Divaricatol
Divaricatol is an orally ative chromone natural product and an active component in Saposhnikovia divaricata. Divaricatol reduces the release of pro-inflammatory cytokines and restores immune homeostasis by stably binding to 5KIR (a target of the TNF/IL-17 pathway). Divaricatol exerts analgesic effects in mouse models. Divaricatol can be used in the research of pain, diarrhea-predominant irritable bowel syndrome (IBS-D) and qi deficiency syndrome.
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- CAS No.: 331433-08-0
- Formule: C17H18O7
- Masse moléculaire:334.32
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Activité biologique
Description
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ddy (Male, 4 weeks old, 24–36 g, acetic acid-induced writhing model)[1]
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Dosage:1, 5 mg/kg
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Administration:p.o.; single dose
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Result:Showed potent analgesic effect at oral doses of 1 and 5 mg/kg.
Chemical Information
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CAS No. 331433-08-0
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Masse moléculaire 334.32
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Formule C17H18O7
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SMILES
OC1=C2C(OC(C)([C@H](C2)OC(C)=O)C)=CC3=C1C(C=C(O3)CO)=O
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Structure Classification
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Initial Source
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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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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
Pureté et documentation
Références
[1]. Okuyama E, et al. Analgesic components of saposhnikovia root (Saposhnikovia divaricata). Chem Pharm Bull (Tokyo). 2001;49(2):154-160. [Content Brief]
[2]. Yu D, et al. Deciphering the microbiological mechanism of Tongxie Yaofang in treating IBS-D: a multimodal mechanistic study in mice integrating network pharmacology, computational simulation, and 16S rRNA sequencing. Exp Biol Med (Maywood). 2025;250:10725. Published 2025 Oct 3. [Content Brief]
[3]. Zhao Z, et al. Integration of serum metabolomics and network pharmacology reveals the immunoenhancing mechanisms of Qishenbuqi capsules. Toxicol Res (Camb). 2023;12(2):201-215. Published 2023 Feb 14. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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