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Neovascular age-related macular degeneration (AMD) causes blindness by causing new blood vessels to form beneath the retina – known as wet AMD. Its cause lies within choroidal neovascularization which in turn may lead to swelling, hemorrhaging, retinal pigment epithelium (RPE) cell damage due to leakage causing leakage within its blood vessels.

Aflibercept

Aflibercept (Eylea) is a synthetic human monoclonal antibody designed to block vascular endothelial growth factor (VEGF), preventing its binding and the subsequent formation of abnormal blood vessels beneath the retina. These abnormal blood vessels may lead to fluid leakage from the retina and decrease visual acuity, known as wet AMD (neovascular age-related macular degeneration). Wet AMD may have worse prognosis than its dry counterpart. Macular Edema in Wet AMD refers to fluid and blood leakage from retinal blood vessels into the macular region, often an early indicator of advanced disease that can quickly lead to loss of vision. Slit lamp microscopy and color fundus photography can be used to diagnose this condition while Ocular Coherence Tomography can uncover areas of choroidal neovascularisation not visible by conventional microscopy alone.

Recent real-world clinical outcomes indicate that intravitreal aflibercept treatment with the TnE protocol can effectively treat neovascular age-related macular disease and polypoidal choroidal vasculopathy (PCV). The research team reviewed medical records of those treated at National Taiwan University Hospital with 2 mg aflibercept given in three monthly loading injections followed by TnE protocol; results demonstrated this treatment regimen improved visual acuity while decreasing macular edema; however frequent injections and assessments may place undue stress upon both patients and caregivers alike.

Researchers concluded from this study that the findings indicate aflibercept combined with TnE can achieve similar morphological and functional results as ranibizumab in real-world clinical settings, yet is significantly safer and requires fewer injections than bevacizumab; additionally it appears effective against both occult CNV as well as minimally classic CNV cases.

The VIEW trial was a two-year, double-blind, randomized controlled clinical trial that compared intravitreal aflibercept with bevacizumab for treating wet AMD. The primary efficacy objective was the percentage of eyes without macular fluid; secondary objectives included changes in anatomic measures and vision changes. Aflibercept produced greater visual improvement rates than its bevacizumab counterpart and over 44 weeks no safety signals were reported in either group.

Faricimab

Intravitreal Faricimab is an innovative new treatment for retinal neovascularization in patients suffering from wet age related macular degeneration (wAMD) and diabetic macular edema (DME). This drug blocks two primary angiogenesis pathways in retinal angiogenesis and has proven safe and effective through multiple clinical trials; even though relatively new, its effectiveness and safety has already made a considerable impactful statement about managing these complex conditions.

Retrospective results of a retrospective study demonstrate that intravitreal faricimab-loading therapy can significantly increase visual acuity for patients suffering from neovascular wet AMD. Researchers observed a decline in central foveal thickness at 1, 2, and 3 months post faricimab administration, and no adverse events occurred as part of this trial.

The STAIRWAY trial was a multicenter, randomized, active comparator-controlled phase 2 clinical trial conducted across multiple centers. The primary objectives were to ascertain whether one injection of faricimab would reduce fluid accumulation while maintaining anatomic and functional outcomes in eyes with treatment-naive choroidal neovascularization secondary to neovascular AMD. Furthermore, efficacy comparisons between faricimab and another anti-VEGF agent, Aflibercept were made.

One major limitation of this study was its relatively small sample size, making comparison between patient subgroups difficult. Furthermore, OCT and fundus autofluorescence results could only partially assess faricimab’s effect in stabilizing vascular blood flow.

Faricimab is a bispecific antibody designed to target both vascular endothelial growth factor A and angiopoietin-2 simultaneously and independently through binding. Approved by FDA, MHRA and EMA for treating age-related macular degeneration, diabetic macular edema and retinal vein occlusion; intravitreal injection available under brand name Vabysmo(r)

Recent studies comparing aflibercept with individualised faricimab dosing every 16 weeks was performed on patients suffering from neovascular AMD and diabetic macular edema. They discovered that faricimab could maintain robust anatomic and visual outcomes after two years in those suffering neovascular AMD, further extending treatment intervals than current anti-VEGF agents; more research is necessary to understand why its benefits exceed those of aflibercept in this patient cohort.

Tie2

Angiopoietin (ANG)-TIE growth factor receptor pathway regulates vascular permeability and pathological remodelling during inflammation, tumour angiogenesis and atherosclerosis. Drugs targeting this pathway have emerged as attractive therapeutic targets in ophthalmology and oncology as VEGF-based anti-angiogenic therapies fail to provide relief; hence targeting this pathway has emerged as attractive therapeutic targets in these fields as well. Furthermore, its vascular stabilizing function makes ANG-TIE pathway an attractive target in conditions like sepsis organ transplantation or atherosclerosis.

In the ocular vascular system, one of ANG-2’s key functions is to suppress blood vessel growth by binding to Integrin 41 and encouraging actin stress fibre formation at endothelial cell-endothelial cell (EC-EC) junctions. Furthermore, binding Ang-2 to 41 causes changes to endothelial cells that reduce laminar shear stress while destabilizing their monolayer, an effect thought to play an essential part in age-associated neovascularization processes.

Neovascular age-related macular degeneration, the “wet” form, results from abnormal blood vessel proliferation in the retina. As new vessels proliferate they leak exudate, fluid, and proteins into the macula and obscure vision. Hemangioblasts induced by VEGF form these new vessels with small openings called fenestrae that allow rapid passage of macromolecules through these vessels.

Normal development relies on ang-2 being released by hemangioblasts to control the permeability of newly-formed blood vessels, but an absence of this function in adult eyes causes neovascular age-related macular degeneration and other vascular diseases, with VEGF producing cells failing to maintain adequate permeability of new vessels, leading to leakage exudate and macular oedema as a result of macular oedema and leakage exudate.

Genetic mutations that decrease ANG-2 expression have been found in patients with venous malformations, including primary congenital glaucoma. Heterozygous ANG2 mutations lead to this disease by disrupting Schlemm’s canal, normally responsible for draining away aqueous humor from the anterior chamber, leading to elevated intraocular pressure and neurodegeneration.

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