Diazoxide

Synonyms: Sch-6783, SRG-95213, Proglycem

Diazoxide (Sch-6783, SRG-95213, Proglycem) is a well-known small molecule that activates KATP channels in the smooth muscle of blood vessels and pancreatic beta-cells by increasing membrane permeability to potassium ions.

Diazoxide Chemical Structure

Diazoxide Chemical Structure

CAS: 364-98-7

Selleck's Diazoxide has been cited by 2 publications

Purity & Quality Control

Batch: S463001 DMSO] 46 mg/mL] false] Water] Insoluble] false] Ethanol] Insoluble] false Purity: 99.99%
99.99

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Biological Activity

Description Diazoxide (Sch-6783, SRG-95213, Proglycem) is a well-known small molecule that activates KATP channels in the smooth muscle of blood vessels and pancreatic beta-cells by increasing membrane permeability to potassium ions.
Targets
KATP channels [2]
In vitro
In vitro Diazoxide inhibits microglial inflammatory activity. Diazoxide treatment partially inhibits the inflammatory pattern induced by LPS/IFN-γ in microglial cells, inducing a decrease in NO production that could be because of the decreased expression of iNOS detected. Diazoxide has no effect on microglial phagocytosis[1].
Cell Research Cell lines Mouse microglial cell line BV-2
Concentrations 100 μM
Incubation Time 30 min
Method The phagocytic ability of microglia is determined by the uptake of 2-μm red fluorescent microspheres by BV-2 cells. Cells are treated with diazoxide 100 μM and activated with LPS/IFN-γ and then incubated with microspheres at a concentration of 0.01% for 30 min in the dark at 37°C and 5% CO2. Cells are rinsed twice in PBS solution, pelleted at 1,000 g for 5 min and resuspended in 300 μL PBS. Cells are kept on ice and analyzed by flow cytometry.
In Vivo
In vivo Diazoxide is beneficial on the improvement in cognitive tasks, reduction of anxiety, decrease in the accumulation of amyloid-beta oligomers and hyperphosphorylation of tau proteins. Diazoxide may also exerts neuroprotective effects independently of K+ channel activation by decreasing neuronal excitability and activation of N-methyl-D-aspartate (NMDA) receptors or by increasing currents trough α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Diazoxide-treated animals show a decrease in disease severity a few days after the first clinical signs are observed, corresponding to the acute inflammatory phase of the disease. Daily oral administration of diazoxide in EAE mice during the effector phase of the disease reduces the severity of the clinical signs without any apparent adverse effect. Diazoxide decreases demyelination and axonal loss, reduces tissue damage, inhibits microglial/macrophage and astrocytic activation and preserves neuron integrity. No effects are observed on the number of B and T lymphocytes infiltrating the spinal cord[1].
Animal Research Animal Models Female C57BL/6J mice
Dosages 0.8 mg/kg
Administration oral administration
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03941236 Active not recruiting
Congenital Hyperinsulinism
Zealand Pharma
May 1 2019 Phase 3
NCT00901823 Withdrawn
Hypertriglyceridemia
Essentialis Inc.
March 2011 Phase 1
NCT00696475 Completed
Hypertriglyceridemia
Essentialis Inc.|Medpace Inc.
June 2008 Phase 2
NCT00688857 Completed
Hypertriglyceridemia
Essentialis Inc.|Cetero Research San Antonio
May 2008 Phase 1

Chemical Information & Solubility

Molecular Weight 230.67 Formula

C8H7ClN2O2S

CAS No. 364-98-7 SDF Download Diazoxide SDF
Smiles CC1=NS(=O)(=O)C2=C(N1)C=CC(=C2)Cl
Storage (From the date of receipt)

In vitro
Batch:

DMSO : 46 mg/mL ( (199.41 mM); Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Water : Insoluble

Ethanol : Insoluble


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In vivo
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