CAS NO: | 108409-83-2 |
规格: | ≥98% |
包装 | 价格(元) |
10mg | 电议 |
25mg | 电议 |
50mg | 电议 |
100mg | 电议 |
250mg | 电议 |
500mg | 电议 |
1g | 电议 |
Molecular Weight (MW) | 361.20 |
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Formula | C13H10Cl2N2O4S |
CAS No. | 108409-83-2 |
Storage | -20℃ for 3 years in powder form |
-80℃ for 2 years in solvent | |
Solubility (In vitro) | DMSO: 72 mg/mL (199.3 mM) |
Water: <1 mg/mL | |
Ethanol: <1 mg/mL | |
SMILES Code | O=S(C1=CC(Cl)=CC=C1Cl)(NC2=CC=C([N+]([O-])=O)C=C2C)=O |
Synonyms | FH-535; FH535; FH 535; Chemical Name: 2,5-dichloro-N-(2-methyl-4-nitrophenyl)-benzenesulfonamide InChi Key: AXNUEXXEQGQWPA-UHFFFAOYSA-N InChi Code: InChI=1S/C13H10Cl2N2O4S/c1-8-6-10(17(18)19)3-5-12(8)16-22(20,21)13-7-9(14)2-4-11(13)15/h2-7,16H,1H3 SMILES Code: O=S(C1=CC(Cl)=CC=C1Cl)(NC2=CC=C([N+]([O-])=O)C=C2C)=O |
In Vitro | In vitro activity: FH535 is a potent inhibitor of the Wnt/β-catenin signaling pathway and also a dual PPARγ and PPARδ antagonist. In vitro, FH535 can inhibit the growth of colon, lung, and hepatocellular carcinoma but not normal fibroblasts. FH535 selectively inhibits cell proliferation and potentiates imatinib-induced apoptosis in myeloid leukemia cell lines. It is reported that FH535 has ability to inhibit growth, migration, and invasion of TN breast cancer cell lines (MDA-MB-231 and HCC38) without affecting adhesive abilities of cells to type I collagen. FH535 antagonizes β-Catenin/Tcf–mediated transcription, and inhibits recruitment of the coactivators GRIP1 and β-catenin to PPARδ and PPARγ. FH535 shows selective anti-proliferation effect on some cancer cells expressing high or active Wnt/β-catenin pathway. FH535 increases cigarette smoke condensate cytotoxicity, and causes changes in β-catenin and EGR-1 signaling. FH535 has potential therapeutic value in treatment of liver cancer by targeting liver cancer stem cells and hepatocellular carcinoma cell lines. Kinase Assay: Three copies of the optimized or mutated Tcf-binding element from TOPFLASH or FOPFLASH driving a secreted alkaline phosphatase reporter gene are cloned into pCEP4 plasmid, replacing the cytomegalovirus promoter. The plasmids are transfected into HepG2 cells, and hygromycin-resistant clones are pooled. Library screening is done at 20 μmol/L concentration in HepG2 serum-free media. Hits are tested in the HCT116 cell line for inhibition of TOPFLASH luciferase activity but not for inhibition of a reporter activity controlled from β-actin promoter. Cell Assay: Cell viability is determined by the modified 3H-thymidine incorporation assay. Briefly, cells (HCT116, SW48, RKO, LoVo, COLO205, IEC6, A427, HCC15, NCI-H1703, A549, HepG2, Hep3b, Huh7, Fibroblasts) are plated in 96-well microplates for 24 h and treated in triplicate with various concentrations of the test compound. After 48 h of compound exposure, the cells are incubated for an additional 48 h in compound-free medium. The cells are then incubated in medium containing 3H-thymidine for 24 h, washed and mixed with the scintillant in the 96-well plate. Individual wells are counted with a 96-well scintillation counter and the LC50 is calculated. |
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In Vivo | FH535 (at 25 mg/kg, i.p.) demonstrates a potent anti-tumor effect on pancreatic cancer xenografts in mice. FH535 also represses angiogenesis in pancreatic cancer xenografts. |
Animal model | Female BALB/c athymic nude mice (Four weeks old) |
Formulation & Dosage | Prepared in 100 μL DMSO/DMEM (1:1); 25 mg/kg; i.p. |
References | Mol Cancer Ther. 2008 Mar;7(3):521-9. doi: 10.1158/1535-7163.MCT-07-2063; Int J Toxicol. 2012 Jul-Aug;31(4):380-9; PLoS One. 2014 Jun 18;9(6):e99272; Onco Targets Ther. 2015 Jul 6;8:1651-70. |