UK-based AstraZeneca has initiated the Phase III programme for tralokinumab, a potential treatment for patients with severe, inadequately controlled asthma.
Tralokinumab is an investigational human monoclonal antibody and is developed by the company's global biologics research and development arm MedImmune.
The Phase III programme is designed to evaluate the safety and effectiveness of tralokinumab in reducing the rate of asthma exacerbations (AER) in adults and adolescents with severe, inadequately controlled asthma, despite receiving inhaled corticosteroids plus long-acting ß2-agonist.
In the programme, the effects of tralokinumab will also be evaluated on lung function, patient-reported asthma symptoms and quality of life, and it will also investigate whether potential clinical biomarkers could identify patients who are more likely to respond to the drug.
AstraZeneca Global Medicines Development unit vice-president and head of Inflammation, Neuroscience and Respiratory Bill Mezzanotte said: " We are pleased to begin the tralokinumab Phase III programme in severe asthma, further strengthening the breadth of our portfolio in respiratory disease, one of AstraZeneca's core therapy areas.
"Patients with severe asthma currently have limited treatment options and need more effective therapies to control their disease.
"The development of tralokinumab underscores our commitment to a personalised treatment approach for these patients, to improve their lives.
"Severe asthma is highly heterogeneous; we are working to better understand patient subtypes, identify potential biomarkers, and tailor therapies to cellular and molecular phenotypes to achieve the best clinical outcomes."
The start of the Phase III programme is based on results from a Phase IIb trial conducted by MedImmune.
Tralokinumab is an investigational human monoclonal antibody which potently and selectively neutralises interleukin-13 (IL-13).
IL-13 is a key cytokine, which is believed to contribute to the onset of severe and frequent asthma attacks, impaired lung function and other debilitating asthma symptoms by driving inflammation, airway hyper-responsiveness and excessive mucus production.