Description
Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC50 of 1 to 3 μM. Diphenyleneiodonium chloride selectively inhibits intracellular reactive oxygen species.
Product information
CAS Number: 4673-26-1
Molecular Weight: 314.55
Formula: C12H8ClI
Chemical Name: 8λ³-iodatricyclo[7.4.0.0²,⁷]trideca-1(13),2,4,6,9,11-hexaen-8-ylium chloride
Smiles: [Cl-].C1C=CC=C2[I+]C3=CC=CC=C3C2=1
InChiKey: FCFZKAVCDNTYID-UHFFFAOYSA-M
InChi: InChI=1S/C12H8I.ClH/c1-3-7-11-9(5-1)10-6-2-4-8-12(10)13-11;/h1-8H;1H/q+1;/p-1
Technical Data
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: DMSO : 6 mg/mL (19.07 mM; Need ultrasonic and warming). H2O : 0.1 mg/mL (0.32 mM; Need ultrasonic).
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥12 months if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
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. 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.
In Vivo:
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.
Products are for research use only. Not for human use.
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