Insmed Announces Worldwide License Agreement with AstraZeneca for Oral DPP1 Inhibitor
Bronchiectasis increases susceptibility to nontuberculous mycobacterial (NTM) lung disease, and up to 50 percent of patients with bronchiectasis may also have an active NTM
infection. NTM lung disease is a rare and often chronic infection that is capable of causing irreversible lung damage and can be fatal.
"With this transaction we have added a highly complementary therapy that aligns perfectly with our established expertise in rare pulmonary diseases," said
"We are pleased to be working with
In a phase 1 study of healthy volunteers AZD7986 was well tolerated and demonstrated inhibition of the activity of the NSP neutrophil elastase in a dose and concentration dependent manner. In preclinical studies, AZD7986 was shown to effectively and reversibly inhibit DPP1 and the activation of NSPs within maturing neutrophils.
Under the terms of the agreement,
INS1007 is a small molecule, reversible inhibitor of dipeptidyl peptidase I (DPP1), an enzyme responsible for activating neutrophil serine proteases (NSPs) in neutrophils when they are formed in the bone marrow. Neutrophils are the most common type of white blood cell and play an essential role in pathogen destruction and inflammatory mediation. Neutrophils contain three NSPs (neutrophil elastase, proteinase 3, and cathepsin G) that have been implicated in a variety of inflammatory diseases. In chronic inflammatory lung diseases, neutrophils accumulate in the airways and result in excessive active NSPs that cause lung destruction and inflammation. INS1007 may decrease the damaging effects of inflammatory diseases, such as non-cystic fibrosis bronchiectasis, by inhibiting DPP1 and its activation of NSPs.
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Insmed Incorporated: Susan MescoHead of Investor Relations 908-947-4326
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