Our mission is to bring forward meaningful drugs that work at the root of insidious diseases by modulating the mitochondria directly to attenuate disease progression.
A key thesis to our approach lies in the fact that modulating mitochondria function by increased energy expenditure results in: improved cellular function, improved biomarkers and a reduction in disease state. This has been shown repeatedly in models of energy expenditure. With small increases in energy expenditure, data now exists to show improvements in cognition with Alzheimer’s Disease (Liu, D. 2014), reduction in symptoms associated with Huntington’s Disease (Duan, W 2003), decrease in reactive oxygen species associated with ALS, improve lipid profiles affecting diabetes/heart disease (Perry, RJ 2013) and neuro-protection in ischemic stroke (Pettigrew, C 2012). Overall, increased energy expenditure via mitochondrial regulation can produce disease-modifying affects.