Bromfenac-d4 sodium
Bromfenac-d4 (sodium) is deuterium labeled Bromfenac (sodium). Bromfenac sodium is a potent and orally active inhibitor of COX, with IC50s of 5.56 and 7.45 nM for COX-1 and COX-2, respectively. Bromfenac sodium is a brominated non-steroidal anti-inflammatory/analgesic agent (NSAID), and it is commonly used for the research of postoperative inflammation and pain following cataract surgery, and pseudophakic cystoid macular edema (CME).
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- CAS. Nr.: 2749400-35-7
- Formel: C15H7D4BrNNaO3
- Molecular Weight:360.17
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Anwendung
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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CAS. Nr. 2749400-35-7
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Unlabeled CAS 91714-93-1
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Molecular Weight 360.17
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Formel C15H7D4BrNNaO3
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SMILES
O=C(O[Na])CC1=CC=CC(C(C2=C([2H])C([2H])=C(Br)C([2H])=C2[2H])=O)=C1N
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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
Reinheit & Dokumentation
Verweise
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Schechter BA, et, al. Use of topical bromfenac for treating ocular pain and inflammation beyond cataract surgery: a review of published studies. Clin Ophthalmol. 2019 Aug 1; 13:1439-1460. [Content Brief]
[3]. Nolan JC, et, al. The topical anti-inflammatory and analgesic properties of bromfenac in rodents. Agents Actions. 1988 Aug; 25(1-2): 77-85. [Content Brief]
[4]. Chen K, et, al. Bromfenac Inhibits TGF-β1-Induced Fibrotic Effects in Human Pterygium and Conjunctival Fibroblasts. Invest Ophthalmol Vis Sci. 2019 Mar 1; 60(4): 1156-1164. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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