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众所周知,阿糖胞苷(Ara-C)对白血病、淋巴肉瘤以及体内、体外脱氧核糖核酸(DNA)病毒均有抑制作用。已证实,阿糖胞苷在DNA聚合水平上抑制DNA的合成。阿糖胞苷进行磷酸化转变为5′三磷酸酯时为脱氧胞苷激酶所调节,当该酶的活性显著下降时就发现对阿糖胞苷产生耐性。阿糖胞苷作为抗病毒药物在所用的治疗方案下,产生毒性反应,因而在临床应用上仅限于严重的感染,此外由于脱氨酶的作用在人体内可转变为没有活性的代谢产物——1-β-D-阿糖尿嘧啶,很难维持有效的血浓度。因此,做了许多的工作试图改造阿糖胞苷的
As we all know, cytarabine (Ara-C) on leukemia, lymphosarcoma and in vivo and in vitro deoxyribonucleic (DNA) virus inhibition. It has been demonstrated that cytarabine inhibits DNA synthesis at the level of DNA polymerization. Cytosolic arabinosylation is deoxycytidine kinase when it is phosphorylated to 5 ’triphosphate, and tolerance to cytarabine is found when the enzyme activity is significantly reduced. Cytosine, as an antiviral drug, produces a toxic response under the treatment regimen used and is therefore limited to serious infections in clinical practice. In addition, cytarabine, as an antiviral agent, can be converted into an inactive metabolite in the human body due to the action of deaminase - 1-β-D-arabinouracil, it is difficult to maintain an effective blood concentration. So, a lot of work has been done to try to transform cytarabine