Delving into the Latest Updates on Donanemab-AZBT with Synapse

Overview

Basic Info

Drug Type

Monoclonal antibody

Synonyms

Donanemab, Donanemab (USAN), N3pG-AB-monoclonal-antibody-Eli-Lilly

+ [12]

Target

pGlu3Aβ

Action

inhibitors

Mechanism

3pE-modified Aβ inhibitors

Therapeutic Areas

Nervous System DiseasesOther DiseasesEndocrinology and Metabolic Disease

Active Indication

Cognition DisordersDementia due to Alzheimer's disease (disorder)Mild cognitive disorder+ [7]

Inactive Indication

Alzheimer Disease, Familial, 1

Originator Organization

Eli Lilly & Co.

Active Organization

Eli Lilly & Co.Eli Lilly Australia Pty Ltd.Eli Lilly Nederland BV

+ [2]

Inactive Organization-

License Organization-

Drug Highest PhaseApproved

First Approval Date

United States (02 Jul 2024),

Alzheimer Disease

RegulationPriority Review (United States), Breakthrough Therapy (United States), Priority Review (China), Breakthrough Therapy (China)

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Structure/Sequence

Sequence Code 190619L

Source: *****

Sequence Code 190621H

Source: *****

The goal of this clinical trial is to learn if donanemab can reduce levels of amyloid in the brain, and if donanemab is safe and well-tolerated in participants with Down syndrome.
The main questions it aims to answer are: Does donanemab reduce amyloid in the brain? Is donanemab safe and well-tolerated in people with Down syndrome? Researchers will compare donanemab to a placebo (a look-alike substance that contains no drug) to see if donanemab works to reduce levels of amyloid in the brain.
Participants in the study will be 35-50 years old and will be in the study for 12 months. Participants will then stay in the study for an additional 12 months in an long-term extension where all participants will receive donanemab. Participants who had a reduction in amyloid (measured by amyloid brain scan) by the end of the first 12 months will receive placebo for the long-term extension, while participants who did not have an amyloid reduction will receive study donanemab for the long-term extension. Everyone (participants and study staff) will remain blinded to treatment for the duration of the study.
Participants will:
* Have intravenous (IV) infusions of donanemab (or placebo) every 4 weeks
* Visit the clinic once every other month for checkups and tests. These tests will include brain scans (magnetic resonance imaging [MRI] and positron emission tomography [PET] ), blood draws and memory tests.
* Have a study partner who who can provide information about the participant and can join participant for some of the study visits.

Start Date01 Aug 2026

Sponsor / Collaborator

University of Southern California

[+3]

NCT06996730

/ RecruitingPhase 2/3IIT

A Double-Blind, Placebo-Controlled, Double-Dummy Study of Donanemab and RG6289 in PSEN1 E280A Mutation Carriers, and in Non-Randomized, Placebo-Treated Non-Carriers From the Same Kindred, to Evaluate the Efficacy and Safety of Donanemab, RG6289, or the Combination of Donanemab and RG6289, in the Treatment of Autosomal-Dominant Alzheimer's Disease

The study will be conducted in 2 blinded parts (Part 1 and Part 2). In Part 1, study participants who are mutation carriers will receive active donanemab and non-mutation carriers will receive placebo-donanemab for up to 18 months (76 weeks), with a minimum treatment period of 9 months. Amyloid PET scans will be conducted at screening, 9, and 18 months in Part 1. Participants who are at or below 11 CL at screening or reach complete amyloid plaque clearance as measured by florbetapir F18 PET (defined as ≤11 CL) at 9 months will initiate Part 2. Participants who are ≤11 CL at screening may delay their entry into Part 2 for up to 6 months at the discretion of the Investigator. All remaining participants will start Part 2 after completing 18 months (76 weeks) in Part 1 independent of amyloid results. Non-carriers will receive placebo in both Parts 1 and 2.
In Part 2, study participants who are mutation carriers will be randomized 1:1:1:1 in a full factorial design to receive either RG6289 + placebo-donanemab (RG6289 alone group), donanemab + placebo-RG6289 (donanemab alone group), the combination of RG6289 and donanemab (combination group), or placebo-RG6289 and placebo-donanemab (placebo group). All non-carriers will be assigned to the placebo group. CDR-GS at the end of Part 1 and the amyloid level using the last completed amyloid PET scan in Part 1 will be used for stratification. All study participants will participate in a double-dummy design for the duration of Part 2 receiving both an intravenous (IV) infusion at the required interval for the donanemab or matching placebo as well as a daily oral treatment of RG6289 or matching placebo.
An exploratory outcome of Part 1 is a comparison of the amyloid clearance between this ADAD cohort and historical controls using propensity score matching. The primary outcome in Part 2 is change from the start of Part 2 through the end of Part 2 in brain amyloid load in PSEN1 E280A mutation carriers as measured by amyloid PET imaging. Other endpoints will include fluid and imaging biomarkers and measures of cognition and functioning. The maximum study duration for any individual participant will be 3 years, not including the screening or follow-up periods

Start Date08 Jul 2026

Sponsor / Collaborator

Banner Health

[+2]

JPRN-jRCTs051260074

/ RecruitingNot Applicable

Development of an Optimization Model for Determining the Optimal Timing to Discontinue Donanemab Treatment Based on Amyloid PET Image Evaluation

Start Date10 Jun 2026

Sponsor / Collaborator-

100 Clinical Results associated with Donanemab-AZBT

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100 Translational Medicine associated with Donanemab-AZBT

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100 Patents (Medical) associated with Donanemab-AZBT

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388

Literatures (Medical) associated with Donanemab-AZBT

01 Nov 2026·Neural Regeneration Research

Analysis of the dual role of amyloid-beta in Alzheimer’s disease through multi-omics integration

Article

Author: Wang, Keke ; Lu, Xiaoqin ; Guo, Jingwen ; Xue, Weishuang ; Wang, Yanzhe ; Qiu, Luying ; Fu, Hefei

Accumulation of amyloid-beta is highly important in the development of Alzheimer’s disease. Given the limitations of the amyloid cascade hypothesis and the repeated clinical failures of anti-amyloid-beta therapies, researchers are increasingly exploring the infection hypothesis. This review explores the dual behaviors of amyloid-beta in Alzheimer’s disease, with a particular focus on its protective role against infection by microorganisms and its complicated connections with innate immune system. This new opinion holds that amyloid-beta can play an antimicrobial peptide role. During microbial invasion, its original role is to protect neural tissue, but prolonged accumulation leads to chronic deposition and involvement in pathological processes. Evidence from in vitro experiments, animal models, and clinical studies indicates that amyloid-beta may possess antiviral and antibacterial properties, particularly against infections such as herpes simplex virus, human immunodeficiency virus, and Porphyromonas gingivalis . However, excessive accumulation of amyloid beta triggers a neuroinflammatory cascade that impairs neuronal regeneration and cognitive function. Despite substantial research into Alzheimer’s disease, current treatments have not yielded significant clinical benefits. Although monoclonal antibodies such as Aducanumab , Lecanemab , and Donanemab have been approved for marketing, their strict indications and high costs pose challenges for widespread promotion. The infection hypothesis of amyloid-beta has spurred clinical trials investigating vaccines targeting specific pathogens to assess their potential in preventing or treating Alzheimer’s disease. This highlights the need for further exploring the multifaceted role of amyloid-beta in Alzheimer’s disease. In addition, microbial infections can also trigger or regulate genetic and epigenetic factors, accelerating amyloid beta deposition. Among them, the apolipoprotein E epsilon 4 allele is the strongest genetic risk factor for Alzheimer’s disease, as it exacerbates the accumulation of amyloid beta and promotes neuroinflammation. Strategies targeting epigenetic regulation may provide novel approaches to inhibit Alzheimer’s disease pathology. This review also integrates various technologies such as genomics, proteomics, and metabolomics. This provides a broader system-level understanding of the risk gene loci, protein interaction networks, and metabolic changes associated with amyloid beta under the influence of microbial infections. Such techniques may lead to the identification of new molecular targets, the development of individualized treatment strategies, and the creation of early biomarkers for use in clinical research. In conclusion, this review suggests that amyloid-beta is not merely a pathological by-product but an environmentally responsive molecule with dual functions. A deeper understanding of the dynamic regulation of amyloid-beta, considering infection status and disease stage, can provide new directions for treatment strategies aimed at the prevention and treatment of Alzheimer’s disease.

01 Nov 2026·JPAD-Journal of Prevention of Alzheimers Disease

The missing improvers: Tau pathology, neuroplasticity, and the case for tau-informed patient selection before amyloid immunotherapy

Article

Author: Dinnerstein, Eric

Amyloid immunotherapy with lecanemab and donanemab has been approved on the basis of statistically significant slowing of cognitive and functional decline in early Alzheimer's disease (1,2). Yet clinicians treating individual patients face the everyday challenge of estimating whether a given patient is declining at the rate that would be expected for them, and whether their trajectory reflects a response to treatment. I argue that this difficulty arises in large part because the field cannot yet routinely stratify patients by tau pathology before treatment, even though tau burden is among the strongest available predictors of both the rate of progression and the magnitude of response to amyloid-targeting therapy. Post-hoc and open-label analyses of the Clarity AD and TRAILBLAZER-ALZ 2 programmes suggest that patients with absent, low, or medium tau burden may constitute a biologically distinct group in whom amyloid clearance is most likely to permit clinical stabilization or measurable functional gain. These observations remain hypotheses, generated largely from subgroup, open-label, and biomarker data rather than from prospective trials designed to test them I propose that tau status should be given strong consideration in patient selection, that tau-guided selection should be evaluated prospectively, and that the access, reimbursement, and standardization barriers to tau positron emission tomography (PET) - together with the promise of scalable plasma tau biomarkers - be addressed deliberately as the field moves toward tau-informed treatment. One tau PET tracer is currently approved by the US Food and Drug Administration, and a regulatory decision on a second is anticipated in 2026.

01 Oct 2026·JPAD-Journal of Prevention of Alzheimers Disease

The generalizability gap: anticoagulant exclusions and the "Enhanced Safety" of donanemab in the EU-eligible population

Letter

Author: Ijaz, Azan ; Mohyudin, Ghulam

675

News (Medical) associated with Donanemab-AZBT

15 Sep 2026

·www.fiercebiotech.com

Lilly pledges up to $237M per program in CNS genetic med collab with Canadian biotech

Eli Lilly’s ongoing attempt to strengthen its genetic medicine offering has seen the company pledge up to $237 million in biobucks per program as part of a collaboration with QurCan Therapeutics. The deal focuses on using the Canadian biotech’s TERP—which stands for target-engineered responsive polymer—platform to facilitate the polymer-lipid nanoparticle (PLNP) delivery of genetic medicines to the central nervous system and the peripheral nervous system. The pact will see Lilly and QurCan collaborate on “multiple research programs,” according to a Sept 15. release. QurCan is in charge of optimizing the genetic medicines that will use the TERP platform with Lilly taking responsibility for “further research, clinical development and commercialization of the selected programs.” The companies didn’t offer a detailed breakdown of the financials, but they did say that Lilly would make an undisclosed strategic investment in QurCan as well as an upfront payment. The biotech could potentially be in line for up to $237 million in research, development and commercial milestone payments per program, as well as a slice of the royalties should any resulting drug make it to market. Toronto-based QurCan has touted its TERP platform as being able to aid the “systemic, non-viral and repeat-dosable delivery of genetic medicines to targeted tissues and cells,” including through the blood-brain barrier (BBB). Plenty of Big Pharmas are seeking paths to enter the BBB, with Novartis execs telling Fierce earlier this year that they are “always looking” for new ways to traverse this final frontier of neuroscience. Finding new ways to reach the CNS aligns with Lilly’s interest in neuroscience. As well as the company’s approved Alzheimer’s disease med Kisunla , its clinical-stage portfolio includes the likes of mevidalen, a dopamine D1 receptor positive allosteric modulator being developed for various neurodegenerative disorders, and a GBA1 gene therapy for Parkinson’s disease. Lilly has also been on the lookout for ways to strengthen its genetic medicines offering for a while, most notably when the Big Pharma picked up its gene editing partner Verve Therapeutics for $1 billion upfront last year. In 2026, the drugmaker has teamed up with Profluent to develop AI-designed recombinases to address diseases with severe unmet needs, and is using Seamless Therapeutics’ recombinase platform to create treatments for hearing loss. “This collaboration with Lilly represents a validation of our PLNP technology platform and its potential to address some of the most challenging delivery problems in genetic medicine,” QurCan CEO Mohammad Ali Amini, Ph.D. said in this morning’s release. “The CNS and PNS remain among the most underserved areas in genetic medicine delivery, and we believe our non-viral approach offers a differentiated and versatile solution across various nucleotide cargos,” the CEO added. “We are thrilled to work with Lilly, a company with unparalleled expertise in neuroscience drug development and commercialization, to bring these therapies to patients who urgently need them.”

Gene TherapyOligonucleotide

09 Sep 2026

·www.prnewswire.com

CURE ALZHEIMER'S FUND EXPANDS ITS SCIENTIFIC ADVISORY BOARD

Leading Alzheimer's Disease Research Nonprofit Welcomes Four Renowned Experts in Therapeutics Development WELLESLEY HILLS, Mass., Sept. 9, 2026 /PRNewswire/ -- Cure Alzheimer's Fund (CureAlz) today announced the appointments of Drs. Michelle Arkin, Ronald B. DeMattos, Donna M. Huryn, and Kalpana Merchant to the organization's Scientific Advisory Board (SAB). The SAB provides strategic guidance on CureAlz's scientific direction and research investment strategy. Drawing on extensive experience translating scientific discoveries into therapies, its members help ensure CureAlz's research investments focus on the most promising opportunities to prevent Alzheimer's disease, reduce risk, and accelerate the development of new treatments that can improve the lives of people affected by the disease. "The addition of Drs. Arkin, DeMattos, Huryn, and Merchant further strengthens an already-exceptional Scientific Advisory Board and reinforces our commitment to identifying and funding the highest-impact Alzheimer's research," said Meg Smith, CEO of Cure Alzheimer's Fund. "The SAB's guidance helps ensure every research dollar is invested where it has the greatest potential to accelerate discoveries that lead to more effective treatments for people living with Alzheimer's disease—and ultimately, to a cure." CureAlz does not accept funding or direction from pharmaceutical or biotech companies but values the insights and expertise SAB members developed during their industry tenures. Collectively, the four new SAB members have decades of experience spanning target identification, drug discovery, and clinical development of Alzheimer's treatments. Michelle Arkin, Ph.D., is Professor of Pharmaceutical Chemistry, Vice Dean for Research Technology and Entrepreneurship in the School of Pharmacy, and Executive Director of the Small Molecule Discovery Center at the University of California, San Francisco. Dr. Arkin's chemical biology lab develops methods and molecules to target "undruggable" proteins—drawing on prior industry experience at Sunesis Pharmaceuticals and ongoing roles advising pharmaceutical companies and scientific journals, and as co-founder of four therapeutics startups. Ronald B. DeMattos, Ph.D., previously spent more than 20 years in neuroscience discovery at Eli Lilly, most recently serving as Senior Vice President and Chief Scientific Officer for Neurobiologics. He led the development of numerous therapeutic candidates that advanced to clinical studies in Alzheimer's patients, including donanemab—the FDA-cleared amyloid-lowering antibody for the treatment of early Alzheimer's disease sold under the brand name Kisunla™. Donna M. Huryn, Ph.D., is Professor of Practice in the Department of Chemistry at the University of Pennsylvania. Her laboratory designs small-molecule probes and drug candidates to treat neurodegenerative, kidney, and genetic diseases, building on an earlier career in pharmaceutical drug discovery at Hoffmann-La Roche and Wyeth Research. Dr. Huryn is a Fellow of the American Association for the Advancement of Science and the American Chemical Society (ACS), and was inducted into the ACS Division of Medicinal Chemistry Hall of Fame. Kalpana Merchant, Ph.D. , is a translational neuroscientist with more than 30 years of experience in drug development for neurological disorders and formerly was Chief Scientific Officer for Tailored Therapeutics–Neuroscience at Eli Lilly. She is Founder, President and Chief Science Officer of TransThera Consulting Co., an Adjunct Professor of Neurology at Northwestern University Feinberg School of Medicine, and serves as an advisor and board member for institutes and foundations. About Cure Alzheimer's Fund Cure Alzheimer's Fund (CureAlz) is a nonprofit dedicated to funding the most promising research to prevent, slow, or reverse Alzheimer's disease. Since its founding in 2004, CureAlz has provided $270 million to 400 of the world's leading researchers and has achieved a 100% perfect score and a Four-Star rating for 14 consecutive years from Charity Navigator. The organization's unwavering focus on finding a cure is made possible by our Board of Directors, Trustees, and Sustaining Partners who empower CureAlz operations and allow 100% of your gift to support our research program. For more information, visit CureAlz.org. MEDIA CONTACT: Stephanie Wasco [email protected] 781-304-8614 SOURCE Alzheimer's Disease Research Foundation 21% more press release views with Request a Demo

Executive Change

09 Sep 2026

·www.biospace.com

CURE ALZHEIMER’S FUND EXPANDS ITS SCIENTIFIC ADVISORY BOARD

Leading Alzheimer's Disease Research Nonprofit Welcomes Four Renowned Experts in Therapeutics Development WELLESLEY HILLS, Mass. , Sept. 9, 2026 /PRNewswire/ -- Cure Alzheimer’s Fund (CureAlz) today announced the appointments of Drs. Michelle Arkin, Ronald B. DeMattos, Donna M. Huryn, and Kalpana Merchant to the organization's Scientific Advisory Board (SAB). The SAB provides strategic guidance on CureAlz's scientific direction and research investment strategy. Drawing on extensive experience translating scientific discoveries into therapies, its members help ensure CureAlz's research investments focus on the most promising opportunities to prevent Alzheimer's disease, reduce risk, and accelerate the development of new treatments that can improve the lives of people affected by the disease. "The addition of Drs. Arkin, DeMattos, Huryn, and Merchant further strengthens an already-exceptional Scientific Advisory Board and reinforces our commitment to identifying and funding the highest-impact Alzheimer's research," said Meg Smith, CEO of Cure Alzheimer's Fund. "The SAB's guidance helps ensure every research dollar is invested where it has the greatest potential to accelerate discoveries that lead to more effective treatments for people living with Alzheimer's disease—and ultimately, to a cure." CureAlz does not accept funding or direction from pharmaceutical or biotech companies but values the insights and expertise SAB members developed during their industry tenures. Collectively, the four new SAB members have decades of experience spanning target identification, drug discovery, and clinical development of Alzheimer's treatments. Michelle Arkin, Ph.D . , is Professor of Pharmaceutical Chemistry, Vice Dean for Research Technology and Entrepreneurship in the School of Pharmacy, and Executive Director of the Small Molecule Discovery Center at the University of California, San Francisco. Dr. Arkin's chemical biology lab develops methods and molecules to target "undruggable" proteins—drawing on prior industry experience at Sunesis Pharmaceuticals and ongoing roles advising pharmaceutical companies and scientific journals, and as co-founder of four therapeutics startups. Ronald B. DeMattos, Ph.D. , previously spent more than 20 years in neuroscience discovery at Eli Lilly, most recently serving as Senior Vice President and Chief Scientific Officer for Neurobiologics. He led the development of numerous therapeutic candidates that advanced to clinical studies in Alzheimer's patients, including donanemab—the FDA-cleared amyloid-lowering antibody for the treatment of early Alzheimer's disease sold under the brand name Kisunla™. Donna M. Huryn, Ph.D. , is Professor of Practice in the Department of Chemistry at the University of Pennsylvania. Her laboratory designs small-molecule probes and drug candidates to treat neurodegenerative, kidney, and genetic diseases, building on an earlier career in pharmaceutical drug discovery at Hoffmann-La Roche and Wyeth Research. Dr. Huryn is a Fellow of the American Association for the Advancement of Science and the American Chemical Society (ACS), and was inducted into the ACS Division of Medicinal Chemistry Hall of Fame. Kalpana Merchant, Ph.D. , is a translational neuroscientist with more than 30 years of experience in drug development for neurological disorders and formerly was Chief Scientific Officer for Tailored Therapeutics–Neuroscience at Eli Lilly. She is Founder, President and Chief Science Officer of TransThera Consulting Co., an Adjunct Professor of Neurology at Northwestern University Feinberg School of Medicine, and serves as an advisor and board member for institutes and foundations. About Cure Alzheimer's Fund Cure Alzheimer's Fund (CureAlz) is a nonprofit dedicated to funding the most promising research to prevent, slow, or reverse Alzheimer's disease. Since its founding in 2004, CureAlz has provided $270 million to 400 of the world's leading researchers and has achieved a 100% perfect score and a Four-Star rating for 14 consecutive years from Charity Navigator. The organization's unwavering focus on finding a cure is made possible by our Board of Directors, Trustees, and Sustaining Partners who empower CureAlz operations and allow 100% of your gift to support our research program. For more information, visit CureAlz.org . MEDIA CONTACT: Stephanie Wasco swasco@CureAlz.org 781-304-8614 View original content to download multimedia: SOURCE Alzheimer's Disease Research Foundation

Executive Change

100 Deals associated with Donanemab-AZBT

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External Link

KEGG	Wiki	ATC	Drug Bank
D11500	Donanemab-AZBT	-	-

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Cognition Disorders	Canada	Eli Lilly Canada, Inc.	03 Jul 2026
Dementia due to Alzheimer's disease (disorder)	United Kingdom	Eli Lilly Nederland BV	23 Oct 2024
Dementia due to Alzheimer's disease (disorder)	United Kingdom	Eli Lilly & Co.	23 Oct 2024
Mild cognitive disorder	United Kingdom	Eli Lilly Nederland BV	23 Oct 2024
Mild cognitive disorder	United Kingdom	Eli Lilly & Co.	23 Oct 2024
Alzheimer Disease	United States	Eli Lilly & Co.	02 Jul 2024

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Psychotic Disorders	NDA/BLA	Canada	Eli Lilly Canada, Inc.	-
Plaque, Amyloid	Phase 3	United States	Eli Lilly & Co.	22 May 2026
Plaque, Amyloid	Phase 3	Japan	Eli Lilly & Co.	22 May 2026
Neurocognitive Disorders	Phase 3	China	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	Argentina	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	Australia	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	Poland	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	South Korea	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	Spain	Eli Lilly & Co.	10 Oct 2022
Neurocognitive Disorders	Phase 3	Taiwan Province	Eli Lilly & Co.	10 Oct 2022

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04437511 (TRAILBLAZER-ALZ 2, Pubmed \| Neurol Clin Pract)	Phase 2	Alzheimer Disease	251	Donanemab (Mild cognitive impairment or mild Alzheimer's disease)	pcheyrgtwt(rbryhqqqsl) = oypmchhixd cyafqblwln (ogfgxngdph ) View more	Positive	01 Jun 2026
NCT05738486 (TRAILBLAZER-ALZ 6, CTAD2025)	Phase 3	Alzheimer Disease	840	Donanemab standard dosing regimen	smoextfmxn(ekioodktmb) = ipfnkwvatb ddeuawnqqg (jnwmigujhk ) View more	Positive	01 Dec 2025
NCT05738486 (TRAILBLAZER-ALZ 6, CTgov)	Phase 3	Alzheimer Disease \| Neurocognitive Disorders	1,175	Placebo+Donanemab (1400 mg Donanemab - Standard Regimen)	euolhlzhly = epnajepecr xtvqxhuzdc (jqbspkblzy, ylkafwqijy - sadryfphmi) View more	-	14 Nov 2025
				Placebo+Donanemab (1400 mg Donanemab - Dose Skipping)	euolhlzhly = iiushexrhc xtvqxhuzdc (jqbspkblzy, xzbbhejoze - dydyzcuxsr) View more
NCT04437511 (TRAILBLAZER-ALZ 2, PRNewswire) Manual	Phase 3	Alzheimer Disease	-	Kisunla	nbaefmwzsm(nzajclyoqi): Difference = -0.6 View more	Positive	30 Jul 2025
				Neuroimaging Initiative (untreated external cohort)
NCT05738486 (TRAILBLAZER-ALZ 6, AAIC2025)	Phase 3	Alzheimer Disease	418	Standard regimen (700 mg monthly for first three doses, followed by 1400 mg monthly)	vtbeuwxgnb(zenevvuioj) = yzhpnlbaqe ikvpnsumlz (qvdwhdqttb ) View more	Positive	27 Jul 2025
				Modified regimen (350 mg, 700 mg, and 1050 mg monthly for first three doses, followed by 1400 mg monthly)	vtbeuwxgnb(zenevvuioj) = izcudxmgqh ikvpnsumlz (qvdwhdqttb ) View more
NCT05108922 (TRAILBLAZER-ALZ 4, Pubmed \| Alzheimers Dement)	Phase 3	Alzheimer Disease amyloid plaque clearance	148	Donanemab	hauqvbupcp(tqdceetvlq) = vvnabkemrd benxrdsirk (drjntcewxr ) View more	Positive	01 May 2025
				Aducanumab	hauqvbupcp(tqdceetvlq) = pnnxqpwdag benxrdsirk (drjntcewxr ) View more
NCT05108922 (TRAILBLAZER-ALZ 4, AAIC2025)	Phase 3	Alzheimer Disease	148	Donanemab	canaayhcxl(yyqdmjzaiu) = wagiiwspuf oybgwalqnm (cazvwvduvc ) View more	Positive	01 May 2025
				Aducanumab	canaayhcxl(yyqdmjzaiu) = mykiizhdaq oybgwalqnm (cazvwvduvc ) View more
NCT04437511 \| NCT03367403 (TRAILBLAZER-ALZ and ALZ 2, Pubmed \| JAMA Neurol)	Not Applicable	Alzheimer Disease APOE ε4 allele number \| amyloid levels	3,030	Donanemab	crvyuqplcc(dotaiymfkb) = jjtogxpjhi ibnlmyoeeg (abxjvzfftx ) View more	Positive	01 May 2025
				Placebo	crvyuqplcc(dotaiymfkb) = lhmxqqykdy ibnlmyoeeg (abxjvzfftx ) View more
NCT05738486 (TRAILBLAZER-ALZ 6, AAIC2025)	Phase 3	Alzheimer Disease	843	donanemab (Standard dosing)	uwtbehzkjf(dkclkgmalw) = berypbmiyz mqzvigxwgw (rwgtxoihyt ) View more	Positive	01 Apr 2025
				donanemab (Modified titration dosing)	uwtbehzkjf(dkclkgmalw) = domnyrrrql mqzvigxwgw (rwgtxoihyt ) View more
NCT05738486 (TRAILBLAZER-ALZ 6, Company_Website 1 \| Company_Website 2) Manual	Phase 3	Alzheimer Disease	843	received two vials (700 mg) of donanemab for the first three infusions, then four vials (1400 mg) thereafterdonanemab for the first three infusions, then four vials (1400 mg) thereafter (Standard Dosing Regimen)	vviwlygazf(aaznhhnrls) = uaggwgngad waxakaijne (tmwzrkzhwf ) View more	Positive	29 Oct 2024
				received 1 vial (350 mg) of donanemab for the first infusion, two vials (700 mg) for the second infusion, three vials (1,050 mg) for the third infusion,donanemab for the first infusion, two vials (700 mg) for the second infusion, three vials (1,050 mg) for the third infusion, and four vials (1400 mg) per infusion thereafter (Modified Titration)	vviwlygazf(aaznhhnrls) = oumofmeotr waxakaijne (tmwzrkzhwf ) View more

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