ArticleArthritis research & therapy2019
Conferring extracellular matrix affinity enhances local therapeutic efficacy of anti-TNF-α antibody in a murine model of rheumatoid arthritis.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Collagen hybridizing peptide imaging and delivery of therapeutic antibody in rheumatoid arthritis models.Nature communications · 2026Article
- RNA nanotherapeutics with fibrosis overexpression and retention for MASH treatment.Nature communications · 2024Article
- Recent and future perspectives on engineering interferons and other cytokines as therapeutics.Trends in biochemical sciences · 2023Review
- Modification of mesenchymal stem cells for cartilage-targeted therapy.Journal of translational medicine · 2022Review
- Targeting the Extracellular Matrix in Traumatic Brain Injury Increases Signal Generation from an Activity-Based Nanosensor.ACS nano · 2021Article
- Location, location, location: how the tissue microenvironment affects inflammation in RA.Nature reviews. Rheumatology · 2021Review
- Harnessing molecular recognition for localized drug delivery.Advanced drug delivery reviews · 2021Review
- Dysregulation of Leukocyte Trafficking in Type 2 Diabetes: Mechanisms and Potential Therapeutic Avenues.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough disease in a majority of rheumatoid arthritis (RA) patients is often initially limited to one or a few joints, currently approved medications including anti-tumor necrosis factor-α antibody (α-TNF) are injected systemically. Given that α-TNF systemic injection typically does not cure RA and involves risk of treatment-related adverse events, one possible approach to enhance therapeutic efficacy and reduce α-TNF systemic exposure is to retain the antibodies in arthritic joints after local administration. The aim of this study was to evaluate the approach of conferring extracellular matrix (ECM) binding affinity to α-TNF antibodies in a RA model.
methodsα-TNF was chemically conjugated with a promiscuous ECM-binding peptide derived from placenta growth factor 2 (PlGF-2
resultsPlGF-2
conclusionThese data demonstrate that retention of α-TNF in arthritic joints can suppress arthritis development and enhance therapeutic efficacy. This simple bioengineering approach of ECM-binding peptide conjugation offers a powerful and clinically translational approach to treat RA.
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