TKI resistance is a critical moment in the treatment of CP-CML1
Treatment-resistant patients need a therapy with depth and durability of response in the third line
Cycling second-generation TKIs in resistant patients is associated with reduced response rates and poor survival1-5
aData from the Ibrahim et al (n=7), García‑Gutiérrez et al (n=17), and Garg et al (n=12) publications. Ibrahim et al defined hematologic resistance as either failure to achieve a CHR or loss of a previously achieved CHR. Garg et al included patients with CP‑CML who developed resistance to second‑line TKI treatment without acquiring new BCR::ABL1 mutations. The percentage listed above includes only those patients with CP‑CML who developed resistance to second‑line treatment and had acquired novel BCR::ABL1 mutations after developing resistance. Garg et al defined resistance as failure to achieve a CHR (CP only) or any hematologic response (AP or BP) after 3 months of therapy, persistence of 100% Philadelphia chromosome (Ph)‑positive metaphases after 6 months of therapy, or 35% or more after 12 months of therapy, transformation to AP or BP, or loss of cytogenetic response or CHR at any time during the course of therapy.3-5
Resistance to TKIs occurs by two mechanisms6,7:
- Primary: Lack of response to initial TKI therapy
- Secondary: Loss of response, potentially due to BCR::ABL1 mutations and disease progression
Recognize the critical moment and assess your treatment path forward
For patients heavily pretreated with TKIs, consider ICLUSIG
For patients with CML, regardless of mutations, consider ICLUSIG
ICLUSIG is a third-generation pan-mutational TKI
AP=accelerated phase; BP=blast phase; CCyR=complete cytogenetic response; CHR=complete hematologic response; CP=chronic phase; CP-CML=chronic phase chronic myeloid leukemia; CML=chronic myeloid leukemia; TKI=tyrosine kinase inhibitor.