Diphenyleneiodonium Chloride

Cas No.:	4673-26-1
SMILES:	[Cl-].C1=CC=C2C3=CC=CC=C3[I+]C2=C1
Formula:	C12H8Cli
M.Wt:	314.55
Purity:	>98%
Sotrage:	2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO

Description:	Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC50 of 1 to 3 μM.
Target:	NOX[1] EC50: 1 to 3 μM (TRPA1)[1]
In Vivo:	Intraplantar injection of 2 mM Diphenyleneiodonium chloride to the hindpaw causes licking or biting behavior[1]. 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[2].
In Vitro:	Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC50 of 1 to 3 μM. Application of Diphenyleneiodonium chloride to HEK-TRPA1 cells at a concentration ranges of 0.03 to 10 μM effectively induces a Ca2+ response. However, Diphenyleneiodonium chloride fails to evoke a Ca2+ response in control HEK cells, even at a relatively high dose of 10 μM[1]. When Diphenyleneiodonium chloride is included in the co-cultures, lipopolysaccharide (LPS)-induced preOL apoptosis is significantly inhibited. Treatment with Diphenyleneiodonium chloride is found to significantly attenuate the LPS-induced O2- production by 2.0-fold, reducing it to within 27% of the controls[2].
Cell Assay:	Purified microglia and preOLs are co-cultured using a Transwell culture system. Co-cultured cells are divided into three groups: control, lipopolysaccharide (LPS)-activated, and LPS plus Diphenyleneiodonium chloride. Microglia are cultured in Transwells over established preOL layers and exposed to either LPS (100 ng/mL), LPS+Diphenyleneiodonium chloride (10 μM) or untreated. The medium supernatants and cellular protein fractions from the co-cultures are then collected for further analysis after 48 h incubation[2].
Animal Administration:	The ddy mice (6 to 7 wk of age) are individually placed in transparent cages for 30 min before experiments. An intraplantar injection of 10 μL Diphenyleneiodonium chloride (2 mM, solvent: Kolliphor EL with 20% DMSO) is then injected into the right hindpaw with or without intraperitoneal administration with HC030031 (300 mg/kg at 0.5 h prior to injection of Diphenyleneiodonium chloride; solvent: saline with 0.5% methyl cellulose). The time spent licking or biting the injected paw is recorded for 45 min after injection[1].
References:	[1]. Suzuki H, et al. The NADPH oxidase inhibitor diphenyleneiodonium activates the human TRPA1 nociceptor. Am J Physiol Cell Physiol. 2014 Aug 15;307(4):C384-94. [2]. He YF, et al. Diphenyleneiodonium protects preoligodendrocytes against endotoxin-activated microglial NADPH oxidase-generated peroxynitrite in a neonatal rat model of periventricular leukomalacia. Brain Res. 2013 Jan 25;1492:108-21.