ires-a

IRES-C11 is a specific inhibitor of translation that targets the internal ribosome entry site (IRES) of the c-MYC gene. It functions by blocking the interaction between heterogeneous nuclear ribonucleoprotein A1, a trans-acting factor required for c-MYC IRES activity, and its corresponding IRES. Notably, IRES-C11 does not inhibit the IRES activity of BAG-1, XIAP, and p53.

hVEGF-IN-1 inhibits human VEGF-A translation and has antitumor activity.

MYC-RIBOTAC, a ribonuclease-targeting chimera (RIBOTAC) specific to the MYC internal ribosome entry site (IRES), comprises an MYC mRNA-binding element tethered to a small molecule that recruits and activates RNase L1. This interaction promotes the degradation of MYC mRNA, subsequently reducing MYC protein levels and inducing apoptosis, thereby presenting potential applications in anticancer research [1].

Lupus autoantigen peptide (LAP), a derivative of the autoantigen La found in systemic lupus erythematosus (SLE) patients, spans amino acids 11-28 of La and functions as an antiviral peptide. It primarily blocks the hepatitis C virus (HCV) from interacting with internal ribosome entry site (IRES) trans-acting factors (ITAFs), notably the polypyrimidine tract-binding protein (PTB) and poly(rC)-binding protein 2 (PCBP2). In a Huh7 cell-based reporter assay, LAP at a concentration of 60 µM effectively hampers HCV IRES-mediated translation, a process reversible by adding recombinant forms of PTB and PCBP2.