BILA 1906 BS
BILA 1906 BS is a HIV protease inhibitor. BILA 1906 BS prevents HIV-1 replication via inhibition of viral protease-mediated cleavage of Gag and Gag-Pol polyprotein precursors during virion maturation. BILA 1906 BS blocks maturation of p24 proteins in wild-type HIV-1, impairing polyprotein processing and viral maturation. BILA 1906 BS can be used for the research of human immunodeficiency virus type 1 (HIV-1) infection.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 154612-31-4
- Formel: C41H52N6O4S
- Molecular Weight:724.95
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
BILA 1906 BS (serial twofold dilutions; 3 days) inhibits wild-type HIV-1 replication in acutely infected C8166 T cells with an EC50 of 1 nM[1].
BILA 1906 BS inhibits wild-type HIV-1 protease with a Ki of 1.7 pM, and protease mutations selected by BILA 1906 BS reduce inhibitor binding, with the HIV-1V32I M46I A71V I84A mutant showing a 12,000-fold increase in Ki[1].
BILA 1906 BS (0-1000 nM; 3 days) blocks polyprotein processing in wild-type HIV-1 particles from transfected 293 cells, but has minimal effect on processing in highly resistant HIV-1 clones bearing protease mutations V32I, M46I, A71V, I84A and a p1/p6 cleavage site mutation[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:293 cells (transfected with HIV-1 molecular clones)
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Concentration:0, 10, 100, 1000 nM
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Incubation Time:3 days post-transfection
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Result:Blocked complete p24 production in wild-type HIV-1 particles at 100 nM.
Blocked Pr55gag and Pr160gag-pol processing in wild-type HIV-1 particles at 1 μM.
Showed almost no effect on Gag processing in highly resistant clone 32/46/71/84A at 1 μM, with only a slight appearance of a 49-kDa intermediate at 100 nM and 1 μM.
Chemical Information
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CAS. Nr. 154612-31-4
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Molecular Weight 724.95
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Formel C41H52N6O4S
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SMILES
O=C(N[C@@H](C(C)C)C(N[C@H]([C@@H](CN1[C@@H](C[C@@H](CC1)SCC2=CC=CN=C2)C(NC(C)(C)C)=O)O)CC3=CC=CC=C3)=O)C4=NC5=CC=CC=C5C=C4
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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)