Forest Program

In March 2004 we entered into a collaboration with Forest Laboratories to develop and commercialize novel small molecule therapeutics for autoimmune and inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. The collaboration focuses on CCR1, a specific chemokine receptor involved in inflammation. As part of this agreement, we have maintained the option to participate in the co-development and co-promotion of these products, allowing for the potential increase in royalties and revenues from sales, as well as the continued build out of our development capabilities.

At the center of our collaborative agreement is the CCR1 chemokine receptor. This receptor is one which interacts with members of the subclass of "CC" chemokines. CC chemokines are responsible for activating a variety of immune cells, including monocytes, macrophages, lymphocytes and others implicated in a number of chronic inflammatory diseases. Using high throughput screening technologies exclusive to ChemoCentryx, we have identified small molecule antagonists that block CCR1-associated chemokines from activating migration by CCR1 bearing leukocytes that can attack tissues and cause the autoimmune-associated inflammation underlying rheumatoid arthritis (RA). Working closely with Forest, we are advancing a promising small molecule candidate that would safely block the CCR1 receptor without causing generalized immune system suppression. In vivo studies in which CCR1 is blocked have shown that treatment prevents inflammation, reduces the development of joint destruction as well as the severity of symptoms.

Rheumatoid Arthritis (RA)

Rheumatoid arthritis is a chronic disease afflicting an estimated two million people in the United States alone. The disease is characterized by symmetrical pain and swelling of the small joints of the hands and feet. As RA progresses, it can also result in cartilage and bone destruction leading to permanent deformities. The exact cause of autoimmune diseases such as RA is unknown.

Current therapies for RA such as nonsteroidal anti-inflammatory drugs (NSAIDS) and disease-modifying anti-rheumatic drugs (DMARDS) relieve symptoms by suppressing inflammatory response and thereby preserving joint function, but their usefulness may be limited by considerable long-term toxicities. TNF agonists, which come closer to acting on the root cause of RA, have recently become available. These drugs more effectively help a portion of patients; however, anti-TNF therapies are only available by injection and are very expensive. As a result of the limitations in current therapeutic options, there is significant need for a highly effective, disease modifying small molecule medicines for RA that may be taken orally and may be manufactured at relatively low costs.

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