Quorum sensing-IN-5
Quorum sensing-IN-5 is a RpfF-targeted quorum-sensing inhibitor. Quorum sensing-IN-5 inhibits Xanthomonas oryzae pv oryzae (Xoo) and Xanthomonas axonopodis pv. citri (Xac) with EC50 values of 9.91 μg/mL and 7.04 μg/mL. Quorum sensing-IN-5 has antimicrobial activity.
For research use only. We do not sell to patients.
- Formula: C29H49N3O4
- Molecular Weight:503.72
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Quorum sensing-IN-5 (compound A26) exhibits robust interactions with Glu A: 161 of RpfF. Quorum sensing-IN-5 could inhibit various bacterial virulence factors, including biofilm formation, extracellular polysaccharides (EPS), extracellular enzyme activity, diffusible signal factor (DSF) production, and swimming motility[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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Molecular Weight 503.72
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Formula C29H49N3O4
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SMILES
OC1=CC(CNC(CCCCCCCC)=O)=CC=C1OCC(O)CN2CCC(N3CCCCC3)CC2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)