Imatinib targeted therapy principle

The targeted therapy principle of Imatinib is based on its inhibitory effect on specific tyrosine kinases, especially the targeted inhibition of BCR-ABL fusion proteins. This fusion protein is composed of chromosomes 9 and 22CML) Chromosomal translocations between an> chromosomes result in the so-called "Philadelphia chromosome" (Philadelphia chromosome). BCR-ABLThe fusion protein is an abnormally active tyrosine kinase that causes uncontrolled proliferation and survival of leukemia cells by continuously activating intracellular signaling pathways.

Imatinib binds to the active site ofBCR-ABLtyrosine kinase, blocking its kinase activity and preventing the conduction of downstream signaling pathways, thereby inhibiting the proliferation of leukemia cells and inducing their apoptosis. Unlike traditional chemotherapy drugs, imatinib is highly selective and mainly targets abnormal BCR-ABL proteins, while having less impact on normal cells, so it has better efficacy and lower side effects.

In addition to treating chronic myelogenous leukemia, imatinib is used to treat other tumors with abnormal tyrosine kinase activity, such as gastrointestinal stromal tumors (GIST). In GIST patients, imatinib mainly inhibits the abnormal activity of KIT tyrosine kinase. KIT Gene mutations lead to abnormal activation of tyrosine kinase, promoting the growth and survival of tumor cells. Imatinib blocks the proliferation of tumor cells and promotes their apoptosis by inhibiting the activity of this kinase.

In general, the principle of targeted therapy with imatinib is to inhibit abnormal signaling of cancer cells by inhibiting specific tyrosine kinases, ultimately achieving the effect of inhibiting tumor growth and delaying the progression of the disease. Compared with traditional chemotherapy drugs, targeted therapy is more precise and has fewer side effects, significantly improving patients' quality of life.