The literature provides evidence that metabolic nitric oxide (NO) release mediates the cytotoxic activities (against human leukemia and prostate cancer xenografts in mice) of JS-K, a compound of structure R(2)N-N(O)=NO-Ar for which R(2)N is 4-(ethoxycarbonyl)piperazin-1-yl and Ar is 2,4-dinitrophenyl. Here we present comparative data on the potencies of JS-K and 41 other O(2)-arylated diazeniumdiolates as inhibitors of HL-60 human leukemia cell proliferation, as well as in the NCI 51-cell-line screen for six of them. The data show JS-K to be the most potent of the 42 in both screens and suggest that other features of its structure and metabolism besides NO release may contribute importantly to its activity. Results with control compounds implicate JS-K's arylating ability, and the surprisingly low IC(50) value of the N-(ethoxycarbonyl)piperazine byproduct of NO release suggests a role for the R(2)N moiety. In addition to the above-mentioned in vivo activities, JS-K is shown here to be carcinostatic in a rat liver cancer model.

中文翻译：

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JS-K [O2-（2,4-二硝基苯基）1-[（（4-乙氧基羰基）哌嗪-1-基]重氮-1-1,2-二醇盐]和相关O2-芳基重氮二醇盐的体外抗肿瘤活性和体内。

文献提供的证据表明，新陈代谢的一氧化氮（NO）释放介导了JS-K的细胞毒性活性（针对人类白血病和前列腺癌异种移植），该化合物的结构为R（2）NN（O）= NO-Ar， R（2）N为4-（乙氧羰基）哌嗪-1-基，Ar为2,4-二硝基苯基。在这里，我们介绍了有关JS-K和其他41种O（2）-芳基重氮二醇盐作为HL-60人白血病细胞增殖抑制剂的功效的比较数据，以及在NCI 51细胞系中筛选其中的六个物质。数据显示JS-K在这两个屏幕中都是42种中最有效的，并且表明其结构和新陈代谢中除了NO释放外的其他特征可能对其活性也有重要作用。对照化合物的结果暗示了JS-K的芳基化能力，NO释放的N-（乙氧羰基）哌嗪副产物的IC（50）值低得令人惊讶，这暗示了R（2）N部分的作用。除上述体内活性外，JS-K在大鼠肝癌模型中还显示出一定的抑癌作用。