 The large cytosolic GT-Parsay, dynamic-related protein 1, DRP1, mediates both physiological and pathological mitochondrial fission. When cell stress occurs, DRP1 binds to mitochondrial fees 1, triggering mitochondrial fragmentation, ROS production, metabolic collapse, and ultimately cell death. However, DRP1 can also mediate physiological fission by binding to mitochondrial MFF, sparing physiological mitochondrial fission. To prevent pathological fission, drugs that inhibit DRP1, fees 1 interactions are needed. One such drug, P110, has been shown to reduce pathology in multiple animal models of neurodegeneration, ischemia, and sepsis. Unfortunately, P110 has limited pharmacokinetics, so researchers sought to identify small molecules that mimicked P110's benefits. They identified a small molecule, SC9, that binds to the same region of DRP1 as P110, and found that it reduced pathology in cells and a mouse model of end. This article was authored by Luis Rios, Suman Pocrol, Sinjin Lee, and others. We are article.tv, links in the description below.