Lornoxicam-d4
Lornoxicam-d4 is the deuterium labeled Lornoxicam. Lornoxicam (Chlortenoxicam), a COX-1 and COX-2 inhibitor, is a new nonsteroidal anti-inflammatory agent (NSAID).
For research use only. We do not sell to patients.
- CAS No.: 1216527-48-8
- Formula: C13H6D4ClN3O4S2
- Molecular Weight:375.84
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
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.
Application
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 No. 1216527-48-8
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Unlabeled CAS 70374-39-9
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Molecular Weight 375.84
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Formula C13H6D4ClN3O4S2
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SMILES
OC(C1=C2C=C(S1)Cl)=C(C(NC3=C([2H])C([2H])=C([2H])C([2H])=N3)=O)N(C)S2(=O)=O
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Synonyms
Chlortenoxicam-d4; Ro 13-9297-d4
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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
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Spyra S, et al. COX-2-selective inhibitors celecoxib and deracoxib modulate transient receptor potential vanilloid 3 channels. Br J Pharmacol. 2017 Aug;174(16):2696-2705. [Content Brief]
[3]. Rose, P. and C. Steinhauser, Comparison of Lornoxicam and Rofecoxib in Patients with Activated Osteoarthritis (COLOR Study). Clin Drug Investig, 2004. 24(4): p. 227-36. [Content Brief]
[4]. Bianchi, M. and A.E. Panerai, Effects of lornoxicam, piroxicam, and meloxicam in a model of thermal hindpaw hyperalgesia induced by formalin injection in rat tail. Pharmacol Res, 2002. 45(2): p. 101-5. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)