Mito-LND (Mito-Lonidamine) is an orally active and mitochondria-targeted inhibitor of oxidative phosphorylation (OXPHOS). Mito-LND inhibits mitochondrial bioenergetics, stimulates the formation of reactive oxygen species , and induces autophagic cell death in lung cancer cells. In Vitro Mito-LND blocks lung cancer growth, migration, and invasion. Mito-LND inhibits cell growth of H2030BrM3 and A549 cells with IC 50 values of 0.74 µM and 0.69 µM, respectively. Mito-LND inhibits mitochondrial complex I and II activities with IC 50 values of 1.2 µM and 2.4 µM, respectively in H2030BrM3 cells. Mito-LND (1 µM) increases ROS generation in H2030BrM3 lung cancer cells. Mito-LND potently induces mitochondrial ROS generation in H2030BrM3 lung cancer cells. Mito-LND (2 µM) decreases the levels of phosphorylated AKT. Mito-LND also decreases the phosphorylation of P70S6K and other energy-sensing proteins in both the parental and metastatic lung cancer cell lines, indicating that Mito-LND specifically downregulates mTOR signaling. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Mito-LND (7.5 µmol/kg; oral gavage; 5 days per week; for 3 consecutive weeks) treatment markedly enhanced potency against both lung cancer progression and metastasis . Mito-LND also decreases the rate of growth of A549 tumor xenografts . Mito-LND treatment shows a marked decrease in lung cancer brain metastasis in NOD/SCID mice bearing H2030BrM3 cells . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Athymic nude mice (5 weeks) injected with H2030BrM3 cells Dosage: 7.5 µmol/kg Administration: Oral gavage; 5 days per week; for 3 consecutive weeks Result: Significantly decreased tumor progression. Form:Solid