Scientists at the University of Edinburgh have identified new drug targets within bacterial cells that could help overcome antimicrobial resistance (AMR), opening new possibilities for more effective antibiotic treatments.

The research, conducted in collaboration with Queen Mary University of London and Imperial College London, was supported by the Biotechnology and Biological Sciences Research Council, the Leverhulme Trust and Wellcome. The findings were published in Nature Communications.

Antibiotics typically work by disrupting the production of proteins essential for bacterial growth and survival. However, some bacteria possess a repair mechanism known as Rtc, which enables them to counteract this process and sustain protein production and growth, despite exposure to antibiotics.

Using a combination of computer modelling and laboratory experiments with E. coli – known for developing antibiotic resistance – the researchers identified potential drug targets within the Rtc repair system. They also observed that bacterial responses to antibiotics vary depending on differences in these repair systems between individual cells.

The team suggests that therapies could be tailored to inhibit key components of the Rtc repair pathway, thereby enhancing the efficacy of existing antibiotics and informing the development of next-generation anti-AMR treatments.

AstraZeneca has reported positive full results from its phase 3 NATRON trial evaluating Fasenra (benralizumab) for the treatment of hypereosinophilic syndrome (HES).

HES is a group of rare disorders characterised by persistently elevated levels of eosinophils – a type of white blood cell – in the blood, accompanied by evidence of tissue or organ damage. Symptoms range from fatigue and weight loss to more severe outcomes such as organ failure or coma. Owing to this variety, diagnosis can be challenging; estimates suggest HES affects between 0.04 and 0.17 per 100,000 people in the UK.

The multicentre, randomised, double-blind, placebo-controlled NATRON study assessed the efficacy and safety of 30mg of Fasenra administered subcutaneously every four weeks in eligible patients with HES.

The trial met its primary endpoint, demonstrating a statistically significant and clinically meaningful delay in time to first disease worsening or flare, and a reduction in overall risk of flare compared with placebo.

All key secondary endpoints were also met, including a lower proportion of patients experiencing flare-ups or withdrawing from treatment, and a reduction in the annualised flare rate versus placebo.