Vedaprofen-d3
Vedaprofen-d3 is the deuterium labeled Vedaprofen. Vedaprofen (Quadrisol) is a COX-1 selective nonsteroidal anti-inflammatory agent (NSAID) for serum TxB2 and exudate PGE2 inhibition . Vedaprofen is a Escherichia coli (E. coli) sliding clamp (SC) inhibitor with the IC50 of 222 μM.
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- CAS No.: 1185054-34-5
- 화학식: C19H19D3O2
- 분자량:285.40
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
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.
신청
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. 1185054-34-5
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Unlabeled CAS 71109-09-6
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분자량 285.40
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화학식 C19H19D3O2
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SMILES
C(C(O)=O)(C([2H])([2H])[2H])C=1C2=C(C(=CC1)C3CCCCC3)C=CC=C2
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Synonyms
Quadrisol-d3; CERM 10202-d3; PM 150-d3
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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
순도&문서
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]. P Lees, et al. PK-PD integration and PK-PD modelling of nonsteroidal anti-inflammatory drugs: principles and applications in veterinary pharmacology. J Vet Pharmacol Ther. 2004 Dec;27(6):491-502. [Content Brief]
[3]. Zhou Yin,et al. DNA replication is the target for the antibacterial effects of nonsteroidal anti-inflammatory drugs. Chem Biol. 2014 Apr 24;21(4):481-487. [Content Brief]
[4]. M Hoeijmakers, et al. The pharmacokinetics of Vedaprofen and its enantiomers in dogs after single and multiple dosing. J Vet Pharmacol Ther. 2005 Jun;28(3):305-12. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)