HAE is caused by a mutation of the C1-inhibitor gene. Defective or missing C1-inhibitor permits activation of kallikrein, a protease that is responsible for liberating bradykinin from its precursor kininogen. An excess of bradykinin leads to fluid leakage from blood vessels, causing swelling of tissues typical of HAE.Ecallantide suppresses this pathogenetic mechanism by selectively and reversibly inhibiting the activity of plasma kallikrein.
Ecallantide (Kalbitor [previously, DX-88]; Dyax, Cambridge, MA) is a recombinant protein synthesized in the yeast Pichia pastoris. Ecallantide is a potent and specific inhibitor of plasma kallikrein. In phase 2 trials, symptoms of angioedema improved within 4 hours after treatment with ecallantide.18,21 The Evaluation of DX-88's Effects in Mitigating Angioedema (EDEMA) 3 trial was a randomized, placebo-controlled, phase 3 evaluation of ecallantide for the treatment of acute attacks of angioedema in patients with hereditary angioedema.
Ecallantide for the Treatment of Acute Attacks in Hereditary Angioedema
Hereditary angioedema (HAE) is a rare, debilitating, and potentially fatal disease characterized by acute attacks of swelling that can affect the abdomen/gastrointestinal tract, larynx, face, genitals, and extremities. Ecallantide is a novel plasma kallikrein inhibitor developed for the treatment of acute HAE attacks. Ecallantide provides relief of acute HAE attack symptoms, with rapidity of response commensurate with therapeutic needs for HAE attack locations.
Response time for ecallantide treatment of acute hereditary angioedema attacks
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