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Hello, and welcome to another edition of the Ophthalmology Times EyePod Week in Review podcast. Each week, we bring you the latest cutting-edge news on the latest advancements in the field of ophthalmology. Here are a few headlines from the week.
A Japanese study found that switching to faricimab (Vabysmo, Genentech) treatment using a treat-and-extend regimen seems to maintain the best-corrected visual acuity and extend the injection interval in patients with neovascular age-related macular degeneration, resulting in enhanced satisfaction 6 months after patients were switched.
Taiichi Hikichi, MD, who is in private practice in Sapporo, Japan, reported his findings in the Japanese Journal of Ophthalmology.
Hikichi conducted a retrospective observational study of 48 consecutive eyes of 48 patients with n AMD who were switched to faricimab and followed for 6 months while they were on a TAE regimen. At the 6-month time point, the patients completed the Macular Disease Treatment Satisfaction Questionnaire.
The results showed that the BCVA was maintained 6 months after the patients were switched to the faricimab TAE regimen. In addition, the mean central foveal thickness decreased significantly at 6 months compared to the time at which patients started on faricimab.
The loss of neurons in the retina as a result of trauma or disease leads to a loss of vision which is irreversible in humans. However, some animals, such as fish, have the built-in ability to regenerate retinal neurons by turning another retinal cell type called “Müller glia” into neurons.
According to research by Thomas Reh, PhD, Juliette Wohlschlegel, PhD, and colleagues at the University of Washington, the human Müller glia can be coaxed into changing identity in the laboratory, which could serve as a potential source of new neurons to treat vision loss.
The study was published in the journal Stem Cell Reports.
The researchers noted that in some species, including fish and birds, Müller glia turn into immature retinal cells upon injury and subsequently generate new retinal neurons. In the mammalian retina, Müller glia react to injury with scar formation and inflammation without making new neurons.
According to the study, it is believed that the difference in behavior is based on different genetic programs being activated in fish versus mammalian Müller glia after injury. Artificial activation of a fish-like genetic program can turn mouse Muller glia into retinal neurons according to prior research.
To this point, it has not been determined whether the same strategy can be used to convert human Müller glia into neurons. Setting out to find out, the researchers genetically modified human Müller glia in the lab to switch on neurons-specific genetic programs, as it naturally happens in fish. Indeed, within a week, the genetically modified cells adopted neuron-like characteristics resembling immature retinal neurons.
OKYO Pharma has announced the last patient enrolled in its phase 2 clinical trial of O K-101 to treat dry eye disease (DED) has completed final protocol visit.
The phase 2 trial of OK-101 is a multi-center, randomized, double-masked, and placebo-controlled study evaluating the efficacy and safety of OK-101 ophthalmic solution compared to placebo in subjects with DED.
According to a press release, data analysis plans for the trial have been finalized and submitted to the FDA for feedback, in anticipation of database lock, subsequent data analysis, and reporting of top-line findings on OK-101. According to the company, top-line efficacy and safety data is on track for release in December of 2023.
OK-101 is a lipid conjugated chemerin peptide agonist of the ChemR23 G-protein coupled receptor which is typically found on immune cells of the eye responsible for the inflammatory response. Furthermore, according to the company, OK-101 has been shown to produce anti-inflammatory and pain-reducing activities in mouse models of dry eye disease and corneal neuropathic pain (NCP), respectively.
A new Japanese study evaluated the subclinical effects of anti-vascular endothelial growth factor (VEGF) therapies for neovascular age-relatedmacular degeneration (AMD) and reported that brolucizumab (Beovu, Novartis) may cause transient retinal disturbances undetectable during general ophthalmologic examinations that affect the implicit electroretinography (ERG) times, according to first author Hisashi Matsubara, MD. He is from the Department of Ophthalmology, Mie University Graduate School of Medicine, Mie, Japan.
Clinical studies of brolucizumab have reported intraocular inflammation (IOI) and retinal vascular occlusion, and those studies have spawned a growing interest in determining the cause of the IOI after intravitreal injections of anti-VEGF agents.
In light of those reports, the investigators wanted to determine if subclinical changes in the blood–aqueous barrier and the retinal physiology developed after anti-VEGF treatments with aflibercept (Eylea, Regeneron), brolucizumab, and or faricimab (Vabysmo, Roche), anti-VEGF drugs that are commonly used to treat neovascular AMD.
To that end, they evaluated the anterior chamber based on the aqueous flare value (AFV) and the retina by flicker ERG after the initial intravitreal injections of the 3 drugs. The AFV and flicker ERGs were determined before and 2 and 4 weeks after the injections in 14 eyes of 14 patients for each drug.
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