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monoclonal
332 studies tagged monoclonal, dated 2000 to 2026-09-09. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
332 studies carry this tag.
Date range
2000 to 2026
Top journals
- Alzheimer's & dementia : the journal of the Alzheimer's Association 26
- Journal of Alzheimer's disease : JAD 21
- The journal of prevention of Alzheimer's disease 20
- Alzheimer's research & therapy 18
- Alzheimer's & dementia (New York, N. Y.) 14
148 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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In 2021, aducanumab, an immunotherapy targeting amyloid-β, was approved for Alzheimer's disease (AD) by the US Food and Drug Administration thanks to positive results on a putative biological surrogate marker.
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45/100
With the recent approval by the FDA of the first disease-modifying drug for Alzheimer's Disease (AD), personalized medicine will be increasingly important for appropriate management and counseling of patients with AD and those at risk.
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Based on the data to date, it is difficult to accurately assess the role of aducanumab in patients with MCI or mild AD.
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Strong genetic evidence supports an imbalance between production and clearance of amyloid β-protein (Aβ) in people with Alzheimer disease (AD).
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Upon further refinement and validation, the VWD model could inform strategies for dosing and ARIA monitoring in individuals with an ARIA-E history.
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Aducanumab is a monoclonal antibody selective for amyloid β (Aβ) aggregates.
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The AD drug development pipeline has agents representing a substantial array of treatment mechanisms and targets.
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Research on disease-modifying treatments for Alzheimer's disease has resulted in a series of failures over the past 20 years.
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Alzheimer's disease (AD) is the most prevalent form of age-related dementia in the world, and its main pathological features consist of amyloid-β (Aβ) plaque deposits and neurofibrillary tangles formed by hyperphosphorylated tau protein.
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Slowing the progression of Alzheimer disease (AD) might be the greatest unmet medical need of our time.
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Aβ plaques removal in the brain due to amyloid therapy is strongly correlated with a better clinical response in patients with early Alzheimer's disease and a higher ARIA-E rate for the treatment groups and clinical trials in this meta-analysis.
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Selecting the right dose is a significant challenge in designing clinical development programs, especially for slowly progressing diseases lacking predictive biomarkers of efficacy that may require long-term treatment to assess clinical benefit.
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Despite presence of substantial evidence suggesting the pivotal role of amyloid (Aβ) in Alzheimer's disease (AD), very few therapeutic agents have been able to ameliorate the disease.
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Specifically, recent studies suggest that increased plasma concentrations of lipoprotein-Aβ compromise the brain microvasculature, resulting in extravasation and retention of the lipoprotein-Aβ moiety.
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Alzheimer's disease (AD) is the most common form of dementia affecting millions of individuals, including family members who often take on the role as caregiver.
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Aducanumab (Aduhelm) is approved in the United States for the treatment of patients with mild cognitive impairment due to Alzheimer's disease or mild AD dementia.
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Given the acknowledged lack of success in Alzheimer's disease (AD) drug development over the past two decades, the objective of this review was to derive key insights from the myriad failures to inform future drug development.
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Amyloid-related imaging abnormalities (ARIA) are adverse events reported in Alzheimer's disease trials of anti-amyloid beta (Aβ) therapies.
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Scientific advances over the last four decades have steadily infused the Alzheimer's disease (AD) field with great optimism that therapies targeting Aβ, amyloid, tau, and innate immune activation states in the brain would provide disease modification.
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Three new drugs are presented: dostarlimab, loncastuximab tesirine, and aducanumab.
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Our results suggest that the risk-benefit profile of mAbs remains unclear.
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39/100
Alzheimer’s disease is a major cause of morbidity and mortality.
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Aducanumab, a human monoclonal antibody, was approved in June of 2021 as the first disease-modifying treatment for Alzheimer’s disease by the United States Food and Drug Administration (U.S. FDA).
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Between July 22, 2014, and May 17, 2018, 261 participants entered the open-label phase. 211 were randomly assigned losartan (n=105) or placebo (n=106).
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DISCLOSURES: Funding for this summary was contributed by Arnold Ventures, The Donaghue Foundation, Harvard Pilgrim Health Care, and Kaiser Foundation Health Plan to the Institute for Clinical and Economic Review (ICER), an independent organization that evaluates the evidence on the value of health care interventions.
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Aducanumab is a human immunoglobulin G1 anti‐amyloid beta (Aβ) antibody currently being evaluated for potential treatment of patients with early Alzheimer’s disease.
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Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in ageing, affecting around 46 million people worldwide but few treatments are currently available.
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Alzheimer’s disease (AD) is the most common form of dementia with global burden projected to triple by 2050.
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Alzheimer's disease (AD) is the most common cause for dementia worldwide.
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En junio, la Agencia de Alimentos y medicamentos de los Estados Unidos (FDA) otorgó aprobación mediante vía acelerada al medicamento aducanumab, desarrollado por Biogen, Inc. para tratamiento de la enfermedad de Alzheimer (EA).
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In vivo biomarker abnormalities provide measures to monitor therapeutic interventions targeting amyloid-β pathology as well as its effects on downstream processes associated with Alzheimer's disease pathophysiology.
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On 7 June , the FDA approved aducanumab, the first new drug for Alzheimer’s disease in almost 20 years—and notably, the first drug with a putative disease‐modifying mechanism for the treatment of this devastating disorder, namely the removal of β‐amyloid (or Aβ) plaques from the brain.
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40/100
Aducanumab (aducanumab-avwa; Aduhelm™) is a human, immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid β.
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Aducanumab has recently been licensed by the Food and Drug Administration (FDA) in the USA under its ‘accelerated approval’ pathway (to provide earlier access to treatments that fulfil an unmet need based on a surrogate endpoint) for treatment of Alzheimer's disease.
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The US FDA approved Aducanumab in June 2021 as the first Alzheimer's disease (AD) drug under its accelerated approval pathway.
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Dominantly inherited Alzheimer's disease (DIAD) causes predictable biological changes decades before the onset of clinical symptoms, enabling testing of interventions in the asymptomatic and symptomatic stages to delay or slow disease progression.
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A large body of clinical and nonclinical evidence supports the role of neurotoxic soluble beta amyloid (amyloid, Aβ) oligomers as upstream pathogenic drivers of Alzheimer's disease (AD).
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Patients with early symptomatic Alzheimer's disease showed less cognitive and functional decline with donanemab compared with placebo in a Phase 2 study offering up to 72 weeks of treatment.
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This pipeline analysis shows that target biological processes are more diversified, biomarkers are more regularly used, and repurposed agents are being explored to determine their utility for the treatment of AD.
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Based on a structured search on the ClinicalTrials.gov and the EudraCT databases, we identified 13 clinical trials testing 11 different approved anticancer agents (five tyrosine kinase inhibitors, two retinoid X receptor agonists, two immunomodulatory agents, one histone deacetylase inhibitor, and one monoclonal antibody) in the AD continuum.
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The calibrated model predicts that endogenous plaque turnover is slow, with an estimated half-life of 2.75 years.
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In this meta-analysis of phase III trials in AD, we found that monoclonal antibodies against Aβ induced clinical improvements of small effect sizes, biomarker improvements of large effect sizes, and increases in risk for the hallmark adverse event, ARIA, by a large effect size, when all drugs were pooled together.
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Drug development for Alzheimer disease and other neurodegenerative dementias, including frontotemporal dementia, has experienced a long history of phase 2 and phase 3 clinical trials that failed to show efficacy of investigational drugs.
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Pooled evidence from available trials reporting both reduction in amyloid levels and change in cognition suggests that amyloid reduction strategies do not substantially improve cognition.
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Aducanumab has been approved by the US Food and Drug Administration for treatment of Alzheimer's disease (AD).
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Donanemab was generally well tolerated up to 10 mg/kg.
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Treatment with donanemab resulted in rapid reduction of amyloid, even after a single dose.
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The dominant theory of Alzheimer disease (AD) has been that amyloid-β (Aβ) accumulation in the brain is the initial cause of the degeneration leading to cognitive and functional deficits.
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Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder characterized by cognitive decline and by the presence of amyloid β plaques and neurofibrillary tangles in the brain.
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Aducanumab recently underwent two large phase III clinical trials that were stopped prematurely by the sponsor Biogen.
From across this tag
8 of the 332 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
- Lecanemab for early Alzheimer's disease: Appropriate use recommendations from the French federation of memory clinics
- TRAILBLAZER-ALZ 4: A phase 3 trial comparing donanemab with aducanumab on amyloid plaque clearance in early, symptomatic Alzheimer's disease
- Profiling aducanumab as a treatment option for Alzheimer's disease: an overview of efficacy, safety and tolerability
- Aducanumab 36-month data from PRIME: a randomized, double-blind, placebo-controlled Phase 1b study in patients with prodromal or mild Alzheimer’s disease (S2.004)
- IVIg protects the 3xTg-AD mouse model of Alzheimer's disease from memory deficit and Aβ pathology
- Advances of therapeutic strategies for Alzheimer's disease
- Anti-Amyloid Monoclonal Antibodies are Transformative Treatments that Redefine Alzheimer's Disease Therapeutics
- Overview of Alzheimer's Disease Neuroimaging Initiative and future clinical trials