iCRT3 Wnt/beta-catenin antagonist

Cat.No.S8647

iCRT3 is an antagonist of Wnt/β-catenin signaling with an IC50 of 8.2 nM in the Wnt responsive STF16-luc reporter assays.
iCRT3 Wnt/beta-catenin antagonist Chemical Structure

Chemical Structure

Molecular Weight: 394.53

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 394.53 Formula

C23H26N2O2S

Storage (From the date of receipt)
CAS No. 901751-47-1 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CCC1=CC=C(C=C1)C2=NC(=C(O2)C)CSCC(=O)NCCC3=CC=CC=C3

Solubility

In vitro
Batch:

DMSO : 78 mg/mL (197.7 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 78 mg/mL

Water : Insoluble

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Mass Concentration Volume Molecular Weight

In vivo
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Mechanism of Action

Targets/IC50/Ki
Wnt/β-catenin [1]
(in STF16 assay)
8.2 nM
In vitro
iCRT3 is a small molecule inhibitor of the Wnt pathway which binds to β-catenin interfering with its interaction with TCF. This compound significantly reduces the LPS-induced Wnt/β-catenin activity and also inhibits TNF-α production and IκB degradation in a dose-dependent manner. It does not influence the transcriptional activity of FOP-Flash luciferase reporter, which harbors mutations in the DNA binding sites for TCF (β-cat response element), showing specificity of the response. It inhibits cytokine production in LPS-stimulated macrophages[1][2].
In vivo
Intraperitoneal administration of iCRT3 to C57BL/6 mice, subjected to cecal ligation and puncture-induced sepsis, decreases the plasma levels of proinflammatory cytokines and organ injury markers in a dose-dependent manner. The histological integrity of the lungs is improved with this compound treatment, along with reduced lung collagen deposition and apoptosis. In addition, this treatment also decreases the expression of the cytokines, neutrophil chemoattractants, as well as the MPO activity in the lungs of septic mice[2].
References

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Signaling Pathway Map