We have compared the anti-proliferative activity in vitro, of R₂SnGala (1–3) [R = Me, n-Bu, pH] and novel R₃SnGala (4, 5) [R = Me, n-Bu] with D-(+)-Galacturonic acid [HGala; Gala^q-, q = (2) and (1) for R₂SnGala and R₃SnGala, respectively] compounds, towards human tumor cell lines of intestinal carcinoma (HCT-116) and breast adenocarcinoma (MCF-7).

The new synthesized 4 and 5 compounds were characterized, in solution, by ¹H,¹³C and ¹¹⁹Sn NMR, that showed that HGala acts as monoanionic moiety and evidenced the dynamic behavior of the compounds, due to inter-conversions involving the anomeric carbon atom of the ligand.

Cell viability, apoptosis induction and cell cycle distribution were analyzed by MTT colorimetric assay and flow cytometry, respectively. The cytotoxicity of the compounds, in the micro-submicromolar range, changed in the order of the organotin(IV) moieties, according to 5 > 3 > 2, while 1 and 4, containing Me_nSn(IV) (n = 2,3) moieties, were ineffective. Compound 5 showed peculiar cytotoxic effects. It did not cause time dependent inhibition of cell growth nor accumulated into the cells.

Cell death induced by the active 2, 3, and 5, was shown to be apoptotic by measuring the exposure of phosphatidylserine to the outer membrane and the loss of mitochondrial potential. All the cytotoxic compounds induced an accumulation of cells in the subG0/G1phase, while only 2 and 3 perturbed the cell cycle confining viable cells in G0/G1phase. Finally, none of the compounds investigated affected the viability of normal intestinal or liver cells, indicating selectivity towards tumor cells.

我们已经比较了R ₂ SnGala（1-3）[R = Me，n-Bu，pH]和新型R ₃ SnGala（4，5）[R = Me，n-Bu]的体外抗增殖活性。用D-（+）-半乳糖醛酸[HGala; 对于肠道癌（HCT-116）和乳腺癌（MCF-7）的人肿瘤细胞系，R ₂ SnGala和R ₃ SnGala的化合物分别分别为Gala ^q-，q =（2）和（1 ）。

通过溶液的¹ H，¹³ C和¹¹⁹ Sn NMR对新合成的4和5化合物进行表征，结果表明HGala充当单阴离子部分，并由于涉及异头碳的相互转化而证明了化合物的动态行为。配体的原子。

通过MTT比色法和流式细胞术分别分析细胞活力，凋亡诱导和细胞周期分布。化合物的细胞毒性在亚微摩尔范围内，按照5  >  3  >  2的顺序依次变化为有机锡（IV）部分，而1和4含Me _n Sn（IV）（n  = 2， 3）部分，无效。化合物5显示出独特的细胞毒性作用。它不会引起时间依赖性的细胞生长抑制，也不会累积到细胞中。

细胞死亡诱导活性2，3和5中，示出通过测量磷脂酰丝氨酸的暴露于外膜和线粒体电位的丧失是凋亡。所有的细胞毒性化合物都诱导subG0 / G1期的细胞蓄积，而只有2个和3个扰动了细胞周期，将活细胞限制在G0 / G1期。最后，所研究的化合物均未影响正常肠或肝细胞的活力，表明其对肿瘤细胞的选择性。