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
Currently, all HAE therapies are either injected on an acute basis or infused prophylactically. Neither therapy is ideal, and it can take time for HAE patients to learn what works best for them.
Our Phase 1 study for KVD900 suggested the compound displays a profile well-suited for use as an oral, on-demand therapy for acute attacks, with a combination of rapid uptake into the plasma and high plasma concentrations.
In addition to KVD900, we continue to develop additional candidates for the HAE portfolio. We believe KalVista can design oral programs to satisfy other segments of the HAE market with high unmet need, such as prophylactic therapy. We anticipate adding at least one more candidate to the clinic this year and potentially more molecules in 2019.
We’re excited by the possibility of developing one or more best-in-class oral therapies for HAE and an alternative for HAE patients facing repeated angioedema attacks. We look forward to your interest as our research continues.