2,5-dimethylcelecoxib

2,5-dimethylcelecoxib (2,5-MeC) is a small molecule derivative of the non-steroidal anti-inflammatory drug (NSAID) celecoxib. Unlike its parent compound, 2,5-MeC lacks cyclooxygenase-2 (COX-2) inhibitory activity but retains and often enhances the anti-proliferative and pro-apoptotic properties of celecoxib. It has been extensively studied as an experimental antineoplastic agent across various cancer types. In the specific context of TP53-aberrant endometrial cancer, 2,5-MeC acts as a potent inducer of the nucleolar translocation of Eukaryotic Translation Initiation Factor 1A X-linked (EIF1AX). This translocation promotes the recruitment of DDX21 to form nucleolar aggregates, which suppresses ribosomal DNA (rDNA) transcription and induces cellular senescence. Furthermore, 2,5-MeC has demonstrated synthetic lethality when combined with histone deacetylase (HDAC) inhibitors such as dacinostat, a process mediated through the activation of the JNK/MAPK signaling pathway.

Other names

2,5-dimethyl-celecoxib4-[5-(2,5-dimethylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide