Division of Cancer Prevention, Department of Medicine, Stony Brook University, Stony Brook, NY 11794-8175, USA.
Carcinogenesis. 2013 Apr;34(4):943-51. doi: 10.1093/carcin/bgs394. Epub 2013 Jan 21.
We have synthesized a novel derivative of indomethacin, phospho-tyrosol-indomethacin (PTI; MPI-621), and evaluated its anticancer efficacy in vitro and in vivo. PTI inhibited the growth of human colon, breast and lung cancer cell lines 6-30-fold more potently than indomethacin. In vivo, in contrast to indomethacin that was unable to inhibit colon cancer xenograft growth, PTI inhibited the growth of colon (69% at 10mg/kg/day, P < 0.01) and lung (91% at 15mg/kg/day, P < 0.01) subcutaneous cancer xenografts in immunodeficient mice, suppressing cell proliferation by 33% and inducing apoptosis by 75% (P < 0.05, for both). Regarding its pharmacokinetics in mice, after a single intraperitoneal injection of PTI, its plasma levels reached the maximum concentration (Cmax = 46 μM) at 2h (Tmax) and became undetectable at 4h. Indomethacin is the major metabolite of PTI, with plasma Cmax = 378 μM and Tmax = 2.5h; it became undetectable 24h postadministration. The cellular uptake of PTI (50-200 μM) at 6h was about 200-fold greater than that of indomethacin. Regarding its safety, PTI had no significant genotoxicity, showed less gastrointestinal toxicity than indomethacin and presented no cardiac toxicity. Mechanistically, PTI suppressed prostaglandin E2 production in A549 human lung cancer cells and strongly inhibited nuclear factor-κB activation in A549 xenografts. These findings indicate that PTI merits further evaluation as an anticancer agent.
我们合成了一种新型的吲哚美辛衍生物,磷酸酪氨酸吲哚美辛(PTI;MPI-621),并评估了其在体外和体内的抗癌功效。PTI 对人结肠、乳腺和肺癌细胞系的生长抑制作用比吲哚美辛强 6-30 倍。在体内,与不能抑制结肠癌异种移植生长的吲哚美辛相反,PTI 抑制了免疫缺陷小鼠中结肠(每天 10mg/kg 时抑制率为 69%,P < 0.01)和肺(每天 15mg/kg 时抑制率为 91%,P < 0.01)皮下癌症异种移植的生长,抑制细胞增殖 33%,诱导凋亡 75%(P < 0.05,两者均)。关于其在小鼠中的药代动力学,单次腹腔注射 PTI 后,其血浆水平在 2h(Tmax)达到最大浓度(Cmax = 46 μM),4h 后无法检测到。吲哚美辛是 PTI 的主要代谢物,其血浆 Cmax = 378 μM,Tmax = 2.5h;给药后 24h 无法检测到。PTI(50-200 μM)在 6h 的细胞摄取量约为吲哚美辛的 200 倍。关于其安全性,PTI 没有明显的遗传毒性,比吲哚美辛显示出更少的胃肠道毒性,并且没有心脏毒性。在机制上,PTI 抑制 A549 人肺癌细胞中环氧化酶-2(COX-2)的表达和前列腺素 E2(PGE2)的产生,并强烈抑制 A549 异种移植物中核因子-κB(NF-κB)的激活。这些发现表明 PTI 作为抗癌剂值得进一步评估。