Delphinidin

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.

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.

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.

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.

Delphinidin reduces intracellular oxygen radicals and increases nitric oxide synthase expression in human endothelial cells in culture, pointing to a potential cardiovascular protective mechanism.

Delphinidin-3-glucoside inhibits platelet activation and reduces thrombus formation in animal models, suggesting anticoagulant properties at concentrations tested in vivo.

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.

Oral bioavailability of delphinidin-3-rutinoside is approximately 0.49% in pharmacokinetic studies; peak plasma concentration occurs around two hours after ingestion.