Vitexin-4''-O-glucoside
Based on 1 Customer Validation
Vitexin-4''-O-glucoside (4''-O-Glucosylvitexin) is an orally active natural flavonoid component with multiple pharmacological effects including antioxidation, anti-inflammation, cytoprotection and anti-apoptosis. Vitexin-4''-O-glucoside regulates the MAPK signaling pathway by downregulating the phosphorylation levels of JNK and p38, thereby blocking endoplasmic reticulum stress responses. Vitexin-4''-O-glucoside alleviates oxidative stress by reducing MDA content and upregulating the activities of SOD and CAT, attenuates inflammation by downregulating the expressions of inflammatory factors TNF-α, IL-1β and IL-6, and also reduces LDH release and inhibits caspase-3 activation. Vitexin-4''-O-glucoside effectively improves drug-induced acute liver injury and exerts significant protective effects against myocardial hypoxia/reoxygenation injury. Vitexin-4''-O-glucoside can be used in studies on acute liver injury, cardiovascular diseases and myocardial hypoxia-reoxygenation injury.
For research use only. We do not sell to patients.
- Purity : 99.81%
- CAS No.: 178468-00-3
- Formula: C27H30O15
- Molecular Weight:594.52
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Storage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
All Caspase Isoforms
More
Biological Activity
Description
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JNK |
p38 |
IL-6 |
IL-1β |
TNF-α |
Caspase 3 |
In Vitro
Vitexin-4''-O-glucoside (VOG) (1.25-40 μg/mL) alleviates Tunicamycin (HY-A0098) -induced endoplasmic reticulum stress and cell damage in AML-12 mouse hepatocytes, with significant protective effects observed at concentrations of 5.00 μg/mL and higher[1].
Vitexin-4''-O-glucoside (120 μM; 24 h pretreatment) prevents hydrogen peroxide-induced apoptotic nuclear morphological changes in human adipose-derived stem cells[2].
Vitexin-4''-O-glucoside (30-480 μM; 24-72 h) is non-cytotoxic to human adipose-derived stem cells at concentrations up to 480 μM over 72 h[2].
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:human adipose-derived stem cells (hADSCs)
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Concentration:30 μM; 60 μM; 120 μM; 240 μM; 480 μM
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Incubation Time:24 h; 48 h; 72 h
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Result:Showed no cytotoxic effect on hADSCs at concentrations up to 480 μM across all incubation times.
Promoted hADSC viability.
Significantly increased hADSC viability.
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Cell Line:human adipose-derived stem cells (hADSCs)
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Concentration:120 μM
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Incubation Time:24 h (pretreatment)
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Result:Reduced hydrogen peroxide-induced percentage of hADSCs in early apoptosis and late apoptosis/necrosis .
Parmacokinetics
| Species | Dose | Route | T1/2 (Distribution) | T1/2β | AUC0-t | AUC0-∞ | MRT0-t | MRT0-∞ | CL | Vd | Cmax |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Rat[4] | 1.73 mg/kg | i.v. | 0.11 h | 0.87 h | 15,602.08 μg·h/mL | 15,626.16 μg·h/mL | 1.17 h | 1.19 h | 0.002 L/h/kg | 0.003 L/kg | 17,706.47 μg/L |
In Vivo
Vitexin-4''-O-glucoside (VGL) (1.73 mg/kg; i.v.; single dose) exhibits a three-compartment pharmacokinetic profile in healthy male Sprague-Dawley rats[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (8-week-old male, 20 g, acetaminophen-induced acute liver injury)[1]
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Dosage:30 mg/kg; 60 mg/kg
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Administration:p.o.; single dose; 2 hours prior to acetaminophen injection
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Result:Lowered plasma ALT and AST levels in a dose-dependent manner, with 60 mg/kg showing stronger effects than 30 mg/kg.
Alleviated hepatocyte vacuolation and inflammatory infiltration, and achieved better morphological improvement at 60 mg/kg.
Decreased hepatic MDA content and elevated SOD and CAT activities, with more notable antioxidant effects at the higher dose.
Suppressed hepatic IL-1β, IL-6 and TNF-α expression, and 60 mg/kg produced a more potent anti-inflammatory effect.
Inhibited phosphorylation of JNK and p38 in a dose-dependent fashion.
Downregulated the expression of IRE-1α, GRP78 and XBP1s, and 60 mg/kg exerted superior regulatory effects on IRE-1α and GRP78.
Chemical Information
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CAS No. 178468-00-3
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Appearance Solid
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Molecular Weight 594.52
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Formula C27H30O15
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Color Light yellow to yellow
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SMILES
O=C1C=C(C2=CC=C(O)C=C2)OC3=C([C@H]4[C@@H]([C@H]([C@@H]([C@@H](CO)O4)O[C@H]5[C@@H]([C@H]([C@@H]([C@@H](CO)O5)O)O)O)O)O)C(O)=CC(O)=C13
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Synonyms
4''-O-Glucosylvitexin
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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
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (168.20 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (4.21 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (4.21 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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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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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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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
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Data Sheet (288 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Dong F, et al. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2025;54(3):307-317. [Content Brief]
[2]. Wei W, et al. Effects of vitexin-2"-O-rhamnoside and vitexin-4"-O-glucoside on growth and oxidative stress-induced cell apoptosis of human adipose-derived stem cells. J Pharm Pharmacol. 2014;66(7):988-997. [Content Brief]
[3]. Ying XX, et al. Pharmacokinetics of vitexin-4″-O-glucoside in rats after intravenous application. Eur J Drug Metab Pharmacokinet. 2012;37(2):109-115. [Content Brief]
[4]. Zhang W, et al. Simultaneous determination of vitexin-4''-O-glucoside, vitexin-2''-O-rhamnoside, rutin and vitexin from hawthorn leaves flavonoids in rat plasma by UPLC-ESI-MS/MS. J Chromatogr B Analyt Technol Biomed Life Sci. 2010;878(21):1837-1844. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.6820 mL | 8.4101 mL | 16.8203 mL | 42.0507 mL |
| 5 mM | 0.3364 mL | 1.6820 mL | 3.3641 mL | 8.4101 mL | |
| 10 mM | 0.1682 mL | 0.8410 mL | 1.6820 mL | 4.2051 mL | |
| 15 mM | 0.1121 mL | 0.5607 mL | 1.1214 mL | 2.8034 mL | |
| 20 mM | 0.0841 mL | 0.4205 mL | 0.8410 mL | 2.1025 mL | |
| 25 mM | 0.0673 mL | 0.3364 mL | 0.6728 mL | 1.6820 mL | |
| 30 mM | 0.0561 mL | 0.2803 mL | 0.5607 mL | 1.4017 mL | |
| 40 mM | 0.0421 mL | 0.2103 mL | 0.4205 mL | 1.0513 mL | |
| 50 mM | 0.0336 mL | 0.1682 mL | 0.3364 mL | 0.8410 mL | |
| 60 mM | 0.0280 mL | 0.1402 mL | 0.2803 mL | 0.7008 mL | |
| 80 mM | 0.0210 mL | 0.1051 mL | 0.2103 mL | 0.5256 mL | |
| 100 mM | 0.0168 mL | 0.0841 mL | 0.1682 mL | 0.4205 mL |
Keywords
- Vitexin-4''-O-glucoside
- 178468-00-3
- 4''-O-Glucosylvitexin
- JNK
- p38 MAPK
- Interleukin Related
- TNF Receptor
- Caspase
- Lactate Dehydrogenase
- Apoptosis
- AML-12 mouse hepatocytes
- Sprague-Dawley rats
- p38 mitogen-activated protein kinase
- X-box binding protein 1s
- glucose-regulated protein 78
- endoplasmic reticulum stress
- human adipose-derived stem cells
- c-Jun N-terminal kinase
- MAPK signaling pathway
- inositol-requiring enzyme 1 alpha
- Inhibitor
- inhibitor
- inhibit