TH588 hydrochloride

TH588 hydrochloride (1-2 µM; 72 h) reduces viability of doxycycline-induced A2780 Pol δ replacement cells, with significantly greater cytotoxicity in cells expressing the error-prone or double mutant Pol δ variants^[1].
TH588 hydrochloride (1 µM; 24 h) induces cleaved PARP signalling in doxycycline-induced A2780 Pol δ replacement cells, with significantly higher levels in cells expressing the error-prone Pol δ variant^[1].
TH588 hydrochloride (2 µM; 24 h) induces caspase-mediated apoptosis in doxycycline-induced A2780 Pol δ replacement cells, with significantly higher apoptosis in cells expressing the error-prone Pol δ variant^[1].
TH588 hydrochloride (5 µM; 16 h) triggers mitotic DNA replication in U2OS cells when pre-incubated with RO3306, resulting in a significant increase in mitotic cells with EdU foci^[1].
TH588 hydrochloride (0.1-10 µM; 72 h) reduces viability of U2OS cells in a dose-dependent manner, and this cytotoxicity is completely prevented by co-treatment with reversine^[1].
TH588 hydrochloride (2-6 μM; 5 days) concentration-dependently inhibits the growth of human pancreatic cancer Panc-1 cells over 5 days, and this effect is independent of oxidative stress^[2].
TH588 hydrochloride (1-3 μM; 7 days) significantly enhances H₂O₂-induced growth inhibition of human pancreatic cancer Panc-1 cells over 7 days, despite having no effect on cell growth when used alone^[2].
TH588 hydrochloride (1-3 μM; 5 days) significantly enhances doxorubicin-induced growth inhibition of human pancreatic cancer MIAPaCa-2 cells over 5 days^[2].
TH588 hydrochloride (1-3 μM; 5 days) significantly enhances PEITC-induced growth inhibition of human pancreatic cancer MIAPaCa-2 cells over 5 days, with the combination showing greater efficacy than other ROS inducer-TH588 pairings^[2].
TH588 hydrochloride (2 μM; 2 days), combined with 4 μM PEITC, induces caspase-dependent cell death in human pancreatic cancer MIAPaCa-2 cells over 2 days^[2].
TH588 hydrochloride (0.2-0.6 μM; 5 days) significantly enhances PEITC-induced growth inhibition of human leukemia NB4 cells over 5 days, regardless of relatively low MTH1 mRNA expression^[2].
TH588 hydrochloride (0.2-0.6 μM; 5 days) significantly enhances PEITC-induced growth inhibition of human lymphoma BALM3 cells over 5 days^[2].
TH588 hydrochloride (1-2 μM; 56 hours) induces nuclear formation of 8-oxo-dG and pH2AX (markers of oxidative DNA damage) in human pancreatic cancer MIAPaCa-2 cells after 56 hours of incubation^[2].
TH588 hydrochloride (0.4 μM; 56 hours), combined with 2 μM PEITC, cooperatively induces nuclear formation of 8-oxo-dG and γH2AX foci in human pancreatic cancer MIAPaCa-2 cells after 56 hours of incubation^[2].
TH588 hydrochloride (1-8 µM; 2 hours) concentration-dependently disrupts centrosome separation, spindle bipolarity, and chromosome congression in unsynchronized mitotic H460 human lung cancer cells, with 4 µM inducing monopolar spindles in over 50% of mitotic cells^[3].
TH588 hydrochloride (4-6 µM; 24 hours) induces G2/M phase cell cycle arrest in H460 human lung cancer cells, with 4 µM increasing G2/M phase cells to ~42% and 6 µM increasing G2/M phase cells to ~35%^[3].
TH588 hydrochloride (4-7 µM; 48 total hours) concentration-dependently induces G1 arrest and prevents cell cycle re-entry in H460 human lung cancer cells, with 7 µM causing G1 arrest in ~70% of cells^[3].
TH588 hydrochloride (6 µM; 48 total hours) shows that TP53 and USP28 are required for TH588-induced G₁ arrest in H460 human lung cancer cells, with TP53 knockout reducing 6 µM TH588-induced G₁ arrest from ~40% to ~10%^[3].
TH588 hydrochloride (2-8 µM; 24 hours) concentration-dependently increases p53 levels in H460 human lung cancer cells, and this activation is dependent on USP28, as USP28-knockout clones show no p53 induction^[3].

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