<unk>  works by binding to an enzyme within the plasma, kallikrein, to inhibit its activity. Kallikrein is a protease that functions to cleave kininogen, subsequently creating kininogen and bradykinin, a potent vasodilator. Patients suffer from hereditary angioedema (HAE) because of a deficiency or dysfunctional C1 inhibitor, which is an enzyme that regulates the activity of the kallikrein-kinin cascade. Poor regulation of the C1 inhibitor results in increased levels of kallikrein and subsequent proteolysis of kininogen. The proteolysis of the kininogen forces an upscaled production of bradykinin and kininogen within the patient. Increased bradykinin levels cause vasodilation, increased vascular permeability, and the succeeding angioedema and pain associated with hereditary angioedema attacks.
Lanadelumab
Ustekinumab
Olaratumab
Alirocumab
Evolocumab
Tralokinumab
Evinacumab
Emapalumab