BEPP hydrochloride

BEPP (1-100 μM; 1-5 days) hydrochloride potently inhibits the growth of MEF/PKR ^(+/+) cells with an IC₅₀ of 1.4 μM, and its efficacy is 10-fold that against MEF/PKR ^(-/-) cells^[1].
BEPP (2.5-10 μM; 72 h) hydrochloride induces apoptosis-related caspase-3 cleavage, upregulation of BAX expression, and downregulation of Bcl-2 expression in MEF/PKR ^(+/+) cells, but exerts no such effects on MEF/PKR ^(-/-) cells^[1].
BEPP (2.5-10 μM; 72 h) hydrochloride activates the PKR pathway in MEF/PKR ^(+/+) cells, increases the levels of phosphorylated PKR and eIF2α, reduces the level of cyclin D1, and elevates the level of phosphorylated AKT, but fails to activate eIF2α in MEF/PKR ^(-/-) cells^[1].
BEPP (2.5-10 μM; 24-72 h) hydrochloride induces apoptosis in MEF/PKR ^(+/+) cells in a dose- and time-dependent manner, while MEF/PKR ^(-/-) cells show no significant apoptotic response^[1].
BEPP (0.3-100 μM; 72 h) hydrochloride potently inhibits the growth of H226B human lung cancer cells overexpressing PKR, with an IC₅₀ of 4.6 μM, and its inhibitory activity is stronger than that against H460, A549, H1299 and HBE cells^[1].
BEPP (7.5 μM; 48 h pretreatment) hydrochloride reduces the replication level of vaccinia virus (vSP) in HeLa cells by approximately 100-fold, and induces activation of the PKR pathway, as evidenced by increased levels of phosphorylated PKR and eIF2α^[1].

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