Bcr-Abl is a target of tyrosine kinase inhibitor drugs, such as imatinib.

An Overview of Bcr-Abl

Human abl gene is located on the long arm of chromosome 9 and has 12 exons. The length of two mRNAs of human abl transcriptional formation is 7kb and 6kb, respectively. The molecular weight of the two proteins synthesized is about 145. The former is located in the cell membrane, while the latter is mainly located in the nucleus. The main structure of Abl is N terminal srchomology-2 (SH2), binding phosphorylation of tyrosine residues. SH1 has tyrosine kinase activity. The near C-terminal is rich in acidic amino acid residues and can be combined with DNA. ABL protein regulates cell cycle. In G 0 phase, the protein complex of abl-Rb binds to DNA. During the G1 -S transition, Rb was isolated and activated by phosphorylated abl, which phosphorylated RNA polymerase and promoted transcription. The breakpoints of cell entering S phase. BCR gene are concentrated in three regions: major bcr (M-bcr) minor bcr (m-bcr), and μ (μ -bcr) region . 90% Chronic Myelogenous Le. The breaking point of bcr gene of bcr/abl fusion gene in the blood cells of patients with ukemia is usually located in M-bcrs, mainly b2a2 and b3a2, and the molecular weight of protein is 210 kb.

Bcr-Abl and diseases

BCR-Abl fusion gene is a necessary element for the pathogenesis of chronic myeloid leukemia. In up to 95% of the cases, chromosome translocation of t(9;22) (q34;q11) resulted in BCR-Abl fusion gene. The translocation occurred on the Philadelphia chromosome (Ph). In rare cases of chronic myeloid leukemia without classical t (9;22) translocation, other translocations also lead to BCR-ABL1 fusion genes, which sometimes involve multiple chromosomes.

Inhibition of Bcr-Abl

A specific abl tyrosine kinase inhibitor, STI-571 ( was obtained by modifying the structure of imatinib.


Li Linyi, Xu Yungen. BCR-ABL kinase inhibitor [J]. Chinese Modern Applied Pharmacy: 2016 (07): 954-962.

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