ArticleFrontiers in immunology2011
Generation and characterization of anti-AA amyloid-specific monoclonal antibodies.
Article in Frontiers in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Efficacy and Safety of Anselamimab in Immunoglobulin Light Chain Amyloidosis: Results From the Randomized CARES Trials.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Trial
- The antibody-peptide fusion protein, AT-02, is an effective opsonin with pan-amyloid reactivity.npj drug discovery · 2025Article
- Targeting Amyloid Fibrils by Passive Immunotherapy in Systemic Amyloidosis.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2022Review
- Serum Amyloid A Protein-Associated Kidney Disease: Presentation, Diagnosis, and Management.Kidney medicine · 2022Review
- Phase 1a/b study of monoclonal antibody CAEL-101 (11-1F4) in patients with AL amyloidosis.Blood · 2021Article
- Understanding Mesangial Pathobiology in AL-Amyloidosis and Monoclonal Ig Light Chain Deposition Disease.Kidney international reports · 2020Review
- Emerging Therapeutics for the Treatment of Light Chain and Transthyretin Amyloidosis.JACC. Basic to translational science · 2019Review
- AL amyloid imaging and therapy with a monoclonal antibody to a cryptic epitope on amyloid fibrils.PloS one · 2012Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AA amyloidosis results from the pathologic deposition in the kidneys and other organs of fibrils composed of N-terminal fragments of serum amyloid A protein (SAA). Given that there are only limited means to visualize these deposits, we have developed a series of mAbs, 2A4, 7D8, and 8G9, that bind specifically with nanomolar affinity to a carboxy-terminal epitope generated following proteolysis of SAA that yields the predominant component of AA amyloid deposits. Notably, these antibodies do not recognize native SAA, they retain their immunoreactivity when radiolabeled with I-125 and, after injection into AA amyloidotic mice, localize, as evidenced by autoradiography and micro-single photon emission computed tomography imaging, to histologically confirmed areas of amyloid deposition; namely, spleen, liver, and pancreas. The results of our in vitro and in vivo studies demonstrate the AA fibril-selectivity of mAbs 2A4, 7D8, and 8G9 and warrant further investigation into their role as novel diagnostic agents for patients with AA amyloidosis.
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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.