Name: BAN2401
Therapy Type: Immunotherapy (passive) (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 2)
Company: Biogen, Eisai Co., Ltd.


BAN2401 is a humanized IgG1 monoclonal antibody that binds selectively to large, soluble Aβ protofibrils and is thought to lead to their clearance or neutralize their toxicity. The therapeutic antibody was originally developed at the biotech company BioArctic Neuroscience following the discovery of the “Arctic” mutation in APP, which leads to a form of clinically typical Alzheimer's disease that is marked by particularly high levels of Aβ protofibrils (see Nilsberth et al., 2001). BAN2401 was licensed to Eisai, which in March 2014 signed a collaboration agreement with Biogen Idec for joint development of this antibody therapeutic.


A multicenter Phase 1 trial tested the safety, tolerability, and pharmacokinetics of single and multiple ascending intravenous doses of BAN2401 in 80 people with mild to moderate AD. Changes in Aβ levels were also tested. BAN2401 was reported to be well-tolerated at all doses tested up to 10mg/kg every two weeks, without incidents of amyloid-related imaging abnormalities (ARIA). The antibody entered the CSF and showed dose-dependent exposure.

A Phase 2, 18-month U.S. trial is testing five different intravenous doses of BAN2401 in a Bayesian adaptive design, where allocation of subsequent enrollees to different groups will be adjusted in response to frequent interim analyses, the first to be done in late 2015 after the first 200 patients have entered the trial. This trial is enrolling up to 800 people who either have early stage AD as defined by the proposed NIA-AA diagnostic criteria of mild cognitive impairment due to AD, or who meet NIA-AA criteria for probable AD and whose diagnosis is confirmed by a positive amyloid PET scan. As a primary outcome, the trial will measure change in a composite of cognitive tests. See clinical trials of BAN2401 at

Clinical Trial Timeline

  • Phase 1
  • Phase 2
  • Study completed / Planned end date
  • Planned end date unavailable
  • Study aborted
Sponsor Clinical Trial 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028
Eisai Co., Ltd. NCT01230853
Eisai Co., Ltd. NCT01767311


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Mutations Citations

  1. APP E693G (Arctic)

Paper Citations

  1. . The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation. Nat Neurosci. 2001 Sep;4(9):887-93. PubMed.

External Citations


Further Reading


  1. . A highly insoluble state of Abeta similar to that of Alzheimer's disease brain is found in Arctic APP transgenic mice. Neurobiol Aging. 2009 Sep;30(9):1393-405. PubMed.
  2. . Perspectives on future Alzheimer therapies: amyloid-β protofibrils - a new target for immunotherapy with BAN2401 in Alzheimer's disease. Alzheimers Res Ther. 2014;6(2):16. Epub 2014 Mar 24 PubMed.