A fully soluble ubiquinone formulation for mitochondrial diseases
A new formulation of ubiquinone that will improve delivery efficiency for supplementation in mitochondrial diseases has been developed at McGill University.
In the mitochondria, the electron transport chain produces the molecule responsible for driving most of the body’s enzymatic reactions: ATP. An integral molecule in this process is the lipid ubiquinone. A deficiency in ubiquinone is commonly associated as being a factor in heart diseases, fetal mitochondrial diseases, and Parkinson’s disease. Unfortunately, the currently available formulations are not very effective because they are very hydrophobic and essentially insoluble in aqueous solutions. Therefore, very little of the administered ubiquinone reaches the organs that need the molecule for the synthesis of ATP.
In this invention, a new formulation of ubiquinone was developed using only non-toxic and FDA-approved components. Since this improved form of ubiquinone is a fully soluble molecule that can be administered in a variety of ways, it will be able to reach the organs affected by mitochondrial diseases: the heart, muscles, kidney, and brain. A proof of concept was verified in animal models of ubiquinone deficiency, while mitochondrial disease models are underway.
- Fully soluble ubiquinone that successfully reaches mitochondria in target organs
- Successful administration in ubiquinone deficiency animal models