Rhinovirus-IN-1
Rhinovirus-IN-1 is a selective anti-Rhinovirus compound. Rhinovirus-IN-1 inhibits the cytopathic effect induced by rhinovirus. Rhinovirus-IN-1 can be used in the research of rhinovirus infection.
For research use only. We do not sell to patients.
- Formula: C26H23F3N4O4
- Molecular Weight:512.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Rhinovirus-IN-1 (Compound 1q) (72 h) inhibits RV-A2 replication in HeLa cells with an IC50 of 1.09 μM and RV-B14 replication with an IC50 of 3.28 μM, while showing no cytotoxicity at concentrations up to 100 μM, resulting in high selectivity indices[1].
Rhinovirus-IN-1 exhibits correlated motion with both sets of entrance loops in VP1 from RV-A2 and RV-B14, indicating stable binding to the hydrophobic pocket of both viral capsid proteins, which correlates with its broad anti-rhinovirus activity[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:HeLa cells infected with rhinovirus A2 (RV-A2) and rhinovirus B14 (RV-B14)
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Concentration:Various concentrations
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Incubation Time:72 h (cytotoxicity); 3 days (antiviral activity)
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Result:Exhibited a mean 50% cytotoxic concentration (CC50) of >100 μM in HeLa cells.
Inhibited RV-A2 replication with a median 50% inhibitory concentration (IC50) of 1.09 μM, resulting in a selectivity index (SI) of >92.
Inhibited RV-B14 replication with a median IC50 of 3.28 μM, with an SI of >31.
Chemical Information
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Molecular Weight 512.48
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Formula C26H23F3N4O4
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SMILES
CC1=C(C=CC(C2=NOC(C(F)(F)F)=N2)=C1)OCCCC3=CC(C(N4CCC5=CC=CC=C5C4)=O)=NO3
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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)