ArticleMolecular cancer therapeutics2026
QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp-overexpressing cancer models.
Article in Molecular cancer therapeutics, 2026. 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
Drug resistance driven by efflux transporters and altered tubulin dynamics limits the clinical efficacy of taxanes and vincristine in high-risk neuroblastoma (NB) and castration-resistant prostate cancer (CRPC). We developed QW-5-70, a colchicine-binding-site inhibitor (CBSI), engineered to retain low-nanomolar potency in both parental and drug-resistant cancer cells by showing minimal dependence on P-glycoprotein (P-gp)-mediated efflux. QW-5-70 binds to the colchicine site on tubulin, inhibits tubulin polymerization, disrupts microtubule networks, and induces mitotic arrest. Across a panel of NB and prostate cancer lines, QW-5-70 maintained low-nanomolar activity and remained effective in vincristine-resistant BE2C/VCR and paclitaxel-resistant PC-3/TxR cells. Unlike vincristine and paclitaxel, QW-5-70's activity and intracellular accumulation were unaffected by pharmacologic or genetic inhibition of P-gp, indicating effective circumvention of efflux-mediated resistance. In vitro, QW-5-70 significantly reduced colony formation and impaired migration in both parental and resistant cancer cells, and induced G2/M cell cycle arrest and mitochondrial apoptosis. In vivo, QW-5-70 significantly suppressed tumor growth in drug-resistant PC-3/TxR and BE2C/VCR xenografts, with modest weight loss and no evident histopathology in the major organs. Combination studies revealed a combination index (CI)-defined synergistic interactions at selected dose pairs with the ornithine decarboxylase inhibitor DFMO, and enhanced apoptotic and clonogenic suppression when combined with the Aurora A kinase inhibitor MLN8237. Collectively, QW-5-70 is a potent CBSI that circumvents P-gp-associated resistance, triggers mitotic arrest and apoptosis, and achieves significant antitumor activity in multidrug-resistant tumor models with acceptable tolerability, supporting its further preclinical development alone and in combination with other drugs.
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