IRS1

IRS1 undergoes complete ROS-induced oxidation within 420 min in PBS solution, accompanied by a structural transition from nanoparticles to nanofibers, enabling covalent binding with cysteine; it forms micelles in aqueous solution with a critical micelle concentration of 29.0 μM^[1].
IRS1 (0-400 μM; 72 h) selectively inhibits integrin-overexpressing tumor cells (MuM-2B, HeLa, MDA-MB-231), exhibits extremely low toxicity to normal cells (ARPE-19, 293T), and shows weak activity against integrin-low-expressing OCM-1A cells^[1].
IRS1 (25-200 μM; 24 h) preferentially accumulates at the plasma membrane of MuM-2B cells, forming a dense fibrous network and impairing membrane integrity^[1].
IRS1 (0-100 μM; 24 h) impairs the migration and invasion abilities of MuM-2B cells in a dose-dependent manner, with the inhibitory effect reaching its peak at the concentration of 100 μM^[1].
IRS1 (0-400 μM; 0-72 h) effectively penetrates MuM-2B 3D spheroids and inhibits their growth in a dose-dependent manner, while it exerts minimal effects on integrin-low-expressing ARPE-19 spheroids after 72 h of incubation^[1].
IRS1 (0-200 μM; 24 h) induces apoptosis in MuM-2B cells via activating the extrinsic caspase-8-mediated pathway, and upregulates the expression of DR4 and DR5 in MuM-2B cells^[1].
IRS1 (200 μM; 24 h) triggers a robust transcriptomic response in MuM-2B cells, activates death receptor and apoptosis pathways, and simultaneously inhibits metabolic and DNA replication pathways^[1].

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