Antimicrobial agent-12
Antimicrobial agent-12 is a potent antibacterial agent with SARS-CoV-2 inhibitory activity.
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- 화학식: C69H61Cl2F3N10O25
- 분자량:1558.18
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
Bacteria, SARS-CoV-2[1]
In Vitro
Antimicrobial agent-12 (compound 6) shows inhibitory activity on coronavirus (SARS-CoV-2) replication and spike-mediated pseudovirus entry in Vero E6 cells, with EC50 values of 13 μM[1].
Antimicrobial agent-12 inhibits 3CLPro enzyme activity and the ACE2-spike interaction, with EC50 values of 28 μM and 48 μM respectively[1].
Antimicrobial agent-12 (0-1 μg/mL approximately) shows activity against diverse species of Gram-positive bacteria including drug-resistant strains[1].
Antimicrobial agent-12 (0-100 μM, 2 h) inhibits SARS-CoV-2 pseudovirus entry in Vero and A549-AT cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:S. aureus, E. faecalis, E. faecium, S. epidermidis, S. haemolyticus
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Concentration:0-1 μg/mL approximately
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Incubation Time:
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Result:Inhibited bacteria activities with MIC values of 0.0625-0.27 μg/mL.
Chemical Information
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분자량 1558.18
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화학식 C69H61Cl2F3N10O25
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SMILES
OC1=C(OC2=C(C=C(C=C2)[C@@]([H])(O[C@H]3[C@@H]([C@H]([C@@H]([C@H](O3)CO)O)O)NC(C)=O)[C@]([H])(NC([C@@H]4N5)=O)C(N[C@H](C6=CC(O)=CC(O)=C6C7=CC4=CC=C7O)C(O)=O)=O)Cl)C=C(C=C1OC8=C(C=C(C=C8)C[C@]([H])9NC([C@@H]%10NC(N)=N)=O)Cl)[C@H](C5=O)NC([C@@H](NC9=O)C%11=CC(OC%12=CC%10=CC=C%12O)=CC(O)=C%11)=O.FC(C(O)=O)(F)F
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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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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)