NDLI: Drug Repurposing to Enhance Antitumor Response to PD-1/PD-L1 Immune Checkpoint Inhibitors

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Drug Repurposing to Enhance Antitumor Response to PD-1/PD-L1 Immune Checkpoint Inhibitors

Content Provider	MDPI
Author	Thuru, Xavier Magnez, Romain El-Bouazzati, Hassiba Vergoten, Gérard Quesnel, Bruno Bailly, Christian
Copyright Year	2022
Description	Monoclonal antibodies targeting the PD-1/PD-L1 immune checkpoint have considerably improved the treatment of some cancers, but novel drugs, new combinations, and treatment modalities are needed to reinvigorate immunosurveillance in immune-refractory tumors. An option to elicit antitumor immunity against cancer consists of using approved and marketed drugs known for their capacity to modulate the expression and functioning of the PD-1/PD-L1 checkpoint. Here, we have reviewed several types of drugs known to alter the checkpoint, either directly via the blockade of PD-L1 or indirectly via an action on upstream effectors (such as STAT3) to suppress PD-L1 transcription or to induce its proteasomal degradation. Specifically, the repositioning of the approved drugs liothyronine, azelnidipine (and related dihydropyridine calcium channel blockers), niclosamide, albendazole/flubendazole, and a few other modulators of the PD-1/PD-L1 checkpoint (repaglinide, pimozide, fenofibrate, lonazolac, propranolol) is presented. Their capacity to bind to PD-L1 or to repress its expression and function offer novel perspectives for combination with PD-1 targeted biotherapeutics. These known and affordable drugs could be useful to improve the therapy of cancer.
Starting Page	3368
e-ISSN	20726694
DOI	10.3390/cancers14143368
Journal	Cancers
Issue Number	14
Volume Number	14
Language	English
Publisher	MDPI
Publisher Date	2022-07-11
Access Restriction	Open
Subject Keyword	Cancers Oncology Azelnidipine Cancer Therapy Drug Repurposing Immune Checkpoint Liothyronine Niclosamide Pd-1 Pd-l1 Tumor
Content Type	Text
Resource Type	Article

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