Over the course of the last ten years, targeted small molecule medications have brought about a significant change in the treatment of chronic myeloid leukemia (CML). These medications disrupt the ATP-dependent ABL tyrosine kinase, which in turn disrupts a constitutively active BCR-ABL, which is the agent that is responsible for chronic myeloid leukemia. Despite the fact that tyrosine kinase inhibitors (TKIs) have been shown to be helpful in facilitating a survival rate that is more than 90 percent, these medications do not have any curative effects. In addition to this, the T315I BCR-ABL variant is ineffective against all of the TKIs that are currently licensed. A new generation of TKIs that are capable of binding to T315I is on the horizon, however. The current therapeutics for chronic myeloma, such as TKIs of the first and second generations, as well as potential future therapy techniques, will be reviewed, with a particular focus on the clinical utility of these medications. In recent years, new insights have emerged on the complexity of chronic myelogenous leukemia, notably in the microenvironment of the bone marrow. As a result of the fact that primitive human CML stem cells are not dependent on BCR-ABL, we recommend that strategies that go beyond targeting BCR-ABL will be the key to successfully treating CML. For patients suffering from chronic myeloid leukemia, the use of synthetic lethality or combinations of medications has the potential to transform responses into therapies that are permanent.
