View clinical trials related to Neovascularization, Choroidal.
Filter by:The overall goal of the proposed research project is to provide evidence that a specific subtype of neovascularization that may develop in eyes with age-related macular degeneration (AMD) prevents vision loss. This concept challenges the current view that the development of neovascularizations in AMD represents a harmful event in general. Notably, before the era of anti-vascular endothelial growths factor (VEGF) therapy, destruction and surgical removal of neovascular membranes have been tested as treatment options for neovascular AMD. This research project aims to substantiate the hypothesis that type 1 macular neovascularization (MNV) is intrinsically protective, in sense of a positive response to the degenerative processes in AMD. This concept has actually been proposed by pathologists decades ago but has not been systematically investigated in vivo. With the immense advances in retinal imaging, 'sub-clinical', non-exudative type 1 MNVs that are located beneath the retinal pigment epithelium (RPE) can now be detected non-invasively and characterized in vivo. There is currently a growing body of evidence that photoreceptor and RPE degeneration is indeed slowed down in eyes exhibiting type 1 MNV. However, the proof of a direct protective effect of non-exudative type 1 MNV on visual function in AMD is lacking. Here, the aim is to demonstrate relative preservation of function along with preserved structure in the immediate vicinity of type 1 MNV, while there is progressive loss of sensitivity and degeneration in the surrounding tissue.
This was a Phase II, multicenter, randomized, active comparator-controlled, 52-week study to investigate the efficacy, safety and pharmacokinetics of faricimab (RO6867461; RG7716) administered with extended dosing regimens in treatment-naive participants with neovascular age related macular degeneration (nAMD). Only one eye was chosen as the study eye.
Age-related macular degeneration (AMD) is by far the most common disorder in the group of irreversible causes of visual disability. AMD leads to dysfunction and loss of photoreceptors in the central retina. Neovascular AMD (nAMD) affects visual function early in the disease process and severely compromises the highly developed functions of the macula, such as perception of details, central fixation, color vision, and reading ability. AMD-related visual impairment is associated with a loss of autonomy and quality of life. Current therapeutic approaches target vascular endothelial growth factor (VEGF), which has been identified as a main cytokine in the pathogenesis of nAMD. Ranibizumab, the fab-fragment of an antibody targeting VEGF is approved for the treatment of nAMD applied intravitreally in monthly intervals until the disease activity is stopped. However, a significant proportion of patients with nAMD suffer from persistent or recurring disease with the need of continuous anti-VEGF therapy over months and years, often leading to irreversible changes in the photoreceptor layer and the pigment epithelium. Recent studies regarding the treatment of nAMD utilized different forms of therapies, combining photodynamic therapy with verteporfin (PDT) and ranibizumab, as well as therapeutic regimen containing steroids. Even though these studies did not provide evidence that combination therapies are superior to ranibizumab monotherapy, studies were only conducted with patients with previously untreated nAMD. Therefore, currently there is no alternative therapeutic approach for patients with recurrent or persistent form of nAMD after multiple treatments with ranibizumab monotherapy. The purpose of this study is to assess the treatment effect of reduced fluence PDT and intravitreal ranibizumab versus intravitreal dexamethasone and ranibizumab versus intravitreal ranibizumab monotherapy in patients with persistent or recurrent choroidal neovascularization (CNV) due to AMD. The investigators hypothesis is that these findings will offer new insights in the management of persistent or recurrent CNV secondary to AMD.