Desacetylcephapirin-d6 sodium
Based on 1 Customer Validation
Desacetylcephapirin-d6 sodium (Deacetylcephapirin-d6 sodium) is the deuterium labeled Desacetylcephapirin sodium (HY-131989). Desacetylcephapirin (Deacetylcephapirin) sodium is an active metabolite of Cephapirin (HY-A0153A). Desacetylcephapirin sodium has antimicrobial against S. aureus and coagulase-negative staphylococci mastitis pathogen.
For research use only. We do not sell to patients.
- Formula: C15H8D6N3NaO5S2
- Molecular Weight:409.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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Unlabeled CAS 104557-24-6
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Molecular Weight 409.45
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Formula C15H8D6N3NaO5S2
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SMILES
O=C1[C@H]([C@@]2(N1C(C(O[Na])=O)=C(CS2)CO)[H])NC(C([2H])(SC3=C(C([2H])=NC([2H])=C3[2H])[2H])[2H])=O
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Synonyms
Deacetylcephapirin-d6 sodium
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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 Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. B. E. Cabana, et al. Comparative Pharmacokinetics and Metabolism of Cephapirin in Laboratory Animals and Humans. Antimicrob Agents Chemother. 1976 Aug; 10(2): 307-317. [Content Brief]
[2]. Cristina S Cortinhas, et al. Minimum inhibitory concentrations of cephalosporin compounds and their active metabolites for selected mastitis pathogens. Am J Vet Res. 2013 May;74(5):683-90. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)