NBM-T-BMX-OS01

NBM-T-BMX-OS01 (0-10 μM; 0-72 h) exerts antiproliferative effects on A549 cells and sensitizes A549 cells to 10 μM Cisplatin (HY-17394)^[1].
NBM-T-BMX-OS01 (1 μM; 14 days) enhances the Cisplatin-induced reduction in clonogenic survival rate of A549 cells^[1].
NBM-T-BMX-OS01 (1 μM; 24 h) enhances Cisplatin-induced apoptosis and SubG1 cell cycle arrest in A549 cells^[1].
NBM-T-BMX-OS01 (1 μM) enhances Cisplatin-induced oxidative stress in A549 cells by increasing the production of intracellular and mitochondrial reactive oxygen species (ROS) and reducing the activity of mitochondrial complex I^[1].
NBM-T-BMX-OS01 (1 μM) alone inhibits the phosphorylation of Akt in A549 cells; when combined with Cisplatin, it suppresses Cisplatin-induced phosphorylation of ERK and Akt, while activating AMPK^[1].
NBM-T-BMX-OS01 (1-10 μM; 24 h) inhibits vascular endothelial growth factor (VEGF)-induced viability and proliferation of human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner^[2].
NBM-T-BMX-OS01 (1-5 μM; 16 h) inhibits VEGF-induced migration and capillary tube formation of HUVECs in a concentration-dependent manner^[2].
NBM-T-BMX-OS01 (1-5 μM; 30 min pre-treatment followed by 5 or 30 min VEGF stimulation) concentration-dependently inhibits VEGF-induced activation of VEGFR2 and the activation of downstream signaling kinases (Src, FAK, Akt, ERK1/2) in HUVECs^[2].
NBM-T-BMX-OS01 (1-5 μM; 24 h) modulates the levels of cell cycle regulatory proteins in HUVECs, upregulating p21_cip/Waf1 and downregulating cyclinD1, CDK4 and survivin^[2].
NBM-T-BMX-OS01 (1-10 μM; 24-28 h) reduces the cell viability of HCT116 in a time- and concentration-dependent manner and inhibits serum-induced proliferation^[2].
NBM-T-BMX-OS01 (1-5 μM; 24 h) regulates the levels of cell cycle regulatory proteins in HCT116, upregulating p21_cip/Waf1 and downregulating survivin^[2].

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