-ITD–positive acute myeloid leukemia (AML) harboring an 

 mutation and epigenetic regulatory gene mutations derived a significant benefit with the addition of quizartinib (Vanflyta) plus standard chemotherapy vs placebo plus chemotherapy, according to data from an exploratory analysis of the phase 3 QuANTUM-First trial (NCT02668653) presented during the 

2025 European Hematology Association Congress

-mutated disease who received quizartinib (n = 142) achieved a median overall survival (OS) that was not estimable (NE) compared with 15.1 months in the placebo arm (n = 140; HR, 0.64; 95% CI, 0.46-0.89). Those with 

-mutated disease experienced a median OS of 40.4 months and 9.6 months in the quizartinib (n = 112) and placebo (n = 113) arms, respectively (HR, 0.55; 95% CI, 0.39-0.78). Among patients with 

-mutated disease, the median OS was NE in the quizartinib arm (n = 61) vs 11.3 months in the placebo arm (n = 67; HR, 0.60; 95% CI, 0.37-0.97). Notably, the median OS was NE among patients with 

-mutated disease who received quizartinib (n = 86) vs 9.6 months in the placebo arm (n = 82; HR, 0.47; 95% CI, 0.31-0.71).

 particularly benefited from quizartinib, irrespective of age,” Mark J. Levis, MD, PhD, said during the presentation. 

Levis is the program leader of the Hematologic Malignancies and Bone Marrow Transplant Program, as well as the director of the Adult Leukemia Service at the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center in Baltimore, Maryland. He is also a professor of oncology, medicine, and pharmacology in the Division of Hematologic Malignancies at the Johns Hopkins University School of Medicine.

In July 2023, the FDA approved quizartinib

 in combination with standard cytarabine and anthracycline induction and cytarabine consolidation, and as single-agent maintenance therapy following consolidation chemotherapy, in adult patients with newly diagnosed 

 The regulatory decision was supported by prior data from QuANTUM-First.

Unpacking the Study Design and Baseline Characteristics

QuANTUM-First was a double-blind, randomized, global study that enrolled patients with newly diagnosed 

 Patients were required to be 18 to 75 years old, have a 

-ITD allelic frequency of at least 3%, and an ECOG performance status of 0 to 2.

 All patients initiated 7+3 chemotherapy during screening.

 Random assignment was stratified by region (North America vs Europe vs Asia/other regions), age (<60 years vs ≥60 years), and white blood cell count (<40 

During the induction phase, all patients received cytarabine on days 1 through 7 plus daunorubicin or idarubicin on days 1 through 3, in combination with daily quizartinib at a dose of 35.4 mg on days 8 through 21 or placebo, for up to 2 cycles. Patients received high-dose cytarabine on days 1, 3, and 5 of the consolidation phase in combination with quizartinib or placebo on days 6 through 19, with or without allogeneic hematopoietic stem cell transplantation, for up to 4 cycles. Treatment was then continued with placebo or quizartinib at a starting dose of 26.5 mg which was increased to 53.0 mg once daily for up to 36 cycles.

The primary end point was OS. Secondary end points included composite complete remission (CRc) rate, event-free survival, complete remission rate, and safety.

Baseline gene mutations were assessed by central laboratory testing via bone marrow and peripheral blood samples.

 The mutational statuses of 38 AML-related genes were analyzed using next-generation sequencing; a gene was classified as mutated if it displayed at least 1 somatic mutation with a minimum variant allele frequency of 2.7%. The study authors performed exploratory analyses to determine the effects of individual gene mutations on OS, CRc rate, and relapse-free survival.

At baseline, the most common mutations in the quizartinib arm were 

 (24%). These mutations were reported at respective rates of 54%, 43%, and 26% in the placebo arm. The most common mutations in the quizartinib and placebo arms that were deemed by investigators to be prognostically relevant included 

Notably, 96.5% (n = 500/518) of patients in the overall population had mutated disease. Comutations in 

 were reported in 33.6% (n = 168/500) patients. Most patients (50.2%; n = 251/500) had an 

mutation in combination with a mutation in 

Additional findings revealed that the OS benefit with quizartinib vs placebo persisted in most of the individual mutational subgroups. No individual mutation fully favored the placebo arm compared with the quizartinib arm.

The OS HR for patients with any gene mutations related to myelodysplastic syndrome (MDS) was 0.998 (95% CI, 0.72-1.39). Investigators noted that small sample sizes and wide confidence intervals limited the interpretation of these findings. “There is much more to learn about the MDS mutations and their impact on this patient population,” Levis commented.

Notably, no individual baseline mutation appeared to lead to primary resistance to quizartinib. Patients with mutations in 

 (odds ratio [OR], 7.80; 95% CI, 0.87-70.1), 

 (OR, 3.46; 95% CI, 0.99-12.1) experienced the most significant CRc benefit with quizartinib vs placebo.

-mutated disease (n = 82) experienced a median OS of 9.6 months compared with 26.2 months among those with other mutations (n = 178; HR, 1.51; 95% CI, 1.08-2.10). Those with 

-mutated disease also experienced an OS benefit with quizartinib vs placebo if they were less than 60 years old (HR, 0.32; 95% CI, 0.17-0.60) or at least 60 years old (HR, 0.67; 95% CI, 0.38-1.19). The median OS favored the quizartinib arm in patients with 

-mutated disease with an additional mutation in an epigenetic regulator (HR, 0.57; 95% CI, 0.40-0.81).

“[These data] speak to the need to wait for a mutational analysis before deciding which therapy to choose,” Levis said during his conclusion. “If [a patient] has this version of AML, they may benefit from intensive [chemotherapy] plus quizartinib.”

industry affiliations with Astellas, Daiichi-Sankyo, BMS, GSK, Menarini, Novartis, Syndax, and Takeda. 

Levis MJ, Montesinos P, Kim HJ, et al. The combination of a FLT3-ITD, NPM1mut and an epigenetic regulatory gene mutation confers unique sensitivity to quizartinib: analysis from the QuANTUM-First trial. Presented at: 2025 European Hematology Association Congress; June 12-15, 2025; Milan, Italy. Abstract S140.

FDA approves quizartinib for newly diagnosed acute myeloid leukemia. FDA. July 20, 2023. https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-quizartinib-newly-diagnosed-acute-myeloid-leukemia

Quizartinib with standard of care chemotherapy and as continuation therapy in patients with newly diagnosed FLT3-ITD (+) acute myeloid leukemia (AML) (QuANTUM-First). ClinicalTrials.gov. Updated August 6, 2024. Accessed June 25, 2025. https://clinicaltrials.gov/study/NCT02668653

Articles

Quizartinib, when added to chemotherapy, significantly improved overall survival in patients with FLT3-ITD–positive acute myeloid leukemia (AML) with NPM1 and epigenetic regulatory gene mutations, as shown in the QuANTUM-First trial. The study highlighted the pronounced benefit in patients with triple mutations of FLT3-ITD, NPM1, and DNMT3A. The trial's design included a double-blind, randomized approach with stratification by region, age, and white blood cell count. The findings underscore the importance of mutational analysis in guiding treatment decisions for AML patients.

FLT3-ITD positivity plus mutations in NPM1 and epigenetic regulatory genes led to heightened efficacy of quizartinib plus chemotherapy in newly diagnosed AML.

Quizartinib Plus Chemotherapy Shows Strong Activity in FLT3-ITD–Positive, NPM1-Mutated AML

Since the FLT3 inhibitor quizartinib (Vanflyta) has shown efficacy in both patients with 

-ITD–positive acute myeloid leukemia (AML) and those with 

-ITD–negative AML, ongoing research aims to answer questions regarding this agent’s mechanism of action and the predictive value of 

 gene expression, according to David M. Swoboda, MD.

 in combination with standard induction and consolidation chemotherapy, and as maintenance monotherapy following consolidation chemotherapy, for the treatment of adult patients with newly diagnosed, 

 In the pivotal phase 3 QuANTUM-First trial (NCT02668653), patients who received quizartinib plus chemotherapy (n = 268) achieved a statistically significant overall survival (OS) improvement vs those who received placebo plus chemotherapy (n = 271; HR, 0.78; 95% CI, 0.62-0.98; 2-sided 

The phase 2 QUIWI trial (NCT04107727) showed the efficacy of quizartinib in patients with 

 At a median follow-up of 39.4 months, the median event-free survival (EFS) was 18.8 months with quizartinib plus induction and consolidation chemotherapy (n = 180) vs 9.9 months with placebo plus chemotherapy (n = 93; HR, 0.732; 95% CI, 0.533-1.005; 

= .0455). The median OS was not reached vs 29.3 months in the quizartinib and placebo arms, respectively (HR, 0.625; 95% CI, 0.436-0.897; 

Based on the positive findings from QUIWI, the ongoing, confirmatory, phase 3 QuANTUM-Wild trial (NCT06578247) is evaluating quizartinib plus chemotherapy vs placebo plus chemotherapy in patients with newly diagnosed, 

 OS will serve as the primary end point. Key secondary end points will include EFS, duration of response, recurrence-free survival, complete response (CR) rate, rate of CR with minimal residual disease, and safety.

“We have to understand what specific mutations occur [in each patient] to better understand their prognosis and give them the best treatment options possible,” Swoboda said in an interview with 

In the interview, Swoboda discussed the evolution of FLT3-targeted therapies for patients with 

-positive AML, data with quizartinib in patients with 

-negative AML stemming from the QUIWI trial, and how the QUIWI findings provided the rationale for the QuANTUM-Wild trial.

Swoboda is a hematologist oncologist at Tampa General Hospital (TGH) and clinical director of Leukemia at TGH Cancer Institute in Florida.

: What is the importance of distinguishing between the 

: We now use [somatic] genetic testing to understand how best to diagnose a patient [with AML], put them in a prognostic category, and treat them. [This is] not genetic testing that [assesses genetics that are] passed down from one generation to another. [I am referring to testing for] mutations that people acquire—generally as they age—that ultimately lead to [the development of] this disease.

 mutations, which are one of the most common mutations in AML, [are found in approximately] 30% of patients. There are 2 different [types of] 

-TKD mutations. They are vastly different [from each other]. Patients with 

-ITD–mutated disease tend to have more aggressive disease compared with those with 

-TKD mutations, and they respond differently to different therapies.

Therapeutic intervention [for patients with AML] has changed and is [now] molecularly based and targeted. We have established different drugs, some of which target FLT3 and some of which target other gene mutations, like 

. Some of those drugs that target FLT3 target both the ITD and TKD mutations, whereas others target the ITD mutations alone.

Quizartinib—one of the newest FDA-approved drugs [for patients with AML]—was approved based on the QuANTUM-First data. [This agent] specifically targets 

-ITD–positive disease, whereas gilteritinib [Xospata]—a drug that was approved based on the phase 3 ADMIRAL study [NCT02421939] in relapsed/refractory AML—can be used in both 

-ITD– and -TKD–positive disease. Midostaurin [Rydapt], which was the [first] drug approved for [patients with 

What was the rationale for the QUIWI study investigating quizartinib in patients with 

We [have historically thought we could design] targeted therapies to specifically target a mutation, and then we could design trials to focus on that mutational subgroup. The story for the FLT3 inhibitor quizartinib was that most clinical trials have to—at least initially as proof of concept—include both patients with mutations, as well as those with wild-type disease, because we want to understand: Does a drug work in patients with mutations? Does it not work in patients who lack a particular mutation.

Similar to most targetable agents, we found that quizartinib worked well in patients with 

 mutations, so we expanded that cohort into a large, randomized phase 3 clinical trial of 7+3 chemotherapy plus quizartinib vs standard-of-care [SOC] induction with 7+3 chemotherapy [alone]. We found that patients with 

-ITD–mutant AML had better overall outcomes if they received quizartinib in combination with SOC [vs SOC alone]. Interestingly, we realized that 

-negative—or wild-type—patients also seemed to initially have better outcomes with this drug [than with SOC alone].

We spent additional time and research investigating that wild-type cohort. Why are those patients responding to therapy that's targeting a mutation they lack? Ultimately, we wanted to see whether [quizartinib] could improve treatment efficacy for patients [with 

-negative disease]. Therefore, we launched the QUIWI study, which is a randomized phase 2 clinical trial. It was similar to QuANTUM-First, but we enrolled patients with 

-ITD–negative [disease]. We found that, similarly to in the 

-ITD–mutant subset of patients, the addition of quizartinib to SOC chemotherapy led to improved OS in patients with 

What questions did the QUIWI trial findings raise about the mechanism of action of quizartinib?

When we launch a study, we [typically] enroll a broad population of patients with AML, and then eventually take [the investigational agent] down its path [toward] approval. However, rarely do we go back and [evaluate the agent's efficacy] outside that approval [indication], [especially with an agent] that is supposed to be selective for a particular mutation. [The QUIWI findings made us ask]: What is the mechanism of action [of quizartinib]? Why, in 

-negative patients, were we seeing better and more durable responses [vs SOC chemotherapy alone]? Why was this occurring when we originally thought and still do feel like quizartinib is primarily a FLT3-targeting agent?

[The expansion of this research] has led to a better understanding that not all patients who lack [a 

] mutation are created equal. That's where gene expression—specifically expression of FLT3—[becomes relevant]. We found through correlative analysis that [some] patients with 

-negative disease ultimately have [FLT3] expression levels similar to those we see in patients with 

-positive disease. Patients don't necessarily have to have a 

 mutation to respond to a FLT3-targeted therapy.

How might the efficacy of quizartinib in patients with 

-negative AML affect genetic testing practices and the clinical use of this agent?

The QUIWI study led by the PETHEMA Foundation was a larger proof-of-concept trial has now led to the global, randomized [QuANTUM-Wild] clinical trial. Can we [replicate the QUIWI trial findings] in a large, international study [that is also comparing] SOC plus quizartinib vs SOC alone? Interestingly, at least in most clinics—even academic clinics—we do not necessarily look at FLT3 expression. A lot of times, we also do not necessarily use what is considered the best test for FLT3 testing. Sometimes we even miss patients with 

-positive disease if we don't use the appropriate test, which is not necessarily large-panel sequencing, but a lot of times is polymerase chain reaction–based testing specifically for that 

-positive disease should probably receive a FLT3 inhibitor. That [decision] is easy. Then, [we need to] tease out which patients within the non-mutant group would benefit most from a FLT3 inhibitor vs potentially a non-FLT3–targeted therapeutic option [or combination] we're trying to develop [for patients with] multiple mutations. [In the future, we may] better understand gene expression and which 

-negative patients are most likely to respond to FLT3 inhibitors. Then, we may ultimately prefer initially giving those patients FLT3-targeted therapy.

What makes the QuANTUM-Wild trial objectives unique compared with typical clinical trials in AML?

The [sponsoring] company is interested in doing large-scale correlative analyses to figure out which patients are most likely to respond to [FLT3-targeted] therapies. [I and the other] investigators on the QuANTUM-Wild study are focused on the research aspect of the trial. [This is] not a normal, large phase 3 clinical trial where we're only using SOC [in the control arm] and are not heavily invested in the correlative side of things. The correlative analysis is important [for this trial] so we can have a large, strong dataset to answer some of these more challenging questions when this trial is done.

FDA approves quizartinib for newly diagnosed acute myeloid leukemia. FDA. July 20, 2023. Accessed March 17, 2025. https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-quizartinib-newly-diagnosed-acute-myeloid-leukemia

Final results of Quiwi: a double blinded, randomized Pethema trial comparing standard chemotherapy plus quizartinib versus placebo in adult patients with newly diagnosed 

. 2024;144(suppl 1):1512. doi:10.1182/blood-2024-204770

Quizartinib or placebo plus chemotherapy in newly diagnosed patients with FLT3-ITD negative AML (QuANTUM-WILD). ClinicalTrials.gov. Updated February 19, 2025. Accessed March 18, 2025. https://clinicaltrials.gov/study/NCT06578247

David M. Swoboda, MD, discusses data with quizartinib in FLT3-negative AML from the QUIWI trial and the rationale for the QuANTUM-Wild trial.

QuANTUM-Wild Trial to Explore Correlative Outcomes With Quizartinib in FLT3-Negative AML

Following encouraging data from the phase 2 QUIWI trial (NCT04107727), investigators will examine the FLT3 inhibitor quizartinib (Vanflyta) in combination with chemotherapy for the treatment of patients newly diagnosed with 

-ITD–negative acute myeloid leukemia (AML) in the phase 3 QuANTUM-Wild study (NCT06578247).

“[Adding] a FLT3 inhibitor to intensive chemotherapy can improve the survival of patients with AML that harbors a 

-ITD or -TKD mutation,” Harry P. Erba, MD, PhD, said in an interview with 

. “The FLT3 receptor [also] plays an important role in normal hematopoiesis. When the FLT3 ligand binds to the extracellular domain of the FLT3 receptor, it causes dimerization of the receptor and activation of the intracellular tyrosine kinase, [setting off] a cascade of events leading to survival and proliferation of those cells. AML cells express the FLT3 receptor, and activation of this receptor can enhance leukemic survival and proliferation. Preclinical data show that the expression of FLT3 on the cell surface of blasts and the level of FLT3 ligand can be associated with prognosis in AML.”

Erba is a professor of medicine in the Department of Hematologic Malignancies and Cellular Therapy and a member of the Duke Cancer Institute at Duke Health in Durham, North Carolina.

In July 2023, the FDA approved quizartinib with standard cytarabine and anthracycline induction and cytarabine consolidation, and as maintenance monotherapy following consolidation chemotherapy, for the treatment of patients with newly diagnosed AML that is 

 The approval was based on data from the phase 3 QuANTUM-First trial (NCT02668653), which demonstrated that those who received quizartinib experienced a statistically significant and clinically meaningful improvement in overall survival (OS) vs those given chemotherapy plus placebo (HR, 0.78; 95% CI, 0.62-0.98; 2-sided 

 = .0324). However, accumulating data suggest the FLT3 inhibitor may have a larger role than originally hypothesized.

QUIWI Data Support Further Evaluation of Quizartinib/Chemotherapy Combination

QUIWI evaluated quizartinib in combination with chemotherapy in patients 18 to 70 years old with newly diagnosed 

 Patients were randomly assigned 2:1 to receive quizartinib or placebo, both in combination with 7+3 chemotherapy. The primary end point was event-free survival (EFS), and OS was the key secondary end point.

Final results from QUIWI presented during the 

 showed that for patients who received quizartinib (n = 180) there was a 28% reduction in the risk of having an EFS event (n = 93; HR, 0.72; 95% CI, 0.53-1.0; 2-sided 

 = .0455). Patients in the quizartinib arm achieved higher 1-, 2-, 3-, and 4-year EFS rates than those in the placebo arm, at 58.3% vs 47.3%, 49.2% vs 36.6%, 44.6% vs 32.1%, and 44.6% vs 32.1%, respectively.

Patients in the quizartinib arm also experienced a 37% reduction in the risk of death compared with those in the placebo arm (HR, 0.63; 95% CI, 0.44-0.91; 2-sided 

 = .0121). The 4-year OS rates were 57.1% and 44.3% with quizartinib and placebo, respectively. The complete remission (CR)/CR with incomplete count recovery (CRi) rates after 2 cycles were 77.2% and 76.3%, respectively.

“A survival benefit was seen only in the patients with European LeukemiaNet 2017 [criteria] favorable- and intermediate-risk disease, not in patients with adverse-risk disease,” Erba commented. “Other subset analyses have shown the benefit was seen predominantly in patients with [an] 

] gene expression signature that has been used to identify patients who have a higher chance of benefit in terms of survival with the addition of quizartinib [to chemotherapy].”

Previous findings from a 2023 subgroup analysis of QUIWI showed that patients with a FLT3-like gene signature (n = 80) experienced a benefit in terms of EFS (HR, 0.45; 95% CI, 0.25-0.82; 

 = .009), OS (HR, 0.41; 95% CI, 0.20-0.84; 

 = .01), and relapse-free survival (RFS; HR, 0.37; 95% CI, 0.18-0.79; 

 Among patients without a FLT3-like gene signature, there were no significant differences between the 2 arms in terms of the total number of deaths, EFS, RFS, or OS.

Safety data from QUIWI revealed that 7 patients died during the first induction cycle in the quizartinib arm compared with 5 in the placebo group.

 Patients received allogeneic stem cell transplantation after first CR/CRi at rates of 32.2% and 30.1% in the quizartinib and placebo arms, respectively. The most common any-grade adverse effects (AEs) in the quizartinib group included febrile neutropenia (81%), rash (63%), and diarrhea (56%). In the placebo arm, common any-grade AEs included febrile neutropenia (78%), rash (60%), and mucositis (47%).

“There was no difference in early death rates between the 2 groups, including in patients over the age of 60 [years],” Erba noted. “The safety of quizartinib combined with intensive chemotherapy was felt to be manageable by investigators, [and] there were no new safety signals.”

Quizartinib Plus Chemotherapy Set for Phase 3 Study

In light of the encouraging results from QUIWI, QuANTUM-Wild was initiated to evaluate quizartinib in combination with chemotherapy in patients newly diagnosed with 

The ongoing study is enrolling adult patients aged 18 to 70 years with an ECOG performance status of 0 to 2 who are receiving a standard 7+3 induction chemotherapy regimen. Prior leukapheresis, hydroxyurea for the treatment of hyperleukocytosis, cranial radiotherapy for central nervous system leukostasis, prophylactic intrathecal chemotherapy, and growth factor/cytokine support are the only prior treatments for AML permitted.

The study includes induction, consolidation, and maintenance phases.

 In the induction phase, all patients will receive a standard 7+3 chemotherapy regimen of cytarabine on days 1 to 7, an anthracycline on days 1 to 3, and quizartinib or placebo on days 8 to 21. Patients with a CR or CRi will enter the consolidation phase and receive high-dose cytarabine with quizartinib or placebo for 1 to 4 cycles, or 1 cycle followed by allogeneic hematopoietic stem cell transplant at the investigator’s discretion. Patients will then enter the maintenance phase to receive quizartinib or placebo.

Eligible patients will be randomly assigned 2:2:1 to receive quizartinib in all phases (arm A), quizartinib placebo in all phases (arm B), or quizartinib during induction and consolidation followed by placebo during the maintenance phase (arm C). Oral quizartinib will be administered at a dose of 60 mg per day for 14 days following the completion of chemotherapy in the induction and consolidation phases, except in patients who are also receiving concomitant strong CYP3A inhibitors—they will receive 30 mg of quizartinib.

 In the maintenance phase, patients will receive quizartinib once daily for up to 36 cycles of 28 days. Those receiving placebo will have the same dosing schedule as quizartinib.

 Secondary end points include EFS, duration of complete response, RFS, CR rate, CR with minimal or measurable residual disease negativity, and treatment-emergent AEs. All end points will be assessed in terms of arms A vs B.

In December 2024, Daiichi Sankyo announced that the first patient had been dosed in QuANTUM-Wild.

 The estimated target enrollment is 700 patients, and the estimated primary completion of the study is June 2030.

“This is an important area of investigation; FLT3 is ubiquitously expressed on AML blasts and appears to play an important role in the pathogenesis of the disease, even when there isn’t an ITD or TKD mutation,” Erba said. “Quizartinib is a potent inhibitor of FLT3 in its inactive confirmation [and] may improve the survival of patients, [including those without] this target. However, this benefit may [only] pertain to a specific subset of patients. No benefit was seen in patients with adverse-risk karyotype, where FLT3 potentially doesn’t play as important a role. There [also] appears to be an expression signature that will potentially allow us to identify patients who may benefit from the addition of quizartinib to intensive chemotherapy.”

Quizartinib or placebo plus chemotherapy in newly diagnosed patients with FLT3-ITD negative AML (QuANTUM-WILD). ClinicalTrials.gov. Updated February 19, 2025. Accessed February 26, 2025. https://clinicaltrials.gov/study/NCT06578247

FDA approves quizartinib for newly diagnosed acute myeloid leukemia. News release. FDA. July 20, 2023. Accessed February 28, 2025. 

https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-quizartinib-newly-diagnosed-acute-myeloid-leukemia

Montesinos P, Rodriguez-Veiga R, Bergua Burgues JM, et al. Final results of QUIWI: a double blinded, randomized PETHEMA trial comparing standard chemotherapy plus quizartinib versus placebo in adult patients with newly diagnosed 

. 2024;144(suppl 1):1512. doi:10.1182/blood-2024-204779

Orgueira AM, Encinas MP, Diaz Arias JA, et al. The FLT3-like gene expression signature predicts response to quizartinib in wild-type FLT3 acute myeloid leukemia: an analysis of the PETHEMA QUIWI trial. 

. 2023;142(suppl 1):974. doi:10.1182/blood-2023-180482

Montesinos P, Cheong JW, Daver N, et al. Trial in progress: the phase 3, randomized, double-blind, placebo-controlled QuANTUM-Wild study of quizartinib in combination with chemotherapy and as single-agent maintenance in newly diagnosed, 

. 2024;144(suppl 1):1504.3. doi:10.1182/blood-2024-205101

QuANTUM-Wild phase 3 trial of Vanflyta initiated in patients with newly diagnosed FLT3-ITD negative AML. News release. Daiichi Sankyo. December 10, 2024. Accessed February 26, 2025. https://daiichisankyo.us/press-releases/-/article/quantum-wild-phase-3-trial-of-vanflyta-initiated-in-patients-with-newly-diagnosed-flt3-itd-negative-aml

Quizartinib with 7+3 chemotherapy was safe and effective in patients with FLT3-ITD–negative AML, leading to the initiation of the phase 3 QuANTUM-Wild trial.

FLT3 Inhibition Fuels Improved Outcomes in Newly Diagnosed FLT3-ITD–Negative AML | Supplements and Featured Publications

Quizartinib Plus Chemotherapy Shows Strong Activity in FLT3-ITD–Positive, NPM1-Mutated AML

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Quizartinib Plus Chemotherapy Is Set to Be Evaluated in FLT3-ITD-Negative AML in Phase 3 Trial