ArticleScientific reports2020
Development of the clinical candidate PBD-C06, a humanized pGlu3-Aβ-specific antibody against Alzheimer's disease with reduced complement activation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Amyloid-related imaging abnormalities (ARIA) in anti-amyloid therapies for Alzheimer's disease: An update from the Alzheimer's Association ARIA workgroup.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Identification of common genes associated with diabetic nephropathy and diabetic retinopathy.Frontiers in cell and developmental biology · 2026Article
- Complement Cascades and Brain Disorders.Biomolecules · 2025Review
- An Overview of Glutaminyl Cyclase as a Promising Drug Target for Alzheimer's Disease.Biomedicines · 2025Article
- Immunotherapies: A Treasure Trove of Alzheimer's Disease.Current pharmaceutical biotechnology · 2025Review
- The role of IL-1 family of cytokines in the pathogenesis and therapy of Alzheimer's disease.Inflammopharmacology · 2024Review
- Screening of [ACS pharmacology & translational science · 2024Article
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond.Current neuropharmacology · 2024Article
- Immunotherapies for Alzheimer's Disease-A Review.Vaccines · 2022Review
- The Complement System, Aging, and Aging-Related Diseases.International journal of molecular sciences · 2022Review
- Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.Pharmacological reviews · 2022Review
- Pyroglutamate Aβ cascade as drug target in Alzheimer's disease.Molecular psychiatry · 2022Review
- Complement System in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Combination of the Glutaminyl Cyclase Inhibitor PQ912 (Varoglutamstat) and the Murine Monoclonal Antibody PBD-C06 (m6) Shows Additive Effects on Brain Aβ Pathology in Transgenic Mice.International journal of molecular sciences · 2021Article
- Focused ultrasound with anti-pGlu3 Aβ enhances efficacy in Alzheimer's disease-like mice via recruitment of peripheral immune cells.Journal of controlled release : official journal of the Controlled Release Society · 2021Article
- A vaccine to prevent initial loss of cognition and eventual Alzheimer's disease in elderly persons.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Kinetic fingerprints differentiate the mechanisms of action of anti-Aβ antibodies.Nature structural & molecular biology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In clinical trials with early Alzheimer's patients, administration of anti-amyloid antibodies reduced amyloid deposits, suggesting that immunotherapies may be promising disease-modifying interventions against Alzheimer's disease (AD). Specific forms of amyloid beta (Aβ) peptides, for example post-translationally modified Aβ peptides with a pyroglutamate at the N-terminus (pGlu3, pE3), are attractive antibody targets, due to pGlu3-Aβ's neo-epitope character and its propensity to form neurotoxic oligomeric aggregates. We have generated a novel anti-pGlu3-Aβ antibody, PBD-C06, which is based on a murine precursor antibody that binds with high specificity to pGlu3-Aβ monomers, oligomers and fibrils, including mixed aggregates of unmodified Aβ and pGlu3-Aβ peptides. PBD-C06 was generated by first grafting the murine antigen binding sequences onto suitable human variable light and heavy chains. Subsequently, the humanized antibody was de-immunized and site-specific mutations were introduced to restore original target binding, to eliminate complement activation and to improve protein stability. PBD-C06 binds with the same specificity and avidity as its murine precursor antibody and elimination of C1q binding did not compromise Fcγ-receptor binding or in vitro phagocytosis. Thus, PBD-C06 was specifically designed to target neurotoxic aggregates and to avoid complement-mediated inflammatory responses, in order to lower the risk for vasogenic edemas in the clinic.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.