ArticleAnnals of the rheumatic diseases2019
Humanised effector-null FcγRIIA antibody inhibits immune complex-mediated proinflammatory responses.
Article in Annals of the rheumatic diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Monovalent Anti-FcγRIIA Antibody Blocks Immune-Mediated Thrombocytopenia and Thrombosis With Minimal Adverse Side Effects in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Depletion and recovery of IgG following treatment with an anti-FcRn antibody and IdeS in pigtail macaques.Clinical and experimental immunology · 2026Article
- Review
- Depletion and recovery of IgG following treatment with Rozanoliximab and Imlifidase in pigtail macaques.bioRxiv : the preprint server for biology · 2025Article
- The anti-inflammatory activity of IgG is enhanced by co-engagement of type I and II Fc receptors.Science (New York, N.Y.) · 2025Article
- Platelet signaling in immune landscape: comprehensive mechanism and clinical therapy.Biomarker research · 2024Review
- Inflammation and autoimmune myasthenia gravis.Frontiers in immunology · 2023Review
- Anchoring IgG-degrading enzymes to the surface of platelets selectively neutralizes antiplatelet antibodies.Blood advances · 2022Article
- Measurement of procoagulant platelets provides mechanistic insight and diagnostic potential in heparin-induced thrombocytopenia.Journal of thrombosis and haemostasis : JTH · 2022Article
- Review
- Leveraging Heterogeneity in Systemic Lupus Erythematosus for New Therapies.Trends in molecular medicine · 2021Review
- Autoimmunity in 2019.Clinical reviews in allergy & immunology · 2020Review
- From Classical to Unconventional: The Immune Receptors Facilitating Platelet Responses to Infection and Inflammation.Biology · 2020Review
- FcRn is a CD32a coreceptor that determines susceptibility to IgG immune complex-driven autoimmunity.The Journal of experimental medicine · 2020Article
- High-Dose IV Administration of Rasburicase Suppresses Anti-rasburicase Antibodies, Depletes Rasburicase-Specific Lymphocytes, and Upregulates Treg Cells.The AAPS journal · 2020Article
- Systemic lupus erythematosus and diffuse alveolar hemorrhage, etiology and novel treatment strategies.Lupus · 2020Review
- Receptor targeting drug delivery strategies and prospects in the treatment of rheumatoid arthritis.Research in pharmaceutical sciences · 2019Review
- Early Host Interactions That Drive the Dysregulated Response in Sepsis.Frontiers in immunology · 2019Review
- Article
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Authors and funding
31 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveImmune complexes (ICs) play a critical role in the pathology of autoimmune diseases. The aim of this study was to generate and characterise a first-in-class anti-FcγRIIA antibody (Ab) VIB9600 (previously known as MEDI9600) that blocks IgG immune complex-mediated cellular activation for clinical development.
methodsVIB9600 was humanised and optimised from the IV.3 Ab. Binding affinity and specificity were determined by Biacore and ELISA. Confocal microscopy, Flow Cytometry-based assays and binding competition assays were used to assess the mode of action of the antibody. In vitro cell-based assays were used to demonstrate suppression of IC-mediated inflammatory responses. In vivo target suppression and efficacy was demonstrated in FcγRIIA-transgenic mice. Single-dose pharmacokinetic (PK)/pharmacodynamic study multiple dose Good Laboratory Practice (GLP) toxicity studies were conducted in non-human primates.
resultsWe generated a humanised effector-deficient anti-FcγRIIA antibody (VIB9600) that potently blocks autoantibody and IC-mediated proinflammatory responses. VIB9600 suppresses FcγRIIA activation by blocking ligand engagement and by internalising FcγRIIA from the cell surface. VIB9600 inhibits IC-induced type I interferons from plasmacytoid dendritic cells (involved in SLE), antineutrophil cytoplasmic antibody (ANCA)-induced production of reactive oxygen species by neutrophils (involved in ANCA-associated vasculitis) and IC-induced tumour necrosis factor α and interleukin-6 production (involved in rheumatoid arthritis). In FcγRIIA transgenic mice, VIB9600 suppressed antiplatelet antibody-induced thrombocytopaenia, acute anti-GBM Ab-induced nephritis and anticollagen Ab-induced arthritis. VIB9600 also exhibited favourable PK and safety profiles in cynomolgus monkey studies.
conclusionsVIB9600 is a specific humanised antibody antagonist of FcγRIIA with null effector function that warrants further clinical development for the treatment of IC-mediated diseases.
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