SARS-CoV-2 nsp14-IN-10
SARS-CoV-2 nsp14-IN-10 is a highly potent and selective NSP14 (IC50 = 0.34 µM) S-adenosylmethionine (SAM) binding pocket inhibitor. SARS-CoV-2 nsp14-IN-10 demonstrates robust antiviral activity against SARS-CoV-2. SARS-CoV-2 nsp14-IN-10 exhibits broad-spectrum activity against other betacoronaviruses and inhibits SARS-CoV-2 at the replication stage. SARS-CoV-2 nsp14-IN-10 suppresses viral translation and exhibits immunostimulatory effects. SARS-CoV-2 nsp14-IN-10 specifically reverses NSP14-mediated alterations inhost transcriptome. SARS-CoV-2 nsp14-IN-10 can be used for the study of SARS-CoV-2.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C24H22F3N7O3S
- Molecular Weight:545.54
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Help & FAQs
Biologische Aktivität
Beschreibung
In Vitro
SARS-CoV-2 nsp14-IN-10 (Compound C10) (20-500 µM) specifically binds to the SAM recognition pocket of NSP14 (KD = 187 nM) in a competitive manner with SAM[1].
SARS-CoV-2 nsp14-IN-10 (5-25 μM, 8 h) enhances the thermostability of NSP14 protein in HEK293-NSP14 cells, indicating that it binds to the target in living cells[1].
SARS-CoV-2 nsp14-IN-10 (24 h) significantly reduces the infection rates of the original SARS-CoV-2 strain, Delta, and Omicron variants in A549-ACE2 cells (EC50 values of 0.31 μM, 0.50 μM and 0.06 μM, respectively)[1].
SARS-CoV-2 nsp14-IN-10 (10 µM, 24 h) potently inhibits the replication phase of SARS-CoV-2 in HeLa cells[1].
SARS-CoV-2 nsp14-IN-10 (3-20 μM, 0-24 h) shows strong inhibitory activity in A549-ACE2 cells infected with SARS-CoV-2 trVLP during both full-time and post-entry treatments, while entry treatment shows no significant inhibition[1].
SARS-CoV-2 nsp14-IN-10 (20-40 μM, 8 h) inhibits the translation initiation of SARS-CoV-2 mRNA in A549-ACE2 cells infected with trVLP, specifically by cap maturation, selectively impairing[1].
SARS-CoV-2 nsp14-IN-10 (20-40 µM, 8 h) selectively inhibits viral translation in A549-ACE2 cells infected with SARS-CoV-2 trVLP[1].
SARS-CoV-2 nsp14-IN-10 (20 μM, 24 h) significantly reduced the expression levels of Spike mRNA and protein in A549-ACE2 cells infected with SARS-CoV-2 trVLP[1].
SARS-CoV-2 nsp14-IN-10 (20 μM, 24 h) upregulates the expression of interferon-stimulated genes (ISGs) such as RSAD2, IFI6, and IRF7 in A549-ACE2 cells[1].
SARS-CoV-2 nsp14-IN-10 (5-20 μM, 48 h) reverses host transcriptome changes induced by NSP14 expression in HEK293-NSP14 cells[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:HEK293-NSP14 cells
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Concentration:5 μM, 10 μM, 15 μM, 20 μM, 25 μM
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Incubation Time:8 h
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Result:Enhanced the thermal stability of NSP14 protein.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:The six- to eight-week-old male K18-hACE2 transgenic mice (18-20 g) were inoculated intranasally with 5 × 103 focus-forming units of SARS-CoV-2 nCoV-SH01 strain[1].
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Dosage:60 mg/kg, 120 mg/kg, 180 mg/kg
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Administration:I.p., twice daily for 3 days
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Result:120 mg/kg significantly reduced pulmonary viral titer.
60 mg/kg showed a decreasing trend, but the effect was not statistically significant.
Reduced alveolar wall thickening, congestion, and inflammatory infiltration.
The positive signal of the SARS-CoV-2 nucleocapsid protein was significantly reduced.
Chemical Information
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Molecular Weight 545.54
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Formel C24H22F3N7O3S
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SMILES
O=C(NC1CCN(C2=C3N=CNC3=NC=N2)CC1)C4=CC=CC(NS(=O)(C5=CC=C(C(F)(F)F)C=C5)=O)=C4
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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