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ASH 2024 | The LODEFI trial: low-dose deferasirox in LR-MDS resistant or relapsing after ESAs
Sophie Park, MD, PhD, CHU Grenoble Alpes, Grenoble, France, discusses findings from the Phase II LODEFI trial (NCT03387475), which is evaluating low-dose deferasirox in patients with lower-risk myelodysplastic syndrome (LR-MDS) who are resistant or relapsing after erythropoietin-stimulating agents (ESAs). Prof. Park notes that low-dose deferasirox increased erythroid progenitor proliferation and achieved 47% transfusion independence at month 2. She suggests a mechanism beyond traditional iron chelation, potentially involving the reduction of oxidative stress and activation of the NF-κB pathway. This interview took place at the 66th ASH Annual Meeting and Exposition, held in San Diego, CA.
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Transcript (AI-generated)
And for the second abstract, the LODEFI trial, the background is that you know that when you collate MDS patients with anemia, you have about 20-30% of patients who had erythroid response. So we have set an in vitro study where we have evaluated the deferasirox and the proliferation of erythroid progenitors. And we have observed that low-dose deferasirox, three micromolar, increases the proliferation of erythroid progenitors...
And for the second abstract, the LODEFI trial, the background is that you know that when you collate MDS patients with anemia, you have about 20-30% of patients who had erythroid response. So we have set an in vitro study where we have evaluated the deferasirox and the proliferation of erythroid progenitors. And we have observed that low-dose deferasirox, three micromolar, increases the proliferation of erythroid progenitors. So we translated that in a clinical trial, in a Phase II clinical trial, where we evaluated the low dose of deferasirox, 3.5 mg per kilo per day of deferasirox instead of the traditional chelating dose of 17 mg per kilo. So the patients were relapsing or refractory to ESA and we administered deferasirox low dose in these patients. So in this trial there were 38 patients having received the treatment. And we observed, interestingly, that there was 47% of transfusion independence at month 2 in this trial. And perhaps the mechanism is not iron chelation, but it is diminishing, decreasing of ROS oxidative stress and increase of NF-κB pathway for the proliferation of erythroid progenitors. And so we will see later results at month 18 to see the longer effects of deferasirox.
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Disclosures
Janssen: Research Funding; BMS/Celgene: Honoraria, Other: Travel Support & Meetings, Research Funding; Novartis: Honoraria, Research Funding; Pfizer: Honoraria, Other: Travel Support & Meetings, Research Funding.
