[Novel inhibitors of Bcr-Abl].
[Novel inhibitors of Bcr-Abl].
复制标题
[Bcr-Abl 的新型抑制剂]。
DOI：
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
M. Czyż
中科院分区：
文献类型：
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作者：
Justyna Jakubowska;M. Czyż
STI 571（伊马替尼; Gleevec）是专门针对费城染色体阳性慢性粒细胞白血病（CML）中Bcr-Abl蛋白的酪氨酸激酶活性而开发的。它还抑制c-Kit和PDGFR的活性。它是新诊断的CML的一线药物，对这种癌症的慢性期患者具有显著疗效。然而，处于加速期或急变期的CML患者经常由于耐药而复发。STI 571未能根除白血病干细胞和BCR-ABL（+）。在大多数患者中仍然可以检测到细胞。对STI 571耐药白血病的替代或额外治疗的必要性导致了第二代靶向治疗药物的开发。在这篇综述中，文献综述的替代抑制剂，旨在推翻STI 571耐药性和降低异常的激酶活性的Bcr-Abl蛋白，以更高的效率。
STI571 (imatinib; Gleevec) was developed to specifically target the tyrosine kinase activity of the Bcr-Abl protein in Philadelphia chromosome-positive chronic myeloid leukemia (CML). It also inhibits the activity of c-Kit and PDGFR. It is the first-line drug for newly diagnosed CML, with remarkable efficacy to patients in the chronic phase of this cancer. However, CML patients in the accelerated phase or blast crisis often relapse due to drug resistance. STI571 fails to eradicate leukemic stem cells, and BCR-ABL(+). cells remain detectable in the majority of patients. The necessity for alternative or additional treatment for STI571-resistant leukemia resulted in the development of a second generation of drugs for targeted therapies. In this review a literature overview of the alternative inhibitors which were designed to override STI571 resistance and decrease the aberrant kinase activity of Bcr-Abl protein with higher efficiency is presented.