Quantcast

ChemoCentryx Reports Positive Phase I Study Results for CCX354 at the Annual European Congress of Rheumatology (EULAR)

June 17, 2010

MOUNTAIN VIEW, Calif., June 17 /PRNewswire/ — ChemoCentryx, Inc., today announced that it reported positive Phase I results for its novel drug candidate CCX354 at the Annual European Congress of Rheumatology (EULAR). CCX354 is the Company’s orally-active small molecule drug candidate designed to specifically target the CCR1 chemokine receptor for the treatment of patients with rheumatoid arthritis (RA). Data demonstrating that CCX354 was safe and well tolerated with a clear pharmacokinetic to pharmacodynamic relationship were presented today by Daniel Dairaghi, Ph.D., Director, Molecular Pharmacology of ChemoCentryx, in a poster presentation entitled “A Novel CCR1 Antagonist CCX354-C for Rheumatoid Arthritis” in Rome, Italy. CCX354 is currently in Phase II clinical trials for the treatment of patients with RA.

Study results showed that CCX354 was well tolerated and displayed a linear dose-exposure profile in single-dose and multiple-dose Phase I studies in healthy volunteers. Plasma levels far exceeded those required for adequate receptor blockade. High levels of receptor coverage (>90%) at the 12-hour time point were achieved after a single dose of 100 mg of CCX354.

“Our data and the reports of other labs now show that a high degree of CCR1 receptor coverage is essential to achieve a therapeutic effect in inflammatory diseases such as RA,” stated Thomas J. Schall, Ph.D., President and Chief Executive Officer of ChemoCentryx. “We are very pleased that this study demonstrated the unique ability of CCX354 to selectively and sufficiently block the CCR1 receptor – objectives that other molecules in this class have been unable to achieve to date. As such, we believe our CCR1 antagonist is best-in-class, with the potential to offer an effective drug for the treatment of patients with RA.”

CCX354 is a highly potent and selective antagonist of CCR1, a chemokine receptor that drives the recruitment of inflammatory monocytes and macrophages into the joints of patients with RA. By selectively blocking the CCR1 receptor, CCX354 is designed to reduce the infiltration of inflammatory cells into the joints of RA patients and inhibiting the inflammation, swelling, pain, and associated joint destruction while minimizing the potential for off-target effects, thus providing a wider therapeutic window than currently approved therapies.

About Rheumatoid Arthritis and CCX354

Rheumatoid arthritis (RA) is a chronic and debilitating inflammatory disease which causes pain, stiffness, swelling and limitation in the motion and function of multiple joints. RA is estimated to affect more than two million people in the U.S. and is a leading cause of morbidity and work disability. The exact cause of RA is unknown, but is believed to reflect the body’s immune system attack on the synovium, the tissue that lines the joints. Although treatment options have improved over the last 25 years, there is no cure and still no single therapy that is effective for all patients. Treatment of RA can be divided into Disease-Modifying Antirheumatic Drugs (DMARDs), anti-inflammatory agents and analgesics, addressing a $10 billion market.

During the development and progression of RA, the recruitment of inflammatory cells, both innate and adaptive, into affected joints plays a key role in the inflammatory process and the ensuing joint destruction. There is strong evidence implicating CCR1 in the pathology of RA. ChemoCentryx’s approach to specifically target the CCR1 receptor with CCX354 represents a new mechanism of action in the potential treatment of RA. CCX354 falls within the scope of the strategic alliance with GlaxoSmithKline through its Center of Excellence for External Drug Discovery (CEEDD).

About ChemoCentryx

ChemoCentryx, Inc., is a clinical-stage biopharmaceutical company focused on discovering, developing and commercializing orally-administered therapeutics that target the chemokine and chemoattractant systems in order to treat autoimmune diseases, inflammatory disorders and cancer. The chemokine system is a biological network that regulates inflammation via a collection of secreted chemokine molecules, or ligands, and their specific cell surface receptors. Based on its proprietary drug discovery and drug development platform, ChemoCentryx has internally generated multiple clinical and preclinical-stage programs, each targeting distinct chemokine and chemoattractant receptors with different small molecule compounds. ChemoCentryx’s lead compound, Traficet-EN, a specific CCR9 antagonist, completed a Phase II/III multi-national clinical trial, called PROTECT-1, in patients with moderate-to-severe Crohn’s disease, where it demonstrated the ability to induce a clinical response and to maintain clinical remission over the course of the trial. In addition, CCX025, also a CCR9 antagonist, has successfully completed a Phase I clinical program. Other clinical programs include CCX140, which targets the CCR2 receptor, in Phase II clinical development for the treatment of type 2 diabetes mellitus; CCX354, a CCR1 antagonist in a Phase II clinical trial for the treatment of rheumatoid arthritis; and CCX168, a C5aR antagonist, in Phase I clinical development. ChemoCentryx also has several programs in preclinical development. ChemoCentryx is privately held. For more information, please refer to www.chemocentryx.com.

Certain statements in this press release may constitute “forward-looking statements”. These statements are made on the basis of current expectations, forecasts and assumptions that involve risks and uncertainties, including, but not limited to, economic, competitive, governmental and technological factors outside of our control, that may cause our business, strategy or actual results to differ materially from those expressed or implied. We do not intend, and undertake no obligation, to update any forward-looking statements, whether as a result of new information, future events or otherwise.

SOURCE ChemoCentryx, Inc.


Source: newswire



comments powered by Disqus