Abstract
Plasma kallikrein (pKal) is a serine protease responsible for generating the vasodilator bradykinin, and is mainly regulated by C1 inhibitor (C1-INH). Patients with hereditary angioedema (HAE) have deficient levels of functional C1-INH, leading to unpredictable attacks of debilitating edema via dysregulated pKal-mediated bradykinin generation. Inhibition of pKal is a viable therapeutic option for HAE, as demonstrated by the efficacy of ecallantide, a specific pKal inhibitor, for treatment of acute HAE attacks.
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