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).

开始日期2016-06-01

申办/合作机构

Eli Lilly & Co.

NCT02614131 / Terminated临床1期

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.

开始日期2015-12-01

申办/合作机构

Eli Lilly & Co.

100 项与苏兰珠单抗相关的临床结果

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100 项与苏兰珠单抗相关的转化医学

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100 项与苏兰珠单抗相关的专利（医药）

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591

项与苏兰珠单抗相关的文献（医药）

2024-12-01·PHYTOMEDICINE

Osmundacetone ameliorates Alzheimer's-like pathologies by inhibiting β-amyloid fibrillation, oxidative damage and neuroinflammation in APP/PS1 transgenic mice

Article

作者: Zhang, Qi ; Zhao, Ling-Xiao ; Fan, Yong-Gang ; Wu, Ting-Yao ; Su, Jing-Yang ; Wang, Zhan-You ; Ren, Hang ; He, Da-Long ; Zhang, Yan-Hui

BACKGROUND:

β-Amyloid (Aβ) fibrillation is critical for Aβ deposition and cytotoxicity during the progression of Alzheimer's disease (AD). Consequently, anti-Aβ monoclonal antibody drugs targeting Aβ oligomers and aggregation are considered potential therapeutic strategies for AD treatment. Similar to the working mechanisms of anti-Aβ monoclonal antibody drugs, our study identified osmundacetone (OAC), a small-molecule compound isolated from the traditional Chinese medicine Rhizoma Osmundae, as exerting anti-AD effects by targeting Aβ.

PURPOSE:

This study sought to determine whether OAC influences the Aβ burden in APP/PS1 mice and to identify potential regulatory mechanisms.

METHODS:

Five-month-old APP/PS1 mice were injected intraperitoneally with OAC at a dose of 1 mg/kg for 12 weeks. The cognitive functions of the mice were assessed via the Morris water maze test and the open field test. Osmundacetone was analyzed via molecular docking, an isothermal dose‒response fingerprint-cellular context thermal shift assay, a thioflavine T fluorescence assay, and an atomic force microscopy assay to analyze the effects of OAC on Aβ fibrillation. Immunofluorescence, immunoblotting, and immunohistochemistry were used to assess Aβ clearance, AD pathology, oxidative stress, and inflammatory responses.

RESULTS:

The innovative biochemical and physical data illustrated that the ability of OAC to inhibit Aβ fibrillation was accomplished by binding directly to Aβ, which differed from the majority of previously reported natural polyphenols that modulate the Aβ content and structure in an indirect manner. The inhibition of Aβ fibrosis by OAC subsequently promoted Aβ lysosomal degradation, resulting in a decreased Aβ burden in APP/PS1 mice. Furthermore, OAC treatment inhibited oxidative damage by upregulating glutathione peroxidase expression and attenuated the production of inflammatory factors by downregulating nuclear factor-kB phosphorylation in APP/PS1 mice.

CONCLUSION:

These findings demonstrate, for the first time, that OAC could reduce the brain Aβ burden in APP/PS1 mice by inhibiting Aβ fibrillation through direct binding to Aβ and improve cognitive dysfunction by attenuating oxidative damage and neuroinflammation. These findings indicate that OAC may be a promising candidate for the treatment of AD.

2024-10-03·BRAIN

Increases in amyloid-β42 slow cognitive and clinical decline in Alzheimer’s disease trials

Article

作者: Imbimbo, Bruno P ; Espay, Alberto J ; Dwivedi, Alok K ; Abanto, Jesus

Abstract:

Positive effects of new anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer’s disease (AD) have been attributed to brain amyloid reduction. However, most anti-Aβ antibodies also increase the CSF levels of the 42-amino acid isoform (Aβ42). We evaluated the associations of changes in CSF Aβ42 and brain Aβ-PET with cognitive and clinical end points in randomized trials of anti-Aβ drugs that lowered (β- and γ-secretase inhibitors) or increased CSF Aβ42 levels (anti-Aβ monoclonal antibodies) to test the hypothesis that post-treatment increases in CSF Aβ42 levels are independently associated with cognitive and clinical outcomes.From long-term (≥12 months) randomized placebo-controlled clinical trials of anti-Aβ drugs published until November 2023, we calculated the post-treatment versus baseline difference in ADAS-Cog (cognitive subscale of the Alzheimer’s Disease Assessment Scale) and CDR-SB (Clinical Dementia Rate-Sum of Boxes) and z-standardized changes in CSF Aβ42 and Aβ-PET Centiloids (CL). We estimated the effect size [regression coefficients (RCs) and confidence intervals (CIs)] and the heterogeneity (I2) of the associations between AD biomarkers and cognitive and clinical end points using random-effects meta-regression models.We included 25 966 subjects with AD from 24 trials. In random-effects analysis, increases in CSF Aβ42 were associated with slower decline in ADAS-Cog (RC: −0.55; 95% CI: −0.89, −0.21, P = 0.003, I2 = 61.4%) and CDR-SB (RC: −0.16; 95% CI: −0.26, −0.06, P = 0.002, I2 = 34.5%). Similarly, decreases in Aβ–PET were associated with slower decline in ADAS-Cog (RC: 0.69; 95% CI: 0.48, 0.89, P < 0.001, I2 = 0%) and CDR-SB (RC: 0.26; 95% CI: 0.18, 0.33, P < 0.001, I2 = 0%). Sensitivity analyses yielded similar results.Higher CSF Aβ42 levels after exposure to anti-Aβ drugs are independently associated with slowing cognitive impairment and clinical decline. Increases in Aβ42 may represent a mechanism of potential benefit of anti-Aβ monoclonal antibodies in AD.

2024-10-01·Brain and nerve = Shinkei kenkyu no shinpo

[Anti-Amyloid Antibody Therapy for Alzheimer's Disease].

Review

作者: Ono, Kenjiro ; Shinohara, Moeko

Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death. Aβ monomers aggregate to form oligomers, protofibrils, and mature fibrils. Previously, the mature fibrils and plaques were implicated as contributors to neurotoxicity and neurodegeneration. However, a growing body of evidence proves stronger toxicity of oligomers and protofibrils. Among the many recent phase 3 clinical trials that have investigated the role of anti-Aβ antibodies in AD, some have shown the clinical efficacy of aducanumab, lecanemab, and donanemab in these patients. Lecanemab showed selectivity towards protofibrils over fibrils, and donanemab was specifically directed against Aβ only in brain-specific amyloid plaques. In contrast, other anti-Aβ antibodies did not show efficacy in AD.

208

项与苏兰珠单抗相关的新闻（医药）

2024-10-29

·GlobeNewswire-Health Care

Eledon Pharmaceuticals Announces Positive Initial Data from Subjects with Type 1 Diabetes Treated with Tegoprubart as Part of an Immunosuppression Regimen Following Islet Transplantation in Investigator-Initiated Trial at UChicago Medicine

- First two out of three subjects treated with tegoprubart as part of immunosuppression regimen to prevent transplant rejection achieved insulin independence and remain insulin free, with glucose control in the normal range; Third subject was recently transplanted and is on trajectory for insulin independence - Islet engraftment in the first two subjects with tegoprubart estimated three to five times higher than engraftment in three comparable subjects receiving standard of care tacrolimus-based immunosuppression - Treatment with tegoprubart was generally well tolerated - Study data to be presented by UChicago Medicine’s team in oral presentation at the 5th IPITA/HSCI/Breakthrough T1D Stem Cells Summit IRVINE, Calif., Oct. 29, 2024 (GLOBE NEWSWIRE) -- Eledon Pharmaceuticals, Inc. (“Eledon”) (NASDAQ: ELDN) today announced positive data for the first three islet transplant recipients treated with an immunosuppression regimen that includes tegoprubart, the Company’s investigational anti-CD40L antibody, for prevention of islet transplant rejection in subjects with type 1 diabetes (T1D). The investigator-initiated trial, conducted by the research team at the University of Chicago Medicine’s Transplantation Institute, demonstrated potentially the first human cases of insulin independence achieved using an anti-CD40L monoclonal antibody therapy without the use of tacrolimus, the current standard of care for prevention of transplant rejection. The first two subjects achieved insulin independence and normal hemoglobin A1C (HbA1c) levels, a measure of average blood glucose, post-transplant. The third subject, who recently received an islet transplant, decreased insulin use by more than 60% three days following the procedure and continues on an insulin independence trajectory. Subjects on study received islet transplants combined with induction therapy, mycophenolate mofetil (MMF), and tegoprubart, given every third week by intravenous (IV) infusion. The first two subjects achieved insulin independence and presented stable islet graft function at approximately three months and six months post-transplant, respectively. Islet engraftment, measured by graft function standardized to the number of islets infused, was three to five times higher than three comparable subjects outside this study who received tacrolimus-based immunosuppression, suggesting treatment with tegoprubart is less toxic to transplanted islets resulting in improved graft survival and function. Treatment was generally well tolerated in all subjects with no unexpected adverse events or hypoglycemic episodes. After initial islet transplant, the first participant reduced insulin requirements by over 60% and normalized blood glucose control. The first patient then achieved insulin independence approximately two weeks after the second islet transplantation procedure. The data are being featured in an oral presentation at the International Pancreas and Islet Transplantation Association (IPITA), Harvard Stem Cell Institute (HSCI), and Breakthrough T1D (formerly JDRF) 5th Annual Summit on Stem Cell Derived Islets on Tuesday, October 29, 2024. “We are very pleased that tegoprubart played a pivotal role in yet another landmark advance in transplantation research through the work of Dr. Witkowski, Dr. Fung and their team at UChicago Medicine,” said David-Alexandre C. Gros, M.D., Chief Executive Officer of Eledon. “Following promising results in kidney allotransplant procedures as well as heart and kidney xenograft procedures, these data from subjects following islet transplantation further demonstrate tegoprubart’s potential to protect transplanted organs and cells. Dr. Witkowski’s study also further reinforces prior study results showing that tegoprubart may offer a favorable safety and efficacy profile compared to tacrolimus-based immunosuppression regimens.” “These data are another step in our quest to achieve a path for functional cures in type 1 diabetes,” said Piotr Witkowski, M.D., Ph.D., Director, Pancreas and Islet Transplant Program, UChicago Medicine and one of the study’s lead investigators. “For more than 30 years, we have been looking for options that can deliver target levels of immunosuppression without the side effects associated with standard of care, including toxicity to the kidneys, central nervous system and islet cells, and increased risk of diabetes and hypertension. These data further support tegoprubart as a novel immunosuppression option that can play a central role in advancing islets transplantation as a potentially transformational alternative for subjects with type 1 diabetes.” “Breakthrough T1D is proud to fund and support this research and is encouraged by the tegoprubart study showing that subjects who received islet transplants with a tacrolimus-free immunosuppressive regimen are making insulin again,” said Breakthrough T1D Chief Scientific Officer Sanjoy Dutta, Ph.D. “Islet replacement therapies are a key priority for Breakthrough T1D, and we’re committed to driving research that moves us toward a world where these therapies are available to the broader T1D community. Achieving this goal requires novel approaches to keep transplanted cells functional with a tolerable immunosuppression regimen. These results are an important step toward that goal, and we look forward to seeing additional data.” Efficacy and Safety Results The first participant was a 42-year-old female with a baseline weight of 88 kg/194 lbs (BMI of 30). At 90 days post-transplant, the participant’s HbA1c level improved to 6.0% (from 8.4% at baseline) and daily insulin dose decreased to 16 units per day (from 80 units per day at baseline). After 16 weeks, the participant received a second islet transplant, and approximately two weeks later achieved insulin independence, maintaining improved HbA1c levels of 5.4% afterwards. The second participant was a 30-year-old female with a baseline weight of 50 kg/110 lbs (BMI of 21). This patient stopped insulin support (from 60 units per day at baseline) four weeks after the islet transplant. Her HbA1c levels improved to 5.8% and below (from 8.5% at baseline) starting at seven weeks after the transplant. The third participant was a 37-year-old male with a baseline weight of 92 kg/203 lbs (BMI of 30) with a baseline HbA1C of 9.3%. This patient was discharged home on day three post-transplant, requiring 29 units of insulin (from 90 units per day at baseline). The treatment was generally well tolerated in all subjects with no unexpected adverse events, severe hypoglycemic episodes, or graft rejection. In January 2024, Eledon announced that it would be supplying tegoprubart for this investigator-led clinical trial with the UChicago Medicine Transplantation Institute for pancreatic islet transplantation in subjects with type 1 diabetes (NCT06305286). Tegoprubart is the cornerstone component of the chronic immunosuppressive regimen for trial participants and is being evaluated for the prevention of transplant rejection in the trial. Funding for the study includes grants from Breakthrough T1D (formerly known as JDRF) and The Cure Alliance. About Islet Transplantation for Type 1 Diabetes Pancreatic islet transplantation is a minimally invasive procedure developed to provide blood glucose control for subjects with type 1 diabetes and minimize or eliminate dependence on insulin. During the procedure, pancreatic islets containing insulin-producing beta cells are isolated from the pancreas of a deceased organ donor and infused through a small catheter into the patient’s liver. The islet cells lodge in small blood vessels in the liver and release insulin. Post-procedure, subjects remain on immunosuppression therapy to prevent transplant rejection. About Eledon Pharmaceuticals and tegoprubart Eledon Pharmaceuticals, Inc. is a clinical stage biotechnology company that is developing immune-modulating therapies for the management and treatment of life-threatening conditions. The Company’s lead investigational product is tegoprubart, an anti-CD40L antibody with high affinity for the CD40 Ligand, a well-validated biological target that has broad therapeutic potential. The central role of CD40L signaling in both adaptive and innate immune cell activation and function positions it as an attractive target for non-lymphocyte depleting, immunomodulatory therapeutic intervention. The Company is building upon a deep historical knowledge of anti-CD40 Ligand biology to conduct preclinical and clinical studies in kidney allograft transplantation, xenotransplantation, and amyotrophic lateral sclerosis (ALS). Eledon is headquartered in Irvine, California. For more information, please visit the Company’s website at www.eledon.com. Follow Eledon Pharmaceuticals on social media: LinkedIn; Twitter Forward-Looking Statements This press release contains forward-looking statements that involve substantial risks and uncertainties. Any statements about the company’s future expectations, plans and prospects, including statements about planned clinical trials, the development of product candidates, expected timing for initiation of future clinical trials, expected timing for receipt of data from clinical trials, expected or future results of tegoprubart trials and its ability to prevent rejection in connection with islet cell transplantation or kidney transplantation, as well as other statements containing the words “believes,” “anticipates,” “plans,” “expects,” “estimates,” “intends,” “predicts,” “projects,” “targets,” “looks forward,” “could,” “may,” and similar expressions, constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements are inherently uncertain and are subject to numerous risks and uncertainties, including: risks relating to the safety and efficacy of our drug candidates; risks relating to clinical development timelines, including interactions with regulators and clinical sites, as well as patient enrollment; and risks relating to costs of clinical trials and the sufficiency of the company’s capital resources to fund planned clinical trials. Actual results may differ materially from those indicated by such forward-looking statements as a result of various factors. These risks and uncertainties, as well as other risks and uncertainties that could cause the company’s actual results to differ significantly from the forward-looking statements contained herein, are discussed in our quarterly 10-Q, annual 10-K, and other filings with the U.S. Securities and Exchange Commission, which can be found at www.sec.gov. Any forward-looking statements contained in this press release speak only as of the date hereof and not of any future date, and the company expressly disclaims any intent to update any forward-looking statements, whether as a result of new information, future events or otherwise. Investor Contact: Stephen JasperGilmartin Group(858) 525 2047stephen@gilmartinir.com Media Contact: Jenna UrbanBerry & Company Public Relations(212) 253 8881jurban@berrypr.com Source: Eledon Pharmaceuticals

临床结果免疫疗法临床研究

2024-10-29

·Endpoints

Two type 1 diabetes patients are insulin-free after Eledon's immunosuppressant and an islet transplant

Eledon Pharmaceuticals’ experimental immunosuppressant helped two patients with type 1 diabetes go insulin-free following an islet cell transplant, the company announced Tuesday. The company’s stock $ELDN rose about 12% on Tuesday morning after Eledon announced the data and an $85 million offering . It said the investigator-initiated trial, which is being conducted by researchers at UChicago Medicine Transplant Institute, could have produced the first results showing that two patients became insulin-independent after undergoing treatment with an anti-CD40L monoclonal antibody and without taking tacrolimus, which is the current standard of care to prevent transplant rejections. Tacrolimus, a type of immunosuppressant, comes with a laundry list of toxicity issues, including kidney and beta cell toxicity, post-transplant new-onset diabetes, hypertension, brain fog and tremors, according to Eledon CEO David-Alexandre Gros. “We’re trying to get people off insulin, and yet, right when we’re giving them new islet cells, we’re giving them a drug that is going to harm,” Gros told Endpoints News . “We’re looking to develop a new generation of immunomodulator, one that will be both more effective as well as safer than the current standard of care.” Gros pointed to Vertex’s work in stem cell-derived islet cell therapy — the company announced over the summer that three of its patients had gone insulin-free using VX-880 — but patients also have to be on chronic immunosuppressive therapy. Vertex is working on VX-264, which is designed to treat patients without immunosuppressants, but Gros thinks there will be a place for Eledon’s drug, called tegoprubart, if VX-264 fails. “What we’re hoping to do is to unlock this market if tegoprubart can provide as good or better protection but without all of the side effects,” Gros said. “And so far, the data is very encouraging.” In the study, patients received islet transplants combined with induction therapy — mycophenolate mofetil plus tegoprubart — every three weeks by an IV infusion. The company said treatment with tegoprubart was “generally well-tolerated” in all subjects, with no unexpected adverse events, graft rejection or hypoglycemic episodes. A third patient decreased their insulin use by more than 60% three days after the transplant procedure. Along with achieving insulin independence at approximately three months and six months post-transplant, the first two patients also recorded normal HbA1c levels. All three patients saw improved islet engraftment — engraftment was three to five times higher than three comparable subjects who received only tacrolimus — and Eledon said this suggests that tegoprubart is “less toxic” to transplanted islets and led to improved graft survival and function. Back in 2020, Eledon bought tegoprubart through its acquisition of Anelixis, though the ALS Therapy Development Institute had discovered the drug. Eledon first ran a Phase 2 trial with the drug in ALS patients before pivoting to transplant rejection. It still has plans to develop the drug in ALS. The company is continuing the trial in islet cell transplant, which is designed for up to nine patients, and it has three ongoing trials in kidney transplantation. Editor’s note: This story has been updated with the name of the UChicago Medicine Transplant Institute.

临床结果细胞疗法临床2期并购免疫疗法

2024-10-24

·GlobeNewswire-Health Care

Biogen to Present New Data at the Clinical Trials on Alzheimer's Disease (CTAD) 2024 Annual Conference

CAMBRIDGE, Mass., Oct. 24, 2024 (GLOBE NEWSWIRE) -- Biogen Inc. (Nasdaq: BIIB) announced upcoming data presentations and programming at the Clinical Trials on Alzheimer’s Disease (CTAD) annual conference, taking place October 29 - November 1, in Madrid, Spain. The presentations will include updates on new scientific findings from Biogen’s Alzheimer’s portfolio, highlighting data on different aspects of treatment and data examining preclinical Alzheimer’s disease and race. “These data showcase the breadth of our Alzheimer’s disease research and our ongoing commitment to scientific innovation,” said Priya Singhal, M.D., M.P.H., Head of Development at Biogen. “We remain dedicated to advancing the field of research and treatment for this disease in order to better serve the millions of patients, families and providers in the Alzheimer’s community.” Key Presentations and Symposia: Transitioning from Clinical Trial to Clinical Practice for Long-Term Lecanemab Treatment in Early Alzheimer's Disease: Perspectives from an Alzheimer's Disease Treatment Center, Tuesday, October 29The AHEAD 3-45 Study: Design and Results of a Novel Screening Process for a Preclinical AD Trial, Tuesday, October 29, 6:10 PMDoes the Current Evidence Base Support Continued Dosing with Lecanemab for Early Alzheimer's Disease? Wednesday, October 30, 9:40 AMLecanemab for the Treatment of Mild Cognitive Impairment and Mild Dementia Due to Alzheimer's Disease in Adults That Are Apoliprotein E ɛ4 Heterozygotes or Non-Carriers, Wednesday, October 30, 11:20 AMOne-Year Experience on the Use of Lecanemab in Clinical Practice, Wednesday, October 30, 3:30 PMAI-Derived Prognostic Covariates Enhance the Precision of Lecanemab Efficacy Assessments and Optimize Alzheimer's Disease Clinical Trials, Thursday, October 31, 3:25 PMEstimating by race and APOE Ɛ4 carrier status counts of US adults with subjective cognitive decline with preclinical Alzheimer’s disease, Friday, November 1 Virtual Experience on Tau PathologyAt the meeting, Biogen will also host a virtual booth for attendees exploring the role of tau in Alzheimer’s disease, including an interactive medical education e-learning module on knowtau.com which has more information on tau pathophysiology. For more information, please see the CTAD 2024 program and visit the Biogen CTAD virtual booth. About LEQEMBI® (lecanemab)LEQEMBI (lecanemab) is the result of a strategic research alliance between Eisai and BioArctic. LEQEMBI is a humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). LEQEMBI is an amyloid beta-directed antibody for the treatment for Alzheimer’s disease (AD) in the U.S. The U.S. Food and Drug Administration (FDA) granted LEQEMBI traditional approval on July 6, 2023. LEQEMBI is indicated for the treatment of Alzheimer’s disease. Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was initiated in clinical trials. Eisai and Biogen have been collaborating on the joint development and commercialization of AD treatments since 2014. Eisai serves as the lead of LEQEMBI development and regulatory submissions globally with both companies co-commercializing and co-promoting the product and Eisai having final decision-making authority. Please see full U.S. Prescribing Information for LEQEMBI, including Boxed WARNING and Medication Guide. About BiogenFounded in 1978, Biogen is a leading biotechnology company that pioneers innovative science to deliver new medicines to transform patient’s lives and to create value for shareholders and our communities. We apply deep understanding of human biology and leverage different modalities to advance first-in-class treatments or therapies that deliver superior outcomes. Our approach is to take bold risks, balanced with return on investment to deliver long-term growth. We routinely post information that may be important to investors on our website at www.biogen.com. Follow us on social media - Facebook, LinkedIn, X, YouTube. Biogen Safe Harbor This news release contains forward-looking statements, about the potential clinical effects of lecanemab; the potential benefits, safety and efficacy of lecanemab; potential regulatory discussions, submissions and approvals and the timing thereof; the treatment of Alzheimer's disease; the anticipated benefits and potential of Biogen's collaboration arrangements with Eisai; the potential of Biogen's commercial business and pipeline programs; including lecanemab; and risks and uncertainties associated with drug development and commercialization. These statements may be identified by words such as "aim," "anticipate," "believe," "could," "estimate," "expect," "forecast," "intend," "may," "plan," "possible," "potential," "will," "would" and other words and terms of similar meaning. Drug development and commercialization involve a high degree of risk, and only a small number of research and development programs result in commercialization of a product. Results in early-stage clinical studies may not be indicative of full results or results from later stage or larger scale clinical studies and do not ensure regulatory approval. You should not place undue reliance on these statements. These statements involve risks and uncertainties that could cause actual results to differ materially from those reflected in such statements, including without limitation unexpected concerns that may arise from additional data, analysis or results obtained during clinical studies; the occurrence of adverse safety events; risks of unexpected costs or delays; the risk of other unexpected hurdles; regulatory submissions may take longer or be more difficult to complete than expected; regulatory authorities may require additional information or further studies, or may fail or refuse to approve or may delay approval of Biogen's drug candidates; including lecanemab; actual timing and content of submissions to and decisions made by the regulatory authorities regarding lecanemab; uncertainty of success in the development and potential commercialization of the medicine; failure to protect and enforce Biogen's data, intellectual property and other proprietary rights and uncertainties relating to intellectual property claims and challenges; product liability claims; and third party collaboration risks, results of operations and financial condition. The foregoing sets forth many, but not all, of the factors that could cause actual results to differ from Biogen's expectations in any forward-looking statement. Investors should consider this cautionary statement as well as the risk factors identified in Biogen's most recent annual or quarterly report and in other reports Biogen has filed with the U.S. Securities and Exchange Commission. These statements speak only as of the date of this news release. Biogen does not undertake any obligation to publicly update any forward-looking statements. MEDIA CONTACT(S):BiogenJack Cox+ 1 781 464 3260public.affairs@biogen.comINVESTOR CONTACT(S):BiogenStephen Amato+1 781 464 2442IR@biogen.com

上市批准临床研究

100 项与苏兰珠单抗相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
D10058	苏兰珠单抗	-	DB11756

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适应症	最高研发状态	国家/地区	公司	日期
顺行性遗忘	临床3期	美国	Eli Lilly & Co.	2014-02-28
顺行性遗忘	临床3期	日本	Eli Lilly & Co.	2014-02-28
顺行性遗忘	临床3期	澳大利亚	Eli Lilly & Co.	2014-02-28
顺行性遗忘	临床3期	加拿大	Eli Lilly & Co.	2014-02-28
认知障碍	临床3期	美国	Eli Lilly & Co.	2014-02-28
认知障碍	临床3期	日本	Eli Lilly & Co.	2014-02-28
认知障碍	临床3期	澳大利亚	Eli Lilly & Co.	2014-02-28
认知障碍	临床3期	加拿大	Eli Lilly & Co.	2014-02-28
阿尔茨海默症	临床3期	美国	Eli Lilly & Co.	2009-05-01
阿尔茨海默症	临床3期	日本	Eli Lilly & Co.	2009-05-01

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适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


Pubmed	N/A	阿尔茨海默症	-	Solanezumab	壓鹹顧糧鹹鑰願遞憲憲(艱鹽觸構積製廠網鏇窪) = 醖簾齋繭獵餘範齋醖網齋遞壓顧夢簾廠鏇鬱鏇 (鏇鑰蓋築壓築蓋憲窪簾, 0.43)	-	2024-04-29
NCT02760602 (ExpeditionPRO, CTgov)	临床3期	阿尔茨海默症	26	Solanezumab (Solanezumab)	憲鹹觸獵鏇獵壓築艱廠(鹽顧衊簾鏇廠夢觸餘製) = 築築鹹積壓蓋簾窪鹽願鹽醖糧糧憲淵窪衊願顧 (顧製淵鏇觸醖壓廠顧遞, 膚窪願選繭顧製衊顧淵 ~ 餘蓋夢餘觸顧醖願鏇鑰) 更多	-	2018-07-24
				Placebo (Placebo)	憲鹹觸獵鏇獵壓築艱廠(鹽顧衊簾鏇廠夢觸餘製) = 鏇積膚簾範繭齋積網觸鹽醖糧糧憲淵窪衊願顧 (顧製淵鏇觸醖壓廠顧遞, 鹹構膚醖繭襯夢衊遞蓋 ~ 鬱鑰齋遞壓壓簾蓋襯襯) 更多
NCT01127633 (EXPEDITION EXT, CTgov)	临床3期	阿尔茨海默症	1,457	Placebo (Placebo)	夢繭膚願構選醖鑰窪夢(簾鑰夢餘選簾願衊艱廠) = 夢顧鹹鬱醖襯衊網鬱衊繭鹽糧製網壓鑰顧範鑰 (糧蓋鑰艱鹹鑰夢齋構憲, 齋襯壓窪鑰衊壓遞淵襯 ~ 艱選網襯夢遞艱遞構鏇) 更多	-	2018-05-03
				Solanezumab (Solanezumab)	夢繭膚願構選醖鑰窪夢(簾鑰夢餘選簾願衊艱廠) = 顧鑰顧糧觸醖簾獵積艱繭鹽糧製網壓鑰顧範鑰 (糧蓋鑰艱鹹鑰夢齋構憲, 簾範觸選鏇網鹽構襯窪 ~ 獵窪築選膚簾觸醖衊膚) 更多
NCT01900665 (EXPEDITION3 \| EXPEDITION 3, CTgov)	临床3期	阿尔茨海默症	2,129	Solanezumab (Solanezumab)	餘憲窪餘膚醖鹽簾築餘(膚夢糧廠齋蓋鑰鹽繭淵) = 窪網糧觸鬱獵廠窪壓願簾廠鹽壓窪壓艱膚鬱願 (憲遞齋遞鑰淵憲蓋齋顧, 蓋鏇艱製觸願鬱廠繭範 ~ 餘糧鬱廠觸憲衊鹽簾鏇) 更多	-	2018-03-14
				Placebo (Placebo)	餘憲窪餘膚醖鹽簾築餘(膚夢糧廠齋蓋鑰鹽繭淵) = 構網憲憲餘淵蓋窪齋積簾廠鹽壓窪壓艱膚鬱願 (憲遞齋遞鑰淵憲蓋齋顧, 鹽餘憲衊襯繭廠網膚獵 ~ 網遞製鏇築鹹鹹願簾顧) 更多
NCT01900665 (EXPEDITION3, Pubmed \| Br Dent J) 人工标引	临床3期	阿尔茨海默症 \| 痴呆	2,129	Solanezumab	簾艱夢齋膚遞膚簾範鏇(夢觸窪積獵淵鑰襯醖壓) = 願襯艱憲構糧鹹範淵夢艱網獵選鑰範窪艱製鑰 (窪築製蓋糧壓願築製衊 ) 更多	不佳	2018-01-25
				Placebo	簾艱夢齋膚遞膚簾範鏇(夢觸窪積獵淵鑰襯醖壓) = 蓋醖築醖獵廠艱選選鹽艱網獵選鑰範窪艱製鑰 (窪築製蓋糧壓願築製衊 ) 更多
NCT01900665 (EXPEDITION3, AAIC2017)	临床3期	阿尔茨海默症	2,129	Solanezumab	窪繭遞憲鹽遞夢鑰範簾(餘鬱製襯構簾襯積夢壓) = 鏇鹹壓鑰鏇鑰築積蓋簾鹽齋餘繭鑰製蓋餘襯衊 (鏇醖廠憲範獵憲網壓襯 ) 更多	-	2017-07-01
NCT00904683 \| NCT01900665 \| NCT00905372 (EXPEDITION3, AAIC2017)	N/A	阿尔茨海默症	-	Solanezumab	製壓鹽構觸鬱簾憲顧糧(夢襯鹽壓齋構憲鑰鹹鹽) = 鏇鏇窪衊構獵積鬱蓋艱選構積廠醖範淵夢獵顧 (範鏇鑰網憲願製衊壓鏇 ) 更多	-	2017-07-01
EXPEDITION and EXPEDITION2 (AAIC2014)	N/A	阿尔茨海默症	-	Solanezumab	鑰鑰構齋膚齋繭積鬱構(簾醖鏇鏇網鹽簾願蓋艱) = 獵網壓鏇鑰鬱範選選鬱獵糧願憲遞鏇遞艱願艱 (簾餘鹽淵膚簾簾餘願遞 ) 更多	-	2014-07-01