ZXH-8-004
ZXH-8-004 is a DENV E PROTAC degrader with a DC50 value of 0.21 µM in Huh7.5 cells. ZXH-8-004 induces CRBN- and proteasome-dependent degradation of intracellular dengue virus envelope protein. ZXH-8-004 inhibits envelope-mediated membrane fusion during viral entry and reduces the production of infectious dengue virus particles. ZXH-8-004 can be used in studies related to dengue virus infection, Zika virus infection, Japanese encephalitis virus infection, West Nile virus infection, and yellow fever virus infection.
(Pink: Dengue Virus ligand (HY-161807); Blue: Cereblon ligand (HY-103596); Black: linker (HY-42149)).
For research use only. We do not sell to patients.
- Formula: C38H33F6N7O10
- Molecular Weight:861.70
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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
In Vitro
ZXH-8-004 (2-12-2-deg) (0.07-20 μM; 24 h) induces CRBN- and proteasome-dependent depletion of intracellular DENV2 E protein in infected wild-type Huh7.5 cells, with a DC50 of 0.21 μM and a maximum depletion rate of up to 95%[1].
ZXH-8-004 (0.01-100 μM; 24 h) exerts CRBN-dependent enhanced anti-DENV2 activity in wild-type Huh7.5 cells, with an EC90 of 1.67 μM[1].
ZXH-8-004 (2-12-2-deg) (0.01-100 μM; 24 h) exhibits broad-spectrum and enhanced antiviral activity against ZIKV, JEV, WNV-Kunjin and YFV in Huh7.5 cells, with EC90 values ranging from 4.77 μM to 22.14 μM[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:Infected wild-type Huh7.5 cells
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Concentration:0.07, 0.15, 0.3, 0.6, 1.2, 2.5, 5, 10, 20 μM
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Incubation Time:24 h
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Result:Induced CRBN- and proteasome-dependent depletion of intracellular DENV2 E protein.
Chemical Information
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Molecular Weight 861.70
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Formula C38H33F6N7O10
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SMILES
FC(F)(F)OC1=CC=C(NC2=CC=NC(NC3=CC=C(C(NCCOCCOCCOC4=C5C(C(N(C6CCC(NC6=O)=O)C5=O)=O)=CC=C4)=O)C=C3OC(F)(F)F)=N2)C=C1
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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)