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Exon skipping and dystrophin restoration in patients with Duchenne muscular dystrophy after systemic phosphorodiamidate morpholino oligomer treatment: an open-label, phase 2, dose-escalation study.

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TLDR
The safety and biochemical efficacy presented show the potential of AVI-4658 to become a disease-modifying drug for Duchenne muscular dystrophy.
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This article is published in The Lancet.The article was published on 2011-08-13 and is currently open access. It has received 847 citations till now. The article focuses on the topics: Duchenne muscular dystrophy & Drisapersen.

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LC-MS of oligonucleotides: applications in biomedical research

TL;DR: The current applications of LC-MS in the analysis of oligonucleotides, with an emphasis on RNA therapeutics and biomarkers, will be examined and the theoretical framework of olig onucleotide ESI is carefully inspected with the purpose of identifying the contributing factors to MS signal intensity.
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Exon skipping restores dystrophin expression, but fails to prevent disease progression in later stage dystrophic dko mice

TL;DR: The PPMO treatment alleviated the disease pathology and significantly prolonged the life span of the mice receiving treatment at younger age with mild phenotype, however, restoration of high levels of dystrophin expression failed to prevent disease progression to the mice received treatment when disease was already at advanced stage.
Patent

Antisense molecules and methods for treating pathologies

TL;DR: An antisense molecule capable of binding to a selected target site to induce exon skipping in the dystrophin gene, as set forth in SEQ ID NO: 1 to 59, was presented in this article.
Journal ArticleDOI

Antisense oligonucleotide therapeutics in clinical trials for the treatment of inherited retinal diseases.

TL;DR: Antisense oligonucleotides hold great therapeutic potential for numerous other inherited retinal diseases with common deep-intronic and dominant gain-of-function mutations, and would complement viral vector-mediated gene augmentation which is generally limited by the size of the transgene and to the treatment of recessive diseases.
References
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Journal ArticleDOI

Dystrophin: The protein product of the duchenne muscular dystrophy locus

TL;DR: The identification of the mdx mouse as an animal model for DMD has important implications with regard to the etiology of the lethal DMD phenotype, and the protein dystrophin is named because of its identification via the isolation of the Duchenne muscular dystrophy locus.
Journal ArticleDOI

Local Dystrophin Restoration with Antisense Oligonucleotide PRO051

TL;DR: Intramuscular injection of antisense oligonucleotide PRO051 induced dystrophin synthesis in four patients with Duchenne's muscular dystrophy who had suitable mutations, suggesting that further studies might be feasible.
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