Niflumic acid

製品コードS3018 バッチS301801

化学情報

	Synonyms	Nifluril	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₁₃H₉F₃N₂O₂
	分子量	282.22	CAS No.	4394-00-7
Solubility (25°C)*	体外	DMSO	56 mg/mL (198.42 mM)
		Water	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

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生物活性

製品説明	Niflumic acid is an inhibitor of cyclooxygenase-2 used for joint and muscular pain.
in vitro	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. ^[1] 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. ^[2] Niflumic acid dose-dependently and reversibly activates large conductance calcium-activated K+ (KCa) channels. ^[3] 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. ^[4] 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. ^[5]

製品説明

Niflumic acid is an inhibitor of cyclooxygenase-2 used for joint and muscular pain.

in vitro

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. ^[1] 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. ^[2] Niflumic acid dose-dependently and reversibly activates large conductance calcium-activated K+ (KCa) channels. ^[3] 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. ^[4] 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. ^[5]

プロトコル(参考用のみ)

参考

[4] Hogg RC, et al. Br J Pharmacol, 1994, 112(3), 977-984.

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Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

The TGF-β1/COX-2-dependant pathway serves a key role in the generation of OKC-induced M2-polarized macrophage-like cells and angiogenesis [ Oncol Lett, 2020, 20(4):39]	PubMed: 32788934

The TGF-β1/COX-2-dependant pathway serves a key role in the generation of OKC-induced M2-polarized macrophage-like cells and angiogenesis [ Oncol Lett, 2020, 20(4):39]

PubMed: 32788934

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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