Anti-Human TNF alpha (Infliximab) (T770-200ug)

TNFα is a 17.5 kD protein that mediates inflammation and immunity caused by the invasion of viruses, bacteria, and parasites by initiating a cascade of cytokines that increase vascular permeability, thus bringing macrophages and neutrophils to the site of infection. TNFα secreted by macrophages cause the blood to clot which provides containment of an infection. TNFα is also associated with autoimmune diseases and its inactivation is important in downregulating inflammatory reactions associated with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, moderate to severe chronic psoriasis, and juvenile idiopathic arthritis. Infliximab is used in the clinical setting to treat immune-mediated inflammatory disorders and is a particularly efficacious treatment for inflammatory bowel disease1. Infliximab, and its biosimilar ABP-710, suppresses inflammation primarily by binding and neutralizing sTNFα2. ABP-710 and infliximab are analytically similar regarding amino acid sequence, primary peptide structure, secondary structure, tertiary structure, conformation, thermal stability, and glycan mapping1,2. ABP-710 and infliximab biological functions are also similar2. Like infliximab, ABP-710 inhibits sTNFα-induced apoptosis and mediates effector functions such as antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis, and complement-dependent cytotoxicity when interacting with membrane bound TNFα.