Figures & data
Figure 1 Mode of action of imatinib mesylate. The phosphorylation of a substrate is shown schematically. ATP occupies the pocket in the ABL component of BCR-ABL oncoprotein. The substrate then detaches itself from the BCR-ABL oncoprotein and makes functional contact with a further downstream effector molecule. When imatinib occupies the ATP binding site, it prevents phosphorylation of the substrate. This molecule in turn fails to make contact with the effector protein and the signal transduction pathway that would otherwise transmit the leukemia signal is interrupted. Reproduced with permission from Goldman and Mughal.Citation70
Figure 2 Development of osteoblasts and osteoclasts from bone marrow progenitors. Factors affecting the development and function of these cells, bone resorption by osteoclast, and new bone formation by osteoblasts. Copyright © 2006. Reproduced with permission from Valsamis et al; licensee BioMed Central Ltd. Alsamis HA, et al. Antiepileptic drugs and bone metabolism. Nutr Metab. 2006;3:36. doi:10.1186/1743-7075-3-36.Citation71
Table 1 Most frequently reported adverse effects in patients with CML in CP treated with imatinib
Table 2 Imatinib and reproduction: suggested recommendations to providers for patients taking imatinib by gender
Table 3 Incidence of notable short- and long-term reported toxicities of imatinib