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Diflunisal COX inhibitor

Cat.No.S4609

Diflunisal (Dolobid, Dolobis, Flovacil, Fluniget, MK-647) is a difluorophenyl derivate of salicylic acid and a nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, analgesic and anti-inflammatory properties. The mechanism of action of this compound is as a Cyclooxygenase Inhibitor.
Diflunisal COX inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 250.20

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Quality Control

Batch: Purity: 99.99%
99.99

Solubility

In vitro
Batch:

DMSO : 50 mg/mL (199.84 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 50 mg/mL

Water : Insoluble

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In vivo
Batch:

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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
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Chemical Information, Storage & Stability

Molecular Weight 250.20 Formula

C13H8F2O3

Storage (From the date of receipt)
CAS No. 22494-42-4 Download SDF Storage of Stock Solutions

Synonyms Dolobid, Dolobis, Flovacil, Fluniget,MK-647 Smiles C1=CC(=C(C=C1C2=C(C=C(C=C2)F)F)C(=O)O)O

Mechanism of Action

Targets/IC50/Ki
COX
p300
996 μM
In vitro

Diflunisal, an FDA-approved drug containing a salicylic acid substructure, inhibited CBP/p300 more potently than salicylate. This compound exhibits anti-tumor activity against a specific leukemia carrying a t(8;21) translocation, a tumor previously reported to be dependent on p300 in vitro and in vivo.

In vivo

Diflunisal-mediated kinetic stabilization of TTR(Rate-limiting transthyretin) should ameliorate TTR amyloidoses, provided that the nonsteroidal anti-inflammatory drug liabilities of this compound can be managed clinically.

References

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