ArticleDisease models & mechanisms2017
Trimebutine, a small molecule mimetic agonist of adhesion molecule L1, contributes to functional recovery after spinal cord injury in mice.
Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Depletion of Cell Adhesion Molecule L1 from Microglia and Macrophages Reduces Recovery After Spinal Cord Injury.International journal of molecular sciences · 2025Article
- The Use of Small-Molecule Compounds for Cell Adhesion and Migration in Regenerative Medicine.Biomedicines · 2023Review
- The Interactions of the 70 kDa Fragment of Cell Adhesion Molecule L1 with Topoisomerase 1, Peroxisome Proliferator-Activated Receptor γ and NADH Dehydrogenase (Ubiquinone) Flavoprotein 2 Are Involved in Gene Expression and Neuronal L1-Dependent Functions.International journal of molecular sciences · 2023Article
- Functional trajectories during innate spinal cord repair.Frontiers in molecular neuroscience · 2023Article
- Antagonistic L1 Adhesion Molecule Mimetic Compounds Inhibit Glioblastoma Cell Migration In Vitro.Biomolecules · 2022Article
- Honokiol improves depression-like behaviors in rats by HIF-1α- VEGF signaling pathway activation.Frontiers in pharmacology · 2022Article
- Amelioration of the abnormal phenotype of a new L1 syndrome mouse mutation with L1 mimetics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Adhesion Molecule L1 Agonist Mimetics Protect Against the Pesticide Paraquat-Induced Locomotor Deficits and Biochemical Alterations in Zebrafish.Frontiers in neuroscience · 2020Article
- Glycan Mimetics from Natural Products: New Therapeutic Opportunities for Neurodegenerative Disease.Molecules (Basel, Switzerland) · 2019Review
- Enhanced Neuronal Survival and Neurite Outgrowth Triggered by Novel Small Organic Compounds Mimicking the LewisX Glycan.Molecular neurobiology · 2018Article
- Small Molecules: Therapeutic Application in Neuropsychiatric and Neurodegenerative Disorders.Molecules (Basel, Switzerland) · 2018Review
- ROCK Inhibitor Y27632 Induced Morphological Shift and Enhanced Neurite Outgrowth-Promoting Property of Olfactory Ensheathing Cells via YAP-Dependent Up-Regulation of L1-CAM.Frontiers in cellular neuroscience · 2018Article
- Trimebutine Promotes Glioma Cell Apoptosis as a Potential Anti-tumor Agent.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Curing spinal cord injury (SCI) in mammals is a daunting task because of the lack of permissive mechanisms and strong inhibitory responses at and around the lesion. The neural cell adhesion molecule L1CAM (L1) has been shown to favor axonal regrowth and enhance neuronal survival and synaptic plasticity but delivery of full-length L1 or its extracellular domain could encounter difficulties in translation to therapy in humans. We have, therefore, identified several small organic compounds that bind to L1 and stimulate neuronal survival, neuronal migration and neurite outgrowth in an L1-dependent manner. Here, we assessed the functions of two L1 mimetics, trimebutine and honokiol, in regeneration following SCI in young adult mice. Using the Basso Mouse Scale (BMS) score, we found that ground locomotion in trimebutine-treated mice recovered better than honokiol-treated or vehicle-receiving mice. Enhanced hindlimb locomotor functions in the trimebutine group were observed at 6 weeks after SCI. Immunohistology of the spinal cords rostral and caudal to the lesion site showed reduced areas and intensities of glial fibrillary acidic protein immunoreactivity in both trimebutine and honokiol groups, whereas increased regrowth of axons was observed only in the trimebutine-treated group. Both L1- and L1 mimetic-mediated intracellular signaling cascades in the spinal cord lesion sites were activated by trimebutine and honokiol, with trimebutine being more effective than honokiol. These observations suggest that trimebutine and, to a lesser extent under the present experimental conditions, honokiol have a potential for therapy in regeneration of mammalian spinal cord injuries.
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Registered trials
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