Vanflyta (quizartinib) / Daiichi Sankyo - LARVOL DELTA

FLT3 testing and guideline concordance in Acute Myeloid Leukemia across an Indiana health system (ASH 2025) - "Current guidelines recommend FLT3 mutation testing at diagnosis to inform risk stratification and guide the use of FLT3 inhibitors such as midostaurin, quizartinib, and gilteritinib...The most frequently used induction therapies included venetoclax in combination with a hypomethylating agent (30%), 7+3 (15.7%), and a combination regimen consisting of fludarabine, cytarabine, idarubicin, and granulocyte colony-stimulating factor (FLAG IDA; 13.8%)... FLT3 testing was commonly performed in this cohort, yet notable variability in guideline adherence was observed. Guideline-concordant induction regimen selection was marginally higher for patients with FLT3 mutations. These findings underscore the need for institutional quality improvement initiatives aimed at enhancing the documentation of FLT3 status and optimizing the integration of guideline-directed therapies in AML management."

Discordant • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3

Enhanced antileukemic activity of momelotinib in combination with venetoclax and azacitidine compared to gilteritinib-based combination (ASH 2025) - "Despite extensive genomic insights, conventional chemotherapies, specifically anthracyclines and cytarabine , have remained the cornerstone of treatment for the past four decades...In contrast, selective inhibitors of JAK-STAT (ruxolitinib) or FLT3 (gilteritinib or quizartinib) alone failed to demonstrate comparable synergy, highlighting the distinct polypharmacological profile of momelotinib in mediating the cytotoxic response...Notably, while the efficacy of gilteritinib-based regimens was restricted to FLT3-mutant AML, the momelotinib combination demonstrated activity across both FLT3 mutant and FLT3 wild-type contexts. Altogether these preclinical data support clinical evaluation of momelotinib in combination with venetoclax and azacitidine as a potential effective treatment in AML."

Combination therapy • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • ACVR1 • FLT3 • IRAK1

Inhibitors of RAD51 as potential novel therapies in Acute Myeloid Leukemia (ASH 2025) - "Furthermore, these compounds often exhibit strong synergy and at least additivity in combination with both on-label and off-label use of FDA-approved compounds, as well as investigational molecularly-targeted agents, in relevant cell lines; these include FLT3 inhibitors quizartinib, gilteritinib and tuspetinib ((in MV-4-11 and HL60 cell lines) and BCR/ABL inhibitors (imatinib and regorafenib) in the K562 cell line (AACR 2025)...We have confirmed the IBRs inhibit multiple RAD51 functions including hydroxyurea-induced RAD51 focus formation, HRR by DR-GFP assay, and RS protection by RPA focus formation and a DNA fibre assay...JKYN-1 is a partially optimized (more soluble and more potent) version of IBR120 but is not resistant to degradation by liver microsomes or sufficiently capable of entry into target cells...Treatment dose and combinations will be pre-screened using a highly predictive cell line as a surrogate of human cancer stem cells for subsequently AML patient..."

Acute Myelogenous Leukemia • Colorectal Cancer • Hematological Malignancies • Leukemia • Solid Tumor • BRCA1 • BRCA2 • FLT3 • HRD • RAD51

Chromomycin A2 exhibits antileukemic effects by coordinated disruption of survival pathways (ASH 2025) - "A total of 22 leukemia-derived cell lines were analyzed, including myeloid (n = 13) and lymphoid (n = 9) models, with subsets with acquired resistant to venetoclax (n = 2), quizartinib (n = 1), and ATRA (n = 1). Taken together, these findings support the therapeutic potential of chromomycin A2 in hematologic malignancies and provide a strong rationale for further preclinical studies. Supported by FAPESP, CAPES, and CNPq."

Acute Lymphocytic Leukemia • Acute Myelogenous Leukemia • Gastric Adenocarcinoma • Hematological Malignancies • Leukemia • Melanoma • Solid Tumor • ANXA5 • SQSTM1

High-intensity purine analogue-based therapy for refractory/relapsed Acute Myeloid Leukemia (RR-AML): A single-institution experience (ASH 2025) - "For medically fit patients, high-intensity salvage regimens such as CLAG or FLAG-IDA incorporate purine analogues (cladribine or fludarabine) with high-dose cytarabine and granulocyte colony-stimulating factor (G-CSF), achieving complete remission (CR) rates between 30% and 60% in the relapsed setting...Five patients (29%) received FLAG-IDA (2 of them received a concomitant FLT3 inhibitor: midostaurin and quizartinib), 7 patients (41%) received FLAG-IDA + venetoclax, 4 (24%) received CLAG-IDA + Venetoclax, and 1 patient (6%) received CLAG + VEN... Our single-institution experience demonstrates that high-intensity purine analogue-based therapy is safe and active in patients with RR-AML and can achieve meaningful remission rates in a heavily pretreated, predominantly adverse risk population. These outcomes compare favorably to historic expectations and support the use of purine analogue regimens as an effective salvage strategy. Prospective studies and continued real-world..."

Clinical • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Infectious Disease • Leukemia • Neutropenia • FLT3 • IDH1 • TP53

Comparative safety and efficacy of first- and second-generation FLT3 inhibitors in newly diagnosed and relapsed AML: A meta-analysis stratified by molecular biomarkers (ASH 2025) - "First-generation (sorafenib and midostaurin) and second-generation (gilteritinib, quizartinib, and crenolanib) FLT inhibitors demonstrated efficacy and safety across disease stages and are now used as a standard of treatment for FLT3-mutated AML. Conclusions Second-generation FLT inhibitors exhibit enhanced efficacy in relapsed-refractory AML scenarios and comparable outcomes to first-generation inhibitors in newly diagnosed AML.Stratification using ITD allelic ratio and NPM1 co-mutation is emerging as a critical factor. In light of these findings, it's imperative to integrate second-generation inhibitors in salvage settings and Biomarker-guided treatment decisions in front-line FLT3 mutant-AML"

Biomarker • Retrospective data • Acute Myelogenous Leukemia • Cardiovascular • Hematological Disorders • Hypertension • Neutropenia • FLT3 • NPM1

Maintenance with hypomethylating agent + venetoclax after intensive induction chemotherapy in patients with newly diagnosed Acute Myeloid Leukemia (ASH 2025) - "Background Consolidative therapy with high/intermediate-dose cytarabine is standard practice for fit patients with newly diagnosed acute myeloid leukemia (ND-AML) who achieve complete remission (CR) after receiving intensive induction chemotherapy (IC). Oral azacitidine is approved as maintenance therapy in patients who achieve CR after IC but are unable to complete intensive consolidation therapy...Five patients (20%) received a FLT3 inhibitor with HMA and VEN (3 quizartinib, 2 gilteritinib), and 1 patient (4%) received an IDH-2 inhibitor (enasidenib)...These findings must be interpreted in the context of several limitations: a relatively small sample size, a median of one maintenance cycle, and the absence of scheduled repeat disease assessments. Larger, prospective studies are needed to confirm these observations and better define the role of HMA + VEN in this setting."

Clinical • Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Chronic Graft versus Host Disease • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • FLT3 • IDH1 • IDH2 • TP53

Development of HPB-092: A novel dual kinase inhibitor targeting FLT3 and IRAK4 for the treatment of relapsed/refractory Acute Myeloid Leukemia (RR-AML) (ASH 2025) - "Compared to the approved FLT3 inhibitors gilteritinib and quizartinib, as well as the clinical-stage dual inhibitor CA-4948, HPB-092 displayed comparable or superior potency against mutant FLT3 and IRAK4, improved kinome selectivity (selectivity score 50 μM), and no hERG inhibition (IC50 > 10 μM), along with an excellent overall safety profile in nonclinical species. The study has been approved by the Institutional Review Board (IRB) and has also been submitted to ClinicalTrials.gov, currently pending final approval. The first patient is anticipated to be enrolled in the fourth quarter of 2025."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • IRAK4 • SF3B1 • U2AF1

Unveiling FLT3 in B-ALL: Molecular drivers and targeted treatment opportunities (ASH 2025) - "In vitro assays withincreasing concentrations of 6 FLT3i for 24, 48, 72h [Gilteritinib (Gil), Midostaurin, Crenolanib, Sorafenib,Quizartinib, Ponatinib (Pon)] and Venetoclax (Ven) were performed on primary patient samples (n=29; FLT3-mut n=5/29), 11 B-ALL wt cell lines, 2 B-ALL mut (NALM6-mut, KASUMI-10), and 4 AML cell lines (OCI-AML3 wt; MV-4-11, MOLM-13, MONO-MAC6 FLT3-mut). FLT3 alterations define a novel Ph-negative B-ALL subgroup withtherapeutic relevance. Given the responses in FLT3-wt in addition to the mutated models, FLT3i may alsobenefit patients without FLT3 muts. Thanks to: Ricerca Corrente by the Italian MoH L3P1946 andAILTreviso."

Acute Lymphocytic Leukemia • Acute Myelogenous Leukemia • B Acute Lymphoblastic Leukemia • Bone Marrow Transplantation • Hematological Malignancies • Leukemia • T Acute Lymphoblastic Leukemia • FLT3 • IKZF1 • KMT2A • PBX1 • TCF3 • TP53 • ZNF384

Preliminary safety and efficacy of the frida study: Iadademstat and gilteritinib in FLT3-mutated relapsed/refractory acute myeloid leukemia (ASH 2025) - P1 | "Preclinically, iada is synergistic with gilteritinib in FLT3 mut AML cells and in derivedcell lines resistant to venetoclax, azacitidine or other FLT3is (Sacilotto et al., 2022 Eur J. of Cancer 174S1).More than 140 pts have been treated with iada, including treatment-naïve AML pts in the ALICE studywhere, in combination with azacitidine, iada produced rapid, durable, and deep responses with amanageable safety profile (Salamero et al., Lancet Hematol...The FRIDA Phase 1 study(NCT05546580) aims to establish the safety, tolerability, and the recommended Phase 2 dose (RP2D) ofthe combination of iada plus gilteritinib in FLT3 mut R/R AML.Adult pts with ≤ 2 prior lines of therapy (including quizartinib and gilteritinib if not refractory), receivediada PO at doses of 50 to 100 μg on a 5 days ON- 2 days OFF (5+2) schedule for 3 or 4 weeks (wks), in 28-day cycles with continuous gilteritinib PO at 120 mg/day...The combination of iada and gilteritinib at the tested doses..."

Clinical • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Febrile Neutropenia • Gene Therapies • Hematological Malignancies • Leukemia • Neutropenia • FLT3

FLT3-ITD drives poor prognosis in NPM1 mutated AML via BCAT1-dependent epigenetic regulation (ASH 2025) - "FLT3-ITDknock-in OCI-AML3 cells (with NPM1mut) demonstrated significant upregulation of BCAT1 expression,while AC220 (quizartinib) treatment substantially reduced BCAT1 expression...These combined effects render NPM1mutFLT3ITD cells apoptosis-resistant yet paradoxicallyvulnerable to apoptosis-inducing agents, providing a possible mechanistic rationale for combininghypomethylating agents with Bcl-2 inhibitors in this AML subtype. Furthermore, compromised TP53-mediated DNA damage response suggests potential susceptibility to DNA repair inhibitors (such as PARPinhibitors) in this patient subset, offering novel therapeutic opportunities."

IO biomarker • Acute Myelogenous Leukemia • AATK • BCAT1 • FLT3 • NPM1 • TET2

FLT3/ITD-driven noncanonical STAT1 S727 phosphorylation upregulates CD276, mediating CD8positive- T cell exhaustion and immune evasion in AML (ASH 2025) - "Multipleximmunohistochemical confirmed elevated pS727-STAT1+CD276+ blasts and reduced CD8+ T cells inFLT3/ITD patient samples, linking FLT3/ITD–STAT1 signaling to CD276 transactivation and immunesuppression.Pharmacologic (fludarabine) and genetic approaches showed dose-dependent suppression of CD276mRNA and protein in FLT3/ITD models. In FLT3/ITDPDX models, quizartinib + MGA271/MG009 achieved a 99% complete remission rate, with excellenttolerability, validating CD276 blockade as a potent synergistic strategy with FLT3 inhibition.In summary, FLT3/ITD drives CD8+ T cell exhaustion via tumor-intrinsic CD276 upregulation, mediated bySTAT1 S727 phosphorylation. Co-targeting FLT3 and CD276 synergistically restores T-cell function anderadicates leukemia in vivo, offering a translatable immunotherapy strategy for AML."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • CD276 • CD8 • FLT3 • GZMB • IFNG • STAT1 • STAT5

Phase l dose escalation and expansion of ziftomenib in combination with quizartinib in AML (ASH 2025) - P1 | "Secondary objectives include assessment of the composite complete remission rate, duration ofresponse, event-free and overall survival and concordance of genetic (NGS, Invivoscribe, USA) and flowMRD. This trial includes longitudinal collection of samples, with exploratory objectives focused onimproving MRD detection, and understand of response and resistance using cytometry by time of flight.This study, currently enrolling patients at MD Anderson, could lead to a novel all-oral targeted therapycombination for the largest subset of patients with AML."

Combination therapy • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • KMT2A • MEIS1 • NPM1 • NUP98

Treatment intensity may alter the prognostic impact of baseline co-mutations in newly diagnosed FLT3-ITD AML treated with FLT3 inhibitor-based therapy (ASH 2025) - " A total of 213 pts were included; 83 received IC + FLT3i [sorafenib in 56 (68%), midostaurin in 1(1%), gilteritinib in 23 (28%), and quizartinib in 3 (4%)] while 130 received LIT + FLT3i [including sorafenibin 32 (25%), midostaurin in 1 (1%), gilteritinib in 48 (37%), and quizartinib in 49 (38%)]. The impact of baseline co-mut on frontline FLT3i-based therapy in ND FLT3-ITD mut AMLmay vary by the nature of the induction regimen. The presence of NPM1 mut +/- epigenetic regulator mutwas associated with improved outcomes with IC + FLT3i, consistent with findings from QuANTUM-1, butimportantly, we noted that co-mut in RAS pathway and MR genes portended a poorer prognosis. Incontrast, co-mut in NPM1 and MR genes did not influence outcomes with LIT + FLT3i regimens (with orwithout VEN)."

Acute Myelogenous Leukemia • Myelodysplastic Syndrome • ASXL1 • DNMT3A • FLT3 • IDH1 • IDH2 • KRAS • NPM1 • NRAS • PTPN11 • RUNX1 • TET2 • WT1

Quizartinib enhances conditioning for hematopoietic stem cell transplantation via transcriptional suppression of DNA repair pathways (ASH 2025) - "To assess HSC transplantation efficacy, mice were conditioned with 700 or1000 Rads of TBI, transplanted with 2 million CD45.1 bone marrow (BM) cells, and monitored for donorcell engraftment for 4 months. Quizartinib synergized with DNA damaging chemotherapeutic agents (cyclophosphamide,carboplatin, cisplatin, temozolomide, and mitoxantrone) to deplete HSPC populations. Quizartinib sensitizes HSPCs to DNA-damaging therapies via downregulation of DNA repairgenes and impaired resolution of DNA damage, resulting in enhanced HSPC depletion. This quizartinib-driven sensitization demonstrated improved engraftment after HSCT in murine models. These resultsprovide a rationale for incorporating quizartinib into reduced-intensity, myeloablative conditioningregimens to improve transplant outcomes while minimizing non-hematopoietic toxicity."

Bone Marrow Transplantation • Transplantation • BRCA1 • BRCA2 • CD34 • FLT3 • NBN • PTPRC • RAD51

Sphingosine-1-phosphate receptor modulators overcome FLT3 inhibitor resistance in Acute Myeloid Leukemia with FLT3-ITD and NRAS mutations through sphingosine kinase 1/AKT pathway downregulation. (ASH 2025) - "SphK1 is linked toFLT3 inhibitor resistance, as prolonged sorafenib exposure was shown to activate the Sphk1/S1P axis.Here we studied the efficacy of targeting Sphk1 with sphingosine-1-phosphate receptor (S1PR)modulators in conjunction with FLT3 inhibitors to overcome FLT3 inhibitor resistance mediated by NRASmutations in AML cells with FLT3-ITD. MethodsMOLM-14 and MV4-11 human FLT3-ITD AML cell lines with NRAS mutations including G12D, G12S, G12C,Q61K and Q61H and FLT3-ITD AML patient blasts with G13V and G13D mutations were cultured with theFLT3 inhibitors gilteritinib (10 nM) or quizartinib (1 nM) and/or the S1PR modulators fingolimod (FTY720; 2.5 μM) or mocravimod (KRP203; 5 μM)...ConclusionsThe S1PR agonists fingolimod (FTY720) and mocravimod (KRP203) resensitize FLT3-ITD AML cellsharboring G12D, G12S, Q61K, and Q61H, but not G12C, NRAS mutations to FLT3 inhibitors. The datasupport potential clinical efficacy of combination regimens with these clinically applicable..."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • ANXA5 • BAD • FLT3 • NRAS • SPHK1 • STAT5

Determining sensitivity to FLT3 inhibitors prior to therapy in FLT3 mutant acute myelogenous leukemia (ASH 2025) - "For ex-vivo sensitivity assays, AML cells were treated with several dilutions of a FLT3i(Sorafenib, Midostaurin, Crenolanib, Quizartinib, Gilteritinib, Tuspetinib and MAX-40279 (a dualFLT3/FGFR inhibitor)) and cell viability was assessed with CellTiter-Glo® (Promega). Using our MS-based proteomics measurements and sensitivity results with our proprietary MLmodel, we processed both AML patient samples (N=57) and patient-derived cell lines (N=59), and wewere able to identify 7 distinct clusters. Previously we demonstrated that RPPA proteomics could discriminate FLT3i sensitive andresistant cases and here we present orthogonal confirmation by MS proteomics and ex-vivo sensitivityassays. Moreover, we show that the expression of only three proteins forms a robust biomarker topredict FLT3i sensitivity of FLT3-MUT AML patients prior to therapy. We also identified AML cell lines thatmimic both FLT3i resistance and sensitivity, and combined with deep proteomics data, these..."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • CD34 • FLT3 • PXN • SMARCA2

ESAM is functionally involved in the activity of cancer stem-like cells in human acute myeloid leukemia (ASH 2025) - "However, upon treatment with FLT3 inhibitors (CEP701 and quizartinib), ESAM-expressingcells retained heigh drug sensitivity. ESAM enhances biological activity of AML LSCs, likely through modulation ofsignaling pathways and interactions with junctional and membrane-associated proteins. These findingsidentify ESAM as a key regulator of LSC behavior and a potential therapeutic target in AML."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Lymphoma • Oncology • Targeted Protein Degradation • FLT3 • TJP1 • ZKSCAN1 • ZNF23

Negative feedback regulation of nfkb, MAPK, and JAK-STAT drives adaptive resistance to gilteritinib in AML (ASH 2025) - "Patients treated with highly selective inhibitors such asgilteritinib, crenolanib, and quizartinib usually relapse within eight to twelve months. These findings explain how elevated AP1 and NF-κB/JAK-STAT activitiestranscriptionally induce negative regulators to favor cellular survival, as unchecked MAPK signaling wouldotherwise trigger apoptosis. Collectively, these data strongly support the rationale for evaluating thecombination of gilteritinib and venetoclax with momelotinib as a therapeutic strategy to achieve effectiveand durable responses in AML."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • IRAK1 • MAPK8 • STAT5 • TET2

Clinical impact of FLT3 microclones on outcomes in patients with newly diagnosed FLT3-ITD negative AML: A subanalysis from the pethema quiwi trial (ASH 2025) - P2 | "The PETHEMA group conducted the QUIWI trial(NCT04107727), a 2:1 randomized, double-blind, placebo-controlled (PBO) phase II study evaluating theaddition of quizartinib (Quiz) to intensive chemotherapy in patients with FLT3-ITD-negative AML (i.e.,allelic ratio <0.03)... In the QUIWI trial, patients randomized to Quiz had improved outcomes irrespectively of thepresence of FLT3 microclones. Acknowledging that the study is limited by the sample size, there was anapparent improvement in DoR among microclone-pos patients randomized to Quiz as compared withPBO."

Clinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • NPM1

Prognosis of FLT3 ligand level in newly diagnosed FLT3-ITD negative Acute Myeloid Leukemia patients enrolled in the pethema QUIWI trial (ASH 2025) - P2 | "The trial enrolled patients withnewly diagnosed AML who received standard 3+7 induction chemotherapy (idarubicin and cytarabine),followed by quizartinib or placebo from day +8 to day +21, between September 2019 and October 2022.Plasma levels of FL (expressed in pg/mL) were measured by ELISA before starting and on day +15 ofinduction therapy. The Quiz arm showed anumerically higher proportion of patients achieving ≥1000 pg/mL FL level, and we observed a trend forprolonged DoR among Low FL patients randomized to Quiz. Larger studies are needed to elucidate thebiology and prognostic impact of FL levels after chemotherapy in AML."

Clinical • Acute Myelogenous Leukemia • Aplastic Anemia • Hematological Disorders • Hematological Malignancies • Leukemia • FLT3

Healthcare resource utilization in patients receiving quizartinib or placebo in combination with chemotherapy for newly diagnosed, FLT3-ITD+ acute myeloid leukemia: An analysis from the QuANTUM-first trial (ASH 2025) - P3 | "HRU was generally comparable between arms across all phases of therapy, predominantlydue to the intensity of the backbone chemotherapy used in induction and consolidation. Notably, in themaintenance phase, Quiz monotherapy was associated with a numerically lower mean proportion ofdays hospitalized vs Pbo, regardless of HSCT status. These outcomes indicate that the addition of Quiz,and its class effect of myelosuppression, did not result in a clinically meaningful increase in HRU in termsof days hospitalized or transfusion burden, supporting the tolerability of Quiz in combination withinduction and consolidation, and especially during maintenance monotherapy."

Clinical • Combination therapy • HEOR • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Hematological Disorders • Hematological Malignancies • Leukemia • Neutropenia • Thrombocytopenia

Diagnostic evaluation methods and prognostic impact of FLT3-ITD microclones in Acute Myeloid Leukemia (AML): A retrospective multicenter study on behalf of the EHA AML-specialized working group (SWG) (ASH 2025) - "In two largetrials combining intensive chemotherapy with the FLT3 inhibitors midostaurin (RATIFY) and quizartinib(QuANTUM-First), the AR threshold to define FLT3-ITD+ was conventionally set at 0.05 and 0.03,respectively. Our data show that FLT3-ITDm are associated with older age, secondary-type AML and higher frequencyof MR-gene mutations vs AML with FLT3-ITD >0.05. The potential benefit of FLT3 inhibitors in patientswith FLT3-ITDm needs to be evaluated in randomized clinical trials."

Retrospective data • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • DNMT3A • FLT3 • NPM1

Acute myeloid leukemia drug resistance: targetable nodes and the clinical trajectory of small-molecule inhibitors. (PubMed, Front Pharmacol) - "Over the past decade, six targeted or pathway-directed small molecules-midostaurin, gilteritinib, quizartinib, ivosidenib, enasidenib, venetoclax and glasdegib-have changed frontline and relapsed/refractory (R/R) practice in genomically defined subgroups or in patients unfit for intensive chemotherapy. Here we integrate mechanistic insights with clinical evidence to: (i) map resistance biology onto targetable nodes (apoptosis control; signalling kinases; chromatin/lineage programmes; RNA splicing; DNA-damage response; nuclear export; niche adhesion and innate immune evasion); (ii) summarise the clinical trajectory and current limits of approved and emerging small molecules (including menin and LSD1 inhibitors); (iii) propose rules for rational doublets and triplets that are biologically orthogonal yet clinically tolerable; (iv) outline a regulatory timeline for key AML small molecules; and (v) prioritise where drug development should go next, including next-generation..."

Journal • Review • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology

MODULE 3: Role of FLT3 Inhibitors in AML Management (ASH 2024) - "This program is supported by educational grants from AbbVie Inc, Astellas, and Daiichi Sankyo Inc.Pharmacologic similarities and differences among available FLT3 inhibitors for AML; implications for potency, activity and tolerability Principal findings from the Phase III QuANTUM-First study evaluating the addition of quizartinib to chemotherapy and its continuation as a single agent for patients with newly diagnosed AML with a FLT3-ITD mutation FDA approval of quizartinib for previously untreated AML with a FLT3-ITD mutation; clinical role Long-term outcomes reported with gilteritinib versus salvage chemotherapy for patients with relapsed/refractory (R/R) AML with a FLT3 mutation; optimal integration into routine practice Early data with gilteritinib combined with standard intensive chemotherapy or venetoclax-based therapy for AML with a FLT3 mutation Available data with and ongoing investigations of other novel FLT3 inhibitors, such as crenolanib and BMF-500, for AML..."

Acute Myelogenous Leukemia • FLT3