Jun15702
Jun15702 is a PROTAC degrader targeting the capsid protein VP1 of enterovirus D68. Jun15702 recruits the Cereblon (CRBN) E3 ligase and activates the ubiquitin-proteasome pathway. Jun15702 inhibits viral entry and exerts inhibitory effects during the early, middle and late stages of viral replication. Jun15702 exhibits antiviral activity against multiple wild-type enterovirus D68 strains, and also shows submicromolar antiviral activity against the Pleconaril (HY-19952)-resistant enterovirus D68 variant rMO-VP1 F159V. Jun15702 can be used in studies related to enterovirus D68 (EV-D68) infection.
(Pink: Enterovirus ligand (HY-183010); Blue: Cereblon ligand (HY-183011); Black: linker).
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- Formule: C47H54F3N7O11
- Masse moléculaire:949.97
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
IC50 & Target
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Cereblon |
In Vitro
Jun15702 (10 μM; 0-8 h) depletes VP1 levels in EV-D68 US/MO/14-18947-infected RD cells when added before, during, or after viral entry, and effectively degrades the pleconaril-resistant VP1F159V mutant protein[1].
Jun15702 (0.3-30 μM; 2-10 h) induces dose-dependent, CRBN-mediated degradation of VP1 protein in EV-D68 US/MO/14-18947-infected RD cells, as confirmed by Western blot analysis[1].
Jun15702 (range; 60 h) has a CC50 of 81.8 μM in RD cells, showing no significant cytotoxicity at concentrations below 50 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:EV-D68 US/MO/14-18947-infected RD cells, rMO-VP1 F159V EV-D68-infected RD cells
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Concentration:10 μM
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Incubation Time:-1-8 h, 0-8 h, 1-8 h, 2-8 h, 3-8 h, 4-8 h, 5-8 h, 6-8 h, 7-8 h (relative to infection; wild-type testing); 2-8 hpi (mutant strain testing)
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Result:Nearly completely depleted VP1 levels when added before or during viral entry (-1-8 h, 0-8 h).
Retained potent inhibitory activity when added post-entry (2-8 h, 3-8 h, 4-8 h, 5-8 hpi), only gradually losing activity at 6-8 h and 7-8 hpi.
Dramatically reduced VP1 immunofluorescence signals when added at 2-8 hpi to rMO-VP1 F159V-infected cells, whereas pleconaril showed no inhibition.
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Cell Line:EV-D68 US/MO/14-18947-infected RD cells
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Concentration:0, 0.3, 1, 3, 10, 30 μM; 10 μM lenalidomide-5-Br combined with increasing concentrations of Jun15702
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Incubation Time:2-10 hpi
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Result:Caused a dose-dependent reduction in VP1 protein levels, whereas pleconaril and lenalidomide-5-Br did not induce VP1 degradation.
Preserved VP1 degradation at concentrations above 3 μM when combined with 10 μM lenalidomide-5-Br.
Chemical Information
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Masse moléculaire 949.97
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Formule C47H54F3N7O11
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SMILES
O=C(NCCCOCCOCCOCCCNC(C1=NOC(CCCOC2=C(C=C(C=C2C)C3=NOC(C(F)(F)F)=N3)C)=C1)=O)CCCC#CC4=CC=C(CN(C5CCC(NC5=O)=O)C6=O)C6=C4
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)