| Size | Price | Stock | Qty |
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| 50mg |
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| 100mg |
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| 250mg | |||
| 500mg | |||
| Other Sizes |
Purity: =99.69%
| Targets |
p65
Schisantherin A targets multiple signaling pathways involved in inflammation and oxidative stress. It inhibits the activation of NF-κB and mitogen-activated protein kinases (MAPKs), including p38, ERK, and JNK, which are key mediators of inflammatory responses. By suppressing these pathways, schisantherin A reduces the production of pro-inflammatory cytokines and protects cells from inflammatory damage. The compound also exhibits antioxidant activity by scavenging reactive oxygen species and enhancing cellular defense mechanisms. Additionally, schisantherin A is a mechanism-based inhibitor of CYP3A4, competitively inhibiting and irreversibly inactivating this important drug-metabolizing enzyme. |
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| ln Vitro |
The concentrations of TNF-α and IL-6 in the supernatant of cells pretreated with 2.5 or 25 mg/L of Schisantherin A are significantly decreased compared to the LPS control group (p<0.05, p<0.01). The MTT assay is used to assess the potential cytotoxicity of Schisantherin A after cells are incubated for 24 hours in the presence or absence of LPS. The results show that the cytokines do not affect cell viability at the used concentrations (0.5, 2.5, and 25 mg/L). Schisantherin A is pre-incubated for 1 hour with RAW 264.7 murine macrophage cells before stimulation with 1 mg/L LPS is applied for 12 hours. In the control group, neither LPS nor the samples are treated. Schisantherin A is found to reduce NO and PGE2 production in a dose-dependent manner after the cell culture media are collected, nitrite levels, and PGE2 levels are assessed[1].
In vitro, schisantherin A suppresses interleukin-1β-induced inflammation in human chondrocytes by inhibiting NF-κB and MAPKs activation. It reduces the expression of inflammatory mediators such as iNOS and COX-2. The compound also exhibits antioxidant activity by reducing the production of reactive oxygen species. Schisantherin A has been shown to inhibit the formation of advanced glycation end products (AGEs) in vitro. These in vitro studies confirm the anti-inflammatory, antioxidant, and chondroprotective activities of schisantherin A. |
| ln Vivo |
Schisantherin A, a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera, has been reported to have a variety of positive pharmacological effects. Schisantherin A prevents lipopolysaccharide-induced acute respiratory distress syndrome in mice by blocking the NF-κB and MAPK signaling pathways. Pretreatment with Schisantherin A significantly lessens the histopathologic changes brought on by LPS and lowers the levels of TNF-α, IL-6, and IL-1β in the BALF. Additionally, Schisantherin A inhibits the phosphorylation of NF-κB p65, IκB-α, JNK, ERK and p38 induced by LPS. At 7 hours following the intranasal administration of LPS, the lung wet/dry weight ratio is assessed. Schisantherin A (40 mg/kg) and the control groups did not differ in any way, according to the results (p>0.05). In comparison to the control group, LPS significantly increases the lung wet/dry weight ratio (p<0.01). Compared to those in the LPS group, schistantherin A dose-dependently lowers the lung wet/dry weight ratio (p<0.05)[1].
In vivo, schisantherin A protects against lipopolysaccharide-induced acute respiratory distress syndrome in mice through inhibition of NF-κB and MAPKs signaling pathways. The compound has also demonstrated hepatoprotective, neuroprotective, and cardioprotective effects in animal models. Its anti-inflammatory and antioxidant activities contribute to its protective effects in various tissues. Schisantherin A is used in traditional East Asian medicine for its health-promoting properties. |
| Enzyme Assay |
The in vitro enzyme/receptor binding (non-cellular) assays for schisantherin A include assays to measure its ability to inhibit CYP3A4 activity. In these assays, schisantherin A is incubated with CYP3A4 and a substrate, and the rate of substrate metabolism is measured. The compound's mechanism-based inhibition is characterized by time- and NADPH-dependent inactivation. Additionally, the compound's ability to inhibit NF-κB activation or MAPK phosphorylation can be assessed using cell-free assays such as kinase activity assays or NF-κB DNA binding assays.
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| Cell Assay |
Cell viability is assessed using the MTT assay. RAW 264. Mechanically scraped 7 cells are seeded at a density of 4×105 cells per mL in 96-well plates, and they are then incubated in a 37 °C, 5% CO2 incubator over night. Cells are stimulated with 50 μL LPS for 18 h after being exposed to different concentrations of Schisantherin A (0–25 mg/L) for 50 μL for 1 h. The cells are then incubated for 4 hours after 20 μL of 5 mg/mL MTT in FBS-free medium is added to each well. 150 L of DMSO per well is used to dissolve MTT. Using a microplate reader, the optical density at 570 nm is calculated. This triplicate experiment measures concentrations in three wells of each sample[1].
In vitro cellular assays for schisantherin A are performed using human chondrocytes or other cell types. Cells are stimulated with inflammatory agents such as interleukin-1β or lipopolysaccharide in the presence or absence of schisantherin A. The expression of inflammatory mediators such as iNOS, COX-2, TNF-α, and IL-6 is measured by quantitative PCR or ELISA. The phosphorylation of NF-κB and MAPKs is assessed by Western blotting. Cell viability is evaluated using MTT assays to ensure that the observed effects are not due to cytotoxicity. |
| Animal Protocol |
Mice: Male BALB/c mice, 6-8 weeks old, are used. The six groups consist of the control group, the Schisantherin A (40 mg/kg) group, the LPS group, the Schisantherin A (10, 20 and 40 mg/kg)+LPS group, and the Dexamethasone (DEX)+LPS group. A positive control is the DEX+LPS group. Intraperitoneally administered Schisantherin A and DEX (5 mg/kg). A comparable amount of PBS is administered to the mice in the control and LPS groups. In order to cause lung damage, mice are given 10 g of LPS in 50 μL of PBS an hour after being given a light anesthetic (diethyl ether) inhalation. Instead of LPS, 50 L of PBS are given to control mice. Following a 7-hour LPS treatment, all mice are still alive[1].
In vivo animal experiments for schisantherin A have been conducted in mouse models of acute respiratory distress syndrome. Mice are administered schisantherin A prior to or following lipopolysaccharide challenge, and lung inflammation, oxidative stress, and histopathological changes are assessed. Other models may include studies of hepatoprotection, neuroprotection, or cardioprotection. Endpoints include measurement of inflammatory cytokines in serum or tissue, assessment of tissue damage, and evaluation of functional outcomes. |
| ADME/Pharmacokinetics |
Schisantherin A has a molecular weight of 536.56 g/mol and a molecular formula of C30H32O9. Detailed pharmacokinetic properties such as bioavailability, half-life, and tissue distribution have not been extensively reported in the available literature. As a lignan, schisantherin A may have moderate oral bioavailability and may undergo extensive metabolism. The compound's mechanism-based inhibition of CYP3A4 suggests potential for drug-drug interactions, which would need to be considered in its pharmacokinetic profile.
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| Toxicity/Toxicokinetics |
Schisantherin A has been evaluated in preclinical studies and has been reported to be well-tolerated at effective doses. No significant toxicity has been reported in the available literature. However, as a mechanism-based inhibitor of CYP3A4, schisantherin A may have the potential to cause drug-drug interactions by inhibiting the metabolism of other drugs. Comprehensive toxicology studies would be necessary to fully assess the compound's safety profile for clinical development.
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| References |
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| Additional Infomation |
Gomisin A is a tannin. It has been reported to be found in Schisandra chinensis, Schisandra chinensis, and other organisms with relevant data. See also: Schisandra chinensis fruit (partial).
Schisantherin A is a dibenzocyclooctadiene lignan isolated from *Schisandra chinensis* and *Schisandra sphenanthera* fruits. It exhibits a wide range of biological activities, including anti-inflammatory, antioxidant, neuroprotective, hepatoprotective, and cardioprotective effects. Schisantherin A suppresses inflammation by inhibiting NF-κB and MAPKs activation and protects against acute respiratory distress syndrome in mice. It is also a mechanism-based inhibitor of CYP3A4. Schisantherin A is a research compound with potential applications in inflammatory and oxidative stress-related diseases. |
| Molecular Formula |
C30H32O9
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|---|---|
| Molecular Weight |
536.57
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| Exact Mass |
536.204
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| Elemental Analysis |
C, 67.15; H, 6.01; O, 26.84
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| CAS # |
58546-56-8
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| Related CAS # |
58546-56-8
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| PubChem CID |
151529
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
675.6±55.0 °C at 760 mmHg
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| Flash Point |
218.9±25.0 °C
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| Vapour Pressure |
0.0±2.2 mmHg at 25°C
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| Index of Refraction |
1.623
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| LogP |
6.38
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
39
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| Complexity |
833
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| Defined Atom Stereocenter Count |
3
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| SMILES |
O([H])[C@]1(C([H])([H])[H])[C@]([H])(C2=C([H])C(=C(C(=C2C2=C(C3=C(C([H])=C2C([H])([H])[C@]1([H])C([H])([H])[H])OC([H])([H])O3)OC([H])([H])[H])OC([H])([H])[H])OC([H])([H])[H])OC([H])([H])[H])OC(C1C([H])=C([H])C([H])=C([H])C=1[H])=O
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| InChi Key |
UFCGDBKFOKKVAC-DSASHONVSA-N
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| InChi Code |
InChI=1S/C30H32O9/c1-16-12-18-13-21-25(38-15-37-21)26(35-5)22(18)23-19(14-20(33-3)24(34-4)27(23)36-6)28(30(16,2)32)39-29(31)17-10-8-7-9-11-17/h7-11,13-14,16,28,32H,12,15H2,1-6H3/t16-,28-,30-/m0/s1
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| Chemical Name |
[(8S,9S,10S)-9-hydroxy-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-8-yl] benzoate
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| Synonyms |
Gomisin C; Schisantherin A
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| HS Tariff Code |
2934.99.03.00
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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: ≥ 100 mg/mL (~186.4 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.66 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 (4.66 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.8637 mL | 9.3184 mL | 18.6369 mL | |
| 5 mM | 0.3727 mL | 1.8637 mL | 3.7274 mL | |
| 10 mM | 0.1864 mL | 0.9318 mL | 1.8637 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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