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 indications

The beneficial effects of intravitreal injections of ranibizumab (Lucentis, Genentech, Inc., South San Francisco, CA, and Novartis, Basel, Switzerland) and aflibercept in the treatment of neovascular AMD (nv-AMD) have been widely evidenced showing significant improvements in visual acuity and quality of life [2, 3]. [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]
To determine whether bevacizumab is as effective and safe as ranibizumab, numerous randomised, controlled clinical trials (RCTs) and retrospective studies have been performed over the past five years, such as the Comparison of Age-related macular degeneration Treatments Trials (CATT), the Alternative treatments to Inhibit VEGF in Age-related choroidal Neovascularization (IVAN), the Multicenter Anti-VEGF Trial in Austria (MANTA), and the Groupe d'Etude Français Avastin versus Lucentis dans la DMLA néovasculaire (GEFAL). [source, 2014]
To date, neither the general nor the regional effects of Lucentis injections on the ECM in patients with CNV/AMD have been described, and to the best of our knowledge, this is the first study to examine these effects. [source, 2014]
The effect of the Lucentis injection on the change in expression of the collagen and laminin genes is presented in Table 3. [source, 2014]
The major clinical trials first reported that ranibizumab (Lucentis, Genentech Inc, South San Francisco, CA) was effective in improving visual acuity for patients with age-related macular degeneration. [source, 2012]
We next compared the effect of Dz13 against a clinically-used approach such as VEGF-A antibodies (akin to Lucentis) in this model. [source, 2012]
A recent study from the Comparison of AMD Treatments Trials (CATT) involving 1208 patients with neovascular age-related macular degeneration demonstrated that Avastin and Lucentis are equally effective in treating AMD, with mean change in visual acuity at 1 year the primary outcome [40]. [source, 2012]
Among all anti-VEGF therapeutic agents, the anti-VEGF antibody drugs ranibizumab (Lucentis, Genentech) and bevacizumab (Avastin, Genentech) are most broadly used to treat AMD with similar efficacy and side effects [6,7]. [source, 2012]
Similarly, while recurrent intravitreal injections of the monoclonal anti-VEGF antibody ranibizumab (Lucentis) is the standard of care for age-related macular degeneration where the majority of patients show visual stabilization [8], isolated cases of macular ischemia and persistent elevation in intraocular pressure following treatment have been reported [45], [46] and the long term effects of drug resistance, tolerance or ancillary effects in targeting this pathway have yet to be addressed. [source, 2012]