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Enterprise Therapeutics’ First Potentiator Program for Treatment of Respiratory Diseases Acquired by Roche

Enterprise Therapeutics’ First Potentiator Program for Treatment of Respiratory Diseases Acquired by Roche content piece image
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Enterprise Therapeutics Ltd (Enterprise), a biopharmaceutical company today announced its novel TMEM16A potentiator portfolio has been fully acquired by Roche and will be developed by Genentech, a member of the Roche Group. The portfolio includes ETD002 which recently entered Phase 1 trials.

Enterprise’s shareholders received an upfront payment of £75 million and are eligible to receive additional contingent payments, to be made based on the achievement of certain predetermined milestones.

The TMEM16A portfolio is focused toward treating all people with cystic fibrosis (CF), with potential to benefit people with other severe respiratory diseases characterised by excessive mucus congestion.

Dr John Ford, CEO, Enterprise Therapeutics, said: “Roche and Genentech have a proven track record of bringing new medicines to people with respiratory diseases, and have recognised the opportunity that our TMEM16A potentiator portfolio presents. I am very proud of the team at Enterprise for identifying and developing this innovative approach to treat patients, with ETD002 the first of our compounds to reach clinical stage. TMEM16A potentiation has the potential to significantly increase the quality of life for people living with cystic fibrosis, for many of whom existing therapies are not effective.”

Dr James Sabry, MD, PhD, Global Head of Pharma Partnering, Roche, commented: “We are excited to add Enterprise’s TMEM16A potentiator program to our existing respiratory portfolio. We have deep capabilities in this area and look forward to a robust program focused on helping cystic fibrosis patients and patients suffering from other muco-obstructive disorders as quickly as possible.”

CF is estimated to affect 75,000 people globally. One of the main causes of difficulty in breathing and increased risk of infection is mucus congestion in the lungs. The ETD002 compound targets the underlying mechanisms of mucus congestion, and is expected to restore lung function, reduce the frequency of lung infections and improve patient quality of life. CF is caused by loss of function mutations in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) gene, that normally produces an anion channel highly expressed by the airway epithelium. Increasing anion conductance via CFTR modulation is a clinically validated approach for treating CF, however it is not currently available or effective for all people with CF.

In pre-clinical models, Enterprise has demonstrated that ETD002 enhances the activity of TMEM16A, an alternative anion channel present in airway epithelial cells, and by doing so increases anion and fluid flow into the airways, thinning the mucus and increasing its clearance. As TMEM16A potentiation is independent of the mutational status of CFTR, this makes the approach potentially applicable to all people with CF, and perhaps patients with non-CF muco-obstructive lung disease.

Moelis acted as financial advisor and Goodwin Procter acted as legal counsel to Enterprise Therapeutics.