No abstract

Chronic myeloid leukemia is a type of cancer which affects hematopoetic cells, causing excessive proliferation of white blood cells which eventually leads to loss of function and resistance to apoptosis (stage known as acute leukemia). Researchers have shown that many CML cases are associated with mutant transcripts of the Philadelphia chromosome (i.e. BCR-ABL), whose effects are pharmacologically treated. The first successful drug in that matter is imatinib, a competitive inhibitor which caused groundbreaking advances in the treatment of CML. However, many patients develop resistance to the therapeutic effects of this drug. To solve this problem, several new drugs similar to imatinib have been developed in search for a new revolutionary molecule, with the same therapeutic potential. In this work, we study two second-generation inhibitors, dasatinib and afatinib, and compare their interactions with those of imatinib. Furthermore, we calculated the inhibition constant of afatinib, which is currently not used in this particular protein.