Eisai to Present New Data From LEQEMBI® (lecanemab-irmb) Phase 3 Clarity AD Study and Other Alzheimer's Disease Pipeline Research at the Clinical Trials on Alzheimer's Disease (CTAD) Conference

Update on LEQEMBI Investigational Subcutaneous Formulation

TOKYO, Oct. 15, 2023 /PRNewswire/ -- Eisai Co. Ltd (Headquarters: Tokyo, CEO: Haruo Naito, "Eisai") announced today that the company will present new data from the phase 3 Clarity AD study for its Alzheimer's disease (AD) treatment LEQEMBI® (lecanemab-irmb) 100 mg/mL injection for intravenous use and new data on the subcutaneous formulation in development at the 16th annual Clinical Trials on Alzheimer's Disease (CTAD) conference. The conference will be held in Boston, Massachusetts, United States and virtually from October 24 to 27, 2023. In addition to the data presented on Eisai's anti-amyloid beta (Aβ) protofibril* antibody LEQEMBI, phase 1 data for E2511, an investigational tropomyosin receptor Kinase A (TrkA) positive allosteric modulator (PAM), will be presented as well as other research from the company's AD pipeline. At the conference, Eisai will present data and research in five oral and ten poster presentations. BioArctic will give an oral presentation on lecanemab.

U.S. journalists may experience the full interactive Multichannel News Release here: https://www.multivu.com/players/English/9211051-eisai-at-ctad2023/

Late-Breaking Symposium 4 – Lecanemab for early Alzheimer's Disease: Long-Term Outcomes, Predictive Biomarkers, and Novel Subcutaneous Administration

  • In a late-breaking symposium on October 25 from 17:25-18:05 EDT, Eisai will present the latest data from the Clarity AD optional tau PET longitudinal substudy. The presentation will include a post-hoc analysis of the low and intermediate + high-tau subgroups, with the low-tau subgroup representing early stages of disease studied specifically in the phase 3 core study, and the open-label extension study. An update on the investigational subcutaneous formulation, including interim safety and effect on amyloid in the brain measured by amyloid PET, will be provided.
  • Distinguished faculty members Christopher van Dyck M.D., Keith Johnson M.D. and Reisa Sperling M.D. will discuss the findings in a panel led by Michael Irizarry, M.D., MPH, Eisai.
  • A live webcast of this symposium can be viewed on the Eisai Co., Ltd. website.

"Alzheimer's disease is a progressive and relentless condition that requires early diagnosis1,2,3 and continued treatment. LEQEMBI supports neuronal function in Alzheimer's disease1,4,5 by clearing highly toxic protofibrils3,4 that can continue to cause neuronal injury and death well after plaques are cleared,"5,6,7,8 said Michael Irizarry, MD, MPH, Senior Vice President, Clinical Research, Neurology, Deputy Chief Clinical Officer, Clinical Evidence Generation, Eisai. "We look forward to sharing the new LEQEMBI low-tau subgroup data and subcutaneous data at CTAD 2023."

Other major oral presentations include:

  • Lecanemab: Binding profiles of lecanemab and donanemab to different amyloid-beta species (OC19, presentation by BioArctic).
  • E2511, a novel TrkA modulator, engages its CNS cholinergic target in a phase 1 clinical study (OC34).
  • Novel CSF tau biomarkers can be used for disease staging of sporadic Alzheimer's disease (OC2).

The full list of presentations about Eisai assets and research follows.

Late Breaking Symposium 4
The Symposium title: Lecanemab for Early Alzheimer's Disease: Long-Term Outcomes, Predictive Biomarkers and Novel Subcutaneous Administration from 17:25 to 18:05 EDT on October 25, 2023.

Presentation Title

Clarity AD: Review of the Mechanism-Based Rationale and Results of the Lecanemab Phase 3 Trial

Biomarker Assessments from Clarity AD: A Focus on Downstream Implications of Targeting Protofibrils* and Tau as a Predictive Biomarker

Lecanemab for the Treatment of Early Alzheimer's Disease: The Extension of Efficacy Results from Clarity AD

Preliminary Update on Lecanemab Safety in Clarity AD Open-Label Extension, Including Subcutaneous Formulation

Panel discussion, Q&A

■ Oral Presentations

Asset/Project,

Presentation Time (EDT)

Presentation Number, Title

Lecanemab

October 26 (Thu) 14:50-15:05

OC19

Binding Profiles of Lecanemab and Donanemab to Different Amyloid-beta Species

(presentation by BioArctic)

Lecanemab

October 26 (Thu) 17:05-17:45

(Late breaking symposium 6)

Presentation 3 in Late breaking symposium 6

Aβ42/Aβ40 and Phospho-tau217 Concentration Ratios Increase the Accuracy of Amyloid PET Classification
in Preclinical Alzheimer's Disease

E2511
October 27 (Fri) 14:45-14:55

OC34

E2511, a Novel TrkA Modulator, Engages its CNS Cholinergic Target in a Phase 1 Clinical Study

Biomarker

October 25 (Wed) 8:45-9:00

LB7

PrecivityAD2™ Blood Test: An Analytically and Clinically Validated Test Combining p-Tau217/np-Tau217
and Aβ42/40 Ratios to Identify Brain Amyloid

(presentation by C2N)

Biomarker

October 25 (Wed) 11:35-11:50

OC2

Novel CSF Tau Biomarkers Can Be Used for Disease Staging of Sporadic Alzheimer's Disease

AD general

October 27 (Fri) 11:45-12:00

OC29
AI-based Enrichment Tools to Increase Efficiency of Alzheimer's Disease Clinical Trials

Poster Presentations

Asset/Project

Presentation Number, Title

Lecanemab

P018

Recruitment Source, Eligibility and Reason for Prescreen-Fail Across Sex, Race and Ethnicity: Preliminary Analysis of
Prescreening Data from the AHEAD Study

Lecanemab

P045

ARIA by Clinical Subgroup and Baseline Amyloid PET Centiloid Levels from the Lecanemab Clarity AD

Lecanemab

LP011

Impact of a Site Supplemental Funding Program to Alleviate Recruitment Burden: Experiences in the Preclinical Alzheimer's
Disease AHEAD Study

E2511

P044

Safety and Pharmacokinetics of Multiple Ascending Doses of E2511, a Novel TrkA Allosteric Modulator, in Healthy Volunteers

Biomarker

P070

Systematic Literature Review of the Clinical and Non-clinical Value of Imaging and Fluid Biomarker Testing to Diagnose,
Identify and Monitor Patients with Alzheimer's Disease

AD general

P032

Planning the Next Generation of Alzheimer's Disease Clinical Trials Using Diverse Patient-level Database from the
Critical Path for Alzheimer's Disease (CPAD) Consortium

AD general

P033

Critical Path for Alzheimer's Disease (CPAD) Consortium: Data-Driven Solutions for Clinical Trial Design and
Informed Decision Making

AD general

LP003

Implications of Missing Data and Dropouts in Randomized Clinical Trials in Early Alzheimer's Disease

AD general

P145

Age-Specific Relative Comorbidity Burden of MCI: a US Database Study

AD general

P179

Development of a Mild Cognitive Impairment Risk Prediction Model Using Electronic Health Record Data

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.

*Protofibrils

  • One of the AD pathological features is the accumulation of clusters (plaques) of amyloid beta (Aβ) in the brain. The formation of these plaques is the result of a continuous process by which individual Aβ proteins join together, latching onto each other, one at a time, like adding links to a chain.9 In the early part of this process these small chains of Aβ are soluble and are toxic to the nerves within the brain.10,11
  • The most toxic of the soluble chains is called a protofibril.3 Protofibrils are believed to contribute to the brain injury that occurs with AD and are considered to be the most toxic form of Aβ, having a primary role in the cognitive decline associated with this progressive, debilitating condition.1,2
  • 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.12

INDICATION
LEQEMBI is indicated for the treatment of Alzheimer's disease. Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was initiated in clinical trials.

WARNING: AMYLOID RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of amyloid beta, including LEQEMBI, can cause amyloid related imaging abnormalities (ARIA), characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events rarely can occur. Serious intracerebral hemorrhages >1 cm, some of which have been fatal, have been observed in patients treated with this class of medications.
    • Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (approximately 15% of Alzheimer's disease patients) treated with this class of medications, including LEQEMBI, have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.
  • Consider the benefit of LEQEMBI for the treatment of Alzheimer's disease and potential risk of serious adverse events associated with ARIA when deciding to initiate treatment with LEQEMBI


CONTRAINDICATION
LEQEMBI is contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients of LEQEMBI. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS
Amyloid Related Imaging Abnormalities

  • LEQEMBI can cause ARIA-E and ARIA-H. ARIA-E can be observed on MRI as brain edema or sulcal effusions, and ARIA-H as microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with Alzheimer's disease. ARIA-H associated with monoclonal antibodies directed against aggregated forms of beta amyloid generally occurs in association with an occurrence of ARIA-E. ARIA-H and ARIA-E can occur together. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, rarely can occur. Reported symptoms associated with ARIA may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms associated with ARIA usually resolve over time.

ARIA Monitoring and Dose Management Guidelines

  • Obtain recent baseline brain magnetic resonance imaging (MRI) prior to initiating treatment with LEQEMBI. Obtain an MRI prior to the 5th, 7th and 14th infusions.
  • Recommendations for dosing in patients with ARIA-E and ARIA-H depend on clinical symptoms and radiographic severity. Depending on ARIA severity, use clinical judgment in considering whether to continue dosing, temporarily discontinue treatment, or permanently discontinue LEQEMBI.
  • Enhanced clinical vigilance for ARIA is recommended during the first 14 weeks of treatment with LEQEMBI. If a patient experiences symptoms suggestive of ARIA, clinical evaluation should be performed, including MRI if indicated. If ARIA is observed on MRI, careful clinical evaluation should be performed prior to continuing treatment.
  • There is no experience in patients who continued dosing through symptomatic ARIA-E or through asymptomatic, but radiographically severe, ARIA-E. There is limited experience in patients who continued dosing through asymptomatic but radiographically mild to moderate ARIA-E. There are limited data in dosing patients who experienced recurrent ARIA-E.

Incidence of ARIA

  • In Study 2, symptomatic ARIA occurred in 3% (29/898) of LEQEMBI-treated patients. Serious symptoms associated with ARIA were reported in 0.7% (6/898) of patients treated with LEQEMBI. Clinical symptoms associated with ARIA resolved in 79% (23/29) of patients during the period of observation.
  • Including asymptomatic radiographic events, ARIA was observed in LEQEMBI: 21% (191/898); placebo: 9% (84/897). ARIA-E was observed in LEQEMBI: 13% (113/898); placebo: 2% (15/897). ARIA-H was observed in LEQEMBI: 17% (152/898); placebo: 9% (80/897). There was no increase in isolated ARIA-H for LEQEMBI vs placebo.

ApoE ε4 Carrier Status and Risk of ARIA

  • In Study 2, 16% (141/898) of patients in the LEQEMBI arm were ApoE ε4 homozygotes, 53% (479/898) were heterozygotes, and 31% (278/898) were noncarriers.
  • The incidence of ARIA was higher in ApoE ε4 homozygotes (LEQEMBI: 45%; placebo: 22%) than in heterozygotes (LEQEMBI: 19%; placebo: 9%) and noncarriers (LEQEMBI: 13%; placebo: 4%). Among patients treated with LEQEMBI, symptomatic ARIA-E occurred in 9% of ApoE ε4 homozygotes compared with 2% of heterozygotes and 1% noncarriers. Serious events of ARIA occurred in 3% of ApoE ε4 homozygotes, and approximately 1% of heterozygotes and noncarriers.
  • The recommendations on management of ARIA do not differ between ApoE ε4 carriers and noncarriers.

Radiographic Findings

  • The majority of ARIA-E radiographic events occurred early in treatment (within the first 7 doses), although ARIA can occur at any time and patients can have more than 1 episode. The maximum radiographic severity of ARIA-E in patients treated with LEQEMBI was mild in 4% (37/898), moderate in 7% (66/898), and severe in 1% (9/898). Resolution on MRI occurred in 52% of ARIA-E patients by 12 weeks, 81% by 17 weeks, and 100% overall after detection. The maximum radiographic severity of ARIA-H microhemorrhage in LEQEMBI-treated patients was mild in 9% (79/898), moderate in 2% (19/898), and severe in 3% (28/898) of patients; superficial siderosis was mild in 4% (38/898), moderate in 1% (8/898) , and severe in 0.4% (4/898). Among LEQEMBI-treated patients, the rate of severe radiographic ARIA-E was highest in ApoE ε4 homozygotes 5% (7/141), compared to heterozygotes 0.4% (2/479) or noncarriers 0% (0/278). Among LEQEMBI-treated patients, the rate of severe radiographic ARIA-H was highest in ApoE ε4 homozygotes 13.5% (19/141), compared to heterozygotes 2.1% (10/479) or noncarriers 1.1% (3/278).

Intracerebral Hemorrhage

  • Intracerebral hemorrhage >1 cm in diameter was reported in 0.7% (6/898) of patients in Study 2 after treatment with LEQEMBI compared to 0.1% (1/897) on placebo. Fatal events of intracerebral hemorrhage in patients taking LEQEMBI have been reported.

Concomitant Antithrombotic Medication:

  • In Study 2, baseline use of antithrombotic medication (aspirin, other antiplatelets, or anticoagulants) was allowed if the patient was on a stable dose. The majority of exposures to antithrombotic medications were to aspirin. Antithrombotic medications did not increase the risk of ARIA with LEQEMBI. The incidence of intracerebral hemorrhage was 0.9% (3/328 patients) in patients taking LEQEMBI with a concomitant antithrombotic medication at the time of the event compared to 0.6% (3/545 patients) in those who did not receive an antithrombotic. Patients taking LEQEMBI with an anticoagulant alone or combined with an antiplatelet medication or aspirin had an incidence of intracerebral hemorrhage of 2.5% (2/79 patients) compared to none in patients who received placebo.
  • Because intracerebral hemorrhages >1 cm in diameter have been observed in patients taking LEQEMBI, additional caution should be exercised when considering the administration of anticoagulants or a thrombolytic agent (e.g., tissue plasminogen activator) to a patient already being treated with LEQEMBI.

Other Risk Factors for Intracerebral Hemorrhage:

  • Patients were excluded from enrollment in Study 2 for findings on neuroimaging that indicated an increased risk for intracerebral hemorrhage. These included findings suggestive of cerebral amyloid angiopathy (prior cerebral hemorrhage >1 cm in greatest diameter, >4 microhemorrhages, superficial siderosis, vasogenic edema) or other lesions (aneurysm, vascular malformation) that could potentially increase the risk of intracerebral hemorrhage. The presence of an ApoE ε4 allele is also associated with cerebral amyloid angiopathy, which has an increased risk for intracerebral hemorrhage. Caution should be exercised when considering the use of LEQEMBI in patients with factors that indicate an increased risk for intracerebral hemorrhage and in particular for patients who need to be on anticoagulant therapy.

Hypersensitivity Reactions
Hypersensitivity reactions, including angioedema, bronchospasm, and anaphylaxis, have occurred in LEQEMBI-treated patients. Promptly discontinue the infusion upon the first observation of any signs or symptoms consistent with a hypersensitivity reaction, and initiate appropriate therapy.

Infusion-Related Reactions

  • In Study 2, infusion-related reactions were observed in LEQEMBI: 26% (237/898); placebo: 7% (66/897), and the majority of cases in LEQEMBI-treated patients (75%, 178/237) occurred with the first infusion. Infusion-related reactions were mostly mild (69%) or moderate (28%) in severity. Infusion-related reactions resulted in discontinuations in 1% (12/898) of LEQEMBI-treated patients. Symptoms of infusion-related reactions included fever and flu-like symptoms (chills, generalized aches, feeling shaky, and joint pain), nausea, vomiting, hypotension, hypertension, and oxygen desaturation.
  • In the event of an infusion-related reaction, the infusion rate may be reduced, or the infusion may be discontinued, and appropriate therapy initiated as clinically indicated. Prophylactic treatment with antihistamines, acetaminophen, nonsteroidal anti-inflammatory drugs, or corticosteroids prior to future infusions may be considered.

ADVERSE REACTIONS

  • In Study 2, the most common adverse reactions leading to discontinuation of LEQEMBI was ARIA-H microhemorrhages that led to discontinuation in 2% (15/898) of patients treated with LEQEMBI compared to <1% (1/897) of patients on placebo.
  • In Study 2, the most common adverse reactions reported in ≥5% of patients treated with LEQEMBI (N=898) and ≥2% higher than placebo (N=897) were infusion-related reactions (LEQEMBI: 26%; placebo: 7%), ARIA-H (LEQEMBI: 14%; placebo: 8%), ARIA-E (LEQEMBI: 13%; placebo: 2%), headache (LEQEMBI: 11%; placebo: 8%), superficial siderosis of central nervous system (LEQEMBI: 6%; placebo: 3%), rash (LEQEMBI: 6%; placebo: 4%), and nausea/vomiting (LEQEMBI: 6%; placebo: 4%).

Please see full Prescribing Information for LEQEMBI, including Boxed WARNING.

[Notes to editors]

1. About Lecanemab (generic name, U.S. brand name: LEQEMBI®),
Lecanemab is the result of a strategic research alliance between Eisai and BioArctic. Lecanemab is a humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). In the U.S., LEQEMBI was granted traditional approval by the U.S. Food and Drug Administration (FDA) on July 6, 2023. LEQEMBI is an amyloid beta-directed antibody indicated as a disease-modifying treatment for Alzheimer's disease (AD) in the U.S. Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment (MCI) or mild dementia stage of disease, the population in which treatment was initiated in clinical trials. There are no safety or effectiveness data on initiating treatment at earlier or later stages of the disease than were studied. In Japan, Eisai received approval from the Ministry of Health, Labour and Welfare (MHLW) on September 25, 2023 to manufacture and market lecaenmab as a treatment for slowing progression of MCI and mild dementia due to AD.

Please see full Prescribing Information, including Boxed WARNING in the United States.

Eisai has also submitted applications for approval of lecanemab in EU, China, Canada, Great Britain, Australia, Switzerland, South Korea and Israel. In China and Israel, the applications have been designated for priority review, and in Great Britain, lecanemab has been designated for the Innovative Licensing and Access Pathway (ILAP), which aims to reduce the time to market for innovative medicines.

Eisai has completed a lecanemab subcutaneous bioavailability study, and subcutaneous dosing is currently being evaluated in the Clarity AD (Study 301) open-label extension (OLE). A maintenance dosing regimen has been evaluated as part of Study 201.

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.

2. About E2511
E2511 is Eisai' s in-house discovered and developed investigational novel molecule that directly binds to tropomyosin receptor kinase A (TrkA); a nerve growth factor (NGF) located on the neural cell membrane. E2511 could potentially promote recovery and synaptic remodeling of damaged cholinergic neurons. A Phase 1 study for E2511 is underway.

3. About the Collaboration between Eisai and Biogen for Alzheimer's Disease
Eisai and Biogen have been collaborating on the joint development and commercialization of AD treatments since 2014. 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. In Japan, Eisai and Biogen Japan will co-promote lecanemab, with Eisai distributing the product as the Marketing Authorization Holder.

4. About the Collaboration between Eisai and BioArctic for Alzheimer's Disease
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 LEQEMBI for the treatment of AD pursuant to an agreement with BioArctic in December 2007. The development and commercialization agreement on the antibody LEQEMBI back-up was signed in May 2015.

References

  1. LEQEMBI US Prescribing Information under Traditional Approval
  2. Alzheimer's Association, Facts & Figures 2023. https://www.alz.org/media/Documents/alzheimers-facts-and-figures.pdf Accessed October 12, 2023.
  3. Hampel, H., Hardy, J., Blennow, K. et al. The Amyloid-β Pathway in Alzheimer's Disease. Mol Psychiatry. 2021;26:5481–5503. https://doi.org/10.1038/s41380-021-01249-0
  4. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in early Alzheimer's disease. N Engl J Med. 2023;388(1):9-21.
  5. Brendza RP, et al. Anti-Aβ antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice. J Clin Invest. 2005;115(2):428-433. https://doi.org/10.1172/JCI23269.
  6. 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.
  7. Söderberg L, et al. Lecanemab, Aducanumab, and Gantenerumab — Binding Profiles to Different Forms of Amyloid–Beta Might Explain Efficacy and Side Effects in Clinical Trials for Alzheimer's Disease. Neurotherapeutics. 2023;20:195–206 https://doi.org/10.1007/s13311-022-01308-6 Accessed October 12, 2023.
  8. Hartley DM, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM, Teplow DB, Selkoe DJ. Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J Neurosci. 1999;19(20):8876-84. doi: 10.1523/JNEUROSCI.19-20-08876.1999. PMID: 10516307; PMCID: PMC6782787.
  9. Alzheimer's Association. (2022). Brain Tour Part 2 - Alzheimer's Effect. Retrieved September 27, 2023, from https://www.alz.org/alzheimers-dementia/what-is-alzheimers/brain_tour_part_2
  10. Chen, Gf., Xu, Th., Yan, Y. et al. Amyloid beta: structure, biology and structure-based therapeutic development. Acta Pharmacol. 2017;38:1205. https://doi.org/10.1038/aps.2017.28
  11. Habashi M., Vulta S., Tripathi K., et al. Early diagnosis and treatment of Alzheimer's disease by targeting toxic soluble Aβ oligomers. Biophysics and Computational Biology. 2022;10.1073. https://www.pnas.org/doi/epdf/10.1073/pnas.2210766119
  12. 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

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SOURCE Eisai Inc.

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