Product name: Schizandrol B
Synonym name: schisandrol B; Wuweizi alcohol B; Besigomsin; Wuweizi alcohol B; Gomisin A
Catalogue No.: BP1266
Cas No.: 58546-54-6
Formula: C₂₃H₂₈O₇
Mol Weight: 416.47
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:

Gomisin A has anti-inflammatory, antihypertensive, neuroprotective, and anti-proliferation properties, it induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. Gomisin A inhibits COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation.

References:

Int J Mol Med. 2013 Apr;31(4):888-98.    

Protective effects of gomisin A isolated from Schisandra chinensis against CCl(4)-induced hepatic and renal injury.  

The aim of the present study was to investigate the protective effects of Gomisin A, a lignan compound isolated from Schisandra chinensis, against liver and kidney damage induced by CCl(4) exposure. 

METHODS AND RESULTS:

We assessed alterations in organ weights, levels of serum biochemical indicators, and activation of the caspase-3 and MAPK signaling pathways and carried out histological analysis of liver and kidney tissue in rats pretreated with Gomisin A for four days. In the Gomisin A/CCl(4)-treated group, only the liver experienced a significant increase in weight, whereas the other organs did not undergo any changes. Five biochemical indicators in serum indicated that liver and kidney toxicity dramatically decreased upon Gomisin A pretreatment, although the decrease in ratios varied. Upon histological analysis, the Gomisin A/CCl(4)-treated group showed less hepatocellular necrosis, a poorly dilated central vein in the liver section, decreased diameter of the glomerulus, a lower number of capillaries, and a convoluted tubule in the kidney section. Furthermore, the formation of active caspase-3 was inhibited by Gomisin A pretreatment in the Gomisin A/CCl(4)-treated group, whereas the expression level of Bax protein was slightly increased. Western blot analysis revealed that there were differences between the liver and kidney in terms of activation of the MAPK signaling pathway. In the liver, Gomisin A pretreatment increased phosphorylation of three members of the MAPK pathway when compared to that in the vehicle pretreatment group. However, in the kidney, only the phosphorylation level of p38 was elevated upon Gomisin A pretreatment, whereas levels of the other two members were decreased. 

CONCLUSIONS:

These results suggest that Gomisin A induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway.    

Biol Pharm Bull. 2012;35(11):1997-2003.    

Gomisin A enhances tumor necrosis factor-α-induced G1 cell cycle arrest via signal transducer and activator of transcription 1-mediated phosphorylation of retinoblastoma protein.

Gomisin A, a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra chinensis, has been reported as an anti-cancer substance. In this study, we investigated the effects of Gomisin Aon cancer cell proliferation and cell cycle arrest in HeLa cells. 

METHODS AND RESULTS:

Gomisin A significantly inhibited cell proliferation in a dose-dependent manner after 72 h treatment, especially in the presence of tumor necrosis factor-α (TNF-α), due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation. In addition, Gomisin A in combination with TNF-α strongly suppressed the expression of signal transducer and activator of transcription 1 (STAT1). 

CONCLUSIONS:

Inhibition of STAT1 pathways by a small-interfering RNA against STAT1 and AG490 Janus kinase (JAK) kinase inhibitor AG490 reduced the cyclin D1 expression and RB phosphorylation, indicating that JAK-mediated STAT1 activation is involved in Gomisin A-induced G1 cell cycle arrest.    

Biol Pharm Bull. 2012;35(2):171-7.    

The molecular mechanisms of the hepatoprotective effect of gomisin A against oxidative stress and inflammatory response in rats with carbon tetrachloride-induced acute liver injury.

Oxidative damage and inflammation are implicated in the pathogenesis of liver injury and fibrosis. In the present study, we investigated the molecular mechanism by which Gomisin A conferred a hepatoprotective effect, focusing on its antioxidant and anti-inflammatory effects using rats with carbon tetrachloride (CCl(4))-induced acute liver injury. 

METHODS AND RESULTS:

Pretreatment with Gomisin A prior to the administration of CCl(4) markedly prevented an increase in alanine aminotransferase, aspartate aminotransferase, and histological hepatic lesions. Gomisin A was also associated with a decrease in hepatic lipid peroxidation, and increased superoxide dismutase activity, suggesting that Gomisin A has an antioxidant effect. In addition Gomisin A treatment ameliorated mRNA levels of CCl(4)-induced inflammatory mediators, including tumor necrosis factor-α, interleukin-1β and inducible nitric oxide (NO) synthase, and the protein levels of transcriptional upregulator nuclear factor kappa B (NF-κB) and phospho-inhibitor of NF-κB (IκB). Furthermore, α-smooth muscle actin (α-SMA), a myofibroblast marker, was also inhibited by Gomisin A treatment. 

CONCLUSIONS:

These results suggest that Gomisin A inhibits the oxidative stress and activation of NF-κB, leading to down-regulation of pro-inflammatory mediators and amelioration of fibrogenesis.    

HPLC of Schizandrol B

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

Introduction/Overview

Schizandrol B (CAS No.: 58546-54-6) is a naturally occurring diterpene compound isolated from Schisandra chinensis. As a traditional Chinese medicinal herb, Schisandra has been widely studied and applied due to its diverse pharmacological effects. In recent years, with the continuous rise in the incidence of neurodegenerative diseases, the search for natural products with neuroprotective effects has become an important direction for drug development. Schisandra ethyl has gradually become a research hotspot due to its remarkable neuroprotective potential. This paper aims to systematically review the chemical structure and physicochemical properties of schisandra alcohol ethyl, plant origin and extraction methods, pharmacological activity, mechanism of action and molecular targets, druggability evaluation, and pharmacokinetic characteristics, and to explore its clinical application prospects and future development directions.

Chemical structure and physicochemical properties

The molecular formula of Schisandra Alcohol B is C_24H_32O_6, with a molecular weight of 416.4700. Its structure belongs to the dicyclic diterpene class, featuring multiple hydroxyl and methoxy substituents, giving it a relatively complex stereotype. Its LogP value is 3.0996, indicating moderate lipid solubility that facilitates penetration of cell membranes and the blood-brain barrier. TPSA (Topological Polar Surface Area) is 75.6100, indicating moderate polarity and both hydrophilic and hydrophobic properties. Its low water solubility (0.0052 mg/mL) somewhat limits its bioavailability, but its high blood-brain barrier penetration offers potential advantages for treating neurological diseases. The hERG suppression test results were negative, indicating a low risk of cardiotoxicity. The Ames test result was 0.6, indicating a low genotoxicity risk and meeting safety requirements.

Plant Origins and Extraction Methods

Schisandra alcohol 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 Russian Far East. Traditionally, Schisandra fruit is used in medicine in dried form, with effects such as nourishing the liver and kidneys, astringing the lungs, and generating fluids.

Common methods for extracting schisandra alcohol ethyl include solvent extraction, ultrasound-assisted extraction, and high-performance liquid chromatography separation. Ethanol or methanol is generally used as the extraction solvent, and high-purity schisandra alcohol ethyl is obtained through a multi-step separation and purification process. In recent years, supercritical CO_2 extraction technology has been introduced due to its green environmental friendliness and efficient selectivity, significantly improving extraction efficiency and purity. Additionally, techniques such as column chromatography and reversed-phase high-performance liquid chromatography (RP-HPLC) are commonly used for purification and quantitative analysis.

Pharmacological activity research

Schisandra ethyl exhibits significant pharmacological activity in various in vitro and in vivo models, especially in the field of neuroprotection.

1. Neuroprotective effects
   Schisandra Ethyl can reduce oxidative stress and inflammatory responses, protecting neurons from damage. In Alzheimer's disease (AD) and Parkinson's disease (PD) models, schisandra alcohol ethyl improves cognitive function and motor impairment by modulating multiple signaling pathways. Its antioxidant activity mainly works by activating the NRF2 signaling pathway, enhancing intracellular antioxidant enzyme expression and reducing the accumulation of reactive oxygen species (ROS).

2. Anti-inflammatory effects
   Schisandra alcohol can inhibit the release of inflammatory mediators and reduce neuroinflammation levels. By inhibiting the MAPK1 (ERK2) and NF-κB signaling pathways, the expression of pro-inflammatory cytokines such as TNF-α and IL-1β is reduced, thereby alleviating inflammatory responses in the nervous system.

3. Anti-apoptotic effects
   This compound regulates the expression of BCL2 family proteins, inhibits CASP3 activation, halts neuronal apoptosis, and protects neuronal survival.

4. Neurotransmitter regulation
   Schisandra ethylcholinesterase (ACHE) has certain inhibitory effects, may improve neurotransmitter balance, enhance nerve signal transmission, and aid in the recovery of cognitive function.

Mechanism of action and molecular targets

The neuroprotective effect of schisandra alcohol ethyl involves coordinated regulation of multiple targets and pathways, with the specific mechanisms as follows:

• BCL2 (anti-apoptotic protein): Schisandra alcohol e-regulates BCL2 expression, enhancing cellular resistance to apoptosis and preventing programmed neuronal death.
• APP (amyloid precursor protein) and BACE1 (β-secretase 1): By regulating APP metabolism and inhibiting BACE1 activity, they reduce β-amyloid (Aβ) deposition and lessen the pathological burden of AD.
• MAP (microtubule-associated protein Tau): regulates the phosphorylation state of tau protein, inhibits nerve fiber tangle formation, and maintains the stability of neuronal microtubule structures.
• SIRT1 (Silent Information Regulatory Factor 2-Related Enzyme 1): Activates SIRT1, promotes cellular metabolism and antioxidant capacity, and delays neurodegenerative changes.
• MAPK1 (mitogen-activated protein kinase 1): Inhibits excessive activation of MAPK1, reduces inflammation and cellular stress responses.
• ACE (Acetylcholinesterase): Moderately inhibits ACHE, increases acetylcholine levels, and improves neural signal transmission.
• CASP3 (caspase-3): Inhibits CASP3 activity and prevents apoptotic cascade reactions.
• SNCA (α-synuclein): Regulates SNCA expression and aggregation, slowing neurotoxicity associated with Parkinson's disease.
• NRF2 (Nuclear Factor 2-Related Factor 2): Activates the NRF2 signaling pathway, enhances antioxidant defenses, and reduces oxidative damage.

The integrated regulation of these molecular targets enables Schisandra Alcohol Eto to demonstrate multidimensional therapeutic potential in the field of neuroprotection.

Druggability evaluation and pharmacokinetics

The druggability parameters of Schisandol Ethyl indicate that it has promising potential for drug development. The molecular weight of 416.47 meets the Lipinski rule, with a LogP of 3.0996, indicating moderate lipid solubility, which is beneficial for oral absorption and blood-brain barrier penetration. TPSA was 75.61, indicating moderate polarity and favorable cell membrane permeability.

Low water solubility (0.0052 mg/mL) is a major challenge to druggability and may affect oral bioavailability. To address this issue, formulation technology improvements can be implemented, such as nanoparticle carriers and solid dispersions, to enhance solubility and absorption rates.

The high penetration ability of the blood-brain barrier provides important advantages in treating central nervous system diseases. hERG inhibitor is negative and carries low genotoxicity risk, indicating good safety.

In terms of pharmacokinetics, existing studies show that Schisandol E-is is rapidly absorbed orally, has a moderate plasma half-life, and is mainly metabolized by the liver, with excretion primarily via bile and urine. Its high concentration in brain tissue provides the foundation for its neuroprotective effects in vivo.

Prospects and outlooks for clinical applications

With the increasing number of patients with neurodegenerative diseases, the development of safe and effective neuroprotective drugs is urgently needed. With its multi-target regulation and significant neuroprotective effects, schisandra alcohol ethyl shows broad clinical application prospects.

Future research should focus on the following aspects:

1. Preclinical safety and efficacy evaluation
   Systematic toxicological research and multi-animal model validation were strengthened to clarify the safety and efficacy of long-term medication.

2. Formulation development and route of administration optimization
   By integrating modern pharmaceutical technologies, we enhance water solubility and bioavailability, exploring various approaches such as oral administration, injection, and nasal administration.

3. In-depth analysis of mechanisms
   By utilizing multi-omics and systems biology approaches, we further reveal its network of action and potential new targets, facilitating the development of precision therapy strategies.

4. Clinical trial design
   Phase I to III clinical trials are progressively advancing to evaluate efficacy and safety in Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases.

5. Combination drug studies
   Explore synergies with existing neuroprotective or anti-inflammatory drugs to enhance treatment outcomes and reduce adverse reactions.

Conclusion

As an important active ingredient in Schisandra, Schisandra Alcohol E, with its unique chemical structure and excellent neuroprotective activity, has become a research hotspot in the field of natural product pharmacology. Its multi-target and multi-pathway mechanisms offer new ideas and potential drug candidates for the treatment of neurodegenerative diseases. Despite challenges such as low water solubility and limited bioavailability, modern formulation technology and in-depth mechanism research are expected to overcome these bottlenecks and achieve clinical translation. In the future, Schisandra Alcohol B is expected to become an important drug in the field of neuroprotection, contributing to improving patients' quality of life.