Product name: Schizantherin A
Synonym name: Gomisin C; Schisantherin A; Wuweizi ester A
Catalogue No.: BP1267
Cas No.: 58546-56-8
Formula: C₃₀H₃₂O₉
Mol Weight: 536.577
Botanical Source: Schisandra chinensis（Turcz.）Baill.
Physical Description:
Type of Compound: Lignans

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle

Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.

The product could be supplied from milligrams to grams
Inquire for bulk scale.

Description:

Schisantherin A exhibits anti-tussive, sedative, anti-inflammatory, antioxidant, anti-osteoporotic, neuroprotective, cognition enhancing, and cardioprotective activities. Schisantherin A can significantly attenuate Aβ1-42-induced learning and memory impairment and noticeably improve the histopathological changes in the hippocampus. Schisantherin A exhibits neuroprotection against 1-methyl-4-phenylpyridinium ion (MPP(+)) through the regulation of two distinct pathways including increasing CREB-mediated Bcl-2 expression and activating PI3K/Akt survival signaling.

References:

PLoS One. 2013 Apr 19;8(4):e61590.    

Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats.  

METHODS AND RESULTS:

Anesthetized male rats were treated once with deoxyschizandrin(DSD) and Schisantherin A(STA) (each 40 μmol/kg) through the tail vein after 45 min of ischemia, followed by 2-h reperfusion. Cardiac function, infarct size, biochemical markers, histopathology and apoptosis were measured and mRNA expression of gp91 (phox) in myocardial tissue assessed by RT-PCR. Neonatal rat cardiomyocytes were pretreated with DSD and STA and then damaged by H2O2. Cell apoptosis was tested by a flow cytometric assay. Compared with the I/R group: (i) DSD and STA could significantly reduce the abnormalities of LVSP, LVEDP, ±dp/dtmax and arrhythmias, thereby showing their protective roles in cardiac function; (ii) DSD and STA could significantly attenuate the infarct size and MDA release while increasing SOD activity, suggesting a role in reducing myocardial injury; (iii) tissue morphology and myocardial textual analysis revealed that DSD and STA mitigated changes in myocardial histopathology; (iv) DSD and STA decreased apoptosis (33.56±2.58% to 10.28±2.80% and 10.98±1.99%, respectively) and caspase-3 activity in the myocardium (0.62±0.02 OD/mg to 0.38±0.02 OD/mg and 0.32±0.02 OD/mg, respectively), showing their protective effects upon cardiomyocytes; and (v) DSD and STA had similar protective effects on I/R injury as those seen with the positive control metoprolol. In vitro, DSD and STA could significantly decrease the apoptosis of neonatal cardiomyocytes. 

CONCLUSIONS:

These data suggest that DSD and STA can protect against myocardial I/R injury. The underlining mechanism may be related to their role in inhibiting cardiomyocyte apoptosis.    

Biochem Biophys Res Commun. 2014 Jul 4;449(3):344-50.    

Schisantherin A suppresses osteoclast formation and wear particle-induced osteolysis via modulating RANKL signaling pathways.   

Receptor activator of NF-κB ligand (RANKL) plays critical role in osteoclastogenesis. Targeting RANKL signaling pathways has been a promising strategy for treating osteoclast related bone diseases such as osteoporosis and aseptic prosthetic loosening. Schisantherin A (SA), a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera, has been used as an antitussive, tonic, and sedative agent, but its effect on osteoclasts has been hitherto unknown. 

METHODS AND RESULTS:

In the present study, SA was found to inhibit RANKL-induced osteoclast formation and bone resorption. The osteoclastic specific marker genes induced by RANKL including c-Src, SA inhibited OSCAR, cathepsin K and TRAP in a dose dependent manner. Further signal transduction studies revealed that SA down-regulate RANKL-induced nuclear factor-kappaB (NF-κB) signaling activation by suppressing the phosphorylation and degradation of IκBα, and subsequently preventing the NF-κB transcriptional activity. Moreover, SA also decreased the RANKL-induced MAPKs signaling pathway, including JNK and ERK1/2 posphorylation while had no obvious effects on p38 activation. Finally, SA suppressed the NF-κB and MAPKs subsequent gene expression of NFATc1 and c-Fos. In vivo studies, SA inhibited osteoclast function and exhibited bone protection effect in wear-particle-induced bone erosion model. Taken together, SA could attenuate osteoclast formation and wear particle-induced osteolysis by mediating RANKL signaling pathways.

CONCLUSIONS:

These data indicated that SA is a promising therapeutic natural compound for the treatment of osteoclast-related prosthesis loosening.    

HPLC of Schizantherin A

Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃

Introduction/Overview

Schizantherin A is a natural tannic acid compound derived from Schisandra chinensis, exhibiting significant biological activity and showing broad pharmacological potential, especially in the field of liver protection. As a traditional Chinese medicinal herb, Schisandra has long been used to treat liver diseases, enhance physical strength, and regulate immune function. Its active ingredient, Schisandra ester A, has become a hot topic in pharmacological research of natural products in recent years due to its unique chemical structure and biological effects. This paper systematically reviews the chemical properties, plant origins, pharmacological activity, mechanism of action, druggability evaluation, and clinical application prospects of Schisandra Ester, aiming to provide a theoretical basis and research direction for subsequent drug development and clinical translation.

Chemical structure and physicochemical properties

The molecular formula of Schisandra Ester A is C_29H_36O_10, with a molecular weight of 536.5770 and CAS number 58546-56-8. Its chemical structure belongs to the tannic acid class, containing multiple phenolic hydroxyl and ester groups, giving it strong antioxidant capacity. The compound had a LogP value of 3.9499, indicating moderate lipid solubility, which is beneficial for cell membrane penetration and distribution in vivo. TPSA (Topological Polar Surface Area) is 101.9100, indicating a certain balance between polar and non-polar environments, which helps bind to multiple biological targets.

Schisandra ester A has low water solubility (0.0016 mg/mL), which may limit its oral bioavailability, but its high blood-brain barrier permeability suggests the compound can enter the central nervous system and has potential neuroprotective effects. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test result was 0.0, indicating no significant genotoxicity and relatively high safety.

Plant Origins and Extraction Methods

Schisandra ester A is mainly found in the fruit of Schisandra, a plant of the Magnoliaceae family, genus Schisandra, widely distributed in Northeast China, North China, and the Korean Peninsula. Traditionally, Schisandra fruit was used clinically by methods such as boiling in water and soaking in wine, but modern research mostly uses organic solvents to extract and enrich the active components.

Common extraction methods include:

1. Organic solvent extraction: Using solvents such as ethanol, methanol, or ethyl acetate, dried Schisandra fruit is extracted and extracted, then purified by liquid-liquid separation and column chromatography.
2. Ultrasound-assisted extraction: Using ultrasound to enhance solvent penetration and solute diffusion, improving extraction efficiency and purity.
3. High-performance liquid chromatography (HPLC) separation: used for further purification and quantitative analysis of Schisandra Ester A.

In recent years, with the promotion of green chemistry concepts, new technologies such as supercritical CO_2 extraction and microwave-assisted extraction have gradually been applied to the extraction of active components of Schisandra, improving extraction efficiency and environmental friendliness.

Pharmacological activity research

The pharmacological activity of Schisandra ester A mainly focuses on liver protection, and its antioxidant, anti-inflammatory, and anti-fibrotic mechanisms provide scientific evidence for the prevention and treatment of liver diseases.

Hepatoprotective effects

1. Antioxidant effects: Schisandra ester A can significantly enhance antioxidant enzyme activity in the body, such as superoxide dismutase (SOD1, SOD2), catalase (CAT), glutathione peroxidase (GPX1), and hemoglobin oxygenase (HMOX1), effectively scavenging free radicals and reducing oxidative stress damage to liver cells.
2. Anti-inflammatory effect: By regulating the activation of transcription factor NRF2, it suppresses the expression of pro-inflammatory cytokines such as transforming growth factor β1 (TGFB1), thereby reducing liver inflammation.
3. Anti-fibrotic effect: Schisandra ester A can inhibit hepatic stellate cell activation, reduce actin α2 (ACTA2) expression, and block the process of liver fibrosis.
4. Matrix metalloproteinase regulation: By regulating MMP9 activity, it promotes the remodeling and repair of the liver tissue matrix.

Other potential pharmacological activities

In addition to liver protection, Schisandra ester A, due to its excellent blood-brain barrier permeability, may have potential for neuroprotection and resistance to neurodegenerative diseases, and related research is still in its early stages.

Mechanism of action and molecular targets

The hepatoprotective effect of Schisandra ester A is mainly achieved through multi-target coordinated regulation:

• NRF2 signaling pathway: As a core regulator of cellular antioxidant defense, NRF2 activates upregulate the expression of antioxidant enzyme genes such as NQO1 and HMOX1, enhancing the cell's ability to resist oxidative damage. Schisandra ester A promotes NRF2 nuclear translocation, activating its downstream target gene.
• Antioxidant enzyme system: Enzymes such as SOD1, SOD2, CAT, and GPX1 remove superoxide anions and hydrogen peroxide, reduce oxidative stress, and protect the structural integrity of liver cell membranes.
• Anti-fibrotic target: By inhibiting the TGFB1 signaling pathway, it reduces activation of hepatic stellate cells and collagen deposition, thereby preventing the progression of liver fibrosis.
• Matrix metalloproteinase MMP9: Regulates the degradation and remodeling of the extracellular matrix, promoting repair of damaged liver tissue.
• Actin α2 (ACTA2): As a marker of hepatic stellate cell activation, Schisandra ester A weakens fibrosis by inhibiting its expression.

In summary, Schisandra ester A forms a complex and effective liver protection network through multi-target and multi-pathway synergistic effects.

Druggability evaluation and pharmacokinetics

The druggability parameters of Schisandra Ester A indicate that it has certain potential for drug development:

• The molecular weight (536.5770) is slightly above the 500 Da limit recommended by the Lipinski rule, but still within an acceptable range.
• LogP (3.9499) indicates moderate lipid solubility, which facilitates cell membrane penetration.
• TPSA (101.9100) is moderate, indicating good distribution capability in both polar and non-polar environments.
• Water solubility is extremely low (0.0016 mg/mL), which may limit oral absorption and requires formulation optimization or improved bioavailability through drug carrier systems.
• The high permeability of the blood-brain barrier opens up its potential for applications in central nervous system diseases.
• hERG channel inhibition is negative, indicating good cardiac safety.
• Non-genotoxic (Ames test negative), relatively safe.

Pharmacokinetic studies show that Schisandra ester A has a long half-life in the body and is widely distributed, especially enriched in the liver, meeting the targeted requirements for hepatoprotective effects. The metabolic pathway mainly involves oxidation of hepatic enzymes and hydrolysis of ester bonds, and the safety of these metabolites still requires further evaluation.

Prospects and outlooks for clinical applications

As a natural tannic acid compound, Schisandra ester A demonstrates broad therapeutic potential for liver diseases thanks to its remarkable antioxidant, anti-inflammatory, and anti-fibrotic effects. Especially in the adjunctive treatment of chronic hepatitis, liver fibrosis, and cirrhosis, Schisandra A is expected to become an effective natural medicine candidate.

Future research directions include:

1. In-depth mechanism research: Further clarifying the specific mechanisms of Schisandra ester A in cell signaling, gene regulation, and metabolic regulation.
2. Pharmacokinetics and toxicology studies: Systematic evaluation of in vivo metabolic pathways, long-term safety, and potential toxicity.
3. Formulation and delivery route optimization: Enhancing bioavailability and targeting through novel drug delivery systems such as nanocarriers and liposomes.
4. Clinical trial design: Conduct multicenter, randomized, double-blind clinical trials to verify the efficacy and safety of liver disease treatment.
5. Multi-target combined application: Combining modern drug design concepts to explore the synergistic effects of Schisandra Ester A and other anti-liver disease drugs.

Additionally, given its excellent blood-brain barrier permeability, the potential applications of Schisandra ester A in neurological diseases are also worth attention.

Conclusion

As an important active ingredient in Schisandra, Schisandra ester A has become a research hotspot in the field of natural product pharmacology due to its unique chemical structure and multi-target hepatoprotective mechanism. Its excellent safety and druggability parameters lay a solid foundation for its clinical translation. In the future, through multidisciplinary collaboration and combining modern medicinal chemistry, molecular biology, and clinical medical research methods, Schisandra Ester A is expected to develop into an innovative natural medicine for treating liver diseases, contributing new strength to human health.