CF-Vanillin
CF-Vanillin is an orally active hypolipidemic/hepatic protector with strong binding affinity for PPAR-α. CF-Vanillin exerts antioxidant and anti-inflammatory effects by activating the Nrf2/HO-1 signaling pathway. CF-Vanillin reduces triglyceride and total cholesterol levels and alleviates liver injury. CF-Vanillin can be used in the research of diseases such as hyperlipidemia and liver injury.
For research use only. We do not sell to patients.
- CAS No.: 1323378-95-5
- Formula: C18H17ClO5
- Molecular Weight:348.78
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
PPARα |
IL-6 |
HO-1 |
In Vivo
CF-Vanillin (1.65 mmol/kg; i.g.; 30 days) can alleviate oxidative stress and inflammation by upregulating the Nrf2/HO-1 signaling pathway, thereby significantly reducing liver injury in healthy mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Triton WR 1339-induced hyperlipidemic mice[1]
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Dosage:0.534 mmol/kg; 0.267 mmol/kg; 0.1335 mmol/kg
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Administration:once daily; 7 days
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Result:Reduced serum TG by 28.82% and serum TC by 37.23% at 0.534 mmol/kg.
Reduced serum TG by 24.32% and serum TC by 29.51% at 0.267 mmol/kg.
Reduced serum TG by 21.83% and serum TC by 19.07% at 0.1335 mmol/kg.
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Animal Model:Healthy mice[1]
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Dosage:1.65 mmol/kg
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Administration:i.g.; once daily; 30 days
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Result:Showed no significant difference in body weight relative to control or CF groups.
Significantly reduced liver weight and liver coefficient relative to the CF group.
Significantly reduced serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels relative to the CF group.
Reduced serum alkaline phosphatase (AKP) levels but not significantly.
Significantly increased serum superoxide dismutase (SOD) levels relative to the CF group, significantly increased serum glutathione (GSH) levels relative to the CF group, and significantly reduced serum malondialdehyde (MDA) levels relative to the CF group.
Significantly reduced liver tissue tumor necrosis factor-alpha (TNF-α) protein expression relative to the CF group.
Reduced interleukin-6 (IL-6) protein expression but not significantly.
Showed no inflammatory cell infiltration and only mild hepatocyte swelling, compared to marked hepatocyte swelling, necrosis, nuclear degeneration/dissolution, and inflammatory cell infiltration in the CF group.
Significantly upregulated liver tissue Nrf2 protein expression relative to the CF group, and significantly upregulated HO-1 protein expression relative to the CF group.
Chemical Information
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CAS No. 1323378-95-5
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Molecular Weight 348.78
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Formula C18H17ClO5
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SMILES
ClC1=CC=C(OC(C)(C)C(OC2=C(OC)C=C(C=O)C=C2)=O)C=C1
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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 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)