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GA can unravel your
patients’ lives1-3

GA is relentlessly progressive4

Vision loss

Vision loss from GA can occur before lesions reach the fovea5,6

Early detection and referral of GA is critical7,8

Foveal encroachment can happen as quickly as 1.5 years4*

Every millimeter matters9,10

Lesion foveal encroachment can result in irreversible photoreceptor loss

*In a retrospective analysis of the IRIS registry database, the average time for foveal encroachment in the study eye was: 16.9 months in patients with GA in the fellow eye (n=3,800), and 15.6 months in patients with nAMD in the fellow eye (n=1,540).4

"TIME CAN TAKE AWAY TISSUE."

"When it comes to a confirmed GA diagnosis, the clock is ticking. Time can take away tissue."

Dr Deepak Sambhara, MD makes early identification of GA a key priority. Hear how he ensures that his patients are diagnosed and referred to a specialist as soon as possible to discuss treatment to slow their GA progression.

View Transcript   ▼

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

  • SYFOVRE is contraindicated in patients with ocular or periocular infections, in patients with active intraocular inflammation, and in patients with hypersensitivity to pegcetacoplan or any of the excipients in SYFOVRE. Systemic hypersensitivity reactions (e.g., anaphylaxis, rash, urticaria) have occurred.

Please stay tuned for additional Important Safety Information and please see accompanying full Prescribing Information.

Assessing GA on Retinal Scans

Hi, I’m Dr Deepak Sambhara. I’m a retina specialist at the Eye Clinic of Wisconsin, where I’ve been in clinical practice since 2019.

Since SYFOVRE was FDA approved, I've made identifying and assessing patients with geographic atrophy, secondary to AMD, a key priority.

There are very early signs of geographic atrophy, or GA, that can be observed on retinal scans, and when it comes to the identification and referral of GA, I believe that earlier is better.

At my large tertiary care practice with satellite offices, I work closely with the optometrists to ensure patients who have GA, and those who are at risk of developing GA, get retinal scanning or referral as appropriate.

GA Starts With Changes to the Retinal Tissue

In the past, before there was an approved treatment, we might have overlooked GA, because GA doesn’t start with changes to visual acuity. It starts with changes to the retinal tissue.

In fact, retinal scans can reveal very early changes to the retina, that show clear risk of GA developing. These changes include subsidence of the outer plexiform layer and the inner nuclear layer and a wedge-shaped band, what I think is almost like bird wings, within the boundaries of the outer plexiform layer.

These changes are not always characterized by absolute scotomas. But some damage may be there.

This is why retinal scans are so important in assessing GA. When it comes to GA, the tissue is the issue. GA is defined by damaged retinal tissue as opposed to measures of functional vision such as BCVA. GA causes relentless and irreversible destruction of retinal tissue.

So for patients with GA, I want to orient the entire care team around retinal scanning as our primary assessment tool.

I ask my optometrist colleagues, “Do you have patients who you see with GA, or who might be at risk for GA, who have the same best-corrected visual acuity this year as last year, and yet report symptoms of visual difficulty?”

They might have difficulty adapting to low light, for example.

That might be a sign that they’re experiencing GA progression.

Instead of telling these patients, “see you in 12 months,” we should discuss the difficulty they're having and ensure that they get retinal scans as soon as possible to confirm a possible GA diagnosis. I also follow up in 3 to 6 months for additional monitoring.

When I'm assessing a patient with confirmed GA, or suspected GA for the first time, I’m like most retina specialists who work in a large network: I prefer to see them at our main campus where we keep the latest and greatest equipment. That’s where I know I’ll have access to the full array of imaging modalities. But that isn’t the case at every location.

Work With the Scanning Equipment You Have

It’s important to work with the tools you have. Some of our satellite offices don’t have FAF scanning available, and many of our referring clinicians, who are on the front lines when it comes to assessing GA, may be only using OCT. And if all you have available is OCT, it still is a great tool.

For example, choroidal hypertransmission defects can be used to identify GA on OCT, particularly when FAF scanning isn’t available.

In the absence of photoreceptors and hyperreflective retinal pigment epithelium, or RPE, there's less light being reflected, so more light passes through into the choroid. This creates the hypertransmission defect highlighted on this image.

Here we have a scan of a different eye with earlier disease.

Intraretinal hyperreflective foci are another risk factor for GA.

This eye has evidence of higher-than-normal metabolic processing, resulting in a migration of RPE.

And in these scans of the same eye captured 3 years later, we can see there has been extensive GA progression.

Now, let’s move to images from a third patient.

Pseudodrusen are another important risk factor for GA. They often appear as a starry sky pattern on NIR imaging. They can look like little peppered areas.

Drusen typically exist underneath the retina. On OCT, when you see drusen above the level of the RPE, as shown here in these red circles, that's usually atypical, and may indicate GA.

When we go to the following slide, you can see that over the course of time, GA has progressed, and this eye developed a subfoveal GA lesion.

Talking to Your Patients About GA Progression

When we observe scans like these, it's our cue to confirm whether there is a diagnosis of GA secondary to AMD. Then, a confirmed diagnosis is our cue to start the conversation about the potential to slow down the GA lesion progression with SYFOVRE treatment.

The patient may need time to process the diagnosis and consider the treatment decision, but they also need to understand the urgency: any damage to the retina is irreversible.

When it comes to a confirmed GA diagnosis, the clock is ticking. Time can take away tissue. In a retrospective analysis of the AREDS dataset, of the 397 patients who developed GA, the median time to development of central GA was just 2.5 years.

And the vision loss from GA can take place before lesions even reach the fovea.

So I tell my patients it’s important to ensure they come back for follow-up scans in 3 to 6 months rather than one or more years down the line, so we can assess GA progression and continue the dialogue about initiating treatment for appropriate patients.

To help ensure a seamless approach for our shared patients, I work closely with the optometrists in my network to ensure the patient conversation is continued and supported on their end.

These days, it's important to definitively identify GA as early as possible using retinal scanning. A watch and wait approach, where a year might pass by before the next scan, is no longer in the best interest of a patient who may have GA secondary to AMD. Today, we can take action with SYFOVRE.

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

  • SYFOVRE is contraindicated in patients with ocular or periocular infections, in patients with active intraocular inflammation, and in patients with hypersensitivity to pegcetacoplan or any of the excipients in SYFOVRE. Systemic hypersensitivity reactions (e.g., anaphylaxis, rash, urticaria) have occurred.

WARNINGS AND PRECAUTIONS

  • Endophthalmitis and Retinal Detachments
    • Intravitreal injections, including those with SYFOVRE, may be associated with endophthalmitis and retinal detachments. Proper aseptic injection technique must always be used when administering SYFOVRE to minimize the risk of endophthalmitis. Patients should be instructed to report any symptoms suggestive of endophthalmitis or retinal detachment without delay and should be managed appropriately.
  • Retinal Vasculitis and/or Retinal Vascular Occlusion
    • Retinal vasculitis and/or retinal vascular occlusion, typically in the presence of intraocular inflammation, have been reported with the use of SYFOVRE. Cases may occur with the first dose of SYFOVRE and may result in severe vision loss. Discontinue treatment with SYFOVRE in patients who develop these events. Patients should be instructed to report any change in vision without delay.
  • Neovascular AMD
    • In clinical trials, use of SYFOVRE was associated with increased rates of neovascular (wet) AMD or choroidal neovascularization (12% when administered monthly, 7% when administered every other month and 3% in the control group) by Month 24. Patients receiving SYFOVRE should be monitored for signs of neovascular AMD. In case anti-Vascular Endothelial Growth Factor (anti-VEGF) is required, it should be given separately from SYFOVRE administration.
  • Intraocular Inflammation
    • In clinical trials, use of SYFOVRE was associated with episodes of intraocular inflammation including: vitritis, vitreal cells, iridocyclitis, uveitis, anterior chamber cells, iritis, and anterior chamber flare. After inflammation resolves, patients may resume treatment with SYFOVRE.
  • Increased Intraocular Pressure
    • Acute increase in IOP may occur within minutes of any intravitreal injection, including with SYFOVRE. Perfusion of the optic nerve head should be monitored following the injection and managed as needed.

ADVERSE REACTIONS

  • Most common adverse reactions (incidence ≥5%) are ocular discomfort, neovascular age-related macular degeneration, vitreous floaters, conjunctival hemorrhage.

Please see accompanying full Prescribing Information, also available on SyfovreECP.com.

Slowing GA lesion growth is critical to delaying further irreversible retinal tissue loss11

Identifying AMD and GA on OCT scans

Click on the tabs below to learn more.

  • Medium-sized drusen >63 µm and ≤125 µm
  • No pigmentary abnormalities

Few medium-sized drusen

Early AMD

©2018. This work is licensed under a CC BY 4.0 license. "Advanced imaging for the diagnosis of age-related macular degeneration: a case vignettes study", "Figure 2 Case 1", Ly A, Nivision-Smith L, Zangerl B, Assad N, Kalloniatis M. Clin Exp Optom.

  • Large drusen >125 µm and/or pigmentary abnormalities
  • Can lead to GA, nAMD, or both GA and nAMD

Drusen grow larger with disease progression

Hyperreflective foci representing RPE migration

Intermediate AMD

©2023. This work is licensed under a CC BY 4.0 license. “Correlation between hyperreflective foci and visual function testing in eyes with intermediate age-related macular degeneration”, "Figure 1", Liu TYA, Wang J, Csaky KG. Int J Retina Vitreous.

GA

  • Atrophy of photoreceptors and the loss of RPE can lead to increased reflectivity below Bruch’s membrane and resulting hypertransmission15,16
  • Even if visual acuity or BCVA is relatively unchanged, functional vision continues to decline as lesions progress1,6,17
  • Patients with GA can also naturally develop nAMD and vice versa. Up to 29% of patients with GA develop nAMD in about 2 years (N=12,309)18†

Hypertransmission seen in GA

Loss of RPE and photoreceptors

Advanced AMD

Neovascular AMD (nAMD)

  • Distinguished by abnormal blood vessels that may cause fluid or blood to leak into the macula16
  • Up to 37% of patients with nAMD develop GA in about 2 years (n=35)19‡

Fluid leakage extending from the choroidal vessels through Bruch’s membrane

Choroidal neovascular membrane

Advanced nAMD

Image courtesy of Mohammad Rafieetary, OD, Charles Retina Institute.

Retrospective analysis (N=12,309) of the Intelligent Research in Sight (IRIS) Registry database in patients with GA in the study eye and nAMD in the fellow eye (n=3607/12,309).18

Images courtesy of Dr Juan David Arias and Dr Andrea Hoyos, Colombia.

SYFOVRE is only indicated for the treatment of GA secondary to AMD.

Retrospective cohort analysis (N=94 eyes) to assess growth of GA in patients with nAMD treated with anti-VEGF therapy.19

GA
nAMD

Patients with GA may experience one or more of these symptoms5,20

Straight lines that appear crooked
Hazy or blurred vision
Blurry spots in the center of vision
Dull or washed-out colors
Difficulty seeing in low light
Missing spots in vision

Know the key risk factors for the development of GA

Key GA risk factors include:

Genetics21
  • Family history (genetic predisposition)
Physiology21
  • Obesity
  • Certain dyslipidemias
  • Cardiovascular disease/hypertension
Lifestyle/Environment21
  • History of smoking
  • Diet
Clinical findings from imaging
  • GA in fellow eye15
  • Increased drusen volume23
Age: From age 50 and onwards, the prevalence of GA quadruples every 10 years22

Identify and refer early—GA can progress faster than you think

AMD=age-related macular degeneration; BCVA=best-corrected visual acuity; GA=geographic atrophy; nAMD=neovascular age-related macular degeneration; OCT=optical coherence tomography; RPE=retinal pigment epithelium; VEGF=vascular endothelial growth factor.

References:  1. Boyer DS, Schmidt-Erfurth U, van Lookeren Campagne M, Henry EC, Brittain C. The pathophysiology of geographic atrophy secondary to age-related macular degeneration and the complement pathway as a therapeutic target. Retina. 2017;37(5):819-835. doi:10.1097/iae.0000000000001392. 2. Pfau M, von der Emde L, de Sisternes L, et al. Progression of photoreceptor degeneration in geographic atrophy secondary to age-related macular degeneration. JAMA Ophthalmol. 2020;138(10):1026-1034. 3. Bird AC, Phillips RL, Hageman GS. Geographic atrophy: a histopathological assessment. JAMA Ophthalmol. 2014;132(3):338-345. 4. Rahimy E, Khan MA, Ho AC, et al; Progression of geographic atrophy: retrospective analysis of patients from the IRIS® Registry (Intelligent Research in Sight). Ophthalmol Sci. 2023;3(4):100318. doi:10.1016/j.xops.2023.100318. 5. Sacconi R, Corbelli E, Querques L, Bandello F, Querques G. A review of current and future management of geographic atrophy. Ophthalmol Ther. 2017;6(1):69-77. doi:10.1007/s40123-017-0086-6. 6. Sunness JS, Margalit E, Srikumaran D, et al. The long-term natural history of geographic atrophy from age-related macular degeneration: enlargement of atrophy and implications for interventional clinical trials. Ophthalmology. 2007;114(2):271-277. doi:10.1016/j.ophtha.2006.09.016. 7. Neely DC, Bray KJ, Huisingh CE, et al. Prevalence of undiagnosed age-related macular degeneration in primary eye care. JAMA Ophthalmol. 2017;135(6):570-575. doi:10.1001/jamaophthalmol.2017.0830. 8. Kaiser PK, Karpecki PM, Regillo CD, et al. Geographic Atrophy Management Consensus (GA-MAC): a Delphi panel study on identification, diagnosis and treatment. BMJ Open Ophthalmol. 2023;8(1):e001395. doi:10.1136/bmjophth-2023-001395. 9. Wells-Gray EM, Choi SS, Bries A, Doble N. Variation in rod and cone density from the fovea to the mid-periphery in healthy human retinas using adaptive optics scanning laser ophthalmoscopy. Eye (Lond). 2016;30(8):1135-1143. 10. van Lookeren Campagne M, LeCouter J, Yaspan BL, Ye W. Mechanisms of age-related macular degeneration and therapeutic opportunities. J Pathol. 2014;232(2):151-164. doi:10.1002/path.4266. 11. Bakri SJ, Bektas M, Sharp D, Luo R, Sarda SP, Khan S. Geographic atrophy: mechanism of disease, pathophysiology, and role of the complement system. J Manag Care Spec Pharm. 2023;29(5-a Suppl):S2-S11. doi:10.18553/jmcp.2023.29.5-a.s2. 12. Ferris FL 3rd, Wilkinson CP, Bird A, et al. Beckman Initiative for Macular Research Classification Committee. Clinical classification of age-related macular degeneration. Ophthalmology. 2013;120(4):844-851. doi:10.1016/j.ophtha.2012.10.036. 13. Ruan Y, Jiang S, Gericke A. Age-related macular degeneration: role of oxidative stress and blood vessels. Int J Mol Sci. 2021;22(3):1296. doi:10.3390/ijms22031296. 14. Jager RD, Mieler WF, Miller JW. Age-related macular degeneration. N Engl J Med. 2008; 358(24):2606-2617. doi:10.1056/NEJMra0801537. 15. Fleckenstein M, Mitchell P, Freund KB, et al. The progression of geographic atrophy secondary to age-related macular degeneration. Ophthalmology. 2018;125(3):369-390. doi:10.1016/j.ophtha.08.038. 16. Chakravarthy U, Bailey CC, Scanlon PH, et al. Progression from early/intermediate to advanced forms of age-related macular degeneration in a large UK cohort: rates and risk factors. Ophthalmol Retina. 2020;4(7):662-672. doi:10.1016/j.oret.2020.01.012. 17. Kimel M, Leidy NK, Tschosik E, et al. Functional reading independence (FRI) index: a new patient-reported outcome measure for patients with geographic atrophy. Invest Ophthalmol Vis Sci. 2016;57(14):6298-6304. doi:10.1167/iovs.16-20361. 18. Rahimy E. Evaluating geographic atrophy in real-world clinical practice: new findings from the IRIS registry. Presented at: American Academy of Ophthalmology Meeting; November 14, 2020; virtual meeting. 19. Xu L, Mrejen S, Jung JJ, et al. Geographic atrophy in patients receiving anti-vascular endothelial growth factor for neovascular age-related macular degeneration. Retina. 2015;35(2):176-186. doi:10.1097/IAE.0000000000000374. 20. Schultz NM, Bhardwaj S, Barclay C, Gaspar L, Schwartz J. Global burden of dry age-related macular degeneration: a targeted literature review. Clin Ther. 2021;43(10):1792-1818. doi:10.1016/j.clinthera.2021.08.011. 21. Sobrin L, Seddon JM. Nature and nurture- genes and environment- predict onset and progression of macular degeneration. Prog Retin Eye Res. 2014;40:1-15. doi:10.1016/j.preteyeres.2013.12.004. 22. Rudnicka AR, Jarrar Z, Wormald R, Cook DG, Fletcher A, Owen CG. Age and gender variations in age-related macular degeneration prevalence in populations of European ancestry: a meta-analysis. Ophthalmology. 2012;119:571-580. doi:10.1016/j.ophtha.2011.09.027. 23. Lad EM, Finger RP, Guymer R. Biomarkers for the progression of intermediate age-related macular degeneration. Ophthalmol Ther. 2023;12:2917-2941. doi:10.1007/s40123-023-00807-9.

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IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

  • SYFOVRE is contraindicated in patients with ocular or periocular infections, in patients with active intraocular inflammation, and in patients with hypersensitivity to pegcetacoplan or any of the excipients in SYFOVRE. Systemic hypersensitivity reactions (e.g., anaphylaxis, rash, urticaria) have occurred.

WARNINGS AND PRECAUTIONS

  • Endophthalmitis and Retinal Detachments
    • Intravitreal injections, including those with SYFOVRE, may be associated with endophthalmitis and retinal detachments. Proper aseptic injection technique must always be used when administering SYFOVRE to minimize the risk of endophthalmitis. Patients should be instructed to report any symptoms suggestive of endophthalmitis or retinal detachment without delay and should be managed appropriately.
  • Retinal Vasculitis and/or Retinal Vascular Occlusion
    • Retinal vasculitis and/or retinal vascular occlusion, typically in the presence of intraocular inflammation, have been reported with the use of SYFOVRE. Cases may occur with the first dose of SYFOVRE and may result in severe vision loss. Discontinue treatment with SYFOVRE in patients who develop these events. Patients should be instructed to report any change in vision without delay.
  • Neovascular AMD
    • In clinical trials, use of SYFOVRE was associated with increased rates of neovascular (wet) AMD or choroidal neovascularization (12% when administered monthly, 7% when administered every other month and 3% in the control group) by Month 24. Patients receiving SYFOVRE should be monitored for signs of neovascular AMD. In case anti-Vascular Endothelial Growth Factor (anti-VEGF) is required, it should be given separately from SYFOVRE administration.
  • Intraocular Inflammation
    • In clinical trials, use of SYFOVRE was associated with episodes of intraocular inflammation including: vitritis, vitreal cells, iridocyclitis, uveitis, anterior chamber cells, iritis, and anterior chamber flare. After inflammation resolves, patients may resume treatment with SYFOVRE.
  • Increased Intraocular Pressure
    • Acute increase in IOP may occur within minutes of any intravitreal injection, including with SYFOVRE. Perfusion of the optic nerve head should be monitored following the injection and managed as needed.

ADVERSE REACTIONS

  • Most common adverse reactions (incidence ≥5%) are ocular discomfort, neovascular age-related macular degeneration, vitreous floaters, conjunctival hemorrhage.

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).

Please see full Prescribing Information for more information.

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

  • SYFOVRE is contraindicated in patients with ocular or periocular infections, in patients with active intraocular inflammation, and in patients with hypersensitivity to pegcetacoplan or any of the excipients in SYFOVRE. Systemic hypersensitivity reactions (e.g., anaphylaxis, rash, urticaria) have occurred.

WARNINGS AND PRECAUTIONS

  • Endophthalmitis and Retinal Detachments
    • Intravitreal injections, including those with SYFOVRE, may be associated with endophthalmitis and retinal detachments. Proper aseptic injection technique must always be used when administering SYFOVRE to minimize the risk of endophthalmitis. Patients should be instructed to report any symptoms suggestive of endophthalmitis or retinal detachment without delay and should be managed appropriately.
  • Retinal Vasculitis and/or Retinal Vascular Occlusion
    • Retinal vasculitis and/or retinal vascular occlusion, typically in the presence of intraocular inflammation, have been reported with the use of SYFOVRE. Cases may occur with the first dose of SYFOVRE and may result in severe vision loss. Discontinue treatment with SYFOVRE in patients who develop these events. Patients should be instructed to report any change in vision without delay.
  • Neovascular AMD
    • In clinical trials, use of SYFOVRE was associated with increased rates of neovascular (wet) AMD or choroidal neovascularization (12% when administered monthly, 7% when administered every other month and 3% in the control group) by Month 24. Patients receiving SYFOVRE should be monitored for signs of neovascular AMD. In case anti-Vascular Endothelial Growth Factor (anti-VEGF) is required, it should be given separately from SYFOVRE administration.
  • Intraocular Inflammation
    • In clinical trials, use of SYFOVRE was associated with episodes of intraocular inflammation including: vitritis, vitreal cells, iridocyclitis, uveitis, anterior chamber cells, iritis, and anterior chamber flare. After inflammation resolves, patients may resume treatment with SYFOVRE.
  • Increased Intraocular Pressure
    • Acute increase in IOP may occur within minutes of any intravitreal injection, including with SYFOVRE. Perfusion of the optic nerve head should be monitored following the injection and managed as needed.

ADVERSE REACTIONS

  • Most common adverse reactions (incidence ≥5%) are ocular discomfort, neovascular age-related macular degeneration, vitreous floaters, conjunctival hemorrhage.

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).

Please see full Prescribing Information for more information.

INDICATION

SYFOVRE® (pegcetacoplan injection) is indicated for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD).