Ranibizumab CAS 347396-82-1 API
Ranibizumab injection 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.
Description
Ranibizumab injection 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.
Basic Information
|
Chemical Name |
Ranibizumab |
|
CAS NO. |
347396-82-1 |
|
Appearance |
Colorless Liquid |
|
Molecular Formula |
C2158H3282N562O681S12 |
|
Molecular Weight |
N/A |
|
Purity by Genohope |
99% |
|
Annual Capacity by Genohope |
100 g/year |
|
Process by Genohope |
E.coli Fermented |
Brief Introduction
Ranibizumab, sold under the brand name Lucentis among others, is a monoclonal antibody fragment (Fab) created from the same parent mouse antibody as bevacizumab.
It is an anti-angiogenic that is approved to treat the "wet" type of age-related macular degeneration (AMD, also ARMD), diabetic retinopathy, and macular edema due to branch retinal vein occlusion or central retinal vein occlusion.
Ranibizumab was developed by Genentech and marketed by them in the United States, and elsewhere by Novartis, under the brand name Lucentis.
Ranibizumab (Lucentis) was approved for medical use in the United States in June 2006, and in the European Union in January 2007.
Indication and Usage
Ranibizumab, also called LUCENTIS, is indicated for the treatment of patients with neovascular (wet) age-related macular degeneration.
Mechanism of Action
Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, VEGF110. VEGF-A has been shown to cause neovascularization and leakage in models of ocular angiogenesis and is thought to contribute to the progression of the neovascular form of age-related macular degeneration
(AMD). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.
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