The definitive guide to gene editing.
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Disease · Rare genetic disease

Hereditary Angioedema

A rare disorder causing sudden, unpredictable and sometimes life-threatening swelling attacks — and the setting for the first positive Phase 3 result for any in vivo gene-editing therapy.

Phase III liverin vivoKLKB1
Clinical research Being tested in people in registered clinical trials. Being in trials is not evidence that a treatment works or is safe.

Simple explanation

People with hereditary angioedema have attacks of severe swelling that arrive without warning — in the face, the limbs, the gut, or dangerously in the airway. The cause is a missing brake on one of the body's signalling systems, which lets a molecule called bradykinin accumulate and make blood vessels leak. An in vivo gene-editing treatment aims to remove a different protein in that pathway permanently, with a single infusion, so the attacks stop happening.

Go deeper

Hereditary angioedema most often results from SERPING1 mutations causing C1-esterase inhibitor deficiency, leading to unregulated kallikrein activity and excess bradykinin. Attacks are episodic, unpredictable and potentially fatal when laryngeal. Lonvoguran ziclumeran (lonvo-z, NTLA-2002) uses lipid-nanoparticle-delivered CRISPR-Cas9 to knock out KLKB1, which encodes prekallikrein, in hepatocytes — removing the substrate upstream of bradykinin generation rather than replacing the missing inhibitor.

Why this result matters beyond the disease

Intellia reported positive results from the global Phase 3 HAELO study of lonvo-z, described by the company as the first positive Phase 3 readout for an in vivo gene-editing therapy anywhere. Enrolment completed and a biologics licence application was signalled for the second half of 2026.

Whatever happens next, the significance is structural: it is the first evidence that editing a gene inside a living person's body can carry a treatment through a registrational trial. Every in vivo programme in every other disease is watching that regulatory path.

What patients use now

Existing treatment is effective and burdensome: C1-inhibitor replacement, the kallikrein inhibitor lanadelumab, berotralstat orally, and icatibant for acute attacks. Most require indefinite regular administration. A single-dose alternative would change the shape of the disease rather than only its severity — which is why this indication attracted an editing programme despite effective drugs already existing.

Sources

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Educational information only This page is a reference, not medical advice. Research and regulatory status change; check the last-updated date above and confirm anything important against the primary sources listed.