Cycloneroside A
Cycloneroside A is a sesquiterpene aminoglycoside compound discovered from Trichoderma sp. SCSIOW21. Cycloneroside A has the activity of inhibiting the production of NO. In the experiment with macrophage RAW 264.7 cells, its IC50 value for inhibiting the production of NO is approximately 100 µM. Cycloneroside A can be used in the research of the anti-inflammatory field.
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- CAS No.: 3075431-04-5
- Formule: C23H41NO7
- Masse moléculaire:443.57
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Chemical Information
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CAS No. 3075431-04-5
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Masse moléculaire 443.57
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Formule C23H41NO7
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SMILES
CC(N[C@H]([C@H]([C@@H]1O)O)[C@H](O[C@@H]1CO)O[C@@]([C@H]2C)(CC[C@@]2([H])[C@](C)(O)CC/C=C(C)/C)C)=O
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Structure Classification
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Initial Source
Trichoderma sp.
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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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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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)