The main purpose of this study is to investigate the safety and efficacy of the study drug solanezumab in participants with prodromal Alzheimer's disease (AD).

Start Date01 Jun 2016

Sponsor / Collaborator

Eli Lilly & Co.

NCT02614131

/ TerminatedPhase 1

Single-Dose and Multiple-Dose, Dose-Escalation Study With LY2599666 to Evaluate the Safety, Pharmacokinetics, and Tolerability in Healthy Subjects and Patients With Mild Cognitive Impairment Due to Alzheimer's Disease and Mild-to-Moderate Alzheimer's Disease

The main purpose of this study is to evaluate the safety and tolerability of the study drug known as LY2599666 in different groups of people - those who are healthy, those who have mild cognitive impairment due to Alzheimer's Disease (AD), and those with mild-to-moderate AD. The study will measure how much LY2599666 gets into the bloodstream and how long it takes the body to get rid of it. It will also evaluate how LY2599666 affects the body. The study has three parts. Part A will last about 2 months. Parts B and C will each last about 23 weeks. Participants may only enroll in one part.

Start Date01 Dec 2015

Sponsor / Collaborator

Eli Lilly & Co.

100 Clinical Results associated with Solanezumab

100 Translational Medicine associated with Solanezumab

100 Patents (Medical) associated with Solanezumab

302

Literatures (Medical) associated with Solanezumab

01 Feb 2026·Neural Regeneration Research

Insights into the transcriptomic heterogeneity of brain endothelial cells in normal aging and Alzheimer’s disease

Article

Author: Hoi, Maggie Pui Man ; Lei, Chon Lok ; Yue, Qian ; Wan, Huaibin ; Zhang, Zaijun ; Li, Shang

Drug development for Alzheimer’s disease is extremely challenging, as demonstrated by the repeated failures of amyloid-β-targeted therapeutics and the controversies surrounding the amyloid-β cascade hypothesis. More recently, advances in the development of Lecanemab, an anti-amyloid-β monoclonal antibody, have shown positive results in reducing brain A burden and slowing cognitive decline in patients with early-stage Alzheimer’s disease in the Phase III clinical trial (Clarity Alzheimer’s disease). Despite these promising results, side effects such as amyloid-related imaging abnormalities (ARIA) may limit its usage. ARIA can manifest as ARIA-E (cerebral edema or effusions) and ARIA-H (microhemorrhages or superficial siderosis) and is thought to be caused by increased vascular permeability due to inflammatory responses, leading to leakages of blood products and protein-rich fluid into brain parenchyma. Endothelial dysfunction is an early pathological feature of Alzheimer’s disease, and the blood–brain barrier becomes increasingly leaky as the disease progresses. In addition, APOE4, the strongest genetic risk factor for Alzheimer’s disease, is associated with higher vascular amyloid burden, increased ARIA incidence, and accelerated blood–brain barrier disruptions. These interconnected vascular abnormalities highlight the importance of vascular contributions to the pathophysiology of Alzheimer’s disease. Here, we will closely examine recent research evaluating the heterogeneity of brain endothelial cells in the microvasculature of different brain regions and their relationships with Alzheimer’s disease progression.

01 Aug 2025·Japanese Journal of Radiology

Practical brain MRI guidelines for anti-Aβ antibody treatment in early symptomatic Alzheimer’s disease

Review

Author: Mori, Harushi ; Abe, Osamu ; Miki, Yukio ; Kakeda, Shingo ; Tokumaru, Aya M ; Kudo, Kohsuke ; Aoki, Shigeki

Abstract:

Purpose:

These guidelines aim to support magnetic resonance imaging (MRI) diagnosis in patients receiving anti-amyloid β (Aβ) antibody treatment without restricting treatment eligibility.

Materials and methods:

These guidelines were collaboratively established by Japan Radiological Society, The Japanese Society of Neuroradiology, and Japanese Society for Magnetic Resonance in Medicine by reviewing existing literature and the results of clinical trials.

Results:

Facility standards should comply with the “Optimal Use Promotion Guidelines” of Japan, and physicians should possess comprehensive knowledge of amyloid-related imaging abnormalities (ARIA) and expertise in brain MRI interpretation. The acquisition of knowledge regarding amyloid-related imaging abnormalities, brain MRI, anti-Aβ antibody introduction, and post-treatment diagnosis are also recommended.

Conclusion:

These guidelines facilitate the accurate diagnosis and effective management of ARIA; ensure the safe administration of anti-Aβ drugs; and provide a framework for MRI facilities, includes staffing requirements and the use of MRI management systems.

24 Jun 2025·NEUROLOGY

Changes in Daily Functioning in Association With Tau and Amyloid Among Unimpaired Older Adults With and Without Elevated Amyloid

Article

Author: Amariglio, Rebecca ; Rentz, Dorene M. ; Donohue, Michael C. ; Sperling, Reisa Anne ; Marshall, Gad A. ; Liu, Andy ; Langford, Oliver ; Dubbelman, Mark A. ; Aisen, Paul S. ; Raman, Rema

BACKGROUND AND OBJECTIVES:

Everyday functioning declines gradually over time in Alzheimer disease (AD), with the earliest changes potentially occurring at the preclinical stage. We investigated how changes in everyday functioning relate to (changes in) amyloid and tau in a large sample of cognitively unimpaired older adults, most of whom had elevated amyloid levels at the start of the study.

METHODS:

This prospective study included participants from a 240-week randomized controlled trial of an anti-amyloid drug, solanezumab, and individuals who screen-failed because of a negative amyloid PET scan. A subset (n = 434) underwent repeated tau PET scans. Participants and their study partners completed the Alzheimer's Disease Cooperative Study Activities of Daily Living Prevention Instrument multiple times during the double-blind phase of the trial. Using generalized least-squares models, fit by restricted maximum likelihood, we analyzed how changes in everyday functioning related to amyloid and tau PET. We also correlated changes in amyloid and tau PET with changes in everyday functioning.

RESULTS:

A total of 1,707 participants (71.5 ± 4.7 years, 60% female) showed a marginal decline in everyday functioning. Among individuals with elevated amyloid, those with the highest levels of neocortical and medial temporal tau showed the largest decline in everyday functioning, as reported by the participants and their study partners. Increases in neocortical and medial temporal tau correlated moderately (correlation coefficient ranging from -0.2 to -0.5) with a decline in ADCS ADL-PI scores. Functional changes were not evident with amyloid alone. At the item level, participants and their study partners were most likely to report increased difficulty at the last visit with completing complex activities and selecting and paying for items when shopping.

DISCUSSION:

Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning. These findings demonstrate the utility of including sensitive measures of everyday functioning in clinical practice and clinical trials at the stage of preclinical AD.

TRIAL REGISTRATION INFORMATION:

The A4 study, ClinicalTrials.gov ID: NCT02008357; and Longitudinal Evaluation of Amyloid Risk and Neurodegeneration, ClinicalTrials.gov ID: NCT02488720.

News (Medical) associated with Solanezumab

04 Aug 2025

·www.einpresswire.com

Biomed Industries Presents Four Breakthrough Studies on Alzheimer’s, Rett Syndrome, and Obesity Therapies at AAIC 2025

Biomed Industries, Inc. Presents Four Pivotal Studies at AAIC 2025 Highlighting Breakthrough Therapies for Alzheimer’s, Rett Syndrome, and Obesity NA-831 is the only drug to date that has halted Alzheimer’s disease progression. Combining it with existing drugs like Donanemab could optimize therapeutic efficacy and reduce serious side effects.” — Dr. Lloyd L. Tran, CEO of Biomed SAN JOSE, CA, UNITED STATES, August 4, 2025 / EINPresswire.com / -- Biomed Industries, Inc., a leading biopharmaceutical innovator developing transformative therapies for neurological and metabolic diseases, today announced the presentation of four major scientific papers at the Alzheimer’s Association International Conference (AAIC), held July 27–31, 2025, in Toronto, Canada. The presentations featured Biomed’s next-generation oral therapies for Alzheimer’s disease, Rett syndrome, and obesity, with a focus on novel combination strategies designed to enhance safety, efficacy, and accessibility. Featured AAIC 2025 Presentations: 1. The End of the Amyloid Era? Evidence for a Paradigm Shift in the Quest to Treat Alzheimer’s Disease 2. A Phase 3 Clinical Protocol of NA-831 Combined with Donanemab in Early Alzheimer’s Disease: A Placebo-Controlled, Double-Blind Study 3. Associations Between Alzheimer’s Disease and Rett Syndrome: Clinical Trials of NA-831 and NA-921 4. Neuro-Metabolic Link Between Alzheimer’s Disease and Obesity: Clinical Evaluation of NA-831 and NA-931 1. PRESENTATION: The End of the Amyloid Era? A Paradigm Shift in Alzheimer’s Research For over three decades, the “amyloid hypothesis” has dominated Alzheimer’s disease (AD) research, asserting that amyloid-β accumulation is a primary driver of neurodegeneration. Biomed’s comprehensive analysis of Phase 3 trial data from seven anti-amyloid drugs — including aducanumab, lecanemab, donanemab, gantenerumab, bapineuzumab, crenezumab, and solanezumab — challenges this paradigm. Across all trials, both treatment and placebo groups exhibited similar cognitive decline, as measured by CDR-SB and ADAS-Cog. The average differences between treatment and placebo arms were minor and not clinically significant (CDR-SB: -0.25; ADAS-Cog: -0.79). Slope comparisons further revealed near-identical rates of decline between groups. “Our analysis of Phase 3 clinical trial data for seven anti-amyloid drugs, including FDA-approved Aducanumab, Lecanemab, and Donanemab, indicates that none could halt disease progression in a clinically meaningful way — and all carried serious safety concerns,” said Dr. Zung Tran, VP of Biostatistics and AI at Biomed. 2. PRESENTATION: Phase 3 Clinical Protocol of NA-831 Combined with Donanemab NA-831, Biomed’s lead oral candidate, is a first-in-class therapy that promotes neuroprotection, neurogenesis, and memory enhancement. Phase 2 trials demonstrated its disease-modifying potential with a favorable safety profile compared to traditional anti-amyloid drugs. In this upcoming Phase 3 study, NA-831 will be evaluated in combination with Donanemab, a recently FDA-approved monoclonal antibody, to explore synergistic effects. The goal is to lower Donanemab dosing, thereby reducing risks such as cerebral edema and microbleeds, while enhancing cognitive outcomes. “NA-831 is the only drug to date that has halted disease progression in Phase 2 trials,” said Dr. Lloyd Tran, CEO of Biomed Industries. “Combining it with existing drugs like Donanemab could optimize therapeutic efficacy and reduce serious side effects.” 3. PRESENTATION: Alzheimer’s and Rett Syndrome: Shared Mechanisms and Dual Therapeutic Potential Biomed also presented findings on NA-921, a structural analog of NA-831 developed for Rett syndrome, a rare X-linked neurodevelopmental disorder. NA-921 modulates MeCP2 expression, targeting the disorder’s core epigenetic dysfunction. A double-blind, placebo-controlled Phase 2/3 trial (ClinicalTrials.gov ID: NCT06849973) demonstrated promising results: Clinical Global Impression–Improvement (CGI-I) at week 12: NA-921: 3.60 | Placebo: 3.83 | P = 0.0020 | Effect size = 0.42 NA-921 was well tolerated, with a significantly improved safety profile compared to trofinetide: - Diarrhea: Trofinetide 82%, NA-921 24%, Placebo 19% - Vomiting: Trofinetide 29%, NA-921 9%, Placebo 11% - Fever: Trofinetide 9%, NA-921 5%, Placebo 4% These findings underscore a possible biological link between Alzheimer’s disease and Rett syndrome, opening new cross-indication opportunities for NA-831 and NA-921. 4. PRESENTATION: Neuro-Metabolic Connections: NA-831 and NA-931 in Alzheimer’s and Obesity Biomed’s data also revealed compelling evidence of a neuro-metabolic bridge between Alzheimer’s disease, diabetes, and obesity. In addition to NA-831’s CNS benefits, Biomed is advancing NA-931, an oral quadruple receptor agonist (IGF-1, GLP-1, GIP, and glucagon) designed to treat obesity. In a 13-week Multiple Ascending Dose (MAD) study: - Mean body weight reduction: Up to 13.8% at 150 mg daily, 12.4% greater than placebo - ≥12% weight loss achieved by 72% of NA-931-treated patients vs. 2% in placebo group NA-931 demonstrated a strong safety profile, with mild and transient GI-related adverse events, and no observed muscle loss. “Our pipeline shows how targeting interconnected pathways across the CNS and metabolic systems can unlock significant clinical potential,” said Michael Willis, VP of Business Development. “With six active programs across Alzheimer’s, ALS, Rett syndrome, stroke, obesity, and MASH, we are building a diversified platform to accelerate innovation and value creation.” ABOUT BIOMED INDUSTRIES, INC. Biomed Industries, Inc. is a pioneering biopharmaceutical company committed to developing novel therapeutics that address unmet medical needs. Its innovative research platform has produced treatments for conditions including Alzheimer’s disease, ALS, Traumatic Brain Injury, Major Depressive Disorder, Diabetes, Obesity, MASH, Stroke, and rare diseases such as Huntington Disease and Rett Syndrome. (Website: https://www.biomedind.com ) Michael Willis Biomed Industries, Inc. email us here Visit us on social media: LinkedIn X Biomed introduction video Legal Disclaimer: EIN Presswire provides this news content "as is" without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the author above.

Clinical ResultPhase 2Phase 3

29 Apr 2025

·www.biospace.com

AstraZeneca Abandons Neuroscience, Prioritizes Weight Loss, Immunology

iStock, hapabapa Following the recent discontinuations of assets in Alzheimer’s and migraine, AstraZeneca is stepping away from neuro altogether. AstraZeneca will no longer play in the neuroscience space, company executives said in an investor call on Tuesday, presenting the pharma’s first-quarter 2025 earnings report. “There’s a lot of things we can’t fund and we cannot be everywhere,” CEO Pascal Soriot said during the call. “CNS really is probably better managed by other companies that have a focus on that.” In the quarter, AstraZeneca discontinued the development of MEDI1814, an early-stage anti-amyloid beta antibody for Alzheimer’s disease, and MEDI0618, a Phase II monoclonal antibody for migraine, according to its latest pipeline document . These moves leave the company with no active neuroscience program. “We have closed our neuro programs and identified partners for some of them,” noted Sharon Barr, executive vice president of BioPharmaceuticals R&D at AstraZeneca. “This represents the closure of our neuroscience group at AstraZeneca,” which will allow the company to focus on its “core therapeutic priorities and fund our high-value programs.” The move away from neuroscience, according to Barr, will allow the pharma to instead channel its resources into weight management, dyslipidemia, respiratory diseases and immunology indications. “This prioritization allows us to reinvest in the programs that we think are important for AstraZeneca.” In the first three months of 2025, AstraZeneca recorded 10% revenue growth , nearly hitting $13.6 billion. The pharma’s performance in the quarter fell short of the analyst forecast , however, which pegged its Q1 sales to hit $13.68 billion. On a per-share basis, on the other hand, AstraZeneca came out ahead, earning $1.88 in the quarter versus the consensus of $1.10. Cancer remained the pharma’s strongest area, racking up more than $5.6 billion in sales across its various products. While its top-selling product was the type 2 diabetes therapy Farxiga—which surged 15% year-on-year to bring in more than $2 billion in Q1—most of its main growth drivers come from its oncology business. The kinase inhibitor Tagrisso, for instance, brought in nearly $1.7 billion in the quarter, a 12% increase from the same period last year. Imfinzi, a PD-1 blocker indicated for lung cancer, earned $1.26 billion in Q1, while the lymphoma drug Calquence and the PARP inhibitor Lynparza raked in $762 million and $726 million, respectively. Looking ahead to the rest of the year, AstraZeneca expects its total revenue to grow by a high single-digit percentage, while core earnings per share will increase by a low double-digit percentage. Tariffs Unlikely To Have Major Impact AstraZeneca executives on Tuesday refused to commit to a substantial investment package in the U.S., emphasizing that the potential effects of tariffs on its business would be “manageable,” particularly since the majority of its products in the U.S. are being manufactured domestically, Chief Financial Officer Aradhana Sarin said during the investor call. The pharma made a $3.5 billion injection into its U.S. footprint last November, money that it earmarked for an R&D facility in Massachusetts and a couple of manufacturing facilities. “We’ve said this year that our [capital expenditure] would be 50% higher than last year, but going forward, we need to look at how the portfolio develops,” Sarin added. For instance, before making any major infrastructure investments, the pharma will first want to see how its oral GLP-1 drug performs in clinical trials and how its breast cancer candidate camizestrant progresses, Sarin said. “We will then start to plan for success for these molecules and we’ll build and manage supply accordingly.” Several of AstraZeneca’s Big Pharma peers have in recent weeks announced hefty multi-billion investments in the U.S., largely in response to the threat of tariffs from President Donald Trump. Eli Lilly was first out the door in February with a $27 billion pledge to construct four new plants. J&J was close behind, with a $55 billion commitment that it will make over the next four years. Novartis , Roche and Regeneron have all also announced U.S.-based investments.

Phase 2Financial StatementPhase 1

12 Jun 2024

·firstwordpharma.com

With fresh $100M, Alzheon lays out strategy for Alzheimer’s approval next year

Despite a pair of drug approvals within the last three years and millions of patients in need, Alzheimer’s disease treatments have struggled with a gamut of safety, efficacy, and accessibility problems. As a third anti-beta amyloid antibody – Eli Lilly’s donanemab – nears FDA clearance, Alzheon is taking a different tack with its lead programme that it thinks will address all three pain points that have plagued drug development in the field.On Wednesday, the biotech raised a $100-million series E to wrap up the APOLLOE4 Phase III study of valiltramiprosate (ALZ-801) in patients with early Alzheimer’s, and ready it for commercialisation. The round, led by Alerce Medical Technology Partners, brings Alzheon’s total equity financing to $185 million.The pivotal trial is expected to read out in the third quarter, and the company plans to begin a regulatory submission to the FDA by year-end. If all goes well, CEO Martin Tolar expects the oral small molecule to be available to US patients in 2025. “We truly are at the dawn of a new era,” he said. “We understand the biology [of Alzhiemer’s] and we have an opportunity to transform the standard of care with our treatment.”Genetically defined diseaseAlzheon was founded over a decade ago to develop a treatment for Alzheimer’s by methodically determining which toxic agent is driving the disease, and which biomarkers are effective at tracking progression and gauging the efficacy of a given treatment.Notably, Alzheon’s clinical programme is initially enrolling patients who are homozygous for APOE4, a strong genetic risk factor of the disease.Around two-thirds of patients with Alzheimer’s have one copy of the gene, but in people with two copies, “virtually everybody” will develop the disease, Tolar said. About 15% of Alzheimer’s patients are homozygous for APOE4. While the high-risk group might seem the most likely to benefit from treatment, both of Biogen and Eisai’s anti-beta amyloid antibodies, Leqembi (lecanemab) and the now-abandoned Aduhelm (aducanumab), as well as Lilly’s donenamab, have not been as effective in APOE4-homozygous patients and in fact had increased side effects in this population. Plaque precursorsWhile Alzheon has also landed on beta amyloid as the main cause of Alzheimer’s, the team importantly singled out small, soluble amyloid aggregates – the precursors of the plaques targeted by most antibody therapeutics – as the molecules responsible for disease pathology. Beta amyloid is a key neurological protein that responds to damage, but as we age, levels of the monomer increase and the brain becomes less efficient at clearing it. As the molecule accumulates, it can misfold and begin aggregating into toxic, soluble oligomers that cause damage to the brain, Tolar explained.The brain will then sequester these aggregates into insoluble amyloid plaques, which have been the target for much of the drugs in development for Alzheimer’s.But, Tolar said, plaques are “the wrong target” to achieve cognitive and functional improvement, which the company says it has demonstrated in multiple published studies. Rather, the key is to prevent these plaques from forming in the first place – valiltramiprosate accomplishes by blocking beta amyloid from clumping into oligomers.Positive safety, efficacy signsSo far, clinical data seem to support Alzheon’s tactic. While Leqembi and donanemab led to patient improvements of 27% and 29%, versus placebo, respectively, on the Clinical Dementia Rating scale, Phase II results for valiltramiprosate demonstrated an 81% functional benefit on the same measurement. “These patients usually are at the edge of a cliff. They are a little forgetful. But in a year and a half they don't recognise their children, their spouses. And we can keep them stable for two years,” Tolar commented. “These are the data that really gave us confidence [in valiltramiprosate], and in fact helped us raise $100 million at a time where nobody can raise money.”Additionally, because plaques can occur in blood vessel walls, they could also be the reason why amyloid-related imaging abnormalities (ARIA), which can cause both brain oedema and haemorrhage, are a serious side effect associated with both Leqembi and donanemab. However, since valiltramiprosate doesn’t act on plaques, it could be a safer option. “We have shown in over 3000 patients, in a three-year follow-up, that we don't have an increase in brain haemorrhages,” Tolar said. Another potential benefit of valiltramiprosate is simply by virtue of its oral administration, which would make it cheaper and easier for patients to take for years to stave off disease progression, rather than an antibody IV infusion.

Phase 2Phase 3Clinical ResultDrug Approval

100 Deals associated with Solanezumab

External Link

KEGG	Wiki	ATC	Drug Bank
D10058	Solanezumab	-	DB11756

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Amnesia	Phase 3	United States	Eli Lilly & Co.	28 Feb 2014
Amnesia	Phase 3	Japan	Eli Lilly & Co.	28 Feb 2014
Amnesia	Phase 3	Australia	Eli Lilly & Co.	28 Feb 2014
Amnesia	Phase 3	Canada	Eli Lilly & Co.	28 Feb 2014
Cognition Disorders	Phase 3	United States	Eli Lilly & Co.	28 Feb 2014
Cognition Disorders	Phase 3	Japan	Eli Lilly & Co.	28 Feb 2014
Cognition Disorders	Phase 3	Australia	Eli Lilly & Co.	28 Feb 2014
Cognition Disorders	Phase 3	Canada	Eli Lilly & Co.	28 Feb 2014
Alzheimer Disease	Phase 3	United States	Eli Lilly & Co.	01 May 2009
Alzheimer Disease	Phase 3	Japan	Eli Lilly & Co.	01 May 2009

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04623242 (Pubmed)	Phase 2/3	Alzheimer Disease	-	Solanezumab	xorjatueyp(gdikpftkrw) = miywwiwobr kubxkzlhio (buxycwjnwb, 0.43)	-	29 Apr 2024
NCT02008357 (A4, Pubmed \| N Engl J Med)	Phase 3	Alzheimer Disease	1,169	Solanezumab	jynqccjfeg(ujkbaizuka) = zbiqetsasc twpivbbsve (ayylcrcnoo )	Negative	21 Sep 2023
				Placebo	jynqccjfeg(ujkbaizuka) = pjieunkxyn twpivbbsve (ayylcrcnoo )
NCT02760602 (ExpeditionPRO, CTgov)	Phase 3	Alzheimer Disease	26	Solanezumab (Solanezumab)	epsixllcyy(kgcnlqqjjo) = rjeesmdubr valzsozpbw (gdfvuxqvfn, vmqplrpssb - jxfoowejsw) View more	-	24 Jul 2018
				Placebo (Placebo)	epsixllcyy(kgcnlqqjjo) = tauoxykhyq valzsozpbw (gdfvuxqvfn, fkspanapak - vsodfcrhrn) View more
NCT01127633 (EXPEDITION EXT, CTgov)	Phase 3	Alzheimer Disease	1,457	Placebo (Placebo)	sfufyrohtq = wyjgnytudv ehmegcwgqb (myyuebrbkq, ouzwfukbla - pkyqiawodi) View more	-	03 May 2018
				Solanezumab (Solanezumab)	sfufyrohtq = fkeegnawti ehmegcwgqb (myyuebrbkq, xdycgffkzv - kznhosvcyj) View more
NCT01900665 (EXPEDITION3 \| EXPEDITION 3, CTgov)	Phase 3	Alzheimer Disease	2,129	Solanezumab (Solanezumab)	joacddwykb(pxpagadqqs) = rosjxxsysf sishbxxdwb (blyhrfatum, 0.355) View more	-	14 Mar 2018
				Placebo (Placebo)	joacddwykb(pxpagadqqs) = pkfouxpiuk sishbxxdwb (blyhrfatum, 0.356) View more
NCT01900665 (EXPEDITION3, Pubmed \| Br Dent J \| N Engl J Med) Manual	Phase 3	Alzheimer Disease \| Dementia	2,129	Solanezumab	uaklxbviav(dccvcchzma) = vqbqhlonfr rhfdddhjia (nucxgxmugc ) View more	Negative	25 Jan 2018
				Placebo	uaklxbviav(dccvcchzma) = uztqgfkcav rhfdddhjia (nucxgxmugc ) View more
NCT00904683 \| NCT01900665 \| NCT00905372 (EXPEDITION3, AAIC2017)	Phase 3	Alzheimer Disease amyloid pathology	-	Solanezumab	ilxxbwolgw(cysrtcurte) = aqluvywrur mwsmbfqbqb (pheaslopkc ) View more	-	01 Jul 2017

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