Tubulin polymerization-IN-82

Tubulin polymerization-IN-82 (Compound 9n) (0.039-2.5 μM, 72 h) displays antiproliferative activities against different cells with IC₅₀s of 0.09 μM (HepG-2), 0.25 μM (NCI-H460) , 0.20 μM (HCT-116) and 0.18 μM (SK-OV-3)^[1].

Tubulin polymerization-IN-82 (0.039-2.5 μM, 72 h) has antiproliferative effect on drug-resistant cells with IC₅₀s of 0.29 μM (A549/CDDP), 0.45 μM (A549/ Paclitaxel) and 0.51 μM (MCF-7/DOX)^[1].

Tubulin polymerization-IN-82 (1.25-20 μM, 5-65 min) inhibits tubulin polymerization of purified tubulin, with an IC₅₀ of 3.56 μM^[1].

Tubulin polymerization-IN-82 (1.25 μM, 2.5 μM, 24 h) induces apoptosis of HepG-2 cells through a mitochondrial-mediated pathway and endoplasmic reticulum stress , disrupts the microtubule network in HepG-2 cells ^[1].

Tubulin polymerization-IN-82 (1.25 μM, 2.5 μM, 24 h) causes cell cycle arrest at the G2/M phase of HepG-2 cells in a concentration-dependent manner^[1].

Tubulin polymerization-IN-82 (1.25 μM, 2.5 μM, 24 h) decreases the MMP of HepG-2 cells, induces ROS generation^[1].

Tubulin polymerization-IN-82 (1.25 μM, 2.5 μM, 24 h) enhances intracellular Ca2+ levels and increases the expression levels of p-PERK, p-eIF2α, and CHOP in HepG-2 cells^[1].

Tubulin polymerization-IN-82 (1.25 μM, 2.5 μM, 24 h) inhibits the cell colony formation, and inhibits cell migration and invasion of HepG-2 cells^[1].

Tubulin polymerization-IN-82 was hydrolyzed by esterase after exposure to carboxylesterase for 4 h^[1].

Tubulin polymerization-IN-82 remains stable at 24, 48 or 72 h under both PBS (pH = 7.4) and DMEM containing 1 % DMF^[1].

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