Euryachin E
Euryachin E is an antimicrobial and antiviral agent found in Eurya chinensis. It exhibits a MIC of 6.25 μg/mL against B. cereus and 0.78 μg/mL against S. aureus. Its IC50 against COVID-19 is 6.41 μM. Euryachin E can be utilized for research in the fields of infection and inflammation.
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- 화학식: C39H54O6
- 분자량:618.84
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
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Biological Activity
제품 설명
Chemical Information
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분자량 618.84
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화학식 C39H54O6
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SMILES
CC([C@@H]1CC[C@]2(C(O)=O)CC[C@@]3(C)[C@]4(C)CCC5[C@](C)(COC(/C=C/C6=CC=C(O)C=C6)=O)[C@](O)([H])CC[C@]5(C)C4CCC3C21)=C
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Structure Classification
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Initial Source
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Euryachin E Related Classifications
HY-N15344 Related Classifications
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