DPI (Diphenyleneiodonium chloride)

Catalog No.S8639 Batch:S863902

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Technical Data

Formula

C12H8I.Cl
Molecular Weight 314.55 CAS No. 4673-26-1
Solubility (25°C)* In vitro DMSO 18 mg/mL (57.22 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
3%DMSO 40%PEG300 2%Tween80 55%ddH2O
0.5mg/ml Taking the 1 mL working solution as an example, add 30 μL of clarified DMSO stock solution of 16.6666666666667 mg/ml to 400 μL of PEG300, mix evenly to clarify it; add 20 μL of Tween80 to the above system, mix evenly to clarify it; then continue to add 550 μL of ddH2O to make it clear. Volume up to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description DPI (Diphenyleneiodonium chloride) is an inhibitor of NADPH oxidase and also a potent, irreversible, and time-, temperature-dependent iNOS/eNOS inhibitor. Diphenyleneiodonium chloride (DPI) also functions as a TRPA1 activator and selectively inhibits intracellular reactive oxygen species (ROS).
Targets
NADPH oxidase [1]
In vitro

DPI inhibits the activity of NADPH oxidase, nitric oxide synthase, xanthine oxidase and NADPH cytochrome P450 oxidoreductase[4].

Femtomolar concentrations of DPI exert potent anti-inflammatory and neuroprotective effects by inhibiting microglial activation through the inhibition of ERK-regulated PHOX activity[1].

DPI has frequently been used to inhibit ROS production mediated by various flavoenzymes, including NAD(P)H oxidase, quinone oxidoreductase, cytochrome P450 reductase and nitric oxide synthase[2].

NADPH, NADP+, and 2'5'-ADP blocks the inhibitory action of DPI[3].

DPI treatment in ARPE-19 cells evoked a dose- and time-dependent growth inhibition, and also induced DNA fragmentation and protein content of the proapoptotic factor Bax. In addition, DPI significantly induced the expression and phosphorylation of p53, which induces proapoptotic genes in response to DNA damage or irreparable cell cycle arrest. ROS have been implicated as a key factor in the activation of p53 by many chemotherapeutic drugs[4].
In vivo

Diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, inhibited the production of pro-inflammatory cytokines, (TNF-α and IL-6), reduced macrophage infiltration and classical polarization, and induced the ROS generation.

Protocol (from reference)

Cell Assay:

[4]
  • Cell lines

    ARPE-19 cells

  • Concentrations

    0.1, 1, and 10 μM

  • Incubation Time

    6, 12, 24, and 48 h

  • Method

    ARPE-19 cells are plated at 1×106 cells per 60-mm dishes and incubated for 24 h. Cells are cultured in presence or absence of different concentrations of DPI in fresh DMEM/F12 medium supplemented with 10% FBS. After incubation, the cells are trypsinized, washed with phosphate-buffered saline (PBS) and the viable cells were scored by the trypan blue dye exclusion method using a hemocytometer.
Animal Study:

[5]
  • Animal Models

    Male C57BL/6 mice

  • Dosages

    1 mg/kg

  • Administration

    i.p.

Selleck's DPI (Diphenyleneiodonium chloride) has been cited by 45 publications

Bacillus cereus cereolysin O induces pyroptosis in an undecapeptide-dependent manner [ Cell Death Discov, 2024, 10(1):122] PubMed: 38458999
The novel roles of RNA m6A modification in regulating the development, infection, and oxidative DNA damage repair of Phytophthora sojae [ PLoS Pathog, 2024, 20(9):e1012553] PubMed: 39312577
NOX2 deficiency promotes GSDME-related pyroptosis by reducing AMPK activation in neutrophils [ Int Immunopharmacol, 2024, 143(Pt 2):113504] PubMed: 39476568
Fusobacterium nucleatum-triggered neutrophil extracellular traps facilitate colorectal carcinoma progression [ J Exp Clin Cancer Res, 2023, 42(1):236] PubMed: 37684625
Fusobacterium nucleatum-triggered neutrophil extracellular traps facilitate colorectal carcinoma progression [ J Exp Clin Cancer Res, 2023, 42(1):236] PubMed: 37684625
Bi-fluorescent Staphylococcus aureus infection enables single-cell analysis of intracellular killing in vivo [ Front Immunol, 2023, 14:1089111] PubMed: 36756129
Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH [ Apoptosis, 2023, 1-14.] PubMed: 37306805
Multiparametric Profiling of Neutrophil Function via a High-Throughput Flow Cytometry-Based Assay [ Cells, 2023, 12(5)743] PubMed: 36899878
Targeting NADPH Oxidase and Integrin α5β1 to Inhibit Neutrophil Extracellular Traps-Mediated Metastasis in Colorectal Cancer [ Int J Mol Sci, 2023, 10.3390/ijms242116001] PubMed: 37958984
Imaging of innate immunity activation in vivo with a redox-tuned PET reporter [ Nat Biotechnol, 2022, 10.1038/s41587-021-01169-y] PubMed: 35190688

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.