Flufenamic acid

Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca2+ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

Product information

CAS Number: 530-78-9

Molecular Weight: 281.23

Formula: C14H10F3NO2

Chemical Name: 2-{[3-(trifluoromethyl)phenyl]amino}benzoic acid

Smiles: OC(=O)C1=CC=CC=C1NC1C=C(C=CC=1)C(F)(F)F

InChiKey: LPEPZBJOKDYZAD-UHFFFAOYSA-N

InChi: InChI=1S/C14H10F3NO2/c15-14(16,17)9-4-3-5-10(8-9)18-12-7-2-1-6-11(12)13(19)20/h1-8,18H,(H,19,20)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 100 mg/mL (355.58 mM; Need ultrasonic).

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

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.

References:

1. Guinamard R, et al. Flufenamic acid as an ion channel modulator. Pharmacol Ther. 2013 May;138(2):272-84.
2. Pongkorpsakol P, et al. Flufenamic acid protects against intestinal fluid secretion and barrier leakage in a mouse model of Vibrio cholerae infection through NF-κB inhibition and AMPK activation. Eur J Pharmacol. 2017 Mar 5;798:94-104.
3. Pongkorpsakol P, et al. Cellular mechanisms underlying the inhibitory effect of flufenamic acid on chloride secretion in human intestinal epithelial cells. J Pharmacol Sci. 2017 Jun;134(2):93-100.

Products are for research use only. Not for human use.