Age-related macular degeneration (AMD)
remains one of the most prevalent eye problems among the elderly worldwide.
With an overall prevalence of 8.7%, it is projected to affect 288 million by 2040.1 To medical retina specialist
Dr. Kelvin Teo Yi Chong from the Singapore National Eye Centre, treating neovascular AMD (nAMD) is commonplace. “I see about two to three new cases per week in my practice.
In Singapore, the incidence of late AMD is about 0.5%,” he said. Some background on antiVEGF drugs Neovascular AMD is a type of late AMD characterized ลาวสามัคคี
by choroidal neovascularization with intraretinal or subretinal leakage, hemorrhage and retinal pigment epithelial (RPE) detachment.
Despite therapeutic advances in the management of nAMD, none of the currently used treatments cures the disease or reverses its course.2
Nevertheless, the introduction of vascular endothelial growth factor inhibitors — known as anti-VEGF — have brought forth significant advancement in nAMD treatment.
This has altered the prognosis from blindness to a significant chance (about 30%)3 of visual acuity improvement, at least during
the first two years of treatment.4-6 Some of the more common antiVEGF agents include pegaptanib, bevacizumab, ranibizumab, aflibercept and brolucizumab.
Pegaptanib sodium was the first intravitreal anti-VEGF treatment developed for nAMD.
It is a pegylated oligoribonucleotide (aptamer) that binds with high specificity and affinity to VEGF 165, sequestering and therefore preventing VEGF 165 from activating its receptor.
It is no longer recommended for treating exudative AMD as it is less effective compared to other anti-VEGF drugs.
Ranibizumab is a fully humanized monoclonal antibody fragment that binds to multiple isoforms of VEGF-A. It was originally approved for treating nAMD.
The efficacy and safety of fixed regimens of ranibizumab have been evaluated in various trials, including ANCHOR, MARINA, PIER and EXCITE.
Aflibercept is a fusion protein (115 kDa) comprising the second Ig domain of human VEGFR1, the third Ig domain of human VEGFR2, and the Fc region of a human IgG1.
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