Informed Clinical Decision-Making in CP-CML or Ph+ ALL

EP: 1.Current Standards of Care in Patients with Chronic Phase Chronic Myeloid Leukemia (CP-CML) and Philadelphia Chromosome-Positive ALL (Ph+ ALL)

EP: 2.Goals of Treatment for Patients with CP-CML and Acute Phase CML

EP: 3.Factors Impacting CML Treatment Selection

EP: 4.IRIS Trial Highlighting Role of Imatinib in CML Treatment

EP: 5.OPTIC Trial Overview

EP: 6.Unmet Needs Surrounding CP-CML and Ph+ ALL

EP: 7.Effects of TKI Resistance and Intolerance

EP: 8.Identifying TKI Resistance in Patients

EP: 9.Challenges in Treating Resistant CP-CML or Ph+ ALL

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EP: 10.Informed Clinical Decision-Making in CP-CML or Ph+ ALL

EP: 11.Considerations for Second and Third Generation TKI Treatment

EP: 12.Novel Agents as Third-Line Treatment Options

Neal Dave, PharmD: Mutationaltesting occurs typically when a patient progresses from chronic phase to acute or blast phase. And so that would be the time to possibly see if there is a mutation that’s causing the resistance or for treatment to not work.

Having mutational testing information earlier would definitely help. You can make that choice early in therapy, you can monitor that patient a lot closer. I don’t know if there are data on starting patients on a TKI [tyrosine kinase inhibitor] that works specifically on a mutation, but that’s potentially an option. You would run through your options for drug therapy if you start on a later-generation TKI. But I think you’d have a more informed decision when you’re starting that patient on a therapy and possibly you could be a bit more vigilant with monitoring and identifying when a patient is resistant.

For therapy options that would be available for patients who have a T315I mutation, one option would be ponatinib. I think that would be my first go to. Asciminib is another treatment option that has become available recently. There’s also the subcutaneous Synribo [omacetaxine mepesuccinate]. That’s a twice daily injection. I think the first 2 I mentioned are better options than the subcutaneous version.

There could be resistance without a mutation, but you wouldn’t know it if you haven’t tested. But I think you need to identify the cause of the resistance. That’s the big need, identifying, is it a compliance issue? With orals, it can be a problem. Or is it an adverse effect or a drug interaction that’s causing that? Then you can make a decision on which drug therapy to utilize for this patient. It does need to be tailored to each individual patient and why they’re having resistance to a drug therapy that they were initially prescribed.

Transcript edited for clarity.