Cycloneroside E
Cycloneroside E is a sesquiterpene aminoglycoside compound discovered from Trichoderma sp. SCSIOW21. Cycloneroside E has the activity of inhibiting the production of NO. In macrophage RAW 264.7 cells, its IC50 value for inhibiting the production of NO is 48.0 µM. Cycloneroside E can be used in the research of the anti-inflammatory field.
For research use only. We do not sell to patients.
- CAS No.: 3075431-08-9
- Formula: C23H39NO8
- Molecular Weight:457.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 3075431-08-9
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Molecular Weight 457.56
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Formula C23H39NO8
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SMILES
C[C@@](CCC1=O)([C@@](CC[C@](C)2O[C@@H](O[C@@H]3CO)[C@@H]([C@H]([C@@H]3O)O)NC(C)=O)([H])[C@@H]2C)OC1(C)C
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Structure Classification
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Initial Source
Trichoderma sp.
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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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Phagocytosis Functional Assay
A phagocytosis functional assay measures the ability of phagocytic cells, such as neutrophils, macrophages, monocytes, or microglia/macrophages, to bind and internalize particulate targets including bacteria, yeast particles, beads, or myelin particles. Fluorescent flow-cytometry assays detect target uptake as fluorescence associated with gated phagocytes, while pH-sensitive dyes such as pHrodo increase signal in acidic phagosomal compartments and therefore preferentially report internalized particles rather than particles remaining outside the cell. Microscopy or high-content imaging can be used to confirm intracellular localization and, in some protocols, to follow uptake kinetics.
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)