Schizandrin ACAS# 61281-38-7 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 61281-38-7 | SDF | Download SDF |
PubChem ID | 155256 | Appearance | White powder |
Formula | C24H32O6 | M.Wt | 416.51 |
Type of Compound | Lignans | Storage | Desiccate at -20°C |
Synonyms | Schizandrin-A; Wuweizisu-A; Deoxyschizandrin | ||
Solubility | DMSO : 50 mg/mL (120.05 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
Chemical Name | (9R,10S)-3,4,5,14,15,16-hexamethoxy-9,10-dimethyltricyclo[10.4.0.02,7]hexadeca-1(16),2,4,6,12,14-hexaene | ||
SMILES | CC1CC2=CC(=C(C(=C2C3=C(C(=C(C=C3CC1C)OC)OC)OC)OC)OC)OC | ||
Standard InChIKey | JEJFTTRHGBKKEI-OKILXGFUSA-N | ||
Standard InChI | InChI=1S/C24H32O6/c1-13-9-15-11-17(25-3)21(27-5)23(29-7)19(15)20-16(10-14(13)2)12-18(26-4)22(28-6)24(20)30-8/h11-14H,9-10H2,1-8H3/t13-,14+ | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Schisandrin A , an agonist of the adiponectin receptor 2 (AdipoR2) with the IC50 value of 3.5 μM, has neuroprotective, anti-inflammatory, liver-protective, antitumor, and antioxidant activities. It alleviated microglia-mediated neuroinflammation injury through inhibiting the TRAF6-IKKβ-NF-κB and Jak2-Stat3 signaling pathways. It inhibited CYP3A activity with an IC50 of 6.60 μM and Ki of 5.83 μM, respectively. |
Targets | ERK | JNK | p38MAPK | Caspase | NO | TNF-α | IL Receptor | NOS | COX | JAK | STAT | NF-kB | IkB | P-gp | P450 (e.g. CYP17) | IKK |
In vitro | Neuroprotective effect of schizandrin A on oxygen and glucose deprivation/reperfusion-induced cell injury in primary culture of rat cortical neurons.[Pubmed: 24986222]J Physiol Biochem. 2014 Sep;70(3):735-47.Brain ischemia appears to be associated with innate immunity. Recent reports showed that C3a and C5a, as potent targets, might protect against ischemia induced cell death. In traditional Chinese medicine, the fruit of Schizandra chinesis Baill (Fructus schizandrae) has been widely used as a tonic.
Reversing mechanism of schizandrin A on multi-drug resistance of K562/ADR,HL60/ADR,MCF-7/ADR cell lines.[Reference: WebLink]Chinese Pharmacological Bulletin, 2011, 27(3): 329-34.To study the reversal effect of Schizandrin A(schA) on the K562/ADR,HL60/ADR,MCF-7/ADR,and explore its reversal mechanism.
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Kinase Assay | Effects of schizandrin A on the activity of CYP3A in rat liver microsomes.[Reference: WebLink]Chinese Journal of Clinical Pharmacology & Therapeutics, 2009, 14(11):1275-80.To study the effects of Schizandrin A on CYP3A by in vitro drug metabolism experiments. |
Cell Research | Schizandrin A Inhibits Microglia-Mediated Neuroninflammation through Inhibiting TRAF6-NF-κB and Jak2-Stat3 Signaling Pathways.[Pubmed: 26919063]PLoS One. 2016 Feb 26;11(2):e0149991.Microglial-mediated neuroinflammation has been established as playing a vital role in pathogenesis of neurodegenerative disorders. Thus, rational regulation of microglia functions to inhibit inflammation injury may be a logical and promising approach to neurodegenerative disease therapy. The purposes of the present study were to explore the neuroprotective effects and potential molecular mechanism of Schizandrin A (Sch A), a lignin compound isolated from Schisandra chinesnesis. |
Schizandrin A Dilution Calculator
Schizandrin A Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.4009 mL | 12.0045 mL | 24.009 mL | 48.0181 mL | 60.0226 mL |
5 mM | 0.4802 mL | 2.4009 mL | 4.8018 mL | 9.6036 mL | 12.0045 mL |
10 mM | 0.2401 mL | 1.2005 mL | 2.4009 mL | 4.8018 mL | 6.0023 mL |
50 mM | 0.048 mL | 0.2401 mL | 0.4802 mL | 0.9604 mL | 1.2005 mL |
100 mM | 0.024 mL | 0.12 mL | 0.2401 mL | 0.4802 mL | 0.6002 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Schisandrin A inhibits CYP3A activity with an IC50 of 6.60 μM and Ki of 5.83 μM, respectively.
In Vitro:Schisandrin A (Sch A) strongly inhibits microsomal midazolam 1-hydroxylation catalyzed by CYP3A, with an IC50 of 6.60 μM. The recovery of enzyme activity in the absence or presence of Schisandrin A is shown in dilution assay plots. The Ki value for Schisandrin A is obtained from the Dixon plots and is 5.83 μM. The inactivation of rat liver microsomal midazolam 1-hydroxylation activity by Schisandrin A in the presence of NADPH is found to be time- and concentration-dependent. The Kinact and Ki are estimated to be 0.134/min and 4.51 μM, respectively for Schisandrin A[1].
In Vivo:Schisandrin A (SchA) significantly inhibits CYP3A activity in rat hepatic microsomes and Vmax value of each group in a concentration-dependent manner. The double-reciprocal plots and the secondary plot show that Schisandrin A inhibits CYP3A activity, with an apparent Ki value of 30.67 mg/kg. In each Schisandrin A-treated group, Schisandrin A also significantly decreases 1-hydroxymidazolam plasma concentrations compared with the negative group (to levels similar to the positive group)[2].
References:
[1]. Li WL, et al. Inhibitory effects of Schisandrin A and Schisandrin B on CYP3A activity. Methods Find Exp Clin Pharmacol. 2010 Apr;32(3):163-9.
[2]. Li WL, et al. Inhibitory effects of continuous ingestion of Schisandrin A on CYP3A in the rat. Basic Clin Pharmacol Toxicol. 2012 Feb;110(2):187-92.
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Neuroprotective effect of schizandrin A on oxygen and glucose deprivation/reperfusion-induced cell injury in primary culture of rat cortical neurons.[Pubmed:24986222]
J Physiol Biochem. 2014 Sep;70(3):735-47.
Brain ischemia appears to be associated with innate immunity. Recent reports showed that C3a and C5a, as potent targets, might protect against ischemia induced cell death. In traditional Chinese medicine, the fruit of Schizandra chinesis Baill (Fructus schizandrae) has been widely used as a tonic. In the present study, we sought to evaluate the neuroprotective effects of Schizandrin A, a composition of S. chinesis Baill, against oxygen and glucose deprivation followed by reperfusion (OGD/R)-induced cell death in primary culture of rat cortical neurons, and to test whether C3a and C5a affected cortical neuron recovery from ischemic injury after Schizandrin A treatment. The results showed that Schizandrin A significantly reduced cell apoptosis and necrosis, increased cell survival, and decreased intracellular calcium concentration ([Ca(2+)]i) and lactate dehydrogenase (LDH) release in primary culture of rat cortical neurons after OGD/R. Mechanism studies suggested that the modulation of extracellular-regulated kinase (ERK), c-Jun NH2-terminal kinases (JNK), and p38, as well as caspase-3 activity played an important role on the progress of neuronal apoptosis. C5aR participated in the neuroprotective effect of Schizandrin A in primary culture of rat cortical neurons after OGD/R. Our findings suggested that Schizandrin A might act as a candidate therapeutic target drug used for brain ischemia and related diseases.
Schizandrin A Inhibits Microglia-Mediated Neuroninflammation through Inhibiting TRAF6-NF-kappaB and Jak2-Stat3 Signaling Pathways.[Pubmed:26919063]
PLoS One. 2016 Feb 26;11(2):e0149991.
Microglial-mediated neuroinflammation has been established as playing a vital role in pathogenesis of neurodegenerative disorders. Thus, rational regulation of microglia functions to inhibit inflammation injury may be a logical and promising approach to neurodegenerative disease therapy. The purposes of the present study were to explore the neuroprotective effects and potential molecular mechanism of Schizandrin A (Sch A), a lignin compound isolated from Schisandra chinesnesis. Our observations showed that Sch A could significantly down-regulate the increased production of nitric oxide (NO), tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 induced by lipopolysaccharide (LPS) both in BV-2 cells and primary microglia cells. Moreover, Sch A exerted obvious neuroprotective effects against inflammatory injury in neurons when exposed to microglia-conditioned medium. Investigations of the mechanism showed the anti-inflammatory effect of Sch A involved the inhibition of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression levels and inhibition of the LPS-induced TRAF6-IKKbeta-NF-kappaB pathway. Furthermore, inhibition of Jak2-Stat3 pathway activation and Stat3 nuclear translocation also was observed. In conclusion, SchA can exert anti-inflammatory and neuroprotective effects by alleviating microglia-mediated neuroinflammation injury through inhibiting the TRAF6-IKKbeta-NF-kappaB and Jak2-Stat3 signaling pathways.