Mechanism-of-action

Mitochondria in Health and Disease

Mitochondria are the cell’s source of energy and play an essential role in the proper functioning of cells and organs. Healthy mitochondria generate adenosine triphosphate (ATP), the energy molecule required by our cells and organs to function properly. Mitochondria also produce a minimal level of reactive oxygen species (ROS) as secondary products of respiration.

When mitochondria dysfunction, ATP production is reduced and ROS production is increased, with an accompanying increase in oxidative stress. The increased ROS that dysfunctional mitochondria produce can damage multiple cellular components (including DNA, proteins, lipids and the mitochondria themselves), which results in the disruption of normal biological functioning and disease.

Mitochondrial dysfunction is believed to arise either as a result of inherited genetic defects or through damage-signals encountered during disease. In either case, the result is the generation of excessive ROS and reduced ATP production. Dysfunctional mitochondria are a key element in a variety of serious diseases (both rare and common), and thus a promising therapeutic target.

Mitochondrial Medicines

The development of Mitochondrial Medicines is challenged by the difficulty of targeting the mitochondria (passing both the cellular membrane and the mitochondrial outer membrane) without affecting the mitochondrial membrane potential or causing mitochondrial toxicity. Our compound SUL-109 appears to target and protect dysfunctional mitochondria without affecting healthy mitochondria and cells. Want to read more about the mechanism of action? Download the manuscript of Dr. G. Krenning (UMCG) which explains all about our SUL compound:

Publication Dr. G. Krenning (UMCG) through Science Direct: The 6-chromanol derivate SUL-109 enables prolonged hypothermic storage of adipose tissue-derived stem cells