ChemoCentryx Reports Positive Phase I Results for CCX168, a Novel C5aR Antagonist, at the Annual American College of Rheumatology Mee... (e in a class by itself. We think t...)

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ChemoCentryx Reports Positive Phase I Results for CCX168, a Novel C5aR Antagonist, at the Annual American College of Rheumatology Meeting (ACR)

Date:11/10/2010

e in a class by itself. We think that this new agent has extraordinary potential in treating previously intractable conditions such as the devastating vasculitis seen in autoimmune diseases."

CCX168 Study Results and ANCA-Associated Vasculitis

In Phase I clinical trials CCX168 was safe and well tolerated, with excellent oral bioavailability and dose-proportional exposure increases in human subjects. Pharmacokinetic and pharmacodynamic data indicated that 30 to 50 mg of CCX168 given orally twice daily in humans results in greater than 90% C5aR coverage in blood at all times, and this is considered optimal for CCX168 evaluation in Phase II trials in vasculitis.

Supporting the Phase I data are results from a mouse model of anti-neutrophil cytoplasmic autoantibody (ANCA) associated glomerulonephritis (GN). In this study, human C5aR transgenic mice were employed, and ANCA kidney disease was profoundly inhibited by doses of CCX168 that are very similar to those achieved safely in the human Phase I studies.

CCX168 is a highly potent and very selective compound that specifically targets the receptor for the anaphylotoxin designated C5a, a component of the body's complement system and a potent driver of the inflammatory response associated with ANCA-associated vasculitis and other autoimmune disease. In ANCA disease, auto-antibodies lead to the activation and increased adhesiveness of neutrophils to endothelial cells that line the interior surfaces of blood vessels in the kidney and other organs. These adhering neutrophils accumulate inside the blood vessels and initiate an inflammatory cascade. Activation of the complement pathway occurs as a consequence, with production of C5a, one of the most potent pro-inflammatory mediators of the complement system. C5a, through binding to its receptor C5aR, induces expression of additional adhesion molecules and chemotactic factors, thus
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SOURCE ChemoCentryx, Inc.
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