ZIKV-IN-9
ZIKV-IN-9 is a ZIKV inhibitor that blocks the early binding of viral particles to the cell surface. ZIKV-IN-9 inhibits ZIKV in various cell models. ZIKV-IN-9 is applicable to research related to Zika virus infection.
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- 화학식: C19H21NO6S
- 분자량:391.44
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
ZIKV-IN-9 (compound 5v) (10 μM; 96 h) reduces ZIKV-induced cytopathic effect by 88.84% and maintains 88.91% cell viability in Vero cells[1].
ZIKV-IN-9 (96 h) potently inhibits ZIKV in Vero cells with an EC50 of 3.25 μM and no detectable cytotoxicity at tested concentrations[1].
ZIKV-IN-9 (24 h) inhibits ZIKV in A549 cells with an EC50 of 6.32 μM, a CC50 > 100 μM, and a selectivity index > 15[1].
ZIKV-IN-9 (10 μM; 24 h) inhibits ZIKV RNA synthesis and envelope protein expression in U251 cells, with an EC50 of 4.30 μM, a CC50 > 40 μM, and a selectivity index > 9[1].
ZIKV-IN-9 (5-20 μM; 24 h) potently inhibits both ZIKV MR766 and HPF2013 strains in A549 cells in vitro in a dose-dependent manner[1].
ZIKV-IN-9 (20 μM) mainly targets the early adsorption stage of the ZIKV life cycle in A549 cells and blocks viral particle attachment to the cell surface, confirming its function as a ZIKV entry inhibitor[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:Vero cells (African green monkey kidney cells)
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Concentration:10 μM
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Incubation Time:96 h
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Result:Reduced ZIKV-induced CPE by 88.84%.
Maintained 88.91% cell viability in uninfected Vero cells.
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Cell Line:Vero cells
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Concentration:Log -0.5, Log 0, Log 0.5, Log 1, Log 1.5 μM
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Incubation Time:96 h
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Result:Exhibited concentration-dependent protection against ZIKV-induced CPE.
Achieved an EC50 of 3.25 μM.
Showed no detectable cytotoxicity at tested concentrations.
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Cell Line:U251 human glioblastoma cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Significantly suppressed ZIKV RNA synthesis at 10 μM.
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Cell Line:U251 human glioblastoma cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Significantly suppressed ZIKV envelope protein expression at 10 μM.
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Cell Line:A549 human lung epithelial cells
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Concentration:5, 10, 20 μM
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Incubation Time:24 h
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Result:Significantly reduced viral RNA replication across all tested concentrations.
Showed the strongest effects at 20 μM.
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Cell Line:A549 human lung epithelial cells
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Concentration:5, 10, 20 μM
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Incubation Time:24 h
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Result:Significantly reduced envelope protein expression across all tested concentrations.
Showed the strongest effects at 20 μM.
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Cell Line:A549 human lung epithelial cells
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Concentration:20 μM
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Incubation Time:1 h (pre-incubation before infection); added 1 h post-infection, incubated until 12 hpi
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Result:Exhibited strong inhibitory activity when administered before viral adsorption.
Showed substantially diminished potency when added after adsorption.
Matched the inhibitory pattern of a ZIKV envelope protein-neutralizing antibody.
Chemical Information
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분자량 391.44
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화학식 C19H21NO6S
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SMILES
O=C(OCC)C1=C(NC(C2=CC=CO2)=O)SC3=C1CCC(C(OCC)=O)C3
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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)
ZIKV-IN-9 Related Classifications
HY-183314 Related Classifications
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