Value Proposition:
· Drug treats mitochondrial dysfunction by promoting mitochondrial fission and mitophagy.
· Decreases fat levels and represses glucose production in the liver to effectively treat diabetes, obesity, and non-alcoholic fatty liver disease.
· Possesses antitumor activity via p53-mediated apoptosis
Unmet Need
· Approximately 1 in every 4,300 individuals in the United States has a mitochondrial disease (Children’s Hospital of Philadelphia). Metabolic disorders that occur as a result of mitochondrial dysfunction include diabetes, obesity, and non-alcoholic fatty liver disease (NAFLD). While therapies including metformin and GLP1 antagonists exist for these metabolic disorders, side effects can be potent and disease burden remains high. There is an unmet need for additional therapeutics that target the mitochondrial dysfunction underlying many metabolic diseases.
Technology Description
· Researchers at Johns Hopkins have developed three peptides designed to act on the AMPK pathway: a master regulator of energy homeostasis that is compromised in metabolic disease and elderly patients. By increasing AMPK kinase activity, data in animal models have shown improvements in mitochondrial function; improvement in hyperglycemia in obese mice; and reduction in hepatocyte fat levels in obese mice. The researchers’ peptide activates AMPK (counteracting the negative hyperphosphorylation of AMPK in human cancers), which has been shown to trigger apoptosis of human tumor cells.
Stage of Development
· In vitro assays, cellular assays, animal tests, and testing on human tissue samples have already been conducted
Data Availability
· Available on Request
Publication
· Cell Chemical Biology - Blocking AMPKαS496 phosphorylation improves mitochondrial dynamics and hyperglycemia in aging and obesity
