Fenamic acid

Fenamic acid (N-Phenylanthranilic acid, NPAA) is an orally active chloride channel blocker. Fenamic acid is the basic constituent of non-steroidal anti-inflammatory agents (NSAIA), and derives into mefenamic, tofenacin, flufenac acid and melofenac acid. Fenamic acid also acts as antibacterial and analgesic agent^[1]-[6]. IC50 & Target:Chloride Channel^[1] In Vitro: Fenamic acid (N-Phenylanthranilic acid, NPAA) (2.5 mM; 3 h) inhibits Cl^- transportation and blocks ³⁶C1^- uptake and efflux in endothelial cells^[1][2].
Fenamic acid exhibits selectivity to AKR1B10 (the tumor-marker) over human AR, and inhibits AKR1B10 with IC₅₀s of 0.76 μM (Flufenamic acid), 1.6 μM (Mefenamic acid), 9.89 μM (Meclofenamic acid), respectively^[4].
Fenamic acid (4-16 μg/mL; 72 h) inhibits 50% of Neisseria gonorrhoeae with an MIC₅₀ value from 4 to 16 μg/mL (tolfenamic acid, flufenamic acid, and meclofenamic acid) in a low frequency of resistance^[5].
Fenamic acid (2-8 μg/mL; 8 h) reduces the expression of the porinflammatory cytokines (IL-8, IL-6 and IL-β) by infected endocervical cells without (>128 μg/mL; 24 h) inhibition towards commensal Lactobacillus spp. belonging healthy female genital microbiota^[5]. In Vivo: RPA-1 is a biomarker in the detection of collecting duct injury in papillary necrosis in male rats^[3].
Fenamic acid (N-Phenylanthranilic acid, NPAA) (350-700 mg/kg/day; p.o.; 4 d, 8 d, and 15 d) causes renal papillary necrosis and increases urinary renal papillary antigen-1 (RPA-1) in rats^[3].
Fenamic acid (20 g/0.2 mL; i.p.) shows inhibitory effect against the abdominal constriction induced by acetic acid in mice^[6].