National Institute on Aging

STOCKHOLM, June 30, 2026 /PRNewswire/ -- BioArctic AB's (publ) (NASDAQ STOCKHOLM: BIOA B) partner Eisai will present new clinical and real-world evidence on lecanemab (Leqembi®) at the Alzheimer's Association International Conference (AAIC) in London, July 12-15, including data on its subcutaneous formulation, long-term use across diverse patient groups, maintenance dosing, and at-home administration. BioArctic will also participate in the Plenary Session "Prevalence of Alzheimer's Disease Pathology in the Community," taking place on 14 July (11:00am to 12:15pm BST). In a presentation called "Outcomes of Clinical Progression for Clinical Trials of People with Neuronal Synucleinopathy with Cognitive Impairment", strategies for assessing clinical progression in people with cognitive impairment related to α-synuclein pathology will be discussed, primarily across Parkinson's disease (PD), Parkinson's disease dementia (PDD), and dementia with Lewy bodies (DLB). Key oral lecanemab presentations at AAIC Subcutaneous treatment data: On Sunday, July 12, as part of the "Developing Topics Session: Lecanemab Subcutaneous Formulation in Early Alzheimer's Disease: Emerging Clinical Evidence and Practical Use Considerations" (4:15-5:45pm BST), emerging clinical evidence and practical use considerations for the subcutaneous formulation of lecanemab will be presented, including clinical trial and real-world patient experience. LEADER study – real-world evidence from US clinical practice: On Tuesday, July 14, as part of the "Featured Research Session: Lecanemab Three Years Post Approval: A Comprehensive Multicenter, Real-World, Retrospective Study (LEADER) in Diverse US Clinical Settings" (4:15-5:45pm BST), data from the LEADER study evaluating real-world lecanemab use in diverse US clinical settings three years post-approval, will be presented. It will include results on maintenance dosing with IV treatment every four weeks and the first reported findings of at-home subcutaneous administration. Preclinical Alzheimer's Disease: Presentations on the Phase 3 AHEAD 3-45 study in preclinical Alzheimer's Disease will highlight progress of the trial, including updates on participant retention and engagement. Additional oral presentations Poster presentations on lecanemab Poster viewing time is set from 7:30am – 4:15pm BST on the date of presentation Eisai-Sponsored Symposium Symposium is intended for HCPs only The information was released for public disclosure, through the agency of the contact person below, on June 30, 2026, at 8am CET. For further information, please contact: Oskar Bosson, Chief Investor Relations & Communications Officer E-mail: [email protected] Telephone: +46 704 107 180 Jenny Ljunggren, External Communications and Investor Relations Manager E-mail: [email protected] Telephone: +46 76 013 86 08 About Leqembi ® (lecanemab) Leqembi is the result of a strategic research alliance between BioArctic and Eisai. It is a humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). Leqembi is approved in 53 countries and is under regulatory review in 6 countries. Following the initial phase with treatment every two weeks for 18 months, intravenous (IV) maintenance dosing with treatment every four weeks is approved in 8 countries, including the United Kingdom, China, the US and Japan, and applications have been filed in 12 countries and regions. In the US, Leqembi Iqlik™ is approved for subcutaneous dosing with an autoinjector for maintenance treatment of early Alzheimer's disease. In November 2025, a new drug application for subcutaneous formulation of Leqembi was submitted in Japan. In December 2025, Leqembi was included in the "Commercial Insurance Innovative Drug List", recently introduced by the National Healthcare Security Administration (NHSA) of China. In January 2026, Eisai's supplemental Biologics License Application (sBLA) regarding a subcutaneous starting dose with Leqembi Iqlik was granted Priority Review by the US FDA. The sBLA has been assigned an extended PDUFA date of August 24, 2026. In January 2026, the Biologics License Application for subcutaneous formulation of Leqembi was accepted in China and in February, the application was designated for priority review. Since July 2020, Eisai's Phase 3 clinical study (AHEAD 3-45) with lecanemab in individuals with preclinical Alzheimer's disease meaning they are clinically normal and have intermediate or elevated levels of amyloid in their brains, is ongoing. The study was fully recruited in October 2024. AHEAD 3-45 is a four-year study conducted as a public-private partnership between Eisai, Biogen and the Alzheimer's Clinical Trial Consortium that provides the infrastructure for academic clinical trials in Alzheimer's disease and related dementias in the US, funded by the National Institute on Aging, part of the National Institutes of Health. Since January 2022, the Tau NexGen clinical study for Dominantly Inherited Alzheimer's disease (DIAD), that is conducted by Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU), led by Washington University School of Medicine in St. Louis, is ongoing and includes lecanemab as the backbone anti-amyloid therapy. About the collaboration between BioArctic and Eisai Since 2005, BioArctic has a long-term collaboration with Eisai regarding the development and commercialization of drugs for the treatment of Alzheimer's disease. The most important agreements are the Development and Commercialization agreement for the lecanemab antibody, which was signed 2007, and the Development and Commercialization agreement for the antibody lecanemab back-up for Alzheimer's disease, which was signed 2015. In 2014, Eisai and Biogen entered into a joint development and commercialization agreement for lecanemab. Eisai is responsible for the clinical development, application for market approval and commercialization of the products for Alzheimer's disease. BioArctic has the right to commercialize lecanemab in the Nordic region and is currently preparing for commercialization in the Nordics together with Eisai. BioArctic has no development costs for lecanemab in Alzheimer's disease and is entitled to payments in connection with sales milestones as well as royalties on global sales. About BioArctic AB BioArctic AB (publ) is a Swedish research-based biopharma company focusing on innovative treatments that can delay or stop the progression of neurodegenerative diseases. The company invented Leqembi® (lecanemab) – the world's first drug proven to slow the progression of the disease and reduce cognitive impairment in early Alzheimer's disease. Leqembi has been developed together with BioArctic's partner Eisai, who are responsible for regulatory interactions and commercialization globally. In addition to Leqembi, BioArctic has a broad research portfolio with antibodies against Parkinson's disease and ALS as well as additional projects against Alzheimer's disease. Several of the projects utilize the company's proprietary BrainTransporter™ technology, which has the potential to actively transport antibodies across the blood-brain barrier to enhance the efficacy of the treatment. BioArctic's B share (BIOA B) is listed on Nasdaq Stockholm Large Cap. For further information, please visit . This information was brought to you by Cision The following files are available for download: 21% more press release views with Request a Demo

A common brain protein may be giving Alzheimer’s disease an unexpected way to spread, carrying toxic Tau proteins from damaged neurons into healthy ones. By blocking these harmful protein packages before they reach new cells, researchers believe it may one day be possible to slow the disease's relentless progression.Alzheimer's disease is marked by the buildup of a toxic protein called Tau, which damages and eventually kills brain cells. As this harmful protein moves into new areas of the brain, the disease progresses, leading to worsening memory loss and cognitive decline. Now, researchers have uncovered an unexpected player in that process. In a study of mice, they found that a brain protein called Arc, which normally helps neurons communicate, also appears to help toxic Tau spread from diseased brain cells to healthy ones. The discovery points to a possible new strategy for slowing Alzheimer's disease. Rather than trying to eliminate Tau entirely, future treatments might stop it from reaching healthy brain cells in the first place. "I'm excited by the fact that we've identified a new way of potentially stopping the progression of Alzheimer's disease," says Jason Shepherd, PhD, professor of neurobiology at University of Utah Health and senior author of the study. The findings were published in the journal Cell. How Arc Helps Toxic Tau Travel To investigate how Alzheimer's spreads, the researchers compared mouse models of the disease with and without the Arc protein. Their experiments showed that Arc is essential for moving toxic Tau between neurons. Under normal conditions, Arc plays an important role in brain function. The protein packages itself inside tiny membrane bound sacs known as extracellular vesicles (EVs), which travel from one neuron to another carrying important cellular signals. The researchers found that toxic Tau can exploit this natural communication system. By attaching itself to Arc inside these microscopic vesicles, Tau is able to travel from an unhealthy neuron into a healthy one, where it can continue spreading disease. Tau Turns Healthy Brain Cells Toxic Every neuron contains Tau, but in Alzheimer's disease the protein begins clumping into large, sticky tangles that interfere with the cell's internal transport system before eventually killing the neuron. Mitali Tyagi, PhD, postdoctoral research associate at Washington University in St. Louis and first author of the study, who conducted the research while a neuroscience graduate student in the Shepherd Lab at U of U Health, compares these tangles to "glue monsters." "They glue together and block transportation within the neuron," Tyagi explains. "But they can break down into smaller glue monsters, called Tau seeds, which can then get transferred to a new neuron. And once this Tau seed comes into contact with healthy Tau, it is able to corrupt it. So, the pathology starts all over again in a healthy neuron." In the Alzheimer's mouse model, the team found extracellular vesicles containing both Arc and "sticky" Tau in brain tissue. These vesicles were capable of entering healthy cells and triggering the formation of new Tau tangles. The picture changed dramatically when Arc was removed. Mice lacking the protein had extracellular vesicles containing very little Tau, and the disease could no longer spread effectively to neighboring brain cells. "When we removed Arc, we saw that the transfer of Tau was severely, severely reduced," Tyagi says. "It was almost gone." Arc Has Both Harmful and Helpful Effects Although blocking Arc might sound like an obvious treatment strategy, the researchers discovered that the protein also performs an important protective role during the early stages of disease. By helping neurons expel excess toxic Tau, Arc appears to allow damaged cells to survive longer. In mice without Arc, toxic Tau remained trapped inside neurons, causing those already sick cells to die more quickly. "When Arc is absent, Tau becomes trapped inside neurons and accumulates to toxic levels. When Arc is present, Tau can be released in extracellular vesicles. While this helps reduce Tau buildup within the original neuron, the released Tau can be taken up by neighboring healthy neurons, promoting the spread of pathology," Tyagi says. These findings suggest that the most effective treatment may not be preventing diseased cells from releasing Tau. Instead, it may be better to stop those toxic extracellular vesicles from entering healthy neurons. A Potential New Target for Alzheimer's Therapies The researchers also found extracellular vesicles containing both Arc and Tau in human brain tissue, suggesting the same mechanism could exist in people. However, they stress that much more research is needed before any potential therapy reaches patients. "Most of the work we've been doing is in mice, not in humans," Shepherd says. "We have some clues that whatever is happening in these mice could also be happening in humans, but we don't know that yet. And we're far away from saying that we're developing a treatment for anything. But it could open new avenues to get to that point." One promising possibility would be to intercept Tau containing extracellular vesicles after they leave diseased neurons but before they reach healthy ones. While such an approach would not reverse existing brain damage, it could potentially slow or prevent further spread of Alzheimer's disease. "If we could target these particular EVs, that would be a really useful therapy strategy," Shepherd says. "For someone with early-onset Alzheimer's or dementia, if we could stop the spread, then we could prevent further damage and cognitive decline." The study, titled "Arc mediates intercellular tau transmission via extracellular vesicles," was published in Cell. The research was supported by the National Institutes of Health, including the Director's Office Transformative Research Award (R01 NS115716), the National Institute of Neurological Disorders and Stroke (DSPAN F99), and the National Institute on Aging (AG073236), the Chan-Zuckerberg Initiative Ben Barres Early Acceleration Award, the Alzheimer's Association, the McKnight Brain Disorders Award, the Jon M. Huntsman Presidential Endowed Chair fund, the Max Planck Society, AIRC IG 26229, PRIN 2022EMZJL4, the Rainwater Foundation, the JPB Foundation, and the Cure Alzheimer Fund. The Massachusetts Alzheimer's Disease Research Center, supported by the National Institute on Aging (P30AG062421) provided human samples. Shepherd is a co-founder of VNV, LLC and holds stock in and is a consultant for Aera Therapeutics, Inc., which licenses intellectual property and patents that include Arc capsids.

TOKYO, June 29, 2026 /PRNewswire/ -- Eisai Co., Ltd. announced today the company will present the latest findings from its Alzheimer's disease (AD) research, including lecanemab (brand name: LEQEMBI®), our anti-amyloid beta (Aβ) protofibril antibody for the treatment of Alzheimer's disease (AD) and anti-MTBR (microtubule binding region) tau antibody, etalanetug (E2814), at the Alzheimer's Association International Conference ® 2026 (AAIC ®) from July 12-15 in London and online. Eisai will present 52 abstracts across its AD portfolio at AAIC. Highlights include a Developing Topics Session and a Featured Research Session on lecanemab, featuring four and six oral presentations, respectively, alongside 10 additional key oral presentations and 32 posters. Eisai will also host a symposium on early intervention in AD. Key Presentations A Developing Topics Session will feature emerging clinical evidence and practical use considerations for the subcutaneous formulation of lecanemab, including clinical trial and real-world patient experience. A Featured Research Session will highlight data from the LEADER study evaluating real-world lecanemab use in diverse US clinical settings three years post-approval, including results on maintenance dosing with IV treatment every four weeks and the first reported findings of at-home subcutaneous administration. Presentations on the Phase 3 AHEAD 3-45 study in preclinical AD will highlight progress of the trial including updates on participant retention and engagement. Additional oral presentations will highlight a Phase 2 trial of etalanetug with background lecanemab, and the effect on tau pathology. "We are sharing a broad and robust data set at AAIC spanning the Alzheimer's disease continuum, multiple therapeutic targets, and modes of administration, underscoring our commitment to advancing care for this complex disease," said Lynn D. Kramer, M.D., FAAN, Chief Clinical Officer, Deep Human Biology Learning (DHBL), Eisai. "Growing real-world experience with lecanemab, along with insights from patients, care partners, and clinicians, continues to add to our understanding of the value of early intervention, long-term treatment, and patient choice in care delivery." AAIC 2026 Presentations Relating to Eisai's Key Compounds and Research Developing Topics Session #1-32-FRS-C: Lecanemab Subcutaneous Formulation in Early Alzheimer's Disease: Emerging Clinical Evidence and Practical Use Considerations 4:15-5:45 PM BST, Sunday, July 12 Featured Research S ession #4-33-FRS-A: Lecanemab Three Years Post-Approval: A Comprehensive Multicenter, Real-World, Retrospective Study (LEADER) in Diverse US Clinical Settings 4:15-5:45 PM BST, Tuesday, July 14 Additional Oral Presentations Poster Presentations **Poster viewing time is set from 7:30 AM – 4:15 PM BST on the date of presentation Eisai-Sponsored Symposium ***Symposium is intended for HCPs only Eisai serves as the lead of lecanemab development and regulatory submissions globally with both Eisai and Biogen co-commercializing and co-promoting the product and Eisai having final decision-making authority. This release discusses investigational uses of agents in development and is not intended to convey conclusions about efficacy or safety. There is no guarantee that such investigational agents will successfully complete clinical development or gain health authority approval. MEDIA CONTACTS Public Relations Department, Eisai Co., Ltd. +81-(0)3-3817-5120 Eisai Europe, Ltd. (Europe, Australia, New Zealand and Russia) EMEA Communications Department +44 (0) 7739-600-678 [email protected] Eisai, Inc. (U.S.) Julie Edelman +1-862-213-5915 Julie [email protected] [Notes to editors] About lecanemab (generic name, brand name: LEQEMBI®) Lecanemab is the result of a strategic research alliance between Eisai and BioArctic. It is a humanized immunoglobulin gamma (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). Lecanemab has been approved in 53 countries and regions including Japan, the United States, China, Europe, South Korea, Taiwan, and Saudi Arabia, and is under regulatory review in 6 countries. Following the initial phase with treatment every two weeks for 18 months, intravenous (IV) maintenance dosing with treatment every four weeks was approved in 8 countries including the U.S., China, the UK, and others, and applications have been filed in 12 countries and regions. The U.S. FDA approved Eisai's Biologics License Application (BLA) for subcutaneous maintenance dosing with LEQEMBI IQLIK in August 2025. A Supplemental Biologics License Application (sBLA) for initiation treatment was accepted in January 2026 and granted Priority Review. The sBLA has been assigned an extended Prescription Drug User Fee Act (PDUFA) action date of August 24, 2026. In November 2025, an application for a subcutaneous injectable formulation in Japan was submitted. In January 2026, the Biologics License Application (BLA) for the subcutaneous formulation was accepted in China. In December 2025, Lecanemab (IV) has been included in the "Commercial Insurance Innovative Drug List", recently introduced by the National Healthcare Security Administration (NHSA) of China. Since July 2020 the Phase 3 clinical study (AHEAD 3-45) for individuals with preclinical AD, meaning they are clinically normal and have intermediate or elevated levels of amyloid in their brains, is ongoing. AHEAD 3-45 is conducted as a public-private partnership between the Alzheimer's Clinical Trial Consortium that provides the infrastructure for academic clinical trials in AD and related dementias in the U.S, funded by the National Institute on Aging, part of the National Institutes of Health, Eisai and Biogen. Since January 2022, the Tau NexGen clinical study for Dominantly Inherited AD (DIAD), that is conducted by Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU), led by Washington University School of Medicine in St. Louis, is ongoing and includes lecanemab as the backbone anti-amyloid therapy. About Protofibrils Protofibrils are believed to contribute to the brain injury that occurs with AD and are considered to be the most toxic form of soluble Aβ, having a primary role in the cognitive decline associated with this progressive, debilitating condition.1 Protofibrils cause injury to neurons in the brain, which in turn, can negatively impact cognitive function via multiple mechanisms, not only increasing the development of insoluble Aβ plaques but also increasing direct damage to brain cell membranes and the connections that transmit signals between nerve cells or nerve cells and other cells. It is believed the reduction of protofibrils may prevent the progression of AD by reducing damage to neurons in the brain and cognitive dysfunction.2 About etalanetug (E2814) Etalanetug is an anti-MTBR (microtubule-binding region) tau antibody discovered through collaborative research between Eisai and University College London. It is designed to inhibit the propagation of tau seeds within the brain. Etalanetug is being developed as a potential disease-modifying therapy for tauopathies, including sporadic Alzheimer's disease (AD). Currently, etalanetug is being evaluated in two ongoing clinical studies: the Tau NexGen Phase 2/3 trial in dominantly inherited Alzheimer's disease (DIAD), conducted under the Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU) and led by Washington University School of Medicine in St. Louis, added to the standard-of-care anti-Aβ protofibril antibody lecanemab (brand name: LEQEMBI), and the Phase 2 Study 202, a global randomized trial in individuals with early sporadic AD, also assessing etalanetug added to lecanemab. In September 2025, etalanetug received Fast Track designation from the U.S. Food and Drug Administration (FDA). About the Collaboration between Eisai and Biogen for AD Eisai and Biogen have been collaborating on the joint development and commercialization of AD treatments since 2014. Eisai serves as the lead of LEQEMBI development and regulatory submissions globally with both companies co-commercializing and co-promoting the product and Eisai having final decision-making authority. About the Collaboration between Eisai and BioArctic for AD Since 2005, Eisai and BioArctic have had a long-term collaboration regarding the development and commercialization of AD treatments. Eisai obtained the global rights to study, develop, manufacture and market lecanemab for the treatment of AD pursuant to an agreement with BioArctic in December 2007. The development and commercialization agreement on the antibody lecanemab back-up was signed in May 2015. References Amin L, Harris DA. Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers. Nat Commun. 2021;12: 3451. doi:10.1038/s41467-021-23507-z. Ono K, Tsuji M. Protofibrils of Amyloid-β are Important Targets of a Disease-Modifying Approach for Alzheimer's Disease. Int J Mol Sci. 2020;21(3):952. doi: 10.3390/ijms21030952. PMID: 32023927; PMCID: PMC7037706. SOURCE Eisai Inc. 21% more press release views with Request a Demo