BSS-Et

BSS-Et (30 μM; 1.5 h) induces reactive oxygen species generation in hypoxic 4T1 mouse breast cancer cells upon 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) reduces viability of hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) induces DNA double-strand breaks in hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) reduces mitochondrial membrane potential and induces apoptosis in hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) induces mitochondrial permeability transition pore opening and apoptosis in hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) induces apoptosis in 40.2% of hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min^[1].
BSS-Et (30 μM; 2 h) increases γ-H2AX (1.6-fold) and Cleaved Caspase-3 (1.3-fold) expression in hypoxic 4T1 mouse breast cancer cells when combined with 808 nm laser irradiation at 1.5 W·cm⁻² for 5 min, indicating enhanced DNA damage and apoptosis^[1].

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