108409-83-2

FH-535 (108409-83-2) suppresses Wnt/β-catenin signaling. It antagonizes PPARγ and PPARδ ligand-dependent activation which is mediated by inhibition of recruitment of the coactivators β-catenin and GRIP1 but not the corepressors NCoR and SMRT.1?Inhibits the migration and growth of breast cancer cell lines2 as well as colon, lung and liver cell lines1. FH-535 is a useful tool for probing the involvement of Wnt signaling pathway.3,4

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A cell-permeable compound that inhibits Wnt/β-catenin and PPAR

Antagonizes Wnt/β-catenin/Tcf-mediated transcription as well as PPARγ and δ activity. Able to inhibit the recruitment of the co-activators β-catenin and GRIP1, both of which are activators for both pathways.

ChEBI: 2,5-dichloro-N-(2-methyl-4-nitrophenyl)benzenesulfonamide is a sulfonamide.

FH535 has the ability to block the development of colon cancer cells. It can change several cancer-associated biological processes. FH535 can also prevent PARylation of Axin2 in osteosarcoma cells.

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1) Handeli et al. (2008), A small-molecule inhibitor of Tcf/beta-catenin signaling down-regulates PPARgamma and PPARdelta activities; Mol. Cancer Ther., 7 521 2) Iida et al. (2012), FH535 inhibited migration and growth of breast cancer cells; PLoS One, 7 e44418 3) Frewer et al. (2013), A role for WISP2 in colorectal cancer cell invasion and motility; Cancer Genomics Proteomics, 10 187 4) Polk et al. (2012), FH535 potentiation of cigarette smoke condensate cytotoxicity is associated with changes in β-catenin and EGR-1 signaling; Int. J. Toxicol., 31 380 5) Morita and Hayashi (2018), Tumor Progression is Mediated by Thymosin-β4 through a TGFβ/MRTF Signaling Axis; Mol. Cancer Res. 16(5) 880