TrxR1-IN-3

TrxR1-IN-3 (Compound 6M) (Gradient concentrations; 72 h) potently inhibits the proliferation of MCF7, MDA-MB-231, MDA-MB-468, and BT474 breast cancer cells with IC₅₀ values ranging from 0.94 μM to 2.53 μM, and exhibits low cytotoxicity toward normal MCF-10A breast epithelial cells with a selectivity index exceeding 10 for all tested cancer cell lines^[1].
TrxR1-IN-3 (Gradient concentrations; 2 h) potently inhibits purified rat TrxR1 activity with an IC₅₀ of 1.19 μM, primarily targeting the Sec-498 residue, as evidenced by its drastically reduced inhibitory potency (IC₅₀ > 10 μM) against the human U498C TrxR1 mutant^[1].
TrxR1-IN-3 (1-10 μM) selectively inhibits cellular TrxR activity in MCF7 cells with an IC₅₀ of 2.99 μM, while having minimal inhibitory effects on GR and GPx even at 10 μM^[1].
TrxR1-IN-3 (1-5 μM; 24 h) dose-dependently inhibits intracellular TrxR activity in MCF7 and MDA-MB-231 breast cancer cells^[1].
TrxR1-IN-3 (1-5 μM; 24 h) dose-dependently reduces the clonogenic capacity of MCF7 and MDA-MB-231 breast cancer cells^[1].
TrxR1-IN-3 (3-5 μM; 24 h) dose-dependently induces apoptosis in MCF7 and MDA-MB-231 breast cancer cells^[1].
TrxR1-IN-3 (3-5 μM) induces caspase-dependent apoptosis in MCF7 and MDA-MB-231 breast cancer cells via activation of both extrinsic and intrinsic pathways, as evidenced by cleavage of caspase-8, caspase-9, and PARP, with this effect blocked by pre-incubation with the pan-caspase inhibitor Z-VAD^[1].
TrxR1-IN-3 (1-5 μM; 24 h) dose-dependently elevates intracellular ROS levels in MCF7 and MDA-MB-231 breast cancer cells^[1].

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