Bapineuzumab

A new report trying to settle a decades-old debate about Alzheimer’s disease has reached a dramatic conclusion: Antibody drugs that target sticky amyloid beta proteins in the brain simply don’t work. The meta-analysis, which compiles data from more than 20,000 patients across 17 clinical trials, determined that treatment with amyloid antibodies resulted in “little to no difference” in cognitive function, dementia severity and functional ability. The authors concluded that future Alzheimer’s drugs “should focus on other mechanisms of action.” But the study is filled with limitations sure to send many neuroscientists who have devoted their lives to these drugs into a tizzy. It overlooks the strongest arguments about why so many older attempts have failed; it ignores recent technological breakthroughs in delivering these kinds of drugs into the brain more efficiently; and it skirts over bigger and longer clinical trials that are still ongoing but promise to provide the most conclusive evidence on amyloid drugs yet. “I don’t think this changes the overall view of these therapies,” Eric McDade, a neurologist who studies these drugs and others at the WashU Medicine Memory Diagnostic Center in St. Louis, told Endpoints News . When asked if the meta-analysis would move the needle on the broader debate about the amyloid hypothesis, he said he “highly doubts it.” The study , published in the Cochrane Database of Systematic Reviews on Wednesday night, quickly spurred numerous headlines proclaiming the amyloid drugs useless or suggesting that the study will further fuel the ongoing debate about whether the marginal benefits of the medicines outweigh their risks, which can include brain bleeding and swelling. But several researchers contacted by Endpoints News were quick to point out what they see as a major methodological flaw. Only two clinical trials included in the review centered on the two amyloid antibodies that are commercially available in the US: Leqembi, sold by Biogen and Eisai; and Kisunla, made by Eli Lilly. Twelve clinical trials in the meta-analysis focused on drugs that failed their pivotal trials, including Genentech’s crenezumab, Johnson & Johnson’s bapineuzumab, Lilly’s solanezumab and Roche’s gantenerumab. Another three studies focused on Aduhelm, the controversial Biogen drug that the FDA approved against the will of its scientific advisors because it failed one of its two pivotal studies. The drug was subsequently withdrawn from the market after abysmal sales. “It should be no surprise that if you average 15 studies for drugs that don’t work with two studies for drugs that do work, that the average result shows that, as a class, these drugs don’t work,” Andrew Budson, associate director of the Boston University Alzheimer’s Disease Research Center, told Endpoints. “I just don’t think that this review is relevant for people living with Alzheimer’s disease.” For decades, much of the Alzheimer’s field has centered on the problematic protein known as amyloid beta. Scientists now know that the protein begins accumulating in our brains a decade or two before the first signs of memory loss set in. By that point, amyloid has formed plaques in the brain that trigger a cascade of other problems, including toxic tangles of a protein called tau and rampant inflammation. At least, that’s the gist of what scientists who adhere to the amyloid hypothesis of Alzheimer’s believe is happening. It’s an interpretation backed by reams of laboratory data and tantalizing genetic clues. Yet despite the billions of dollars that drugmakers have spent trying to clear out amyloid, they’ve barely made a dent in the disease. The dispute over whether amyloid has led the field astray — or worse, hijacked and blocked out promising alternative theories — has been roiling for years. Neuroscientists who are sticking to their guns often note that the earliest studies of amyloid-targeting drugs were tested in people already in the throes of dementia. In retrospect, scientists say those treatments were too little too late. There’s a variety of other arguments for why earlier attempts to target amyloid have failed. Some studies were done in people who had memory loss but turned out to not have amyloid plaques in the brain. Today, many companies use imaging molecules to make sure the patients they enroll in their studies actually have brains full of the plaques they are trying to remove. The type of amyloid that the drug targets may be important too. Older drugs like Lilly’s solanezumab that targeted free-floating forms of the protein failed to show a benefit in clinical studies. The commercialized drugs targeting smaller clumps of the protein, like Leqembi, or specific forms of the plaques, like Kisunla, showed modest but statistically significant slowing of cognitive decline. An Eisai spokesperson told Endpoints that the Cochrane review was “scientifically deeply flawed by inappropriately combining ineffective antibodies and failed studies with effective, regulatory-approved anti-amyloid treatments.” A Lilly spokesperson echoed that sentiment and said that pooling failed drugs with approved ones “dilutes the observed benefit and produces class-level conclusions that do not reflect the evidence for any individual approved therapy.” But combining data from disparate drugs may have had an unintended effect: making the medicines look safer than they really are. The risks of brain bleeding and swelling have only become prominent with the FDA-approved medicines. The Cochrane review concluded that there was probably “little to no difference” in symptomatic brain bleeding and swelling, risks that have been at the heart of the debate about whether the modest benefits of the drugs are worth it. McDade said that pooling all these studies together “underestimates the risk and benefit” of the two commercialized medicines, which “have the most consistent clinical benefit, which was modest and has been recognized as modest.” The Cochrane review authors, based at the Institute of Neurological Sciences of Bologna in Italy, did not immediately respond to questions from Endpoints. Whether the amyloid hypothesis proves to be the right one, drugmakers are marching down that road as ardently as ever. The trials included in the Cochrane review focused on people with mild cognitive impairment or in the early stages of dementia. Eisai and Lilly believe that their drugs will work better when given even earlier. Both companies are conducting large and lengthy clinical trials in seemingly healthy people who have evidence of amyloid accumulation, but no outward signs of memory loss. They hope that treating these so-called asymptomatic patients will more dramatically slow the disease. Results could come in the next couple of years. Other companies, including Roche, are working on next-generation versions of amyloid antibodies designed to better cross the protective blood-brain barrier — something that the existing medicines do rather poorly. Early results from Roche’s drug suggest greater and faster amyloid plaque reduction with far lower rates of brain bleeding and swelling. Several big pharma companies, including AbbVie, Bristol Myers Squibb and Novartis, have begun their own work on similar brain-targeting amyloid antibodies. Dozens of smaller companies have jumped on the trend as well. Marc Diamond, founding director of the Center for Alzheimer’s and Neurodegenerative Diseases at UT Southwestern Medical Center, doesn’t think the Cochrane review’s conclusions have any bearing on these new kinds of studies that are rejuvenating the often-dreary field. And although it’s too soon to know whether they will find success where so many others have failed, he is hopeful. “Stay tuned,” he said. “It is likely they will have a bigger effect.” Endpoints is fielding the next Biopharma Sentiment Index (BPSI) — a concise, three-minute survey that distills thousands of industry views into a clear quarterly benchmark. This year is pivotal for biopharma, and we need your perspective on where things are going. Take the survey here.

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.