ZK-Thiazolidinone

ZK-Thiazolidinone (4 d) inhibits the proliferation of various human and mouse tumor cell lines in vitro, with an IC₅₀ value ranging from 0.2 to 1.3 μM^[1].
Treatment of HeLa S3 cells with ZK-Thiazolidinone (1 μM; 12 h-48 h) for 12 h induces reversible G₂/M cell cycle arrest, whereas prolonged treatment (48 h) leads to cell death; treatment of MCF7 cells with this compound for 24 h under concentration-increasing conditions also induces G₂/M arrest^[1].
ZK-Thiazolidinone (1 μM; 12 h) induces spindle assembly checkpoint-dependent prometaphase arrest and generates monopolar spindles in HeLa S3 cells^[1].
ZK-Thiazolidinone (1 μM; 12 h) disrupts centrosome maturation in HeLa S3 cells by inhibiting the recruitment of γ-tubulin and Aurora A to centrosomes, without altering the localization and related protein levels of Eg5^[1].
ZK-Thiazolidinone (1 μM; 0-120 min) disrupts the maintenance of bipolar spindles in metaphase-synchronized HeLa S3 cells, thereby causing spindle collapse into a monopolar spindle array within 120 min^[1].
ZK-Thiazolidinone (1 μM; 10-12 h) impairs the stability of K-fibers in HeLa S3 cells and inhibits the separation of sister chromatid arms^[1].
ZK-Thiazolidinone (1 μM; 12 h) induces the spreading of Plk1 and PICH along chromatid arms in HeLa S3 cells, and the redistribution of Plk1 requires the involvement of PICH^[1].
ZK-Thiazolidinone (1 μM) induces cytokinesis failure in HeLa S3 cells in vitro in a mitotic stage-dependent manner by inhibiting the localization of RhoA and ECT2 to their respective cytokinesis-related sites^[1].
ZK-Thiazolidinone (1 μM; 30 min) disrupts the central spindle structure in HeLa cells, inhibits Plk1-dependent phosphorylation and localization of PRC1 and Mklp2, and reduces the interaction between Plk1 and PRC1 in anaphase cells, without altering Aurora B-dependent Mklp1 phosphorylation^[1].

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