Flufenamic acid (Arlef) is an anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically.

Under peak amyloid fibril formation conditions (pH 4.4), Flufenamic acid binds to wild-type transthyretin (KD1=30 nM, KD2=255 nM), V30M transthyretin (KD1=41 nM, KD2=320 nM), and L55P transthyretin (KD1=74 nM, KD2=682 nM) with high affinity and negative cooperativity (pH value 7.6), fully inhibiting fibril formation at a concentration of 10.8 μM. In Xenopus oocytes, Flufenamic acid reversibly suppresses ICl(Ca) in a dose-dependent manner, with an IC50 of 28 mM, without affecting the shape of the current-voltage curve in response to depolarizing voltage. Flufenamic acid inhibits the calcium-activated non-selective cation channels in the basolateral membrane of rat pancreatic exocrine cells activated by an inward-outward patch with an IC50 of 10 μM. The compound also inhibits currents activated by intracellular ADP-ribose in recombinant human TRPM2 (hTRPM2) channels and the CRI-G1 rat insulinoma cell line. Additionally, it reversibly inhibits (IC50=13.8 μM) DAP and phase discharge in rat suprachiasmatic neurons with similar kinetics, without significantly affecting membrane potential, spike threshold, or input resistance (P > 0.05), nor does it significantly affect the frequency and amplitude of spontaneous synaptic potentials.