Difenamizole
Difenamizole (Pasalin) is an orally active pyrazole non-steroidal anti-inflammatory agent and pain inhibitor, which capable of crossing the blood-brain barrier. Difenamizole inhibits the release of catecholamines by monoaminergic neurons, reduces the concentrations of dopamine metabolites and normetanephrine (NE) in the striatum, and thereby regulates the levels of dopamine and norepinephrine in the brain. Difenamizole is not only antagonized by dopamine in the brain, but also exerts synergistic effects with Oxidopamine (6-OHDA) (HY-B1081/A), Phenoxybenzamine (HY-B0431), Reserpine (HY-N0480), and other agents. Difenamizole inhibits conditioned, emotional and aggressive behaviors in rodents, and can be used in studies of pain and related neurobehaviors.
For research use only. We do not sell to patients.
- CAS No.: 20170-20-1
- Formula: C20H22N4O
- Molecular Weight:334.42
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Dopamine Receptor Isoforms
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Biological Activity
Description
In Vivo
Difenamizole (50 mg/kg; p.o.; single dose) significantly reduces striatal 3-MT and HVA concentrations 60 minutes post-administration in healthy male ddY mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ddY (male, 20-22 g)[1]
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Dosage:50 mg/kg
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Administration:p.o.; single dose
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Result:Increased striatal dopamine levels to 4735.2 ng/g wet weight.
Decreased striatal 3-MT levels to 218.8 ng/g wet weight.
Decreased striatal homovanillic acid (HVA) levels to 461.0 ng/g wet weight.
Chemical Information
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CAS No. 20170-20-1
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Molecular Weight 334.42
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Formula C20H22N4O
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SMILES
O=C(NC1=CC(=NN1C=2C=CC=CC2)C=3C=CC=CC3)C(N(C)C)C
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Synonyms
Pasalin
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)