Resveratrol 12-C-β-glucopyranoside
Resveratrol 12-C-β-glucopyranoside is a stilbene-type natural secondary metabolite. Resveratrol 12-C-β-glucopyranoside has the potential to target TNF-α, TGF-β1, and PPAR-α. As one of the core active components of MESR, Resveratrol 12-C-β-glucopyranoside exerts hepatoprotective, anti-inflammatory, and antioxidant effects in a rat liver injury model induced by Isoniazid (HY-B0329). Resveratrol 12-C-β-glucopyranoside can be used for studies related to drug-induced liver injury.
For research use only. We do not sell to patients.
- CAS No.: 163527-00-2
- Formula: C20H22O8
- Molecular Weight:390.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
In Vitro
Resveratrol 12-C-β-glucopyranoside shows high binding affinity to recombinant human TNF-α (-9.9 kcal/mol) and TGF-β1 (-10.0 kcal/mol), as well as moderate binding affinity to PPAR-α according to molecular docking results, which suggests it may exert potential hepatoprotective effects via regulating these pivotal targets[1].
Resveratrol 12-C-β-glucopyranoside is a compound isolated from the stem bark of Shorea hemsleyana, with a C-β-glucopyranosyl group attached at the C-12 position of Resveratrol (HY-16561)[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 163527-00-2
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Molecular Weight 390.38
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Formula C20H22O8
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SMILES
OC1=C([C@@H]2O[C@@H]([C@H]([C@@H]([C@H]2O)O)O)CO)C(O)=CC(/C=C/C3=CC=C(C=C3)O)=C1
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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 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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Hepatotoxicity Study
This protocol evaluates hepatotoxicity using complementary in vivo mouse APAP acute liver injury and in vitro hepatocyte-based cytotoxicity readouts. In vivo APAP injury is assessed by serum ALT/AST, liver histology, hepatic glutathione, protein adducts, necrosis, inflammation, and regeneration-related endpoints. In vitro hepatotoxicity is assessed by loss of viability, leakage of ALT/AST/LDH, oxidative-stress markers, mitochondrial function, nuclear morphology, intracellular calcium, and high-content imaging endpoints.
Purity & Documentation
References
[1]. Samantaray B, et al. Hepatoprotective Mechanism of Shorea Robusta Gaertn. f. Against Isoniazid-induced Hepatotoxicity by Targeting TNF-α, TGF-β1, and PPAR-α: Insights from Computational Profiling To Immunohistochemical Confirmation. Cell biochemistry and biophysics. 2026 Jun;84(2):2209-2239. [Content Brief]
[2]. Ito T, et al. Stilbenoids isolated from stem bark of Shorea hemsleyana. Chemical & pharmaceutical bulletin. 2000 Jul;48(7):1001-5. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)