For research use only
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ICG-001 is an inhibitor of β-catenin/TCF mediated transcription. ICG-001 works by specifically binding to cyclic AMP response element-binding protein with an IC50 of 3 μM. ICG-001 selectively blocks the β-catenin/CBP interaction without interfering with the β-catenin/p300 interaction.
|IC50 & Target|
IC50: 3 μM (CBP)
ICG-001 (5 mg/kg per day) significantly inhibits beta-catenin signaling in mice, while concurrently preserving the epithelium. Administration of a water-soluble analog of ICG-001 for 9 weeks reduces the formation of colon and small intestinal polyps by 42% as effectively as the nonsteroidal antiinflammatory agent MK-231, which has consistently demonstrated efficacy in this model. ICG-001 (150 mg/kg, i.v.) demonstrates a dramatic reduction in tumor volume over the 19-day course of treatment, with no mortality or weight loss in the SW620 nude mouse xenograft model of tumor regression.
ICG-001 (5μM) inhibits leptin-induced EMT, invasion and tumorsphere formation in MCF7 cells. ICG-001 can phenotypically rescue normal nerve growth factor (NGF)-induced neuronal differentiation and neurite outgrowth in the presenilin-1 mutant cells, emphasizing the importance of the TCF/β-catenin signaling pathway on neurite outgrowth and neuronal differentiation. ICG-001 (25μM) treatment reduces the steady-state levels of Survivin and Cyclin D1 RNA and protein in SW480 cells, both of which can be up-regulated by β-catenin. ICG-001 selectively induces apoptosis in transformed cells but not in normal colon cells, and reduces in vitro growth of colon carcinoma cells.
|In solvent||-80°C||6 months|
. Yan D, et al, Leptin-induced epithelial-mesenchymal transition in breast cancer cells requires β-catenin activation via Akt/GSK3- and MTA1/Wnt1 protein-dependent pathways. J Biol Chem, 2012, 287(11), 8598-8612.