Fig. 1
From: Complement mediators: key regulators of airway tissue remodeling in asthma
Model shows active mediators of the complement cascade during inflammation in airway asthma. Further, it highlights activation of inflammatory cells (Basophils, PMNs and Macrophages) through complement receptor binding and downstream release of inflammatory mediators. As shown, all these mediators contribute in tissue damage and remodeling. APL-1 and APL-2, are derivatives of Compstatin, bind to and inhibit complement activation at the C3 level, thus blocking all major effector pathways of complement activation. (Both APL-1 and APL-2 are under clinical trials).