Trabectedin 是一种四氢异喹啉生物碱，有抗肿瘤的活性， 通过与 DNA 的小沟结合，阻断应激诱导的蛋白质的转录，诱导 DNA 骨架裂解和癌细胞凋亡，并增加 MCF-7 和 MDA-MB-453 细胞中ROS的生成。Trabectedin 在软组织肉瘤和卵巢癌中具有的研究价值。

Trabectedin has potent antitumor activity and the potential for soft tissue sarcoma and ovarian cancer research. Trabectedin inhibits cell growth of MX-1, MCF7 and MCF7/DXR cells with IC50 values of 0.1 nM, 1.5 nM and 3.7 nM, respectively.

In MCF7 cells, Trabectedin (10 nM; 24-72 hours) results in cell accumulation in late S to G2 phase[1]. Trabectedin induces cytotoxicity and apoptosis in both breast cancer cells in a time and concentration-dependent manner. In MDA-MB-453 cells, the mitochondrial pathway related pro-apoptotic proteins Bax, Bad, Cytochrome c, Smac/DIABLO, and Cleaved Caspase-3 expressions are induced by 4.2-, 3.6-, 4.8-, 4.5-, and 4.4-fold, and the expression levels of anti-apoptotic proteins Bcl-2 and Bcl-XL are reduced by 4.8- and 5.2-fold. In MCF-7 cells, the expression levels of the death receptor pathway molecules, TRAIL-R1/DR4, TRAIL-R2/DR5, FAS/TNFRSF6, TNF RI/TNFRSF1A, and FADD are significantly increased by 2.6-, 3.1-, 1.7-, 11.2- and 4.0-fold by Trabectedin treatment[2]. Trabectedin selectively inhibits the production of CCL2, CXCL8, IL-6, VEGF, and PTX3 by myxoid liposarcoma (MLS) primary tumor cultures and/or cell lines[3].

In female athymic nude mice, Trabectedin (30-50 μg/kg; intravenous injection; every three days) increased the antitumor effects in nude mice bearing MX-1 mammary carcinoma xenografts without increasing toxicity[1]. In a xenograft mouse model of human myxoid liposarcoma (MLS), Trabectedin reduced CCL2, CXCL8, CD68+ infiltrating macrophages, CD31+ tumor vessels, and partial decreased PTX3[3].

114899-77-3

C39H43N3O11S

761.84

ET-743;Ecteinascidin 743;曲贝替定

DMSO:33.33 mg/mL (43.75 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years