NPPB is a blocker of the outwardly rectifying chloride channel (ORCC). Dose-dependent inhibition of chloride currents is observed with a 50% inhibitory concentration (IC50) of 125 μM NPPB. NPPB itself also shows cytotoxicity against glioma cells with a GI50 of approximately 500 μM. TMZ(Temozolomide)-NPPB blocked chloride currents in U373MG, a severely invasive human glioma cell line, and suppressed migration and invasion of U373MG cells[1]. NPPB treatment inhibited proliferation, migration, cell cycle progression and synthesis of the ECM(extracellular matrix), while promoting apoptosis in HConFs(human conjunctival fibroblasts), by inhibiting the PI3K̸AKT(phosphoinositide 3-kinase/protein kinase B) signaling pathway[2]. NPPB triggered Ca(2+) efflux from mature zone of tea root and significantly increased relative CaM in tea roots. Besides, pretreatment with the Ca(2+) chelator (EGTA) and CaM antagonists (CPZ and TFP) suppressed NPPB-elevated cytosolic Ca(2+) fluorescence intensity and CaM concentration in tea roots, respectively[3]. NPPB could significantly prevent the formation of peritoneal adhesion in rats and inhibit the proliferation of AFB in a concentration-dependent manner. NPPB also reduced the migration of AFB (adhesion fibroblasts) cells with an IC50 of 53.09 μM. Moreover, 100 μM NPPB almost completely eliminated the capacity of regulatory volume decrease (RVD) in these cells[4].
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