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Eprenetapopt

CAS No. : 5291-32-7

MCE 国际站：Eprenetapopt

产品活性：Eprenetapopt (APR-246) 是首创的在 TP53 突变细胞中恢复野生型p53功能的小分子。Eprenetapopt 引发肿瘤细胞凋亡。Eprenetapopt 还抑制硒蛋白硫氧还蛋白还原酶 1 (TrxR1)。

研究领域：Apoptosis  |  Autophagy

作用靶点：MDM-2/p53  |  Autophagy  |  Apoptosis  |  Ferroptosis

In Vitro: Eprenetapopt inhibits both recombinant TrxR1 in vitro and TrxR1 in cells. Cellular TrxR1 activity is inhibited by Eprenetapopt irrespective of p53 status. Eprenetapopt can directly affect cellular redox status via targeting of TrxR1. Several small molecules have been shown to restore wild-type activity to mutant p53, including CP-31398, PRIMA-1 and Eprenetapopt, MIRA, STIMA, PhiKan-083 and NSC319726. PRIMA-1 and its methylated analog Eprenetapopt promote correct folding of mutant p53, induce cell death by apoptosis, and inhibit tumor growth in mice. Eprenetapopt has also been shown to reactivate mutant forms of the p63 and p73 proteins that share high structural homology with p53.
Eprenetapopt is a powerful apoptosis-inducing agent. Eprenetapopt can enhance apoptosis in mutant p53 carrying cells, compared to the p53 null parental cells. Most p53 mutants are in complex with Hsp70 proteins. Eprenetapopt treatment increases Hsp70 expression and nucleolar translocation, in parallel with the induction of nucleolar accumulation of mutant p53. Several lines of evidence suggest that Eprenetapopt can also act independently of the p53 status of the cell. It can radiosensitize prostate carcinoma cell lines with mutant or wild type p53 and p53^-/- cells as well. Introduction of mutant p53 (p53ser249 or p53gln248) into p53^-/- hepatocarcinoma cells increases sensitivity to Eprenetapopt without the induction of p53 target genes.Eprenetapopt regularly induces apoptosis in mutant p53 expressing cells.

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