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G. Cumberlidge, H. Saragovi, K. J. Lane, M. B. Abelson; An Evaluation of D3, a Novel TrkA Receptor Agonist, for Ability to Prevent Retinal Ganglion Cell Loss in a Rat Model of Glaucoma. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4367.
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To evaluate D3, a TrkA specific partial agonist, for ability to prevent RGC loss in the rat episcleral cauterization model of glaucomatous optic neuropathy.
To induce elevated intraocular pressure, the right eye of each rat was subjected the episcleral vessel cauterization. Animals were randomized to receive no treatment, treatment with a topical hypotensive agent (betaxolol 0.5%, beginning 14 days after cauterization and continued through the study), treatment with 1 microgram D3 (injected intravitreally at 14 and 21 days after cauterization), or combined treatment with both topical betaxolol 0.5% and intravitreal D3 (as described above). An untreated control group was sacrificed at Day 14 to determine extent of RGC loss prior to therapeutic intervention. Remaining animals were sacrificed at Day 42, 28 days after initiating treatment. Percent RGC loss was calculated.
At Day 14, untreated cauterized animals demonstrated 8% RGC loss compared to normotensive controls. By Day 42, 36% RGC loss was exhibited in untreated animals. Animals treated with betaxolol beginning at Day 14 demonstrated 21% RCG loss at Day 42. Animals treated with D3 at Day 14 and Day 21 exhibited 29% RCG loss at Day 42. Animals that received both the topical hypotensive and intravitreal D3 demonstrated only 11% RCG loss at Day 42.
Treatment with D3 in combination with topical betaxolol was significantly more effective at preventing RGC loss than treatment with betaxolol alone (p<0.05). Given that RCG loss continues following normalization of IOP, a neuroprotective agent acting at the TrkA receptor holds significant therapeutic potential, acting in an additive or synergistic fashion with the topical hypotensive to prevent additional RCG loss.
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