WR-1065 dihydrochloride can protect normal tissues from the toxic effects of certain cancer drugs and activate p53 through a JNK-dependent signaling pathway. IC50 & Target: p53^[1] In Vitro: The DNA-binding activity is increased in a WR-1065 dihydrochloride (WR-1065) concentration-dependent manner. Cells treated with 1 mM WR-1065 dihydrochloride for 24 h reveal that all of the p53-induced genes analyzed are transactivated following WR-1065 dihydrochloride treatment, in a p53-dependent manner. Significantly, treatment with WR-1065 dihydrochloride leads to a 3-fold increase in luciferase expression driven by AP-1, and a 5-fold increase when this reporter gene is driven by NF-κB, when these values are normalized to the level of the cotransfected β-galactosidase gene^[2]. In Vivo: The results show that wR-1065 dihydrochloride (WR-1065) attenuates the severity of 6-OHDA-induced catalepsy (P<0.001) when compare with 6-OHDA-lesioned rats. Also it has been observed that WR-1065 dihydrochloride improves catalepsy in dose dependent manner (P<0.001). Pretreatment with three different doses of WR-1065 dihydrochloride (20, 40 and 80 μg/2 μL/rat) for 3 days before 6-OHDA administration, significantly (P<0.001) elevates SOD activity and restores it to normal range compare with 6-OHDA lesioned rats^[3].