What is the role of Quizartinib (Acrylamide derivative) in the treatment of Acute Myeloid Leukemia (AML) with FLT3-ITD mutations?

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Last updated: November 27, 2025View editorial policy

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Quizartinib in FLT3-ITD-Positive Acute Myeloid Leukemia

Quizartinib is a highly potent and selective FLT3 inhibitor approved for treating FLT3-ITD-positive AML in two distinct settings: as combination therapy with chemotherapy for newly diagnosed patients, and as monotherapy for relapsed/refractory disease, with demonstrated survival benefits in both contexts. 1, 2

Mechanism and Pharmacology

Quizartinib is a second-generation type II FLT3 tyrosine kinase inhibitor that binds to the ATP binding domain of FLT3, preventing autophosphorylation and blocking downstream signaling pathways (RAS/RAF/MEK, MAPK/ERK, PI3K/AKT/mTOR, and JAK/STAT5). 2, 3 The drug achieves steady-state concentrations by day 15 with once-daily dosing, has 71% oral bioavailability, and exhibits an effective half-life of 81 hours during maintenance therapy. 2

First-Line Treatment (Newly Diagnosed FLT3-ITD-Positive AML)

For adults aged 18-75 years with newly diagnosed FLT3-ITD-positive AML, quizartinib should be combined with standard 7+3 induction chemotherapy (cytarabine plus anthracycline), continued through consolidation, and maintained as monotherapy for up to 3 years. 1, 4

Dosing Regimen for Newly Diagnosed Disease

  • Induction: 35.4 mg orally once daily starting on day 8 of chemotherapy, continuing for 14 days 2
  • Consolidation: 35.4 mg orally once daily starting on day 8, continuing for 14 days with each cycle 2
  • Maintenance: 53 mg orally once daily for up to 3 years (but not after allogeneic HCT in the United States) 2

Efficacy in Newly Diagnosed Patients

The QuANTUM-First trial demonstrated that quizartinib plus chemotherapy significantly improved overall survival compared to placebo plus chemotherapy (median OS 31.9 months vs 15.1 months; HR 0.78,95% CI 0.62-0.98, p=0.032). 4 This survival benefit was maintained even when patients proceeded to allogeneic hematopoietic cell transplantation. 4

Relapsed/Refractory FLT3-ITD-Positive AML

For patients with relapsed or refractory FLT3-ITD-positive AML, quizartinib monotherapy provides a survival benefit over salvage chemotherapy, though gilteritinib is preferred when available based on superior overall survival data. 5

Comparative Efficacy in Relapsed/Refractory Disease

Quizartinib monotherapy showed a survival benefit in relapsed/refractory FLT3-ITD-mutated patients (median OS 6.2 months vs 4.7 months with chemotherapy), though this was less robust than gilteritinib's benefit (median OS 9.3 months vs 5.6 months). 5 The composite complete remission rate with quizartinib monotherapy was 56% in FLT3-ITD-positive patients aged ≥60 years with early relapse, and 46% in those with relapse after salvage therapy or transplant. 6

Dosing for Relapsed/Refractory Disease

The approved dose for relapsed/refractory disease is 60 mg orally once daily (based on QuANTUM-R trial), though earlier phase 2 studies used sex-based dosing (135 mg/day for men, 90 mg/day for women). 5, 6

Post-Transplant Relapse

For patients with FLT3-mutated AML relapsing after allogeneic HCT, both quizartinib and gilteritinib show encouraging results as monotherapy, with the potential to bridge patients to a second allogeneic HCT or donor lymphocyte infusion. 5 This represents a critical treatment option for a population with otherwise dismal prognosis, particularly for those relapsing later than 5 months post-transplant. 5

Safety Profile and Monitoring Requirements

Common Adverse Events

The most frequent adverse events with quizartinib are infectious complications and QT prolongation. 5

Infectious complications:

  • Sepsis/septic shock: 19% (grade 3-5) 5
  • Pneumonia: 12% (grade 3 or higher: 9-13%) 5
  • Febrile neutropenia: 37-41% (grade 3-4) 5

Cardiac toxicity:

  • QTcF prolongation (grade 3): 3-4% of patients 5
  • Median QTcF prolongation: 18-24 ms at therapeutic doses 2
  • One case of torsades de pointes reported in phase 2 studies 6

Critical Monitoring and Management

Monitor ECG at baseline, on days 8 and 15 of cycle 1, and regularly thereafter; avoid concomitant QT-prolonging medications and maintain electrolytes (potassium, magnesium) within normal limits. 2 The drug should be held if QTcF exceeds 500 ms or increases >60 ms from baseline. 2

Antimicrobial Prophylaxis Recommendations

No specific antimicrobial prophylaxis is required when quizartinib is given as monotherapy; standard of care prophylaxis should be applied when combined with intensive chemotherapy. 5 Standard neutropenic fever protocols apply for diagnostic workup and treatment of infections. 5

Drug Interactions

Avoid strong CYP3A4 inhibitors (azole antifungals, clarithromycin, protease inhibitors) and strong CYP3A4 inducers (rifampin) due to significant alterations in quizartinib exposure. 5 If azole antifungals are necessary, close monitoring for QT prolongation is essential, though alternative antifungal agents should be considered when possible. 5

Dose Modifications

No dose adjustment is required for mild-to-moderate renal impairment (CrCl 30-89 mL/min) or mild-to-moderate hepatic impairment (Child-Pugh A or B). 2 The drug has not been studied in severe renal impairment (CrCl <30 mL/min) or severe hepatic impairment (Child-Pugh C). 2

Regulatory Status and Clinical Context

Quizartinib is approved in the United States, Japan, Europe, and United Kingdom for newly diagnosed FLT3-ITD-positive AML in combination with chemotherapy. 1, 3 For relapsed/refractory disease, it is approved only in Japan, while gilteritinib holds broader approval and is generally preferred in this setting based on superior survival data. 5 The European Medicines Agency has not approved quizartinib for relapsed/refractory disease despite demonstrated survival benefit. 5

Resistance Mechanisms

Resistance to quizartinib typically develops through on-target FLT3 kinase domain mutations (particularly D835 and F691 mutations) or activation of alternative signaling pathways. 3 This underscores the importance of combination strategies and sequential use of different FLT3 inhibitors with distinct resistance profiles. 3

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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