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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:MK03_HUMAN
Synonyms:
ERK-1
ERT2
Extracellular signal-regulated kinase 1
Insulin-stimulated MAP2 kinase
MAP kinase 1
MAPK 1
Microtubule-associated protein 2 kinase
Mitogen-activated protein kinase 3
p44-ERK1
p44-MAPK
EC-Numbers:2.7.11.24
Organism:Homo sapiens
Human
PDB IDs:2ZOQ
Structure:
2ZOQ

Binding Affinities:

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

References:

12566304
Sulindac sulfide inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cells.. Pamela L Rice; Michele Washington; Shea Schleman; K Scott Beard; Linda J Driggers; Dennis J Ahnen (2003) Cancer research display abstract
Colorectal cancer is the second leading cause of cancer death in the United States. Nonsteroidal anti-inflammatory drugs including sulindac are promising chemopreventive agents for colorectal cancer. Sulindac and selective cyclooxygenase (COX)-2 inhibitors cause regression of colonic polyps in familial polyposis patients. Sulindac induces apoptotic cell death in cancer cells in vitro and in vivo. In tumor cells, activation of extracellular-regulated kinase (ERK) 1/2 results in phosphorylation of several ERK1/2 effectors, including the proapoptotic protein Bad. Phosphorylation of Ser112 by ERK1/2 inactivates Bad and protects the tumor cell from apoptosis. Sulindac metabolites and other nonsteroidal anti-inflammatory drugs selectively inhibit ERK1/2 phosphorylation in human colon cancer cells. In this study we show that epidermal growth factor (EGF) strongly induces phosphorylation of ERK1/2 and Bad in HT29 colon cancer cells. EGF-stimulated phosphorylation of ERK and Bad is blocked by pretreatment with U0126, a selective MAP kinase kinase (MKK)1/2 inhibitor. Similarly, pretreatment with sulindac sulfide blocks the ability of EGF to induce ERK1/2 and Bad phosphorylation, but also down-regulates total Bad but not ERK1/2 protein levels. The ability of sulindac to block ERK1/2 signaling by the EGF receptor may account for at least part of its potent growth-inhibitory effects against cancer cells.