Only VANFLYTA specifically targets the FLT3-ITD mutation, one of the most aggressive threats in AML

Discover how VANFLYTA worked in eligible patients with newly diagnosed FLT3-ITD+ AML

VANFLYTA is a potent and selective therapy that acts on the FLT3-ITD mutation1,2

Mechanism of Action for VANFLYTA1,3

Image representing mechanism of action for VANFLYTA

Adapted from Grafone et al, 2012.

VANFLYTA binds to the inactive conformation of the FLT3 receptor leading to inhibition of downstream signaling. VANFLYTA interacts with the juxtamembrane region adjacent to the ATP binding site that is only accessible when the receptor is inactive, therefore preventing receptor activation.1,3

ATP=adenosine triphosphate.

VANFLYTA is a targeted treatment with minimal impact on off-target kinases1,2

FLT3 Selectivity in VANFLYTA2,4

Image representing FLT3 selectivity in VANFLYTA Legend for the FLT3 selectivity in VANFLYTA image

Reprinted from Blood, Vol 114, Zarrinkar P et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML), Pages 2984-2992, Copyright 2009, with permission from Elsevier.

VANFLYTA is potent and selective, with high kinase inhibition of the FLT3 signaling pathway, which harbors the FLT3-ITD mutation1,2

QuANTUM-First is the only pivotal trial to specifically study FLT3-ITD+ AML patients over a 5-year period1,5,6

VANFLYTA is the first FLT3 inhibitor indicated across all 3 treatment phases.1,5,6

VANFLYTA is not indicated as maintenance monotherapy following allogeneic HSCT; improvement in overall survival with VANFLYTA in this setting has not been demonstrated.1

The efficacy and safety of VANFLYTA vs placebo were studied in a Phase 3, randomized, double-blind, placebo-controlled, multicenter global study of patients with newly diagnosed FLT3-ITD+ AML. 1,3

QuANTUM-First Study Design and Endpoints 1,3,4

QuANTUM-First Study Design & Endpoints for VANFLYTA QuANTUM-First Study Design & Endpoints for VANFLYTA


overall survival1


EFS, CR, and CRc1,3


RFS and DoCR1,3

Standard chemotherapy included cytarabine- and anthracycline-based induction and consolidation regimens (either daunorubicin or idarubicin). Eligible patients, including those who underwent allogeneic HSCT, continued with single agent VANFLYTA or standard chemotherapy. There was no re-randomization at the start of post-consolidation therapy.1,3

A second course of induction was administered to 20% of the patients; 65% initiated at least 1 cycle of consolidation; and 39% initiated maintenance treatment with VANFLYTA1

  • Among the patients who entered maintenance, 64% completed at least 12 cycles, 36% completed at least 24 cycles, and 16% completed all 36 planned cycles of maintenance
  • 29% (157/539) of the patients underwent HSCT in first CR

*Patients were stratified by age (<60 vs ≥60 years), white blood cell count at diagnosis (<40x109/L vs ≥40x109/L), and region (North America, Europe vs Asia, other regions).1

Patients received 35.4 mg orally once daily on Days 8-21 of 7+3 (cytarabine [100 or 200 mg/m2/day], on Days 1-7 plus daunorubicin [60 mg/m2/day] or idarubicin [12 mg/m2/day] on Days 1-3), and on Days 8-21 or 6-19 of an optional second induction (7+3 or 5+2 [5 days cytarabine plus 2 days daunorubicin or idarubicin], respectively).1

Consolidation chemotherapy consisted of 35.4 mg orally once daily on Days 6-19 of high-dose cytarabine (1.5 to 3 g/m2 every 12 hours on Days 1, 3, and 5) for up to 4 cycles.1

CR=complete remission; CRc=composite complete remission; DoCR=duration of complete remission; EFS=event-free survival; HiDAC=high-dose cytarabine; HSCT=hematopoietic stem cell transplantation; RFS=relapse-free survival.

VANFLYTA was studied in the largest and longest trial of patients with newly diagnosed FLT3-ITD+ AML1,3


Chart representing baseline patient characteristics for VANFLYTA Chart representing baseline patient characteristics for VANFLYTA
  • Of the 539 randomized patients:
    • The majority of the patients (72%) had intermediate risk cytogenetics at baseline
    • FLT3-ITD VAF was 3-25% in 36% of patients, >25-50% in 52% of patients, and >50% in 12% of patients
    • NPM1 mutations were identified in 52% of patients

*Three patients in the ITT set were randomized but not treated in each arm.4

One patient in the placebo group was missing an ECOG status.4

Favorable: inv(16), t(16;16), t(8;21), or t(15;17); intermediate: normal, 8, 6, or −Y; unfavorable: deI(5q), −5, del(7q), −7, or complex karyotype.

ECOG=Eastern Cooperative Oncology Group; ITT=intent-to-treat; NPM1=nucleophosmin; VAF=variant allelic frequency.


1. VANFLYTA [package insert]. Basking Ridge, NJ: Daiichi Sankyo, Inc; 2023. 2. Aikawa T, Togashi N, Iwanaga K, et al. Quizartinib, a selective FLT3 inhibitor, maintains antileukemic activity in preclinical models of RAS-mediated midostaurin-resistant acute myeloid leukemia cells. Oncotarget. 2020;11(11):943-955. doi:10.18632/oncotarget.27489 3. Larrosa-Garcia M, Baer MR. FLT3 inhibitors in acute myeloid leukemia: Current status and future directions. Mol Cancer Ther. 2017;16(6):991-1001. doi:10.1158/1535-7163.MCT-16-0876 4. Zarrinkar P, Gunawardane R, Cramer M, et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood. 2009;114(14):2984-2992. doi:10.1182/blood-2009-05-222034