Synthesis and evaluation of small molecule C5a receptor antagonists

ORGN 278

J. Kent Barbay, kbarbay@prdus.jnj.com1, Mieke Buntinx2, Yong Gong1, Jian Li1, Concha Claes2, Pamela J. Hornby1, Guy van Lommen2, Jean van Wauwe2, and Wei He1. (1) Johnson & Johnson Pharmaceutical Research & Development, L.L.C, Welsh & McKean Roads, P.O. Box 776, Spring House, PA 19477-0776, (2) Johnson & Johnson Pharmaceutical Research & Development, L.L.C., Beerse, Belgium
Activation of the complement system plays a role in the normal inflammatory and immune response. In response to certain stimuli a proteolytic cascade is initiated, resulting in formation of bioactive peptides including C5a. This peptide binds to a specific G-protein coupled receptor (C5aR) on target cells (neutrophils, monocytes, macrophages, and others), recruiting them to sites of inflammation and stimulating release of additional pro-inflammatory mediators. Antagonists of C5aR are sought as potential therapeutic agents for autoimmune and inflammatory conditions involving over-activation of the complement system. The discovery, synthesis, and optimization of a series of non-peptidic, small molecule C5aR antagonists will be disclosed. Data pertaining to antagonism of C5a binding and functional activity, early ADME properties, rat pharmacokinetics, and species selectivity of the compounds will be presented.