Opitor-0

Opitor-0 (50 μM; 6-24 h) induces mitochondrial fragmentation in MCF10A, MCF10AT1 and MCF10CA1h breast cells; it selectively reduces mitochondrial respiratory efficiency and ATP-coupled respiration in metastatic MCF10CA1h and MCF10CA1a breast cancer cells^[1].
Opitor-0 (1-50 μM; 5 h) induces concentration-dependent mitochondrial fragmentation in mtYFP-expressing MEF cells and HeLa cells^[2].
Opitor-0 (50 μM; 20 h) selectively impairs the migratory capacity of metastatic MCF10CA1h and MCF10CA1a breast cancer cells, without affecting non-metastatic MCF10A and MCF10AT1 breast cancer cells^[1].
Opitor-0 (50 μM; 24 h) selectively reduces the proliferative capacity of highly metastatic MCF10CA1a breast cancer cells, without affecting non-metastatic MCF10A, MCF10AT1 or moderately metastatic MCF10CA1h breast cancer cells^[1].
Opitor-0 (50 μM) does not induce cell death in any tested breast cancer cell lines after 24 h of treatment, but causes a small yet significant increase in the level of cell death in metastatic MCF10CA1h and MCF10CA1a breast cancer cells after 72 h of treatment, without affecting non-metastatic MCF10A and MCF10AT1 breast cancer cells^[1].
Opitor-0 potently inhibits the GTPase activity of wild-type mini-rOpa1, with an IC₅₀ of 3.0 μM^[2].
Opitor-0 (25-125 μM; 30 min) potently enhances cBID-mediated cytochrome c release from purified mouse liver mitochondria^[2].
Opitor-0 (5-100 μM; administered for 5 h after 12 h of preincubation with 10-20 μM ABT-737) exerts a strong synergistic effect with the Bcl-2 inhibitor ABT-737 (HY-50907) to induce caspase-dependent apoptosis in MDA-MB-231 triple-negative breast cancer cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.