Eltenac
Based on 1 Customer Validation
Eltenac, a non-steroidal anti-inflammatory drug (NSAID), is a COX inhibitor. Eltenac shows IC50 of 0.03 μM for both COX-1 and COX-2 in isolated human whole blood.
Para uso exclusivo en investigación. No vendemos a pacientes.
- No. CAS: 72895-88-6
- Fòrmula: C12H9Cl2NO2S
- Peso molecular:302.18
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Almacenamiento:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Actividad biológica
Descripciòn
IC50 & Target
[1]|
COX-1 0.03 μM (IC50) |
COX-2 0.03 μM (IC50) |
In Vitro
Eltenac (10 mg/kg; p.o.; Female Sprague-Dawley rats weighing150-190; rat paw edema model) efficaciously reduces the increase in paw volume by 52%[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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No. CAS 72895-88-6
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Unlabeled CAS 72895-88-6
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Appearance Solid
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Peso molecular 302.18
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Fòrmula C12H9Cl2NO2S
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SMILES
O=C(O)CC1=CSC=C1NC2=C(Cl)C=CC=C2Cl
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocolo
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)