Xylopine is an aporphine alkaloid with cytotoxic activity on cancer cells. Xylopine induces oxidative stress, causes G2/M cell cycle arrest and apoptosis in cancer cells[1].

Xylopine (3.5 μM-14 μM; 24-48 hours) displays potent cytotoxicity in a time- and does-depenpent manner[1].Xylopine (72 h) has cytotoxic activity, with IC50 values ranging from 6.4 to 26.6 μM in eight different cancer cell lines (MCF7, HCT116, HepG2, SCC-9, HSC-3, HL-60, K-562, and B16-F10)[1].Xylopine (3.5 μM-14 μM; 24-48 hours) causes cell cycle block at the phase G2/M, which is followed by internucleosomal DNA fragmentation[1].Xylopine (3.5 μM-14 μM; 24-48 hours) significantly increases the early and late apoptosis, induces mitochondrial depolarization, and increases caspase-3 activation[1].Xylopine also causes an increase in the production of reactive oxygen/nitrogen species (ROS/RNS), including hydrogen peroxide and nitric oxide, but not superoxide anion, and reduces glutathione levels are decreased in Xylopine-treated HCT116 cells[1].HCT116 cells[1]3.5 μM, 7 μM, and 14 μM 24 hours, 48 hoursInduced G2/M phase arrest.HCT116 cells[1]3.5 μM, 7 μM, and 14 μM 24 hours, 48 hoursSignificantly increased the early and late apoptosis.

[1]. Luciano de Souza Santos, et al. Xylopine Induces Oxidative Stress and Causes G 2/M Phase Arrest, Triggering Caspase-Mediated Apoptosis by p53-Independent Pathway in HCT116 Cells. Oxid Med Cell Longev. 2017;2017:7126872.