Immune-modulating enzyme indoleamine 2,3-dioxygenase is effectively inhibited by targeting its apo-form

Micah T. Nelp(Princeton University), Patrick A. Kates(Princeton University), John T. Hunt(Bristol-Myers Squibb (United States)), John A. Newitt(Bristol-Myers Squibb (United States)), Aaron Balog(Bristol-Myers Squibb (United States)), Derrick Maley(Bristol-Myers Squibb (United States)), Xiao Bing Zhu(Bristol-Myers Squibb (United States)), Lynn M. Abell(Bristol-Myers Squibb (United States)), Alban J. Allentoff(Bristol-Myers Squibb (United States)), R. M. Borzilleri(Bristol-Myers Squibb (United States)), H.A. Lewis(Bristol-Myers Squibb (United States)), Zeyu Lin(Bristol-Myers Squibb (United States)), Steven P. Seitz(Bristol-Myers Squibb (United States)), Chunhong Yan(Bristol-Myers Squibb (United States)), John T. Groves(Princeton University)
Proceedings of the National Academy of Sciences
March 12, 2018
Cited by 208Open Access
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Abstract

-formylkynurenine. On deformylation, kynurenine and downstream metabolites suppress T cell function. The importance of this immunosuppressive mechanism has spurred intense interest in the development of clinical IDO1 inhibitors. Herein, we describe the mechanism by which a class of compounds effectively and specifically inhibits IDO1 by targeting its apo-form. We show that the in vitro kinetics of inhibition coincide with an unusually high rate of intrinsic enzyme-heme dissociation, especially in the ferric form. X-ray crystal structures of the inhibitor-enzyme complexes show that heme is displaced from the enzyme and blocked from rebinding by these compounds. The results reveal that apo-IDO1 serves as a unique target for inhibition and that heme lability plays an important role in posttranslational regulation.


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