Coversin inhibits both C5 activation and binds tightly to the proinflammatory mediator LTB4. Akari believes that this unique dual mode of action may make Coversin a particularly effective inhibitor of inflammation in disease conditions where both C5 activation and LTB4 have a causative role in disease pathology, and in particular where C5 and LTB4 are upregulated independently of one another. Scientific evidence for the involvement of both inflammatory mediators in a wide range of diseases is emerging at an ever-increasing rate. Akari is undertaking work to identify conditions where combined inhibition of C5 and LTB4 may be of greatest benefit.
Akari plans to initiate a human trial in a disease where both C5 and LTB4 are believed to drive pathology in the second-half of 2017.