Product name: Vicine
Synonym name: Divicine β-D-glucopyranoside
Catalogue No.: BP3639
Cas No.: 152-93-2
Formula: C10H16N4O7
Mol Weight: 304.259
Botanical Source:
Physical Description:
Type of Compound:
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
The product could be supplied from milligrams to grams. Inquire for bulk scale.
We provide solution to improve the water-solubility of compounds, thereby facilitating the variety of activity tests and clinic uses.
For Reference Standard and R&D, Not for Human Use Directly.
Description:
Vicine is important natural fungicide. "High levels" of vicine or convicine or both might have shortened the birds' survival time by enhancing the neurotoxicity induced by "lower levels" of beta-cyanoalanine.
References:
J Sci Food Agric. 1978 Feb;29(2):136-40.
Favism-inducing toxins in broad beans (Vicia faba). Determination of vicine content and investigation of other non-protein nitrogenous compounds in different broad bean cultivars.
Vicine contents of seed coats and cotyledons of 58 cultivars of broad beans are reported.
METHODS AND RESULTS:
Seed coats contained up to 0.07% and cotyledons between 0.23 and 0.61 % a Vicine. Non-protein nitrogenous compounds in broad beans were analysed by thin-layer chromatography. Five compounds other than Vicine were isolated from broad bean extracts. These are, in order of increasing RF value, FLG, B1, D1, B2 and D2. The possibility of existence of these compounds in different cultivars was investigated. Their ultra-violet absorption spectra in three different pH conditions are reported.
Rostlinna Vyroba, 2002, 48(12):543-547.
Fungitoxicity of natural heterocycle glucoside vicine obtained from Vicia faba L. against selected microscopic filamentous fungi
Vicine and conVicine were isolated from mature seeds of Vicia faba L.
METHODS AND RESULTS:
These compounds were separated from the relevant fractions by HPLC and identified by IR, MS and NMR. Obtained Vicine was used for all bioassays. Vicine in concentra-tion of 25 μg in 1 ml of medium had significant toxic effect. The concentration of 5 μg of Vicine in 1 ml of medium had significant fungistatic effect for fungi Fusarium culmorum and Alternaria alternata. The concentration of 500 ng of Vicine in 1 ml of medium had significant fungistatic effect for fungi Cladosporium herbarum and Botrytis cinerea. The effective concentration of Vicine in our test was significantly lower than is the concentration of Vicine in seeds and pods of V. faba. The toxicity of Vicine comparing with the toxicity of insecticide Actellic was higher by one order. Also, the fungicide Impact had a lower toxicity than Vicine. Fungitoxic and fungistatic effect of Vicine was comparable with some other test-ed fungicides and with the plant saponin digitonin.
CONCLUSIONS:
Our results confirmed that Vicine is important natural fungicide.
HPLC of Vicine
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
197.1700
-2.5195
-2.5203
6.9258
.3684
.0592
Low
21.0612
4.0581
Yes
No
No
No
Yes
No
1.2
Yes
No
Yes
Yes
Vicine (CAS number: 152-93-2) is an alkaloid glycoside naturally found in fava beans (Vicia faba), which has attracted widespread attention due to its unique biological activity and toxicological properties. As an inactive precursor compound, savomarin is hydrolyzed by the human gut microbiota into an active metabolite with high free radical production capacity—aglycone divovi. This active metabolite can induce oxidative stress, especially in patients with hereditary glucose-6-phosphate dehydrogenase (G6PD) deficiency, causing hemolytic anemia, becoming an important risk factor in clinical prevention and treatment of genetic diseases. In recent years, with in-depth research into the pharmacological mechanisms of natural products, the potential therapeutic effects of favismarin in neurodegenerative diseases, especially Parkinson's disease (PD), have attracted great interest from the scientific community. By regulating various neurotransmitter-related targets, including monoamine oxidase B (MAOB), dopamine receptors (DRD1, DRD3), and α-synuclein (SNCA), it demonstrates certain neuroprotective potential.
This paper aims to systematically review the chemical structure and physicochemical properties of savavvy, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics. Combined with research progress in the field of Parkinson's disease, it explores its clinical application prospects and future directions, providing theoretical basis and research reference for natural product pharmacology and related drug development.
The molecular formula of vovisin is C14H18N4O7, with a molecular weight of 304.2590, and it belongs to the alkaloid glycoside class. Its structural features mainly include a pyrimidine alkaloid core connected to a glycoside segment. The presence of glycosidic bonds gives it high hydrophilicity and strong molecular polarity. Its topological pole surface area (TPSA) is calculated to be 197.1700, indicating strong polarity and potential hydrogen bond donor/acceptor capacity.
In terms of physicochemical properties, the LogP value of favismarin was -2.5195, indicating strong hydrophilicity, difficulty crossing lipid membranes, and low blood-brain barrier (BBB) permeability, suggesting possible limited direct action in the central nervous system. Water solubility is 6.9258, indicating good solubility in the aqueous phase, which is beneficial for absorption and distribution in the body. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test value was 1.2, indicating a low genotoxicity risk and relatively good safety.
Structurally, the glycoside portion of vovisin releases active aglycone after hydrolysis of the gut microbiota, which can exert biological effects by generating free radical-mediated oxidative stress. This metabolic process is key to its toxicity and pharmacological activity.
Favisin is mainly found in the seeds of broad bean (Vicia faba L.), and its content is greatly affected by variety, maturity, and growing environment. As an important food and feed crop, fava beans have seeds rich in various bioactive components, among which favisin is one of the main alkaloid glycosides and holds high research and application value.
Common methods for extracting savavvy include water extraction, alcohol extraction, and their combination technologies. Traditional processes typically use hot water extraction combined with ultrasound-assisted extraction or microwave-assisted extraction to improve extraction efficiency. Through steps such as concentration and cooling for crystallization, the extract yields high-purity favismarin crystals. Modern separation technologies such as high-performance liquid chromatography (HPLC), countercurrent chromatography, and membrane separation techniques are also applied for the purification and quantitative analysis of favisin.
Optimization of extraction processes mainly focuses on parameters such as solvent selection, temperature, time, and solid-liquid ratio, aiming to maximize the recovery rate and purity of favisin while reducing the formation of impurities and degradation products.
The best known toxicological effect of favisin is its hemolytic anemia in patients with G6PD deficiency. This pathological process originates from aglycone free radical products released by favisin after hydrolysis of the intestinal microbiota, leading to increased oxidative stress in red blood cells and peroxidation of membrane lipids, ultimately causing red blood cell rupture. Research on this toxic effect not only reveals the mechanism of interaction between hereditary metabolic defects and natural products, but also provides a theoretical basis for clinical prevention of favism.
In recent years, the potential pharmacological activity of fava dariin in neurodegenerative diseases has gradually been discovered. Parkinson's disease is characterized by degenerative loss of dopaminergic neurons. MAOB, a key enzyme in dopamine metabolism, is overactive and leads to increased oxidative stress and neurotoxicity. It was found that savomarin and its metabolites can regulate MAOB activity and reduce oxidative stress damage, thus demonstrating certain potential for resistance to Parkinson's disease.
Additionally, favisin regulates targets such as dopamine receptors DRD1, DRD3, and α-synuclein (SNCA), which may further exert neuroprotective effects by improving neurotransmitter balance and inhibiting abnormal protein aggregation. In vitro and animal model studies have shown that favisin can alleviate movement disorders and slow the progression of neurodegenerative diseases.
Besides the nervous system, the antioxidant, anti-inflammatory, and immunomodulatory effects of favisin have also been gradually reported. By regulating intracellular redox status and inflammatory factor expression, it may have adjunctive therapeutic value for various chronic diseases.
The biological effects of favisin mainly depend on the free radical production capacity of its metabolite aglycone. This radical induces intracellular oxidative stress, affecting various signaling pathways and molecular targets. The specific mechanism is as follows:
MAOB inhibition: MAOB is a key enzyme for dopamine metabolism and oxidative stress in Parkinson's disease. Favismarin metabolites directly or indirectly inhibit MAOB activity, reducing harmful hydrogen peroxide and free radical production, and protecting dopaminergic neurons.
Dopamine receptor regulation (DRD1, DRD3): Defamin affects the expression and function of dopamine receptors, regulates neurotransmitter signaling, and improves motor function and neuronal survival.
α-Synuclein (SNCA) regulation: Abnormal SNCA aggregation is a key part of Parkinson's disease pathogenesis. Savadin may slow neurotoxicity by regulating SNCA expression or inhibiting its aggregation.
Tyrosine hydroxylase (TH) activity effect: TH is a rate-limiting enzyme for dopamine synthesis, and its regulation of expression and activity in favismarin helps maintain stable dopamine levels.
Oxidative stress and inflammatory signaling pathways: Favisin alleviates neuroinflammation and oxidative damage by regulating the Nrf2/ARE antioxidant pathway and the NF-κB inflammatory pathway.
In summary, saviarine exerts its neuroprotective and regulatory functions through multi-target and multi-pathway synergistic effects.
Druggability evaluations of favisin show good safety and water solubility, but its low blood-brain barrier permeability limits its ability to act directly on the central nervous system. Its molecular weight (304.2590) is moderate, and its hydrophilicity is strong (LogP -2.5195), meeting certain requirements for pharmacochemical properties.
The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. Ames trial results showed low genotoxicity risk and good safety. Its high TPSA (197.1700) and low blood-brain barrier permeability suggest that improving central nervous system bioavailability through molecular structure modification or drug delivery systems (such as nanocarriers and liposomes) is a future research direction.
Pharmacokinetics: after oral administration, favismarin is mainly hydrolyzed by the gut microbiota, producing the active metabolite aglycone, which is then absorbed into the bloodstream. Its distribution, metabolism, and excretion in the body require further systematic research, especially regarding the interaction between metabolic kinetics and metabolic enzymes.
As a natural product, savomarin faces both challenges and opportunities in clinical applications due to its unique toxicological properties and potential neuroprotective effects. For patients with G6PD deficiency, the intake of favisin must be strictly controlled to prevent hemolytic anemia, and there are clear dietary contraindications in clinical practice.
On the other hand, research on favisin in the field of Parkinson's disease provides a theoretical foundation for the development of novel neuroprotective drugs. In the future, through structural modification, improvements in drug delivery technology, and combination drug strategies, it is expected to overcome the limitations of poor blood-brain barrier permeability and enhance efficacy in the central nervous system.
In addition, the antioxidant and anti-inflammatory effects of favisin also offer potential applications in other neurodegenerative diseases and chronic inflammatory diseases. By combining modern drug screening techniques with multi-omics research, in-depth analysis of its mechanisms of action and target networks will help promote the clinical translation of favomacin-related drugs.
As an important alkaloid glycoside in fava beans, favisin holds significant research value in the fields of hereditary G6PD deficiency and neurodegenerative diseases due to its unique chemical structure and biological activity. The active free radical products generated through the metabolism of the gut microbiota are both the source of toxicological risk and the basis of potential pharmacological activity.
This paper systematically reviews the chemical and physicochemical properties, plant origin, extraction methods, pharmacological activity, mechanism of action, and druggability evaluation of favismarin, with a focus on its multi-target regulatory role in the fight against Parkinson's disease. In the future, combining molecular modification with advanced drug delivery technologies, favisiin is expected to become an important candidate molecule in the development of natural product drugs.
With further in-depth research into its pharmacokinetic characteristics and clinical efficacy, the safety and efficacy of favisin will be evaluated more comprehensively, laying a solid foundation for its clinical application and new drug development. The continued development of natural product pharmacology will further promote the innovative application of favisin and its derivatives in modern medicine.
