2. PI3K/Akt/mTOR Stem Cell/Wnt Neuronal Signaling Apoptosis Immunology/Inflammation
  3. PI3K Akt mTOR GSK-3 Tau Protein TNF Receptor Interleukin Related Apoptosis
  4. Schisantherin B

Schisantherin B  (Synonyms: Gomisin-B; Wuweizi ester-B; Schisantherin-B)

Cat. No.: HY-N0695 Purity: 99.75%
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Schisantherin B (Gomisin-B) is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression.

For research use only. We do not sell to patients.

Schisantherin B

Schisantherin B Chemical Structure

CAS No. : 58546-55-7

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Solid + Solvent (Highly Recommended)
10 mM * 1 mL in DMSO
ready for reconstitution
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Based on 1 publication(s) in Google Scholar

Other Forms of Schisantherin B:

Schisantherin B Related Antibodies

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1 Publications Citing Use of MCE Schisantherin B

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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GSK-3 GSK-3α GSK-3β

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TNFRSF1A/CD120a TNFRSF3/CD18 TNFRSF4 TNFRSF5/CD40 TNFRSF6/Fas/CD95 TNFRSF7/CD27 TNFRSF8/CD30 TNFRSF9/4-1BB/CD137 TNFRSF10B/DR5/CD262 TNFRSF12A/TWEAK TNFRSF16/NGF Receptor/CD271 TNFRSF18/GITR/CD357

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IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Schisantherin B (Gomisin-B) is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression[1][2][3].

In Vitro

Schisantherin B (25 μM; 4 h) increases viability, inhibits apoptosis, and activates the PI3K/AKT pathway in H2O2-treated PC12 cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Schisantherin B Related Antibodies

Cell Viability Assay[2]

Cell Line: PC12 cells
Concentration: 25 μM (co-incubated with 90 μM H2O2)
Incubation Time: 4 hours
Result: Increased PC12 cell viability to 66.15% (compared to 40.86% in the H2O2-only group).
Reduced the apoptotic cell percentage to 5.84% (compared to 10.81% in the H2O2-only group).
Significantly decreased mean fluorescence intensity (MFI) of cleaved caspase-3.
Significantly upregulated MFI of phosphorylated PI3K (p-PI3K) and phosphorylated AKT (p-AKT) compared to the H2O2-only group.
In Vivo

Schisantherin B (15 mg/kg; i.p.; once daily for 10 consecutive days) exerts antidepressant-like effects in mice with depression induced by the forced swim test (FST), ameliorates FST-induced short-term memory impairment, and restores the activities of hippocampal GLT-1 and the PI3K/AKT/mTOR pathway[1].
Schisantherin B (15 mg/kg; intravenous injection; three times daily) improves motor function, alleviates tissue damage, inhibits apoptosis and inflammatory responses, and activates the PI3K/AKT pathway to mitigate secondary injury, thereby promoting recovery in a mouse model of spinal cord injury[2].
Schisantherin B (0.015-0.15 mg/kg; intracerebroventricular injection; once daily for 5 consecutive days) dose-dependently ameliorates Aβ1-42-induced cognitive decline and neuronal damage in mice by restoring the functions of GLT-1 and GSK3β and reducing excessive tau phosphorylation[3].
Schisantherin B (0.15 mg/kg; intracerebroventricular injection, once daily for 5 consecutive days) enhances spatial learning ability in healthy mice without altering their basal motor activity or inducing neuronal or biochemical abnormalities[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: KM mice (male, 10-week old, 20-25 g, forced swimming test-induced depression)[1]
Dosage: 15 mg/kg
Administration: i.p.; daily; 10 days
Result: Significantly reduced immobility time and climbing time, and significantly increased swimming time relative to the control group.
Significantly increased spontaneous alternation behavior relative to the control group on day 19; by day 20, spontaneous alternation behavior was comparable to the normal (non-FST) group; by day 27, no differences in alternation behavior were observed between groups.
Significantly increased total distance traveled relative to the control group on day 20.
Significantly restored hippocampal levels of GLT-1, P-PI3K/PI3K, P-AKT/AKT, and P-mTOR/mTOR relative to the control group on day 19.
Animal Model: C57BL/6J Nifdc (8-10-week-old; spinal cord injury model via 12.5 g weight-drop procedure under ketamine/xylazine anesthesia)[2]
Dosage: 15 mg/kg
Administration: i.v.; three times daily
Result: Increased Basso Mouse Scale scores significantly at 21 and 28 days post-injury compared to untreated mice.
Increased hindlimb stride length to ~36 mm and reduced stride width to ~21 mm compared to untreated mice.
Reduced spinal cord cavity size, preserved spinal cord tissue integrity, and increased the number of surviving ventral horn motor neurons.
Reduced the percentage of apoptotic cells and suppressed microglial activation.
Decreased concentrations of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α, and increased concentrations of anti-inflammatory cytokine IL-10.
Increased the proportion of p-PI3K-positive neurons to ~0.5, p-AKT-positive neurons to ~0.45, and upregulated p-PI3K/PI3K and p-AKT/AKT protein expression ratios compared to untreated mice.
Animal Model: KM mice (male, 10-week-old, 25-30 g, intracerebroventricular injection of aggregated Aβ1-42 peptide)[3]
Dosage: 0.015 mg/kg; 0.15 mg/kg
Administration: i.c.v.; daily; 5 days
Result: Showed no significant effect on locomotor activity.
Significantly relieved Aβ1-42-induced reduction in spontaneous alternation behavior in the Y-maze test, with 0.15 mg/kg showing greater efficacy than 0.015 mg/kg.
Significantly ameliorated Aβ1-42-induced increases in escape latency and escape distance in the Morris water maze place navigation test on days 4 and 5 at 0.15 mg/kg.
Restored hippocampal GLT-1 levels to 58.18 pg/mL, cerebral cortex GLT-1 levels to 98.05 pg/mL, reduced hippocampal GSK3β levels to 80.56 pmol/l, cerebral cortex GSK3β levels to 181.22 pmol/l, and restored hippocampal p-GSK3β levels to 217.24 ng/l, cerebral cortex p-GSK3β levels to 215.83 ng/l at 0.15 mg/kg.
Reduced hippocampal p-tau levels to 192.32 ng/l and cerebral cortex p-tau levels to 179.43 ng/l at 0.15 mg/kg.
Normalized hippocampal and cerebral cortex Aβ1-42 levels at 0.15 mg/kg.
Restored hippocampal GLT-1/β-actin, GSK3β/β-actin, p-GSK3β/β-actin, and p-tau/β-actin ratios to near-normal levels at 0.15 mg/kg.
Inhibited Aβ1-42-induced hippocampal neuronal damage (shrunken nuclei, swollen neuronal bodies) as observed via H.E.
and Nissl staining at 0.15 mg/kg.
Reduced escape latency in the Morris water maze place navigation test in healthy mice treated with 0.15 mg/kg compared to normal untreated mice.
Maintained near-normal hippocampal and cerebral cortex GLT-1, GSK3β, p-GSK3β, Aβ1-42, and p-tau levels in healthy mice treated with 0.15 mg/kg.
Showed intact, ordered hippocampal neurons in healthy mice treated with 0.15 mg/kg.
Animal Model: KM mice (male, 10-week-old, 25-30 g)[3]
Dosage: 0.15 mg/kg
Administration: i.c.v.; daily; 5 days
Result: Showed no significant effect on locomotor activity or Y-maze spontaneous alternation behavior.
Reduced escape latency in the Morris water maze place navigation test compared to normal untreated mice.
Spent more time in the target quadrant during the Morris water maze spatial probe test.
Maintained near-normal hippocampal and cerebral cortex GLT-1, GSK3β, p-GSK3β, Aβ1-42, and p-tau levels.
Showed intact, ordered hippocampal neurons.
Molecular Weight

514.56

Formula

C28H34O9
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C(OC(C(C)(O)C(C)C1)C2=CC(OC)=C(OC)C(OC)=C2C3=C1C=C4OCOC4=C3OC)/C(C)=C/C
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (97.17 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.9434 mL 9.7170 mL 19.4341 mL
5 mM 0.3887 mL 1.9434 mL 3.8868 mL
View the 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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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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.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    90% Corn Oil

    Solubility: ≥ 2.5 mg/mL (4.86 mM); Clear solution

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

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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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
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.
Purity & Documentation

Purity: 99.75%

SDS (252 KB)

COA (257 KB) HNMR (321 KB) LCMS (114 KB)

Handling Instructions (2659 KB)
References

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. 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 1.9434 mL 9.7170 mL 19.4341 mL 48.5852 mL
5 mM 0.3887 mL 1.9434 mL 3.8868 mL 9.7170 mL
10 mM 0.1943 mL 0.9717 mL 1.9434 mL 4.8585 mL
15 mM 0.1296 mL 0.6478 mL 1.2956 mL 3.2390 mL
20 mM 0.0972 mL 0.4859 mL 0.9717 mL 2.4293 mL
25 mM 0.0777 mL 0.3887 mL 0.7774 mL 1.9434 mL
30 mM 0.0648 mL 0.3239 mL 0.6478 mL 1.6195 mL
40 mM 0.0486 mL 0.2429 mL 0.4859 mL 1.2146 mL
50 mM 0.0389 mL 0.1943 mL 0.3887 mL 0.9717 mL
60 mM 0.0324 mL 0.1620 mL 0.3239 mL 0.8098 mL
80 mM 0.0243 mL 0.1215 mL 0.2429 mL 0.6073 mL
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Schisantherin B58546-55-7Gomisin-B Wuweizi ester-B Schisantherin-BPI3KAktmTORGSK-3Tau ProteinTNF ReceptorInterleukin RelatedApoptosisPhosphoinositide 3-kinasePKBProtein kinase BMammalian target of RapamycinGlycogen synthase kinase-3Glycogen synthase kinase 3Tumor Necrosis Factor ReceptorTNFRILIL-1βtau hyperphosphorylationhippocampal tissueIL-6TNF-αcerebral cortical tissueGLT-1GSK3βPI3K/AKT/mTOR pathwayPI3K/AKT signalingInhibitorinhibitorinhibit

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