A disintegrin and metalloproteinase 17 (ADAM17 (also commonly called TACE))

A disintegrin and metalloproteinase 17 (ADAM17), also known as tumor necrosis factor alpha-converting enzyme (TACE), is a membrane-anchored metalloproteinase enzyme responsible for the proteolytic release (“shedding”) of several important cell-surface proteins, including pro-inflammatory cytokines (notably TNF-alpha), cytokine receptors (such as TNF receptors), and growth factor precursors[1][3][5]. ADAM17 is ubiquitously expressed and has a complex, multidomain structure that enables it to regulate key biological processes related to inflammation, immune response, tissue repair, and signal transduction[1][4][5][8]. Its dysregulation or increased activity is implicated in a range of inflammatory, cardiovascular, oncological, and metabolic diseases, making it an attractive, though challenging, therapeutic target for drug development[1][4][5][9]. ADAM17 inhibitors are being explored for conditions involving pathological cytokine activation, but clinical translation is limited by safety concerns due to the enzyme’s broad range of substrates and physiological roles[5][9].

Other names

Tumor necrosis factor alpha-converting enzymeTACECD156bMetalloproteinase disintegrinDisintegrin and metalloproteinase domain-containing protein 17

Inhibition of metalloproteinase catalytic activity to block cytokine or receptor ectodomain shedding; Reduction of soluble TNF-alpha production; Modulation of cell surface receptor signaling by preventing their cleavage