C1r, C1s, kallikrein, factor XIIa, and factor XIa

These are serine proteases vital to the initiation and propagation of the classical complement pathway and the contact activation (kallikrein-kinin) system. C1r and C1s form part of the C1 complex that activates complement in response to immune complexes, sequentially cleaving C1s, C4, and C2[4][6][8]. Kallikrein and factors XIIa/XIa participate in both clotting and inflammation, activating each other and precursors to generate bradykinin (vasodilation) and trigger further complement and coagulation activity[5][7]. Their enzymatic activity is tightly regulated by endogenous inhibitors like C1-INH, and dysregulation may result in hereditary angioedema, thrombosis, or chronic inflammation[1][3][7].

Other names

C1r esteraseactivated complement C1rComplement component 1rActivated complement C1sComplement component 1sPlasma kallikreinKLKB1Activated Factor XIIHageman factor (activated)Activated Factor XI

Serine protease inhibition: Drugs and endogenous inhibitors (e.g., C1-INH) neutralize enzyme activity, block proteolytic activation Prevention of substrate cleavage: Stop activation of downstream components or formation of inflammatory mediators such as bradykinin