C18H26ClN3O
DB01611
DivK1c_000942
EINECS 204-249-8
Ethanol, 2-((4-((7-chloro-4-quinolinyl)amino)pentyl)ethylamino)-
Ethanol, 2-((4-((7-chloro-4-quinolyl)amino)pentyl)ethylamino)-
Ethanol, 2-[[4-[(7-chloro-4-quinolinyl)amino]pentyl]ethylamino]-
Gen-Hydroxychloroquine 200mg Tablets
HCQ
Hidroxicloroquina [INN-Spanish]
Hydroxychlorochin
Hydroxychloroguine
Hydroxychloroquine
Hydroxychloroquine sulfate
Hydroxychloroquine Sulfate (1:1) Salt
Hydroxychloroquine [INN:BAN]
Hydroxychloroquinum [INN-Latin]
IDI1_000942
Idrossiclorochina [DCIT]
KBio1_000942
LS-66614
NCGC00159483-02
NINDS_000942
NSC4375 (MONOSULFATE SALT)
Oxichlorochinum
Oxichloroquine
Oxychlorochin
Oxychloroquine
Plaquenil
SBB012559
SPBio_001116
Spectrum2_001238
Spectrum5_001697
ST072188
WIN 1258
ATC-Codes:
Side-Effects:
Side-EffectFrequency
allergic reaction0
erythema0
tinnitus0
thrombocytopenia0
stevens - johnson syndrome0
visual field defect0
retinopathy0
psychosis0
psoriasis0
pruritus0
porphyria0
urticaria0
vertigo0
abnormal pigmentation0
cardiomyopathy0
paralysis0
blindness0
photosensitivity0
blurred vision0
photophobia0
hepatic failure0
weight loss0
vomiting0
weakness0
nystagmus0
nightmares0
convulsions0
bronchospasm0
ataxia0
asthenia0
anorexia0
angioedema0
aplastic anemia0
anemia0
alopecia0
agranulocytosis0
deafness0
exfoliative dermatitis0
neuromyopathy0
nervousness0
nausea0
myopathy0
leukopenia0
irritability0
headache0
edema0
dizziness0
diarrhea0
abdominal cramps0

Target

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Uniprot ID:ICE_DROME
Synonyms:
Caspase
drICE
EC-Numbers:3.4.22.-
Organism:Drosophila melanogaster
Fruit fly
PDB IDs:-

Binding Affinities:

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

References:

16734620
Hydroxychloroquine potentiates Fas-mediated apoptosis of rheumatoid synoviocytes.. W-U Kim; S-A Yoo; S-Y Min; S-H Park; H-S Koh; S-W Song; C-S Cho (2006) Clinical and experimental immunology display abstract
Inadequate apoptosis may contribute to the synovial hyperplasia associated with rheumatoid arthritis (RA). The Fas-associated death domain protein (FADD)-like interleukin (IL)-1beta-converting enzyme (FLICE)-inhibitory protein (FLIP), which is an apoptotic inhibitor, has been implicated in the resistance to Fas-mediated apoptosis of synoviocytes. This study investigated whether hydroxychloroquine (HCQ), an anti-rheumatic drug, induces the apoptosis of rheumatoid synoviocytes, and modulates the expression of FLIP. Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and were cultured with various concentrations of HCQ in the presence or absence of the IgM anti-Fas monoclonal antibodies (mAb) (CH11). Treatment with HCQ, ranging from 1 to 100 microM, induced the apoptosis of FLS in a dose- and time-dependent manner. The increase in synoviocytes apoptosis by HCQ was associated with caspase-3 activation. A combined treatment of HCQ and anti-Fas mAb increased FLS apoptosis and caspase-3 activity synergistically, compared with either anti-Fas mAb or HCQ alone. The Fas expression level in the FLS was not increased by the HCQ treatment, while the FLIP mRNA and protein levels were decreased rapidly by the HCQ treatment. Moreover, time kinetics analysis revealed that the decreased expression of FLIP by HCQ preceded the apoptotic event that was triggered by HCQ plus anti-Fas mAb. Taken together, HCQ increases the apoptosis of rheumatoid synoviocytes by activating caspase-3, and also sensitizes rheumatoid synoviocytes to Fas-mediated apoptosis. Our data suggest that HCQ may exert its anti-rheumatic effect in rheumatoid joints through these mechanisms.