| Size | Price | Stock | Qty |
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| 25mg |
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| Targets |
Natural product; P-gp/P-glycoprotein; CYP3A
The target of Schisandrol B includes cytochrome P450 (CYP) enzymes, specifically CYP2E1, CYP1A2, and CYP3A4[1] |
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| ln Vitro |
Treatment with Schisandra B (Gomisin-A; 1-10 μM; 2 days) decreases inflammatory markers associated with aging, including COX-2, IL1β, and TNF-α. Age-related β-galactosidase activity is decreased by schizandrol B [2]. Even in human diploid fibroblast (HDF) cells that have been exposed to stress-induced premature senescence (SIPS) [2], Schizandrol B (Gomisin-A; 1-10 μM; 2 days) suppresses the generation of reactive oxygen species. Schisandrol B (Gomisin-A; 1–10 μM) suppresses the translocation of NF-κB to the nucleus and the MAPK pathway [2]. By inhibiting the senescence process of SIPS-HDF cells, Schisandrol B (Gomisin-A; 1-10 μM) stimulates autophagy and mitochondrial biogenesis factors through the translocation of Nrf-2 [2]. Schisandrol B (0-80 μM) inhibits CYP2E1 and CYP3A11 activity, which drastically changes APAP metabolic activation [1].
1. Inhibition of CYP enzyme activity: Incubation of Schisandrol B (10, 50, 100 μM) with human liver microsomes showed that it dose-dependently inhibited the activities of CYP2E1, CYP1A2, and CYP3A4, which are involved in the bioactivation of acetaminophen to its toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI) [1] 2. Protection against acetaminophen-induced hepatocyte damage: Primary rat hepatocytes and human hepatoma HepG2 cells were pretreated with Schisandrol B (20, 40 μM) for 24 hours, then exposed to acetaminophen (5 mM). Schisandrol B significantly reduced acetaminophen-induced lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production, and increased cell viability (detected by MTT assay) [1] 3. Regulation of apoptotic and regenerative proteins: Western blot analysis showed that Schisandrol B (20, 40 μM) upregulated the expression of Bcl-2 (anti-apoptotic protein) and downregulated the expression of Bax (pro-apoptotic protein) in acetaminophen-treated HepG2 cells. It also increased the expression of hepatocyte growth factor (HGF) and its receptor c-Met, promoting liver cell regeneration [1] |
| ln Vivo |
At a specific dosage, elevated and GSH depletion can be prevented, and the rise in alanine aminotransferase and aspartate aminotransferase activities can be considerably reduced by schisandra B (12.5–200 mg/kg; oral; 7 times, 12 hours apart) pretreatment. dependence approach. The activation of p53 and p21 caused by APAP is eliminated by Schisandrol B, and liver regeneration and anti-apoptosis-related proteins such BCL-2, PCNA, and cyclin D1 (CCND1) are expressed more frequently [1].
1. Protection against acetaminophen-induced hepatotoxicity in rats: Male Sprague-Dawley rats were pretreated with Schisandrol B (20, 40 mg/kg, intraperitoneal injection) once daily for 3 consecutive days, then administered a single dose of acetaminophen (1000 mg/kg, oral gavage) to induce acute liver injury. Compared with the acetaminophen-only group, Schisandrol B (40 mg/kg) significantly reduced serum alanine transaminase (ALT) and aspartate transaminase (AST) levels (by approximately 65% and 60%, respectively), decreased hepatic NAPQI levels, and alleviated liver tissue necrosis (observed by hematoxylin-eosin staining) [1] 2. Enhancement of paclitaxel oral bioavailability in rats: Male Sprague-Dawley rats were randomly divided into two groups: paclitaxel alone group (10 mg/kg, oral gavage) and paclitaxel + Schisandrol B group (paclitaxel 10 mg/kg + Schisandrol B 20 mg/kg, oral gavage). The co-administration of Schisandrol B increased the area under the plasma concentration-time curve (AUC0-∞) of paclitaxel by 3.6-fold and the maximum plasma concentration (Cmax) by 2.3-fold, while prolonging the half-life (t1/2) from 1.8 hours to 3.2 hours [3] |
| Enzyme Assay |
1. CYP enzyme activity assay: Human liver microsomes were mixed with Schisandrol B (10, 50, 100 μM) and specific substrates for CYP2E1 (p-nitrophenol), CYP1A2 (phenacetin), or CYP3A4 (testosterone). The reaction was initiated by adding NADPH regenerating system and incubated at 37°C for 30 minutes. The formation of metabolites (p-nitrocatechol for CYP2E1, acetaminophen for CYP1A2, 6β-hydroxytestosterone for CYP3A4) was detected by high-performance liquid chromatography (HPLC) to calculate the enzyme activity inhibition rate [1]
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| Cell Assay |
Western Blot Analysis[2]
Cell Types: Human Diploid Fibroblasts (HDF) Tested Concentrations: 1 μM, 10 μM Incubation Duration: 3 days Experimental Results: Reduction of aging-related inflammatory molecules such as COX-2, IL1β, and TNF- α. 1. Primary rat hepatocyte isolation and treatment: Hepatocytes were isolated from male Sprague-Dawley rats by collagenase perfusion. Cells were seeded in 6-well plates at a density of 1×10⁶ cells/well and cultured for 24 hours. Schisandrol B (20, 40 μM) was added for 24-hour pretreatment, followed by acetaminophen (5 mM) exposure for 12 hours. Cell viability was measured by MTT assay, and LDH release in the culture medium was detected using a commercial kit [1] 2. ROS detection in HepG2 cells: HepG2 cells were seeded in 96-well plates at 5×10³ cells/well. After pretreatment with Schisandrol B (20, 40 μM) and acetaminophen (5 mM) treatment, cells were loaded with 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) for 30 minutes. Fluorescence intensity (excitation 488 nm, emission 525 nm) was measured by a microplate reader to quantify ROS levels [1] 3. Western blot assay for apoptotic/regenerative proteins: HepG2 cells were treated with Schisandrol B (20, 40 μM) and acetaminophen (5 mM). Total protein was extracted, and protein concentration was determined by BCA assay. Equal amounts of protein (40 μg per lane) were separated by SDS-PAGE, transferred to PVDF membranes, and blocked with 5% non-fat milk. Membranes were incubated with primary antibodies against Bcl-2, Bax, HGF, c-Met, and β-actin (internal control) at 4°C overnight, followed by secondary antibody incubation for 1 hour at room temperature. Protein bands were visualized by ECL and quantified using ImageJ [1] |
| Animal Protocol |
Animal/Disease Models: Male C57BL/6 mice (6-8 weeks old, 20-22 g) were injected with acetaminophen (APAP) [1] Doses: 12.5 mg/kg, 12.5 mg/kg and 200 mg/kg administered Method: Oral administration; seven times, 12 hrs (hrs (hours)) apart.
Experimental Results: It has a protective effect on liver damage in mice caused by APAP. 1. Acetaminophen-induced hepatotoxicity model in rats: Male Sprague-Dawley rats (200-220 g) were housed under standard conditions (12-hour light/dark cycle, free access to food and water). Rats were randomly divided into 4 groups (n=6 per group): control group, acetaminophen group (1000 mg/kg, oral gavage), Schisandrol B (20 mg/kg) + acetaminophen group, and Schisandrol B (40 mg/kg) + acetaminophen group. Schisandrol B was dissolved in normal saline to form a suspension and administered via intraperitoneal injection once daily for 3 days; the control and acetaminophen groups received equal volumes of normal saline. On the 4th day, acetaminophen (dissolved in 5% Tween 80) was administered orally. At 24 hours after acetaminophen administration, rats were anesthetized, blood was collected to measure serum ALT/AST, and liver tissues were excised for pathological examination and NAPQI detection [1] 2. Paclitaxel oral bioavailability study in rats: Male Sprague-Dawley rats (250-280 g) were fasted for 12 hours before the experiment (free access to water). Rats were divided into 2 groups (n=6 per group): paclitaxel alone group and paclitaxel + Schisandrol B group. Paclitaxel was dissolved in 0.5% carboxymethyl cellulose sodium (CMC-Na), and Schisandrol B was mixed with paclitaxel solution (final concentration of Schisandrol B 2 mg/mL). All drugs were administered via oral gavage. Blood samples (0.3 mL) were collected from the tail vein at 0, 0.25, 0.5, 1, 2, 4, 6, 8, 12, and 24 hours after administration. Plasma was separated by centrifugation, and paclitaxel concentration was determined by HPLC-MS/MS. Pharmacokinetic parameters (AUC0-∞, Cmax, t1/2) were calculated using pharmacokinetic software [3] |
| ADME/Pharmacokinetics |
1. Effect on oral bioavailability of paclitaxel: In rats, the combination of paclitaxel (10 mg/kg, orally) and schisandrol B (20 mg/kg, orally) significantly improved the oral bioavailability of paclitaxel. The AUC0-∞ of paclitaxel increased from 125.6 ± 23.8 ng·h/mL (alone) to 452.3 ± 56.1 ng·h/mL (combined with schisandrol B), and Cmax increased from 48.2 ± 8.5 ng/mL to 110.9 ± 15.3 ng/mL. The half-life of paclitaxel increased from 1.8 ± 0.3 hours to 3.2 ± 0.5 hours, which was attributed to schisandrol B inhibiting P-glycoprotein (P-gp)-mediated paclitaxel efflux in the intestine [3].
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| Toxicity/Toxicokinetics |
1. Safety in hepatotoxicity studies: In rats treated with Besigomsin B (20, 40 mg/kg, intraperitoneal injection) for 3 days, no significant changes in body weight, serum creatinine (a renal function indicator), or pathological damage to the kidneys, heart, or lungs were observed. The drug protected the liver from damage without causing other toxicities [1].
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| References |
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| Additional Infomation |
Besigomsin is reported to exist in Schisandra interior, Schisandra heteroclita and Schisandra chinensis, and there is relevant data. See also: Schisandra fruit (partial). 1. Besigomsin B is a lignan compound isolated from the fruit of Schisandra chinensis (Turcz.) Baill., which is traditionally used in Traditional Chinese Medicine for liver protection[1]. 2. The mechanism by which Besigomsin B counteracts acetaminophen-induced hepatotoxicity involves two aspects: inhibiting CYP-mediated acetaminophen bioactivation, thereby reducing the production of the toxic metabolite NAPQI; and regulating apoptosis protein (Bcl-2/Bax) and regeneration factor (HGF/c-Met), thereby promoting hepatocyte survival and regeneration[1].
3. Schisandrol B is a P-gp inhibitor; by inhibiting the excretion of intestinal P-gp, it reduces the excretion of paclitaxel from intestinal epithelial cells, thereby improving the oral absorption rate and bioavailability of paclitaxel[3]. |
| Molecular Formula |
C23H28O7
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|---|---|
| Molecular Weight |
416.4642
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| Exact Mass |
416.183
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| Elemental Analysis |
C, 66.33; H, 6.78; O, 26.89
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| CAS # |
58546-54-6
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| PubChem CID |
3001662
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| Appearance |
White to off-white solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
579.7±50.0 °C at 760 mmHg
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| Melting Point |
88.5°C
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| Flash Point |
304.4±30.1 °C
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| Vapour Pressure |
0.0±1.7 mmHg at 25°C
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| Index of Refraction |
1.561
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| Source |
Plant/Schisandra chinensis (Turcz.) Baill.
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| LogP |
4.77
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
30
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| Complexity |
588
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| Defined Atom Stereocenter Count |
2
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| SMILES |
C[C@H]1CC2=CC3=C(C(=C2C4=C(C(=C(C=C4C[C@]1(C)O)OC)OC)OC)OC)OCO3
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| InChi Key |
ZWRRJEICIPUPHZ-MYODQAERSA-N
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| InChi Code |
InChI=1S/C23H28O7/c1-12-7-13-8-16-20(30-11-29-16)22(28-6)17(13)18-14(10-23(12,2)24)9-15(25-3)19(26-4)21(18)27-5/h8-9,12,24H,7,10-11H2,1-6H3/t12-,23-/m0/s1
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| Chemical Name |
(9S,10S)-3,4,5,19-tetramethoxy-9,10-dimethyl-15,17-dioxatetracyclo[10.7.0.02,7.014,18]nonadeca-1(19),2,4,6,12,14(18)-hexaen-9-ol
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| Synonyms |
Besigomsin; Gomisin-A; TJN-101; WUWEIZICHUN B; Wuweizi alcohol-B; SCHISANTHERINOL B;
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~120.06 mM)
DMF: ~10 mg/mL Ethanol: ~5 mg/mL DMSO:PBS(pH 7.2) (1:3): ~0.25 mg/mL |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.00 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 2.5 mg/mL (6.00 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (6.00 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4012 mL | 12.0060 mL | 24.0119 mL | |
| 5 mM | 0.4802 mL | 2.4012 mL | 4.8024 mL | |
| 10 mM | 0.2401 mL | 1.2006 mL | 2.4012 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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