ArticleCell death & disease2025
Inhibiting microtubule polymerization with EAPB02303, a prodrug activated by catechol-O-methyl transferase, enhances paclitaxel effect in pancreatic cancer models.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The Imiqualines family is an original group of small heterocyclic compounds, diversely substituted around different scaffolds. Among these compounds, the lead EAPB02303 displays outstanding cytotoxic activity at nanomolar concentrations comparable to those of standard-of-care chemotherapy drugs in different cancer cell lines, including Pancreatic Ductal AdenoCarcinoma (PDAC) cell lines. Due to its high aggressiveness and resistance to therapies, PDAC has an extremely poor prognosis with limited treatment options. Here, we demonstrated the cytotoxic activities of EAPB02303 alone or combined with standard chemotherapy drugs in several PDAC cell lines and confirmed these results in patient-derived xenograft mouse models. EAPB02303 potently induced cell cycle arrest in the G2/M phase and in mitosis followed by apoptosis. Then, using a combination of transcriptomic, proteomic, biochemical and cellular assay, we found that EAPB02303 mechanism of action relies on its bioactivation by catechol-O-methyltransferase, resulting in the production of a methylated compound that effectively inhibits microtubule polymerization. Moreover, EAPB02303 had a synergistic effect when combined with paclitaxel (the standard-of-care agent in PDAC) providing the rationale to continue the development of EAPB02303 combination strategies for the treatment of catechol-O-methyltransferase-overexpressing PDAC.
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