Evidence map›Paper›PMID 36544184›Full record

Trial reportAlzheimer's research & therapy2022

Lecanemab in patients with early Alzheimer's disease: detailed results on biomarker, cognitive, and clinical effects from the randomized and open-label extension of the phase 2 proof-of-concept study.

Eric McDade, Jeffrey L Cummings, Shobha Dhadda, Chad J Swanson, Larisa Reyderman, Michio Kanekiyo, Akihiko Koyama, Michael Irizarry, Lynn D Kramer, Randall J Bateman

2 registry-linked trialsOpen access · goldAbstract readRandomized Controlled TrialClinical Trial, Phase II
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Alzheimer's research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 169 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed, 5 pooled it
29.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT01767311 phase2completednot on this map

A Placebo-Controlled, Double-Blind, Parallel-Group, Bayesian Adaptive Randomization Design and Dose Regimen-finding Study With an Open-Label Extension Phase to Evaluate Safety, Tolerability and Efficacy of BAN2401 in Subjects With Early Alzheimer's Disease

TypeinterventionalSponsorEisai Inc.Ran2012 to 2024Enrolled856ConditionsAlzheimer's DiseaseArmsLecanemab 2.5 mg/kg, Lecanemab 5.0 mg/kg, Lecanemab 10 mg/kg, Placebo
NCT06384573 phase3active not recruitingnot on this mapstarted 2024, after this paper: background citation

The Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU) Amyloid Removal Trial (ART): A Phase IIIb/IV Open-Label Study of Lecanemab to Evaluate Prevention and Progression of Dominantly Inherited Alzheimer's Disease

TypeinterventionalSponsorWashington University School of MedicineRan2024 to 2030Enrolled40ConditionsAlzheimer's Disease, Dementia, Alzheimer's Disease, FamilialArmslecanemab
3 · Its place in the literature

Who cites it

169 citing papers in PubMed, 5 syntheses or guidelines pooled it, 265 citations in OpenAlex.

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  3. The efficacy and safety of lecanemab 10 mg/kg biweekly compared to a placebo in patients with Alzheimer's disease: a systematic review and meta-analysis of randomized controlled trials.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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  12. The relationship of soluble tau species with Alzheimer's disease amyloid plaque removal and tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  18. The value of timely treatment with anti-amyloid therapy for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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109 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Eric McDadeThe DIAN-TU, Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.
Jeffrey L CummingsChambers-Grundy Center for Transformative Neuroscience, Quirk Brain Health and Biomarker Laboratory, Department of Brain Health, School of Integrated Health Sciences, University of Nevada Las Vegas, Las Vegas, NV, USA.
Shobha DhaddaEisai Inc., Nutley, NJ, USA.
Chad J SwansonEisai Inc., Nutley, NJ, USA.
Larisa ReydermanEisai Inc., Nutley, NJ, USA.
Michio KanekiyoEisai Inc., Nutley, NJ, USA.
Akihiko KoyamaEisai Inc., Nutley, NJ, USA.
Michael IrizarryEisai Inc., Nutley, NJ, USA.
Lynn D KramerEisai Inc., Nutley, NJ, USA.
Randall J BatemanThe DIAN-TU, Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA. batemanr@wustl.edu.
Eisai (United States) · USSaint Louis University · USUniversity of Nevada, Las Vegas · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLecanemab, a humanized IgG1 monoclonal antibody that targets soluble aggregated Aβ species (protofibrils), has demonstrated robust brain fibrillar amyloid reduction and slowing of clinical decline in early AD. The objective of this analysis is to report results from study 201 blinded period (core), the open-label extension (OLE), and gap period (between core and OLE) supporting the effectiveness of lecanemab.

methodsThe lecanemab study 201 core was a double-blind, randomized, placebo-controlled study of 856 patients randomized to one of five dose regimens or placebo. An OLE of study 201 was initiated to allow patients to receive open-label lecanemab 10mg/kg biweekly for up to 24 months, with an intervening off-treatment period (gap period) ranging from 9 to 59 months (mean 24 months).

resultsAt 12 and 18 months of treatment in the core, lecanemab 10 mg/kg biweekly demonstrated dose-dependent reductions of brain amyloid measured PET and corresponding changes in plasma biomarkers and slowing of cognitive decline. The rates of clinical progression during the gap were similar in lecanemab and placebo subjects, with clinical treatment differences maintained after discontinued dosing over an average of 24 months in the gap period. During the gap, plasma Aβ42/40 ratio and p-tau181 levels began to return towards pre-randomization levels more quickly than amyloid PET. At OLE baseline, treatment differences vs placebo at 18 months in the randomized period were maintained across 3 clinical assessments. In the OLE, lecanemab 10 mg/kg biweekly treatment produced dose-dependent reductions in amyloid PET SUVr, improvements in plasma Aβ42/40 ratio, and reductions in plasma p-tau181.

conclusionsLecanemab treatment resulted in significant reduction in amyloid plaques and a slowing of clinical decline. Data indicate that rapid and pronounced amyloid reduction correlates with clinical benefit and potential disease-modifying effects, as well as the potential to use plasma biomarkers to monitor for lecanemab treatment effects.

trial registrationClinicalTrials.gov NCT01767311 .

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloidogenic ProteinsAntibodies, Monoclonal, HumanizedBiomarkersBrainCognitionHumansAmyloid beta-PeptidesAmyloidogenic ProteinsAntibodies, Monoclonal, HumanizedBiomarkerslecanemab

Identifiers

PMID36544184
PMCPMC9768996
OpenAlexW4312128797

What OpenQuestion holds

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LicenceCC BY
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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.