Other inflammatory pathways also contribute to GA pathogenesis. Activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 inflammasome leads to assembly of the multiprotein complex and activation of caspase-1, which promotes maturation and release of the proinflammatory cytokines interleukin-1b and interleukin-18 and induces pyroptotic cell death.²¹ Although activation of the inflammasome has been associated with RPE cell death, the exact mechanism remains unclear.²² The accumulation of ribonucleic acid, drusen components (e.g., C1q), and other complement components such as C3a and C5a have been implicated in inflammasome activation.²²

 

Upregulation of mitochondrial dysfunction pathways has been identified in GA.²³ Accumulation of reactive oxygen species (ROS) can impair mitochondrial function in RPE cells, leading to increased inflammation that amplifies ROS production, creating a positive feedback loop.²⁴ This oxidative damage leads to RPE dysfunction and apoptosis, which precipitates photoreceptor degeneration.²⁴ Defective energy metabolism, mitophagy, and increased ROS production contribute to cellular stress, inflammation, and apoptosis in the RPE and outer retina.²⁵ The resulting RPE dysfunction, combined with complement activation, leads to degeneration of the choriocapillaris. The choriocapillaris, the primary vascular supply to the outer retina, classically degenerates in GA alongside RPE and photoreceptor loss.²⁶ Indeed, deficits in choriocapillaris flow have been associated with faster GA lesion growth and reduced central visual function.²⁷⁻²⁸ The extent of choriocapillaris impairment often exceeds the boundaries of atrophy, allowing for its use in quantitative imaging as a marker of risk and progression.²⁹ Ultimately, the combination of chronic RPE dysfunction, oxidative stress, complement-mediated inflammation, and loss of support from the choriocapillaris leads to irreversible photoreceptor atrophy.

 

GA is also characterized by abnormal lipid metabolism. The accumulation of ceramides and decline in phospholipids signify significant disruption of lipid homeostasis.³⁰⁻³¹ Genes involved in lipid metabolism, including ABCA1 and GPX4, have been identified as potential drug targets in AMD.³² Impaired lipid transport, accumulation of lipoproteins, and dysregulated cholesterol efflux in the RPE all contribute to the production of drusen.³³

 

The genetic variants that most strongly affect GA risk are related to the complement pathway, including CFH, CFB, FHR1-FHR3, and C3.8,³⁴ Several genes have been implicated in the risk for GA progression. The age-related maculopathy susceptibility 2 (ARMS2) and high-temperature requirement A serine peptidase 1 (HTRA1) gene risk alleles, particularly the single-nucleotide polymorphism rs10490924, have been associated with faster enlargement of GA lesions. The ARMS2 and HTRA1 genes are tightly linked. Patients with two risk alleles (TT) had the greatest rate of GA lesion enlargement (0.317 mm/year, 95% CI 0.279 to 0.355), followed by one allele (GT; 0.298, 95% CI 0.271 to 0.324) and no risk alleles (GG; 0.224, 95% CI 0.195 to 0.252, P<0.0001).³⁵ Increased enlargement was most pronounced in eyes with small lesions.³⁵ The exact function of the ARMS2 protein is unknown, although it may regulate mitochondrial homeostasis and the extracellular matrix.³⁶ Conversely, HTRA serine protease, coded by HTRA1, regulates cell growth, and overexpression has been linked to inflammation and neovascularization, particularly at the RPE-Bruch membrane interface.³⁷ The protein arginine methyltransferase 6 rs1184959 and lanosterol synthase rs2839127 loci have also been associated with disease progression.³⁸ The PRMT6 protein, which is involved in post-translational protein modification, contributes to normal retinal structure. PRMT6 is expressed more in the peripheral RPE and choroid than the central region, and dysregulation may affect GA lesion localization.³⁸ Finally, the LSS protein is an enzyme used for cholesterol synthesis and is necessary for normal retinal vasculature.³⁸ Together, these loci serve as potential targets for risk stratification and future treatments.

 

Imaging and Biomarkers in Diagnosis

​

Multimodal retinal imaging is important for the diagnosis and monitoring of GA. In recent years, studies harnessing machine learning models have confirmed and identified several important biomarkers of severity and progression. Optical coherence tomography (OCT) and fundus autofluorescence (FAF) are the most common modalities used in GA surveillance.³⁹⁻⁴⁰ OCT provides high-resolution cross-sectional visualization of retinal layers and can reliably diagnose GA. Numerous terms established by the Classification of Atrophy Meetings program are now employed to capture the severity of possible GA lesions on OCT, including complete RPE and outer retinal atrophy (cRORA), incomplete RPE and outer retinal atrophy (iRORA), complete outer retinal atrophy (cORA), and incomplete outer retinal atrophy (iORA).⁴¹ cRORA is defined as homogeneous choroidal hypertransmission and absence of the RPE band measuring ≥250 μm, accompanied by overlying outer retinal thinning and photoreceptor loss. iRORA is defined as a region of choroidal hypertransmission and corresponding attenuation or disruption of the RPE with overlying photoreceptor degeneration that does not meet the definition of cRORA. Despite their prognostic value, there are limitations to the detection of iRORA, including variations in OCT devices and difficulties in accurately measuring size to distinguish from cRORA when lesions span the border of adjacent scans.⁴²⁻⁴³ OCT also allows for the detection of drusen, RPD, and hyperreflective foci, which have been identified as risk factors for GA onset and progression.⁴²⁺⁴⁴⁻⁴⁶ Loss of the ellipsoid zone and/or RPE, and thinning of the outer nuclear layer are also indicative of GA progression.¹⁵⁺⁴⁷⁻⁴⁸

 

FAF visualizes the autofluorescent properties of lipofuscin, an accumulated byproduct of photoreceptor damage.³⁹ Although lipofuscin accumulates with age, GA lesions lack lipofuscin due to RPE atrophy, appearing as hypofluorescent areas on FAF.³⁹ On colour fundus photography, drusen appear as yellowish-whitish deposits, whereas on FAF they may demonstrate decreased auto­fluorescence, correlating with outer retinal thinning.⁴⁹ RPD appear as interlacing networks of hypoautofluorescent lesions, namely dots or ribbons, against a background with mildly reduced or iso-autofluorescence.⁵⁰⁻⁵¹ Vitelliform lesions typically show intense hyperautofluorescence in early stages, but become hypoautofluorescent as atrophy develops.⁵²

 

Lifestyle Modifications

​

Several important modifiable risk factors should be targeted in patients with dry AMD, including GA. Smoking cessation is incredibly important among patients who are at risk for AMD and those who already have AMD.¹⁵⁺⁵³ A 40 pack-year smoking history was associated with >3 times greater odds of developing GA, and current smokers have a 3-fold increase in risk for AMD compared to patients who never smoked.¹⁵⁺⁵³ Further, some studies suggest that the increased risk can be partially reversed upon smoking cessation.¹⁵ Dietary modifications, particularly adherence to a Mediterranean diet, have been associated with decreased progression to late AMD.⁵⁴ Increased physical activity may be associated with reduced incidence and slowed progression of AMD.⁵⁵

 

Current Treatments

​

For patients with bilateral intermediate AMD or one eye with intermediate and the other with advanced AMD, the Age-Related Eye Disease Study (AREDS) and AREDS2 studies showed that oral micronutrient supplementation can reduce the progression of AMD.⁵⁶ A 2025 post hoc analysis of AREDS2 participants found that randomization to lutein and zeaxanthin reduced proximity-based progression of GA compared to controls (-34.3 μm/year; 95% confidence interval [CI] -60.8 to -7.8; P=0.011), although there was no significant difference in area-based progression.⁵⁷ This study provided the first large-scale evidence that use of AREDS2 vitamin supplementation impacted the extent to which GA grew towards the fovea. Importantly, AREDS2 supplementation is not a treatment that reverses established GA.

 

Beyond the preventive benefits of AREDS/AREDS2, there were until recently no evidence-based treatments to slow the progression of GA. In 2023, pegcetacoplan and avacincaptad pegol (ACP) were approved by the United States (US) Food and Drug Administration (FDA) for the treatment of GA secondary to AMD.⁵⁸ Both drugs target the complement cascade; pegcetacoplan targets complement component 3 (C3), and ACP targets C5.⁵⁸ The evidence to date suggests that the benefits of these treatments are largely anatomical and limited to slowing GA progression without being able to reverse GA. Longer-term follow-up may be required to demonstrate a preventive effect, with pivotal clinical trials only beginning to report data beyond 24 months.⁵⁹ As of August 2026, neither drug has been approved for use in patients with GA by Health Canada, although ACP is currently under review.⁶⁰⁻⁶¹

 

ACP

​

The primary evidence in support of ACP is the GATHER1 and GATHER2 trials.⁶²⁻⁶³ GATHER1 was a 2-part study that randomized 77 eyes 1:1:1 to ACP 1 mg, ACP 2 mg, or sham intravitreal injection and 209 eyes 1:2:2 to ACP 2 mg, 4 mg, and sham, all with monthly dosing.62 In eyes receiving ACP 4 mg, the least-squares mean (LSM) GA lesion growth was -0.167 mm² (95% CI -0.273 to -0.062), representing a difference of -30.0% compared to sham, while the difference in LSM lesion growth was -28.1% (-0.168 mm²; 95% CI -0.271 to -0.066) in eyes receiving ACP 2 mg compared to sham. Both ACP 2 mg and 4 mg showed numeric improvement in best-corrected visual acuity (BCVA) and low light VA compared to sham, although the results were not statistically significant. ACP was well tolerated, with most adverse events (AEs) relating to the injection procedure. There was 1 case of intraocular inflammation in the ACP 2 mg group (1.5%) and no cases of endophthalmitis. There was 1 severe ocular AE in each intervention group: optic ischemic neuropathy in ACP 2 mg (1.5%) and retinal detachment in ACP 4 mg (1.2%). New-onset nAMD was observed in 8 eyes (11.9%) in the ACP 2 mg group, 9 eyes (10.7%) in the ACP 4 mg group, and 2 eyes (1.8%) in the sham group. Choroidal neovascularization was identified in 4 eyes (4.8%) of the ACP 4 mg group and in 1 eye (0.9%) of the sham group.

 

GATHER2 randomized 448 eyes 1:1 to ACP 2 mg monthly or sham.63 At 12 months, eyes receiving ACP 2 mg were re-randomized 1:1 to continue ACP 2 mg monthly or switch to ACP 2 mg every other month (EOM). The LSM difference in GA lesion growth in the ACP 2 mg monthly group vs sham was -0.724 mm² (-14%; 95% CI -1.315 to -0.133; P=0.017), and was -0.976 mm² (-19%; 95% CI -1.575 to -0.377; P=0.002) for ACP 2 mg EOM vs sham at 24 months. By 24 months, the difference in change in BCVA was -0.83 Early Treatment Diabetic Retinopathy Study (ETDRS) letters (95% CI -3.79 to 2.12, P=0.58). ACP was generally well tolerated, although more cases of ocular treatment-emergent AEs were related to ACP in the study eye in the ACP 2 mg group (n=7; 3.1%) versus sham (n=2; 0.9%). Over 24 months, there was 1 event (0.4%) of intraocular inflammation in the treatment group and 1 (0.4%) confirmed event of endophthalmitis. There were 26 (11.6%) new-onset events of choroidal neovascularization in the ACP 2 mg group and 20 (9.0%) in the sham group.

 

Pegcetacoplan

​

The pivotal evidence for pegcetacoplan comes from the Phase III OAKS and DERBY trials, which randomized a combined 1258 eyes and analyzed 1211 (96.3%) in the modified intention-to-treat (mITT) population.⁶⁴ Participants were randomized 2:2:1:1 to receive 15 mg intravitreal injections of pegcetacoplan monthly, pegcetacoplan EOM, sham monthly, or sham EOM. Over 24 months, the LSM change in lesion area vs sham was -0.82 mm² (-21%; 95% CI -1.11 to -0.54; P<0.0001) among eyes receiving monthly pegcetacoplan and -0.69 mm² (-17%; 95% CI -0.97 to -0.40; P<0.0001) among eyes receiving EOM pegcetacoplan. The greatest reduction occurred in parafoveal and perifoveal regions (monthly pegcetacoplan vs sham -26%; P<0.0001; EOM pegcetacoplan vs sham -22%; P<0.0001) rather than subfoveal regions (monthly pegcetacoplan vs sham -19%; P<0.0001; EOM pegcetacoplan vs sham -16%; P=0.0003). A post hoc analysis of GA OCT features found detectable differences in RPE loss and outer retinal atrophy as early as 3 months between pegcetacoplan and sham, which persisted every month until 24 months.⁶⁵ However, there were no significant differences between treated and sham groups in functional endpoints—change in VA, maximum reading speed, National Eye Institute Visual Functioning Questionnaire 25 distance activity score, and macular sensitivity—at 24 months.⁶⁴ Pegcetacoplan had a generally acceptable tolerability, although there were several notable AEs. New-onset nAMD was reported in a higher proportion of eyes receiving pegcetacoplan monthly (OAKS n=24 [11.3%], 25 events; DERBY n=27 [13.1%], 30  events) and EOM (OAKS n=16 [7.6%], 17 events; DERBY n=12 [5.8%], 12 events) vs sham (OAKS n=4 [1.9%], 4 events; DERBY n=9 [4.4%], 11 events). Intraocular inflammation was reported at a rate of 0.24% per injection at 24 months, with most cases classified as mild or moderate.⁶⁴ Infectious endophthalmitis rates per injection were 0.05% at 12 months and 0.03% at 24 months, which is consistent with other intravitreal injection therapies.⁵⁷⁺⁶⁶ Serious treatment-emergent ocular AEs were low, with 5 (2.3%), 4 (1.9%), and 1 (0.5%) in OAKS and 4 (1.9%), 2 (1.0%), and 2 (1.0%) in DERBY eyes receiving pegcetacoplan monthly, pegcetacoplan EOM, and sham, respectively.⁶⁴ These included endophthalmitis (3 eyes [1.4%] in OAKS pegcetacoplan EOM and 2 eyes [0.9%] in OAKS pegcetacoplan monthly) and ischemic optic neuropathy (2 eyes [0.9%] in OAKS pegcetacoplan monthly and 1 eye [0.5%] in DERBY pegcetacoplan monthly). The GALE 12-month open-label extension to OAKS and DERBY provided data to 36 months of treatment with pegcetacoplan.⁶⁷ Efficacy aligned with the findings from OAKS and DERBY; i.e., increased reduction in overall GA lesion growth in the pegcetacoplan monthly (-25%, -1.49 mm²) and EOM (-20%, -1.21 mm²) versus sham, with increased reduction in nonsubfoveal regions.⁶⁷ Microperimetry analysis found an 18% reduction (P=0.0156) in the number of new scotomatous points in the pegcetacoplan monthly group versus sham, while the EOM group did not reach a statistically significant decrease (12%; P=0.1233).

 

A post-marketing report from the American Society of Retina Specialists Research and Safety in Therapeutics Committee confirmed retinal vasculitis in 14 eyes of 13 patients presenting within a median of 10.5 days (range 8–23) of pegcetacoplan initiation.⁶⁸ VA declined by >15 ETDRS letters in 8 eyes (57.1%), by >30 letters in 6 eyes (42.9%), and 2 eyes (14.3%) required enucleation. Overall, 12 eyes (85.7%) had vitritis, 6 eyes (42.9%) developed neovascularization, and all 11 cases of retinal vasculitis that could be graded involved the retinal veins.

 

Evidence synthesis

​

Pegcetacoplan and ACP have demonstrated statistically significant reductions in GA lesion growth compared to sham, although neither showed evidence of a significant improvement in visual function by 24 months. Pegcetacoplan appeared to be associated with a broader spectrum of ocular AEs than ACP, including increased rates of retinal vasculitis. A study using matching-adjusted indirect comparisons between OAKS, DERBY, and GATHER2 found that pegcetacoplan monthly had significantly less lesion growth than those receiving ACP monthly (-0.589 mm²; -30%; 95% CI -1.164 to -0.015; P=0.04).⁶⁹ A numerically greater reduction in lesion size (-0.415 mm²; -21%; 95% CI -1.130 to 0.300; P=0.25) was determined for pegcetacoplan EOM vs ACP monthly, suggesting that pegcetacoplan EOM may be more suitable to reduce treatment burden for patients and their caregivers. However, this analysis relied on a narrower sample size to balance baseline differences between trials, which may limit the generalizability of its findings to the broader population of patients with GA.

 

A real-world comparative observational study of pegcetacoplan (n=52) and ACP (n=60) found no significant differences between the interventions in any effectiveness outcomes over 12 months, including change in VA from baseline (pegcetacoplan -0.09 logarithm of the minimum angle of resolution (logMAR) [95% CI -0.13 to -0.05]; ACP -0.10 logMAR [95% CI -0.16 to -0.04]; P=0.57) and change in GA lesion size from baseline (P=0.61).⁷⁰ There was no significant difference in the incidence of macular neovascularization (pegcetacoplan 4 events [7.7%], ACP 7 events [11.7%]; P=0.66). There were no retinal vasculitis, vitritis, endophthalmitis, or vitreous hemorrhage events for any participant. Of note, the pegcetacoplan group had a much lower number of complement inhibition injections (5.96 versus ACP 9.05; P<0.01), which remained when including anti-vascular endothelial growth factor injections (pegcetacoplan 6.31 vs ACP 9.58; P<0.01). Ultimately, comparison of the safety profiles of these 2 drugs requires large-scale pharmacovigilance studies.

 

The disconnect of anatomic improvement without yet-apparent functional benefit raises questions about the clinical relevance of slowing GA without functional improvements. One hypothesis for this discrepancy is that the location of GA lesions may be more consequential than the size alone.⁷¹ Long-term longitudinal data will be needed to determine if lesion growth inhibition ultimately leads to a significant preservation of VA.

 

Emerging Therapies

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There are several therapies for GA in clinical development. Aside from targeting C3 and C5, other components of the complement system could serve as therapeutic targets to prevent the complement cascade that leads to cell death in GA. Complement factors B, D, H, I, and the membrane attack complex have all been investigated as potential targets.⁷² To date, most of these investigations have been unfruitful, including antisense oligonucleotides that target complement factors B (sefaxersen),⁷³ D (lampalizumab),⁷⁴ H (GEM103),⁷⁵ and I (GT005).⁷⁴ JNJ-81201887 is an investigational adeno-associated viral vector that delivers CD59 via intravitreal injection to inhibit membrane attack complex formation and reduce cell damage and death. After demonstrating a manageable safety profile in a Phase I trial, it is under investigation in a Phase II trial estimated to be completed by the end of 2026.⁷⁶⁻⁷⁷ Pozelimab, a monoclonal antibody C5 inhibitor approved in the US for CD55-deficient protein-losing enteropathy, is being investigated as a subcutaneous injection in the Phase III SIENNA trial (estimated completion May 2032) and an intravitreal injection in the Phase I VIENNA study (estimated completion July 2028).⁷⁸⁻⁷⁹

 

Some neuroprotective therapies have also been investigated. ONL1204, an apoptosis inhibitor that targets the Fas receptor via intravitreal injection, may prevent retinal cell inflammation and death.⁸⁰ In a Phase Ib trial (N=28), ONL1204 demonstrated a favourable short-term safety profile and slower GA lesion growth over 6 months.⁸¹ A Phase II study is underway, with completion estimated to be in 2028.⁸²

 

Visual cycle modulators, which slow biochemical reactions in the eye, may be useful in GA by reducing the rate of toxic metabolite accumulation. Tinlarebant, a once-daily oral tablet that inhibits the retinol-binding protein 4–retinol complex, is being investigated for GA in the Phase III PHOENIX trial, with expected completion in August 2027.⁸³

 

Photobiomodulation therapy may improve mitochondrial function and enhance cellular respiration by exposing the retina to low-intensity light. The LIGHTSITE III trial (N=148 eyes), investigating eyes with dry AMD without centre-involving GA, demonstrated a significant difference in BCVA between the Valeda Light Delivery System (VLDS) and sham (between-group difference 2.4 letters; 95% CI 0.1 to 4.7; P=0.02), and fewer patients receiving VLDS developed GA (1.1%, n=1) versus sham (10.0%, n=5; P=0.024).⁸⁴ The VLDS is approved for use in patients with dry AMD and without central-involving GA.⁸⁵

 

By replacing damaged RPE cells, allogeneic stem-cell-based therapies delivered via subretinal surgical implantation may restore visual function. ASP7317, a human embryonic stem cell (hESC)-derived RPE cell therapy, is currently undergoing a Phase I trial.⁸⁶ OpRegen, a similar hESC-derived therapy, demonstrated meaningful disease stabilization and even some functional improvement in a Phase I/IIa clinical study; a Phase II trial is estimated to be completed by 2031.⁸⁷⁻⁸⁸

 

Conclusion

​

GA is a progressive manifestation of late AMD driven by complex interactions between complement dysregulation, inflammation, oxidative stress, and genetic susceptibility. Complement inhibitors, including pegcetacoplan and ACP, represent an important advance by slowing GA lesion growth, although significant functional benefits have not yet been demonstrated. Future therapies targeting complementary pathways, neuroprotection, visual cycle modulation, and retinal cell replacement may further improve management and ultimately help preserve meaningful visual function in patients with GA.

​

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75. Gemini Therapeutics, Inc. A multicenter, open-label, multiple dose study in patients with geographic atrophy secondary to dry age-related macular degeneration to evaluate the safety, tolerability, pharmacodynamics, and immunogenicity of repeat intravitreal injections of GEM103. Available at: https://clinicaltrials.gov/study/NCT04643886. Accessed on February 20, 2026.

76. Janssen Research & Development, LLC. A phase 2b, randomized, double-masked, multicenter, dose-ranging, sham-controlled clinical trial to evaluate intravitreal JNJ-81201887 (AAVCAGsCD59) compared to sham procedure for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD). Available at: https://clinicaltrials.gov/study/NCT05811351. Accessed on February 20, 2026.

77. Heier JS, Cohen MN, Chao DL, et al. Phase 1 study of JNJ-81201887 gene therapy in geographic atrophy secondary to age-related macular degeneration. Ophthalmology. 2024;131(12):1377-1388.

78. Regeneron Pharmaceuticals. A multicenter, randomized, double-masked, placebo-controlled phase 3 study of the efficacy, safety, and tolerability of subcutaneously administered pozelimab in combination with cemdisiran or cemdisiran alone in participants with geographic atrophy secondary to age-related macular degeneration. Available at: https://clinicaltrials.gov/study/NCT06541704. Accessed on March 5, 2026.

79. Regeneron Pharmaceuticals. A phase 1 dose-escalation and repeated-dose study of the safety and tolerability of intravitreal pozelimab in participants with geographic atrophy. Available at: https://clinicaltrials.gov/study/NCT07230834. Accessed on March 5, 2026.

80. Kocab AJ, Cano M, Bacellar-Galdino M, et al. In vivo characterization of ONL1204, a small peptide inhibitor of the Fas receptor, as a potential neuroprotective therapy for geographic atrophy and dry age-related macular degeneration. Biomedicines. 2025;13(9):2052.

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82. ONL Therapeutics. A phase 2 multicenter, randomized, double-masked, sham-controlled, reference-arm study to evaluate efficacy and safety of ONL1204 in patients with geographic atrophy (GA) associated with age-related macular degeneration (AMD). Available at: https://clinicaltrials.gov/study/NCT06659445. Accessed on February 20, 2026.

83. Belite Bio, Inc. Phase 3, multicenter, randomized, double-masked, placebo-controlled study of tinlarebant to explore safety and efficacy in the treatment of geographic atrophy (the PHOENIX Study). Available at: https://clinicaltrials.gov/study/NCT05949593. Accessed on March 5, 2026.

84. Boyer D, Hu A, Warrow D, et al. LIGHTSITE III: 13-month efficacy and safety evaluation of multiwavelength photobiomodulation in nonexudative (dry) age-related macular degeneration using the LumiThera Valeda light delivery system. Retina. 2024;44(3):487.

85. Russell MW, Rachitskaya AV. Photobiomodulation therapy for management of retinal diseases. Curr Ophthalmol Rep. 2025;13(1):13.

86. Astellas Institute for Regenerative Medicine. A phase 1b, multicenter, dose escalation, evaluation of safety and tolerability of ASP7317 for geographic atrophy secondary to age-related macular degeneration. Available at: https://clinicaltrials.gov/study/NCT03178149. Accessed on February 20, 2026.

87. Ho AC, Banin E, Barak A, et al. Safety and efficacy of a phase 1/2a clinical trial of transplanted allogeneic retinal pigmented epithelium (RPE, OpRegen) cells in advanced dry age-related macular degeneration (AMD). Invest Ophthalmol Vis Sci. 2022;63(7):1862-1862.

88. Genentech, Inc. A phase IIa, multicenter, open-label, single-arm study to optimize subretinal surgical delivery and to evaluate safety and activity of OpRegen in patients with geographic atrophy secondary to age-related macular degeneration. Available at: https://clinicaltrials.gov/study/NCT05626114. Accessed on February 20, 2026.

 

Mr. Gou is a Doctor of Medicine Candidate, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario.

Dr. Tao is a Resident Physician, Department of Ophthalmology & Vision Sciences, University of Toronto, Toronto, Ontario.

Dr. Popovic is a Retina Specialist, St. Michael’s Hospital and Kensington Vision and Research Centre, Toronto, Ontario.

 

Conflicts of Interest: Dr. Popovic reports being a consultant to or a member of an advisory board for Astellas, Bayer, Roche, and Sandoz, as well as financial support (to institution) from Bayer, Fighting Blindness Canada, and PSI Foundation. Mr. Gou and Dr. Tao stated that they have no disclosures to report in association with the contents of this issue.