ChemoCentryx代理，ChemoCentryx中國代理，ChemoCentryx上海代理，ChemoCentryx北京代理，ChemoCentryx廣州代理，ChemoCentryx代理，ChemoCentryx

CCR2 Program

Our lead independent drug candidate, CCX140, which targets the chemokine receptor known as CCR2, has successfully completed a Phase II clinical trial in type 2 diabetics and is currently in two Phase II clinical trials in patients with diabetic nephropathy, a form of kidney disease. It is believed that CCR2 plays an important role in the inflammatory response associated with diseases such as diabetic nephropathy andType 2 diabetes. Studies have shown that CCR2 may also be implicated in the development of multiple sclerosis (MS) and inflammatory diseases of the cardiovascular system such as vascular restenosis. CCX140 is being developed as an orally delivered therapy for the treatment of diabetic nephropathy.

Data from preclinical studies indicate that CCX140 is a potent and selective antagonist of CCR2 which is required for monocytes to infiltrate the inflamed kidney, where they differentiate into macrophages. While CCX140 is not the first CCR2 antagonist to advance into clinical trials, it is chemically distinct from all publicly known antagonists of CCR2. We believe that CCX140 is unique in a number of ways, including its high selectivity for CCR2 relative to other chemokine receptors such as CCR5, even when the compound is given at high doses. We believe that CCX140 also distinguishes itself from other CCR2 antagonists in that it has been shown preclinically to be free of the cardiovascular safety signals associated with other CCR2 antagonists. CCX140 has been shown in a number of preclinical toxicology studies to be suitable for evaluation in humans for chronic use in diabetic nephropathy.

Based on the data from our preclinical studies to date, we believe that CCX140 has a favorable safety and pharmacokinetic profile.

ChemoCentryx completed a Phase II clinical trial in subjects with Type 2 diabetes mellitus. A total of 159 subjects, on stable doses of metformin, were randomized to receive placebo, 5mg CCX140, 10mg CCX140, or 30mg pioglitazone hydrochloride once daily for 4 weeks. Fasting plasma glucose decreased dose-dependently with CCX140 treatment. Hemoglobin A1c changes from baseline to Week 4 were -0.09%, -0.09%, -0.23% (p= 0.045 vs. placebo), and -0.13% for the placebo, 5mg, 10mg CCX140, and pioglitazone groups, respectively. Plasma CCL2 and circulating monocyte levels were unchanged by CCX140 treatment. CCX140 was generally well tolerated and safe in this study.

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