C1INH exerts an inhibitory effect on several proteases (target proteases) of the contact and complement systems. The effect of conestat alpha on target proteases such as activated C1s, kallikrein, factor XIIa and factor XIa, was assessed in vitro. Inhibition kinetics were found to be comparable with those observed for plasma-derived human C1INH. Patients with hereditary angioedema (HAE) have a heterozygous deficiency of the plasma protein C1INH. As a result they may suffer from uncontrolled activation of contact and complement systems, with formation of inflammatory mediators, which clinically becomes manifest as the occurrence of acute angioedema attacks.