Icariside E4
Based on 1 Customer Validation
Icariside E4 is an antinociceptive agent, and can be isolated from Tabebuia roseo-alba. Icariside E4 has peripheral analgesic activity by ATP-sensitive K+ channel-dependent mechanisms. Icariside E4 also has anti-oxidant, anti-Alzheimer and anti-inflammatory effects.
For research use only. We do not sell to patients.
- Purity : 98.13%
- CAS No.: 126253-42-7
- Formula: C26H34O10
- Molecular Weight:506.54
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Storage:
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Caco-2 | IC50 |
<5 μg/mL
Compound: Icariside E4
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Cytotoxicity against human Caco2 cells after 72 hrs by MTS assay
Cytotoxicity against human Caco2 cells after 72 hrs by MTS assay
|
[PMID: 22032697] |
| CCD-18Co | IC50 |
<5 μg/mL
Compound: Icariside E4
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Cytotoxicity against human CCD-18Co cells after 72 hrs by MTS assay
Cytotoxicity against human CCD-18Co cells after 72 hrs by MTS assay
|
[PMID: 22032697] |
| HCT-116 | IC50 |
<5 μg/mL
Compound: Icariside E4
|
Cytotoxicity against human HCT116 cells after 72 hrs by MTS assay
Cytotoxicity against human HCT116 cells after 72 hrs by MTS assay
|
[PMID: 22032697] |
Chemical Information
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CAS No. 126253-42-7
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Appearance Solid
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Molecular Weight 506.54
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Formula C26H34O10
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Color White to off-white
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SMILES
OC[C@@H]1C2=CC(CCCO)=CC(OC)=C2O[C@@]1([H])C3=CC(OC)=C(C=C3)O[C@H]4[C@@H]([C@@H]([C@H]([C@@H](O4)C)O)O)O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Protocols
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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
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Data Sheet (269 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Veiga TA, et al. Furoquinoline alkaloids isolated from Balfourodendron riedelianum as photosynthetic inhibitors in spinach chloroplasts. J Photochem Photobiol B. 2013 Mar 5;120:36-43. [Content Brief]
[2]. Suh JY, et al. Hypolipogenic effects of Icariside E4 via phosphorylation of AMPK and inhibition of MID1IP1 in HepG2 cells. Phytother Res. 2023 Jan;37(1):7-14. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)