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TED-347 YAP inhibitor

Cat.No.S8951

TED-347 is a potent, irreversible, covalent and allosteric inhibitor of the TEAD⋅Yap protein-protein interaction. This compound inhibits TEAD4⋅Yap1 protein-protein interaction with an apparent EC50 of 5.9 μM.
TED-347 YAP inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 313.70

Quality Control

Batch: S895101 DMSO]69 mg/mL]false]Ethanol]25 mg/mL]false]Water]˂1 mg/mL]false Purity: 99.72%
99.72

Chemical Information, Storage & Stability

Molecular Weight 313.70 Formula

C15H11ClF3NO

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 2378626-29-8 -- Storage of Stock Solutions

Synonyms N/A Smiles C1=CC=C(C(=C1)C(=O)CCl)NC2=CC=CC(=C2)C(F)(F)F

Solubility

In vitro
Batch:

DMSO : 69 mg/mL (219.95 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 25 mg/mL

Water : ˂1 mg/mL

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

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.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
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Mechanism of Action

Targets/IC50/Ki
TEAD4⋅Yap1 [1]
(Cell-free assay)
5.9 μM(EC50)
In vitro

TED-347 is found to inhibit the protein-protein interaction in a time-dependent manner. This compound is shown to functionally disrupt the TEAD·Yap1 interaction in cells and to reduce the viability of patient-derived glioblastoma cell lines.[1]

References

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