BMS-986144 (non-deuterated)
BMS-986144 non-deuterated is the non-tritium form of BMS-986144 (HY-131905S). BMS-986144 is an orally active inhibitor of HCV NS3/4A protease. BMS-986144 binds to the active site of HCV NS3/4A protease and induces conformational changes in the protease. BMS-986144 reduces time-dependent CYP3A4 inhibition, exhibits hepatic microsomal metabolic stability, and undergoes oxidation of the macrocyclic linker chain. BMS-986144 can be used in studies related to hepatitis C virus infection.
For research use only. We do not sell to patients.
- CAS No.: 1410114-25-8
- Formula: C40H51F4N5O9S
- Molecular Weight:853.92
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
BMS-986144 non-deuterated is the non-tritium form of BMS-986144 (HY-131905S)[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. 1410114-25-8
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Molecular Weight 853.92
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Formula C40H51F4N5O9S
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SMILES
O=C(OC(C)(C)C(F)(F)F)N[C@H]1[C@H](CC)C[C@H](C)CC/C=C\[C@@]2([H])[C@](C2)(C(NS(=O)(C3(C)CC3)=O)=O)NC([C@@](C[C@@H](OC4=NC=CC5=C4C=C(F)C(OC)=C5)C6)([H])N6C1=O)=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)