Satranidazole-d3
Satranidazole-d3 is the deuterium labeled Satranidazole. Satranidazole is an orally active insecticide and antimicrobial agent with high electron affinity. Satranidazole forms reduced nitro intermediates, which interact with DNA, causing helix instability, strand breakage and release of thymidine derivatives. Satranidazole exhibits antitrichomonal activity against Trichomonas vaginalis and Trichomonas foetus, and antiamoebic activity in rodent models of hepatic amoebiasis and caecal amoebiasis. Satranidazole inhibits the replication of bacteriophage φX174 DNA. Satranidazole can be used in research related to caecal amoebiasis, trichomoniasis and anaerobic bacterial infections.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C8H8D3N5O5S
- Molecular Weight:292.29
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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.
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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Unlabeled CAS 56302-13-7
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Molecular Weight 292.29
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Formel C8H8D3N5O5S
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SMILES
O=C1N(CCN1C2=NC=C(N2C([2H])([2H])[2H])[N+]([O-])=O)S(=O)(C)=O
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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 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.
Reinheit & Dokumentation
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)