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This is the first preclinical study to demonstrate that semaglutide, a drug in late-stage clinical development for NASH, reduces hepatic tumor burden in a translational mouse model of NASH-HCC

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[1] Unlike NAD+ building blocks (NMN, NR), it targets the enzyme bottleneck itself instead of adding more raw material

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As discussed, the anti-hyperglycaemic effects of DPP-4 inhibition are mediated via enhancing levels of endogenous DPP-4 substrates, since the inhibitors themselves do not possess any inherent glucose-lowering activity