PROTAC HBeAg degrader-1
PROTAC HBeAg degrader-1 is a HBeAg-targeting PROTAC degrader that recruits VHL. PROTAC HBeAg degrader-1 degrades HBeAg and reduces HBcAg levels in a largely VHL-independent manner, and inhibits secreted HBeAg in a concentration-dependent manner, with particularly stronger inhibitory activity against the HAP-resistant (HBVT109I mutation) strain. PROTAC HBeAg degrader-1 can be used in studies related to hepatitis B virus infection.
(Pink: HBeAg ligand (HY-174857); Blue: VHL ligand (HY-125845); Black: linker).
For research use only. We do not sell to patients.
- Formula: C48H57ClFN9O7S2
- Molecular Weight:990.60
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All PROTACs Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
HBeAg |
HBcAg |
In Vitro
PROTAC HBeAg degrader-1 (compound LH-3) (10 μM; 24 h) reduces the level of total non-secretory HiBiT-tagged HBeAg in HEK293T HiBiT-HBeAg-NS cells to less than 30% of that in the DMSO control group[1].
PROTAC HBeAg degrader-1 (20 μM; 24 h) reduces the level of secreted HiBiT-tagged HBeAg in HEK293T HiBiT-HBeAg-S cells to < 7% of that in the DMSO control group, and decreases the level of intracellular HiBiT-tagged HBeAg to 46% of that in the DMSO control group[1].
PROTAC HBeAg degrader-1 (10 μM; 24 h) reduces secreted and intracellular HiBiT-tagged HBeAg in HEK293T HiBiT-HBeAg-S and HEK293T VHL KO HiBiT-HBeAg-S cells, indicating that this degradation is largely independent of VHL[1].
PROTAC HBeAg degrader-1 (10 μM; 24 h) reduces secreted HiBiT-tagged HBeAg to 8% of the DMSO control level and intracellular HiBiT-tagged HBeAg to 44% of the DMSO control level in HEK293T HiBiT-HBeAg-S cells, and this activity depends on the key motif in the VH032 domain[1].
PROTAC HBeAg degrader-1 (10 μM; 24 h) reduces secreted HiBiT-tagged HBeAg to 9% of the DMSO control level and intracellular HiBiT-tagged HBeAg to 45% of the DMSO control level in HEK293T HiBiT-HBeAg-S cells[1].
PROTAC HBeAg degrader-1 (10 μM; 6 days) reduces the level of HBcAg (p21) in HBV-expressing HepAD38 cells[1].
PROTAC HBeAg degrader-1 (10 μM; 24 h) reduces the level of secreted HBeAg in wild-type HBV-transfected Huh7 cells to approximately 8% of that in untreated cells, and reduces the level of this protein in HBVT109I mutant-transfected Huh7 cells to approximately 11.5% of that in untreated cells[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:HepAD38 HBV-expressing cells
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Concentration:10 μM
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Incubation Time:6 days
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Result:Caused a strong reduction in HBcAg (p21) levels relative to DMSO control.
Chemical Information
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Molecular Weight 990.60
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Formula C48H57ClFN9O7S2
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SMILES
O=C(C1=C(CN2CCN(C(CCCCC(N[C@@H](C(C)(C)C)C(N3[C@H](C(NCC4=CC=C(C5=C(C)N=CS5)C=C4)=O)C[C@@H](O)C3)=O)=O)=O)CC2)NC(C6=NC=CS6)=N[C@H]1C7=CC=C(F)C=C7Cl)OC
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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.
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)