Scientists at the University of Bath have developed a new technology that could allow protein-based drugs to be taken orally, potentially replacing injections for treatments such as growth hormone, immunotherapy and diabetes medications including Wegovy and Ozempic.

Protein-based drugs cannot currently be taken as pills because they are broken down in the stomach. This means patients must rely on injections, which can be painful and inconvenient, especially for those with chronic conditions.

The Bath team has created a system that transports therapeutic proteins across the gut wall into the bloodstream. This could enable oral delivery of drugs that previously required injection.

Professor Randy Mrsny, from the University of Bath’s Department of Life Sciences, led the study. He said: “Whilst it’s not the first system to replace injections, ours is the first platform to work safely and consistently, delivering the drug at effective doses and using a well understood pathway.”

The system mimics a natural mechanism used by gut bacteria. Researchers linked human growth hormone to a non-toxic carrier molecule derived from bacteria associated with cholera.

This carrier binds to a receptor on intestinal cells, moves the drug across the gut lining and releases it into the bloodstream. The system consistently delivered 5–10% of the drug, which is sufficient for commercial viability.

Professor Mrsny said: “This pathway is well understood and has been derived from events in the human intestine, so we know it will work in patients.”

He added: “Unlike previous systems, our method doesn’t damage the epithelium and can generically transport a large range of medications, including hormones and cancer treatments that can currently only be injected.”

Initial human testing could begin within two years, pending further optimisation with pharmaceutical partners.

Eisai has presented new clinical data showing that patients with early Alzheimer’s disease continue to benefit from four years of treatment with Leqembi (lecanemab). Findings were shared at the Alzheimer’s Association International Conference 2025, held in Toronto and virtually.

Results from the Clarity AD open label extension show that lecanemab slowed clinical decline by 1.75 points on the Clinical Dementia Rating-Sum of Boxes scale, compared to expected decline in the ADNI cohort. This effect was observed across all apolipoprotein E ε4 genotypes.

The benefit increased over time. At three years, lecanemab reduced decline by 1.01 points vs ADNI, rising to 1.75 points at four years. Against the BioFINDER cohort, the reduction was 1.40 points at three years and 2.17 points at four years.

Lecanemab is an amyloid-beta monoclonal antibody that targets and clears toxic protofibrils and reduces amyloid plaques. These aggregates are linked to neuronal injury in Alzheimer’s disease.

In the EU and UK, lecanemab is indicated for adults with mild cognitive impairment or mild dementia due to Alzheimer’s disease, who are ApoE ε4 non-carriers or heterozygotes with confirmed amyloid pathology.

A total of 478 patients who completed the 18-month Clarity AD core study continued treatment for four years in the extension phase. No new safety findings were reported during this period.

Rates of amyloid-related imaging abnormalities decreased after the first year and remained stable throughout treatment. The most common adverse events in the phase 3 trial included infusion reactions, ARIA-H, ARIA-E, headache and fall.