STOCKHOLM, Nov. 19, 2025 — Leads & Copy — BioArctic AB’s partner, Eisai, will present the latest findings on lecanemab (Leqembi®) at the Clinical Trials on Alzheimer’s Disease (CTAD) conference in San Diego, December 1-4.
Presentations will feature data on long-term treatment, estimated time savings over 10 years, safety, and potential benefits of subcutaneous administration of lecanemab for initiation dosing. Data on the effects of lecanemab on soluble amyloid-beta (Aβ) protofibrils and insights from real-world clinical practice studies, including the US ALZ-NET registry, will also be shared.
Key oral presentations include:
Continued treatment: New analyses on the benefits of continued therapy and estimated time savings over 10 years of lecanemab treatment based on Phase 3 clinical data (LB12, LB21) will be presented on Tuesday, Dec. 2, at 5:05 PM PT and Wednesday, Dec. 3, at 2:40 PM PT.
Subcutaneous initiation dosing: A late-breaking symposium, “Lecanemab Subcutaneous Formulation for Treatment Initiation in Early Alzheimer’s Disease: Optimizing Patient Care with a Potential New Option” (LB Symposium 2), will explore potential benefits of subcutaneous lecanemab initiation dosing as well as pharmacokinetic and safety findings on Wednesday, Dec. 3, from 3:10 – 3:50 PM PT.
Real-world experience: Findings from an interim analysis of a post-marketing observational study of lecanemab in Japan (OC30) will be shared on Thursday, Dec. 4, at 11:40 AM PT.
Mechanism-related: The effects of lecanemab treatment on soluble Aβ protofibrils in the Clarity AD clinical trial (OC5) will be reviewed on Tuesday, Dec. 2, at 1:40 PM PT.
A key lecanemab poster presentation will provide an overview of baseline characteristics and preliminary safety findings from a study of lecanemab in Alzheimer’s disease (AD) using the ALZ-NET registry during the poster session on Monday, Dec. 1, at 3:00 PM PT and Tuesday, Dec. 2, at 5:30 PM PT (Poster 055).
Additional lecanemab poster presentations include:
Characterizing Enrollment Patterns in a Preclinical Alzheimer’s Disease Trial (P006); Stability and Improvement in Early Alzheimer’s Disease with Lecanemab: Sub-analysis from a United States Multicenter, Retrospective Real-World Study (P049); Long-Term Benefit of Lecanemab in Patients with Low Baseline Amyloid: Estimation of Time Saved (P052); Patient, Care Partner, and Health Care Professional Acceptability of the Autoinjector for the Subcutaneous Delivery of Lecanemab in Patients with Early Alzheimer’s Disease in the US (P053); Real-World Clinical, Safety and Patient-Reported Outcomes of Treatment with Lecanemab in a New England Alzheimer’s Disease Center (P072); Comparison of Amyloid-related Imaging Abnormalities Risk for Lecanemab versus Donanemab and the Potential Implications (P096); Binding profiles of lecanemab and other amyloid-beta antibodies to amyloid-beta species isolated from Alzheimer’s disease brain (P292); C2N Eligibility, APOE Genotype Identification, Amyloid Confirmation Results from the AHEAD 3-45 Programme at Neuroclin Glasgow (P256); A Simulation of Long-Term Lecanemab Treatment Effect on the Alzheimer’s Disease Progression in ApoE4 Non-Carriers and Heterozygous Carriers (P278); Neuro-Dynamic Quantitative Systems Pharmacology (QSP) Model Predicts Increasing Benefits of Continued Lecanemab Treatment with Clarity AD 48-Month Data (P279); Clinical Outcomes and Patient Experience of Subcutaneous Lecanemab Administration from an Alzheimer’s Disease Treatment Center (P342); and Societal Cost and Efficiency Comparison of Subcutaneous vs Intravenous Lecanemab for Early Alzheimer’s Disease in the United States (P361).
Leqembi is the result of a collaboration between BioArctic and Eisai. BioArctic developed the antibody, and Eisai is responsible for clinical development, market approval applications, and commercialization. BioArctic has the right to commercialize Leqembi in the Nordic region with Eisai.
Lecanemab is approved in 51 countries and is under regulatory review in 9 countries. The U.S. FDA has initiated a rolling sBLA application for subcutaneous initiation dosing with Leqembi Iqlik.
Oskar Bosson, VP Communications and Investor Relations, can be reached at oskar.bosson@bioarctic.com or +46 704 107 180.
Protofibrils are thought to be the most toxic Aβ species contributing to brain damage in AD and play a major role in the cognitive decline of this progressive and devastating disease. It is believed that reducing protofibrils may reduce neuronal damage and cognitive impairment, potentially preventing the progression of AD.
Source: BioArctic AB
