ArticlemAbs2026
Preclinical characterization of AZD1163, a first-in-class anti-PAD2/4 bispecific antibody for the treatment of rheumatoid arthritis.
Article in mAbs, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
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Who cites it
3 citing papers in PubMed.
- Autoantibodies and T Cells Target Citrullinated and Homocitrullinated Antigens in Rheumatoid Arthritis.Immunological reviews · 2026Review
- NLRP3 inflammasome promotes PAD2/PAD4 release and protein citrullination in rheumatoid arthritis.Communications biology · 2026Article
- Fibrinogen in extracellular matrix remodeling: functional switching, source heterogeneity, and biomaterial translation.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
27 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-citrullinated protein autoantibodies promote inflammation and joint tissue injury and define a poor prognostic group of patients with rheumatoid arthritis (RA). Citrullinated autoantigens that drive this autoimmune response are generated by peptidylarginine deiminase (PAD) enzymes, which are predominately expressed and released by neutrophils and monocytes. Accordingly, blocking the enzymatic activity of PADs to curb the generation of citrullinated autoantigens that drive autoimmunity and tissue injury may provide therapeutic benefit. Herein, we developed a high affinity, bispecific, anti-PAD2/4, effector-null antibody, AZD1163, which potently inhibits recombinant PAD2 and PAD4 activity in both histone H3 and fibrinogen citrullination assays. AZD1163 inhibited all endogenous PAD activity in the serum of patients with RA irrespective of the presence of anti-PAD4 autoantibodies, and neutralized PAD activity in synovial fluid. AZD1163 also bound and internalized PADs expressed on cell membranes into low pH endosomes for degradation, reducing the surface expression and catalytic potential. Binding of AZD1163 to neutrophils and monocytes did not trigger complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, or the production of proinflammatory cytokines, or otherwise impact neutrophil phagocytosis, production of reactive oxygen species, or NETosis. In a non-human primate study of pharmacokinetics (PK) and pharmacodynamics, a single dose of AZD1163 exhibited PK consistent with a half-life extended antibody and a rapid and durable suppression of endogenous PAD activity. AZD1163 has a favorable preclinical safety profile. Collectively, these in vitro and in vivo pharmacology and safety data support the clinical development of AZD1163 as a novel therapeutic strategy for RA by reducing autoantigen load.
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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.