Coenzyme A (CoA) is a vital cofactor in cellular metabolism, particularly in the mitochondria, where it plays a central role in the oxidation of fatty acids and the citric acid cycle (Krebs cycle). These pathways are fundamental for the production of adenosine triphosphate (ATP), the primary energy currency of the cell. Scientific studies have elucidated the biochemical necessity of CoA for mitochondrial energy metabolism: it is required for the formation of acetyl-CoA, which enters the citric acid cycle, and for the β-oxidation of fatty acids within the mitochondrial matrix.

However, while the essential role of endogenous CoA in mitochondrial function is well established, evidence supporting oral Coenzyme A supplementation to "support" mitochondrial function in healthy individuals is less robust. Most clinical research focuses on CoA’s metabolic functions and its deficiency states, with limited data directly linking supplemental CoA to enhanced mitochondrial performance or health outcomes in humans. Some preclinical and animal studies suggest that boosting CoA precursors may optimize metabolic processes under certain conditions, but high-quality human trials are sparse.

In summary, Coenzyme A is scientifically validated as indispensable for mitochondrial metabolism, but the translation of this knowledge to the efficacy of supplemental CoA for mitochondrial "support" in people is not yet conclusively demonstrated. The ingredient’s use for mitochondrial health is thus grounded in strong mechanistic science, but direct supplementation evidence is limited.