Surprisingly, a single application of CeNPs at P15 reduced the number of TUNEL+ profiles by half for up to 7 dpi. Because a large percentage of rod cells in the P23H-1 rat retina are destined to die early and fast, we hypothesize that CeNPs are delaying the initiation of the apoptotic death of these rod cells. Because CeNPs possess catalytic ROS scavenging activities, we hypothesize that CeNPs are able to maintain the redox balance of these ��sick�� cells for a longer period. The catalytic activity of CeNPs continued for the next 14 days, albeit at a much reduced level. We observed small although not statistically significant reduction even at 21 dpi. From this study, we conclude that the pharmacodynamics of CeNPs is maximal between 3 and 7 days post injection in the P23H-1 rats at the dosage applied and the catalytic activity of CeNPs becomes limiting at 14 dpi. An alternative, but not mutually exclusive, interpretation is that the smaller reduction in cell death index at the later time points reflects a different cause of rod cell death that cannot be alleviated by the ROS scavenging activity of CeNPs. Furthermore, to determine if the dose of CeNPs is limiting, we can increase the initial dosage or apply a second dose 7 days after the first dose and perform the TUNEL assay at equivalent time intervals. Even though we have demonstrated that 94% of injected CeNPs are taken up by retinal cells within one hour of intravitreal injection, it is still unknown how quickly cellular effects can be detected after CeNPs application in vivo. In primary rat retinal cell cultures, the earliest effect of CeNPs mediated reduction of ROS induced by hydrogen peroxide treatment was found to be at 12 hours post incubation and not at 30 min. Using this cell death index paradigm, we are confident that one can determine when CeNPs start to exert their catalytic activity after intravitreal injection. Renal cell carcinoma is the most common malignancy of the kidney. It��s the seventh most common CT99021 cancer in males and the ninth most common cancer in females, with a worldwide incidence of over 210,000 cases, resulting in 102,000 deaths per year. RCC is refractory to traditional cytotoxic chemotherapy and radiotherapy. Recently, treatment options for advanced RCC have been expanded by the approval of molecularly-targeted LY2157299 clinical trial inhibitors of protein kinases. An important molecular target for RCC is the mechanistic target of rapamycin, which is a pivotal regulator of cell proliferation and survival.