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阿糖胞苷对某些恶性肿瘤有效,并已广泛应用于临床,由于二个现象最终限制其使用:(1)正常组织中的胞嘧啶脱氨酶可使其迅速脱氨变为尿嘧啶阿糖胞苷,而失去抗肿瘤活性,为了维持其有效的血浓度,必需多次和连续用药。最近研究表明,在阿糖胞苷治疗后,肿瘤细胞的胞嘧啶核苷脱氨酶的活力增加,提示耐药机理可能包括增快药物的代谢;(2)阿糖胞苷耐药的迅速发生是由于脱氧胞嘧啶核苷激酶的丢失,此酶可将阿糖胞苷转化为其有活性的磷酸形式。为了克服上述缺点,对阿糖胞苷基本分子作了
Cytarabine is effective for certain malignancies and has been widely used in clinical settings due to two phenomena that ultimately limit its use: (1) Cytosine deaminase in normal tissues can rapidly deammoniate to uracil Cytosine, and loss of anti-tumor activity, in order to maintain its effective blood concentration, must be repeated and continuous medication. Recent studies have shown that cytarabine deaminase activity in tumor cells increases after cytarabine treatment, suggesting that drug resistance mechanisms may include increased drug metabolism; (2) rapid cytarabine resistance Is due to the loss of a deoxycytidine kinase that converts cytarabine into its active phosphate form. In order to overcome the above shortcomings, the basic molecule of cytarabine was made