P53R3 is a potent p53 reactivator and restores sequence-specific DNA binding of p53 hot spot mutants, including p53 R175H , p53 R248W and p53 R273H. P53R3 induces p53-dependent antiproliferative effects with much higher specificity than PRIMA-1. P53R3 enhances the recruitment of wild-type p53 and p53 M237I to several target gene promoters. P53R3 strongly enhances the mRNA, total protein and cell surface expression of the death receptor death receptor 5 (DR5). P53R3 is used for cancer research. In Vitro P53R3 (10 μg/ml; 24 hours; in the absence or presence of the unlabelled p53 consensus oligonucleotide) restores p53-specific DNA binding activity to p53 R273H (a DNA contact mutant) and p53R175H (a structural mutant) in WiDr colon tumour cells harbouring p53 R273H and KLE cells with p53R175H. P53R3 (1-33 μg/ml; 24 hours) inhibits the proliferation of the LN-308 sublines expressing mutant p53 plasmids in a p53-dependent manner. The p53 R175H -dependent effects are strong over a broad range of concentrations, but p53 R273H -dependent effects are weaker and requires high concentrations of P53R3. P53R3 induces p53 R248W reactivation is more pronounced proliferation inhibition than observed with p53 R273H . P53R3 does not exhibit cytotoxic effects even at concentrations close to its solubility limit (33 μg/ml). P53R3 (33 μg/ml; 18 hours) induces a strong decrease in S phase cells and a G0/G1 cell cycle arrest in LN-308 p53 R175H and LN-308 p53 R273H cells. But it does not affect cell cycle distribution of LN-308 p53 R248W cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: p53 LN-308 human glioma cells with a control plasmid or plasmids encoding the mutants p53R175H, p53R248W and p53R273H Concentration: 1-33 μg/mL Incubation Time: 24 hours Result: Induced p53-dependent and -independent antiproliferative and cytotoxic effects in vitro . Form:Solid