Lurbinectedin, a synthetic tetrahydroisoquinoline alkaloid in phase I clinical trials for solid tumors, forms DNA adducts causing double-strand breaks, S-phase accumulation, and apoptosis, with potent cytotoxicity confirmed by a mean GI50 value of 2.7 nM in a 23-cell line panel[2]. Lurbinectedin significantly reduces tumor growth in both chemosensitive and chemoresistant human ovarian clear cell carcinoma (CCC) cells in vitro and in mouse CCC cell xenografts. The combination of lurbinectedin and SN-38 exhibits a remarkable synergistic effect[1].
体内研究
Furthermore, Lurbinectedin markedly diminishes tumor growth in four murine xenograft models of human cancer without causing weight loss in treated animals[2].
Both single lurbinectedin treatments and those combined with NSC 119875 prove effective in NSC 119875-sensitive and -resistant preclinical ovarian tumor models. The most significant synergistic effect occurs in NSC 119875-resistant tumors, with lurbinectedin's effectiveness linked to reduced cell proliferation, increased aberrant mitosis rates, and induced apoptosis[3].
体外研究
Lurbinectedin, a synthetic tetrahydroisoquinoline alkaloid in phase I clinical trials for solid tumors, forms DNA adducts causing double-strand breaks, S-phase accumulation, and apoptosis, with potent cytotoxicity confirmed by a mean GI50 value of 2.7 nM in a 23-cell line panel[2].
Lurbinectedin significantly reduces tumor growth in both chemosensitive and chemoresistant human ovarian clear cell carcinoma (CCC) cells in vitro and in mouse CCC cell xenografts. The combination of lurbinectedin and SN-38 exhibits a remarkable synergistic effect[1].
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