Furin-IN-3
Furin-IN-3 is a non-peptidic furin inhibitor with a dichlorobiphenyl-derived core, with a Ki value of 1.67 nM for furin inhibition and a Ki value of 278 nM for proprotein convertase PC7 inhibition. Furin-IN-3 can be used in the research of influenza A virus infection (H7N7 strain SC35M).
For research use only. We do not sell to patients.
- CAS No.: 3080672-14-3
- Formula: C38H47Cl2F9N4O7
- Molecular Weight:913.69
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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
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furin 1.67 nM (Ki) |
PC7 278 nM (Ki) |
In Vitro
Furin-IN-3 (compound 9) inhibits furin with a Ki value of 12.4 nM in a fluorogenic substrate assay, indicating that it ranks among the moderately potent inhibitors in this series[1].
Furin-IN-3 inhibits PC7 with a Ki value of 278 nM, indicating that it exhibits significantly weaker activity against this related proprotein convertase than against furin[1].
Furin-IN-3 (72 h) demonstrates the most potent antiviral activity against the H7N7 influenza strain SC35M in A549 cells at 5 μM, reducing viral titers by 104 to 105-fold[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3080672-14-3
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Molecular Weight 913.69
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Formula C38H47Cl2F9N4O7
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SMILES
O=C(C(F)(F)F)O.O=C(C)NCC1CCN(CC1)CC2=CC(C3=CC(Cl)=CC(Cl)=C3)=CC(CN4CCC(C5CCNCC5)CC4)=C2.O=C(C(F)(F)F)O.O=C(C(F)(F)F)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)
Furin-IN-3 Related Classifications
HY-180145 Related Classifications
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