BI-1388
BI-1388 is a macrocyclic acylsulfonamide-based HCV NS3-4A protease inhibitor. BI-1388 inhibits clinically relevant drug-resistant mutant strains (KRASD168V gt 1b and KRASR155K gt 1a) and exhibits high liver distribution. BI-1388 is applicable for the research of HCV infection.
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The BI-1388 was designed by Boehringer Ingelheim and could be obtained free of charge through the Boehringer Ingelheim open innovation portal opnMe.com, associated with its negative control.
- CAS No.: 1309952-03-1
- 화학식: C41H53N7O9S
- 분자량:819.97
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보관:
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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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
IC50 & Target
[1]|
K-RAS |
In Vitro
BI-1388 (compound 19) inhibits the replication of HCV genotype 1b D168V variant, with an EC50 of 1.0 nM at 72 h; it also inhibits the replication of HCV genotype 1a R155K variant, with an EC50 of 0.14 nM at 72 h[1].
The half-life of BI-1388 in human liver microsomes is 54 min[1].
The half-life of BI-1388 in rat liver microsomes is 138 min[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
Chemical Information
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CAS No. 1309952-03-1
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분자량 819.97
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화학식 C41H53N7O9S
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SMILES
O=C([C@]([C@]1([H])/C=C\CCCCC[C@@H]2NC(C3=NN(C)C=C3)=O)(C1)NC([C@@](C[C@@H](OC4=CC(OC(C)C)=NC5=C(C)C(OC)=CC=C45)C6)([H])N6C2=O)=O)NS(=O)(C7(C)CC7)=O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BI-1388 Related Classifications
HY-115516 Related Classifications
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