Understanding HAE
A rare but potentially life-threatening disease, HAE is most frequently caused by a genetic disorder where the protein C1-inhibitor esterase is inadequately synthesized or dysfunctional.
C1-inhibitor is a critical mediator of inflammation. With inadequate levels or malfunctioning C1-inhibitor, excess plasma kallikrein can become activated, leading the body to produce the vasopeptide bradykinin in excessive amounts, which in turn leads to increased vascular permeability and sudden onset of angioedema.
Angioedema attacks can occur in the limbs, face, gastrointestinal tract and/or airways. Laryngeal episodes can happen to any patient and are potentially life-threatening.
Ongoing R&D
In addition to sebetralstat, KVD824 is our twice-daily oral plasma kallikrein inhibitor for prevention of HAE attacks. The Phase 2 KOMPLETE clinical trial is intended to evaluate the efficacy and safety of KVD824 as a prophylactic treatment for HAE.
We are excited by the possibility of developing multiple oral therapies for HAE as options for patients. We look forward to your interest as our research continues.