SARS-CoV-2-IN-28
SARS-CoV-2-IN-28 is a two-armed diphosphate ester with C7 alkyl and molecular tweezers with extended length. SARS-CoV-2-IN-28 exhibits antiviral activity with IC50s of 0.4 μM and 1.0 μM against SARS-CoV-2 activity and the spike pseudoparticle transduction, respectively. SARS-CoV-2-IN-28 induces liposomal membrane disruption with an EC50 value of 4.4 μM.
For research use only. We do not sell to patients.
- Formula: C56H60O8P2
- Molecular Weight:923.02
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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
IC50 & Target
IC50: 4.4 μM (viral liposome, SARS-CoV-2)[1]
In Vitro
SARS-CoV-2-IN-28 (CP020) inhibits SARS-CoV-2 (IC50=1.0 μM) with few cytotoxicity (Caco2 cells, CC50=213.1 μM)[1].
SARS-CoV-2-IN-28 (0-15 μM; 2 h) inactivate SARS-CoV-2, shows inhibition against infection with an IC50 value of 0.4 μM[1].
SARS-CoV-2-IN-28 suppresses varies enveloped viruses activity with IC50s of 7.1 μM (respiratory syncytial virus, RSV), 24.5 μM (influenza A virus, IAV), 4.0 μM (measles virus, MeV), 1.6 μM (herpes simplex viruses, HSV-1), respectively[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:Caco2 cells exposed with SARS-CoV-2 (2 h, 37 ℃)
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Concentration:0, 0.23, 0.93, 3.75, 15 μM
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Incubation Time:2 hours; determined infection rates on day 2
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Result:Inhibited SARS-CoV-2 infection activity to Caco2 cells.
Chemical Information
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Molecular Weight 923.02
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Formula C56H60O8P2
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SMILES
OP(OC1=C2C(C3C4=C(C2C3)C=C5C(C6C7=C(C5C6)C=CC=C7)=C4)=C(C8=C1C9C%10=CC(C%11CC%12C%13=C%11C=CC=C%13)=C%12C=C%10C8C9)OP(OCCCCCCC)(O)=O)(OCCCCCCC)=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.
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)
SARS-CoV-2-IN-28 Related Classifications
HY-151274 Related Classifications
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