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However, a phase II clinical trial (NCT03486223) failed to demonstrate its efficacy in treating impaired glucose tolerance, obesity and endocrine system diseases, even though it can inhibit sEH activity in plasma, muscle, and adipose tissue and reduce F2-isoprostanes, a marker of oxidative stress

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Two to six times more ynfA gene expression than tolC gene expression was observed (Sarkar et al., 2015)

In the face of controversies and challenges, it is essential to establish a more efficient translational interface between science, technology, and clinical practice, driving mitochondrial metabolic reprogramming therapy from a potential pathway to clinical reality. Conclusion Mitochondrial metabolic reprogramming plays a central role in the therapeutic failure of CRC