Therapy of Chronic Myeloid Leukemia: Twilight of the Imatinib Era?
Figure 3
Schematic mechanism of IM action. (a) The constitutively active BCR/ABL tyrosine kinase functions by transferring phosphate from ATP to tyrosine residues on various substrates leading to excess proliferation of myeloid cells typical for CML. (b) IM blocks binding of ATP to the BCR/ABL kinase, causing inhibition of its activity.
