IAV-IN-5
IAV-IN-5 is an orally active inhibitor of influenza A virus (IAV). IAV-IN-5 inhibits viral replication, blocks virus-induced apoptosis, oxidative stress and cytokine storm, and regulates host immune signaling pathways. IAV-IN-5 reduces viral load and inflammatory cytokine levels in lung tissues of IAV-infected mouse models, alleviates body weight loss and pulmonary pathological damage. IAV-IN-5 can be used in studies related to influenza A virus infection.
For research use only. We do not sell to patients.
- CAS No.: 3038861-11-6
- Formula: C22H23NO3S
- Molecular Weight:381.49
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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
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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NF-κB |
IL-4 |
IL-6 |
TLR3 |
iNOS |
IAV-IN-5 (compound 3h) (25-100 μM; 24 h post-infection) dose-dependently inhibits RIG-I protein expression and phosphorylated NF-κB levels in A/Weiss/43 (H1N1)-infected A549 cells, blocking activation of the NF-κB inflammatory signaling pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:A549 cells infected with A/Weiss/43 (H1N1)
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Concentration:25, 50, 100 μM
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Incubation Time:24 h post-infection
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Result:Dose-dependently inhibited RIG-I protein expression compared to the virus control group.
Significantly reduced pNF-κB levels compared to the virus control group.
IAV-IN-5 (100 mg/kg/d; i.g.; daily; 6 days) shows excellent in vivo safety in healthy BALB/c mice, with no observable organ toxicity or changes in blood or serum biochemical parameters[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, 5 weeks old, 13-17 g, intranasal inoculation with A/Weiss/43 H1N1 virus)[1]
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Dosage:25 mg/kg/d; 50 mg/kg/d; 100 mg/kg/d
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Administration:i.g.; daily; 6 days
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Result:Alleviated virus-induced weight loss and improved mouse survival.
Reduced hemorrhagic lesions and edema; 100 mg/kg/d caused only mild edema, similar to oseltamivir.
Inhibited lung index by 23.76% (25 mg/kg/d), 38.24% (50 mg/kg/d), and 50.26% (100 mg/kg/d); high-dose inhibition exceeded oseltamivir.
Mitigated alveolar wall thickening, interstitial edema, and inflammatory infiltration; 100 mg/kg/d maintained intact alveolar structure comparable to oseltamivir.
Decreased influenza virus NP protein staining in lung tissue dose-dependently, with the weakest signal at 100 mg/kg/d.
Reduced mRNA levels of viral NP and M2 genes in lung tissue on days 2, 4, and 6 post-infection at all doses.
Downregulated mRNA expression of inflammatory factors (RIG-I, TLR3, IRF3, ASC, iNOS, IL-4, IL-6, IFN-α) in lung tissue on day 6 post-infection at all doses.
Diminished apoptotic cells in lung tissue dose-dependently; 100 mg/kg/d was comparable to oseltamivir.
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Animal Model:BALB/c (female, 5 weeks old, 13-17 g)[1]
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Dosage:100 mg/kg/d
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Administration:i.g.; daily; 6 days
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Result:Showed no obvious pathological changes, tissue damage, cell degeneration/necrosis, or inflammatory cell infiltration.
Maintained routine blood parameters within normal physiological ranges.
Kept serum biochemical indices close to normal control levels.
Chemical Information
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CAS No. 3038861-11-6
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Molecular Weight 381.49
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Formula C22H23NO3S
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SMILES
O=S(C1=CC=C(C)C=C1)(N(C2=C(C)[C@@]3([H])CCCC([C@@]23[H])=O)C4=CC=CC=C4)=O
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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