Sulbactam-d2 sodium
Based on 1 Customer Validation
Sulbactam-d2 (sodium) is the deuterium labeled Sulbactam sodium. Sulbactam (CP45899) sodium is a competitive, irreversible beta-lactamase inhibitor. Sulbactam sodium shows antimicrobial activity against multidrug-resistant (MDR) acinetobacter calcoaceticus--Acinetobacter baumannii (Acb) complex.
For research use only. We do not sell to patients.
- Purity : 95.50%
- CAS No.: 948027-82-5
- Formula: C8H8D2NNaO5S
- Molecular Weight:257.24
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Storage:
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
All Antibiotic 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. 948027-82-5
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Unlabeled CAS 69388-84-7
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Appearance Solid
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Molecular Weight 257.24
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Formula C8H8D2NNaO5S
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Color Off-white to light brown
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SMILES
O=C([C@@H]1N2[C@](C([2H])([2H])C2=O)([H])S(=O)(C1(C)C)=O)O[Na]
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Synonyms
CP45899-d2 sodium
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
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
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Data Sheet (276 KB)
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SDS (419 KB)
- English - EN (419 KB)
- Français - FR (419 KB)
- Deutsch - DE (419 KB)
- Norwegian - NO (419 KB)
- Español - ES (419 KB)
- Swedish - SV (419 KB)
- Italian - IT (419 KB)
- Korean - KR (419 KB)
- Portuguese - PT (419 KB)
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Handling Instructions (2659 KB)
References
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019 Feb;53(2):211-216. [Content Brief]
[2]. Noguchi JK, et al. Sulbactam: a beta-lactamase inhibitor. Clin Pharm. 1988;7(1):37-51. [Content Brief]
[3]. Lin HS, et al. Sulbactam treatment for pneumonia involving multidrug-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii complex. Infect Dis (Lond). 201547(6):370-378. [Content Brief]
[4]. Betrosian AP, et al. Ampicillin-sulbactam: an update on the use of parenteral and oral forms in bacterial infections. Expert Opin Drug Metab Toxicol. 20095(9):1099-1112. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)