Torres-Masjoan Laia, Aguti Sara, Zhou Haiyan, Muntoni Francesco
Genetic Therapy Accelerator Centre, Institute of Neurology, University College London, London WC1N 1EH, UK.
National Institute for Health and Care Research (NIHR) Great Ormond Street Hospital Biomedical Research Centre, London WC1N 1EH, UK; Genetics and Genomic Medicine Research and Teaching Department, Great Ormond Street Institute of Child Health, University College London, London WC1N 1EH, UK.
Mol Ther. 2025 Jun 4;33(6):2689-2704. doi: 10.1016/j.ymthe.2025.04.038. Epub 2025 Apr 30.
Four exon-skipping antisense oligonucleotides (ASOs) have been approved by the US Food and Drug Administration (FDA) for the treatment of Duchenne muscular dystrophy (DMD), including eteplirsen, golodirsen, viltolarsen, and casimersen. Current data from long-term real-world usage of these ASOs suggests a broad safety profile and a delay in muscle deterioration. Nevertheless, the exon-skipping efficacy and dystrophin protein production of these ASOs are limited, suggesting the need for more efficient ASOs. Over the past decade, many studies have focused on improving ASO efficacy by incorporating novel chemical modifications or bioconjugations of a variety of moieties including peptides or antibodies to increase their cellular uptake by muscle cells, their endosomal escape, and their nuclear import to boost therapeutic efficacy. Many of these newly developed exon-skipping ASOs have been studied in clinical trials in DMD patients, and early findings suggest clear improvements in molecular efficacy compared to the earlier version of ASOs, although the safety track record may not be the same as the first-generation compounds. Here, we summarize the recent preclinical and clinical developments of ASOs and discuss the future challenges of exon-skipping therapies for DMD and other neuromuscular diseases.
四种外显子跳跃反义寡核苷酸(ASO)已获美国食品药品监督管理局(FDA)批准用于治疗杜氏肌营养不良症(DMD),包括依特普瑞森、戈洛迪森、维托拉森和卡西默森。这些ASO长期实际应用的当前数据表明其安全性良好且能延缓肌肉退化。然而,这些ASO的外显子跳跃功效和肌营养不良蛋白的产生有限,这表明需要更有效的ASO。在过去十年中,许多研究致力于通过纳入新型化学修饰或与包括肽或抗体在内的各种部分进行生物缀合来提高ASO功效,以增加其被肌肉细胞摄取、从内体逃逸以及核转运,从而提高治疗效果。许多这些新开发的外显子跳跃ASO已在DMD患者的临床试验中进行研究,早期结果表明,与早期版本的ASO相比,分子功效有明显改善,尽管其安全记录可能与第一代化合物不同。在此,我们总结了ASO最近的临床前和临床进展,并讨论了DMD和其他神经肌肉疾病外显子跳跃疗法未来面临的挑战。