IRES-C11

Research use only, not for human use.

A novel, spectfic c-Myc IRES (internal ribosome entry site) function inhibitor that prevents binding of hnRNP A1 to the Myc IRES and specifically inhibits Myc IRES activity in MM cells.

A novel, spectfic c-Myc IRES (internal ribosome entry site) function inhibitor that prevents binding of hnRNP A1 to the Myc IRES and specifically inhibits Myc IRES activity in MM cells; shows no effect on BAG-1, XIAP and p53 IRESes, and has no significant effect on myc translation; significantly inhibits myc expression when combined with ER stress inducers, especially bortezomib; shows synergistic anti-MM cytotoxicity combined with ER stress inducers; also blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic anti-GBM properties combined with PP242.

IRES-C11 blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic anti-glioblastoma properties when combined with the mechanistic target of mTOR PP242.IRES-C11 (50 nM) significantly inhibits both cyclin D1 and c-MYC IRES activity. IRES-C11 treatment induces a significant shift in both cyclin D1 and c-MYC mRNA to monosomal/nonribosomal fractions, whereas actin mRNA distribution is unaffected. IRES-C11 inhibits both cyclin D1 and c-MYC IRES-mediated mRNA translation, leading to reductions in protein levels.Mechanistic studies with IRES-C11 reveal binding of the inhibitors within the UP1 fragment of heterogeneous nuclear ribonucleoprotein A1.

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IRES inhibitor C11

Cell Cycle/DNA Damage

c-Myc

c-Myc

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342416-30-2

316.134

C13H11Cl2NO4

>98% (HPLC)

In Vitro:?DMSO : 250 mg/mL (790.79 mM)

COC1=CC(=C(C=C1)CN2C(=O)C(=C(C2=O)Cl)Cl)OC

3,4-dichloro-1-(2,4-dimethoxybenzyl)-1H-pyrrole-2,5-dione

(-20℃)

With Ice Pack

≥ 2 years