ArticleCellular and molecular life sciences : CMLS2022
Moxifloxacin rescues SMA phenotypes in patient-derived cells and animal model.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Haloperidol induces neuroprotection and enhances neuromuscular function in both murine and human models of spinal muscular atrophy.Experimental & molecular medicine · 2026Article
- Suppressive effect of topical moxifloxacin on imiquimod-induced model of psoriasis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Patient-specific responses toMolecular therapy. Methods & clinical development · 2024Article
- GLNNMDA: a multimodal prediction model for microbe-drug associations based on global and local features.Scientific reports · 2024Article
- A novel microbe-drug association prediction model based on graph attention networks and bilayer random forest.BMC bioinformatics · 2024Article
- Unlocking the Complexity of Neuromuscular Diseases: Insights from Human Pluripotent Stem Cell-Derived Neuromuscular Junctions.International journal of molecular sciences · 2023Review
- Elucidation of bioinformatic-guided high-prospect drug repositioning candidates for DMD via Swanson linking of target-focused latent knowledge from text-mined categorical metadata.Frontiers in cell and developmental biology · 2023Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Spinal muscular atrophy (SMA) is a genetic disease resulting in the loss of α-motoneurons followed by muscle atrophy. It is caused by knock-out mutations in the survival of motor neuron 1 (SMN1) gene, which has an unaffected, but due to preferential exon 7 skipping, only partially functional human-specific SMN2 copy. We previously described a Drosophila-based screening of FDA-approved drugs that led us to discover moxifloxacin. We showed its positive effect on the SMN2 exon 7 splicing in SMA patient-derived skin cells and its ability to increase the SMN protein level. Here, we focus on moxifloxacin's therapeutic potential in additional SMA cellular and animal models. We demonstrate that moxifloxacin rescues the SMA-related molecular and phenotypical defects in muscle cells and motoneurons by improving the SMN2 splicing. The consequent increase of SMN levels was higher than in case of risdiplam, a potent exon 7 splicing modifier, and exceeded the threshold necessary for a survival improvement. We also demonstrate that daily subcutaneous injections of moxifloxacin in a severe SMA murine model reduces its characteristic neuroinflammation and increases the SMN levels in various tissues, leading to improved motor skills and extended lifespan. We show that moxifloxacin, originally used as an antibiotic, can be potentially repositioned for the SMA treatment.
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