NIP 502
NIP 502 is a pyridazinone derivative with orally active anti-inflammation and anti-immunology effects. NIP 502 can be used for the research of asthma.
For research use only. We do not sell to patients.
- CAS No.: 108616-42-8
- Formula: C14H16ClN3O3
- Molecular Weight:309.75
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
NIP 502 (30-300 μM, 5 mins) significantly inhibits FMLP (HY-P0224)-induced superoxide anion production by guinea pig alveolar macrophages[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NIP-502 (30 mg/kg, p.o., 1 h before each ovalbumin aerosol inhalation) inhibits the Ovalbumin (HY-W250978)-induced increase in the number of macrophages, eosinophils, and neutrophils in the bronchoalveolar lavage fluid of guinea pigs[1].
NIP-502 (30-50 mg/kg, p.o., 1 h before antigen challenge) inhibits the passive cutaneous anaphylactic reaction in rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 108616-42-8
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Molecular Weight 309.75
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Formula C14H16ClN3O3
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SMILES
CCOC1=C(C=CC(CNC2=C(C(NN=C2)=O)Cl)=C1)OC
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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)