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Pifithrin-α (PFTα),63208-82-2,IC-0228497
Pifithrin-α(PFT-α) is a p53 inhibitor[1]. Pifithrin-α widely used in neuroscience to block neuronal apoptotic cell death[2]. Pifithrin-α is also a potent stimulant of aryl hydrocarbon receptor (AhR) [3]. Pifithrin-α (10 µM;48h) reduces meth-induced degeneration of dopaminergic neurons[4]. Treatment with Pifithrin-α(1 µM; 12-24 h) prevents ROS formation in hMp84-overexpressing A375 cells[5]. The IC50 of TPT for HepG2 cells after 10 µµ PFTα pretreated(1-100 µM; 2 h), was 4.8 to 14.4 folds lower than the effect of TPT alone. PFTα decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells[6]. Pifithrin-α (2 mg/kg; i.v) reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21WAF[7].Delayed Pifithrin-α (0.4µg/µl; 20µl; i.c.v + 0.2mg/100gm, i.p; twice a day for three days) treatment improved locomotor behavior in stroke rats[8]. Pifithrin-α reduced dopaminergic neurodegeneration in animal models of Parkinson s disease(10 µg)[9], prevented cell death of dopaminergic transplants in 6-OHDA-lesioned rats(2 mg/kg/day; i.p ; 5 days)[10], improved the survival of neuroprogenitor cells in subventricular zone of stroke rats, and reduced traumatic brain injury[11].
Pifithrin-α(PFT-α) is a p53 inhibitor[1]. Pifithrin-α widely used in neuroscience to block neuronal apoptotic cell death[2]. Pifithrin-α is also a potent stimulant of aryl hydrocarbon receptor (AhR) [3]. Pifithrin-α (10 µM;48h) reduces meth-induced degeneration of dopaminergic neurons[4]. Treatment with Pifithrin-α(1 µM; 12-24 h) prevents ROS formation in hMp84-overexpressing A375 cells[5]. The IC50 of TPT for HepG2 cells after 10 µµ PFTα pretreated(1-100 µM; 2 h), was 4.8 to 14.4 folds lower than the effect of TPT alone. PFTα decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells[6]. Pifithrin-α (2 mg/kg; i.v) reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21WAF[7].Delayed Pifithrin-α (0.4µg/µl; 20µl; i.c.v + 0.2mg/100gm, i.p; twice a day for three days) treatment improved locomotor behavior in stroke rats[8]. Pifithrin-α reduced dopaminergic neurodegeneration in animal models of Parkinson s disease(10 µg)[9], prevented cell death of dopaminergic transplants in 6-OHDA-lesioned rats(2 mg/kg/day; i.p ; 5 days)[10], improved the survival of neuroprogenitor cells in subventricular zone of stroke rats, and reduced traumatic brain injury[11].
