Niflumic acid, a Ca2+-activated Cl- channel blocker, is an analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.
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Niflumic acid, a drug used for joint and muscular pain, affected Ca²⁺ signaling in different models. In MG63 cells, niflumic acid induced [Ca²⁺]i rises by evoking PLC-dependent (phospholipase C) Ca²⁺ release from the endoplasmic reticulum, and Ca²⁺ entry via PKC-sensitive (protein kinase C) store-operated Ca²⁺ entry. Niflumic acid also induced Ca²⁺-independent cell death[3]. Niflumic acid (10 and 30 mM) also inhibited the noradrenaline-induced increase in perfusion pressure and 30 mM niflumic acid reduced the pressor response to 1 nmol noradrenaline by 34 +/- 6%. The increases in perfusion elicited by 5-HT (0.3 and 3 nmol) were reduced by niflumic acid (10 and 30 mM) in a concentration-dependent manner and 30 mM niflumic acid inhibited responses to 0.3 and 3 nmol 5-HT by, respectively, 49 +/- 8% and 50 +/- 7%. Niflumic acid selectively reduces a component of noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels[4]. Niflumic acid restored core and associated symptoms of peripheral neuropathy by suppressing oxidative-nitrosative stress, inflammatory cytokines (TNF-α, IL-1β) and TRPV1 level in stavudine-induced neuropathic pain in rats. Pharmacological efficacy of niflumic acid (20 mg/kg) was equivalent to pregabalin (30 mg/kg) [5].
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