Avacopan (CCX168) is a C5aR antagonist (IC50=0.1 nM) with selective and oral activity. Avacopan blocks the action of C5a and prevents the development of GN induced by anti-myeloperoxidase antibodies in a mouse model of AAV. Avacopan can be used to treat anti-neutrophil cytoplasmic antibody (ANCA)-related vasculitis.

C5aR:0.1 nM

METHODS: MCF7 cell line was used for cytotoxicity, scratch assay, and flow cytometry analysis to validate the in vitro anti-tumor activity of Beta-Tetralone.
RESULTS: Beta-Tetralone exhibited anticancer activity through dual targeting of MDM2 E3 ubiquitin ligase and Bcl-w anti-apoptotic protein.[1]
METHODS: Beta-Tetralone biotransformation was monitored using KCh 6651 of Mycobacterium sp. at a substrate concentration of 1 g/L.
RESULTS: Biotransformation of Beta-Tetralone yielded high yields of pure (S)-(-)-1,2,3,4-tetrahydro-2-naphthol.[2]

CCX168 (avacopan), an orally administered selective and potent C5aR inhibitor.?CCX168 blocked the C5a binding, C5a-mediated migration, calcium mobilization, and CD11b upregulation in U937 cells as well as in freshly isolated human neutrophils.?CCX168 retains high potency when present in human blood.?A transgenic human C5aR knock-in mouse model allowed comparison of the in vitro and in vivo efficacy of the molecule.?CCX168 effectively blocked migration in in vitro and ex vivo chemotaxis assays, and it blocked the C5a-mediated neutrophil vascular endothelial margination.?CCX168 was effective in migration and neutrophil margination assays in cynomolgus monkeys[1].