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Drug-Target Interaction

Drug

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PubChem ID:5469318
Structure:
Synonyms:
162520-00-5
2-(((2E,6E)-3,7,11-Trimethyl-2,6,10-dodecatrienyl)sulfanyl)benzoic acid
2-[(2E,6E)-3,7,11-trimethyldodeca-2,6,10-trienyl]sulfanylbenzoic acid
AC1NV5Y3
Benzoic acid, 2-(((2E,6E)-3,7,11-trimethyl-2,6,10-dodecatrienyl)thio)-
C093323
CCG-204607
CHEBI:130247
CHEMBL23293
D08995
EU-0100517
F 8175
Farnesylthiosalicylic acid
FTS
Lopac-F-8175
Lopac0_000517
LS-186975
LS-187617
NCGC00015448-01
NCGC00015448-02
NCGC00015448-03
NCGC00093912-01
NCGC00093912-02
NSC685986
S-Farnesylthiosalicylic acid
S-trans,trans-farnesylthiosalicylic acid
Salirasib
Salirasib (INN/USAN)
Salirasib [USAN]
UNII-MZH0OM550M

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:

16239932
Farnesylthiosalicylic acid induces caspase activation and apoptosis in glioblastoma cells.. S Amos; G T Redpath; G Polar; R McPheson; D Schiff; I M Hussaini (2006) Cell death and differentiation display abstract
Primary glioblastomas (GBMs) commonly overexpress the oncogene epidermal growth factor receptor (EGFR), which leads to increased Ras activity. FTA, a novel Ras inhibitor, produced both time- and dose-dependent caspase-mediated apoptosis in GBM cell lines. EGFR-mediated increase in 3H-thymidine uptake was inhibited by FTA. FACS analysis was performed to determine the percent of apoptotic cells. The sub-Go population of GBM cells was increased from 4.5 to 13.8% (control) to over 45-53.6% in FTA-treated cells within 24 h. Furthermore, FTA also increased the activities of both caspase-3 and -9, and PARP cleavage. Treatment of GBMs with FTA before or after EGF addition to the cultures blocked phosphorylation of Akt and mitogen-activated protein kinases (MAPK). FTA also significantly reduced the amount of EGF-induced Ras-GTP as reflected by a decrease in the level of Ras bound to Raf-RBD-GST. This study demonstrates that inhibition of Ras methylation may provide a therapeutic target for the treatment of GBMs overexpressing EGFR.