IndraLab

Statements



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"XREF_BIBR Cl - channel blockers such as mefenamic acid, flufenamic acid, benzoic acid, etc, can inhibit the NLRP3 activation."

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"Mefenamic acid which belongs to fenamate group inhibits the NLRP3 inflammasome by inhibiting efflux of chloride ions and influx of calcium ions through blocking VRAC and TRPM2 respectively."

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"Flufenamic acid and mefenamic acid inhibit NLRP3 inflammasome activation through the suppression of chloride efflux."

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"A few NLRP3 inflammasome inhibitors, including sulforaphane, isoliquiritigenin, beta-hydroxybutyrate (BHB), flufenamic acid, mefenamic acid, 3,4-methylenedioxy-beta-nitrostyrene (MNS), parthenolide, BAY 11-7082, INF39, and MCC950, have been developed, but there is no evidence showing that these compounds can specifically and directly inhibit NLRP3 itself."

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"Various Cl - channel inhibitors, including 4,4 '-diisothiocyano-2,2 ' stilbene-disulfonic acid (DIDS), 5-nitro-(3-phenylpropylamino) benzoic acid (NPPB), flufenamic acid, mefenamic acid, and indanyloxyacetic acid 94 (IAA94), block the NLRP3 inflammasome but can not block the NLRC4 or AIM2 inflammasomes."

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"Different NLRP3 inflammasome inhibitors, including sulforaphane, β-hydroxybutyrate, glyburide, flufenamic acid, mefenamic acid, parthenolide, BAY 11-7082, INF39, and MCC950 have been developed, but there is no evidence demonstrating that these compounds directly and specifically target NLRP3 itself (212)."

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"Studies have shown that, unlike other NSAIDs, fenamates (mefenamic acid, flufenamic acid) selectively inhibit the NLRP3 inflammasome and IL-1beta release via inhibiting the membrane volume regulated anion (Cl -) channel (VRAC), independent of its cyclooxygenase-1 (COX-1) mediated anti-inflammatory activity."