GSTO1-IN-3 is a potent inhibitor of GSTO1-1, with an IC50 value of 0.11 μM, and exhibits selectivity towards GSTO2-2, GSTA1-1, and GSTP1-1 (IC50> 100 μM). It enhances the cytotoxic effects of Cisplatin on human breast cancer cells and inhibits IL-1β release in mouse bone marrow-derived macrophages (BMDM). Additionally, GSTO1-IN-3 reduces inflammation in mice and is applicable for research related to breast cancer and inflammation.

GSTO1-1:0.11 μM

GSTO1-IN-3 (compound 5C-1) demonstrates favorable in vitro safety, as it shows no thiol reactivity in ALARM NMR experiments and lacks mutagenicity in Ames tests with *Salmonella typhimurium* strains TA98 and TA100 at concentrations up to 2 mg/mL. It exhibits greater stability in human liver microsomes compared to mouse microsomes. GSTO1-IN-3 forms a covalent bond with the Cys32 of GSTO1-1, with an inhibition efficiency constant (kᵢₙₐcₜ/Kᵢ) of 3.4 × 10⁴ M⁻¹s⁻¹. At a concentration of 5 μM, GSTO1-IN-3 reduces IL-1β release by 59.2% in mouse bone marrow-derived macrophages (BMDM). Additionally, at 5-50 μM for 24 hours, it exhibits a synergistic effect with Cisplatin, significantly enhancing cytotoxicity in a concentration-dependent manner against human breast cancer MDA-MB-231 cells.

GSTO1-IN-3, when administered intraperitoneally at a dose of 30 mg/kg, 30 minutes prior to LPS injection, can mitigate the inflammation induced by lipopolysaccharide (LPS) in mice.