DB2313 是一种有效的转录因子 PU.1 抑制剂，apoptosis 为 14 nM。DB2313 破坏了 PU.1 与靶基因启动子的相互作用。DB2313 可诱导急性髓细胞性白血病 (AML) 细胞凋亡 (apoptosis)，并具有抗癌作用。

DB2313 is a potent transcription factor PU.1 inhibitor with an apoptosis of 14 nM. DB2313 disrupts the interaction of PU.1 with target gene promoters. DB2313 induces apoptosis of acute myeloid leukemia (AML) cells, and has anticancer effects.

Solid

IC50: 14 nM (PU.1)

DB2313 treatment leads to a profound decrease in the growth of PU.1 URE acute myeloid leukemia (AML) cells (IC50 of 7.1 μM), while showing little effect on normal hematopoietic cells at similar concentrations. DB2313 treatment leads to a 3.5-fold increase in apoptotic cells in murine PU.1 URE AML cells. DB2313 also leads to a significant decrease in clonogenicity in the second and third rounds of plating and a complete disruption of clonogenic capacity in the fourth and higher rounds of plating.
In AML cells, DB2313 decreases PU.1 occupancy on E2f1, Junb, and Csf1r promoters. has not independently confirmed the accuracy of these methods. They are for reference only.

DB2313 (17 mg/kg; i.p.; three times per week; for 3 weeks) treatment decreases leukemia progression and results in increased survival in mice. has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model:

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Iléana Antony-Debré, et al. Pharmacological inhibition of the transcription factor PU.1 in leukemia. J Clin Invest. 2017 Dec 1;127(12):4297-4313.
[2]. Zhang S, Zhao S, Qi Y, et al. SPI1-induced downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner. Mol Ther Nucleic Acids. 2022;27:699-717.

In Vitro: DMSO : 3.7 mg/mL (5.22 mM; ultrasonic and warming and heat to 70°C)配制储备液