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Product name: Fargesin
Synonym name: Methyl pluviatilol; (+)-Fargesin,68296-27-5
Catalogue No.: BP0583
Cas No.: 31008-19-2
Formula: C21H22O6
Mol Weight: 370.401
Botanical Source: Magnoliae flos
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:
Fargesin has anti-inflammatory, anti-cancer, antihypertensive , and anti-bone-resorbing effects, it is widely used in the treatment of managing rhinitis, inflammation, histamine, sinusitis, and headache. Fargesin improves lipid and glucose metabolism in 3T3-L1 adipocytes and high-fat diet-induced obese mice by activating Akt and AMPK in WAT. It as a potential β1 adrenergic receptor antagonist protects the hearts against ischemia/reperfusion injury in rats via attenuating oxidative stress and apoptosis.
References:
Fitoterapia. 2015 May 27;105:16-25.
Fargesin as a potential β1 adrenergic receptor antagonist protects the hearts against ischemia/reperfusion injury in rats via attenuating oxidative stress and apoptosis.
Fargesin displayed similar chromatographic retention peak to metoprolol in the cardiac muscle/cell membrane chromatography (CM/CMC) and β1 adrenergic receptor/cell membrane chromatography (β1AR/CMC) models.
METHODS AND RESULTS:
To provide more biological information about Fargesin, we investigated the effects of Fargesin on isoproterenol-(ISO-) induced cells injury in the high expression β1 adrenergic receptor/Chinese hamster ovary-S (β1AR/CHO-S) cells and occluding the left coronary artery- (LAD-) induced myocardial ischemia/reperfusion (MI/R) injury in rats. The results in vitro showed that ISO-induced canonical cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) levels were decreased by Fargesin in β1AR/CHO-S cells. Fargesin attenuated the serum creatine kinase (CK), lactate dehydrogenase (LDH), and improved histopathological changes of ischemic myocardium compared with the I/R rats. Similar results were obtained with Evans Blue/TTC staining, in which Fargesin notably reduced infarct size. Moreover, compared with the I/R group, Fargesin increased COX release and the activities of some endogenous antioxidative enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), but suppressed malondialdehyde (MDA), and intracellular ROS release. Additionally, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay demonstrated Fargesin suppressed myocardial apoptosis, which may be related to inhibition of caspase-3 activity.
CONCLUSIONS:
Taken together, these results provided substantial evidences that Fargesin as a potential β1AR antagonist through cAMP/PKA pathway could protect against myocardial ischemia/reperfusion injury in rats. The underlining mechanism may be related to inhibiting oxidative stress and myocardial apoptosis.
Phytomedicine. 2017 Jan 15;24:96-103.
Fargesin exerts anti-inflammatory effects in THP-1 monocytes by suppressing PKC-dependent AP-1 and NF-ĸB signaling.
Fargesin is a lignan from Magnolia fargesii, an oriental medicine used in the treatment of nasal congestion and sinusitis. The anti-inflammatory properties of this compound have not been fully elucidated yet. This study focused on assessing the anti-inflammatory effects of Fargesin on phorbal ester (PMA)-stimulated THP-1 human monocytes, and the molecular mechanisms underlying them.
METHODS AND RESULTS:
Cell viability was evaluated by MTS assay. Protein expression levels of inflammatory mediators were analyzed by Western blotting, ELISA, Immunofluorescence assay. mRNA levels were measured by Real-time PCR. Promoter activities were elucidated by Luciferase assay. It was found that pre-treatment with Fargesin attenuated significantly the expression of two major inflammatory mediators, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Fargesin also inhibited the production of pro-inflammation cytokines (IL-1β, TNF-α) and chemokine (CCL-5). Besides, nuclear translocation of transcription factors nuclear factor-kappa B (NF-ĸB) and activator protein-1 (AP-1), which regulate multiple pro-inflammatory genes, was suppressed by Fargesin in a PKC-dependent manner. Furthermore, among the mitogen-activated protein kinases (MAPKs), only c-Jun N-terminal kinase (JNK) was downregulated by Fargesin in a PKC-dependent manner, and this reduction was involved in PMA-induced AP-1 and NF-ĸB nuclear translocation attenuation, demonstrated using a specific JNK inhibitor.
CONCLUSIONS:
Taken together, our results found that Fargesin exhibits anti-inflammation effects on THP-1 cells via suppression of PKC pathway including downstream JNK, nuclear factors AP-1 and NF-ĸB. These results suggest that Fargesin has anti-inflammatory properties with potential applications in drug development against inflammatory disorders.
Invest New Drugs. 2014 Feb;32(1):1-13.
Tetrahydrofurofuran-type lignans inhibit breast cancer-mediated bone destruction by blocking the vicious cycle between cancer cells, osteoblasts and osteoclasts.
Breast cancer frequently spreads to bone. The interaction between bone metastases and microenvironment, referred as the "vicious cycle", increases both tumor burden and bone destruction. Therefore, inhibition at any point in this "vicious cycle" can reduce malignant osteolytic lesions in patients with advanced breast cancer.
METHODS AND RESULTS:
In this study, we evaluated whether tetrahydrofurofuran-type lignans derived from Magnoliae Flos, commonly used in traditional Asian medicine to treat inflammatory diseases, could block breast cancer-mediated bone loss. Aschatin, Fargesin, lirioresinol B dimethyl ether, and magnolin at noncytotoxic concentrations suppressed mRNA expression and secretion of osteolytic factor PTHrP in MDA-MB-231 metastatic human breast cancer cells. Fargesin inhibited TGF-β-stimulated cell viability, migration, and invasion and decreased TGF-β-induced PTHrP production in MDA-MB-231 cells. In addition, these lignans reduced RANKL/OPG ratio in PTHrP-treated hFOB1.19 human osteoblastic cells and inhibited RANKL-mediated osteoclast differentiation in mouse bone marrow macrophages. Aschatin, Fargesin, lirioresinol B dimethyl ether, and magnolin substantially reduced bone-resorbing activity of osteoclasts by inhibiting MMP-9 and cathepsin K activities. Furthermore, orally administered Fargesin inhibited tumor growth and cancer-mediated bone destruction in mice with MDA-MB-231 cells injected into calvarial tissues. Aschatin, Fargesin, lirioresinol B dimethyl ether, and magnolin blocked initiation and progression of the "vicious cycle" between breast cancer metastases and bone microenvironment by inhibiting PTHrP production in breast cancer cells and osteoclastic bone resorption.
CONCLUSIONS:
Therefore, these tetrahydrofurofuran-type lignans have the potential to serve as beneficial agents to prevent and treat cancer-induced bone destruction in breast cancer patients.
Can J Physiol Pharmacol. 2016 Aug;94(8):900-6.
Antihypertensive effects of fargesin in vitro and in vivo via attenuating oxidative stress and promoting nitric oxide release.
Fargesin, a bioactive neolignan isolated from magnolia plants, is widely used in the treatment of managing rhinitis, inflammation, histamine, sinusitis, and headache. To provide more biological information about Fargesin, we investigated the effects of Fargesin on rat aortic rings and 2-kidney, 1-clip (2K1C) hypertensive rats.
METHODS AND RESULTS:
In vitro, Fargesin caused concentration-dependent vasorelaxation in rat isolated aortic rings induced by KCl and norepinephrine. The effect was weakened by endothelium denudation and nitric oxide (NO) synthesis inhibition. In vivo, the evolution of systolic blood pressure (SBP) was followed by weekly measurements. Angiotensin II (Ang II) and endothelin (ET) levels, NO and nitric oxide synthase (NOS), and plasma and liver oxidative stress markers were determined at the end of the experimental period. After 5 weeks of Fargesin treatment, we found that Fargesin treatment reduced SBP, cardiac hypertrophy, and Ang II and ET levels of hypertensive rats. Increased NOS activity and NO level were observed in Fargesin-treated rats. Normalisation of plasma MDA concentrations and improvement of the antioxidant defence system in plasma and liver accompanied the antihypertensive effect of Fargesin.
CONCLUSIONS:
Taken together, these results provided substantial evidences that Fargesin has antihypertensive effect in 2K1C hypertensive rats via inhibiting oxidative stress and promoting NO release.
HPLC of Fargesin
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
55.3800
2.7511
2.7511
.0058
6.0018
15.4760
High
91.1578
3.6285
No
No
Yes
No
Yes
No
0.9
No
Yes
No
Yes
Fargesin (CAS No.: 31008-19-2), a new lignan natural product, was first isolated from Magnoliaceae plants and has attracted widespread attention in recent years due to its remarkable biological activity. Lignin compounds are an important class of plant secondary metabolites, possessing diverse pharmacological activities including anti-inflammatory, antioxidant, antitumor, and neuroprotective effects. As a typical representative, magnolipin demonstrates unique antihypertensive and anti-inflammatory activities, especially showing potential clinical value in the field of anti-allergy.
With in-depth research into the pharmacological mechanisms of natural products, the molecular targets of magnolipin have gradually been revealed, involving various immunomodulator-related factors and signaling pathways, such as ALOX5, HRH1, IL4, IL5, IL13, FCER1A, TBXA2R, STAT6, and TSLP, which play key roles in the occurrence and development of allergic reactions. This paper will systematically review the chemical structure and physicochemical properties of magnolipid, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics, and finally look ahead to its clinical application prospects, providing a theoretical basis and reference for subsequent research and development.
Magnolipin belongs to the neolignan class of compounds, with a molecular formula of C22H26O5 and a molecular weight of 370.4010. Its structural features include two benzene rings connected by oxygen bridges, forming a typical lignan backbone, and containing multiple methoxy and hydroxyl substituents, which impart certain polarity and biological activity. The LogP value of magnolipidin was 2.7511, indicating moderate lipid solubility, which is beneficial for cell membrane penetration and bioavailability. The polar surface area (TPSA) was 55.38 Ų, indicating a certain polarity that facilitates binding to target proteins.
It has relatively low water solubility (0.0058 mg/mL), which somewhat limits its oral bioavailability, but it has good lipid solubility and is suitable for drug delivery via liposomals or nanocarriers. The high permeability of the blood-brain barrier suggests it may have potential for central nervous system function. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity in magnolipid. The Ames test scored 0.9, basically eliminating genotoxicity risk and indicating good safety.
Magnolipin mainly comes from Magnolia family plants, especially the flower buds and bark of Magnolia biondii Pamp., which are abundant. As a traditional Chinese medicinal herb, Magnolia has long been used to treat symptoms such as rhinitis, headaches, and colds. Research on its active components has promoted the discovery and development of Magnolipin Extract.
The extraction method mostly uses organic solvent extraction combined with chromatography separation technology. Common extraction solvents include ethanol, methanol, and ethyl acetate, which use ultrasound-assisted extraction or reflux extraction to improve extraction efficiency. The extract was purified by liquid-liquid distribution, silica gel column chromatography, and high-performance liquid chromatography (HPLC), ultimately obtaining high-purity magnolipin. In recent years, supercritical CO2 extraction and microwave-assisted extraction technologies have also been applied to the extraction of magnolipin, further improving extraction efficiency and environmental friendliness.
Research on the pharmacological activity of magnolipin covers multiple aspects including antihypertensive, anti-inflammatory, and anti-allergic effects.
Research shows that magnolipin can significantly lower blood pressure levels by dilating vascular smooth muscle, inhibiting angiotensin-converting enzyme activity, and regulating endothelial function. Its mechanism of action may involve regulating nitric oxide (NO) synthesis and opening calcium channels, thereby improving vasomotor function. Animal model experiments have shown that magnolipin can effectively lower systolic and diastolic blood pressure in rat hypertension models without significant toxic side effects.
Magnolipin exhibits significant anti-inflammatory activity, inhibiting the release of various inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nitric oxide (NO). Its anti-inflammatory mechanism mainly works by inhibiting activation of the nuclear factor κB (NF-κB) signaling pathway, thereby reducing the expression of inflammatory genes. Additionally, magnolipin can inhibit macrophage activation induced by lipopolysaccharides (LPS), reducing inflammatory responses.
Research on magnolipin in anti-allergy effects is particularly outstanding. Its targets involve key allergenic mediators and signaling molecules such as ALOX5 (5-lipoxygenase), HRH1 (histamine H1 receptor), IL4, IL5, and IL13. By inhibiting ALOX5 activity, magnolipin reduces leukotriene production in allergic reactions, relieving airway inflammation and bronchoconstriction. Antagonism of histamine H1 receptors reduces histamine-mediated vascular permeability and itching symptoms. Additionally, magnolipin regulates IL4, IL5, and IL13 secreted by Th2 cells, inhibits IgE-mediated immune responses, and reduces allergic inflammation.
The mechanism of action of magnolipin involves coordinated regulation of multiple targets and multiple pathways, reflecting its characteristics as a multi-action drug.
ALOX5 is a key enzyme in leukotriene synthesis and is involved in the occurrence of allergic inflammation. Magnolipidin directly inhibits ALOX5 activity, reduces the production of leukotriene B4 (LTB4) and leukotriene C4 (LTC4), alleviates airway inflammation and tissue damage.
Histamine H1 receptors mediate vasodilation and itching in allergic reactions, and the antagonistic effect of magnolipin on HRH1 effectively alleviates allergy symptoms, showing potential as an antihistamine.
IL4, IL5, and IL13 are key cytokines secreted by Th2 cells, promoting IgE synthesis and eosinophil activation. Magnolipidin reduces the expression of these cytokines by inhibiting the STAT6 signaling pathway, regulating immune balance, and alleviating allergic inflammation.
FcεRI is a high-affinity IgE receptor that mediates the initiation of allergic reactions. Magnolipin can inhibit the expression and activation of FcεRI, block the degranulation reactions of mast cells and basophils, and reduce the release of mediators such as histamine.
Magnolipin also affects the platelet-provoking vasoconstrictor receptor TBXA2R, regulating vascular tone and inflammatory responses. TSLP (thymic stromal lymphopoietin) acts as an upstream inflammatory mediator, and its expression is inhibited by magnolipidin, further reducing allergic inflammation.
Druggability evaluation of magnolipin indicates it has promising potential for drug development.
Magnolipin has a moderate molecular weight, and its LogP value indicates good lipid solubility, which facilitates cell membrane penetration. TPSA is moderate, supporting effective binding to target proteins. Low water solubility suggests the need to optimize formulations to improve bioavailability.
The hERG channel inhibition test was negative, reducing the risk of arrhythmias. Ames test results showed no significant genotoxicity and relatively high safety. In animal toxicology studies, magnolipin has shown no significant toxic side effects, supporting its safety foundation for clinical development.
Magnolipidin has a high blood-brain barrier penetration capacity, suggesting its possible role in the central nervous system. Oral absorption is limited by water solubility and has low bioavailability, but new delivery systems such as liposomes and nanoparticles are expected to improve it. The metabolic pathway mainly involves the liver enzyme system, has a moderate half-life, and is suitable for routine administration.
As a multi-target natural product, magnolipin has broad clinical application potential. Its antihypertensive and anti-inflammatory effects offer new approaches for the treatment of cardiovascular and chronic inflammatory diseases. Especially in allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis, magnolipin shows promising therapeutic prospects by regulating immune responses and suppressing allergic mediators.
Future research should focus on the following areas:
Dosage form optimization and drug delivery route exploration: Given the poor water solubility of magnolipin, new carrier systems such as nanoparticles and liposomes were developed to improve bioavailability and targeting.
In-depth mechanism research: Using multi-omics techniques and molecular simulations, further elucidation of the interaction mechanisms between magnolipin and its targets and uncovering potential synergistic targets.
Preclinical and clinical research: Conduct systematic pharmacokinetic, toxicological, and pharmacodynamic evaluations, advance clinical trials, and verify safety and efficacy.
Combination Drug Strategy: Explore the combined use of magnolipin with existing anti-allergy and antihypertensive drugs to achieve synergistic effects and reduce side effects.
Magnolipidin, a new lignan-type natural product derived from plants of the Magnoliaceae family, shows broad prospects for drug development thanks to its unique chemical structure and multi-target pharmacological activity. Its potential applications in antihypertensive, anti-inflammatory, and anti-allergic fields, especially in regulating immune inflammatory responses, provide a new model for pharmacological research of natural products. In the future, through in-depth mechanism analysis, dosage form optimization, and clinical validation, magnolipin is expected to become an innovative drug for treating related diseases, driving the transformation of natural products into clinical practice.
Shenshuai
Wenjing
Hedandan
