C-Phycocyanin, a pigment-protein complex derived from the blue-green algae Spirulina, has been investigated for its potential to support mitochondrial function, mainly due to its antioxidant properties. Several in vitro and animal studies suggest that C-Phycocyanin can scavenge reactive oxygen species (ROS) and reduce oxidative stress, processes that are closely linked to mitochondrial health. By mitigating oxidative damage, C-Phycocyanin may help preserve mitochondrial membrane integrity and support cellular energy production.

However, direct clinical evidence in humans is very limited. Most research to date has focused on mechanistic or preclinical models. In these models, C-Phycocyanin administration has shown protective effects on mitochondria in contexts of induced oxidative damage, such as toxin exposure or ischemia-reperfusion injury. Its capacity to enhance activities of endogenous antioxidant enzymes like superoxide dismutase (SOD) and catalase has also been observed.

Despite promising preclinical data, well-designed human clinical trials are lacking, and therefore, the evidence for C-Phycocyanin’s use specifically for mitochondrial support in humans remains weak. The current scientific consensus is that while there is mechanistic plausibility and some supporting laboratory data, clinical validation is insufficient at this time.