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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
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 番号: 1309952-03-1
- 分子式: C41H53N7O9S
- 分子量:819.97
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保管条件:
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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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
IC50 & Target
[1]|
K-RAS |
体外実験
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
化学情報
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CAS 番号 1309952-03-1
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分子量 819.97
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
BI-1388 関連分類
HY-115516 関連分類
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