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Niflumic acid COX inhibitor

Cat.No.S3018

Niflumic acid (Nifluril) is an inhibitor of cyclooxygenase-2 used for joint and muscular pain.
Niflumic acid COX inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 282.22

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Quality Control

Batch: S301801 DMSO]56 mg/mL]false]Water]Insoluble]false]Ethanol]Insoluble]false Purity: 99.92%
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99.92

Solubility

In vitro
Batch:

DMSO : 56 mg/mL (198.42 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 282.22 Formula

C13H9F3N2O2

Storage (From the date of receipt)
CAS No. 4394-00-7 Download SDF Storage of Stock Solutions

Synonyms Nifluril Smiles C1=CC(=CC(=C1)NC2=C(C=CC=N2)C(=O)O)C(F)(F)F

Mechanism of Action

Targets/IC50/Ki
COX-2
GABA receptor
In vitro

Niflumic acid inhibits Ca2+-activated Cl- channels with inhibition constant of 17 mM. This compound also inhibits ICl(Ca) elicited by bath application of Ca2+ to oocytes permeabilized using the Ca2+ ionophore A23187, demonstrating that the inhibition of ICl(Ca) is due to a direct interaction with the Cl- channel, rather than by interference with Ca2+ entry through voltage-dependent Ca2+ channels. It blocks Ca2+-activated non-selective cation channels in inside-out patches from the basolateral membrane of rat exocrine pancreatic cells with IC50 of 50 μM. This chemical dose-dependently and reversibly activates large conductance calcium-activated K+ (KCa) channels. It produces a concentration-dependent inhibition of spontaneous transient inward current (STIC, calcium-activated chloride current) amplitude. This compound inhibits noradrenaline- and caffeine-evoked IO(Ca) with an ICM50 of 6.6 μM, i.e.is less potent against evoked currents compared to spontaneous currents. It voltage-dependently inhibits spontaneous transient inward current (STIC) amplitude with IC50 of 2.3 μM and 1.1 μM at -50 and +50 mV respectively. It inhibits not only IL-13-induced goblet cell hyperplasia but also airway hyperresponsiveness and eosinophilic infiltration. This chemical suppresses the eotaxin levels in bronchoalveolar lavage fluids and overexpression of the MUC5AC gene, a marker of goblet cell hyperplasia, in the lung after IL-13 instillation. It suppresses JAK2 activation, STAT6 activation, and eotaxin expression in epithelial cells.

References
  • [4] https://pubmed.ncbi.nlm.nih.gov/16528019/

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