QW-5-70

QW-5-70 binds directly to the colchicine-binding site on purified tubulin with a K_d of 10.8 μM, inhibits tubulin polymerization, and disrupts microtubule networks^[1][2].
QW-5-70 exhibits subnanomolar antiproliferative activity in parental and drug-resistant BE2C/VCR, PC-3/TxR, NB, and prostate cancer cells, and evades P-glycoprotein-mediated efflux^[1].
QW-5-70 significantly reduces colony formation, impairs migration, induces G2/M cell cycle arrest and mitochondrial apoptosis in parental and drug-resistant BE2C/VCR, PC-3/TxR, NB, and prostate cancer cells. QW-5-70 enhances apoptosis and reduces clonogenic survival when combined with DFMO (HY-B0744) or MLN8237 (HY-10971)^[1][2].
QW-5-70 inhibits viability of SK-N-BE(2)-C, BE2C/VCR, PC-3, and PC-3/TxR cells with IC₅₀ values of 1.0 nM, 1.8 nM, 1.5 nM, and 1.5 nM, respectively^[2].
QW-5-70 (0.1-15 μM) destabilizes microtubules in SK-N-BE(2)-C, NB-1691, and PC-3 cells, as shown by reduced polymerized β-tubulin and increased soluble β-tubulin levels^[2].
QW-5-70 (2-5 nM) induces G2/M phase cell cycle arrest in SK-N-BE(2)-C, NB-1691, and PC-3/TxR cells, triggers mitotic arrest in BE2C/VCR and PC-3/TxR cells with increased p-Histone H3 (Ser10), cyclin B1, and p-CDK1 (Thr161) levels, and induces apoptosis in BE2C/VCR and PC-3/TxR cells, as evidenced by elevated cleaved caspase-3, cleaved PARP, and phosphorylated BCL2 (Ser70) levels, and reduced total BCL2 expression^[2].

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