Takinib Might Be Starting Point for Therapies Targeting Inflammatory Diseases, Study Finds

Takinib Might Be Starting Point for Therapies Targeting Inflammatory Diseases, Study Finds
Takinib, an inhibitor of the protein TAK1, was found to interrupt the inflammatory response central to a variety of autoimmune disorders, such as Crohn's disease, research shows. The study, “Takinib, a Selective TAK1 Inhibitor, Broadens the Therapeutic Efficacy of TNF-α Inhibition for Cancer and Autoimmune Disease,” was published in the journal Cell Chemical Biology. Takinib is a drug-like molecule that acts to increase cell death and decrease inflammation. TAK1 is part of the TNF-α inflammatory pathway. TNF-α is the major cause of inflammation in autoimmune diseases as it promotes pathways that lead to cell survival and inflammation. When stimulated by TNF-α, TAK1 becomes activated and causes inflammation as well as cell survival. When TAK1 is not activated, TNF-α stimulation causes the cell to undergo cell death (apoptosis). Therefore, the presence of TAK1 determines whether a cell survives or dies when it is stimulated by TNF-α. Patients with autoimmune diseases are generally treated with anti-TNF-α antibodies to control the disease and decrease inflammation. However, during chronic treatment, patients often become resistant to these antibodies and other pharmaceutical drugs that inhibit inflammation. Researchers at Duke University developed the molecule Takinib, which pushes the cell toward apoptosis following TNF-α stimulation in cell models of rheumatoid arthritis and metastatic breast cancer. “The delicate balance between survival and death is often disrupted in disease, and this molecule is able to target the process,”
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