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Iveric Bio is committed to developing innovative therapies that address unmet needs of patients suffering from the progressive symptoms of common and rare retinal diseases, including geographic atrophy, age-related macular degeneration, Stargardt disease, as well as other retinal diseases with specific genetic components.


Adapted from Elsharkawy M, et al. Diagnostics. 2021;11(12):2313, under the terms and conditions of the Creative Commons Attribution (CC BY) license ( © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

AMD is a progressive and degenerative retinal disease that is the leading cause of severe vision loss in individuals >55 years of age in the developed world, accounting for 8.7% of the global population affected globally.1,2

AMD affects the complex of photoreceptors, retinal pigment epithelium (RPE), Bruch’s membrane, and the choroid, altering retinal homeostasis.2,3 The clinical hallmark of AMD is the presence of drusen, which leads to progressive degeneration of photoreceptors and RPE and results in loss of central vision.2

AMD is a disease spectrum ranging from early to late stages, which include geographic atrophy (GA) and wet AMD.3-9


Play the mechanism of disease (MOD) video below to see how GA can develop and progress, potentially leading to irreversible vision loss.


Geographic atrophy (GA) is an advanced form of age-related macular degeneration that results in progressive and irreversible vision loss due to the formation and subsequent growth of atrophic lesions in the macula.7,8,10,11 This disease accounts for ~20% of all cases of legal blindness in North America.12

A2E, N-retinyl-N-retinylidene ethanolamine; ATR, all-trans retinal; GCL, ganglion cell layer; INL, inner nuclear layer; ONL, outer nuclear layer; RPE, retinal pigment epithelium.Reproduced from Holz FG, et al. Geographic atrophy: clinical features and potential therapeutic approaches. Ophthalmology. 2014;121(5):1079-1091, Copyright © 2014, with permission from the American Academy of Ophthalmology. [as adapted with permission by Springer Nature: Sarks et al. Eye. 1988;2:552-577. Copyright 1988].

GA lesions usually begin outside the fovea but then expand into the fovea in a median of 2.5 years post diagnosis.7 Growth rate of GA lesions can be variable and is difficult to predict, but lesion growth may lead to death of the retinal photoreceptors, retinal pigment epithelium, and underlying choriocapillaris, with inflammation highly involved in the mechanism of cell death.7,8,11,13-16

First row: Color fundus photography; second row: Fundus autofluorescence images. Left to right: Annual retinal imaging from baseline through year 4 follow up.Reproduced from Schmitz-Valckenberg S. Ophthalmologica. 2017;237(1):11-20. Copyright © 2017 Karger Publishers, Basel, Switzerland.
Back to GA

    References: 1. Wong WL, et al. Lancet Glob Health. 2014;2:e106-e116. 2. Fleckenstein M, et al. Nat Rev Dis Primers. 2021;7:31. 3. Armento A, et al. Cell Mol Life Sci. 2021:78;4487-4505. 4. Holz FG, et al. J Clin Invest. 2014;124:1430-1438. 5. Flores R, et al. Ophthalmologica. 2021;244:495-511. 6. Ambati J, et al. Nat Rev Immunol. 2013;13:438-451. 7. Boyer DS, et al. Retina. 2017;37:819-835. 8. Fleckenstein M, et al. Ophthalmology. 2018;125:369-390. 9. Elsharkawy M, et al. Diagnostics. 2021;11(12):2313. 10. Arya M, et al. Eye Vis (Lond). 2018;5:22. 11. Sarks JP, et al. Eye (Lond). 1988;2(Pt 5):552-577. 12. Holz FG, et al. Ophthalmology. 2014;121(5):1079-1091. 13. Richard AJ, et al. Curr Opin Ophthalmol. 2021;32(3):247-252. 14. Heesterbeek TJ, et al. Ophthalmic Physiol Opt. 2020;40(2):140-170. 15. Shen LL, et al. Invest Ophthalmol Vis Sci. 2020;61(1):2. 16. Wang J, Ying GS. Ophthalmic Res. 2021;64(2):205-215. 17. Holz FG, et al. Ophthalmology. 2017;124(4):464-478. 18. Chakravarthy U, et al. Ophthalmology. 2018;125(6):842-849. 19. Patel PJ, et al. Clin Ophthalmol. 2020;14:15-28.

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