Infliximab

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Infliximab is a chimeric IgG 1K monoclonal antibody. Its approximate molecular weight is 149,100 daltons. It is composed of human constant and murine variable regions. Infliximab binds specifically to human TNF-α.

Biological effects of infliximab
TNF-α induces proinflammatory cytokines that include IL-1 and IL-6. These cytokines enhance leukocyte migration by increasing endothelial layer permeability and expression of adhesion molecules by endothelial cells and leukocytes, activation of neutrophil and eosinophil functional activity, and induction of acute phase and other liver proteins.
Infliximab neutralizes the biological activity of TNF-α by binding with high affinity to the soluble and transmembrane forms of TNF-α and inhibits binding of TNF-α with its receptors. A related cytokine that utilizes the same receptors as TNF-α, TNF-beta (lymphotoxin α) is not neutralized by infliximab. It has been found to downregulate IL-18 but not IL-12 and IL-13.
It upregulates the expression of CXCchemokine receptor type II and magnifies the proliferative activity of CXCchemokines in human melanocytes. In Crohn’s disease, it decreases levels of IL-10.
Apoptosis of monocytes is not responsible for the therapeutic TNF-alpha Inhibitors. However, some of the therapeutic effects of infliximab may be caused by its ability to downregulate proinflammatory cytokines production by monocytes exposed to bacterial antigens.
Infliximab was first approved by the Food and Drug Administration (FDA) in 1998 as a treatment of moderately to severely active Crohn’s disease. Its initial indication was to reduce the signs and symptoms in patients with Crohn’s. The recommended dose of infliximab for the treatment of severe active Crohn’s disease in refractory patients is 5 mg/kg intravenously as a single dose. In patients with Crohn’s disease with fistula involvement, an initial dose of 5 mg/kg followed by additional 5 mg/kg doses at weeks 2 and 6 is recommended. This dose is often used in other Crohn’s disease patients.
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