For research use only.
CAS No. 108409-83-2
FH535 is a Wnt/β-catenin signaling inhibitor and also a dual PPARγ and PPARδ antagonist.
Selleck's FH535 has been cited by 13 publications
4 Customer Reviews
H. HCCLM3 si-THOR or SMMC7721si-THOR and their control cells were treated with FH535 (40 nM) or not and CD133+ or EpCAM+ hepatoma cells was checked by flow-cytometric assay. I. HCCLM3 si-THOR or SMMC7721si-THOR and their control cells were treated with FH535 (40 nM) or not and subjected to spheroid formation.
Gene, 2019, 684:95-103. FH535 purchased from Selleck.
BrdU assay was used to detect the proliferation level of cells in four groups: the control group, FH535 (15 μM) group, NAM (50 mM) + FH535 (15 μM) group, REV (100 μM) + FH535 (15 μM) group. A. At the next day, the cells were fixed and immunostained for BrdU (red) and with DAPI (blue) then merged the two pictures of the same field. The scale bar is 100 μm. B. The total numbers of cells (DAPI-staining cells) per field in the four groups. C. BrdU-positive rate of C2C12 cells was analyzed. Each value represents the mean ± standard error of the mean of triplicate determinations from three independent cell preparations. *P<0.05, **P<0.01, ***P<0.001 vs the value of the control; n=3; error bars ± standard error of means. Statistical analysis was conducted using one-way ANOVA. Original magnification is ×200.
Int J Clin Exp Pathol, 2016, 9(3):2857-2868.. FH535 purchased from Selleck.
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Choose Selective Wnt/beta-catenin Inhibitors
|Description||FH535 is a Wnt/β-catenin signaling inhibitor and also a dual PPARγ and PPARδ antagonist.|
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. 
High-throughput Library Screen: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.
|In vitro||DMSO||72 mg/mL warmed (199.33 mM)|
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In vivo Formulation Calculator (Clear solution)
|Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)|
|Dosage||mg/kg||Average weight of animals||g||Dosing volume per animal||ul||Number of animals|
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|% DMSO % % Tween 80 % ddH2O|
Working concentration： mg/ml；
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Method for preparing in vivo formulation：Take μL DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH2O，mix and clarify.
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