Premafloxacin
Premafloxacin is a potent antimicrobial agent that exhibits activity against Staphylococcus aureus, Corynebacterium bovis, and Corynebacterium amylocolatum. Premafloxacin demonstrated potent antimicrobial activity against S. aureus by targeting topoisomerase IV, and is a poor substrate for NorA efflux pump. Premafloxacin can be used for antimicrobial research.
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- CAS No.: 143383-65-7
- Formule: C21H26FN3O4
- Masse moléculaire:403.45
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Activité biologique
Description
IC50 & Target
[1]|
TOPO IV |
In Vitro
Premafloxacin (24-48 h) exhibits activity against wild-type S. aureus ISP794 with MIC of 0.004-0.008 μg/mL, while showing 4- to 8-fold decreased activity against various grlA and grlB mutants of these two strains with altered subunits of topoisomrase IV (MIC: 0.032-0.064 μg/mL)[1].
Premafloxacin (2-8× MIC; 48 h) fails to select for resistant single-step mutants of S. aureus ISP794 at 4 × or higher MICs, with resistant mutants only detectable at 2× MIC (mutation frequency: 6.4×10-10 to 4.0×10-7)[1].
Premafloxacin (24 h) exhibits potent in vitro activity against both Corynebacterium bovis and Corynebacterium amylocolatum strains isolated from bovine mammary glands, with MIC90s of 0.015 μg/mL[2].
Premafloxacin (24-48 h) exhibits a 2-fold decreased activity against flqB mutant, which overexpresses NorA efflux pump, indicating that it is a poor substrate for NorA[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 143383-65-7
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Masse moléculaire 403.45
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Formule C21H26FN3O4
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SMILES
O(C)C1=C2N(C=C(C(O)=O)C(=O)C2=CC(F)=C1N3C[C@]([C@@H](NC)C)(CC3)[H])C4CC4
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
[1]. Ince D, et al. Mechanisms and frequency of resistance to premafloxacin in Staphylococcus aureus: novel mutations suggest novel drug-target interactions. Antimicrob Agents Chemother. 2000;44(12):3344-3350. [Content Brief]
[2]. Watts JL, et al. Susceptibilities of Corynebacterium bovis and Corynebacterium amylocolatum isolates from bovine mammary glands to 15 antimicrobial agents. Antimicrob Agents Chemother. 2000;44(12):3476-3477. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Premafloxacin Related Classifications
HY-180414 Related Classifications
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