Amfenac sodium
Amfenac sodium (AHR 5850 sodium) is an orally active and potent anti-inflammatory compound possessing antipyretic and analgesic properties. Amfenac sodium can be used for the research of acute and chronic inflammation.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- CAS No.: 61941-56-8
- Formule: C15H12NNaO3
- Masse moléculaire:277.25
-
Stockage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Activité biologique
Description
Chemical Information
-
CAS No. 61941-56-8
-
Appearance Solid
-
Masse moléculaire 277.25
-
Formule C15H12NNaO3
-
Color Light yellow to yellow
-
SMILES
O=C(CC1=C(N)C(C(C2=CC=CC=C2)=O)=CC=C1)O[Na]
-
Synonyms
AHR 5850 sodium
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocole
-
Cotton Pellet Granuloma
Cotton pellet granuloma is a classical in vivo chronic inflammation model used to evaluate the anti-inflammatory potential of test substances by measuring their ability to inhibit granuloma tissue formation around an implanted foreign body (cotton pellet) in rodents. The method is based on the biological response to a sterile implanted material, which induces proliferative phase inflammation characterized by fibroblast proliferation and collagen-rich granuloma formation, and the final readout reflects the extent of chronic inflammatory tissue growth surrounding the pellet. In multiple preclinical pharmacological evaluations, inhibition of cotton pellet-induced granuloma formation has been used as an indicator of anti-inflammatory activity in both synthetic and natural product screening contexts.
-
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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)