REMS: FDA approved a REMS for quizartinib to ensure that the benefits outweigh the risks. The REMS may apply to one or more preparations of quizartinib and consists of the following: elements to assure safe use and implementation system. See the FDA REMS page ([Web]). |
Quizartinib dihydrochloride, an inhibitor of the receptor tyrosine kinase FLT3, is an antineoplastic agent.1
Quizartinib dihydrochloride is used in combination with standard cytarabine and anthracycline induction and cytarabine consolidation therapies, and as maintenance monotherapy following consolidation chemotherapy, for the treatment of adult patients with newly diagnosed acute myeloid leukemia (AML) that is FLT3 internal tandem duplication (ITD)-positive as detected by an FDA-approved test.1 Quizartinib has been designated an orphan drug by FDA for the treatment of this cancer.2 Quizartinib is not indicated as maintenance monotherapy following allogeneic hematopoietic stem cell transplantation (HSCT), since improvement in overall survival with quizartinib in this setting has not been demonstrated.1
The current indication for quizartinib in the treatment of AML is based principally on the results of a phase 3, double-blind, randomized controlled trial (QuANTUM-First).1, 3 A total of 539 adult patients with newly diagnosed FLT3 -ITD-positive AML were randomly assigned to treatment (at a 1:1 ratio) with either quizartinib or placebo in combination with induction and consolidation therapy and as maintenance therapy.1 Patients received quizartinib 35.4 mg orally once daily or placebo on days 8-21 of a 7+3 induction regimen (cytarabine 100-200 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, respectively).1 Consolidation therapy was initiated in patients who achieved complete remission or complete remission with incomplete neutrophil or platelet recovery during induction.3 For consolidation therapy, patients received quizartinib 35.4 mg orally once daily or placebo on days 6-19 of high dose cytarabine (1.5-3 g/m2 every 12 hours on days 1, 3, and 5).1 For maintenance therapy, patients received placebo or quizartinib 26.5 mg orally once daily on days 1-14 and 53 mg once daily thereafter for up to thirty-six 28-day cycles.1 Patients who underwent HSCT started maintenance therapy (quizartinib or placebo) after recovery from HSCT.1 The primary outcome assessed was overall survival, measured from randomization to death from any cause.1
The median age of patients was 56 years; 54% were female, 60% were white, 29% were Asian, and 84% had an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1.1 Among enrolled patients, 20% received a second course of induction therapy, 65% initiated at least 1 cycle of consolidation, and 39% initiated maintenance therapy.1 For patients given maintenance therapy, 64% completed at least 12 cycles, 36% completed at least 24 cycles, and 16% completed all 36 planned maintenance cycles.1 In the quizartinib and placebo groups respectively, 54 and 47% of patients underwent HSCT.1
Among all randomized patients (intention to treat population), median overall survival with quizartinib was 31.9 months compared to 15.1 months with placebo (hazard ratio 0.78).1, 3 Median follow-up was 39.2 months for both groups.3 In an exploratory subgroup analysis, an overall survival benefit was seen with quizartinib in patients who received maintenance therapy following consolidation chemotherapy (hazard ratio 0.40); however, an overall survival benefit was not observed in patients who received maintenance therapy following HSCT (hazard ratio 1.62).1 Complete remission was seen in 55% of patients in each group, with a duration of complete recovery of 38.6 or 12.4 months for quizartinib or placebo, respectively.1
The National Cancer Institute (NCI) states that the usual treatment option for newly-diagnosed AML is chemotherapy, with most patients undergoing intensive induction chemotherapy unless they are older and/or medically frail.4 Intensive induction chemotherapy regimens include cytarabine plus daunorubicin, cytarabine plus idarubicin, cytarabine plus mitoxantrone, cytarabine plus anthracycline plus midostaurin, and cytarabine plus anthracycline plus gemtuzumab ozogamicin.4 Mutations in the tyrosine kinase domain and internal tandem duplications of the FLT3 gene are common in AML and have been associated with inferior outcomes.4 The addition of an FLT3 inhibitor (e.g., midostaurin, quizartinib) to induction chemotherapy is considered standard of care for patients with FLT3 -mutated AML eligible for intensive chemotherapy.4 Quizartinib is only indicated for patients with FLT3 -ITD mutations, while midostaurin is indicated for patients with any FLT3 mutation.4
Quizartinib is administered orally.1 Administer quizartinib with or without food at approximately the same time each day.1 Swallow the tablets whole.1 Do not cut, crush, or chew.1
If a dose is vomited, do not administer a replacement dose; wait until the next scheduled dose is due.1 If a dose is missed or not taken at the usual time, administer as soon as possible on the same day and return to the usual schedule the following day.1 Do not administer two doses on the same day.1
Store tablets at 20-25°C (excursions permitted between 15-30°C).1
Dosage of quizartinib dihydrochloride is expressed in terms of quizartinib.1
A treatment course consists of up to 2 cycles of quizartinib in combination with induction cytarabine and anthracycline, up to 4 cycles of quizartinib in combination with high-dose cytarabine consolidation, and up to 36 cycles of quizartinib for maintenance therapy or until disease progression or unacceptable toxicity occurs.1 Maintenance therapy should be initiated following consolidation chemotherapy upon blood count recovery of absolute neutrophil count >500 cells/mm3 and platelet count >50,000 cells/mm3.1 The recommended adult dosage is shown in Table 1.1
Induction | Consolidation | Maintenance | |
|---|---|---|---|
Dose | 35.4 mg once daily starting on day 8 (for 7+3 regimen)a | 35.4 mg once daily starting on day 6b | Administer 26.5 mg once daily on days 1-14 of the first cycle if QTcF is ≤450 ms. Increase dosage to 53 mg once daily on day 15 of the first cycle if QTcF is ≤450 ms. Maintain the 26.5 mg once daily dosage if QTcF >500 ms was observed during induction or consolidation. |
Duration (28-day cycles) | Two weeks in each cycle (days 8-21 for 7+3 regimen)a | Two weeks in each cycle (days 6-19)b | Once daily with no break between cycles for up to 36 cycles |
aPatients can receive up to 2 cycles of induction. If a 5+2 regimen is used for the second induction cycle, quizartinib is given on days 6-19.
Dosage Modification for Toxicity
Dosage modifications are recommended for adverse reactions (see Tables 2 and 3).1
Adverse reaction | Recommended Action |
|---|---|
QTcF 450-480 ms (Grade 1) | Continue current dose. |
QTcF 481-500 ms (Grade 2) | Reduce the dosage without interruption (see Table 3). Resume at the previous dosage in the next cycle if QTcF has decreased to <450 ms. Monitor closely for QT prolongation during the first cycle at the increased dosage. |
QTcF >500 ms (Grade 3) | Interrupt quizartinib treatment. Resume at a reduced dose (see Table 3) when QTcF returns to <450 ms. Maintain the 26.5 mg once daily dosage during maintenance if QTcF >500 ms was observed during induction or consolidation. |
Recurrent QTcF >500 ms (Grade 3) | Permanently discontinue quizartinib if QTcF >500 ms recurs despite appropriate dosage reduction and correction/elimination of other risk factors (e.g., serum electrolyte abnormalities, concomitant QT prolonging medications). |
Torsades de pointes, polymorphic ventricular tachycardia, signs/symptoms of life-threatening arrhythmia (Grade 4) | Permanently discontinue quizartinib. |
Grade 3 or 4 hypokalemia (<3 mmol/L) or hypomagnesemia (<0.4 mmol/L or <0.9 mg/dL) | Interrupt quizartinib treatment. Correct hypokalemia and hypomagnesemia according to institutional guidelines. Restart quizartinib at previous dosage when the adverse reaction improves to Grade 2 or less without symptoms. |
Grade 4 neutropenia or thrombocytopenia after achieving remissiona | Reduce quizartinib dosage (see Table 3). |
Grade 3 or 4 non-hematologic adverse reactions | Interrupt quizartinib treatment. Resume treatment at the previous dosage if adverse reaction improves to Grade 1 or less. Resume treatment at a reduced dosage (see Table 3) if adverse reaction improves to Grade 2. Discontinue quizartinib if Grade 3 or 4 adverse reaction persists beyond 28 days. |
Current Dosage | Modified Dosage |
|---|---|
53 mg once daily | 35.4 mg once daily |
35.4 mg once daily | 26.5 mg once daily |
26.5 mg once daily | Interrupt |
17.7 mg once daily | Interrupt |
Dosage Modifications for Concomitant Strong CYP3A Inhibitors
Reduce the dosage of quizartinib when used concomitantly with strong cytochrome P-450 (CYP) 3A inhibitors as shown in Table 4.1 If the current dosage is 17.7 mg once daily, interrupt quizartinib treatment for the duration of strong CYP3A inhibitor use.1 After discontinuation of a strong CYP3A inhibitor for 5 half-lives, resume the quizartinib dosage that was taken before initiating the strong inhibitor.1
Current Dosage | Modified Dosage |
|---|---|
53 mg once daily | 26.5 mg once daily |
35.4 mg once daily | 17.7 mg once daily |
26.5 mg once daily | 17.7 mg once daily |
No dosage adjustment is recommended in patients with mild hepatic impairment (Child-Pugh Class A; total bilirubin ≤ upper limit of normal [ULN] and AST > ULN; or total bilirubin >1 to 1.5 times ULN with any AST) or moderate hepatic impairment (Child-Pugh Class B or total bilirubin >1.5 to 3 times ULN with any AST).1 Quizartinib has not been studied in patients with severe hepatic impairment (Child-Pugh Class C or total bilirubin >3 times ULN with any AST).1
No dosage adjustment is recommended in patients with mild to moderate renal impairment (creatinine clearance [Clcr] 30-89 mL/minute.1 Quizartinib has not been studied in patients with severe renal impairment (Clcr<30 mL/minute).1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
QT Prolongation, Torsades de Pointes, and Cardiac Arrest
A boxed warning about the risk of QT prolongation, torsades de pointes, and cardiac arrest is included in the prescribing information for quizartinib.1 Quizartinib prolongs the QT interval in a dose- and concentration-dependent manner via inhibition of the slow delayed rectifier potassium current.1 The level of QTc prolongation with quizartinib that predicts the risk of cardiac arrhythmias is unclear, as the mechanism of QT prolongation is different from the QT-prolonging mechanism of other QT-prolonging drugs.1 Torsades de pointes, ventricular fibrillation, cardiac arrest, and sudden death have occurred in patients treated with quizartinib.1
Of the 1081 patients with acute myeloid leukemia (AML) treated with quizartinib in clinical trials, torsades de pointes occurred in approximately 0.2% of patients, cardiac arrest occurred in 0.6%, including 0.4% with a fatal outcome, and 0.1% of patients experienced ventricullar fibrillation.1 These severe cardiac arrhythmias occurred predominantly during the induction phase.1
Of the 265 patients with newly-diagnosed FLT3 internal tandem duplication (ITD)-positive AML treated with quizartinib in combination with chemotherapy in a clinical trial, 2.3% were found to have a QT interval corrected by Fridericia's formula (QTcF) >500 ms and 10% of patients had an increase from baseline QTcF >60 ms.1 The clinical trial excluded patients with a QTcF ≥450 ms or other factors that increased risk of QT prolongation or arrhythmic events (e.g., New York Heart Association [NYHA] Class III or IV congestive heart failure, hypokalemia, family history of long QT interval syndrome).1
Do not initiate quizartinib treatment if the patient's QTcF interval is >450 ms.1 Do not use quizartinib in patients with severe hypokalemia, severe hypomagnesemia, long QT syndrome, or in patients with a history of ventricular arrhythmias or torsades de pointes.1 Avoid use in patients who are at significant risk of developing torsades de pointes, including uncontrolled or significant cardiac disease, recent myocardial infarction, heart failure, unstable angina, bradyarrhythmias, tachyarrhythmias, uncontrolled hypertension, high-degree atrioventricular block, severe aortic stenosis, or uncontrolled hypothyroidism.1
Perform an ECG and correct electrolyte abnormalities prior to initiating treatment.1 During induction and consolidation, perform an ECG prior to initiation and then once weekly during treatment or more frequently as clinicially indicated.1 During maintenance, perform ECGs prior to initiation, once weekly for at least the first month following dosage initiation and escalation, and as clinically indicated thereafter.1 Do not escalate the dosage of quizartinib if QTcF is >450 ms.1
Perform ECG monitoring of the QT interval more frequently in patients who are at significant risk of developing QT interval prolongation and torsades de pointes, or following dosage escalation.1
Monitor and correct hypokalemia and hypomagnesemia prior to and during treatment.1 Maintain electrolytes in the normal range.1 Monitor electrolytes and ECG more frequently in patients who experience diarrhea or vomiting.1
Monitor ECG more frequently if concomitant use of quizartinib with drugs known to prolong the QT interval is required.1
Reduce the dosage of quizartinib when used with strong cytochrome P-450 (CYP) 3A inhibitors, as they may increase quizartinib exposure.1 Adjust the dosage of quizartinib if QTc increases to >480 ms; interrupt quizartinib treatment and reduce the dosage if QTc increases to >500 ms.1 Permanently discontinue quizartinib in patients who develop recurrent QTc >500 ms and patients who develop QTc prolongation with signs or symptoms of life-threatening arrhythmia.1
Quizartinib is only available through a restricted distribution program under a Risk Evaluation and Mitigation Strategy (REMS) called the Vanflyta REMS.1 For further information, visit the REMS website (www.vanflytarems.com) or call 1-855-212-6670.1
Other Warnings and Precautions
Fetal/Neonatal Morbidity and Mortality
Based on animal studies and its mechanism of action, quizartinib can cause fetal harm.1 In animal reproduction studies, administration of quizartinib to pregnant rats during organogenesis at exposures 3 times the maximum recommended human dose (MRHD) of 53 mg/day caused structural abnormalities and alterations to growth.1
Advise pregnant women of the potential risk to a fetus.1 Verify pregnancy status in females of reproductive potential within 7 days before starting quizartinib treatment.1
Based on findings from animal studies and its mechanism of action, quizartinib can cause embryo-fetal harm when administered to a pregant woman.1 Advise pregnant women of the potential risk to a fetus.1 Verify pregnancy status in females of reproductive potential within 7 days before starting quizartinib treatment.1
There are no available data on quizartinib use in pregnant women to evaluate for a drug-associated risk.1 In animal reproduction studies, oral administration of quizartinib to pregnant rats during organogenesis at exposures 3 times the MRHD of 53 mg/day caused structural abnormalities (anasarca and edema) and alterations to growth (lower fetal weights and effects on skeletal ossification).1
There are no data on the presence of quizartinib and its metabolites in human milk, or the effects on the breast-fed child or milk production.1 Because of the potential for serious adverse reactions in the breast-fed child, advise women not to breast-feed during quizartinib treatment and for 1 month after the last dose.1
Females and Males of Reproductive Potential
Quizartinib can cause embyro-fetal harm when administered to pregnant women.1 Verify pregnancy status in females of reproductive potential within 7 days before starting treatment.1
Advise females of reproductive potential to use effective contraception during treatment and for 7 months after the last dose.1 Advise male patients with female partners of reproductive potential to use effective contraception during treatment and for 4 months after the last dose.1
Based on animal studies, quizartinib may impair female and male fertility.1 These effects were reversible.1
The safety and effectiveness of quizartinib have not been established in pediatric patients.1
Of the 533 patients with newly-diagnosed AML in the clinical study of quizartinib, 26% were ≥65 years of age and 1 patient was 75 years of age.1 No overall differences in safety or efficacy were observed between patients ≥65 years of age and younger adult patients.1
No dosage adjustment is recommended in patients with mild hepatic impairment (Child-Pugh Class A; total bilirubin ≤ upper limit of normal [ULN] and AST > ULN; or total bilirubin >1 to 1.5 times ULN with any AST) or moderate hepatic impairment (Child-Pugh Class B or total bilirubin >1.5 to 3 times ULN with any AST).1 Mild or moderate hepatic impairment did not have a clinically significant impact on exposure to quizartinib or its active metabolite.1 Quizartinib has not been studied in patients with severe hepatic impairment (Child-Pugh Class C or total bilirubin >3 times ULN with any AST).1
No dosage adjustment is recommended in patients with mild to moderate renal mpairment (creatinine clearance [Clcr] 30-89 mL/minute.1 Mild or moderate renal impairment did not have a clinically significant impact on exposure to quizartinib or its active metabolite.1 Quizartinib has not been studied in patients with severe renal impairment (Clcr<30 mL/minute).1
The most common adverse reactions, occuring in >20% of patients receiving quizartinib in clinical studies, included decreased lymphocytes, decreased potassium, decreased albumin, decreased phosphorus, decreased magnesium, increased alkaline phosphatase, febrile neutropenia, diarrhea, mucositis, nausea, decreased calcium, abdominal pain, sepsis, neutropenia, headache, increased creatine phosphokinase, vomiting, and upper respiratory tract infection.1
Based on in vitro studies, quizartinib is a cytochrome P-450 (CYP) 3A4/5 and P-glycoprotein (P-gp) substrate.1 Quizartinib is not a substrate of breast cancer resistance protein (BCRP), organic anion transporting polypeptide (OATP) 1B1, OATP1B3, organic cation transporter (OCT) 1, organic anion transporter (OAT) 2, multidrug and toxin extrusion (MATE) 1, or multidrug resistance protein (MRP) 2.1 It does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4.1 It does inhibit UDP-glucuronosyltransferase (UGT) 1A1.1 Quizartinib does not induce CYP3A4, CYP1A2, or CYP2B6.1
The active metabolite of quizartinib, AC886, is a substrate for BCRP.1 AC886 is not a substrate for OATP1B1, OATP1B3, MATE1, or MRP2.1 It does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4.1 AC886 does not induce CYP3A4, CYP1A2, or CYP2B6.1
Drugs Affecting or Affected by Hepatic Microsomal Enzymes
Concomitant use of quizartinib with a strong CYP3A inhibitor increases quizartinib systemic exposure, which may increase the risk of quizartinib adverse reactions.1 Reduce the quizartinib dosage when used concomitantly with a strong CYP3A inhibitor.1
The AUC of quizartinib increased by 94% and peak plasma concentration increased by 17% following coadministration of a single 53 mg quizaritnib dose with ketoconazole (a strong CYP3A inhibitor).1 The AUC of the active metabolite of quizarinib (AC886) decreased by 94% and peak plasma concentration decreased by 60%.1 A clinically significant change in quizartinib and metabolite exposure was not observed following coadministration of a single quizartinib dose with fluconazole (a moderate CYP3A inhibitor).1
Strong or Moderate CYP3A Inducers
Concomitant use of quizartinib with a strong or moderate CYP3A inducer decreases quizartinib systemic exposure which may reduce quizartinib efficacy.1 Avoid concomitant use of quizartinib with strong or moderate CYP3A inducers.1
The AUC of quizartinib decreased by 90% and peak plasma concentration decreased by 45% following coadministration of a single 53 mg quizaritnib dose with efavirenz (a moderate CYP3A inducer).1 The AUC of AC886 decreased by 96% and peak plasma concentration decreased by 68%.1
Drugs Affected by Efflux Transport Systems
There were no clinically significant differences in the pharmacokinetics of P-gp substrates (dabigatran etexilate) or UGT1A1 substrates (raltegravir) when used concomitantly with quizartinib.1
Drugs Associated with QT Prolongation
Quizartinib prolongs the QT/QTc interval.1 Coadministration of quizartinib with other drugs that prolong the QT interval may further increase the incidence of QT prolongation.1
Monitor patients more frequently with ECG if coadministration of quizartinib with drugs known to prolong the QT interval (e.g., antifungal azoles, ondansetron, granisetron, azithromycin, pentamidine, doxycycline, moxifloxacin, atovaquone, prochlorperazine, tacrolimus) is required. 1
Drugs Affecting Gastric Acidity
No clinically significant differences in quizartinib pharmacokinetics were observed when used concomitantly with lansoprazole.1
Quizartinib is an inhibitor of the receptor tyrosine kinase FLT3.1 Quizartinib and its active metabolite, AC886, bind to the adenosine triphosphate binding domain of FLT3 with comparable affinity, thereby inhibiting FLT3 kinase activity and preventing autophosphorylation of the receptor.1 This inhibits downstream FLT3 receptor signaling and blocks FLT3 internal tandem duplication (ITD)-dependent cell proliferation.1 Antitumor activity was observed in a mouse model of FLT3 ITD-dependent leukemia.1
In vitro studies have shown that quizartinib is a predominant inhibitor of the slow delayed rectifier potassium current.1 Quizartinib exhibits concentration-dependent QT interval corrected by Fridericia's formula (QTcF) median prolongation of 18 ms and 24 ms at the median steady-state maximum concentrations achieved at the 26.5 mg and 53 mg dosing levels, respectively, during maintenance therapy.1
In patients with acute myeloid leukemia (AML), steady state quizartinib concentrations were achieved at day 15 following once-daily dosing.1 Quizartinib exposure increased proportionally over the dosage range of 17.7-53 mg.1 The mean absolute bioavailability of the oral tablet is 71%.1 The time to peak concentration under fasted conditions was 4 hours (range, 2-8 hours) for quizartinib and 5-6 hours (range, 4-120 hours) for AC886.1 Protein binding of the parent drug and metabolite is ≥99%.1 The mean effective half-lives in patients with newly-diagnosed AML for quizartinib and AC886 are 81 hours and 136 hours, respectively.1 Metabolism of quizartinib is primarily via oxidation by cytochrome P-450 (CYP) 3A4/5.1 AC886 is formed and metabolized by CYP3A4/5.1 A majority of drug is excreted in the feces (76.3%; 4% unchanged), and 1.64% is excreted in urine.1 There were no clinically significant differences in exposure of quizartinib or AC886 based on age (range, 18-91 years), sex, race, or body weight (range, 37-153 kg).1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care. For further information on the handling of antineoplastic agents, see the ASHP Guidelines on Handling Hazardous Drugs at [Web].
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Distribution of quizartinib is restricted (see REMS under Dosage and Administration).1 Quizartinib is available only through the Vanflyta REMS program.1 Contact the manufacturer or consult the manufacturer website for specific availability information.5
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 17.7 mg (of quizartinib) | Vanflyta® | Daiichi Sankyo |
26.5 mg (of quizartinib) | Vanflyta® | Daiichi Sankyo |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions November 10, 2024. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Daiichi Sankyo, Inc. Vanflyta® prescribing information. Basking Ridge, NJ; 2023 Jul. http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=29cdbcfe-497d-4e78-bb7b-2d4acafe8e86
2. US Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. Accessed 2024 Apr 29. http://www.accessdata.fda.gov/scripts/opdlisting/oopd/index.cfm
3. Erba H, Montesinos P, Kim H, et al. Quizartinib plus chemotherapy in newly diagnosed patients with FLT3-internal-tandem-duplication-positive acute myeloid leukaemia (QuANTUM-First): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet . 2023;401:1571-1583.
4. National Cancer Institute. Acute Myeloid Leukemia Treatment (PDQ®)-Health Professional Version. National Cancer Institute. Updated March 6, 2024. Accessed April 29, 2024. http://www.cancer.gov/types/leukemia/hp/adult-aml-treatment-pdq
5. Daiichi-Sankyo. Vanflyta resources and support. Vanflyta HCP website. Accessed April 29, 2024. http://www.vanflytahcp.com/en/resources