Many organ systems and tissues can be compromised by fibrosis and inflammation. Research into the activity of MK2, complemented by successful experiments using Moerae’s selective MK2 inhibitors, suggests a potential role for MK2 in diseases characterized by fibrotic and/or inflammatory activity. Compelling preclinical data with MK2 inhibitors have been generated in models relevant to fibrotic lung disease, obstructive lung disease, fibrosis following myocardial infarction, and acute surgical scar and adhesion formation, as well as vascular graft indications.

Idiopathic Pulmonary Fibrosis (IPF) is a relentlessly progressive and severe disease characterized by excessive scarring and destruction of lung tissue. Activation of the TGF-β, p38 stress activated kinase pathway has been widely implicated in the disease. Activated MK2 is upregulated in human lung tissue in patients with IPF, but is not in individuals who are not afflicted with IPF. MK2 directly activates molecules that stimulate fibrotic and inflammatory
responses.

An inhaled delivery MMI-0100, Moerae’s lead MK2 inhibitor, is being developed for pulmonary disorders characterized by fibrosis and inflammation, such as: IPF, Chronic Obstructive Pulmonary Disease (COPD) and severe asthma.