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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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Patent

Antisense nucleic acids

TL;DR: In this paper, an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene was presented. And a pharmaceutical composition which caused skipping of this exon with high efficiency.
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Efficacy and Safety Profile of Tricyclo-DNA Antisense Oligonucleotides in Duchenne Muscular Dystrophy Mouse Model

TL;DR: It is shown that systemic delivery of 13-mer tcDNA allows restoration of dystrophin in skeletal muscles and to a lower extent in the brain, leading to muscle function improvement and correction of behavioral features linked to the emotional/cognitive deficiency.
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Preventing formation of toxic N-terminal huntingtin fragments through antisense oligonucleotide-mediated protein modification.

TL;DR: The proof of concept shows a completely novel approach to reduce mutant huntingtin toxicity not by reducing its expressing levels, but by modifying the huntingtin protein.
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Innate Immune Response and Off-Target Mis-splicing Are Common Morpholino-Induced Side Effects in Xenopus.

TL;DR: It is concluded that while MOs can be useful to profile loss-of-function phenotypes at a molecular level, careful attention must be paid to their immunogenic and off-target side effects.
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A dystrophic Duchenne mouse model for testing human antisense oligonucleotides.

TL;DR: The del52hDMD/mdx model enables the in vivo analysis of human specific AONs targeting exon 51 or exon 53 on RNA and protein level and muscle quality and function and will be a valuable tool for optimizing human specificAONs and genome editing approaches for DMD.
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.
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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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