TrxR-IN-4

TrxR-IN-4 (Compound 1b) (0.125-2 μM) potently inhibits purified rat liver TrxR with an IC₅₀ of 0.37 μM^[1].
TrxR-IN-4 (72 h) potently inhibits the proliferation of HepG2, SMMC-7721, and Hep3B human hepatocellular carcinoma cells with IC₅₀ values of 5.40 μM, 10.05 μM, and 10.89 μM respectively, shows lower potency against MCF-7 and HT-29 cancer cells, and exhibits selective toxicity toward tumor cells over normal LO₂ liver cells^[1].
TrxR-IN-4 (0.5-10 μM; 24 h) inhibits intracellular TrxR activity in HepG2 human hepatocellular carcinoma cells with an IC₅₀ of 6.51 μM, and dose-dependently reduces TrxR mRNA and protein expression^[1].
TrxR-IN-4 (2.5-10 μM; 24-72 h) induces G2/M phase cell cycle arrest in HepG2 human hepatocellular carcinoma cells after 72 h of treatment, and reduces the expression of Cyclin A and CDK2 proteins at 10 μM after 24 h of treatment^[1].
TrxR-IN-4 (2.5-10 μM; 24-72 h) dose-dependently induces apoptosis in HepG2 human hepatocellular carcinoma cells after 72 h of treatment, and upregulates pro-apoptotic proteins AIF, cytochrome c, and cleaved-PARP/PARP after 24 h of treatment^[1].
TrxR-IN-4 (2.5-10 μM; 24 h) dose-dependently elevates reactive oxygen species levels, increases ROS-endoplasmic reticulum colocalization, and activates endoplasmic reticulum stress via upregulation of CHOP and Calnexin in HepG2 human hepatocellular carcinoma cells^[1].

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