MNS

MNS (NSC 170724), the beta-nitrostyrene derivative, is an orally active tyrosine kinase inhibitor and a broad-spectrum antiplatelet agent. MNS inhibits Src, Syk, and FAK with IC₅₀ of 27.3, 2.8, and 97.6 μM, respectively. MNS inhibits NLRP3 inflammasome and β1 integrin. MNS completely inhibits U46619, ADP-, arachidonic acid-, collagen-, and thrombin-induced platelet aggregation with IC₅₀ values of 2.1, 4.1, 5.8, 7.0, and 12.7 μM, respectively. MNS is cytotoxic to a variety of cells^{[1][2][3][4][5][6][7][8][9]}. In Vitro:MNS (48 h) shows cytotoxicity against human BxPC3, DU145, and KM20L2 cells, with GI₅₀ of 1.7 μg/mL, 1.8 μg/mL, 1.8 μg/mL, respectively^[3].
MNS (1-20 μM, 1-15 h) inhibits adhesion and migration of MDA-MB-231 cells by suppressing β1 integrin function and surface protein disulfide isomerase^[4].
MNS (1-10 μM, 15 min) inhibits NLRP3 inflammasome activation in LPS-primed BMDMs by blocking assembly of the inflammasome^[5].
MNS (2.5-10 μM, 4-24 h) decreases the motility and colony formation of osteosarcoma cells^[6].
In Vivo:MNS (20 mg/kg, i.p.) ameliorates experimental burn wound progression in Wistar rats by inhibiting the NLRP3 inflammasome activation^[7].
MNS (30 mg/kg, p.o., 5 days) alleviates DSS-induced mouse colitis by inhibiting the NLRP3 inflammasome^[8].
MNS (20 mg/kg, i.p., 30 min before reperfusion) significantly protects the kidneys from RIR injury in rats by reducing PANoptosis through specific inhibition of NLRP3^[9].