BP-198
BP-198 is a inhibitor and a SNIPER-class degrader targeting to SARS-CoV-2 main protease (Mpro) , with antiviral activity. BP-198 recruits the IAP ubiquitin ligase complex to degrade target proteins via the ubiquitin-proteasome system. BP-198 also degrades protease mutants resistant to Nirmatrelvir (HY-138687). BP-198 can be used in studies related to COVID-19.
(Pink: SARS-CoV ligand (HY-176442); Blue: IAP ligand (HY-176441); Black: linker (HY-W457968)).
For research use only. We do not sell to patients.
- Formula: C56H72F6N12O10S2
- Molecular Weight:1251.37
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Calu-3 | IC50 |
11.8 μM
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Antiviral activity against SARS-CoV-2 Omicron BA.5 in human Calu-3 cells by reducing infectious viral titer measured via yield-based antiviral assay at 24 h post-infection.
Antiviral activity against SARS-CoV-2 Omicron BA.5 in human Calu-3 cells by reducing infectious viral titer measured via yield-based antiviral assay at 24 h post-infection.
|
40287552 |
| Calu-3 | IC50 |
11.4 μM
|
Antiviral activity against SARS-CoV-2 Omicron BA.5 in human Calu-3 cells by reducing viral genome copy number measured via quantitative RT-PCR at 24 h post-infection.
Antiviral activity against SARS-CoV-2 Omicron BA.5 in human Calu-3 cells by reducing viral genome copy number measured via quantitative RT-PCR at 24 h post-infection.
|
40287552 |
In Vitro
BP-198 (0.5-20 μM; 2-24 h) specifically degrades wildtype SARS-CoV-2 Mpro in HEK293T LVX Mpro-HiBiT reporter cells in a concentration- and time-dependent manner, achieving a 72% reduction in Mpro levels at 20 μM over 24 h[1].
BP-198 (1.25-10 μM; up to 70 h post-infection) exhibits enhanced antiviral activity against wildtype SARS-CoV-2 (VIC-01) in VeroE6/TMPRSS2 and Calu-3 cells, with 2.6-fold higher potency than its non-degrading control BP-206 at 70 h post-infection in VeroE6/TMPRSS2 cells (IC50 = 6.93 μM)[1].
BP-198 (Serial dilutions; 24 h post-infection) demonstrates enhanced antiviral activity against SARS-CoV-2 Omicron BA.5 in Calu-3 cells, with an IC50 of 11.8 μM for reducing infectious viral titer and 11.4 μM for reducing viral genome copy number, showing 2.1-fold higher potency than its non-degrading control BP-206[1].
BP-198 (Serial dilutions; 18 h post-infection) retains enhanced antiviral activity against nirmatrelvir-resistant SARS-CoV-2 Delta (E166V/L50F) in VeroE6/TMPRSS2 cells, with an IC50 of 12.7 μM and only a 25-fold reduction in potency relative to wildtype Delta, compared to a 261-fold reduction for Nirmatrelvir (HY-138687)[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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Molecular Weight 1251.37
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Formula C56H72F6N12O10S2
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SMILES
C[C@@H](C(N[C@@H](C1CCCCC1)C(N2CCC[C@H]2C3=NC(C(C4=CC(OCCCN5N=NC(CSC(C)([C@H](NC(C(F)(F)F)=O)C(N6[C@H](C(N[C@H](C#N)C[C@@H]7CCNC7=O)=O)[C@]8([H])[C@](C8(C)C)([H])C6)=O)C)=C5)=CC=C4)=O)=CS3)=O)=O)NC.OC(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)