June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Topical administration of MRZ-99030, a β-amyloid aggregation modulator, protects retinal ganglion cells and axons in a rodent model of glaucoma
Author Affiliations & Notes
  • Andreas Gravius
    Merz Pharmaceuticals, Frankfurt, Germany
  • Kai-Uwe Klein
    Merz Pharmaceuticals, Frankfurt, Germany
  • Leonard Levin
    McGill University, Montreal, QC, Canada
  • Wolf Lagreze
    University of Freiburg, Freiburg, Germany
  • Nico Wegener
    Merz Pharmaceuticals, Frankfurt, Germany
  • Wojciech Danysz
    Merz Pharmaceuticals, Frankfurt, Germany
  • Footnotes
    Commercial Relationships Andreas Gravius, Merz Pharmaceuticals (E); Kai-Uwe Klein, Merz Pharmaceuticals GmbH (E); Leonard Levin, Quark (C), Inotek (C), Merz (C), Wisconsin Alumni Research Foundation (P), Cytodefense (I), Teva (C), Allergan (C); Wolf Lagreze, Merz (C), Allergan (C); Nico Wegener, Merz Pharmaceuticals (E); Wojciech Danysz, Merz Pharmaceuticals (E)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2625. doi:
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      Andreas Gravius, Kai-Uwe Klein, Leonard Levin, Wolf Lagreze, Nico Wegener, Wojciech Danysz; Topical administration of MRZ-99030, a β-amyloid aggregation modulator, protects retinal ganglion cells and axons in a rodent model of glaucoma. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2625.

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

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Abstract

Purpose: Topical administration of MRZ-99030, a β-amyloid aggregation modulator, protects retinal ganglion cells and axons in a rodent model of glaucoma MRZ-99030 is a small molecule with neuroprotective activity via modulation of β-amyloid (Aβ) aggregation. This compound inhibits Aβ-induced toxicity in multiple in vitro and in vivo models and is currently under Phase I clinical development. The neurotoxic peptide Aβ has recently been implicated in retinal ganglion cell (RGC) apoptosis in glaucoma, with evidence of caspase-3-mediated abnormal amyloid precursor protein processing, increased expression of Aβ in RGCs and optic nerves in experimental glaucoma and increased Aβ in the ganglion cell layer of glaucoma patients. Some forms of aggregated Aβ are able to induce significant RGC apoptosis in vivo and in vitro. Interestingly, it has been shown that targeting different components of the Aβ formation and aggregation pathway can effectively reduce glaucomatous RGC apoptosis in vivo and therefore raises the possibility of neuroprotection in glaucoma. Based on these findings, we assessed the neuroprotective potential of MRZ-99030 after topical administration in a commonly used rodent model of glaucoma

Methods: Ocular hypertension was induced in Brown Norway rats by two injections of hypertonic saline into the episcleral veins. This results in increase of intraocular pressure, with progressive loss of RGCs and axonal degeneration. Topical administration of MRZ-99030 3 times daily for 6 weeks, followed by counting of previously retrograde-labelled RGCs in whole-mounts and assessment of optic nerve sections. All experiments were done with the identity of the topical solution masked. In addition, retina concentrations of MRZ-99030 were assessed in rats and monkeys for evaluation of PK/PD relationship.

Results: MRZ-99030 dose-dependently and significantly reduced loss of RGCs compared to vehicle control with a maximal effect size of 95%. Also axonal degeneration was significantly decreased in drug-treated eyes. Pharmakokinetic studies revealed sufficient retina concentrations of MRZ-99030 above in vitro affinity in both rats and monkeys.

Conclusions: Modulation of Aβ aggregation may be a promising avenue for neuroprotection and axoprotection in glaucoma.

Keywords: 531 ganglion cells • 629 optic nerve  
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