# Delphinidin

**Canonical URL:** https://ingredients.hermeticasuperfoods.com/ingredients/delphinidin
**Data Source:** Hermetica Superfoods Ingredient Encyclopedia
**Updated:** 2026-04-03
**Evidence Score:** 1 / 10
**Category:** Compound
**Also Known As:** 3,5,7,3',4',5'-hexahydroxyflavylium, Delphinidin cation, Dp (abbreviation), Delphinidin aglycone, C.I. Natural Violet 16

## Overview

Delphinidin, a polyhydroxylated anthocyanin flavonoid (MW 303.24 g/mol), exerts concentration-dependent [antioxidant](/ingredients/condition/antioxidant) or prooxidant activity and inhibits key oncogenic enzymes including VEGFR2, PI3K, and CYP3A4, while triggering apoptosis and suppressing angiogenesis in cancer cell lines. Preclinical data demonstrate that delphinidin inhibits tumor cell proliferation at 10–100 µM in vitro and reduces VEGF-driven angiogenesis, though human pharmacokinetic studies show peak plasma concentrations of only 21–64 nmol/L after standardized maqui extract ingestion, underscoring a significant translational gap.

## Health Benefits

- **Antitumor and Antiproliferative Activity**: Delphinidin inhibits proliferation in multiple cancer cell lines (including breast, colorectal, and prostate) at concentrations of 10–100 µM by arresting cell cycle progression and downregulating cyclin D1 and CDK4 expression.
- **Proapoptotic Signaling**: At cytotoxic concentrations (≥50 µM in vitro), delphinidin activates caspase-3 and caspase-9, promotes cytochrome c release from mitochondria, and upregulates the Bax/Bcl-2 ratio, driving intrinsic apoptosis in tumor cells.
- **Antiangiogenic Effects**: Delphinidin suppresses vascular endothelial growth factor (VEGF)-induced phosphorylation of VEGFR2 and downstream Akt/mTOR signaling, reducing endothelial tube formation and migration in in vitro assays.
- **Antioxidant Protection at Low Concentrations**: At concentrations below 1 µM, delphinidin scavenges [reactive oxygen species](/ingredients/condition/antioxidant), increases intracellular [glutathione](/ingredients/condition/detox) levels, and protects endothelial cells from oxidative stress-induced injury through a hormetic mechanism.
- **CYP Enzyme Inhibition**: Delphinidin and its glycosides potently inhibit CYP3A4 (up to 90% inhibition at 100 µM) and moderately inhibit CYP2C9 (≈55%), with implications for modulating drug [metabolism](/ingredients/condition/weight-management) and potentially enhancing bioavailability of co-administered CYP substrates.
- **Anti-[inflammatory Pathway](/ingredients/condition/inflammation) Modulation**: Delphinidin suppresses NF-κB nuclear translocation and reduces expression of pro-inflammatory mediators including COX-2, iNOS, and TNF-α in macrophage and epithelial cell models.
- **Endothelial Cytoprotection via NO Pathway**: At approximately 10 µg/mL (~33 µM), delphinidin activates the NO–guanylyl cyclase pathway in endothelial cells, inhibiting stress-induced apoptosis and potentially contributing to [cardiovascular](/ingredients/condition/heart-health) protective effects observed epidemiologically with anthocyanin-rich diets.

## Mechanism of Action

Delphinidin exhibits concentration-dependent, bidirectional redox activity: at concentrations below 1 µM it acts as a classical antioxidant by donating hydrogen atoms from its polyhydroxyl B-ring to neutralize [reactive oxygen species](/ingredients/condition/antioxidant) and upregulating [glutathione](/ingredients/condition/detox) synthesis, whereas at concentrations of 10–100 µM it generates superoxide and hydroxyl radicals detectable by electron paramagnetic resonance (EPR), creating prooxidant stress that selectively induces apoptosis in rapidly dividing cells. In cancer biology, delphinidin directly inhibits VEGFR2 kinase autophosphorylation and blocks downstream PI3K/Akt and MAPK/ERK signaling cascades, suppressing both tumor cell survival and neoangiogenesis. The compound also inhibits cytochrome P450 enzymes—blocking CYP3A4 activity by approximately 90% at 100 µM and CYP2C9 by roughly 55% for delphinidin glucoside forms—and modulates phase II enzymes including glutathione S-transferases (GSTs), carbonyl reductases (CBRs), and UDP-glucuronosyltransferases (UGTs), collectively altering xenobiotic [metabolism](/ingredients/condition/weight-management). Under physiological conditions (pH 7.4, 37°C), delphinidin degrades rapidly, and its primary metabolite gallic acid independently contributes antioxidant and antitumor activity, suggesting that some observed bioactivities may be mediated indirectly through this degradation product rather than by intact delphinidin.

## Clinical Summary

Human clinical data specific to delphinidin as an isolated compound are essentially absent; the only published pharmacokinetic data come from a bioavailability study of Delphinol® standardized maqui berry extract, which measured peak plasma delphinidin-3-glucoside concentrations of 21.39–63.55 nmol/L at approximately 1 hour post-ingestion, reflecting the characteristically poor (~1%) oral bioavailability of anthocyanins. No clinical trials measuring tumor growth inhibition, apoptosis induction, or antiangiogenic endpoints attributable specifically to delphinidin supplementation have been registered or completed as of the available literature. Studies examining anthocyanin-rich dietary patterns epidemiologically suggest associations with reduced [cardiovascular](/ingredients/condition/heart-health) and cancer risk, but these cannot be attributed to delphinidin alone given the complex polyphenol matrix of whole foods. Confidence in delphinidin's clinical efficacy for any stated indication must therefore be rated as very low, and observed in vitro potency does not translate to established therapeutic benefit at currently achievable human plasma concentrations.

## Nutritional Profile

Delphinidin is a pure polyphenolic compound (molecular formula C15H11O7⁺, MW 303.24 g/mol) and contributes no macronutrients, calories, or minerals when consumed as an isolated compound. In whole food sources, bilberries provide approximately 0.3–0.6 mg delphinidin equivalents per gram fresh weight alongside vitamin C (~10–20 mg/100 g), manganese, and dietary fiber; blackcurrants deliver roughly 1.3–4.0 mg total anthocyanins per gram fresh weight with substantial vitamin C content (~180 mg/100 g). Delphinidin's bioavailability is limited by its glycosidic form in foods (requiring intestinal hydrolysis by β-glucosidases or lactase), rapid degradation at intestinal and physiological pH, extensive first-pass [metabolism](/ingredients/condition/weight-management), and low log P value restricting membrane permeability; estimated oral bioavailability for anthocyanins as a class is approximately 1–2% of ingested dose. Gallic acid, the primary degradation metabolite of delphinidin, is itself bioactive and better absorbed than the parent compound, and may account for a portion of the systemic effects attributed to delphinidin-rich foods.

## Dosage & Preparation

- **Maqui Berry Extract (Delphinol®)**: Standardized powder from Aristotelia chilensis; the most studied commercial form, used in the only published human pharmacokinetic study; no clinically validated dose established.
- **Anthocyanin-Rich Berry Extracts**: Bilberry (Vaccinium myrtillus) and blackcurrant (Ribes nigrum) standardized extracts containing delphinidin alongside other anthocyanins; typical commercial doses 100–500 mg/day of extract, with delphinidin content variable.
- **In Vitro Reference Concentrations**: Antiproliferative effects observed at 10–100 µM in cell culture, equivalent to roughly 3–30 µg/mL of pure delphinidin aglycone; these concentrations are not achievable in human plasma via oral supplementation.
- **Food Sources (Non-Supplemental)**: Bilberries (~300–600 mg anthocyanins/100 g fresh weight), blackcurrants (~130–400 mg/100 g), maqui berries (~138–212 mg delphinidin equivalents/100 g freeze-dried powder).
- **Stability Considerations**: Delphinidin degrades rapidly at physiological pH (7.4) and temperature (37°C); formulations should be stored in acidic, dark, and cool conditions to maximize shelf stability; enteric or encapsulated forms may improve delivery.
- **Timing**: Peak plasma concentrations observed at approximately 1 hour post-oral ingestion in the Delphinol® study; consumption with food may alter absorption kinetics.
- **No Established Therapeutic Dose**: No regulatory body or clinical guideline has established a recommended supplemental dose of isolated delphinidin for any therapeutic indication.

## Safety & Drug Interactions

At dietary concentrations found in whole foods, delphinidin-containing berries and extracts are generally considered safe with no documented serious adverse events in the published literature; however, isolated delphinidin exhibits cytotoxic effects at 100 µM in vitro, reflecting a hormetic dose-response profile that cautions against high-dose supplementation without further safety data. The most clinically significant interaction concern is potent CYP3A4 inhibition (approximately 90% at 100 µM) and moderate CYP2C9 inhibition by delphinidin glycosides; patients taking narrow-therapeutic-index CYP3A4 substrates such as cyclosporine, tacrolimus, some statins, certain benzodiazepines, or direct-acting anticoagulants should exercise caution with high-dose anthocyanin supplementation, though the inhibitory concentrations required may not be achievable via oral supplementation at current commercial doses. Delphinidin also inhibits GSTs and UGTs, potentially affecting conjugation of endogenous and exogenous substrates, and the compound's antiplatelet and vasodilatory properties via the NO pathway theoretically additive with antiplatelet drugs and antihypertensives. No human safety data, maximum tolerated dose, or guidance for pregnancy and lactation exist for supplemental delphinidin; pregnant and lactating individuals should restrict intake to normal dietary levels from whole foods until safety data are available.

## Scientific Research

The evidence base for delphinidin consists almost entirely of in vitro cell culture studies and limited animal models, with no completed, adequately powered randomized controlled trials establishing clinical efficacy for any specific health outcome in humans. In vitro studies across breast, prostate, colorectal, and endothelial cancer cell lines consistently demonstrate antiproliferative and proapoptotic effects in the 10–100 µM range, but these concentrations are 300- to 1000-fold higher than peak plasma concentrations (~21–64 nmol/L) recorded in the sole published human pharmacokinetic study using Delphinol® maqui berry extract in healthy volunteers, for whom the sample size was not fully reported. Animal studies using oral anthocyanin-rich extracts have shown tumor growth reduction and antiangiogenic effects, though isolating delphinidin's specific contribution from the complex mixture remains methodologically challenging. No clinical trials with defined endpoints, control groups, or reported effect sizes for delphinidin as an isolated compound in human disease have been published to date, making all translational claims highly preliminary.

## Historical & Cultural Context

Delphinidin as an isolated chemical entity was not historically recognized or used in traditional medicine; however, the plants richest in delphinidin have centuries-long histories of therapeutic application across multiple cultures. Bilberries were used in European folk medicine from at least the 16th century for diarrhea, urinary complaints, and visual disturbances, with Scandinavian and British herbalists recommending dried berries and leaf decoctions. Maqui berry (Aristotelia chilensis) holds significant cultural importance among the Mapuche people of Chile and Argentina, who consumed the fresh fruit and prepared fermented drinks called 'chicha de maqui' for energy, wound healing, and fever reduction. Roselle (Hibiscus sabdariffa), another delphinidin-rich source, has been used in West African, Caribbean, and Middle Eastern traditions as a tonic tea and natural colorant, with documented use in Ayurvedic and Unani systems for hypertension and liver support.

## Synergistic Combinations

Delphinidin's antitumor and [antioxidant](/ingredients/condition/antioxidant) effects may be synergistically enhanced when combined with other polyphenols sharing complementary mechanistic targets; for example, co-administration with quercetin (a flavonol that inhibits PI3K and HIF-1α) could provide additive suppression of the VEGF/VEGFR2 angiogenic axis at lower individual concentrations. Vitamin C (ascorbic acid) stabilizes delphinidin under physiological conditions by reducing pH-dependent degradation and may preserve anthocyanin bioactivity during intestinal transit, making vitamin C-rich matrices (as naturally found in blackcurrant and maqui berry whole fruit) a rational co-delivery approach. Piperine from black pepper (Piper nigrum), known to inhibit glucuronidation and increase epithelial permeability, has been proposed to enhance anthocyanin bioavailability, though specific data for delphinidin co-administration with piperine remain unpublished.

## Frequently Asked Questions

### What foods are highest in delphinidin?

Bilberries (Vaccinium myrtillus) and blackcurrants (Ribes nigrum) are among the richest dietary sources, with bilberries providing approximately 300–600 mg total anthocyanins per 100 g fresh weight and delphinidin typically comprising 30–50% of that fraction. Maqui berries (Aristotelia chilensis), eggplant skin, roselle calyces, and certain dark-pigmented cowpea varieties are also significant sources, and delphinidin contributes to the blue-violet color of some red wines.

### Can delphinidin kill cancer cells?

Delphinidin induces apoptosis and inhibits proliferation in multiple cancer cell lines—including breast, prostate, and colorectal cancer models—at concentrations of 10–100 µM in laboratory studies, acting via caspase activation, mitochondrial pathway engagement, and VEGFR2 kinase inhibition. However, these effective concentrations are roughly 300–1000 times higher than the peak plasma levels (~21–64 nmol/L) achievable in humans through oral supplementation, meaning no clinical evidence currently supports delphinidin as a cancer treatment.

### How well is delphinidin absorbed by the body?

Delphinidin and anthocyanins as a class have very poor oral bioavailability, estimated at approximately 1–2% of the ingested dose, with peak plasma concentrations of delphinidin-3-glucoside reaching only 21.39–63.55 nmol/L at roughly 1 hour after ingestion of standardized maqui berry extract (Delphinol®) in human volunteers. Rapid degradation at intestinal and physiological pH (7.4), extensive first-pass glucuronidation and sulfation, and low lipophilicity all contribute to this limited systemic exposure; the primary metabolite detected is gallic acid, which may independently contribute to health effects.

### Does delphinidin interact with any medications?

Delphinidin and its glucoside forms are potent inhibitors of CYP3A4 (up to ~90% inhibition at 100 µM in vitro) and moderate inhibitors of CYP2C9 (~55%), raising theoretical concerns about elevated plasma levels of drugs metabolized by these enzymes, such as cyclosporine, tacrolimus, certain statins, and some anticoagulants. While the inhibitory concentrations observed in vitro may exceed what is realistically achieved through typical supplemental doses, individuals taking narrow-therapeutic-index CYP3A4 or CYP2C9 substrates should consult a healthcare provider before using high-dose anthocyanin or delphinidin-rich supplements.

### What is the recommended dose of delphinidin supplement?

No regulatory body has established a recommended or maximum safe supplemental dose for isolated delphinidin, and no clinical trials have defined a therapeutic dose in humans for any specific health condition. Commercial products such as Delphinol® standardized maqui berry extract are sold at varying doses (commonly 60–300 mg of extract per day), but the delphinidin content and its relationship to clinical efficacy remain undefined; consumers should treat any current dosing guidance as empirical rather than evidence-based.

### What is the difference between delphinidin and other anthocyanins?

Delphinidin is one of six major anthocyanins, distinguished by three hydroxyl groups on its B-ring structure, which gives it unique antioxidant and antiproliferative properties compared to cyanidin or malvidin. This structural difference enables delphinidin to more potently inhibit cell cycle regulators like cyclin D1 and CDK4 in cancer cell studies. Research suggests delphinidin may have stronger proapoptotic signaling (caspase activation) than some related anthocyanins at equivalent concentrations.

### Is delphinidin safe for long-term supplementation?

While delphinidin from food sources is considered safe due to its natural presence in berries and vegetables, long-term safety data for concentrated delphinidin supplements in humans is limited. Most safety information comes from in vitro and animal studies; human toxicity or adverse effect thresholds remain undefined. Anyone considering long-term supplementation should consult a healthcare provider, particularly those with bleeding disorders or those taking anticoagulants.

### Who would benefit most from delphinidin supplementation?

Individuals seeking antioxidant support and those interested in cancer chemoprevention may benefit from delphinidin, though clinical evidence in human populations remains limited to observational dietary studies. People with high dietary intake of anthocyanin-rich foods (berries, purple vegetables) already receive delphinidin naturally, making supplementation most relevant for those with restricted access to these sources. Those with metabolic or inflammatory conditions may also benefit, though this application requires further human-based research.

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*Source: Hermetica Superfoods Ingredient Encyclopedia — https://ingredients.hermeticasuperfoods.com*
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