DPI抑制NADPH oxidase、一氧化氮合成酶、黄嘌呤氧化酶和NADPH细胞色素P450氧化还原酶的活性。飞摩尔级别的DPI即可通过抑制ERK调节的PHOX活性、抑制小胶质细胞的激活，发挥其抗炎活性和神经保护作用。DPI常被用于抑制由多种黄素酶介导的ROS生成。NADPH, NADP+, and 2'5'-ADP可阻止DPI的抑制活性。对ARPE-19细胞处理以DPI可引起剂量依赖性和时间依赖性的生长抑制，诱导DNA断裂和促凋亡因子Bax的蛋白水平。除此之外，DPI还可显著地诱导p53的表达和其磷酸化，在DNA损伤或无法修复的DNA周期阻滞中，诱导促凋亡基因的表达。
Intraplantar injection of 2 mM Diphenyleneiodonium chloride to the hindpaw causes licking or biting behavior. Diphenyleneiodonium chloride treatment immediately or 24 h after lipopolysaccharide (LPS) injection significantly attenuates the LPS-induced loss of O4 positive cells. Treatment with Diphenyleneiodonium chloride either immediately or 24 h after LPS injection significantly ameliorates the LPS-induced disorganization of the white matter nerve fibers. However, treatment with DPI 48 h after LPS injection does not appear to correct the LPS-induced white matter damage. DPI treatment either immediately or 24 h after LPS injection significantly reduces the accumulation of both gp91phox and p67phox in the membrane fraction.