IRES-C11 is a spectfic c-MYC internal ribosome entry site (IRES) translation inhibitor. IRES-C11 blocks the interaction of a requisite c-MYC IRES trans-acting factor, heterogeneous nuclear ribonucleoprotein A1, with its IRES. IRES-C11 does not inhibits BAG-1, XIAP and p53 IRESes^[1][2].

IRES-C11 blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic anti-glioblastoma properties when combined with the mechanistic target of mTOR PP242^[1].
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.

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

316.14

C₁₃H₁₁Cl₂NO₄

342416-30-2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Brent Holmes, et al. Mechanistic Target of Rapamycin (mTOR) Inhibition Synergizes with Reduced Internal Ribosome Entry Site (IRES)-mediated Translation of Cyclin D1 and c-MYC mRNAs to Treat Glioblastoma. J Biol Chem. 2016 Jul 1;291(27):14146-14159.

  [2]. Y Shi, et al. Therapeutic potential of targeting IRES-dependent c-myc translation in multiple myeloma cells during ER stress. Oncogene. 2016 Feb 25;35(8):1015-24.