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ASH 2025 | Correlation between treatment-emergent cytopenias and clinical response with imetelstat in LR-MDS
Amer Zeidan, MBBS, MHS, Yale University and Yale Cancer Center, New Haven, CT, discusses the correlation between treatment-emergent cytopenias and clinical response observed in the Phase III IMerge trial (NCT02598661) of imetelstat in patients with lower-risk myelodysplastic syndromes (LR-MDS). Dr Zeidan highlights that patients who experience thrombocytopenia and neutropenia early on after treatment initiation have a higher chance of achieving transfusion independence, reflecting the agent’s mechanism of action. This interview took place at the 67th ASH Annual Meeting and Exposition, held in Orlando, FL.
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Transcript
Another presentation I’m giving on MDS in the lower risk is a subgroup analysis or a secondary analysis from the IMerge trial looking at the use of imetelstat. And imetelstat is an approved drug in refractory/relapsed lower risk MDS after ESA failure. So in this analysis, we actually look at the correlation of the imetelstat-induced neutropenia and thrombocytopenia and the correlation with transfusion independence...
Another presentation I’m giving on MDS in the lower risk is a subgroup analysis or a secondary analysis from the IMerge trial looking at the use of imetelstat. And imetelstat is an approved drug in refractory/relapsed lower risk MDS after ESA failure. So in this analysis, we actually look at the correlation of the imetelstat-induced neutropenia and thrombocytopenia and the correlation with transfusion independence. And what we show is that patients who do get thrombocytopenia and neutropenia early on have a higher chance of achieving transfusion independence, which reflects basically on-target mechanism, which is very reminiscent of what happens with lenalidomide in deletion 5q lower risk MDS. So this could allow people to use this as a predictor for response but most importantly for people not to get too scared when the patient gets thrombocytopenia or neutropenia because it’s part of the mechanism of how the drug works.
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