Abstract:Background
Tryptophan catabolism leading to T cell suppression mediated by indoleamine 2,3-dioxygenase (IDO1) is an important mechanism of tumor immune escape, and IDO1 inhibitors have attracted increasing attention as anticancer therapeutics. However, the phase III clinical trial (ECHO-301/KEYNOTE-252) of epacadostat (INCB024360) had disappointing outcomes. This revealed that purification of IDO1 with high purity is one of the major constraints that limit the development of its inhibitors.
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