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.

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[1].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[1].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)[1].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[1]. Cell Viability Assay[1]Cell Line: p53 null 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 .

922150-12-7

C32H35Cl2N5O2

592.57

P53R3

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years