July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Allele specific knock-down of human P23H rhodopsin mRNA and prevention of retinal degeneration in humanized P23H rhodopsin knock-in mouse, following treatment with an intravitreal GAPmer antisense oligonucleotide (QR-1123)
Author Affiliations & Notes
  • Patricia Biasutto
    ProQR Therapeutics, Leiden, Netherlands
  • Peter S Adamson
    ProQR Therapeutics, Leiden, Netherlands
  • Kalyan Dulla
    ProQR Therapeutics, Leiden, Netherlands
  • Sue Murray
    Ionis Pharmaceuticals, California, United States
  • Brett Monia
    Ionis Pharmaceuticals, California, United States
  • Michael McCaleb
    Ionis Pharmaceuticals, California, United States
  • Footnotes
    Commercial Relationships   Patricia Biasutto, ProQR Therapeutics (E); Peter Adamson, ProQR Therapeutics (E); Kalyan Dulla, ProQR Therapeutics (E); Sue Murray, Ionis Pharmaceuticals (E); Brett Monia, Ionis Pharmaceuticals (E); Michael McCaleb, Ionis Pharmaceuticals (E)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 5719. doi:
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    • Get Citation

      Patricia Biasutto, Peter S Adamson, Kalyan Dulla, Sue Murray, Brett Monia, Michael McCaleb; Allele specific knock-down of human P23H rhodopsin mRNA and prevention of retinal degeneration in humanized P23H rhodopsin knock-in mouse, following treatment with an intravitreal GAPmer antisense oligonucleotide (QR-1123). Invest. Ophthalmol. Vis. Sci. 2019;60(9):5719.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : To demonstrate the allele-selective knockdown of human P23H rhodopsin mRNA using the GAPmer antisense oligonucleotide (ASO) QR-1123 and that, when dosed intravitreally, QR-1123 reduces the rate of retinal loss in a humanized P23H rhodopsin knock-in mouse model of adRP

Methods : HEK293 cells stably expressing human rhodopsin mini-genes with mutation (P23H) or without (WT), were used to determine the selectivity of QR-1123 for the rhodopsin mRNA containing the C-A transversion (P23H). Human P23H/WT transgenic mice (hP23HTg) were created and used to determine the ability of QR-1123 to selectively target the P23H mutant mRNA in vivo following intravitreal delivery, and its ability to limit the retinal degeneration in the P23H rhodopsin expressing mouse

Results : QR-1123 was demonstrated to selectively target the human P23H mutant rhodopsin mRNA, whilst sparing the human WT rhodopsin sequence using an RNAase H1-dependent mechanism in transfected cell lines containing either human rhodopsin mini-gene. When unilaterally dosed by intravitreal injection into humanized rhodopsin knock-in mice expressing either WT or mutated rhodopsin, QR-1123 selectively reduced the P23H human rhodopsin mRNA whilst having little impact in the human WT rhodopsin expressing mice. QR-1123 also showed a capacity to dramatically slow the retinal degeneration in the P23H humanized knock-in model in both inferior and superior retina, when compared to either control non-dosed animals, or in PBS injected contralateral eyes from the same animals

Conclusions : Selective, allele-specific ASO mediated knockdown of human P23H rhodopsin expression by QR-1123 was demonstrated in cell lines containing human rhodopsin sequences and in transgenic human rhodopsin knock-in mice. QR-1123 when dosed intravitreally also slowed the rate of photoreceptor degeneration in the humanized P23H rhodopsin knock-in mouse. These data indicate that ASO treatment is a potentially effective therapy for adRP, arising from P23H mutation in rhodopsin

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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