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4E1RCat

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Chemical Structure| 328998-25-0 同义名 : eIF4E/eIF4G Interaction Inhibitor II
CAS号 : 328998-25-0
货号 : A940826
分子式 : C28H18N2O6
纯度 : 99%+
分子量 : 478.452
MDL号 : MFCD01931282
存储条件：

粉末 Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 16 mg/mL(33.44 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 Eukaryotic translation initiation is tightly regulated at the step of ribosome recruitment. This process involves binding of eukaryotic initiation factor (eIF) 4F complex to mRNA cap structures. eIF4F is composed of: eIF4E, the cap-binding protein; eIF4A, a DEAD-box RNA helicase; and eIF4G, a scaffolding protein that bridges the interaction between eIF4E and eIF4A. 4E1RCat is an inhibitor of eIF4E:eIF4G interaction with an IC50 an of ∼4 μM. It also blocks eIF4E:4E-BP1 interaction. 4E1RCat at 50 μM reduced 80S ribosome complex formation and this inhibition of ribosome recruitment to mRNA by 4E1RCat was cap-specific. 4E1RCat inhibited cap-dependent translation from FF/HCV/Ren in a dose dependent manner. It also inhibited cap-dependent production of Ren Luc from Ren/CrPV/FF. Furthermore, in Jurkat cells, 4E1RCat at 50 μM decreased polysomes, increased the fraction of 80S ribosomal subunits, and decreased levels of Mcl-1 and c-Myc proteins, two eIF4E-dependent mRNAs. In vivo, 4E1RCat (15 mg/kg daily for 5 d) could reverse chemoresistance in a Myc-driven lymphoma model, consistent with the idea that deregulated translation plays a role in this phenomenon[3].
作用机制 eIF4E has five shallow pockets that form an elongated binding site and could support small molecule interactions. 4E1RCat shows potential for binding to four of these pockets[3].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.09mL

0.42mL

0.21mL

10.45mL

2.09mL

1.04mL

20.90mL

4.18mL

2.09mL
参考文献

[1]Salomon JJ, Spahn S,et al. Generation and functional characterization of epithelial cells with stable expression of SLC26A9 Cl- channels. Am J Physiol Lung Cell Mol Physiol. 2016 Apr 1;310(7):L593-602.

[2]Muanprasat C, Sonawane ND, et al. Discovery of glycine hydrazide pore-occluding CFTR inhibitors: mechanism, structure-activity analysis, and in vivo efficacy. J Gen Physiol. 2004 Aug;124(2):125-37.

[3]Cencic R, Hall DR, Robert F, et al. Reversing chemoresistance by small molecule inhibition of the translation initiation complex eIF4F. Proc Natl Acad Sci U S A. 2011;108(3):1046-1051