DS-22-inf-021
DS-22-inf-021 is a neuraminidase (NA) inhibitor. DS-22-inf-021 has antiviral activity against influenza viruses.
For research use only. We do not sell to patients.
- CAS No.: 945170-74-1
- Formula: C20H23N3O2
- Molecular Weight:337.42
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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
DS-22-inf-021 inhibits NA activity of IBV (B/Samara/32/2018 Yamagata lineage) and resistant IAV A/Vladivostok/2/2009 (H1N1 pdm09) carrying the H275Y mutation, with IC50 values of 9.1 μM and 14.7 μM, respectively[1].
DS-22-inf-021 (0.5-50 μM, 10 h) shows antiviral activity in MDCK cells were infected with IAV and IBV strains[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:8-week-old female BALB/c mice, intranasally inoculated with 50 μL of five 50 % mouse lethal doses of IAV and IBV[1].
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Dosage:20, 50 and 100 mg/kg
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Administration:After 2 h post-infection, i.p. injection
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Result:Reached 85 % protection at 100 mg/kg dose. For the B/Samara/32/2018 strain, it was observed that 100 % of mice treated with DS-22-inf-021 at 100 mg/kg.
Chemical Information
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CAS No. 945170-74-1
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Molecular Weight 337.42
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Formula C20H23N3O2
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SMILES
O=C(NC1=CC=C(NC(C2=CC=CC=C2)=O)C=C1)NC3CCCCC3
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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)
DS-22-inf-021 Related Classifications
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