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)。

Eprenetapopt (APR-246) is a first-in-class, small molecule that restores wild-type p53 functions in TP53-mutant cells. Eprenetapopt triggers apoptosis in tumor cells. Eprenetapopt also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance.

Solid

p53 activator
TrxR1 inhibitor

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 wit

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[1]. Peng X, et al. APR-246/PRIMA-1MET inhibits thioredoxin reductase 1 and converts the enzyme to a dedicated NADPH oxidase. Cell Death Dis. 2013 Oct 24;4:e881.
[2]. Stuber G, et al. PRIMA-1MET induces nucleolar translocation of Epstein-Barr virus-encoded EBNA-5 protein. Mol Cancer. 2009 Mar 26;8:23.

In Vitro: DMSO : 100 mg/mL (501.88 mM; Need ultrasonic)H₂O : 50 mg/mL (250.94 mM; Need ultrasonic)配制储备液