Quoromycin
Quoromycin is an orally active SmcR inhibitor with a Kd of 0.697 μM for Vibrio vulnificus SmcR. Quoromycin binds directly to SmcR, reduces its DNA-binding affinity, and inhibits the quorum sensing signaling pathway. Quoromycin is applicable to the research of Vibrio vulnificus infection.
For research use only. We do not sell to patients.
- CAS No.: 205514-29-0
- Formula: C12H8N2O2S
- Molecular Weight:244.27
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Quoromycin (1-50 μM) dose-dependently inhibits the binding of Vibrio vulnificus SmcR to the vvpE promoter DNA without altering SmcR protein levels[1].
Quoromycin (1-50 μM; 25 h) dose-dependently reduces elastase activity in Vibrio vulnificus without inhibiting bacterial growth[1].
Quoromycin (1-50 μM; 12 h) inhibits Vibrio vulnificus vvpE promoter activity with an IC50 of 322 nM[1].
Quoromycin (20 μM) reduces vvpE transcript levels, elastase activity, and exoprotease activity in wild-type Vibrio vulnificus to levels similar to an smcR mutant strain[1].
Quoromycin (1-100 μM; 3 h at 37 °C) dose-dependently reduces Vibrio vulnificus-induced cytotoxicity and bacterial adhesion to INT-407 human intestinal epithelial cells[1].
Quoromycin (20 μM) inhibits quorum sensing in Vibrio harveyi and reduces proteolytic activity in Vibrio anguillarum without inhibiting bacterial growth of either species[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:INT-407 human intestinal epithelial cells infected with Vibrio vulnificus
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Concentration:1, 10, 25, 50, 100 μM
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Incubation Time:3 h at 37 °C
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Result:Reduced Vibrio vulnificus-induced cytotoxicity in INT-407 cells in a dose-dependent manner, with 100 μM quoromycin returning LDH levels to non-infected control levels.
Reduced Vibrio vulnificus adhesion to INT-407 cells in a dose-dependent manner, with 50 μM quoromycin reducing adherent CFUs by half compared to controls.
In Vivo
Quoromycin (122 μg/kg; i.g.; single simultaneous dose with infection) significantly reduces V. vulnificus colonization in mouse small intestine, liver, and spleen, and prevents infection-associated tissue damage[1].
Quoromycin (30-122 μg/kg; i.g.; single dose) shows no acute in vivo cytotoxicity in healthy ICR female mice, with 100% 24-hour survival[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (female, 7-week-old, pathogen-free)[1]
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Dosage:61 μg/kg; 122 μg/kg
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Administration:i.g.; single simultaneous dose with infection
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Result:Conferred 60% 24-hour survival at 122 μg/kg (vs 10% in untreated controls).
Significantly prolonged survival at 61 μg/kg relative to untreated infected mice.
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Animal Model:ICR mice (female, pathogen-free)[1]
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Dosage:122 μg/kg
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Administration:i.g.; single simultaneous dose with infection
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Result:Reduced small intestine colonization index to ~-3 log.
Reduced liver colonization index to ~-4.5 log.
Reduced spleen colonization index to ~-5 log.
Prevented edema, hemorrhage, vasodilation, necrosis, and intestinal inflammation/swelling observed in untreated infected mice.
Chemical Information
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CAS No. 205514-29-0
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Molecular Weight 244.27
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Formula C12H8N2O2S
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SMILES
N#CC1=CN=C(C=C1)S(=O)(=O)C=2C=CC=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)
Quoromycin Related Classifications
HY-W788542 Related Classifications
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