Nur77 modulator 5

Nur77 modulator 5 (Compound 6K) binds directly to the Nur77 ligand-binding domain with an equilibrium dissociation constant (K_D) of 0.62 μM, forming stable hydrogen bonds, π-π stacking, and hydrophobic interactions with key residues in the binding pocket^[1].
Nur77 modulator 5 (48 h) potently inhibits the growth of multiple human cancer cell lines (most potently HGC-27 gastric cancer cells with an IC₅₀ of 0.53 μM) and exhibits minimal cytotoxicity toward normal GES-1 gastric epithelial cells (IC₅₀ = 24.33 μM)^[1].
Nur77 modulator 5 (24-48 h) reduces viability of HGC-27 and AGS gastric cancer cells in a time-dependent manner, with greater potency against HGC-27 cells (IC₅₀ = 1.51 μM) than AGS cells (IC₅₀ = 3.40 μM)^[1].
Nur77 modulator 5 (2.5-5 μM; ~2 weeks) inhibits clonogenic survival of HGC-27 and AGS gastric cancer cells in a concentration-dependent manner, with more pronounced effects in HGC-27 cells^[1].
Nur77 modulator 5 (4 μM; 5 h) induces prominent cytoplasmic vacuolization in HGC-27 and AGS gastric cancer cells^[1].
Nur77 modulator 5 (1.25-5 μM; 24 h) induces apoptosis in HGC-27 gastric cancer cells^[1].
Nur77 modulator 5 (0.625-4 μM; 5 h-2 weeks) induces lysosomal dysfunction and impaired autophagic flux in HGC-27 gastric cancer cells, as evidenced by increased LC3-II/p62 levels, reduced Lyso-Tracker fluorescence, and attenuation of vacuolization and growth inhibition by Bafilomycin A1 (HY-100558)^[1].
Nur77 modulator 5 (0.625-4 μM; 12 h-2 weeks) reduces Nur77 protein levels in HGC-27 gastric cancer cells in a dose-dependent manner, and Nur77 overexpression attenuates Nur77 modulator 5-induced lysosomal dysfunction, apoptotic signaling, and growth inhibition^[1].

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