Scientists compared the changes in macular ganglion cell-inner plexiform layer defects between stable and progressing primary open-angle glaucoma groups, as part of a retrospective, observational study.

A total of 100 POAG eyes with localized retinal nerve fiber layer defect and corresponding macular GCIPL defects were selected for this study. Scientists defined glaucoma progression by structural or functional deterioration. They calculated the number of abnormal superpixels on macular GCIPL deviation maps using a customized MATLAB program, and evaluated GCIPL defect changes by increased angular width and increased area. In addition, they compared defect patterns between the stable and the progression groups.

The rate of angular width increase of GCIPL defects was higher in the progression group than in the stable group (p=0.029). There were no statistically significant differences between the groups’ areas of GCIPL defects (p=0.227). Twenty-seven of 100 (27 percent) eyes showed increased angular width of GCIPL defects. This feature was more frequent in the progression group than in the stable group (p=0.043). Seventeen of 27 (63 percent) eyes showed the away-from-the-horizontal-temporal-raphe-type progression, which was the most common change pattern exhibited by angular width of GCIPL defects.

Scientists reported that increased angular width of GCIPL defects was the most prominent feature of change, and was more frequent in the progression group than in the stable group. Among the types of GCIPL defects classified, they found that the away-from-the-horizontal-temporal-raphe type was the most common.

Researchers determined whether emixustat hydrochloride reduced the rate of geographic atrophy enlargement compared with placebos in subjects with age-related macular degeneration, and evaluated the safety and tolerability of emixustat over 24 months of treatment.

The multicenter, randomized, double-masked, placebo-controlled, Phase IIb/III clinical trial included individuals with GA secondary to AMD, a visual acuity score of at least 35 letters, and GA with a total area of 1.25 to 18 mm². Subjects were randomized (1:1:1:1) to emixustat 2.5 mg, 5 mg, 10 mg or placebo, administered orally once daily for 24 months. Visits included screening, baseline, and months one, two, three, six, nine, 12, 15, 18, 21, 24 and 25.

The primary efficacy end point was the mean annual growth rate of total GA area in the study eye, as measured by a central reading center using fundus autofluorescence images. The change from baseline in normal luminance best-corrected visual acuity was a secondary efficacy end point.

Of 508 randomized subjects, 320 completed the study. Demographics and baseline characteristics were comparable between treatment groups. On average, GA lesions in the study eye grew at a similar rate in each group (emixustat: 1.69 to 1.84 mm²/year; placebo: 1.69 mm²/year; p≥0.81). Changes in NL-BCVA were also comparable between groups. Subjects with a larger low- luminance deficit at baseline (≥20 letters) demonstrated a more rapid growth of GA over 24 months. No relationship was observed between the risk-allele status of the AMD-associated single-nucleotide polymorphisms tested and the growth rate of GA. The most common adverse events in emixustat-treated subjects were delayed dark adaptation (55 percent), chromatopsia (18 percent), visual impairment (15 percent) and erythropsia (15 percent).

Researchers wrote that emixustat didn’t reduce the growth rate of GA in AMD. They noted that the most common adverse events were ocular in nature and likely related to the drug’s mechanism of action. Researchers added that data gained from this study over a two-year period added to the understanding of the natural history of GA and the baseline characteristics affecting the growth rate of GA.