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Ponatinib produced deep responses in patients with chronic myeloid leukaemia or Philadelphia-positive acute lymphoblastic leukaemia whose disease had resisted other kinase inhibitors, including the T315I mutation that no other drug could reach.
Phase 2 study of 449 heavily pretreated patients with chronic, accelerated or blast-phase CML or Ph-positive ALL, including 128 with the T315I gatekeeper mutation, treated with ponatinib 45 mg daily.
In chronic phase, 56 percent achieved a major cytogenetic response (70 percent of those with T315I); responses in accelerated and blast phase were lower and shorter. Arterial occlusive events emerged as the defining toxicity, later prompting dose reduction strategies.
Ponatinib is the drug for T315I-mutated disease and for patients who have failed several inhibitors, including in accelerated and blast phase as a bridge to transplant. Cardiovascular risk must be managed actively.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.
Shares Transplant-free Ph-positive ALL for MRD-negative adults, New England Journal of Medicine.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.
Shares Transplant-free Ph-positive ALL for MRD-negative adults, Ponatinib.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.
Shares Ponatinib, Chronic myeloid leukaemia, accelerated and blast phase.