Millennium, in collaboration with Aventis Pharma, is developing a range of therapies targeted to the disease process underlying inflammatory diseases. Researchers are working to identify mechanisms of action common to multiple inflammatory diseases, and to merge new discoveries about the origins of inflammatory conditions with current models in our extensive knowledge base. With an accurate road map of the inflammatory pathways involved, Millennium scientists concentrate on developing therapies directed against specific points within the series of events that lead to inflammation, potentially addressing the root cause of diseases and their consequences, rather than symptoms alone.

Millennium scientists are investigating several new promising strategies for treat inflammatory diseases. Our pipeline of investigational drugs includes:

MLN02, a humanized monoclonal antibody targeted to a T-cell integrin that is currently being investigated in phase II clinical trials in patients with inflammatory bowel diseases (Crohn's disease and ulcerative colitis).

MLN1202, another humanized monoclonal antibody, in this case targeting the chemokine receptor CCR2, which appears to play an important role in recruiting monocytes and T cells to sites of inflammation. MLN1202 is being developed as a potential treatment for patients with rheumatoid arthritis, and is in phase I clinical trials.

MLN3897, also known as CCR1, is a chemokine receptor expressed on the surface of various cells in the immune system, including macrophages and T-lymphocytes, that participate in inflammatory responses. Several different chemokines can bind to CCR1, including macrophage-inflammatory protein 1-alpha (MIP-1alpha) and RANTES. CCR1 thus plays a role in the recruitment of important inflammatory cells in response to a variety of different signals. MLN3897, the most advanced of these molecules is in Phase I clinical testing, and is being developed as part of our collaboration with Aventis.

For more information, refer to the R&D section of this website.