Antimicrobial agent-12
Antimicrobial agent-12 is a potent antibacterial agent with SARS-CoV-2 inhibitory activity.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 分子式: C69H61Cl2F3N10O25
- 分子量:1558.18
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
IC50 & Target
Bacteria, SARS-CoV-2[1]
体外実験
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.
化学情報
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分子量 1558.18
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)