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Name: Leqembi
Synonyms: Lecanemab-irmb, BAN2401, mAb158
Therapy Type: Immunotherapy (passive) (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Approved)
Company: BioArctic AB, Biogen, Eisai Co., Ltd.


BAN2401 is the humanized IgG1 version of the mouse monoclonal antibody mAb158, which selectively binds to large, soluble Aβ protofibrils. This therapeutic antibody grew out of 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 and relative absence of amyloid plaques (see Nilsberth et al., 2001). mAb158 was originally developed at Uppsala University, Sweden (Englund et al., 2007).

In its preclinical development, mAb158 was found to reduce Aβ protofibrils in brain and CSF of Tg-ArcSwe mice (Lord et al., 2009Tucker et al., 2015). Subsequent studies in mouse neuron-glial co-cultures showed that mAb158 may protect neurons, i.e., reduce Aβ protofibril toxicity, by counteracting the pathological accumulation of these protofibrils in astrocytes (Söllvander et al., 2018). In a direct comparison with the anti-amyloid antibodies aducanumab and gantenerumab, lecanemab was reported to bind most strongly to Aβ protofibrils, while the others preferred more highly aggregated forms (Nov 2021 conference news). Lecanemab was shown to bind to diffusible Aβ fibrils from human brain tissue (Nov 2022 news).

BAN2401 was licensed to Eisai, which in March 2014 signed a collaboration agreement with Biogen for joint development of this therapeutic antibody.

While clinical trials are being conducted in Alzheimer's (see below), preclinical research with postmortem Down's syndrome brain sections indicates binding of lecanemab to Aβ deposits in this disease, as well (Johannesson et al., 2021).

A hexavalent antibody based on mAb158 is being developed, with the goal of enhancing binding strength selectively to Aβ protofibrils (Rofo et al., 2021).


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 measured. BAN2401 was well-tolerated at all doses tested, up to 10mg/kg every two weeks for four months, with amyloid-related imaging abnormalities (ARIA-E, ARIA-H) occurring at the same rate in both placebo and BAN2401. The antibody entered the CSF and showed dose-dependent exposure, though with a short serum elimination half-life of seven days and no clear effect on CSF biomarkers. Results were published (Logovinsky et al., 2016).

Subsequently, a Phase 2, 18-month U.S. trial tested five different intravenous doses of BAN2401 in a Bayesian adaptive design. Allocation of subsequent enrollees to different groups was adjusted in response to frequent interim analyses, the first to be done in late 2015 after the first 196 patients had entered the trial, and again every time 50 more people had enrolled (for detailed description of this innovative trial design see Satlin et al., 2016). This trial enrolled 856 people who had either early stage AD as defined by the proposed NIA-AA diagnostic criteria or mild cognitive impairment due to AD, or who met NIA-AA criteria for probable AD and whose diagnosis was confirmed by a positive amyloid PET scan. As primary outcomes, the trial measured 12-month change from baseline in the new ADCOMS composite of cognitive tests (Wang et al., 2016), and safety.

In 2017 the sponsors announced that BAN2401 had shown no cognitive benefit at this 12-month time point. However, futility conditions had not been met either at the 17 interim analyses conducted until then. Therefore the trial continued to full enrollment of 856 participants, and out to the full treatment period of 18 months (Dec 2017 news). In February 2018, the trial protocol was amended to offer up to five years of additional treatment in an open-label extension phase, in which change on the ADCOMS will be measured at each visit. 

The sponsors announced top-line results of the blinded 18-month treatment phase in July 2018 (see July 2018 news). The highest antibody dose of twice-monthly 10 mg/kg slowed progression on the ADCOMS and reduced brain amyloid accumulation, according to a press release from BioArctic. Full results of this Phase 2b study were presented at AAIC (Jul 2018 news). The antibody reduced brain amyloid by up to 93 percent in the highest-dose group. This dose slowed cognitive decline by 47 percent on the ADAS-Cog, and by 30 percent on the ADCOMS. The next-lower dose, 10 mg/kg monthly, showed a trend toward slower cognitive decline that was not statistically significant. In an analysis of CSF from a subgroup of patients, the treatment caused a dose-dependent rise in CSF Aβ42. MRI scans detected ARIA in just under 10 percent of participants overall, and in fewer than 15 percent of those with ApoE4 in the highest-dose group. Most ARIA occurrences were asymptomatic.

The results were complicated by uneven distribution of ApoE4 carriers between placebo and treatment groups, which was caused by an EMA request during the trial. A subgroup analysis, presented at CTAD, suggested that the treatment benefit was not due to this imbalance (Nov 2018 conference news). Full results were subsequently published (Swanson et al., 2021). Additional analysis of the three cognitive endpoints with six different statistical methods found a consistent positive effect of treatment (Nov 2021 conference news).

An open-label extension to this trial re-enrolled its participants to deliver the highest antibody dose for up to two years total. As reported at AD/PD 2019 in Lisbon, Portugal, Eisai/Biogen planned to treat up to 250 people in this extension, which was to run until August 2021 (May 2019 conference news). Baseline data from 35 participants suggested that brain amyloid load had remained steady during a two-year pause in antibody dosing, but that cognition declined when BAN2401 was discontinued (Dec 2019 conference news). One-year brain imaging data from 76 participants, presented in December 2020 at CTAD, indicated that people previously treated with placebo had large decreases in their brain amyloid since entering the OLE, while those previously treated with antibody maintained low levels of brain amyloid. ARIA-E incidence was comparable to the core study. Most ARIA-E was asymptomatic and resolved within four to 12 weeks. Continuing to dose people with mild to moderate ARIA-E appeared to pose no additional safety issues (Nov 2020 conference news). More one-year OLE data on 180 participants was presented in March 2021 at AD/PD. Brain amyloid fell fastest in those who began the OLE with the highest amyloid. By the end, 80 percent of participants were judged amyloid-negative, with SUVRs below 1.17 (Mar 2021 conference news).

At the July 2021 AAIC, Eisai reported 18-month OLE data on 100 people. It suggested a slowing of cognitive decline in the open-label phase, compared to ADNI historical data. CSF Aβ42/40, which had increased with treatment during the placebo-controlled phase of the trial, started to decline during the dosing gap, but rose again in all participants after open-label treatment began. A post hoc analysis across the entire study duration suggested cognition declined more slowly in people on lecanemab than in those on placebo (Aug 2021 conference news). More data presented at the Nov 2021 CTAD showed a correlation between plaque clearance and slowed decline on ADCOMs in the OLE (Nov 2021 conference news). At the same conference, Eisai reported that changes in plasma ptau181 tracked with changes in amyloid PET and plasma Aβ42/40. OLE results were formally published (McDade et al., 2022), as were details on ARIA in the completed study (Honig et al., 2023), and an explication of the advantages of the Bayesian design (Berry et al., 2023).

In March 2019, Eisai began a Phase 3 trial called Clarity AD, to be run at 250 sites across the world. It aimed to enroll 1,566 people with early symptomatic AD, who received 10 mg/kg drug or placebo infusion every two weeks for 18 months, followed by a two-year open-label extension. The primary outcome in the core study was change in CDR-SB at 18 months, with secondary outcomes of brain amyloid, ADCOMS, and ADAS-Cog14 subscale. In the extension phase, primary outcomes were change in CDR-SB as well as safety. Change in the CSF biomarkers neurogranin, neurofilament light chain, Aβ(1-42), total tau, and phospho-tau from baseline up to 45 months was originally listed as a primary outcome in the trial registration, but this was dropped in July 2019. Plasma and CSF biomarkers, as well as amyloid and tau PET, are being assessed in optional longitudinal substudies.

As of October 2020, Clarity AD had randomized 1,222 participants, with demographic and cognitive scores similar to the Phase 2 study (Nov 2020 conference news). By March 2021, it had exceeded its enrollment goal, at 1,794 patients, the company announced (press release). In 2022, the extension added an option for a weekly subcutaneous injection of 720 mg. The trial is set to run until 2027.

In February 2020, the Alzheimer’s Therapeutic Research Institute announced that the Alzheimer's Clinical Trial Consortium (ACTC) would conduct a large Phase 3 study of lecanemab, called AHEAD 3-45 and co-funded by the NIH and Eisai (press release). It started in July 2020 as a four-year trial that comprises two sub-studies in a combined 1,400 people who are cognitively normal but have elevated brain amyloid. A3 is enrolling 400 people whose amyloid is below the brain-wide threshold for positivity; they will receive 5 mg/kg titrating to 10 mg/kg BAN2401 or placebo every four weeks for 216 weeks, and their primary outcome will be change in brain amyloid PET at that time. A45 is enroll 1,000 participants who have a positive amyloid PET scan. They will receive BAN2401 titrated to 10 mg/kg every two weeks for 96 weeks, followed by 10 mg/kg every four weeks through week 216. Their primary outcome is change from baseline on their Preclinical Alzheimer Cognitive Composite 5 (PACC5) score, also at week 216. Secondary outcomes for A45 include change in brain amyloid PET and cognitive function. Both studies will measure change in tau PET as a secondary outcome. This new study will use blood Aβ42/40 measures to rule out participants unlikely to have elevated brain amyloid before proceeding to PET imaging (for details, see Rafii et al., 2022).The first person was dosed in this trial in September 2020; as of the July 2021 AAIC, 77 people had been randomized. As of November 2022, 107 sites were recruiting around the world. The trial is expected to run until October 2027.

In June 2021, the FDA designated lecanemab a breakthrough therapy, expediting regulatory review, and soon after, Eisai/Biogen began their application for marketing approval (press releaseOct 2021 news). In December 2021, the agency granted fast-track designation (press release).

In September 2021, Eisai began a Phase 1 evaluation of lecanemab subcutaneous administration. The study compared the pharmacokinetics, bioavailability, and safety of a single 700 mg injection under the skin in the abdomen to 10 mg/kg given intravenously in 60 healthy people; it was completed in January 2022. In September 2022, a Phase 1 study started evaluating bioequivalence of a subcutaneous formulation delivered with an auto-injector device; it enrolled 160 healthy participants and finished in January 2023.

In November 2021, the DIAN-TU announced its choice of lecanemab for the first DIAN-TU anti-amyloid/anti-tau concurrent trial (Nov 2021 conference news). It will pair lecanemab with the anti-tau antibody E2814 in the Tau NexGen prevention study in 168 people with familial AD mutations. All will receive lecanemab, while half will get E2814, and half a matching placebo, against a primary outcome of change in tau PET. This trial will run at 40 sites in the Americas, Australia, Japan, and six European countries, until 2027 (Mar 2021 news).

In May 2022, Eisai/Biogen completed lecanemab’s FDA submission, based on the Phase 2 data (May 2022 news). In July 2022, the FDA granted priority review status to the application, with a decision date of January 6, 2023 (Jul 2022 news). 

On September 27, 2022, Biogen and Eisai reported positive top-line results on all primary and secondary outcomes of the Phase 3 Clarity AD study (Sep 2022 news). Results were presented in December at the 2022 CTAD conference, and published the same day (Dec 2022 conference news; van Dyck et al., 2023). Lecanemab slowed decline on the CDR-SB by 27 percent compared to placebo at 18 months. Key secondary endpoints, including the ADAS-Cog14, ADCOMS, and ADCS MCI-ADL, all showed a similar slowing of decline. Two-thirds of the treated group became PET-amyloid negative at 18 months. Tau PET indicated a significant slowing of tangle accumulation in the medial temporal lobe, and trended toward slowing in other brain regions. The astrocytosis biomarker GFAP was reduced on treatment, but markers of neurodegeneration were mixed. Safety was in line with past studies, with amyloid-related ARIA-E detected in 12.6 percent of treated participants vs 1.7 percent of the placebo group. About one-quarter had symptoms, which were typically mild and transient. Three people had severe symptoms, but the company did not say what they were.

Three deaths from brain hemorrhage have been reported in the lecanemab open-label extension (Jan 2023 news). Two of the three people had received blood thinners. In Clarity, macrohemorrhages, defined as any brain bleed larger than 1 cm, occurred in 0.6 percent in the treatment group, and 0.1 percent in the placebo group; for people on anticoagulants and lecanemab, this rate increased to 2.4 percent. According to a news article, the third fatality was a 79-year old woman with preexisting cerebral amyloid angiopathy (Piller, 2023). Published in December 2023, her autopsy report detailed fatal cerebral, Aβ-related arteritis after her third dose of lecanemab (Solopova et al., 2023). A 65-year old woman who received three doses of lecanemab died after being treated with tissue plasminogen activator for acute stroke symptoms; her brain autopsy revealed inflammation in blood vessels with cerebral amyloid angiopathy. The examination also showed evidence of phagocytic clearance of vascular Aβ and parenchymal Aβ plaques, and other changes suggesting Aβ and tau clearance (Castellani et al., 2023Reish et al., 2023).

On January 6, 2023, the FDA approved lecanemab under the Accelerated Approval pathway, based on evidence of effect on the surrogate endpoint of amyloid removal in the Phase 2 trial, and a reasonable likelihood of clinical benefit (FDA press releaseJan 2023 news). Lecanemab is sold under the brand name Leqembi.

In March 2023 , the U.S. Veterans Health Administration announced it would cover the cost of lecanemab for veterans in the early stages of AD, excluding those with two copies of APOE4 (press release; VA use criteria).

Additional efficacy data from the Clarity trial, presented at the March 2023 AD/PD conference and subsequently published, showed benefit on self-reported outcomes capturing quality of life and caregiver burden (April 2023 conference newsCohen et al., 2023). 

In March 2023, Leqembi Appropriate Use Recommendations were published (Cummings et al., 2023). They stipulate that it not be prescribed for people taking anticoagulants, or those with a clotting disorder, strokes, or seizures. People on lecanemab should not be treated with acute thrombolytics such as tPA, though common antiplatelet medications such as aspirin or clopidogrel are allowed. The AUR recommend APOE genotyping prior to therapy, so clinicians can discuss risks with patients, but allow treatment for APOE4 homozygotes. A schedule of monitoring MRIs is recommended to include scans at baseline, and before the fifth, seventh, and 14th biweekly infusions. Scans are recommended at one year for APOE4 carriers and people with any ARIA during the first year.

In June 2023, Beth Israel Deaconess Medical Center in Boston registered a prospective comparative study of monoclonal antibodies for the treatment of AD. This study creates a patient registry, as required for Medicare coverage of Leqembi or other antibodies once approved (see CMS Decision Summary; Jun 2023 news). The study will enroll up to 500 patients at the hospital’s Cognitive Neurology Unit, and follow them for 30 months to determine if the antibodies slow cognitive and functional decline, to identify associations between patient characteristics and side effects, and to establish the time to clinical benefit. Emory University in Atlanta registered a similar study in August 2023.

On July 6, 2023, the FDA granted lecanemab a traditional, full approval (Jul 2023 news).

At the November 2023 CTAD conference, Eisai presented results on subcutaneous dosing of lecanemab in the open-label extension phase of Clarity (Nov 2023 conference news). Participants were administered 720 mg weekly, in two doses, using either an injector pen or syringe and needle. After six months, subcutaneous delivery resulted in 11 percent higher blood exposure and more stable blood levels, compared to IV administration. Amyloid removal increased by 14 percent, and ARIA was slightly higher, both attributed to higher drug exposure. The company plans to apply for FDA licensing by March 2024.

At the same conference, post hoc analyses from Clarity's tau-PET substudy indicated that, among participants who began the study with low tau tangle load, more participants improved on the CDR-SB who were on lecanemab than were on placebo (Nov 2023 conference news).

For all clinical trials of Leqembi/lecanemab, see

Clinical Trial Timeline

  • Phase 1
  • Phase 2
  • Phase 3
  • 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 2029 2030 2031 2032 2033 2034
Eisai Co., Ltd. NCT01230853
Eisai Co., Ltd. NCT01767311
Eisai Co., Ltd. NCT03887455

Last Updated: 20 Dec 2023


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News Citations

  1. No Man’s Land: Neither Early Success nor Failure for BAN2401
  2. Topline Results: 18 Months of BAN2401 Might Work
  3. BAN2401 Removes Brain Amyloid, Possibly Slows Cognitive Decline
  4. Second Look at BAN2401 Data Still Positive, Despite Snafu
  5. Lecanemab Sweeps Up Toxic Aβ Protofibrils, Catches Eyes of Trialists
  6. Keep Your Enthusiasm? Scientists Process Brutal Trial Data
  7. Amyloid Clearance: Check. Cognitive Benefit: Um … Maybe.
  8. BANish Aβ? BAN2401 Antibody Makes Its Move in Phase 3 Program
  9. Shuttle Unloads More Gantenerumab Into the Brain
  10. Lecanemab Post Hoc: Is Continual Treatment Required for Cognitive Benefit?
  11. BAN2401 Forges AHEAD into Phase 3, Preclinical AD
  12. Lecanemab Follows Aduhelm’s Path to Accelerated Approval
  13. Aiming at the Tangle’s Heart? DIAN-TU Trial to Torpedo Tau’s Core
  14. With Aduhelm in Retrenchment, Lecanemab Completes FDA Submission
  15. Lecanemab: FDA Set Accelerated Approval Decision for January 2023
  16. Finally: Big Win on All Outcomes for Lecanemab in Phase 3 Topline Results
  17. Dare We Say Consensus Achieved: Lecanemab Slows the Disease
  18. U.S. FDA Gives Green Light to Leqembi, aka Lecanemab
  19. Next Goals for Immunotherapy: Make It Safer, Less of a Hassle
  20. CMS Sticks to Its Guns on Amyloid Immunotherapy Coverage
  21. FDA Grants Traditional Approval to Leqembi
  22. Gotta Get Rid of It All: Total Plaque Clearance Key for Clinical Benefit
  23. Treat Before ‘Aβ Bothers Tau,’ Scientists Say at CTAD
  24. Short Aβ Fibrils Easily Isolated from Alzheimer's Brain Fluid

Therapeutics Citations

  1. E2814
  2. Aduhelm
  3. Gantenerumab

Research Models Citations

  1. Tg-ArcSwe

Paper Citations

  1. . Safety and tolerability of BAN2401--a clinical study in Alzheimer's disease with a protofibril selective Aβ antibody. Alzheimers Res Ther. 2016 Apr 6;8(1):14. PubMed.
  2. . Design of a Bayesian adaptive phase 2 proof-of-concept trial for BAN2401, a putative disease-modifying monoclonal antibody for the treatment of Alzheimer's disease. Alzheimers Dement (N Y). 2016 Jan;2(1):1-12. Epub 2016 Feb 4 PubMed.
  3. . ADCOMS: a composite clinical outcome for prodromal Alzheimer's disease trials. J Neurol Neurosurg Psychiatry. 2016 Sep;87(9):993-9. Epub 2016 Mar 23 PubMed.
  4. . A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer's disease with lecanemab, an anti-Aβ protofibril antibody. Alzheimers Res Ther. 2021 Apr 17;13(1):80. PubMed. Correction.
  5. . 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. Alzheimers Res Ther. 2022 Dec 21;14(1):191. PubMed.
  6. . ARIA in patients treated with lecanemab (BAN2401) in a phase 2 study in early Alzheimer's disease. Alzheimers Dement (N Y). 2023;9(1):e12377. Epub 2023 Mar 20 PubMed.
  7. . Lecanemab for Patients With Early Alzheimer Disease: Bayesian Analysis of a Phase 2b Dose-Finding Randomized Clinical Trial. JAMA Netw Open. 2023 Apr 3;6(4):e237230. PubMed.
  8. . The AHEAD 3-45 Study: Design of a prevention trial for Alzheimer's disease. Alzheimers Dement. 2022 Aug 15; PubMed.
  9. . Lecanemab in Early Alzheimer's Disease. N Engl J Med. 2023 Jan 5;388(1):9-21. Epub 2022 Nov 29 PubMed.
  10. . Report on trial death stokes Alzheimer's drug fears. Science. 2023 Apr 14;380(6641):122-123. Epub 2023 Apr 13 PubMed.
  11. . Fatal iatrogenic cerebral β-amyloid-related arteritis in a woman treated with lecanemab for Alzheimer's disease. Nat Commun. 2023 Dec 12;14(1):8220. PubMed.
  12. . Neuropathology of Anti-Amyloid-β Immunotherapy: A Case Report. J Alzheimers Dis. 2023;93(2):803-813. PubMed.
  13. . Multiple Cerebral Hemorrhages in a Patient Receiving Lecanemab and Treated with t-PA for Stroke. N Engl J Med. 2023 Jan 4; PubMed.
  14. . Lecanemab Clarity AD: Quality-of-Life Results from a Randomized, Double-Blind Phase 3 Trial in Early Alzheimer's Disease. J Prev Alzheimers Dis. 2023;10(4):771-777. PubMed.
  15. . Lecanemab: Appropriate Use Recommendations. The Journal of Prevention of Alzheimer's Disease
  16. . The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation. Nat Neurosci. 2001 Sep;4(9):887-93. PubMed.
  17. . Sensitive ELISA detection of amyloid-beta protofibrils in biological samples. J Neurochem. 2007 Oct;103(1):334-45. PubMed.
  18. . An amyloid-beta protofibril-selective antibody prevents amyloid formation in a mouse model of Alzheimer's disease. Neurobiol Dis. 2009 Dec;36(3):425-34. PubMed.
  19. . The murine version of BAN2401 (mAb158) selectively reduces amyloid-β protofibrils in brain and cerebrospinal fluid of tg-ArcSwe mice. J Alzheimers Dis. 2015;43(2):575-88. PubMed.
  20. . The Aβ protofibril selective antibody mAb158 prevents accumulation of Aβ in astrocytes and rescues neurons from Aβ-induced cell death. J Neuroinflammation. 2018 Mar 28;15(1):98. PubMed.
  21. . Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease. Mol Cell Neurosci. 2021 Jul;114:103641. Epub 2021 Jun 4 PubMed.
  22. . Novel multivalent design of a monoclonal antibody improves binding strength to soluble aggregates of amyloid beta. Transl Neurodegener. 2021 Sep 28;10(1):38. PubMed.

Other Citations

  1. Jan 2023 news

External Citations

  1. press release from BioArctic.
  2. press release
  3. press release
  4. press release
  5. press release
  6. FDA press release
  7. press release
  8. VA use criteria
  9. CMS Decision Summary

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.
  3. . Are antibodies directed against amyloid-β (Aβ) oligomers the last call for the Aβ hypothesis of Alzheimer's disease?. Immunotherapy. 2019 Jan;11(1):3-6. PubMed.
  4. . SPECT imaging of distribution and retention of a brain-penetrating bispecific amyloid-β antibody in a mouse model of Alzheimer's disease. Transl Neurodegener. 2020 Sep 21;9(1):37. PubMed.
  5. . The Potential Economic Value of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling. Neurol Ther. 2022 Sep;11(3):1285-1307. Epub 2022 Jun 20 PubMed.
  6. . Long-Term Health Outcomes of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling. Neurol Ther. 2022 Jun;11(2):863-880. Epub 2022 Apr 25 PubMed.
  7. . Application of Meta-analysis to Evaluate Relationships Among ARIA-E Rate, Amyloid Reduction Rate, and Clinical Cognitive Response in Amyloid Therapeutic Clinical Trials for Early Alzheimer's Disease. Ther Innov Regul Sci. 2022 May;56(3):501-516. Epub 2022 Mar 23 PubMed.
  8. . 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. 2022 Oct 17; PubMed.
  9. . High-clearance anti-amyloid immunotherapies in Alzheimer's disease. Part 1: Meta-analysis and review of efficacy and safety data, and medico-economical aspects. Rev Neurol (Paris). 2022 Dec;178(10):1011-1030. Epub 2022 Sep 29 PubMed.
  10. . Population pharmacokinetic-pharmacodynamic analyses of amyloid positron emission tomography and plasma biomarkers for lecanemab in subjects with early Alzheimer's disease. CPT Pharmacometrics Syst Pharmacol. 2022 Dec;11(12):1578-1591. Epub 2022 Sep 27 PubMed.
  11. . The Potential Economic Value of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling. Neurol Ther. 2022 Sep;11(3):1285-1307. Epub 2022 Jun 20 PubMed.
  12. . [Causal treatment of Alzheimer's disease: amyloid antibodies]. Inn Med (Heidelb). 2022 Sep;63(9):1000-1008. Epub 2022 Mar 15 PubMed.
  13. . Therapeutic news in Alzheimer’s disease: soon a disease-modifying therapy?. Geriatr Psychol Neuropsychiatr Vieil. 2022 Jun 1;20(2):256-260. PubMed.
  14. . Long-Term Health Outcomes of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling. Neurol Ther. 2022 Jun;11(2):863-880. Epub 2022 Apr 25 PubMed.
  15. . Correction to: A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer's disease with lecanemab, an anti-Aβ protofibril antibody. Alzheimers Res Ther. 2022 May 21;14(1):70. PubMed.
  16. . Lecanemab: First Approval. Drugs. 2023 Mar;83(4):359-365. PubMed.
  17. . Estimated Societal Value of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling. Neurol Ther. 2023 Jun;12(3):795-814. Epub 2023 Mar 16 PubMed.
  18. . A Path to Improved Alzheimer's Care: Simulating Long-Term Health Outcomes of Lecanemab in Early Alzheimer's Disease from the CLARITY AD Trial. Neurol Ther. 2023 Jun;12(3):863-881. Epub 2023 Apr 2 PubMed.
  19. . Eligibility Rates among Racially and Ethnically Diverse US Participants in Phase 2 and Phase 3 Placebo-Controlled, Double-Blind, Randomized Trials of Lecanemab and Elenbecestat in Early Alzheimer Disease. Ann Neurol. 2024 Feb;95(2):288-298. Epub 2023 Oct 25 PubMed.