MAbs to Target IL-9 in Asthma

A new study has demonstrated that interleukin-9 (IL-9) regulates mast cells, which release mediators that cause the bronchi or bronchial airway to constrict. This airway hyperreactivity (AHR) impairs airflow into the lungs, a finding being used to develop a new therapy for asthma.

The findings were presented at the annual meeting of the American Thoracic Society in San Diego (CA, USA) in May 2005 by researchers from MedImmune, Inc. (Gaithersburg, MD, USA). Their data demonstrated that IL-9's effect on AHR depended on the proliferation and maturation of mast cells. In the study, overexpression of mast cells was associated with high lung levels of two mediators: cysteinyl leukotrienes (CystLTs) and prostaglandin E2 (PGE2), which are known to have direct effects on smooth muscle and have been previously associated with changes in intrinsic airway tone, manifesting as AHR.

IL-9 has been associated with symptoms of asthma, including mucous production, lung infiltration of inflammatory cells, and IgE production. MedImmune is evaluating the potential of monoclonal antibodies (MAbs) targeting IL-9 to treat or prevent symptomatic, moderate-to-severe, persistent asthma. The company has already completed a phase I dose-escalation, intravenously administered study in healthy adults with its lead anti-IL-9 MAb. Next, it plans to initiate a subcutaneously administered phase II dose-escalation study.

"We look forward to advancing the development of antibody therapies to block IL-9, which may have the potential to reduce mast cell-derived respiratory factors associated with asthma and other illnesses,” observed Anthony Coyle, Ph.D., senior director, research, at MedImmune.




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