Trilexium (TRX-E-009-1), a third-generation benzopyran structurally related to TRX-E-002-1, increases p21 protein expression, induces apoptosis, depolymerizes microtubules, and demonstrates broad anti-cancer activity [1] [2].

Trilexium exhibits activity against various cancer types. In an evaluation of 240 cell lines using Eurofin's Oncopanel, 10 cell lines showed an IC 50 > 30 μM, while the remaining 230 cell lines had an average IC 50 of 0.428 μM^[1]. Trilexium (300 nM, 4 h) disrupts the microtubule network in HeLa cells^[1]. Trilexium (1-5 μM) increases the protein expression of p21, c-PARP, and c-Caspase 3 in HSJD-DIPG007 cells^[2]. Additionally, Trilexium (0-2 μM) restores H3K27 trimethylation and enhances H3K27 acetylation in HSJD-DIPG007 cells^[2].

Administering Trilexium intravenously at doses ranging from 5-60 mg/kg once daily for 15 consecutive days significantly suppressed tumor growth in a mouse model of A375 melanoma harboring (BRAFV600E), with the highest dose of 60 mg/kg notably enhancing survival rates [1]. Similarly, in other experiments, a regimen of 80 mg/kg daily intravenous injections of Trilexium over 5 days affected the A375-transplanted mouse model by reducing long microtubule filaments, leading to the formation of shorter microtubules and dispersal of microtubule-associated proteins [1].