Latest research on Lucentis

Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab has a molecular weight of approximately 48 kilodaltons and is produced by an E. coli expression system in a nutrient medium containing the antibiotic tetracycline (tetracycline is not detectable in the final product). Ranibizumab is marketed under the name Lucentis®. It is indicated for the treatment of macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema.

Lucentis side effects

In May 2013 NICE recommended ranibizumab (Lucentis, Novartis) as a possible treatment for some people who have sight problems because of macular oedema caused by retinal vein occlusion. [source, 2015]
Subjects were included in the study if they met the following criteria: 1) active subfoveal choroidal neovascularization (CNV) secondary to exudative AMD confirmed by fluorescein angiography; 2) E-ETDRS vision of 25–80 letters (Snellen equivalent of ~20/25 to 20/320); 3) at least one prior injection of 1.25 mg bevacizumab or 0.5 mg ranibizumab (Avastin and Lucentis, respectively; Genentech Inc., South San Francisco, CA, USA) within 3 months of enrollment; and 4) had an initial response on OCT defined as a decrease of retinal edema and/or subretinal fluid to anti-VEGF injections followed by recurrent increase in fluid on OCT (further defined as intraretinal, cystoid, subretinal fluid, or worsening pigment epithelial detachment [PED]) or the presence of a new hemorrhage on clinical examination. [source, 2015]
In the USA, a recent model estimated that the number of cases of legal blindness caused by neovascular AMD would reduce dramatically if monthly ranibizumab (Lucentis, Genentech, Inc., South San Francisco, CA, USA/Novartis AG, Basel, Switzerland) was used when indicated compared with no treatment [9]. [source, 2014]
Among these therapeutic agents, the anti-VEGF antibody drugs, ranibizumab (Lucentis, Genentech, South San Francisco, CA), bevacizumab (Avastin, Genentech), and aflibercept (Eylea, Bayer HealthCare, Berlin, Germany) are most widely used to treat AMD in the clinical setting, and have similar efficacy and side effects [4]–[6]. [source, 2014]
The main inclusion criteria were: (1) active subfoveal choroidal neovascularisation secondary to exudative AMD confirmed by fluorescein angiography; (2) Electronic - Early Treatment In Diabetic Retinopathy Study (E-ETDRS) vision of 25–80 letters (Snellen equivalent of ∼20/25–20/320); (3) at least one prior injection of 1.25 mg bevacizumab, or 0.5 mg ranibizumab (Avastin and Lucentis, respectively; Genentech, South San Francisco, California, USA) within 3 months of enrolment and (4) had an initial response on optical coherence tomography (OCT) defined as a decrease of retinal oedema and/or subretinal fluid to anti-VEGF injections followed by recurrent increase in fluid on OCT (further defined as intraretinal, cystoid, subretinal fluid, or worsening pigment epithelial detachment (PED)) or the presence of new haemorrhage on clinical examination. [source, 2014]
Forty-one days after cataract surgery, a worsening of his CME associated with a progressive decrease of the patient's BCVA (20/50) was present, and this time the LE was first treated with an intravitreal injection of ranibizumab (Lucentis). [source, 2014]
FDA-approved drugs for the treatment of wet AMD include Lucentis (Ranibizumab), Eylea (Aflibercept), and Macugen (Pegaptanib), all of which target VEGF to slow the growth of abnormal blood vessels and reverse the increased vascular permeability associated with new vessel formation [3]–[5]. [source, 2014]
Prospective studies of ranibizumab (Lucentis, Genentech, Inc., South San Francisco, California, USA), a humanised, affinity-matured VEGF antibody fragment that neutralises all isoforms of VEGF-A and their biologically active degradation products in treatment-naïve eyes with ME following BRVO, found that ranibizumab was effective at 2 years after treatment of ME caused by BRVO. [source, 2014]
Increased collagen I occurring after injections of Lucentis may stimulate and sustain angiogenesis, and, as has been shown by Nguyen [23], in the case of illness, activate 2 endopeptidases crucial to the process: gelatinase A (matrix metalloproteinasis-2; MMP-2) and membrane-type metalloproteinase-1 (MMP-14) [23]. [source, 2014]
A decrease in collagen type IV after injection of Lucentis may be considered disadvantageous for the following reasons. [source, 2014]