The use of intravitreal anti-VEGF is becoming increasingly routine in ophthalmological practice today and is responsible for the treatment of numerous ocular pathologies. It basically acts by inhibiting the angiogenesis that this endothelial growth factor promotes. Studies show that VEGF-A is the factor that most induces vascular permeability and is therefore involved in the genesis of ocular neovascularisation, present in diseases such as AMD, diabetic retinopathy, vascular occlusions, among others. There are numerous drugs that are currently used to treat the aforementioned pathologies. These include Pegaptanib (MacugenR), which basically inhibits forms of VEGF longer than 165 amino acids. Bevacizumab, which is a humanised monoclonal antibody (AvastinR), acts directly against VEGF-A and all its isoforms, but its ocular use is off-label.2 Ranibizumab (LucentisR) acts by inhibiting all isoforms of VEGF-A, and because it is a humanised antibody fragment, it easily penetrates the retina.