O Xospata™ (gipritinibe) da Astellas Pharma já está disponível na Irlanda como monoterapia para pacientes adultos com leucemia mieloide aguda (LMA) recidivada ou refratária que apresentam mutação FLT3 – The Irish Medical Times

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Tagged with: acute myeloid leukaemia (AML) Astellas Blood cancert haematology leukaemia Xospata By Editorial Staff 21st October 2025 Astellas Pharma Co Ltd. Ireland today announced that Xospata™ (gilteritinib) 40 mg film-coated tablets for the treatment of relapsed or refractory acute myeloid leukaemia (AML) with a FLT3 mutation is now available in Ireland. Patients with acute myeloid leukemia (AML) whose disease is refractory to, or relapses after, induction chemotherapy have a dismal prognosis with standard chemotherapy. 5 In patients with AML, the presence of the FLT3 ITD mutation adversely affects survival, both at diagnosis and on failure of the initial therapy. 6-8 Gilteritinib was approved by the European Medicines Agency (EMA) in October 2019.9 This approval is based on results from the Phase 3 ADMIRAL trial, which investigated gilteritinib versus salvage chemotherapy in patients with relapsed or refractory FLT3mut+ AML. Patients treated with gilteritinib had significantly longer overall survival (OS) than those who received salvage chemotherapy. Median OS for patients who received gilteritinib was 9.3 months, compared to 5.6 months for patients who received salvage chemotherapy (Hazard Ratio = 0.637 (95% CI 0.490,0.830), P=0.0004). Rates of one-year survival were 37% for patients who received gilteritinib, compared to 16.7% for patients who received salvage chemotherapy² Patients’ FLT3mut+ status can change over the course of AML treatment, even after relapse. Due to the poor outcomes associated with FLT3mut+ AML, patients’ FLT3 mutation status may be confirmed to help inform the best treatment approach. 10-12 About the ADMIRAL Trial The Phase 3 ADMIRAL trial (NCT02421939) was an open-label, multicenter, randomized study of gilteritinib versus salvage chemotherapy in adult patients with FLT3mut+ who are refractory to or have relapsed after first-line AML therapy. The co-primary endpoints of the trial were OS and CR/CRh rates;

OS, the primary endpoint at the trial’s final analysis, was the basis of EC approval. The study enrolled 371 patients with relapsed or refractory AML and FLT3mut+ present in bone marrow or whole blood. Subjects were randomized in a 2: 1 ratio to receive gilteritinib (120 mg) or salvage chemotherapy. 2 The most common adverse events (AEs) across both treatment arms of the ADMIRAL trial were febrile neutropenia (43.7%), anemia (43.4%), and pyrexia (38.6%). Common grade ≥3 AEs related to gilteritinib were anemia (19.5%), febrile neutropenia (15.4%), thrombocytopenia (12.2%), and decreased platelet count (12.2%). Adjusted for exposure duration, serious treatment-emergent AEs per patient year were less common with gilteritinib (7.1%) than salvage chemotherapy (9.2%). 2 About Astellas Astellas Pharma Inc. , based in Tokyo, Japan, is a company dedicated to improving the health of people around the world through the provision of innovative and reliable pharmaceutical products. For more information, please visit our website at https: //www. astellas. com/en. Cautionary Notes In this press release, statements made with respect to current plans, estimates, strategies and beliefs and other statements that are not historical facts are forward-looking statements about the future performance of Astellas. These statements are based on management’s current assumptions and beliefs in light of the information currently available to it and involve known and unknown risks and uncertainties. A number of factors could cause actual results to differ materially from those discussed in the forward-looking statements. Such factors include, but are not limited to: (i) changes in general economic conditions and in laws and regulations, relating to pharmaceutical markets, (ii) currency exchange rate fluctuations, (iii) delays in new product launches, (iv) the inability of Astellas to market existing and new products effectively, Contact for inquiries or additional information: Astellas Pharma Ireland Communications Valerie Quine valerie. quine@astellas. com In the event that patients re-initiate gilteritinib post haematopoietic stem cell transplant (HSCT) as maintenance therapy, gilteritinib treatment should be restricted to patients who are minimal residual disease (MRD)-positive post-transplant1 Gilteritinib is a highly selective, oral FLT3 inhibitor with activity against both FLT3 mutation subtypes (ITD and TKD). 2 the inability of Astellas to continue to effectively research and develop products accepted by customers in highly competitive markets, and (vi) infringements of Astellas’ intellectual property rights by third parties. PCRS Update List – October https: //www. sspcrs. ie/libr/html/monthlyproductupdate. pdf. Perl, A et Gilteritinib significantly prolongs overall survival in patients with FLT3-mutated (FLT3mut+) relapsed/ refractory (R/R) acute myeloid leukemia (AML): Results from the Phase III ADMIRAL trial, N Engl J Med 2019;

381: 1728-40. Roboz GJ, Rosenblat T, Arellano M, et al. International randomized phase III study of elacytarabine versus investigator choice in patients with relapsed/refractory acute myeloid J Clin Oncol 2014; 32: 1919-26. Ravandi F, Ritchie EK, Sayar H, et Vosaroxin plus cytarabine versus placebo plus cytarabine in patients with first relapsed or refractory acute myeloid leukaemia (VALOR): a randomised, controlled, double-blind, multinational, phase 3 study. Lancet Oncol 2015;

16: 1025-36. Megías-Vericat JE, Martínez-Cuadrón D, Sanz MA, Montesinos P. Salvage regimens using conventional chemotherapy agents for relapsed/refractory adult AML patients: a systematic literature Ann Hematol 2018; 97: 1115-53. Nakao M, Yokota S, Iwai T, et Internal tandem duplication of the flt3 gene found in acute myeloid leukemia. Leukemia 1996;

10: 1911-8. Kiyoi H, Towatari M, Yokota S, et Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product. Leukemia 1998; 12: 1333-7. Yamamoto Y, Kiyoi H, Nakano Y, et Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies. Blood 2001;

97: 2434-9. European Medicines Authorization of medicines. Available at: https: //www. ema. europa. eu/about- us/what- we-do/authorisation-medicines. Last accessed October 2025. Nazha A, et al. Activating internal tandem duplication mutations of the fms-like tyrosine kinase-3 (FLT3-ITD) at complete response and relapse in patients with acute myeloid Haematologica 2012;

97(8): 1242-5. Warren M, et Clinical impact of change of FLT3 mutation status in acute myeloid leukemia patients. Mod Pathol 2012; 25(10): 1405-12. McCormick SR, et FLT3 mutations at diagnosis and relapse in acute myeloid leukemia: cytogenetic and pathologic correlations, including cuplike blast morphology. Arch Pathol Lab Med 2010;

134(8): 1143-51. PCRS Update List – October https: //www. sspcrs. ie/libr/html/monthlyproductupdate. pdf. Perl, A et Gilteritinib significantly prolongs overall survival in patients with FLT3-mutated (FLT3mut+) relapsed/ refractory (R/R) acute myeloid leukemia (AML): Results from the Phase III ADMIRAL trial, N Engl J Med 2019;

134(8): 1143-51.