Vescalagin
Vescalagin is a hexahydroxyphenol. Vescalagin is isolable from Camu-camu (Myrciaria dubia) and immature wax apple fruits. Vescalagin exhibits inhibitory activity against a variety of enzymes, with a Ki value of 5.87 nM against AChE, 3.89 nM against BChE, 11.75 nM against hCA I, 16.23 nM against hCA II, and 16.08 nM against α-glucosidase. Vescalagin inhibits hCA I, hCA II and α-glucosidase in a non-competitive manner. Vescalagin downregulates JNK/p38 MAPK to protect pancreatic β-cells and improve insulin secretion in methylglyoxal-treated rats. Vescalagin reduces hyperglycemia and hypertriglyceridemia in rats fed a high-fructose diet. Vescalagin possesses anti-inflammatory and antioxidant properties.
For research use only. We do not sell to patients.
- CAS No.: 36001-47-5
- Formula: C41H26O26
- Molecular Weight:934.63
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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]|
AChE 5.87 nM (Ki) |
BChE 3.89 nM (Ki) |
hCA I 11.75 nM (Ki) |
hCA II 16.23 nM (Ki) |
α‑glucosidase 16.08 nM (Ki) |
In Vitro
Vescalagin is an inhibitor of acetylcholinesterase (AChE) with a Ki value of 5.87 nM[1].
Vescalagin is an inhibitor of butyrylcholinesterase (BChE) with a Ki value of 3.89 nM[1].
Vescalagin acts as a non-competitive inhibitor of α-glucosidase with a Ki value of 16.08 nM[1].
Vescalagin acts as a non-competitive inhibitor of hCA I with a Ki value of 11.75 nM[1].
Vescalagin acts as a non-competitive inhibitor of hCA II with a Ki value of 16.23 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Vescalagin reduces hyperglycemia and hypertriglyceridemia in rats fed a high-fructose diet[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 36001-47-5
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Molecular Weight 934.63
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Formula C41H26O26
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SMILES
OC1=C(O)C(O)=C(C2=C3C=C(O)C(O)=C2O)C=C1C(OC[C@](OC(C4=C(C5=C6C(C7=C(C(O[C@@]8([H])[C@@H]9O)=O)C9=C(O)C(O)=C7O)=C(O)C(O)=C5O)C(O)=C(O)C(O)=C4)=O)([H])[C@@]([C@@H]8OC6=O)([H])OC3=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
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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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)
Vescalagin Related Classifications
HY-N19401 Related Classifications
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