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Synonym name: Myricitroside; Myricetin 3- rhamnoside
Catalogue No.: BP0971
Cas No.: 17912-87-7
Formula: C21H20O12
Mol Weight: 464.379
Botanical Source: Occurs in Mimusops elongi, Rhus spp. and Elaeocarpus floribundus and numerous other plants
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.
Description:
Myricitrin exhibits hepatoprotective, anti-inflammatory,antioxidant, anti-allergic, antinociception, anxiolytic-like, and antipsychotic-like effects. Myricitrin can be used as a drug candidate for the treatment of cardiovascular diseases, by effectively protecting cells from ox-LDL-induced endothelial cell apoptosis and reducing atherosclerotic plaque formation. Myricitrin is also a nitric oxide (NO) and protein kinase C (PKC) inhibitor that has central nervous system activity.
References:
Nat Prod Commun. 2015 Jan;10(1):83-8.
Phytochemical profile of the aerial parts of Sedum sediforme and anti-inflammatory activity of myricitrin.
The aim of this study was to investigate the phytochemical profile of the methanol extract of the aerial parts of Sedum sediforme and to identify its secondary metabolites.
METHODS AND RESULTS:
By means of chromatographic separation and enrichment of compounds, HPLC-ESI-MS, HRMS, 1D-, 2D- NMR and/or comparison with reference compounds, three triterpenes, two sterols, ten flavonoids and twelve phenolic compounds were identified, together with two new compounds, i.e. (2R*, 3R*)-5,7-dihydroxy-2,3-dimethyl-4-chromanone-7-O-β-D-glucoside (27) and butan-2-O-rutinoside (28). Out of the 29 identified secondary metabolites, 18 are described as ingredients of S. sediforme herein for the first time. Furthermore, Myricitrin, one of the major constituents, was tested for its ability to inhibit different enzymes within the arachidonic acid cascade in order to determine its anti-inflammatory properties.
CONCLUSIONS:
Whereas there was only either weak or no inhibition of the microsomal prostaglandin E2 synthase-1 (mPGES-1) and the soluble epoxide hydrolase (sEH), Myricitrin showed strong inhibition of 5-lipoxygenase (5-LO), with an IC50 of 7.8 ± 0.2 μM.
Biochem Biophys Res Commun. 2015 Mar 6;458(2):227-33.
Myricitrin alleviates MPP⁺-induced mitochondrial dysfunction in a DJ-1-dependent manner in SN4741 cells.
Oxidative stress and mitochondrial dysfunction have been linked to Parkinson's disease. DJ-1 is a recessive familial PD gene involved in antioxidative function and mitochondrial maintenance. Myricitrin, a flavanoid isolated from the root bark of Myrica cerifera, has potent antioxidative properties.
METHODS AND RESULTS:
In the present study, we investigated the protective effects of Myricitrin against MPP(+)-induced mitochondrial dysfunction in SN4741 cells and attempted to elucidate the mechanisms underlying this protection. The results showed that incubating SN4741 cells with Myricitrin significantly reduced cell death induced by the neurotoxin MPP(+). Furthermore, Myricitrin protected cells from MPP(+)-induced effects on mitochondrial morphology and function. However, these protective effects were lost under DJ-1-deficient conditions.
CONCLUSIONS:
Thus, our results suggest that Myricitrin alleviates MPP(+)-induced mitochondrial dysfunction and increases cell viability via DJ-1, indicating that Myricitrin is a potential beneficial agent for age-related neurodegenerative diseases, particularly Parkinson's disease.
Vascul Pharmacol. 2015 Apr 4.
Myricitrin attenuates endothelial cell apoptosis to prevent atherosclerosis: An insight into PI3K/Akt activation and STAT3 signaling pathways.
Blood vessel endothelial dysfunction induced by oxidized low-density lipoprotein (ox-LDL) has been implicated in the pathogenesis of atherosclerosis and vasculopathy. The ox-LDL-elicited reactive oxygen species (ROS) release has been assumed to serve a critical function in endothelial damage. Myricitrin (from Myrica cerifera) is a natural antioxidant that has strong anti-oxidative, anti-inflammatory, and anti-nociceptive activities. However, the protective effect of Myricitrin on ROS-induced endothelial cell injury and its related molecular mechanisms have never been investigated.
METHODS AND RESULTS:
This study demonstrates that Myricitrin can inhibit ox-LDL-induced endothelial apoptosis and prevent plaque formation at an early stage in an atherosclerotic mouse model. The administration of Myricitrin in vivo decreases the thickness of the vascular wall in the aortic arch of ApoE-/- mice. In vitro study shows that ox-LDL-induced human umbilical vein endothelial cell apoptosis can be reduced upon receiving Myricitrin pre-treatment. Treatment with Myricitrin significantly attenuated ox-LDL-induced endothelial cell apoptosis by inhibiting LOX-1 expression and by increasing the activation of the STAT3 and PI3K/Akt/eNOS signaling pathways. At the same time, our result demonstrates that Myricitrin treatment optimizes the balance of pro/anti-apoptosis proteins, including Bax, Bad, XIAP, cIAP-2, and survivin.
CONCLUSIONS:
Our study suggests that Myricitrin treatment can effectively protect cells from ox-LDL-induced endothelial cell apoptosis, which results in reduced atherosclerotic plaque formation. This result indicates that Myricitrin can be used as a drug candidate for the treatment of cardiovascular diseases. Nat Prod Res. 2011 Feb;25(4):374-80.
Anti-allergic effect of the flavonoid myricitrin from Myrica rubra leaf extracts in vitro and in vivo.
Flavonoids are ingested by the general population as anti-oxidant and anti-inflammatory agents.
METHODS AND RESULTS:
In this study, we investigated the effects of Myricitrin, a flavonoid rich in Myrica rubra leaf, upon anti-inflammatory action. Myrica rubra leaf extracts inhibited pro-inflammatory TNFα production in a macrophage cell line, Raw264.7 cells. We observed that the serum IgE levels in the leaf extract-treated DO11.10, a mouse allergy model, were down-regulated. HPLC was performed to demonstrate that M. rubra leaf extracts contain a large amount of Myricitrin. We observed an inhibitory effect of HPLC-purified Myricitrin on TNFα production in Raw264.7 cells.
CONCLUSIONS:
Thus, Myricitrin may be of potential interest in the management of inflammatory conditions.
HPLC of Myricetrin
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
210.5100
.6680
.2655
.9142
.5058
.3249
Low
79.3217
4.1491
Yes
No
Yes
No
Yes
No
1.2
Yes
No
Yes
No
Myricetrin, CAS number 17912-87-7, is a typical glycoxoxyflavonoid natural product, mainly formed by myricetin linked by glycosidic bonds to the 3-position α-L-rhamnosyl residue. As an important active ingredient in Myrica rubra, Myrica glycoside has attracted widespread attention in the field of natural product pharmacology in recent years due to its diverse bioactivity and potential medicinal value. Its exhibited multiple pharmacological effects—anti-allergy, antioxidant, anti-inflammatory, and metabolism-regulating—give it unique advantages in research on the prevention and treatment of diabetes and related metabolic diseases. In addition, myricetin inhibits key enzymes such as protein kinase C (PKC) and nitric oxide synthase (NOS), providing important clues for further elucidating their molecular mechanisms.
This paper aims to systematically review the chemical structure and physicochemical properties of myricein (myricetin), plant origin, and extraction methods, explore its pharmacological activity and mechanism of action in depth, evaluate its druggability and pharmacokinetic characteristics, and anticipate its clinical application potential, providing scientific basis for subsequent basic and translational research.
The chemical structure of myricetin is based on the pentahydroxyflavonoid framework of myricetin, with a molecular formula of C21H20O12 and a molecular weight of 464.3790. Its structural feature is that the 3-position hydroxyl group of myricetin connects to the α-L-rhamnosid group residue via glycosidic bonds, forming a stable glycooxyflavone. Myrosesid glycoside is a monosaccharide derivative that combines the polyphenolic properties of flavonoids with the hydrophilicity of glycosides.
In terms of physicochemical properties, the LogP value of myricecide is about 0.6680, indicating a moderate balance of lipophilic and hydrophilic properties. Its topological polar surface area (TPSA) reaches as high as 210.51 Ų, indicating strong molecular polarity and good water solubility (about 0.9142), which is beneficial for its solubility and bioavailability in aqueous environments. However, a higher TPSA value also suggests a lower ability to cross the blood-brain barrier, consistent with its prediction of low blood-brain barrier permeability. The hERG channel inhibition test was negative, indicating that myricetin has a relatively high safety profile in terms of cardiotoxicity. The Ames-induced mutagenic test scored 1.2, indicating a low genotoxicity risk.
In summary, the chemical structure of myricein gives it excellent water solubility and safety, providing a favorable physicochemical basis for it as a drug candidate.
Myrica glycosides are mainly found in Myrica species, with Myrica rubra fruit being the primary source. As an important economic fruit in southern China, bayberries are rich in bayberries and related flavonoids in their fruits, leaves, and bark. Besides bayberries, some other plants such as those in the Myrtaceae and Myrtaceae families have also been reported to contain myrmeside in varying amounts, though at lower levels.
Traditional methods for extracting myricetin mostly use solvent extraction technology, commonly using ethanol-water mixed solvents (such as 70% ethanol) for reflux or ultrasonic-assisted extraction. Extraction conditions have a significant impact on yield and purity; temperature, time, and solvent polarity need to be optimized to maximize myceride recovery. After concentration, separation, and purification of the extract, qualitative and quantitative analysis is often performed using high-performance liquid chromatography (HPLC) combined with mass spectrometry (MS).
In recent years, green and efficient extraction technologies such as supercritical CO2 extraction, microwave-assisted extraction, and membrane separation have gradually been applied to the extraction of myceride, significantly improving extraction efficiency and purity, reducing the use of organic solvents, and aligning with the sustainable development concept of modern natural products.
Research on the pharmacological activity of myricein covers multiple fields including anti-allergy, anti-inflammatory, antioxidant, metabolic regulation, and neuroprotection, demonstrating its multi-target and multi-pathway biological effects.
Myricetin demonstrates significant anti-allergic effects by inhibiting mast cell degranulation and histamine release. In vitro experiments show that myricetin can reduce IgE-mediated mast cell activation and alleviate the inflammatory cascade of allergic reactions. In animal models, myricetin effectively alleviates symptoms of allergic dermatitis and asthma, suggesting its potential therapeutic value in allergic diseases.
As a polyhydroxyflavonoid, myricein has a powerful free radical scavenging ability and can significantly reduce oxidative stress levels. By activating the Nrf2 signaling pathway, it enhances the expression of endogenous antioxidant enzymes (such as SOD, CAT, GPx), protecting cells from oxidative damage. At the same time, myricetin inhibits the NF-κB signaling pathway, reducing the release of pro-inflammatory factors (such as TNF-α, IL-6, IL-1β), and demonstrates good anti-inflammatory effects.
Myricein shows significant blood sugar-lowering and insulin resistance improvement effects in diabetes and metabolic syndrome models. Its mechanism of action is closely related to the activation of AMPK (5' AMP-activated protein kinase), promoting glucose metabolism and lipid oxidation, thereby improving energy metabolism balance. Additionally, myricetin can inhibit SGLT2 (sodium-glucose co-transporter 2), reducing renal glucose reabsorption and assisting blood sugar control. Its regulatory effects on key insulin signaling enzymes GCK (glucokinase) and PTPN1 (protein tyrosine phosphatase 1B) also provide a molecular basis for its anti-diabetic effects.
Although myricetin has low permeability across the blood-brain barrier, it exerts indirect neuroprotective effects by regulating peripheral inflammatory responses and oxidative stress. Some studies have shown that myricetin can inhibit MAOA (monoamine oxidase A) activity, regulate neurotransmitter metabolism, and may have potential as an adjunct therapy for neuropsychiatric disorders such as depression. Additionally, the regulatory effect of myricein on the estrogen receptor ESR2 suggests its promising application in hormone-related diseases.
The multiple pharmacological effects of myricecide are attributed to its regulation of various key enzymes and signaling pathways, involving multiple targets such as protein kinase C (PKC), nitric oxide synthase (NOS), AMPK, SGLT2, GCK, and PTPN1.
PKC plays an important role in cellular signal transduction, inflammatory responses, and metabolic regulation. As an EC class 2.7, 11, and 13 PKC inhibitor, myceride glycoside can block downstream signal transduction mediated by PKC, reduce inflammation and cell damage, and promote cellular homeostasis recovery.
Myricein inhibits EC 1.14.13.39 class nitric oxide synthase, regulates NO production, and affects vasodilation, immune response, and nerve conduction. By regulating NOS activity, myricetin plays an important role in anti-inflammatory and vascular protection.
AMPK acts as an "energy sensor" for cellular energy metabolism, activating and promoting glucose uptake, fatty acid oxidation, and mitochondrial biosynthesis. Myricetin activates AMPK, improves energy metabolism disorders, and reduces insulin resistance, forming the core mechanism of its anti-diabetes and metabolic syndrome effects.
Myricein inhibits kidney SGLT2 function, reduces glucose reabsorption, promotes urinary glucose excretion, and helps control blood sugar. At the same time, by regulating GCK activity, it promotes glucose metabolism in the liver and pancreas, improving insulin sensitivity.
PTPN1, as an enzyme that negatively regulates insulin signaling, has myricetin's inhibitory effect on it to help enhance insulin signaling. MAOA regulates neurotransmitter metabolism, and its inhibition by myricecide may improve neurological dysfunction.
Druggability evaluation of myricetin shows it has good safety and pharmacokinetic characteristics. A moderate molecular weight of 464.3790 and a LogP value of 0.6680 indicate that it possesses a lipophilic and hydrophilic balance suitable for distribution in the body. Although a high TPSA value limits its blood-brain barrier penetration, it reduces the risk of central nervous system toxicity.
hERG ion channel inhibition was negative and Ames tests showed low mutagenicity, indicating low cardiotoxicity and genotoxicity risks and meeting drug safety requirements. It has good water solubility, which is beneficial for the development of oral formulations.
Pharmacokinetic studies show that myricein is absorbed quickly after oral administration, but its bioavailability is limited by glycoside hydrolysis and intestinal metabolism. Metabolism in the body mainly occurs through the liver enzyme system, with metabolites mostly myricetin and its derivatives, which have certain biological activity. Myriatin has a moderate half-life, making it suitable for daily administration.
In the future, structural modification or nanocarrier delivery technologies can further optimize its pharmacokinetic properties, improving in vivo stability and targeting.
Based on the multi-target pharmacological activity of myracein, it has broad application prospects in adjunctive therapy for diabetes and metabolic syndrome. By modulating AMPK, SGLT2, and insulin signaling pathways, myricetin is expected to become a candidate molecule for novel, natural antidiabetic drugs. In addition, its anti-allergic and anti-inflammatory effects offer new treatment approaches for allergic and chronic inflammatory diseases.
Although clinical research on myricein is still in its early stages, its good safety and diverse bioactivity lay the foundation for subsequent clinical trials. In the future, systematic pharmacokinetics, toxicology, and clinical efficacy evaluations are needed to clarify dosage, safety range, and indications.
At the same time, by integrating modern drug design and delivery technologies, the development of myorinin derivatives or compound formulations is expected to enhance efficacy and bioavailability, expanding its applications in diabetes, cardiovascular diseases, neurodegenerative diseases, and immunomodulation.
As a typical glycooxyflavonoid, myricetin demonstrates broad biological functions and promising drug development potential due to its unique chemical structure and multiple pharmacological activities. Its mechanisms of action in anti-allergy, anti-inflammatory, antioxidant, and metabolic regulation are becoming increasingly elucidated, and it has shown significant advantages in the treatment of diabetes and metabolic diseases.
In the future, by combining modern pharmacology, molecular biology, and medicinal chemistry technologies, the targets and signaling pathways of myracein can be deeply explored and its pharmacokinetic properties optimized, providing a solid foundation for clinical translation. With ongoing research, myricetin is expected to become an important representative of natural product drug development, contributing new natural drug resources to human health.
Shenshuai
Wenjing
Hedandan
