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phosphorodiamidate morpholino oligomer AVI-4126

Known as: PMO AVI-4126 
A c-Myc antisense phosphorodiamidate morpholino oligomer (PMO) with potential antineoplastic activity. Phosphorodiamidate morpholino oligomer AVI… Expand
National Institutes of Health

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Highly Cited
2011
Highly Cited
2011
Summary Background We report clinical safety and biochemical efficacy from a dose-ranging study of intravenously administered AVI… Expand
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Highly Cited
2010
Highly Cited
2010
Exon-skipping efficacies of phosphodiamidate morpholino oligomers (PMOs) or the conjugates of PMOs with cell-penetrating peptides… Expand
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Highly Cited
2008
Highly Cited
2008
Cell-penetrating peptides (CPPs), containing arginine (R), 6-aminohexanoic acid (X), and/or beta-alanine (B) conjugated to… Expand
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Highly Cited
2008
Highly Cited
2008
Abstract Antisense oligonucleotides (AOs) have the potential to induce functional dystrophin protein expression via exon skipping… Expand
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Highly Cited
2007
Highly Cited
2007
Morpholino phosphorodiamidate antisense oligonucleotides (MOs) and short interfering RNAs (siRNAs) are commonly used platforms to… Expand
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Highly Cited
2006
Highly Cited
2006
For the majority of Duchenne muscular dystrophy (DMD) mutations, antisense oligonucleotide (AON)-mediated exon skipping has the… Expand
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Highly Cited
2006
Highly Cited
2006
Manipulation of pre-mRNA splicing by antisense oligonucleotides (AOs) offers considerable potential for a number of genetic… Expand
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Highly Cited
2005
Highly Cited
2005
Phosphorodiamidate morpholino oligomers (PMO) inhibit targeted gene expression by preventing ribosomal assembly, thereby… Expand
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Review
2005
Review
2005
The concept of using antisense oligonucleotides to interfere with gene expression offers a new therapeutic strategy for the… Expand
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Highly Cited
2003
Highly Cited
2003
The mdx mouse model of muscular dystrophy arose due to a nonsense mutation in exon 23 of the dystrophin gene. We have previously… Expand
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