What makes us different
Taligen’s product development programs are based on proprietary technologies which allow for the control and regulation of the complement system.
Science
Complement is a series of proteins which make up part of the innate immune system, an evolutionarily ancient system that acts as an “early warning system” to recognize tissue damage and to initiate the inflammatory process.
Once initiated, inflammation proceeds as a cascade, in which a single injury or insult triggers a complex and highly redundant process including the recruitment of inflammatory cells and release effector molecules such as cytokines and enzymes that lead to tissue damage (see figure below). Currently available anti-inflammatory agents target inflammation by blocking mediators far down in the inflammatory cascade (eg: IL-4, IL-13 etc), leaving many other inflammatory mediators unaffected. In contrast, controlling inflammation early in the inflammatory cascade by regulating complement activation results in the down-regulation of multiple downstream effectors of inflammation, thereby more completely controlling the inflammatory response.
Technology
Taligen’s technologies are directed at controlling the amplification or positive feedback loop of complement activation. Controlling only the amplification of complement regulates excessive activation of complement, which characterizes many disease processes, while low levels of physiologically important complement activation are thought to be maintained. Taligen’s lead technology is directed at inhibiting factor B, an essential component of the alternative pathway of complement and a critical step in the amplification of complement activation. Inhibition of factor B disrupts the amplification "loop", thereby dampening the inflammatory response. Taligen’s technologies are also intended to target complement inhibitors specifically to sites where excessive complement activation is occurring, thereby controlling inflammation at a specific tissue site.
Taligen’s technologies are unique because they do not completely block complement activation, but rather modulate it to prevent excessive activation while allowing low levels of physiologically important complement activation to proceed.
Recognition of tissue injury or insult by complement triggers multiple redundant effector mechanisms resulting in inflammation and tissue damage.