Submit articles online
ISMPO
THIEME

Year (Archive)

Year

Issues

Search

Recent Articles

IJMPO—A Journey of a Thousand Miles

Author : Padmaj S. Kulkarni

Coronavirus Disease 2019 Treatment—T-Cells Hold the Key in Severe Cases

Author : Kunal Das, Nitika Agrawal, Mansi Kala, Rakhee Khanduri

Why Is China Importing COVID-19 Vaccine Now?

Author : Purvish M. Parikh

Gilteritinib

CC BY 4.0 · Indian J Med Paediatr Oncol 2025; 46(06): 600-604

DOI: DOI: 10.1055/s-0045-1809991

Author : Harini Raghunathan, Parathan Karunakaran

Abstract

Introduction

Acute myeloid leukemia (AML) is a heterogeneous and aggressive form of blood cancer that affects the myeloid lineage of the cells. Among various genetic mutations associated with AML, the FLT-3 mutation is one of the most common and associated with poor prognosis. Gilteritinib (previously known as ASP2215) is the first tyrosine kinase inhibitor approved as monotherapy for treatment of relapsed/refractory AML.

Areas Covered

We review gilteritinib in detail, including its mechanism of action, pharmacology, efficacy, toxicity profile, and key clinical trials.

Keywords

FLT3 mutation - relapsed/refractory AML - TKI - gilteritinib

Patient Consent

Patient consent is not required.

Publication History

Article published online:
10 July 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India

We recommend


    Abstract

    Introduction

    Acute myeloid leukemia (AML) is a heterogeneous and aggressive form of blood cancer that affects the myeloid lineage of the cells. Among various genetic mutations associated with AML, the FLT-3 mutation is one of the most common and associated with poor prognosis. Gilteritinib (previously known as ASP2215) is the first tyrosine kinase inhibitor approved as monotherapy for treatment of relapsed/refractory AML.

    Areas Covered

    We review gilteritinib in detail, including its mechanism of action, pharmacology, efficacy, toxicity profile, and key clinical trials.

    Keywords

    FLT3 mutation - relapsed/refractory AML - TKI - gilteritinib

    Introduction

    Acute myeloid leukemia (AML) has an annual incidence of approximately 2 to 3 per 100,000 in adults in India. Fms-related tyrosine kinase 3 (FLT3) gene, which encodes type III receptor tyrosine kinase protein, is the most common gene that is mutated in AML.

    FLT3-mutated AML is characterized by a younger age of onset, high white blood cell count, and high blast percentage at presentation, along with an elevated lactate dehydrogenase. It does achieve remission with conventional therapy, but has a pronounced tendency to relapse, relapse quickly, and die sooner.

    Based on the interim results of the ADMIRAL study, gilteritinib was approved by the U.S. Food and Drug Administration (FDA) in November 2018 for the treatment of adults with relapsed and/or refractory (R/R) AML with a FLT3 mutation.[1] It has been available in India since April 2024. [Table 1] summarizes the drugs available with FLT3 activity.

    Table 1

    FDA-approved drugs for FLT3-mutated AML

    Drug

    Type

    FLT3 activity

    Generation

    Selectivity

    Upfront therapy

    Relapsed therapy

    Sorafenib

    2

    Only ITD

    1

    Multikinase inhibitor (FLT3, VEGFR, PDGFR)

    Midostaurin

    1

    ITD and TKD

    1

    Multikinase inhibitor

    As combination

    Quizartinib

    2

    Only ITD

    2

    FLT3

    As combination

    Gilteritinib

    1

    ITD and TKD

    2

    FLT3, ALK, AXL

    Monotherapy
    Abbreviations: AML, acute myeloid leukemia; FDA, Food and Drug Administration; ITD, internal tandem duplication; TKD, tyrosine kinase domain


    Gilteritinib

    Mechanism of Action

    Gilteritinib is a highly selective FLT3 inhibitor, which has activity against both FLT3-ITD and FLT-TKD mutations. In comparison, midostaurin has slightly lower efficacy against FLT3-TKD. Gilteritinib also inhibits ALK and AXL, which is overexpressed in AML and has shown potential role in chemoresistance.[2]

    Pharmacokinetics

    Maximum plasma concentration achieved: 4 to 6 hours. High-fat meal delays it by 2 hours.

    It is metabolized via CYP3A4, and it is excreted mainly via feces. It has a long elimination half-life of 113 hours, permitting once daily dosing.[2]

    Drug Interactions

    Strong CYP3A inhibitors (voriconazole, posaconazole) increase gilteritinib levels by 34.24%. Hence, dose reduction to 80 mg is advised. However, effect on efficacy is not known. It is pertinent to note that the ADMIRAL trial did not utilize these azoles for prophylaxis.[3]

    Safety[1] [4]

    Gilteritinib is generally well-tolerated compared with traditional chemotherapy. Its nonhematological toxicity includes:

    1. Aspartate and alanine aminotransferase elevation was the most commonly reported adverse effect (AE).

    2. QT segment prolongation

      Recommendation is for electrocardiogram monitoring on days 1, 8, and 15 of cycle 1 and day 1 of subsequent cycles. It is advised to withhold the drug if QTc > 500 ms, and restart at a lower dose once the QTc < 480 ms. Periodic potassium and magnesium monitoring is mandated.

    3. Differentiation syndrome (DS)[5]

      DS is a unique side effect initially reported with the use of all-trans retinoic acid in acute promyelocytic leukemia (APML). In the therapy of AML, gilteritinib shares this unique AE with the isocitrate dehydrogenase (IDH) inhibitors. Unlike DS seen in APML, DS occurs less frequently, has a later onset, and is associated with prominent skin involvement, in the form of Sweet's syndrome.

    4. Gastrointestinal (GI) disturbances, muscle pain, fatigue, dizziness, and peripheral edema have also been reported.

    5. Rare but serious toxicities include posterior reversible encephalopathy syndrome and Pancreatitis.


    Clinical Efficacy

    Approval for gilteritinib was obtained based on the results of CHRYSALIS and ADMIRAL trials.

    ADMIRAL Trial[1]

    This global, open-label, phase III trial enrolled 371 adult patients with R/R FLT3-mutated AML. Assigned 2:1 to either gilteritinib or salvage chemotherapy (MEC/FLAG-Ida/azacitidine [Aza]/low dose cytarabine). The median overall survival was 9.3 months in the gilteritinib group compared with 5.6 months in the chemo group. The objective response rate was considerably higher in the gilteritinib group (67.6% vs. 25.8%). Similarly, gilteritinib demonstrated a longer duration of response (11 vs. 1.8 months).

    MORPHO Trial[6]

    This phase 3 trial by the BMT CTN group evaluated gilteritinib as maintenance therapy posttransplant. The strongest benefit was seen in patients who were MRD (measurable residual disease) positive in the peritransplant period, whereas no benefit was observed in patients who were MRD-negative.

    The posttransplant relapse kinetics demonstrated that those who did not receive maintenance relapsed early (64.3% relapsed within 8 weeks and 93.9% by 16 weeks). Whereas clonal eradication due to graft versus leukemia occurred only by 3 to 6 months. Based on these kinetics in MRD-positive cases, it is advised that gilteritinib should be started soon after engraftment.

    Current Uses

    As Monotherapy

    It is the only FLT3 inhibitor approved as monotherapy by the FDA in the relapsed setting.

    As Combination Therapy

    Combination therapy is preferred in the front-line setting. The Lacewing study initially included a monotherapy arm upfront, however, it was dropped midway through the trial, due to changing treatment paradigm. [Table 2] summarizes the trials with gilteritinib combination therapy.


    Table 2

    Trials of combination therapy with gilteritinib

    Trial / Phase

    n

    Patient profile

    ORR

    CR

    OS

    PFS

    Key message

    Venetoclax plus gilteritinib[7]

    phase IB

    61

    Failed > 1 line of AML therapy

    -

    mCRc- 75%a

    10 months

    −

    Ven + Gilt had high mCRc, regardless of prior FLT3 inhibitor exposure

    Triple therapy with venetoclax, FLT3 inhibitor, and decitabine for FLT3-mutated AML[9]–

    Phase II trial

    25

    Newly diagnosed AML

    and

    R/R AML

    Excl. favorable cytogenetics and prior venetoclax exposure

    Newly diagnosed

    67–92%

    R/R AML 26–83%

    Newly diagnosed

    CRc- 92%

    R/R AML

    CRc- 62%

    Newly diagnosed

    OS not reached (2-year OS – 80%)

    R/R AML

    6.8 months

    Newly diagnosed

    18-month PFS-59%

    R/R AML- 58%

    Triplet therapy safe and effective

    Lacewing trial[10]

    Phase III trial

    123

    Newly diagnosed AML patients ineligible for intensive chemotherapy

    Gilt + AZA-

    CRc- 58%

    CR- 16.2%

    AZA

    CRc–26.5%

    CR-14.3%

    Gilt + AZA

    -9.8 months

    AZA- 8.8 months

    EFS

    Gilt + AZA- 4.5 months

    AZA-0.3 months

    Negative study

    Gilteritinib + 3 + 7 chemotherapy[3]

    phase I B trial

    80

    Newly diagnosed, fit for intensive chemotherapy

    Gilt in induction, consolidation, and maintenance

    −

    FLT-3 WT -CRc- 50%

    FLT3–mutated

    CRc-89%

    mOS- 46.1 months

    −

    Gilteritinib can be safely combined with conventional 3 + 7 therapy.

    It induced prolonged myelosuppression.

    Gilteritinib maintenance well tolerated

    Gilt plus CLIA chemotherapy (cladribine, idarubicin, cytarabine) ± venetoclax[11]

    Phase II trial

    18

    Newly diagnosed, fit for intensive chemotherapy

    CLIA + gilteritinib 80%

    Vs.

    CLIA+ gilteritinib +

    venetoclax

    88%

    21. 9 months

    For entire cohort

    (not reached for CLIA + Gil arm and 22.4 months in CLIA + Gil + Ven arm

    Addition of venetoclax produced similar results but prolonged the count recovery
    Abbreviations: Aza, Azacitidine; AML, acute myeloid leukemia; CRh, complete remission; Cri, complete remission with incomplete hematological recovery; CRc, composite CR (CR + Cri + CRh); Gilt, Gilteritinib; ORR, objective response rate; OS, overall survival; PFS, progression-free survival; R/R, relapsed and/or refractory; Ven, Venetoclax.

    1. Gilteritinib with venetoclax[7]

      It is hypothesized that targeting both FLT3 and BCL-2 pathways may enhance cell death in FLT3-mutated AML cells. Pharmacological modeling also suggests higher synergism between gilteritinib and venetoclax in comparison to midostaurin.[8]

    2. Gilteritinib with Aza[9]

      Aza is believed to enhance FLT3 inhibition by reducing cellular proliferation. The combination has shown manageable toxicity in elderly AML. However, the Lacewing study failed to demonstrate survival benefit for the addition of gilteritinib to Aza.[9] GI toxicity, especially, GI hemorrhage, was higher with gilteritinib + Aza.

      1. Triple therapy: Gilteritinib with Aza and venetoclax[10]

        It is the preferred combination and has proven to have the best efficacy. However, it is associated with higher toxicity with a 62% incidence of infection and 38%. febrile neutropenia, More so with R/R AML.

      2. Gilteritinib and chemotherapy[3] [11]

        Adding gilteritinib to standard chemotherapeutic regimens can induce a deeper molecular response by targeting residual disease more effectively than chemotherapy. However, concern exists regarding the efficacy of gilteritinib in this setting, as there is rebound increase in wild-type FLT3, induced by the recovering marrow post-chemotherapy.

    Use of Gilteritinib Post-Failure of Other FLT3i[12]

    There is a concern that prior use of FLT3i can drive the expansion of clones with additional on-target mutations, which may confer resistance to gilteritinib. However, data from the Admiral trial and real-world data clearly demonstrated its efficacy in this population (composite complete remission [CR] rates of ∼50%).


    Maintenance Therapy for Nontransplant patients[13]

    Gilteritinib maintenance is more effective in preventing early relapse at 0.5 to 1 year. However, its utility is limited if the MRD is negative.


    Myeloid Sarcoma[14]

    Shatilova et al have reported superior efficacy of gilteritinib over other FLT3i for the therapy of extramedullary disease.

    Dosing[1] [7] [9] [10] [11]

    The dose of gilteritinib is 120 mg for monotherapy (only FDA-approved dose).

    Dose escalation up to 200 mg was permitted if the patient is not in CR at 28 days of treatment.

    Gilteritinib is used at a dose of 120 mg for doublet combination therapy (either Aza or venetoclax) and 80 mg for triplet combination therapy (Aza + venetoclax + gilteritinib).

    Cost: Monotherapy with 120 mg of gilteritinib for 1 month will cost INR 6.3 lakh.

    Ongoing Phase 3 Trials

    Gilteritinib versus midostaurin in combination with intensive chemotherapy for upfront AML and MDS (HOVON 156 AML trial).[15]


    Important Points about Gilteritinib[15]

    1. Inhibition of FLT3 needs to be near complete and sustained for days, not hours. Gilteritinib has a long half-life—hence, once daily dosing. It is important to minimize drug interruptions.

    2. Lower myelosuppression

      KIT and FLT3 are structurally similar. Gilteritinib selectively inhibits mutated FLT3, it has fivefold less activity against wild-type FLT3 and nil against KIT—hence, lesser myelosuppression compared with other FLT3i.

    3. FLT3-ITD AML evolves from diagnosis to relapse

      Leukemic cells are dependent on FLT3-ITD signaling for survival. This constitutes a small proportion of the total leukemic cell population at the time of diagnosis. However, it is of a large proportion at the time of relapse. Hence, monotherapy works well at relapse, whereas a combination regimen with synergistic cytotoxicity is a better option for therapy upfront.

    4. Gilteritinib acts by a combination of apoptosis and terminal myeloid differentiation

      Apoptosis of peripheral blood blasts results in rapid clearance. However, bone marrow (BM) blasts undergo differentiation. This tends to be a slower process. Hence, the attainment of CR is later than conventional chemotherapy and recovery of normal count is also delayed.

    5. Clinical endpoint: BM aplasia is avoided with gilteritinib monotherapy; however, count recovery is delayed. Cri + CRh (CR with incomplete hematological recovery + CR with partial hematological recovery) were included as a valid endpoint in clinical trials. This trend is seen with monotherapy with other targeted therapies like the IDH1 and 2 inhibitors as well. CRh has been associated with transfusion independence and lower risk of infections. Thus, it is a clinically relevant endpoint.

    6. MRD analysis: Polymerase chain reaction (PCR) is insufficient to analyze MRD in FLT3-mutated AML due to the template bias issue. Hence, a high sensitivity PCR-next-generation sequencing combination method is utilized to test MRD. This is currently not available in India.

    Molecular Spectrum of Action[16]

    Analysis of the molecular makeup of good responders to gilteritinib demonstrates that:

    • Good response was seen with those with concomitant DNMT3A, IDH1/2, and WT-1 mutations.

    • While the best response was seen with dual-mutated DNMT3A and NPM1.

    The impact of FLT3 mutations on response was also assessed:

    • Presence of multiple FLT3-ITD mutations had no impact on response.

    • Longer FLT3 ITD length responded better than shorter ITD length.

    • High allele ratio FLT3 (↑allele burden) is known to have poorer prognosis—gilteritinib was superior to chemotherapy. However, it was not able to fully abrogate the poor risk.

    Treatment resistance to gilteritinib:

    • Failure of gilteritinib therapy can be caused by primary and secondary mechanisms.

    • F691L gatekeeper mutations and RAS/MAPK pathway gene mutations constitute the most common resistance pathway. They both are mutually exclusive.

    • On-target point mutations: D835, F691 (gatekeeper mutation), N676, and FLT-3 juxtamembrane (JMD) E598D mutations.

    • Off-target mutations in Ras/MAPK pathway: NRAS, PTPN11, and KRAS.

    • Nongenetic mechanisms like FGF2-activated FGF1 receptor 1 can also contribute.

    Conclusion

    Gilteritinib is the first oral tyrosine kinase inhibitor approved for the management of AML in the R/R setting. Its tolerance and lack of marrow aplasia makes it an ideal agent for managing AML patients in an outpatient setting. Ongoing clinical trials in combination therapy and in upfront setting will open broader avenues in the management of FLT-3-mutated AML.

    Conflict of Interest

    None declared.

    Patient Consent

    Patient consent is not required.


    References

    1. Perl AE, Martinelli G, Cortes JE. et al. Gilteritinib or chemotherapy for relapsed or refractory  FLT3-mutated AML. N Engl J Med 2019; 381 (18) 1728-1740
      Crossref PubMed Search in Google Scholar
    2. Levis M, Perl AE. Gilteritinib: potent targeting of FLT3 mutations in AML. Blood Adv 2020; 4 (06) 1178-1191
      Crossref PubMed Search in Google Scholar
    3. Pratz KW, Cherry M, Altman JK. et al. Gilteritinib in combination with induction and consolidation chemotherapy and as maintenance therapy: a phase IB study in patients with newly diagnosed AML. J Clin Oncol 2023; 41 (26) 4236-4246
      Crossref PubMed Search in Google Scholar
    4. Astellas Pharma US, Inc. Highlights of prescribing information [Internet]. Northbrook, IL: Astellas Pharma US, Inc.; 2018 . Accessed April 4, 2025 at:  https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/211349s000lbl.pdf
    5. McMahon CM, Canaani J, Rea B. et al. Gilteritinib induces differentiation in relapsed and refractory  FLT3-mutated acute myeloid leukemia. Blood Adv 2019; 3 (10) 1581-1585
      Crossref PubMed Search in Google Scholar
    6. Levis MJ, Hamadani M, Logan B. et al; BMT-CTN 1506/MORPHO Study Investigators. Gilteritinib as post-transplant maintenance for AML with internal tandem duplication mutation of  FLT3 . J Clin Oncol 2024; 42 (15) 1766-1775
      Crossref PubMed Search in Google Scholar
    7. Daver N, Perl AE, Maly J. et al. Venetoclax plus gilteritinib for  FLT3-mutated relapsed/refractory acute myeloid leukemia. J Clin Oncol 2022; 40 (35) 4048-4059
      Crossref PubMed Search in Google Scholar
    8. Janssen M, Schmidt C, Bruch PM. et al. Venetoclax synergizes with gilteritinib in FLT3 wild-type high-risk acute myeloid leukemia by suppressing MCL-1. Blood 2022; 140 (24) 2594-2610
      Crossref PubMed Search in Google Scholar
    9. Wang ES, Montesinos P, Minden MD. et al. Phase 3 trial of gilteritinib plus azacitidine vs azacitidine for newly diagnosed FLT3mut+ AML ineligible for intensive chemotherapy. Blood 2022; 140 (17) 1845-1857
      Crossref PubMed Search in Google Scholar
    10. Maiti A, DiNardo CD, Daver NG. et al. Triplet therapy with venetoclax, FLT3 inhibitor and decitabine for FLT3-mutated acute myeloid leukemia. Blood Cancer J 2021; 11 (02) 25
      Crossref PubMed Search in Google Scholar
    11. Abuasab T, Kantarjian H, Garcia-Manero G. et al. Phase II study of cladribine, idarubicin, cytarabine (CLIA) plus gilteritinib in patients with FLT3 mutated acute myeloid leukemia (AML). Blood 2021; 138 (supplement 1): 2330
      Crossref Search in Google Scholar
    12. Numan Y, Abdel Rahman Z, Grenet J. et al. Gilteritinib clinical activity in relapsed/refractory FLT3 mutated acute myeloid leukemia previously treated with FLT3 inhibitors. Am J Hematol 2022; 97 (03) 322-328
      Crossref PubMed Search in Google Scholar
    13. Gyan E, Minden MD, Kubo K. et al. Maintenance therapy with the FMS-like tyrosine kinase 3 inhibitor gilteritinib in patients with FMS-like tyrosine kinase 3-internal tandem duplication acute myeloid leukemia: a phase 2 study. Cancer 2025; 131 (04) e35746
      Crossref PubMed Search in Google Scholar
    14. Shatilova A, Budaeva I, Matvienko Y. et al. Myeloid sarcoma or extramedullary acute myeloid leukemia: experience in managing single-centre patients cohort. Blood 2024; 144 (supplement 1): 5987
      Crossref Search in Google Scholar
    15. HOVON Foundation. . Gilteritinib versus midostaurin in FLT3 mutated acute myeloid leukemia. ClinicalTrials.gov Identifier: NCT04027309. Amsterdam: HOVON; 2018 [updated June 13, 2023]. Accessed April 08, 2025 at:  https://clinicaltrials.gov/study/NCT04027309
    16. Smith CC, Levis MJ, Perl AE, Hill JE, Rosales M, Bahceci E. Molecular profile of FLT3-mutated relapsed/refractory patients with AML in the phase 3 ADMIRAL study of gilteritinib. Blood Adv 2022; 6 (07) 2144-2155
      Crossref PubMed Search in Google Scholar

    Address for correspondence

    Parathan Karunakaran, MD, DM
    Cancer Institute (WIA)
    38, Sardar Patel Road, Chennai 600 036, Tamil Nadu
    India   

    Publication History

    Article published online:
    10 July 2025

    © 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

    Thieme Medical and Scientific Publishers Pvt. Ltd.
    A-12, 2nd Floor, Sector 2, Noida-201301 UP, India

    We recommend

      References

      1. Perl AE, Martinelli G, Cortes JE. et al. Gilteritinib or chemotherapy for relapsed or refractory  FLT3-mutated AML. N Engl J Med 2019; 381 (18) 1728-1740
        Crossref PubMed Search in Google Scholar
      2. Levis M, Perl AE. Gilteritinib: potent targeting of FLT3 mutations in AML. Blood Adv 2020; 4 (06) 1178-1191
        Crossref PubMed Search in Google Scholar
      3. Pratz KW, Cherry M, Altman JK. et al. Gilteritinib in combination with induction and consolidation chemotherapy and as maintenance therapy: a phase IB study in patients with newly diagnosed AML. J Clin Oncol 2023; 41 (26) 4236-4246
        Crossref PubMed Search in Google Scholar
      4. Astellas Pharma US, Inc. Highlights of prescribing information [Internet]. Northbrook, IL: Astellas Pharma US, Inc.; 2018 . Accessed April 4, 2025 at:  https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/211349s000lbl.pdf
      5. McMahon CM, Canaani J, Rea B. et al. Gilteritinib induces differentiation in relapsed and refractory  FLT3-mutated acute myeloid leukemia. Blood Adv 2019; 3 (10) 1581-1585
        Crossref PubMed Search in Google Scholar
      6. Levis MJ, Hamadani M, Logan B. et al; BMT-CTN 1506/MORPHO Study Investigators. Gilteritinib as post-transplant maintenance for AML with internal tandem duplication mutation of  FLT3 . J Clin Oncol 2024; 42 (15) 1766-1775
        Crossref PubMed Search in Google Scholar
      7. Daver N, Perl AE, Maly J. et al. Venetoclax plus gilteritinib for  FLT3-mutated relapsed/refractory acute myeloid leukemia. J Clin Oncol 2022; 40 (35) 4048-4059
        Crossref PubMed Search in Google Scholar
      8. Janssen M, Schmidt C, Bruch PM. et al. Venetoclax synergizes with gilteritinib in FLT3 wild-type high-risk acute myeloid leukemia by suppressing MCL-1. Blood 2022; 140 (24) 2594-2610
        Crossref PubMed Search in Google Scholar
      9. Wang ES, Montesinos P, Minden MD. et al. Phase 3 trial of gilteritinib plus azacitidine vs azacitidine for newly diagnosed FLT3mut+ AML ineligible for intensive chemotherapy. Blood 2022; 140 (17) 1845-1857
        Crossref PubMed Search in Google Scholar
      10. Maiti A, DiNardo CD, Daver NG. et al. Triplet therapy with venetoclax, FLT3 inhibitor and decitabine for FLT3-mutated acute myeloid leukemia. Blood Cancer J 2021; 11 (02) 25
        Crossref PubMed Search in Google Scholar
      11. Abuasab T, Kantarjian H, Garcia-Manero G. et al. Phase II study of cladribine, idarubicin, cytarabine (CLIA) plus gilteritinib in patients with FLT3 mutated acute myeloid leukemia (AML). Blood 2021; 138 (supplement 1): 2330
        Crossref Search in Google Scholar
      12. Numan Y, Abdel Rahman Z, Grenet J. et al. Gilteritinib clinical activity in relapsed/refractory FLT3 mutated acute myeloid leukemia previously treated with FLT3 inhibitors. Am J Hematol 2022; 97 (03) 322-328
        Crossref PubMed Search in Google Scholar
      13. Gyan E, Minden MD, Kubo K. et al. Maintenance therapy with the FMS-like tyrosine kinase 3 inhibitor gilteritinib in patients with FMS-like tyrosine kinase 3-internal tandem duplication acute myeloid leukemia: a phase 2 study. Cancer 2025; 131 (04) e35746
        Crossref PubMed Search in Google Scholar
      14. Shatilova A, Budaeva I, Matvienko Y. et al. Myeloid sarcoma or extramedullary acute myeloid leukemia: experience in managing single-centre patients cohort. Blood 2024; 144 (supplement 1): 5987
        Crossref Search in Google Scholar
      15. HOVON Foundation. . Gilteritinib versus midostaurin in FLT3 mutated acute myeloid leukemia. ClinicalTrials.gov Identifier: NCT04027309. Amsterdam: HOVON; 2018 [updated June 13, 2023]. Accessed April 08, 2025 at:  https://clinicaltrials.gov/study/NCT04027309
      16. Smith CC, Levis MJ, Perl AE, Hill JE, Rosales M, Bahceci E. Molecular profile of FLT3-mutated relapsed/refractory patients with AML in the phase 3 ADMIRAL study of gilteritinib. Blood Adv 2022; 6 (07) 2144-2155
        Crossref PubMed Search in Google Scholar

      CONTACT US

      QUICK LINKS

      NEWSLETTER

      Get all the information, latest updates delivered directly in your inbox

      © Indian Journal of Medical and Paediatric Oncology. Designed and Developed by Stackloom & Minerrals