ArticleAdvanced therapeutics2022
Classical Complement Pathway Inhibition in a "Human-On-A-Chip" Model of Autoimmune Demyelinating Neuropathies.
Article in Advanced therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 73 citations in OpenAlex.
- Organoids: From Bench to Bedside Applications.MedComm · 2026Review
- Organoids, organ-on-a-chip, and microtumors: Biomimetic 3D tumor models advancing drug development and precision medicine.Acta pharmaceutica Sinica. B · 2026Review
- Respiratory Organ-on-a-Chip for Disease Modeling: From Architecture to Functional Integration.Advanced healthcare materials · 2026Review
- In Vitro and In Vivo Efficacy of Epithelial Barrier-Promoting Barriolides as Potential Therapy for Ulcerative Colitis.Biomedicines · 2026Article
- Need for NAMs: A systematic evidence synthesis revealing over half a century of drug development failure.NAM journal · 2026Article
- Application and prospects of lung organ-on-a-chip in the development of new drugs.Biomedical engineering online · 2025Review
- Review
- Organoid Models to Study Human Infectious Diseases.Cell proliferation · 2025Review
- Advanced Microfluidics for Single Cell-Based Cancer Research.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- Pre-clinical evaluation of mRNA-lipid nanoparticles' potency and toxicity: current practices and future directions.In vitro models · 2025Review
- Head and neck cancer organoids: a panoramic perspective from basic construction to clinical translation.Stem cell research & therapy · 2025Review
- Organoids-on-Chips Technology: Unveiling New Perspectives in Rare-Disease Research.International journal of molecular sciences · 2025Review
- Microglia determine an immune-challenged environment and facilitate ibuprofen action in human retinal organoids.Journal of neuroinflammation · 2025Article
- Multifocal Motor Neuropathy: A Narrative Review.Muscle & nerve · 2025Review
- Complement activation in immunological neurological disorders: mechanisms and therapeutic strategies.Frontiers in neurology · 2025Review
- Review
- Human-based complexFrontiers in cell and developmental biology · 2025Review
- Path dependency and the rescuing of the biomedical research enterprise.Frontiers in medical technology · 2025Review
- Design strategy primer for organ-on-chips.Biomaterials translational · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
Abstract
Chronic autoimmune demyelinating neuropathies are a group of rare neuromuscular disorders with complex, poorly characterized etiology. Here we describe a phenotypic, human-on-a-chip (HoaC) electrical conduction model of two rare autoimmune demyelinating neuropathies, chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN), and explore the efficacy of TNT005, a monoclonal antibody inhibitor of the classical complement pathway. Patient sera was shown to contain anti-GM1 IgM and IgG antibodies capable of binding to human primary Schwann cells and induced pluripotent stem cell derived motoneurons. Patient autoantibody binding was sufficient to activate the classical complement pathway resulting in detection of C3b and C5b-9 deposits. A HoaC model, using a microelectrode array with directed axonal outgrowth over the electrodes treated with patient sera, exhibited reductions in motoneuron action potential frequency and conduction velocity. TNT005 rescued the serum-induced complement deposition and functional deficits while treatment with an isotype control antibody had no rescue effect. These data indicate that complement activation by CIDP and MMN patient serum is sufficient to mimic neurophysiological features of each disease and that complement inhibition with TNT005 was sufficient to rescue these pathological effects and provide efficacy data included in an investigational new drug application, demonstrating the model's translational potential.
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What Socratic holds
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 Socratic graph.