ArticleThe Journal of biological chemistry
A novel soluble complement receptor 1 fragment with enhanced therapeutic potential.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- In Vivo Efficacy of an Inhibitor of Complement and FcRn in Models of Glomerulonephritis and Collagen-Induced Arthritis Using Human C2 Knock-In Mice.International journal of molecular sciences · 2026Article
- CSL305: A Dual Functional Therapeutic Antibody Targeting Complement C2 and FcRn.International journal of molecular sciences · 2026Article
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- A new Drosophila model of prolonged inactivity shortens lifespan and impairs muscle function.Scientific reports · 2025Article
- Complement Receptor 1 Is a Potential Extracerebral Factor Promoting α-Synuclein Pathology.Molecular neurobiology · 2025Article
- Aberrant systemic acute-phase complement responses in conjunction with soluble CR1 attribute to varying grades of dengue disease severity.Frontiers in immunology · 2025Article
- Monocyte uptake of polymeric peptidoglycan is bimodal and governed by complement C3 and C4 opsonins.JCI insight · 2024Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- The Production of Complement Inhibitor Proteins in Mammalian Cell Lines-Light at the End of the Tunnel?Biomedicines · 2024Review
- Complement in human disease: approved and up-and-coming therapeutics.Lancet (London, England) · 2024Review
- The Molecular Mechanisms of Complement Receptor 1-It Is Complicated.Biomolecules · 2023Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Protein therapeutics and their lessons: Expect the unexpected when inhibiting the multi-protein cascade of the complement system.Immunological reviews · 2023Review
- Complement Regulation in Immortalized Fibroblast-like Synoviocytes and Primary Human Endothelial Cells in Response to SARS-CoV-2 Nucleocapsid Protein and Pro-Inflammatory Cytokine TNFα.Life (Basel, Switzerland) · 2022Article
- Complement-targeting therapeutics for ischemia-reperfusion injury in transplantation and the potential forFrontiers in immunology · 2022Review
- A potent truncated form of human soluble CR1 is protective in a mouse model of renal ischemia-reperfusion injury.Scientific reports · 2021Article
- Analysis of carbohydrates and glycoconjugates by matrix-assisted laser desorption/ionization mass spectrometry: An update for 2021-2022.Mass spectrometry reviewsReview
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human complement receptor 1 (HuCR1) is a pivotal regulator of complement activity, acting on all three complement pathways as a membrane-bound receptor of C3b/C4b, C3/C5 convertase decay accelerator, and cofactor for factor I-mediated cleavage of C3b and C4b. In this study, we sought to identify a minimal soluble fragment of HuCR1, which retains the complement regulatory activity of the wildtype protein. To this end, we generated recombinant, soluble, and truncated versions of HuCR1 and compared their ability to inhibit complement activation in vitro using multiple assays. A soluble form of HuCR1, truncated at amino acid 1392 and designated CSL040, was found to be a more potent inhibitor than all other truncation variants tested. CSL040 retained its affinity to both C3b and C4b as well as its cleavage and decay acceleration activity and was found to be stable under a range of buffer conditions. Pharmacokinetic studies in mice demonstrated that the level of sialylation is a major determinant of CSL040 clearance in vivo. CSL040 also showed an improved pharmacokinetic profile compared with the full extracellular domain of HuCR1. The in vivo effects of CSL040 on acute complement-mediated kidney damage were tested in an attenuated passive antiglomerular basement membrane antibody-induced glomerulonephritis model. In this model, CSL040 at 20 and 60 mg/kg significantly attenuated kidney damage at 24 h, with significant reductions in cellular infiltrates and urine albumin, consistent with protection from kidney damage. CSL040 thus represents a potential therapeutic candidate for the treatment of complement-mediated disorders.
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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.