Abstract
Photoreceptor ciliopathies constitute the most common molecular mechanism of the childhood blindness Leber congenital amaurosis. Ten patients with Leber congenital amaurosis carrying the c.2991+1655A>G allele in the ciliopathy gene centrosomal protein 290 (CEP290) were treated (ClinicalTrials.gov no. NCT03140969 ) with intravitreal injections of an antisense oligonucleotide to restore correct splicing. There were no serious adverse events, and vision improved at 3 months. The visual acuity of one exceptional responder improved from light perception to 20/400.
Publication types
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Clinical Trial
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Alleles
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Antigens, Neoplasm / genetics
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Cell Cycle Proteins
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Cilia / drug effects
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Cilia / pathology*
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Cytoskeletal Proteins
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Female
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Humans
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Intravitreal Injections
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Leber Congenital Amaurosis / drug therapy*
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Leber Congenital Amaurosis / physiopathology*
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Male
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Neoplasm Proteins / genetics
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Oligonucleotides, Antisense / administration & dosage*
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Oligonucleotides, Antisense / therapeutic use*
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Photoreceptor Cells, Vertebrate / pathology*
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Vision, Ocular*
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Young Adult
Substances
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Antigens, Neoplasm
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Cell Cycle Proteins
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Cep290 protein, human
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Cytoskeletal Proteins
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Neoplasm Proteins
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Oligonucleotides, Antisense
Associated data
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ClinicalTrials.gov/NCT03140969