Every batch of TumGard is tested for flavonoid content.

H. pylori's primary survival strategy is the urease enzyme. Urease converts urea into ammonia, neutralising stomach acid around the bacteria — creating a protected pocket where it can survive and multiply.

Specific flavonoids — particularly quercetin, myricetin, and catechin — inhibit urease activity. When urease is inhibited, H. pylori loses its ability to neutralise its local environment. Stomach acid can reach the bacteria directly. Its ability to colonise and persist is significantly compromised.

For H. pylori to cause damage, it first needs to attach to the stomach lining. It uses specific surface proteins to anchor itself to gastric epithelial cells — this adhesion is what allows it to persist and cause progressive mucosal damage.

Certain flavonoids — including licorice-derived compounds — interfere with H. pylori's ability to adhere to gastric epithelial cells. Without adhesion, H. pylori cannot embed itself in the mucosal layer and becomes more susceptible to the stomach's natural defences.

This is where flavonoids separate themselves from antibiotics. Antibiotics can eliminate H. pylori. What they cannot do is address the stomach lining damage the bacteria caused during its time in the stomach.

Flavonoids — particularly licorice-derived compounds like glabridin — stimulate prostaglandin E2 production, support mucus-secreting cells, reduce inflammatory cytokines, and activate the EGFR/ERK pathway that promotes repair of stomach epithelial cells. Gastric mucus content increased by up to 73% in studies.

In addition to urease inhibition and anti-adhesion activity, flavonoids have been shown to alter the cell membrane permeability of H. pylori. This affects the bacteria's ability to maintain internal homeostasis — weakening it and increasing susceptibility to the stomach's acid environment and other antimicrobial mechanisms.