| Bioactivity | 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]. |
| Target | Chloride Channel |
| Invitro | 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-ß) 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; o.p.; 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]. Animal Model: |
| Name | Fenamic acid |
| CAS | 91-40-7 |
| Formula | C13H11NO2 |
| Molar Mass | 213.23 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) |
| Reference | [1]. Mandel KG, et al. Characterization of a cyclic AMP-activated Cl-transport pathway in the apical membrane of a human colonic epithelial cell line. J Biol Chem. 1986 Jan 15. 261(2):704-12. [2]. Ueda S, et al. Chloride efflux in cyclic AMP-induced configurational change of bovine pulmonary artery endothelial cells. Circ Res. 1990 Apr. 66(4):957-67. [3]. Betton GR, et, al. Biomarkers of collecting duct injury in Han-Wistar and Sprague-Dawley rats treated with N-phenylanthranilic Acid. Toxicol Pathol. 2012 Jun;40(4):682-94. [4]. Endo S, et al. Selective inhibition of the tumor marker AKR1B10 by antiinflammatory N-phenylanthranilic acids and glycyrrhetic acid. Biol Pharm Bull. 2010. 33(5):886-90. [5]. Seong YJ, et al. Repurposing Fenamic Acid Drugs To Combat Multidrug-Resistant Neisseria gonorrhoeae. Antimicrob Agents Chemother. 2020 Jun 23. 64(7):e02206-19. [6]. Almasirad A, et al. Synthesis and analgesic activity of 2-phenoxybenzoic acid and N-phenylanthranilic acid hydrazides. Biol Pharm Bull. 2006 Jun. 29(6):1180-5. |
Fenamic acid
CAS: 91-40-7 F: C13H11NO2 W: 213.23
Fenamic acid (N-Phenylanthranilic acid, NPAA) is an orally active chloride channel blocker. Fenamic acid is the basic co
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