P53R3 is a potent reactivator of p53, effectively restoring sequence-specific DNA binding to several p53 hot spot mutants, namely p53 R175H, p53 R248W, and p53 R273H. This compound exhibits p53-dependent antiproliferative effects with significantly higher specificity compared to PRIMA-1 and promotes the recruitment of both wild-type p53 and p53 M237I to various target gene promoters. Additionally, P53R3 markedly increases the mRNA, total protein, and cell surface expression of death receptor 5 (DR5), demonstrating its utility in cancer research.

P53R3（10 μg/ml；24小时；在未标记的p53共识寡核苷酸的存在或缺席下）恢复p53 R273H（DNA接触突变体）和p53R175H（结构突变体）在含有p53 R273H的WiDr结肠肿瘤细胞和含有p53R175H的KLE细胞中的p53特异性DNA结合活性[1]。P53R3（1-33 μg/ml；24小时）以p53依赖的方式抑制表达突变p53质粒的LN-308亚系的增殖。p53 R175H依赖的效应在广泛的浓度范围内较强，但p53 R273H依赖的效应较弱，需要较高浓度的P53R3[1]。P53R3诱导的p53 R248W再激活明显比p53 R273H观察到的增殖抑制更为显著。即使在接近其溶解度极限（33 μg/ml）的浓度下，P53R3也不表现出细胞毒作用[1]。P53R3（33 μg/ml；18小时）在LN-308 p53 R175H和LN-308 p53 R273H细胞中引起S期细胞的显著减少以及G0/G1周期停滞，但它不影响LN-308 p53 R248W细胞的细胞周期分布[1]。细胞存活率检测[1] 细胞系：带有控制质粒或编码突变体p53R175H、p53R248W和p53R273H的p53 LN-308人脑胶质瘤细胞 浓度：1-33 μg/mL 孵育时间：24小时 结果：诱导了体外p53依赖和独立的抗增殖和细胞毒效应。