Development Programs and Science
Leveraging Unique Features of Cellular Metabolism in the Disease Process
In various disease states subsets of cells intrinsically, or in response to treatment, exhibit aberrant cellular metabolism. For example, cancer cells often upregulate mitochondrial OxPhos-dependent metabolism that directly supports cell growth and proliferation. Furthermore, the increased OxPhos activity results in tumor microenvironment hypoxia that indirectly limits immune responses directed to the cancer cells. Similarly, cells associated with diseases of fibrosis may adapt an OxPhos-dependent metabolism to support the energy and nutrient demands required for fibroblast activation to myofibroblast, a cell type important to the development of fibrotic disease. ImmunoMet’s lixumistat (IM156) PC1 inhibitor has the potential to target any disease that is, or has become, dependent on mitochondrial OxPhos activity.
Targeting Mitochondria
In various disease states, particular cell types exhibit dysfunctional cellular metabolism. In cancer, immune suppressor cells can adapt a mitochondrial, OxPhos-dependent metabolism that allows the cells to coexist with tumor cells resulting in limiting the full potential of current immunotherapies. In diseases characterized by aberrant fibrosis, fibroblasts may adapt an OxPhos-dependent hyperactive metabolism during differentiation resulting activated cellular functions which lead to fibrosis. ImmunoMet’s lixumistat (IM156) can target any cell types that use mitochondrial OxPhos during disease progression or maintenance.
