ArticleScientific reports2025
Development and in vitro characterization of humanized antibodies for blocking human TRPM4 channel.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Structural mechanism of Necrocide 1 activation of human TRPM4 that triggers necrosis by sodium overload.Nature communications · 2026Article
- Structural mechanism of Necrocide 1 activation of human TRPM4 that triggers necrosis by sodium overload.bioRxiv : the preprint server for biology · 2026Article
- Structural biology of the TRPM4 channel: architecture, modulation, and therapeutic opportunities.Frontiers in pharmacology · 2026Review
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Authors and funding
7 authors.
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Abstract
Transient receptor potential melastatin 4 (TRPM4) channel, a monovalent cation channel, plays a crucial role in various neurological disorders. We previously showed that TRPM4 activity can be blocked by our antibodies: M4P, which targets rat TRPM4 and M4M, against a similar antigenic epitope of human TRPM4. M4P and M4M demonstrated efficacy in mitigating stroke reperfusion injury. To facilitate human application, M4M was humanized through CDR grafting, resulting in human IgG1 antibodies (Ab1-6). These antibodies were evaluated for their binding affinity, surface staining, stability, and functional inhibition of the human TRPM4 channel. Ab6 (renamed as M4H) was selected and inhibited TRPM4 currents in human brain microvascular endothelial cells under ATP depletion conditions. Importantly, Ab6 (M4H) suppressed ATP depletion-induced cell swelling, indicating its potential for managing vascular injury in ischemic brain diseases. Future studies on animal models could advance the development of novel therapies of neurological disorders with vascular injury.
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