FGA145
FGA145 is a dual, selective inhibitor for Mpro and human Cathepsin L, with Kis of 3.71 μM, 9.82 μM and 53 nM, for Mal-Mpro, pET21-Mpro and Cathepsin L, respectively. FGA145 reveals a multitarget effects in the antiviral activity.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C23H30N4O5
- Molecular Weight:442.51
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
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Help & FAQs
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Biologische Aktivität
Beschreibung
IC50 & Target
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cathepsin L 53 nM (Ki) |
Cathepsin B 206 nM (Ki) |
In Vitro
FGA145 reveals weak antiviral activity against SARS-CoV-2 with EC50 of 11.7 μM with low cytotoxicity in Huh-7-ACE2 cells (CC50 over 100 μM)[1].
FGA145 exhibits inhibitory properties towards cysteine proteases RhD, CRZ, Cat L and Cat B, with Kis of 1.63, 12.6, 53 and 206 nM[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:Huh-7-ACE2
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Concentration:0-100 μM
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Incubation Time:24 h
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Result:Exhibited a CC50 of over 100 μM.
Chemical Information
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Molecular Weight 442.51
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Formel C23H30N4O5
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SMILES
O=C(N[C@@H](C[C@@H]1CCNC1=O)/C=C/[N+]([O-])=O)[C@H](CC(C)C)NC(/C=C/C2=CC=CC=C2)=O
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
FGA145 Related Classifications
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