ReviewBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy2022
Targeting Amyloid Fibrils by Passive Immunotherapy in Systemic Amyloidosis.
Review in BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Disease-Modifying Therapies for Hereditary Transthyretin Amyloidosis with Polyneuropathy: Current Status and Future Perspectives.Neurology and therapy · 2026Review
- Biologics for cardiovascular diseases: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- Structure of ATTRv-F64S fibrils isolated from skin tissue of a living patient.Nature communications · 2025Article
- Pan-Amyloid Reactive Peptides p5+14 and p5R Exhibit Specific Charge-Dependent Binding to Glycosaminoglycans.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The antibody-peptide fusion protein, AT-02, is an effective opsonin with pan-amyloid reactivity.npj drug discovery · 2025Article
- Etiological Treatment of Cardiac Amyloidosis: Standard of Care and Future Directions.Current heart failure reports · 2025Review
- Cardiac amyloidosis: Innovations in diagnosis and treatment.European heart journal supplements : journal of the European Society of Cardiology · 2025Article
- Article
- Amyloids and the Heart: An Update.Journal of clinical medicine · 2024Review
- Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology.Current issues in molecular biology · 2024Review
- A Snapshot of the Most Recent Transthyretin Stabilizers.International journal of molecular sciences · 2024Review
- Current Therapies and Future Horizons in Cardiac Amyloidosis Treatment.Current heart failure reports · 2024Review
- Article
- Emerging Therapies for Transthyretin Amyloidosis.Current oncology reports · 2023Review
- Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.European heart journal supplements : journal of the European Society of Cardiology · 2023Article
- Diagnosis and Treatment of AL Amyloidosis.Drugs · 2023Review
- Development and characterization of a prototypic pan-amyloid clearing agent - a novel murine peptide-immunoglobulin fusion.Frontiers in immunology · 2023Article
- Oral Therapy for the Treatment of Transthyretin-Related Amyloid Cardiomyopathy.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Systemic amyloidoses are characterized by the unrelenting deposition of autologous proteins as highly ordered fibrils in target organs. The ensuing, potentially fatal organ dysfunction is the result of the combined damage caused by the proteotoxic effect of prefibrillar species and by the cytotoxicity and the structural alterations produced by the amyloid fibrils. Current therapy is focused on eliminating the amyloid protein, thus extinguishing the amyloid cascade at its origin. While this approach may end the cell damage caused by prefibrillar aggregates and prevent further amyloid accumulation, the noxious effects of the amyloid fibrils persist and may hamper the recovery of organ function, which is the ultimate goal of therapy as it is necessary to improve the quality of life and extend survival. Preclinical studies indicate that the clearance of amyloid deposits can be accelerated by specific antibodies targeting amyloid fibrils that activate complement-mediated macrophages and giant cell phagocytosis, possibly promoting the recovery of organ function. Measuring the therapeutic effect of anti-amyloid agents is still a matter of research. In recent years, several monoclonal antibodies targeting amyloid deposits have been tested in clinical trials with mixed outcomes. Recent encouraging results from phase I/II trials, new anti-amyloid agents, and new antibody engineering offer hope that effective amyloid removal will be accomplished in the near future, accelerating organ recovery and improving quality of life and survival.
Indexed as
Identifiers
What OpenQuestion holds
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.