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CAS No. : 530-78-9
MCE 国际站:Flufenamic acid
产品活性:Flufenamic acid 是一种非甾体类抗炎剂,能够抑制 COX 的活性,激活 AMPK 的活性,调节离子通道,阻滞氯离子通道 (chloride channel) 和 L-型钙离子通道 (L-type Ca2+ channel),调节非选择性阳离子通道,激活钾离子通道 (K+ channel) 等。Flufenamic acid 与TEAD2 YBD 的中央囊袋结合,抑制 TEAD 功能和 TEAD-YAP 依赖性过程,如细胞迁移和增殖。
研究领域:Immunology/Inflammation | PI3K/Akt/mTOR | Epigenetics | Membrane Transporter/Ion Channel | Neuronal Signaling | Anti-infection
作用靶点:COX | AMPK | Potassium Channel | Chloride Channel | Calcium Channel | Parasite
In Vitro: Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), and also modulates ion channels, blocking chloride channels and L-type Ca2+ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid inhibits a wide spectrum of TRP channels, including: C3, C7, M2, M3, M4, M5, M7, M8, V1, V3, and V4 but activates at least two TRP channels (C6 and A1). Flufenamic acid induces AMPK activation in T84 cells, and such an effect is via a direct stimulation of calcium/calmodulin-dependent protein kinase kinase beta (CaMKKβ) activity. Moreover, Flufenamic acid (FFA; 5-50 μM) dose-dependently inhibits cAMP-dependent Cl- secretion in intact T84 cells, suppresses CFTR-mediated apical ICl-, and blocks the Ca2+-dependent Cl- secretion in a dose-dependent manner with IC50 of appr 10 μM and near complete inhibition at 100 μM in T84 cell monolayers, but shows no effect on Na+-K+ ATPase or NKCC in T84 cells.
In Vivo: Flufenamic acid (50 mg/kg, i.p.) has anti-inflammatory effect in a mouse model of Vibrio cholerae El Tor variant (EL)-induced diarrhea and significantly abrogates EL-induced intestinal fluid secretion and barrier disruption at 20 mg/kg. Furthermore, Flufenamic acid suppresses NF-κB nuclear translocation and expression of proinflammatory mediators and promotes AMPK phosphorylation in the EL-infected mouse intestine.
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