Schisanhenol
Based on 1 Customer Validation
Schisanhenol (Schizanhenol), a lignan, is an orally active antioxidant. Schisanhenol reduces AChE activity, increases SIRT1 and PGC-1α expression, and decreases phosphorylated Tau (Ser 396) levels. Schisanhenol increases SOD and glutathione peroxidase activity, decreases malondialdehyde (MDA) content, and inhibits UGT2B7 activitY. Schisanhenol attenuates ox-LDL-induced apoptosis, intracellular reactive oxygen species generation, and cytotoxicity in endothelial cells. Schisanhenol inhibits LDL oxidation, brain mitochondrial and membrane peroxidative damage, and brain mitochondrial swelling and disintegration. Schisanhenol can be used for the research of Alzheimer’s disease, atherosclerosis, brain ischemia, and age-related brain deterioration.
For research use only. We do not sell to patients.
- Purity : 99.99%
- CAS No.: 69363-14-0
- Formula: C23H30O6
- Molecular Weight:402.48
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
Biological Activity
Description
IC50 & Target
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AChE |
SIRT1 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| H9 | EC50 |
5.7 μM
Compound: 6
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Antiviral activity against HIV1 3B in H9 cells after 4 days by p24-antigen ELISA
Antiviral activity against HIV1 3B in H9 cells after 4 days by p24-antigen ELISA
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[PMID: 17190445] |
| H9 | IC50 |
42 μM
Compound: 6
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Cytotoxicity against human H9 cells after 4 days
Cytotoxicity against human H9 cells after 4 days
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[PMID: 17190445] |
In Vitro
Schisanhenol attenuates ox-LDL-induced apoptosis and reactive oxygen species generation in cultured bovine aorta endothelial cells[1].
Schisanhenol scavenges oxygen radicals in cultured human neutrophils[1].
Schisanhenol protects cultured mouse spleen lymphocytes, isolated rat cerebral mitochondria and synaptosomes from oxygen free radical-induced injury[1].
Schisanhenol (10-50 μM; 1 h pre-incubation, then 24 h co-incubation with ox-LDL) protects bovine aorta endothelial cells against ox-LDL-induced cytotoxicity in a dose-dependent manner, with 50 μM producing the strongest effect by preserving cell morphology, increasing cell viability, and reducing LDH leakage[3].
Schisanhenol (10-50 μM; 24 h co-incubation with ox-LDL) inhibits ox-LDL-induced apoptosis in bovine aorta endothelial cells in a dose-dependent manner, with 10 μM producing a stronger reduction in sub-G1 apoptotic cells[3].
Schisanhenol (10-50 μM; 30 min pre-incubation with DCFH-DA, then 15 min stimulation with ox-LDL) inhibits ox-LDL-induced intracellular reactive oxygen species generation in bovine aorta endothelial cells, with 10 μM returning ROS levels to normal control values[3].
Schisanhenol (1-100 μM; 30 min) inhibits Fe2+-cysteine-induced lipid peroxidation and ATPase activity loss in 8-month-old rat brain membrane fractions in vitro in a dose-dependent manner[4].
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:Bovine aorta endothelial cells (BAECs)
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Concentration:5-50 μM
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Incubation Time:1 h pre-incubation, then 24 h co-incubation with ox-LDL
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Result:Increased cell survival.
Reduced LDH leakage.
Preserved normal BAEC morphology.
Did not significantly increase cell viability or reduce LDH leakage at 5 μM.
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Cell Line:Bovine aorta endothelial cells (BAECs)
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Concentration:10 μM, 50 μM
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Incubation Time:24 h co-incubation with ox-LDL
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Result:Reduced ox-LDL-induced chromatin condensation at 10 and 50 μM.
Diminished the intensity of typical internucleosomal DNA laddering at 10 and 50 μM.
Decreased the percentage of apoptotic cells in the sub-G1 phase to 33.9% at 50 μM.
Decreased the percentage of apoptotic cells in the sub-G1 phase to 23.8% at 10 μM.
In Vivo
Schisanhenol (150 mg/kg; p.o.) significantly increases brain cytosol glutathione-peroxidase activity in mice subjected to brain ischemia-reperfusion, with a measured activity of 0.898 nmol/mg/5 min[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Kunming mice (male, 20-30 g) injected with Scopolamine[1]
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Dosage:10 mg/kg; 30 mg/kg; 100 mg/kg
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Administration:i.p.; daily; 7 days
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Result:Significantly reduced escape latency in the Morris water maze.
Significantly increased time spent in the target quadrant during the probe test.
Significantly reduced acetylcholinesterase (AChE) and malondialdehyde (MDA) activity in hippocampal tissue.
Significantly increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) activity in hippocampal tissue.
Significantly increased SIRT1 and PGC-1α protein levels in hippocampal tissue.
Significantly reduced phosphorylated Tau (Ser396) protein levels in hippocampal tissue.
Chemical Information
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CAS No. 69363-14-0
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Appearance Solid
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Molecular Weight 402.48
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Formula C23H30O6
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Color White to off-white
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SMILES
COC(C(OC)=C(OC)C=C1C[C@H](C)[C@H](C)C2)=C1C3=C2C=C(OC)C(OC)=C3O
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Synonyms
Schizanhenol; Gomisin-K3
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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
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Solvent & Solubility
In Vitro:
DMSO : 250 mg/mL (621.15 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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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: ≥ 6.25 mg/mL (15.53 mM); Clear solution
This protocol yields a clear solution of ≥ 6.25 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (62.5 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.
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.
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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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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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Endothelial Tube Formation Assay
Endothelial tube formation assay evaluates the ability of endothelial cells to attach, migrate, align, and organize into capillary-like networks when cultured on gelled basement membrane extract or Matrigel; the readout is the morphology and quantity of tube-like networks, which reflects an in vitro endothelial morphogenesis step related to angiogenesis. Basement membrane extract/Matrigel provides laminin-rich extracellular matrix cues that support endothelial differentiation into capillary-like structures, but it can contain biologically active growth factors, so growth-factor-reduced matrix is preferred when testing defined angiogenic stimulators or inhibitors.
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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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (287 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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Handling Instructions (2659 KB)
References
[1]. Han Y, et al. Schisanhenol improves learning and memory in scopolamine-treated mice by reducing acetylcholinesterase activity and attenuating oxidative damage through SIRT1-PGC-1α-Tau signaling pathway. Int J Neurosci. 2019;129(2):110-118. [Content Brief]
[2]. Song JH, et al. Inhibition of UDP-Glucuronosyltransferases (UGTs) Activity by constituents of Schisandra chinensis. Phytother Res. 2015;29(10):1658-1664. [Content Brief]
[3]. Yu LH, et al. Schisanhenol attenuated ox-LDL-induced apoptosis and reactive oxygen species generation in bovine aorta endothelial cells in vitro. J Asian Nat Prod Res. 2008;10(7-8):799-806. [Content Brief]
[4]. Xue JY, et al. Antioxidant activity of two dibenzocyclooctene lignans on the aged and ischemic brain in rats. Free Radic Biol Med. 1992;12(2):127-135. [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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.4846 mL | 12.4230 mL | 24.8460 mL | 62.1149 mL |
| 5 mM | 0.4969 mL | 2.4846 mL | 4.9692 mL | 12.4230 mL | |
| 10 mM | 0.2485 mL | 1.2423 mL | 2.4846 mL | 6.2115 mL | |
| 15 mM | 0.1656 mL | 0.8282 mL | 1.6564 mL | 4.1410 mL | |
| 20 mM | 0.1242 mL | 0.6211 mL | 1.2423 mL | 3.1057 mL | |
| 25 mM | 0.0994 mL | 0.4969 mL | 0.9938 mL | 2.4846 mL | |
| 30 mM | 0.0828 mL | 0.4141 mL | 0.8282 mL | 2.0705 mL | |
| 40 mM | 0.0621 mL | 0.3106 mL | 0.6211 mL | 1.5529 mL | |
| 50 mM | 0.0497 mL | 0.2485 mL | 0.4969 mL | 1.2423 mL | |
| 60 mM | 0.0414 mL | 0.2070 mL | 0.4141 mL | 1.0352 mL | |
| 80 mM | 0.0311 mL | 0.1553 mL | 0.3106 mL | 0.7764 mL | |
| 100 mM | 0.0248 mL | 0.1242 mL | 0.2485 mL | 0.6211 mL |
Keywords
- Schisanhenol
- 69363-14-0
- Schizanhenol
- Gomisin-K3
- UGT
- Cholinesterase (ChE)
- Tau Protein
- SOD
- Sirtuin
- UDP-glucuronosyltransferase 2B7
- superoxide dismutase
- endothelial cells
- phosphorylated Tau (Ser 396)
- SIRT1
- acetylcholinesterase
- PGC-1α
- bovine aorta endothelial cells
- Alzheimer’s disease
- glutathione peroxidase
- Inhibitor
- inhibitor
- inhibit