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Diphenyleneiodonium (DPI) is an inhibitor of NADPH oxidase (NOX; EC50 = 0.1 µM in HeLa cells).1 It also inhibits nitric oxide synthase (NOS; IC50 = 0.05 µM in isolated mouse peritoneal macrophages).2 DPI (10, 50, and 100 µM) induces the production of reactive oxygen species (ROS) in, and apoptosis of, human umbilical vein endothelial cells (HUVECs).3 It inhibits NETosis induced by phorbol 12-myristate 13-acetate (PMA; Item No. 10008014) in isolated human neutrophils when used at a concentration of 10 µM.4 DPI (2 mg/kg) reduces tumor growth in HT-29 and LS 174T colon cancer mouse xenograft models.5
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1. Preferential inhibition of the plasma membrane NADH oxidase (NOX) activity by diphenyleneiodonium chloride with NADPH as donor. Antioxid. Redox Signal. 4(1), 207-212 (2002).
2. Inhibition of macrophage and endothelial cell nitric oxide synthase by diphenyleneiodonium and its analogs. FASEB J. 5, 98-103 (1991).
3. Induction of apoptosis and modulation of production of reactive oxygen species in human endothelial cells by diphenyleneiodonium. Biochem. Pharmacol. 69(8), 1263-1273 (2005).
4. Different procedures of diphenyleneiodonium chloride addition affect neutrophil extracellular trap formation. Anal. Biochem. 509, 60-66 (2016).
5. Effects of iodonium-
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Activated neutrophil carbamylates albumin via the release of myeloperoxidase and reactive oxygen species regardless of NETosis. Mod. Rheumatol. 30(2), 345-349 (2019).
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