Merck

Last updated January 31, 2026

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Substituted pyridinyl and cyclobutylpyrimidine ido inhibitors: MerckRecent Research Landscape

Tumor-induced immune suppression via tryptophan depletion leads to immunotherapy failure. These specific piperazine amide and imidazopyridine scaffolds restore T-cell activity by blocking the indoleamine 2,3-dioxygenase metabolic pathway.

What technical problems is Merck addressing in Substituted pyridinyl and cyclobutylpyrimidine ido inhibitors?

Tumor immune escape mechanisms

(3)evidences

Excessive enzymatic degradation of tryptophan by IDO and TDO creates a microenvironment that inhibits T-cell activation. Addressing this metabolic depletion prevents the failure of the immune system to recognize and attack malignant cells.

Tumor immune escape

(1)evidences

Excessive tryptophan catabolism by IDO enzymes creates an immunosuppressive environment that prevents T-cell activation against malignant cells. Inhibiting this pathway restores the immune system's ability to recognize and destroy tumors.