No numerical acceptable daily intake set by EU or UK regulators
When the European Food Safety Authority re-evaluated anthocyanins (the broader E163 group, of which delphinidin is one member) in 2013, the panel concluded that the toxicological database was too limited to set a firm daily intake figure. They found no specific cause for concern at the amounts present in food, but noted that long-term studies on chronic toxicity, carcinogenicity, and effects on reproduction were extremely scarce. This leaves regulatory oversight relying on the principle that additive exposure is broadly comparable to ordinary dietary intake from foods naturally rich in anthocyanins.
EFSA concluded that the available toxicological data were inadequate to set a numerical ADI for E163 anthocyanins, citing major gaps in long-term chronic toxicity, carcinogenicity, and reproductive studies.
2013Regulatory reviewEFSA Panel on Food Additives and Nutrient Sources (ANS), Scientific Opinion on the re-evaluation of anthocyanins (E 163), EFSA Journal 11(4):3145
For anthocyanins extracted from sources other than grape skin or blackcurrant, or using non-aqueous methods, EFSA stated the absence of adequate characterisation meant its safety conclusion could not be confirmed.
2013Regulatory reviewEFSA Panel on Food Additives and Nutrient Sources (ANS), Scientific Opinion on the re-evaluation of anthocyanins (E 163), EFSA Journal 11(4):3145
Preclinical cancer research: promising signals, no human evidence
Laboratory and animal studies have found that delphinidin can slow the growth of cancer cells and trigger cell death across a wide range of tumour types. However, the concentrations used in these experiments are hundreds to thousands of times higher than the amounts that reach the bloodstream after eating or drinking foods containing it. No human clinical trials have tested delphinidin for cancer prevention or treatment, so the cell-culture findings cannot be translated into practical health claims.
In vitro studies across multiple cancer cell lines consistently show delphinidin inducing apoptosis and inhibiting cell proliferation through PI3K/AKT, NF-kB, and MAPK pathways, but the effective concentrations used are in the micromolar range, far above realistic human plasma levels.
2026LabFrontiers in Pharmacology: Targeting cancer with delphinidin: from molecular insights to therapeutic implications, PMC13056821
After oral intake, plasma delphinidin concentrations remain in the low nanomolar range, creating a large gap between the doses active in the laboratory and what the body actually absorbs from food.
2021Lab + animalPMC8583959: Delphinidin and Its Glycosides' War on Cancer: Preclinical Perspectives, Nutrients
Antioxidant and cardiovascular effects: mostly lab evidence
Delphinidin is among the more potent antioxidants in the anthocyanin family. Cell and animal studies show it can reduce LDL oxidation, support blood vessel function, and dampen inflammatory signalling. Small human studies have examined specific concentrated extracts rather than delphinidin in isolation, and the results, while positive, cover mostly metabolic markers rather than clinical outcomes such as heart events.
Delphinidin reduces intracellular oxygen radicals and increases nitric oxide synthase expression in human endothelial cells in culture, pointing to a potential cardiovascular protective mechanism.
2017LabPMC5610832: Bioavailable Concentrations of Delphinidin and Gallic Acid Induce Antioxidant Protection in Cultured Endothelial Cells
Delphinidin-3-glucoside inhibits platelet activation and reduces thrombus formation in animal models, suggesting anticoagulant properties at concentrations tested in vivo.
2012Lab + animalPMC3356278: Plant Food Delphinidin-3-Glucoside Significantly Inhibits Platelet Activation and Thrombosis, PLoS ONE
CYP3A4 enzyme interaction: significant in the lab, not at food levels
One laboratory study found delphinidin inhibits CYP3A4, an enzyme responsible for metabolising around half of all prescription drugs, by over 90% at a concentration of 100 micromolar. The concentration needed to produce meaningful inhibition in the lab is many times higher than what reaches the bloodstream after eating, so scientists currently consider clinically significant drug interactions from normal food intake unlikely.
Delphinidin inhibits CYP3A4 by more than 90% at 100 micromolar (IC50 approximately 32 micromolar) in human liver microsome preparations, but dietary exposure concentrations are considerably lower than those required for significant inhibition in vivo.
2014LabPubs.acs.org: Effects of Anthocyanidins and Anthocyanins on CYP2A6, CYP2B6, CYP2C9, and CYP3A4 in Primary Human Hepatocytes and Human Liver Microsomes, Journal of Agricultural and Food Chemistry
Bioavailability is low
Delphinidin is poorly absorbed from the gut. Oral bioavailability of some glycoside forms is below 0.5%. Gut bacteria help break down the glycoside into the active aglycone, but the process is variable between individuals. The compound is also unstable at neutral to alkaline pH, degrading into gallic acid and other breakdown products. This limits how much of what you eat or drink actually reaches target tissues.
Oral bioavailability of delphinidin-3-rutinoside is approximately 0.49% in pharmacokinetic studies; peak plasma concentration occurs around two hours after ingestion.
2022ObservationalPMC8969030: Chemistry and Pharmacological Actions of Delphinidin, Frontiers in Nutrition