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Mito-LND blocks lung cancer growth, migration, and invasion. Mito-LND inhibits cell growth of H2030BrM3 and A549 cells with IC50 values of 0.74 μM and 0.69 μM, respectively[1].Mito-LND inhibits mitochondrial complex I and II activities with IC50 values of 1.2 μM and 2.4 μM, respectively in H2030BrM3 cells[1]. Mito-LND (1 μM) increases ROS generation in H2030BrM3 lung cancer cells. Mito-LND potently induces mitochondrial ROS generation in H2030BrM3 lung cancer cells[1].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[1].

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[1]. Mito-LND also decreases the rate of growth of A549 tumor xenografts[1].Mito-LND treatment shows a marked decrease in lung cancer brain metastasis in NOD/SCID mice bearing H2030BrM3 cells[1].

[1]. Gang Cheng, et al. Targeting lonidamine to mitochondria mitigates lung tumorigenesis and brain metastasis. Nat Commun. 2019 May 17;10(1):2205.

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