Cyanidin 3 Glucoside

• Potent antioxidant activity
• Anti-inflammatory effects
• Metabolic health support
• Cardiovascular protection
• Neuroprotective properties

• Blood glucose regulation
• Improved insulin sensitivity
• Vision health enhancement
• Antimicrobial properties
• Potential anticancer effects
• Gut microbiome modulation

Cyanidin-3-glucoside (C3G) is the most abundant and widely studied anthocyanin in nature, exerting its biological effects through multiple molecular mechanisms that contribute to its diverse health benefits. As a polyphenolic compound with a distinctive chemical structure featuring a sugar moiety (glucose) attached to the C3 position of the flavylium cation, C3G possesses unique properties that distinguish it from other anthocyanins. The primary mechanisms through which C3G exerts its biological effects include: 1) Direct antioxidant activity: C3G acts as a potent free radical scavenger due to its hydroxyl groups, which can donate hydrogen atoms to neutralize reactive oxygen species (ROS) and reactive nitrogen species (RNS). This direct antioxidant activity occurs through multiple mechanisms including hydrogen atom transfer, single electron transfer, and metal ion chelation.

The presence of the ortho-dihydroxyl structure in the B-ring of C3G is particularly important for its radical scavenging capacity. 2) Activation of endogenous antioxidant defense systems: Beyond direct antioxidant effects, C3G upregulates cellular antioxidant defenses by activating the Nrf2 (Nuclear factor erythroid 2-related factor 2) signaling pathway. Upon activation, Nrf2 translocates to the nucleus and binds to antioxidant response elements (AREs), promoting the expression of antioxidant and detoxifying enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1). This indirect antioxidant effect provides more sustained protection against oxidative stress than direct radical scavenging alone.

3) Anti-inflammatory effects: C3G exhibits potent anti-inflammatory properties through inhibition of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathway. By preventing the phosphorylation and degradation of IκB (inhibitor of κB), C3G blocks the nuclear translocation of NF-κB, thereby reducing the expression of pro-inflammatory genes and the production of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Additionally, C3G inhibits the activity of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), further contributing to its anti-inflammatory effects. C3G also modulates MAPK (mitogen-activated protein kinase) signaling pathways, particularly p38 MAPK and JNK (c-Jun N-terminal kinase), which are involved in inflammatory responses.

4) Metabolic regulation through AMPK activation: C3G activates AMP-activated protein kinase (AMPK), a master regulator of cellular energy homeostasis. AMPK activation by C3G occurs through multiple mechanisms, including increased adiponectin signaling, elevated cellular AMP levels, and activation of upstream kinases such as liver kinase B1 (LKB1) and calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ). Once activated, AMPK phosphorylates numerous downstream targets, leading to enhanced glucose uptake in skeletal muscle and adipose tissue through increased GLUT4 translocation, suppressed hepatic gluconeogenesis through phosphorylation of CRTC2 (CREB-regulated transcription coactivator 2) and HDAC5 (histone deacetylase 5), and improved fatty acid oxidation through inhibition of acetyl-CoA carboxylase (ACC). These metabolic effects collectively contribute to C3G’s benefits for insulin sensitivity and glucose homeostasis.

5) Cardiovascular protection: C3G improves endothelial function by enhancing nitric oxide (NO) bioavailability through multiple mechanisms. It activates endothelial nitric oxide synthase (eNOS) via the PI3K/Akt pathway, leading to increased NO production. Simultaneously, C3G’s antioxidant effects reduce superoxide levels, preventing the formation of peroxynitrite and preserving NO bioavailability. C3G also inhibits NADPH oxidase, a major source of vascular superoxide production.

Additionally, C3G protects against LDL oxidation, a key step in atherosclerosis development, and modulates cholesterol metabolism by affecting the expression of genes involved in cholesterol synthesis, transport, and excretion, including CETP (cholesteryl ester transfer protein). C3G also exhibits antiplatelet and antithrombotic effects by inhibiting platelet aggregation and adhesion. 6) Neuroprotective mechanisms: C3G can cross the blood-brain barrier, albeit in limited amounts, and exert neuroprotective effects through multiple mechanisms. It reduces oxidative stress in neuronal cells, inhibits neuroinflammation by suppressing microglial activation, and prevents protein aggregation associated with neurodegenerative diseases.

C3G enhances brain-derived neurotrophic factor (BDNF) levels, supporting neuronal health and plasticity. It also modulates neurotransmitter systems, including dopaminergic, cholinergic, and GABAergic pathways, potentially improving cognitive function and mood. Additionally, C3G inhibits neuronal apoptosis through regulation of Bcl-2 family proteins and caspase activation. 7) Anticancer potential: C3G demonstrates anticancer properties through multiple mechanisms, including induction of cell cycle arrest and apoptosis in cancer cells via activation of p53, modulation of Bcl-2 family proteins, and activation of caspases.

It inhibits cancer cell proliferation by suppressing various signaling pathways including PI3K/Akt/mTOR and MAPK/ERK. C3G also inhibits angiogenesis by reducing VEGF (vascular endothelial growth factor) expression and matrix metalloproteinases (MMPs) activity. Furthermore, C3G exhibits epigenetic regulatory effects by inhibiting DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), potentially reversing aberrant epigenetic modifications associated with cancer. 8) Gut microbiome modulation: C3G influences gut microbiota composition, potentially promoting beneficial bacteria while inhibiting pathogenic species.

It can strengthen intestinal barrier function by enhancing tight junction proteins and reduce intestinal inflammation. Importantly, C3G undergoes extensive metabolism by gut microbiota, producing smaller, more bioavailable metabolites including protocatechuic acid (PCA), phloroglucinaldehyde, and various phenolic acids. These metabolites contribute significantly to the overall biological effects of C3G, often exhibiting distinct bioactivities from the parent compound. 9) Cellular senescence inhibition: Recent research has shown that C3G can attenuate cellular senescence induced by oxidative stress.

It reduces senescence-associated β-galactosidase activity, inhibits the expression of senescence markers (p16, p21, p53), and suppresses the senescence-associated secretory phenotype (SASP), characterized by the secretion of pro-inflammatory cytokines, chemokines, and matrix metalloproteinases. This anti-senescence effect may contribute to C3G’s potential anti-aging properties. 10) Epigenetic regulation: C3G can modulate gene expression through epigenetic mechanisms, including DNA methylation, histone modifications, and microRNA regulation. By inhibiting DNA methyltransferases and histone deacetylases, C3G may reverse aberrant epigenetic modifications associated with various diseases, potentially leading to the restoration of normal gene expression patterns.

The bioactivity of C3G is influenced by its metabolism, with both the parent compound and its metabolites contributing to the observed health benefits. The relative contribution of direct effects of intact C3G versus effects mediated by its metabolites remains an active area of research. Additionally, the complex interplay between C3G and the gut microbiome adds another layer of complexity to its mechanism of action, as individual variations in gut microbiota composition may influence the metabolic fate of C3G and consequently its biological effects.

Determining optimal dosages for cyanidin-3-glucoside (C3G) is challenging due to several factors, including its variable bioavailability, individual differences in metabolism, and the diverse sources from which

it can be obtained. Unlike single-compound pharmaceuticals, C3G is typically consumed as part of complex plant extracts or whole foods with varying C3G content. For general health maintenance and antioxidant support, dietary intake of C3G-rich foods (blackberries, black rice, purple corn, etc.) is often recommended rather than isolated C3G supplements.

When supplemental forms are used, dosages typically range from 50-320 mg of C3G daily, depending on the specific source and the intended health benefit.

Current dosage recommendations for C3G are limited by several factors: 1) Most clinical studies use specific anthocyanin-rich extracts rather than isolated C3G, making

it difficult to establish dose-response relationships for C3G

specifically ; 2) Significant variability in chemical composition and bioavailability between different C3G sources; 3) Limited long-term safety data for isolated C3G supplements at various doses; 4) Individual variability in metabolism and response to C3G; 5) The complex interplay between parent C3G and its metabolites, which may contribute significantly to biological effects; 6) Lack of standardized analytical methods for quantifying C3G in commercial products. More research is needed to establish optimal dosing regimens for specific health conditions and to understand how factors such as formulation, timing, and individual characteristics affect the optimal dose.

Cyanidin-3-glucoside (C3G) has historically been reported to have low bioavailability, with absorption rates typically ranging from 0.1-2% of the ingested dose when measured as intact parent compound in plasma and urine. However, recent research using isotope-labeled C3G has revealed that its bioavailability may be significantly higher (approximately 12%) when considering its extensive metabolism to phenolic acid derivatives and phase II conjugates. C3G can be absorbed in multiple regions of the gastrointestinal tract, with evidence for absorption in the stomach, small intestine, and colon. In the stomach, the acidic environment stabilizes C3G in its flavylium cation form, allowing for some absorption of the intact molecule.

In the small intestine, a portion of C3G may be absorbed directly through passive diffusion or active transport mechanisms involving glucose transporters (due to its glucose moiety). However, the majority of ingested C3G reaches the colon, where it undergoes extensive metabolism by gut microbiota, producing various phenolic acids and other metabolites that are subsequently absorbed and may contribute significantly to its biological effects.

C3G is generally better absorbed when taken on an empty stomach or between meals to minimize interactions with dietary proteins and other food components that can reduce its absorption. However, taking C3G with meals may be preferable when the goal is to reduce the glycemic impact of the meal or to exert local effects in the gastrointestinal tract. For maximum absorption of parent C3G, morning administration may be optimal due to potentially higher intestinal permeability and metabolic activity early in the day. For effects mediated by C3G metabolites, consistent daily intake is more important than specific timing, as it allows for adaptation of the gut microbiota to enhance metabolite production over time.

The timing of C3G intake may also be influenced by the specific health goal; for example, taking C3G before carbohydrate-rich meals may be most effective for managing postprandial glucose responses.

Gastrointestinal Metabolism: In the stomach, C3G is relatively stable due to the acidic environment (pH 1-2), which favors the flavylium cation form. As it moves into the small intestine (pH 5-7), it undergoes structural transformations to less stable forms including the colorless carbinol pseudobase, quinoidal base, and chalcone forms. In the small intestine, C3G can undergo deglycosylation by brush border β-glucosidases, releasing the cyanidin aglycone, which is highly unstable at intestinal pH and rapidly degrades to phenolic acids and aldehydes, primarily protocatechuic acid (PCA) and phloroglucinaldehyde.

Microbial Metabolism: The majority of ingested C3G reaches the colon, where it is extensively metabolized by gut microbiota. Microbial enzymes cleave the glycosidic bond and open the C-ring of the cyanidin structure, producing various phenolic acids including protocatechuic acid, vanillic acid, ferulic acid, and phloroglucinaldehyde. These microbial metabolites have better absorption profiles than the parent C3G and may contribute significantly to the biological effects attributed to C3G consumption. The specific pattern of metabolites produced depends on the individual’s gut microbiome composition.

Hepatic Metabolism: Absorbed C3G and its metabolites undergo phase II metabolism in the liver, primarily glucuronidation, sulfation, and methylation. These conjugated forms are the predominant circulating metabolites in the bloodstream. The specific pattern of conjugation varies depending on individual genetic factors affecting metabolizing enzymes. Protocatechuic acid, a major metabolite of C3G, may undergo further metabolism to vanillic acid through methylation by catechol-O-methyltransferase (COMT).

Elimination: C3G and its metabolites are primarily excreted in urine (for absorbed compounds) and feces (for unabsorbed compounds). The elimination half-life of parent C3G is relatively short (approximately 1.5-3 hours), while certain metabolites may have longer half-lives (up to 24 hours). Biliary excretion and enterohepatic recycling may also play a role in the disposition of C3G metabolites, potentially prolonging their presence in the body.

Absorption Sites: C3G can be absorbed in multiple regions of the gastrointestinal tract. Some absorption occurs in the stomach, where the acidic environment stabilizes the compound. In the small intestine, C3G may be absorbed through passive diffusion or via glucose transporters due to its glucose moiety. The colon is a major site for the absorption of C3G metabolites produced by gut microbiota.

Distribution: After absorption, C3G and its metabolites are distributed throughout the body, with evidence for presence in various tissues including liver, kidney, brain (in limited amounts), adipose tissue, and skeletal muscle. The volume of distribution is relatively large due to extensive tissue distribution. C3G and its metabolites may bind to plasma proteins, which can affect their distribution and elimination.

Peak Plasma Time: Peak plasma concentrations of parent C3G typically occur 1-2 hours after oral administration, reflecting absorption primarily in the upper gastrointestinal tract. Metabolites may show different kinetics, with some appearing rapidly (1-4 hours) and others showing delayed peaks (6-24 hours) due to microbial metabolism in the colon.

Half Life: The elimination half-life of parent C3G is relatively short, approximately 1.5-3 hours. However, certain metabolites, particularly those produced by gut microbiota and subject to enterohepatic recycling, may have longer half-lives ranging from 6-24 hours. This extended presence of metabolites may contribute to the sustained biological effects observed with C3G supplementation.

Despite significant advances in understanding C3G bioavailability, several knowledge gaps remain: 1) Limited data on tissue distribution and cellular uptake of C3G and its metabolites beyond plasma concentrations; 2) Incomplete understanding of the specific gut microbial species responsible for C3G metabolism and how to optimize

this process; 3) Limited information on how chronic consumption affects bioavailability through potential adaptation mechanisms; 4) Need for better analytical methods to comprehensively identify and quantify the diverse array of C3G metabolites in biological samples; 5) Incomplete knowledge of the relative contribution of parent C3G versus its metabolites to the observed health benefits; 6) Limited understanding of how genetic polymorphisms affect C3G metabolism and individual responses; 7) Need for more human studies using isotope-labeled C3G to accurately track its metabolic fate in vivo.

Cyanidin-3-glucoside (C3G) has an excellent safety profile with minimal reported adverse effects at recommended doses. As a naturally occurring compound found in many common foods and beverages, dietary C3G has a long history of consumption with no significant safety concerns. Clinical studies using C3G-rich extracts at doses up to 320 mg of C3G daily have demonstrated good tolerability with few adverse effects. The safety profile of C3G is further supported by its relatively low bioavailability and rapid metabolism and elimination, which limits systemic exposure to high concentrations.

C3G is generally recognized as safe (GRAS) when consumed in amounts consistent with a normal diet rich in berries and other anthocyanin-containing foods.

No definitive upper limit has been established for C3G. Clinical studies have used doses up to 320 mg of C3G daily without significant adverse effects. The European Food Safety Authority (EFSA) has not established a tolerable upper intake level for C3G or anthocyanins in general due to lack of evidence for any adverse effects. Based on available research, doses up to 300 mg of C3G daily appear to be well-tolerated in most individuals.

Higher intakes from food sources (which may exceed 300 mg in diets rich in berries and other C3G-containing foods) have not been associated with adverse effects.

Long-term safety data beyond 12 months of continuous use is limited for concentrated C3G supplements. Available studies lasting up to 12 months have not identified significant safety concerns at doses up to 320 mg of C3G daily. Epidemiological data on populations consuming diets rich in C3G-containing foods suggest long-term safety of dietary C3G. No cumulative toxicity or adverse effects specific to long-term use have been identified in the available literature. Some evidence suggests potential beneficial effects of long-term C3G consumption on markers of oxidative stress, inflammation, and metabolic health.

Acute Toxicity: C3G has very low acute toxicity. Animal studies have shown no significant adverse effects at doses far exceeding those used in human supplementation. The LD50 (lethal dose for 50% of test animals) for various C3G-rich extracts is typically greater than 2000 mg/kg body weight in rodents, indicating a wide margin of safety.

Subchronic Toxicity: 90-day feeding studies in animals have shown no significant adverse effects at doses equivalent to several times the typical human supplemental dose. No-observed-adverse-effect levels (NOAELs) for various C3G-rich extracts typically range from 1000-2000 mg/kg body weight/day in rodents.

Genotoxicity: Standard genotoxicity assays (Ames test, chromosomal aberration tests, micronucleus tests) have been negative for C3G and C3G-rich extracts, indicating no significant mutagenic potential.

Carcinogenicity: No evidence of carcinogenic potential in available studies. Some research suggests potential anti-carcinogenic properties of C3G through various mechanisms including antioxidant activity, modulation of cell signaling pathways, and epigenetic effects.

C3G is generally recognized as safe (GRAS) for food use by regulatory authorities worldwide. In the United States, various C3G-containing extracts are permitted as food additives and dietary supplement ingredients. The European Food Safety Authority (EFSA) has evaluated various anthocyanin-rich extracts for safety but has not established specific intake recommendations or upper limits for C3G specifically. C3G-containing extracts are permitted as food colorants (E163) in the European Union.

No major regulatory warnings exist for C3G-containing foods or supplements when used as directed. Regulatory status may vary for different sources of C3G (blackberry extract, elderberry extract, etc.) and specific formulations.

Fda Status: Cyanidin-3-glucoside (C3G) is not specifically approved as a drug or medical treatment by the FDA. It is generally recognized as safe (GRAS) when consumed in amounts found in conventional foods. C3G-containing extracts are permitted as dietary supplement ingredients under DSHEA (Dietary Supplement Health and Education Act of 1994), provided they comply with all applicable regulations.

Dietary Supplement Status: C3G can be marketed as a dietary supplement ingredient. Manufacturers must ensure product safety and are responsible for determining that claims are substantiated by adequate evidence. Structure/function claims are permitted with appropriate disclaimer, but disease claims are prohibited without FDA approval.

Food Additive Status: Anthocyanins, including C3G, are approved as color additives exempt from certification (21 CFR 73.250 for fruit juice colors and 21 CFR 73.260 for vegetable juice colors). They can be used in food products according to Good Manufacturing Practices (GMP).

Labeling Requirements: Dietary supplements containing C3G must comply with FDA labeling regulations, including Supplement Facts panel, ingredient list, and appropriate disclaimers for any structure/function claims. Claims must be truthful and not misleading.

Recent Developments: No specific regulatory actions targeting C3G have been issued recently. The FDA continues to monitor the safety of dietary supplements, including those containing anthocyanins.

Efsa Status: The European Food Safety Authority (EFSA) has evaluated anthocyanins, including C3G, for safety but has not established specific intake recommendations or upper limits. No approved health claims exist specifically for C3G under Article 13.1 of Regulation (EC) No 1924/2006.

Novel Food Status: C3G from traditional food sources (berries, black rice, etc.) is not considered a novel food. However, highly purified or synthesized C3G, or C3G from non-traditional sources, may require novel food authorization.

Food Additive Status: Anthocyanins are permitted as food colorants (E163) in the European Union under Regulation (EC) No 1333/2008. They can be used in various food categories according to specified conditions.

Supplement Status: C3G can be used in food supplements regulated under Directive 2002/46/EC, provided they comply with all applicable regulations including safety requirements.

Health Claims: No authorized health claims exist specifically for C3G under the EU nutrition and health claims regulation. Any health claims made for products containing C3G must be authorized by EFSA or fall under transitional measures.

Health Canada Status: C3G is not approved as a drug by Health Canada. It can be included in Natural Health Products (NHPs) if they comply with all applicable regulations.

Natural Health Product Status: C3G-containing extracts can be licensed as Natural Health Products if they meet the requirements of the Natural Health Products Regulations. Several C3G-rich extracts have monographs in the Natural Health Products Ingredients Database.

Food Additive Status: Anthocyanins are permitted as food colorants in Canada under the Food and Drug Regulations (C.R.C., c. 870).

Labeling Requirements: Natural Health Products containing C3G must comply with Health Canada labeling regulations, including medicinal and non-medicinal ingredients, recommended use, and appropriate disclaimers.

Tga Status: C3G is not approved as a medicine by the Therapeutic Goods Administration (TGA). It can be included in listed complementary medicines if they comply with all applicable regulations.

Food Standards Status: Anthocyanins are permitted as food additives (160a) under the Australia New Zealand Food Standards Code.

Supplement Status: C3G can be included in listed complementary medicines regulated by the TGA. Manufacturers must ensure products meet quality, safety, and efficacy standards appropriate for listed medicines.

Mhlw Status: C3G is not approved as a pharmaceutical by the Ministry of Health, Labour and Welfare (MHLW). It can be included in Foods with Health Claims if they comply with applicable regulations.

Food With Functional Claims: Products containing C3G may be marketed as Foods with Functional Claims (FFC) if scientific evidence supporting the claims is submitted to the Consumer Affairs Agency. Several C3G-rich extracts have been used in FFC products, particularly for metabolic health claims.

Food Additive Status: Anthocyanins are permitted as food additives in Japan.

Nmpa Status: C3G is not approved as a drug by the National Medical Products Administration (NMPA). It can be included in health food products if they comply with applicable regulations.

Health Food Status: C3G-containing extracts can be used in health food products regulated by the State Administration for Market Regulation (SAMR). Products must obtain health food approval or filing before marketing.

Food Additive Status: Anthocyanins are permitted as food additives in China under the National Food Safety Standard for Food Additives (GB 2760).

Codex Alimentarius: The Codex Alimentarius Commission has established specifications for anthocyanins as food additives (INS 163) but has not set specific regulations for C3G as a supplement ingredient.

Who Status: The World Health Organization has not issued specific recommendations regarding C3G supplementation.

Global Regulatory Trends: There is a global trend toward increased regulation of dietary supplements and functional foods, with growing emphasis on scientific substantiation of claims and safety. This may impact how C3G products are regulated and marketed internationally in the future.

Manufacturing Standards: Manufacturers of C3G supplements should comply with Good Manufacturing Practices (GMP) as required in their jurisdiction. In the US, this means compliance with 21 CFR Part 111 for dietary supplements.

Quality Testing: Appropriate testing for identity, purity, strength, and composition should be conducted. Testing should verify C3G content, absence of contaminants, and stability throughout shelf life.

Adverse Event Reporting: Manufacturers should maintain systems for collecting and reporting adverse events associated with their products as required by local regulations. In the US, serious adverse events must be reported to the FDA.

Claim Substantiation: Scientific evidence supporting any claims made for C3G products should be maintained and be readily available if requested by regulatory authorities.

International Compliance: Companies marketing C3G products internationally should ensure compliance with the specific regulations of each target market, which may require different formulations, labels, or supporting documentation.

Potential Changes: As research on C3G continues to grow, regulatory frameworks may evolve to better address its unique properties and potential health benefits. This could include specific monographs, approved health claims, or standardized testing methods.

Research Needs: Additional safety studies, particularly long-term consumption data and special population studies, would help establish more specific regulatory guidelines for C3G supplementation.

Industry Trends: The supplement industry is increasingly adopting self-regulatory measures for quality and transparency, which may impact how C3G products are manufactured and marketed even in the absence of new regulations.

Pricing Trends: C3G supplement prices have generally decreased over the past 5 years due to increased competition, improved extraction technologies, and growing consumer demand. However, premium formulations with enhanced bioavailability have maintained higher price points due to their technological advantages and patent protection.

Future Projections: Prices for standard C3G extracts are expected to continue declining gradually (3-5% annually) as production scales increase and more suppliers enter the market. Enhanced bioavailability formulations may see more significant price reductions (5-10% annually) as patents expire and technologies become more widely available.

Emerging Sources: Research into alternative C3G sources, including agricultural waste products (grape pomace, berry processing waste) and biotechnological production methods, may significantly reduce costs in the future. These approaches are currently in development stages but show promise for more cost-effective and sustainable C3G production.

Powder Extract: 18-36 months when properly stored

Liquid Extract: 12-24 months when properly stored

Capsules: 24-36 months when properly stored

Tablets: 24-36 months when properly stored

Notes: Shelf life estimates assume proper storage conditions and sealed containers. Actual stability may vary based on specific formulation, processing methods, and storage conditions. C3G is generally more stable in acidified formulations and when protected from light, heat, and oxygen.

Temperature: Store at cool temperatures (4-25°C). Refrigeration (4-8°C) is ideal for long-term storage, particularly for liquid extracts. Avoid temperatures exceeding 30°C as higher temperatures accelerate degradation. Freeze-thaw cycles should be avoided as they can significantly reduce C3G stability.

Humidity: Keep in low humidity environments (<60% relative humidity). C3G can absorb moisture, which accelerates hydrolysis and degradation reactions. Desiccants may be included in packaging to maintain low humidity.

Light: Protect from direct light, especially UV light, which can catalyze oxidation reactions and structural transformations. Amber or opaque containers are essential for preserving C3G stability. If transparent packaging is used for marketing purposes, secondary packaging should provide light protection.

Packaging: Store in airtight, light-resistant containers to minimize exposure to oxygen, moisture, and light. Nitrogen-flushed packaging can further extend shelf life by displacing oxygen. Aluminum foil pouches or HDPE bottles with oxygen scavengers provide optimal protection.

Notes: Once opened, products should ideally be used within 3-6 months, even if the total shelf life is longer. Consider refrigeration after opening, particularly for liquid extracts. For bulk materials, consider dividing into smaller portions to minimize repeated exposure to air and light.

Synthesis Methods

Natural Sources

Extraction Methods

Quality Considerations

Sustainability

Commercial Forms

Cyanidin-3-glucoside (C3G) has been extensively studied in preclinical models, demonstrating significant antioxidant, anti-inflammatory, and metabolic regulatory properties. Human clinical evidence has grown substantially in the past decade, with numerous randomized controlled trials supporting benefits for metabolic health, cardiovascular function, and potentially cognitive performance. Epidemiological studies consistently associate higher intake of C3G-rich foods with reduced risk of type 2 diabetes, cardiovascular disease, and cognitive decline. The strongest clinical evidence exists for metabolic benefits, with moderate to strong evidence for cardiovascular health and emerging but promising evidence for neuroprotection.

While most studies use C3G-rich extracts rather than isolated C3G, advances in analytical techniques and study design have improved our understanding of the specific contributions of C3G to the observed health benefits. Mechanistic studies have elucidated multiple pathways through which C3G exerts its biological effects, including AMPK activation, Nrf2 signaling, and NF-κB inhibition, providing a strong scientific foundation for its therapeutic potential.

Limited studies on isolated C3G versus complex extracts, making it difficult to attribute effects specifically to C3G, Insufficient dose-response studies to establish optimal therapeutic dosages for specific conditions, Limited long-term safety and efficacy data beyond 12 months, Incomplete understanding of the relative contribution of parent C3G versus its metabolites to observed health benefits, Limited research on potential synergistic effects between C3G and other bioactive compounds, Insufficient clinical trials in specific populations such as children, pregnant women, or those with specific chronic diseases, Need for more studies on enhanced bioavailability formulations and their comparative efficacy

Development and clinical testing of enhanced bioavailability formulations to overcome the limited absorption of C3G, Investigation of the role of gut microbiome in determining individual response to C3G and strategies to optimize this aspect, Larger, longer-duration clinical trials for chronic disease prevention and management, Comparative studies of different C3G sources to identify optimal preparations for specific health conditions, Research on direct supplementation with C3G metabolites to bypass variability in gut metabolism, Development of personalized approaches based on individual metabolic profiles and gut microbiome composition, Investigation of potential epigenetic effects of C3G and their long-term implications for health and disease prevention