Macular degeneration (AMD), is a medical condition that may result in blurred or no vision in the center of the visual field. Specifically, The pathophysiological features of AMD are abnormalities in the microcirculation of the retina, resulting in the growth of abnormal vessels characterized by impaired wall integrity. Research shows that Vascular endothelial growth factor (VEGF) is the major mediator responsible for the development of pathophysiological changes in AMD. Here, we will introduce a potent anti-VEGF agent, Aflibercept.

Aflibercept is a potent VEGF inhibitor.

From: Liberski S, et al. Int J Mol Sci. 2022;23(16):9424.

Aflibercept is a recombinant 115 kDa protein. The structure of the Aflibercept molecule allows for competitive binding of all VEGF-A and VEGF-B isoforms with higher affinity than its native receptors. Thus, due to this property, Aflibercept is sometimes also called “VEGF Trap-Eye”. Aflibercept also can bind PlGF-1 and PlGF-2, other members of the VEGF family. These growth factors have the potential to induce retinal neovascular changes.

In vitro, Aflibercept (1, 10 μg/mL, 10 h) inhibits VEGF signaling by reducing VEGF-regulated processes, such as permeability and angiogenesis. Aflibercept also shows an ability to inhibit the proliferation of bovine vascular endothelial cells.

Besides, In vivo, Aflibercept (10 mg/kg, 3 h post-middle cerebral artery occlusion) reduces stroke-induced VEGF-A and VEGFR2 expression, and brain edema, and BBB disruption and improves post-stroke survival in obese mice. Moreover, In adult rats with choroidal neovascularization (CNV) induced by subretinal Matrigel injection, two systemic administrations of Aflibercept, two days before and six days after Matrigel administration, prevent the development of CNV.

In conclusion, as a potent VEGF inhibitor, Aflibercept is a valuable therapeutic option for patients with retinal vascular diseases.


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