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    Niflumic acid
    Niflumic acid

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1064
    CAS #: 4394-00-7Purity ≥98%

    Description: Niflumic acid (Flunir, Donalgin, Niflactol, Niflugel, Nifluril) is a potent inhibitor of cyclooxygenase-2 (COX-2) enzyme with potential anti-inflammatory and analgesic activity. It is an approved medication used for joint and muscular pain as well as rheumatoid arthritis. Niflumic acid acts an inhibitor of COX (cyclooxygenase-2) enzyme, also a Ca2+-activated Cl- channel blocker. In experimental biology, it has been employed to inhibit chloride channels. Niflumic acid has also been reported to act on GABA-A and NMDA channels and to block T-type calcium channels. 

    References: Mol Pharmacol. 1990 May;37(5):720-4; FEBS Lett. 1990 Jul 30;268(1):79-82.

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    Molecular Weight (MW)282.22
    FormulaC13H9F3N2O2 
    CAS No.4394-00-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 56 mg/mL (198.4 mM)
    Water:<1 mg/mL
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: 2-[3-(trifluoromethyl)anilino]pyridine-3-carboxylic acid

    InChi Key: JZFPYUNJRRFVQU-UHFFFAOYSA-N

    InChi Code: InChI=1S/C13H9F3N2O2/c14-13(15,16)8-3-1-4-9(7-8)18-11-10(12(19)20)5-2-6-17-11/h1-7H,(H,17,18)(H,19,20)

    SMILES Code: O=C(C1=CC=CN=C1NC2=CC=CC(C(F)(F)F)=C2)O

    Synonyms

    Flunir, Niflactol, Niflugel, Niflumic Acid, Donalgin, Nifluril


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    In Vitro

    In vitro activity: Niflumic acid inhibits Ca2+-activated Cl- channels with inhibition constant of 17 mM. Niflumic acid 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. Niflumic acid 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. Niflumic acid dose-dependently and reversibly activates large conductance calcium-activated K+ (KCa) channels. Niflumic acid produces a concentration-dependent inhibition of spontaneous transient inward current (STIC, calcium-activated chloride current) amplitude. Niflumic acid 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. Niflumic acid 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. Niflumic acid inhibits not only IL-13-induced goblet cell hyperplasia but also airway hyperresponsiveness and eosinophilic infiltration. Niflumic 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. Niflumic acid suppresses JAK2 activation, STAT6 activation, and eotaxin expression in epithelial cells.

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    References

    Mol Pharmacol. 1990 May;37(5):720-4; FEBS Lett. 1990 Jul 30;268(1):79-82. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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