NEW YORK – Intellia Therapeutics on Thursday said it is laying off employees as part of a plan to "streamline" operations and focus on strategic priorities.
Cambridge, Massachusetts-based Intellia, a gene-editing company cofounded by CRISPR pioneer Jennifer Doudna in 2014, said that following an internal strategic review, it has opted to reduce its workforce by about 15 percent and pause some "exploratory research-stage programs," though it did not name which programs.
Intellia ended 2023 with about $1 billion in cash, cash equivalents, and marketable securities, with cash expected to fund operations into mid-2026.
Intellia also on Thursday outlined its strategic priorities through 2026, including completion of a Phase III study and biologics license application submission to the US Food and Drug Administration for NTLA-2002, an in vivo gene-editing therapy candidate for hereditary angioedema, a genetic disorder characterized by swelling episodes. NTLA-2002 is designed to stop expression of the KLKB1 gene that is needed to produce kallikrein, a reduction in which is associated with fewer swelling attacks. The company expects to launch a pivotal Phase III study of the therapy in the second half of this year, dependent on regulatory feedback.
The firm meanwhile said it is on track to dose the first patient in a pivotal Phase III trial of NTLA-2001, its lead investigational therapy and a candidate for transthyretin amyloidosis with cardiomyopathy, in the first quarter of this year, with plans to complete patient enrollment by 2026. NTLA-2001 is an in vivo gene-editing therapy designed to correct the TTR gene. Mutations there cause the liver to produce abnormal proteins that misfold and build up, causing the rare, progressive disorder.
Also in 2024, Intellia said it expects to dose the first patient in a Phase I study of the in vivo gene-editing candidate NTLA-3001 as a treatment for alpha-1 antitrypsin deficiency (AATD)-associated lung disease, for which it has submitted a clinical trial application for a first-in-human study. The gene-editing therapy aims to insert a functional copy of the SERPINA1 gene, which is perturbed in AATD.