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Related Experiment Video

Updated: May 21, 2025

Pretargeted Radioimmunotherapy Based on the Inverse Electron Demand Diels-Alder Reaction

Pretargeted Radioimmunotherapy Based on the Inverse Electron Demand Diels-Alder Reaction

Published on: January 29, 2019

IDO Believe in Immunotherapy.

Peter D Zang¹, Tanya B Dorff²

¹City of Hope Comprehensive Cancer Center, Duarte, United States.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research

|March 18, 2025

Summary

Indoleamine 2,3-dioxygenase 1 inhibition with linrodostat did not improve PD-1 blockade efficacy in advanced cancers. Tryptophan 2,3 dioxygenase was identified as a resistance mechanism, suggesting dual targeting may be needed.

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Area of Science:

Immunology
Oncology
Pharmacology

Background:

Indoleamine 2,3-dioxygenase 1 (IDO1) plays a key role in immune suppression.
IDO1 activity is implicated in tumor immune evasion and resistance to cancer therapies.

Purpose of the Study:

To evaluate the efficacy of linrodostat, an IDO1 inhibitor, in combination with PD-1 inhibitors (nivolumab ± ipilimumab) in patients with advanced solid tumors.
To explore potential resistance mechanisms to IDO1 inhibition in this patient population.

Main Methods:

Phase I/II clinical trial design.
Combination therapy with linrodostat and nivolumab ± ipilimumab.
Correlative analyses to investigate biomarkers of response and resistance.

Main Results:

The combination therapy did not enhance the efficacy of PD-1 inhibition.
Correlative studies identified tryptophan 2,3 dioxygenase (TDO) as a mechanism of resistance to IDO1 inhibition.
IDO1 inhibition alone did not overcome TDO-mediated resistance.

Conclusions:

Dual targeting of IDO1 and TDO may be required to overcome resistance and improve responses to PD-1 inhibition in advanced solid tumors.
Further investigation into combined IDO1 and TDO blockade is warranted.