/Editas Medicine Presents EDIT-401 Preclinical Data Demonstrating Robust Reductions in LDL-C, Lp(a), and ApoB in Non-Human Primates at the 94th European Atherosclerosis Society Congress
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Editas Medicine Presents EDIT-401 Preclinical Data Demonstrating Robust Reductions in LDL-C, Lp(a), and ApoB in Non-Human Primates at the 94th European Atherosclerosis Society Congress

GlobeNewswire
2026/05/26Health

Editas Medicine Presents EDIT-401 Preclinical Data Demonstrating Robust Reductions in LDL-C, Lp(a), and ApoB in Non-Human Primates at the 94th European Atherosclerosis Society Congress

Single dose of EDIT-401 achieved ~90% or greater mean reductions in LDL-C, Lp(a), and ApoB in non-human primates

Data reinforce differentiated LDLR upregulation approach with rapid, dose-dependent effects on multiple atherogenic lipoproteins

Company on track to submit CTN by mid-2026 for EDIT-401 and achieve early in vivo human proof-of-concept data by the end of 2026

CAMBRIDGE, Mass., May 26, 2026 — Editas Medicine, Inc. (Nasdaq: EDIT), a pioneering gene editing company focused on developing transformative medicines for serious diseases, presented new preclinical data for EDIT-401, its lead in vivo development candidate, in an oral presentation at the 94th European Atherosclerosis Society (EAS) Congress in Athens, Greece on May 25, 2026. In the data presented, EDIT-401 achieved robust reductions in LDL-cholesterol (LDL-C), lipoprotein(a) (Lp(a)), and apolipoprotein B (ApoB) in non-human primates (NHPs), supporting its potential as a best-in-class medicine for hyperlipidemia.

Key EDIT-401 preclinical data in NHPs presented include:

  • A single dose of EDIT-401 achieved ≥90% mean reduction in LDL-C, with rapid and dose-dependent effect.
  • EDIT-401 achieved rapid, dose dependent ~90% mean reduction in Lp(a), an independent risk factor for atherosclerotic cardiovascular disease (ASCVD).
  • EDIT-401 achieved rapid, dose-dependent ~90% mean reduction in ApoB, a key measure of total plaque-causing cholesterol particles and predictive measure for ASCVD.
  • Reductions in LDL-C, Lp(a), and ApoB were highly correlated, supporting a unified mechanism facilitated by LDLR upregulation.

“The consistent reductions of ~≥90 percent with EDIT-401 in LDL-C, Lp(a), and ApoB observed in these preclinical studies highlight the transformative potential of our LDLR upregulation approach to address multiple drivers of cardiovascular risk, including residual risk beyond LDL-C alone,” said Linda C. Burkly, Ph.D., Executive Vice President and Chief Scientific Officer, Editas Medicine. “These robust and consistent reductions across multiple atherogenic lipoproteins with a single dose further support EDIT-401 as a potentially best-in-class in vivo gene editing medicine for people living with hyperlipidemia.”

The abstract can be accessed on the EAS website, and the presentation is available on the Editas Medicine website.

Editas continues to advance preclinical studies for EDIT-401, including an ongoing Good Laboratory Practice (GLP) toxicology study in NHPs. Interim results from this study demonstrated EDIT-401 was well-tolerated with no adverse clinical observations, no notable treatment-related liver enzyme elevations, and no liver histopathology findings in non-GLP toxicology at the therapeutically relevant dose of 1.5 mg/kg.

The Company also received positive pre-IND feedback from the U.S. Food and Drug Administration (FDA) on its nonclinical package, CMC plans, and study design to support an Investigational New Drug Application (IND). The Company plans to submit a Clinical Trial Notification (CTN) in Australia to the Therapeutic Goods Administration (TGA) by mid-2026 to initiate a first-in-human clinical trial of EDIT-401 in patients with Heterozygous Familial Hypercholesterolemia (HeFH) later this year, and is on track to have early in vivo human proof-of-concept data for EDIT-401 by the end of 2026.

About Editas Medicine

As a pioneering gene editing company, Editas Medicine is focused on translating the power and potential of CRISPR genome editing systems into a robust pipeline of transformative in vivo medicines for people living with serious diseases around the world. Editas Medicine aims to discover, develop, manufacture, and commercialize durable, precision in vivo gene editing medicines for a broad class of diseases. Editas Medicine is the exclusive licensee of Broad Institute’s Cas12a patent estate and Broad Institute and Harvard University’s Cas9 patent estates for human medicines. For the latest information and scientific presentations, please visit www.editasmedicine.com.

Summary

Single dose of EDIT-401 achieved ~90% or greater mean reductions in LDL-C, Lp(a), and ApoB in non-human primates