Nicotinamide mononucleotide enhances anti-tumor effect by resetting macrophages toward the inflammatory M1-like phenotype.

NMN supplementation at high doses demonstrated anti-tumor efficacy comparable to PD-1 checkpoint inhibitors in a murine mesothelioma model by reprogramming tumor-associated macrophages toward a pro-inflammatory M1 phenotype rather than enhancing T cell or NK cell responses. This represents a novel immunotherapy mechanism distinct from current checkpoint blockade strategies. The findings suggest NMN may offer an alternative or complementary cancer immunotherapy approach by modulating innate immunity through macrophage phenotype shifting.

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High-dose NMN shifted tumor macrophages toward M1 phenotype, matching PD-1 inhibitor efficacy in mice—suggests innate immune modulation worth monitoring in oncology contexts.

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