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Drug-Target Interaction

Drug

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PubChem ID:5352624
Structure:
Synonyms:
(Z)-5-Fluoro-2-methyl-1-((4-(methylthio)phenyl)methylene)-1H-indene-3-acet
(Z)-5-Fluoro-2-methyl-1-((4-(methylthio)phenyl)methylene)-1H-indene-3-acetic acid
(Z)-5-Fluoro-2-methyl-1-[p-(methylthio)benzylidene]indene-3-acetic acid
(Z)-Sulindac sulfide
1H-Indene-3-acetic acid, 5-fluoro-2-methyl-1-((4-(methylthio)phenyl)methylene)-, (Z)-
49627-27-2
5-fluoro-2-methyl-1-(4-methylthiobenzylidene)inden-3-ylacetic acid
AC-20512
AC1NS2PY
CHEBI:121650
CHEMBL18797
EINECS 256-403-9
NCGC00161601-01
S3131_SIGMA
Sulindac sulfide
UNM-0000306137
UPCMLD-DP020
UPCMLD-DP020:001

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:
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References:

12017300
Sulindac induces apoptosis, inhibits proliferation and activates caspase-3 in Hep G2 cells.. Jian-Jun Liu; Ji-Yao Wang; Erik Hertervig; Ake Nilsson; Rui-Dong Duan (2002) Anticancer research display abstract
BACKGROUND: It has recently been reported that sulindac has an apoptotic effect on KYN-2 cells, an undifferentiated hepatoma cell line. The present work investigates whether sulindac also has an apoptotic effect on well-differentiated hepatoma cells and what its potential mechanism might be. MATERIALS AND METHODS: Hep G2 cells were treated with sulindac at different concentrations. Apoptosis rate, cell proliferation and 3H-thymidine incorporation were measured. The activities of caspase-3, acid and neutral sphingomyelinase and the changes of sphingomyelin content were also assayed. RESULTS: Sulindac dose-dependently induced apoptosis in Hep G2 cells; both sulindac sulfone and sulfide had similar effects. The apoptosis was accompanied by an increase of caspase-3 activity and a decrease of cell proliferation and 3H-thymidine incorporation. No significant change could be observed for the activity of sphingomyelinase and sphingomyelin content. CONCLUSION: Sulindac induces apoptosis and inhibits proliferation in Hep G2 cells. The effect may be mediated by a pathway related to caspase-3 activation but independent of sphingomyelin metabolism