| Description/Background | Natalizumab is characterized as a disease-modifying therapy for multiple sclerosis (a disease of the central nervous system (CNS)), and inflammatory bowel disease. It works by inhibiting the migration of leukocytes to inflammation sites. The VCAM-1 and α4β1-integrin interaction is necessary for leukocyte adhesion, firm attachment, and transmigration across the blood-brain barrier into the CNS. Natalizumab, a recombinant, humanized antibody, binds to α4β1 -integrin and blocks its interaction with VCAM-1. Hence, leukocyte migration into brain tissue is inhibited, thereby reducing inflammation and preventing the formation of multiple sclerosis lesions.1 Inflammation in the gut pertaining to inflammatory bowel disease can be controlled in a similar fashion. Blocking α4β7-integrin with a humanized, monoclonal antibody, specific to the α4β7 heterodimer inhibits the migration of leukocytes into the inflamed intestinal tissue, thus, reducing inflammation in the gut.2 This cost-effective, research-grade Anti-Human CD49D (Natalizumab) utilizes the same variable regions from the therapeutic antibody Natalizumab making it ideal for research projects. |
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