Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside is an anti-inflammatory agent. Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside exerts significant anti-inflammatory effects in LPS (HY-D1056)-induced RAW 264.7 macrophages by inhibiting the NF-κB, MAPK and Akt signaling pathways, thereby reducing the production of inflammatory mediators (NO, PGE2) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
For research use only. We do not sell to patients.
- CAS No.: 131559-50-7
- Formula: C39H50O25
- Molecular Weight:918.80
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Storage:
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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
COX-2 |
iNOS |
IL-6 |
IL-1β |
In Vitro
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-40 μM; 1 h pre-incubation prior to 24 h LPS stimulation) concentration-dependently inhibits LPS-induced NO production in RAW 264.7 cells[1].
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-5 μM; 1 h pre-incubation prior to 24 h LPS stimulation) concentration-dependently inhibits LPS-induced production of PGE2, TNF-α, IL-1β, and IL-6 in RAW 264.7 cells[1].
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-5 μM; 1 h pre-incubation prior to LPS stimulation) concentration-dependently inhibits LPS-induced activation of the NF-κB pathway in RAW 264.7 cells by reducing phosphorylation of NF-κB p65 and IκB and restoring total IκB expression[1].
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-5 μM) concentration-dependently inhibits LPS-induced expression of iNOS and COX-2 proteins in RAW 264.7 cells[1].
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-5 μM) concentration-dependently inhibits LPS-induced activation of the MAPKs pathway in RAW 264.7 cells by reducing phosphorylation of p38, JNK, and Erk[1].
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside (1.25-5 μM) concentration-dependently inhibits LPS-induced activation of the Akt pathway in RAW 264.7 cells by reducing phosphorylation of Akt[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:RAW 264.7
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Concentration:1.25, 2.5, 5, 10, 20 and 40 μM
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Incubation Time:24 h
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Result:Showed no significant effect on cell viability.
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Cell Line:RAW 264.7 (LPS-stimulated)
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Concentration:1.25, 2.5 and 5 μM
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Incubation Time:1 h pre-incubation; 24 h LPS stimulation
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Result:Concentration-dependently reduced LPS-induced production of PGE2, TNF-α, IL-1β, and IL-6, with significant inhibition at all tested concentrations.
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Cell Line:RAW 264.7 (LPS-stimulated)
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Concentration:1.25, 2.5 and 5 μM
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Incubation Time:1 h pre-incubation; LPS stimulation
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Result:Concentration-dependently reduced LPS-induced phosphorylation of NF-κB p65 and IκB.
Concentration-dependently enhanced LPS-reduced total IκB protein expression.
Left total NF-κB p65 levels unaffected.
Chemical Information
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CAS No. 131559-50-7
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Molecular Weight 918.80
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Formula C39H50O25
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SMILES
O[C@H]([C@@H](CO[C@@H]1O[C@@H](C)[C@H](O)[C@@H](O)[C@H]1O)O2)[C@H](O)[C@@H](O[C@H]3[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O3)[C@@H]2OC4=C(C5=CC=C(O)C=C5)OC6=CC(O[C@H]7[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O7)=CC(O)=C6C4=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
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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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
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside Related Classifications
HY-N18025 Related Classifications
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