Synonym name:
Catalogue No.: BP0685
Cas No.: 66280-25-9
Formula: C22H28O6
Mol Weight: 388.46
Botanical Source: fruits of Schizandra chinensis and from Kadsura coccinea
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.
For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.
HPLC of Gomisin J
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
Gomisin J is a natural lignan derived from the traditional Chinese medicinal herb Schisandra chinensis, and has attracted much attention in recent years due to its multi-target and multi-mechanism pharmacological activity. As a traditional Chinese medicine, Schisandra possesses multiple effects such as immune regulation, liver protection, antioxidant properties, and anti-inflammatory effects. Among its key active ingredients, Gometin J exhibits extensive biological activity. Gomisin J can cross the blood-brain barrier, targeting various key molecules such as eNOS, AMPK (including its upstream kinases LKB1 and CaMKIIβ), fetuin-A, NF-κB, and Nrf2/HO-1 signaling pathways, exerting antihypertensive, lipid-regulating, anti-inflammatory, and antioxidant effects, demonstrating potential therapeutic value in hypertension, non-alcoholic fatty liver disease (NAFLD), and cerebral ischemia-reperfusion injury.
This review systematically introduces the chemical structure and physicochemical properties of Gomisin J, its plant origin, and extraction methods, focusing on its pharmacological activity and mechanism of action. Combining druggability parameters and pharmacokinetics, it explores its clinical application prospects and future research directions, aiming to provide references for the pharmacology of natural products and new drug development.
The chemical name of Gomysin J (due to diverse literature, the specific chemical name is indexed here by CAS number 66280-25-9), with a molecular weight of 388.4600, making it a lignan compound. Its structural feature is a multicyclic aromatic framework containing functional groups such as methoxy and hydroxyl groups, endowing it with excellent bioactivity. In terms of physicochemical properties, the LogP value of Gomisin J is 4.1052, indicating good lipid solubility, which facilitates cell membrane penetration and blood-brain barrier passage. The topological pole surface area (TPSA) is 77.38 Ų, and moderate polarity helps with its distribution and targeting ability in vivo. Low water solubility (0.0080 mg/mL) suggests limited solubility in the aqueous phase and may require formulation optimization to improve bioavailability.
In terms of safety, Gomysin J showed no inhibitory activity on the hERG channel, reducing the risk of cardiotoxicity; The Ames test result was 0.6, indicating low mutagenicity and a solid safety foundation. Additionally, Gomisin J can effectively cross the blood-brain barrier (BBB), giving it unique advantages in treating neurological diseases.
Gomisin J is mainly found in the fruit of Schisandra chinensis, a plant of the Magnoliaceae family, genus Schisandra, widely distributed in Northeast China and the Korean Peninsula. Schisandra fruit is rich in lignan compounds and is a major source of gomisin J.
The extraction method typically combines organic solvent extraction with separation and purification. Common extraction solvents include ethanol, methanol, and ethyl acetate, which improve extraction efficiency through ultrasound-assisted extraction or reflux extraction. The crude extract was separated and purified by silica gel column chromatography and reversed-phase high-performance liquid chromatography (RP-HPLC), ultimately yielding high-purity Gomisin J. In recent years, supercritical CO₂ extraction and membrane separation technologies have also been explored to improve extraction efficiency and purity.
Gomisin J promotes nitric oxide (NO) production by activating endothelial-type nitric oxide synthase (eNOS), dilates blood vessels, and lowers blood pressure. Studies have shown that Gomisin J can activate phosphorylation of eNOS, enhance NO bioavailability, and improve vascular endothelial function. Additionally, Gomisin J indirectly promotes vascular homeostasis by activating the AMPK signaling pathway, regulating energy and lipid metabolism.
Gomisin J demonstrated significant lipid-regulating effects in the non-alcoholic fatty liver (NAFLD) model. By activating AMPK and its upstream kinases LKB1 and CaMKIIβ, it promotes fatty acid oxidation, inhibits lipid synthesis, and reduces liver fat deposition. At the same time, Gomisin J inhibits fetuin-A expression, reduces insulin resistance, and improves liver metabolic disorders.
Gomisin J exerts anti-inflammatory effects by inhibiting the nuclear factor κB (NF-κB) signaling pathway, reducing the expression of pro-inflammatory cytokines (such as TNF-α, IL-6, etc.). Its inhibitory effect on fetuin-A also helps reduce inflammatory responses, especially prominent in the liver and vascular system.
Gomisin J activates the nuclear factor E2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway, enhancing cellular antioxidant capacity and reducing oxidative stress damage. In the cerebral ischemia-reperfusion injury model, Gomisin J reduces neuronal apoptosis and protects brain tissue function through the above mechanisms. Moreover, its excellent blood-brain barrier penetration gives it potential advantages in treating neurological diseases.
Although the main pharmacological activity of Gomisin J is concentrated in the cardiovascular, liver, and nervous systems, it also exhibits certain regulatory effects on liver cancer-related targets (such as BCL2, STAT3, MAPK1, EGFR, etc.), indicating its potential for development in tumor therapy.
The multi-target mechanism of Gomisin J forms the basis for its pharmacological diversity. The main targets and their mechanisms of action are as follows:
eNOS (endothelial nitric oxide synthase): Gomisin J promotes activation and phosphorylation of eNOS, enhances NO production, dilates blood vessels, improves hemodynamics, and exerts antihypertensive effects.
AMPK and its upstream kinases LKB1 and CaMKIIβ: AMPK is a key regulator of cellular energy metabolism. Gomisin J activates the AMPK signaling pathway, promotes fatty acid oxidation, inhibits lipid synthesis, regulates energy metabolism, and improves metabolic syndrome-related diseases.
Fetuin-A: As a pro-inflammatory and insulin resistance-related protein, Gometin J inhibits fetuin-A expression, reduces inflammatory responses, and improves insulin sensitivity.
NF-κB signaling pathway: Gomisin J inhibits NF-κB activation, reduces the expression of pro-inflammatory factors, and exerts anti-inflammatory effects.
Nrf2/HO-1 antioxidant pathway: Gomisin J activates Nrf2, inducing HO-1 expression, enhancing cellular antioxidant defenses, and protecting tissues from oxidative stress damage.
In addition, Gomisin J also has a regulatory effect on liver cancer-related signaling molecules such as BCL2, STAT3, MAPK1, and EGFR, potentially exerting anti-tumor effects by controlling cell proliferation, apoptosis, and migration.
The druggability parameters of Gomisin J indicate that it has promising potential for drug development. The molecular weight of 388.46 conforms to the Lipinski rule, and the LogP value of 4.1 indicates moderate lipid solubility, which facilitates cell membrane penetration and blood-brain barrier passage. TPSA is 77.38 Ų, suitable for oral absorption and central nervous system distribution.
Low water solubility (0.0080 mg/mL) may limit its oral bioavailability, and improvements are needed through formulation optimization methods such as nanocarriers and solid dispersions. In terms of safety, it does not inhibit hERG channels, reducing the risk of cardiotoxicity, and the Ames test is negative, indicating a low risk of mutation.
Pharmacokinetic studies have shown that Gomisin J can effectively cross the blood-brain barrier, providing the basis for central nervous system efficacy. Its metabolic pathways in vivo are not fully understood and are mainly processed by hepatic metabolic enzyme systems. Future studies are needed on its metabolic stability and drug interactions.
With its multi-target and multi-mechanism pharmacological activity, Gomesin J demonstrates broad clinical application prospects. Its effectiveness in disease models such as hypertension, non-alcoholic fatty liver, and cerebral ischemia-reperfusion injury offers new ideas for natural drug treatment for these conditions. In particular, its excellent blood-brain barrier penetration gives it unique advantages in neuroprotection and cerebrovascular disease treatment.
Future research should focus on the following directions:
Systematic pharmacokinetic and toxicological evaluation: clarifying the in vivo metabolic pathway, half-life, and long-term safety of Gomisin J, laying the foundation for clinical translation.
In-depth mechanism analysis: By combining multi-omics techniques, the mechanism of Gomisin J's action in cell signaling networks is further revealed, exploring its potential antitumor activity against tumors such as liver cancer.
Optimization of dosage forms and delivery routes: To address its shortcomings of poor water solubility, new delivery systems are developed to improve bioavailability and targeting.
Preclinical and clinical trial design: Conduct animal models and early clinical trials to verify safety and efficacy, promoting the clinical application of Gomisin J.
Combination Drug Studies: Exploring the synergistic effects of Gomisin J with existing drugs, especially its potential for combined therapy in metabolic and neurological disorders.
As an important lignan component in Schisandra, Gomisin J demonstrates multiple biological functions such as antihypertensive, lipid metabolism regulation, anti-inflammation, and neuroprotective effects due to its multi-target and multi-mechanism pharmacological activity. Its excellent druggability parameters and blood-brain barrier penetration provide strong support for the development of novel natural drugs. Although research on Gomisin J is still in the early stages, its positive performance across various disease models signals broad clinical application prospects. In the future, through systematic pharmacokinetic studies, mechanistic exploration, and clinical validation, Gomisin J is expected to become a major breakthrough in the field of natural product pharmacology, providing new strategies and drug candidates for the treatment of related diseases.
