Asiaticoside F
Asiaticoside F is a triterpenoid glycoside found in Centella asiatica. Asiaticoside F can be used in studies related to skin diseases, diarrhea, eye diseases, inflammation, asthma, leprosy and hypertension.
For research use only. We do not sell to patients.
- CAS No.: 593254-83-2
- Formula: C48H78O18
- Molecular Weight:943.12
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| RAW264.7 | IC50 |
100 μM
Compound: 3
|
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess method
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess method
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[PMID: 21353543] |
In Vitro
Asiaticoside F (3 mg; 2 h) yields Glucose (D-Glucose) (HY-B0389) and Rhamnose (HY-N1420) via acid hydrolysis, as confirmed by paper chromatography comparison with authentic standards[1].
Asiaticoside F confirms it is (3β,4α)-3,23-dihydroxyurs-12-en-28-oic acid O-α-L-rhamnopyranosyl-(1→4)-O-β-D-glucopyranosyl-(1→6)-β-D-glucopyranosyl ester, with a molecular formula of C48H78O18 via spectroscopic analysis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 593254-83-2
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Molecular Weight 943.12
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Formula C48H78O18
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SMILES
OC[C@H]([C@H]([C@@H]([C@H]1O)O)O[C@H]2[C@@H]([C@@H]([C@H]([C@@H](O2)C)O)O)O)O[C@H]1OC[C@H]([C@H]([C@@H]([C@H]3O)O)O)O[C@H]3OC([C@]45[C@]([C@H]([C@@H](CC5)C)C)([H])C6=CC[C@@]([C@@]7([C@@]([C@@](C)([C@H](CC7)O)CO)([H])CC8)C)([H])[C@]8(C)[C@@]6(CC4)C)=O
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Structure Classification
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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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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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)