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Mitochondrial metabolism compounds act on the respiratory chain, energy coupling and redox balance of mitochondria. In 1961 Mitchell proposed that phosphorylation is coupled to electron transfer through a chemiosmotic mechanism. In this model a proton gradient across the inner membrane drives adenosine triphosphate (ATP) synthase in oxidative phosphorylation (OXPHOS). Rotenone inhibits complex I of the electron transport chain, and oligomycin A blocks ATP synthase. Gboxin, reported in 2019, is an OXPHOS inhibitor that suppresses the growth of glioblastoma cells. Mito-TEMPO is a mitochondria-targeted antioxidant that scavenges superoxide in the matrix. Meldonium inhibits carnitine biosynthesis and so limits fatty acid transport into mitochondria. The set is mixed and also lists compounds with secondary mitochondrial links, such as the fluoroquinolone ciprofloxacin.
CDPPB is a selective, orally active allosteric modulator of the metabotropic glutamate receptor 5 (mGluR5). It enhances AKT and ERK1/2 signaling and upregulates BDNF mRNA expression. CDPPB also inhibits caspase-3 activation and mitigates mitochondrial dysfunction, demonstrating therapeutic potential in improving cognitive impairment, depression, and Huntington’s disease.
Mitochondrial fusion promoter M1 is a mitochondrial metabolism modulator that enhances mitochondrial function and promotes cellular respiration. This compound plays a critical role in improving energy production by supporting mitochondrial dynamics, which may mitigate cardiac and cerebral damage in models of ischemia/reperfusion injury. Mitochondrial fusion promoter M1 is a valuable tool for research into mitochondrial biology and the development of therapeutic strategies for cardiac and neurological disorders.
