Tumor necrosis factor alpha (soluble form) (TNF-α)

Soluble tumor necrosis factor alpha (sTNF-α) is a 17 kDa cytokine released by proteolytic cleavage of the membrane-bound precursor (transmembrane TNF-α) through the action of TNF-α converting enzyme (TACE). sTNF-α primarily acts as a homotrimer that binds to and activates the tumor necrosis factor receptor 1 (TNFR1; also known as TNFRSF1A), triggering downstream inflammatory and apoptotic signaling pathways. It is a central mediator in the regulation of immune and inflammatory responses, acute phase reaction, and cell survival or death decisions. Excess or chronic production of sTNF-α is implicated in the pathology of autoimmune diseases (such as rheumatoid arthritis, Crohn’s disease, and psoriasis), infectious diseases, some cancers, and metabolic or cardiovascular disorders. Accordingly, sTNF-α is a validated therapeutic target for multiple inflammatory and autoimmune conditions, and is targeted by several monoclonal antibodies and decoy receptors in clinical practice.

Other names

TNF-alphaTNFATNFcachectinsoluble TNF-alphasTNF-α

Neutralization of soluble TNF-α, blocking its interaction with TNF receptors; Inhibition of TNF-α-induced signal transduction; Induction of cell cycle arrest and apoptosis in TNF-α producing cells (for some antibody drugs)