TMEM11 Inhibitors

TMEM11 inhibitors primarily focus on chemicals that influence TMEM11 by targeting various aspects of mitochondrial function and morphogenesis. The first subset of these inhibitors targets mitochondrial division and fusion processes. For instance, Mdivi-1, by inhibiting Drp1, affects mitochondrial fission, a process likely intertwined with TMEM11's function in mitochondrial morphology. Similarly, chemicals like Oligomycin A and Rotenone alter mitochondrial energy metabolism, affecting the energy-dependent processes of mitochondrial morphogenesis. The second subset involves compounds that disrupt the mitochondrial membrane potential and electron transport chain (ETC), such as Carbonyl Cyanide m-Chlorophenylhydrazone, FCCP, and Antimycin A. These compounds lead to a cascade of effects within the mitochondria, including alterations in ATP production and reactive oxygen species (ROS) levels, which are known to influence mitochondrial dynamics. For instance, FCCP, as a protonophore, dissipates the mitochondrial membrane potential, fundamentally altering the mitochondrial environment, thereby impacting TMEM11's function.

Additionally, compounds like Resveratrol and D-α-Tocopheryl Succinate, though not directly targeting mitochondrial dynamics, influence mitochondrial biogenesis and the overall health of mitochondria. This, in turn, could have a downstream effect on TMEM11's role in mitochondrial morphogenesis. By altering the signaling pathways and the mitochondrial landscape, these inhibitors indirectly modulate the activity and function of TMEM11. In summary, TMEM11 inhibitors encompass a diverse range of chemicals that influence mitochondrial dynamics, energy metabolism, and biogenesis.