FLT3 (Fms-related tyrosine kinase 3)

Furthermore, compound 31l displayed a favorable metabolic stability profile in both human and mouse liver microsome screens and an oral bioavailability of 56%. This finding suggests that lead compound 31l is a promising tool for further optimization and development as a potential MERTK/FLT3 dual inhibitor anti-AML drug candidate.

P=N/A, N=111, Completed, The first affiliated hospital, Zhejiang University School of Medicine; The first affiliated hospital, Zhejiang University School of Medicine

The significant increases in serum PDGF-AA and TGF-α, and significant decreases in serum EGF and Flt3 ligand could be explained by post-procedural inflammatory or paraneoplastic mechanisms. Further research into these biomarkers with larger cohorts may enable further understanding of their role pre- and post-operatively in TTPB and their correlation with clinical outcomes. This may be used to develop a clinical tool to predict or identify patients at risk of early post-TTPB complications.

Cells were treated with VEN, the MCL-1 inhibitor S63845 and the mitogen-activated protein kinase (MEK) inhibitor trametinib (TRA), alone or in combination. The presented results highlight the role of MAPK-driven MCL-1 and BCL(x)L expression, which mediates VEN resistance. While dual inhibition of B-cell lymphoma 2 and MCL-1 is already effective, additional MEK inhibition may further improve outcomes in PTPN11-mutated AML.

The patient achieved sustained remission following risk-adapted AML chemotherapy and allogeneic hematopoietic stem cell transplantation (allo-HSCT). This case underscores three critical points in pediatric AML: (1) the essential role of integrated molecular profiling in resolving morphologic ambiguities to prevent misclassification; (2) the complex prognostic impact of FLT3-ITD/NPM1 co-mutations in childhood AML; and (3) the potential therapeutic efficacy of allo-HSCT for rare fusion-driven subtypes.

P2, N=33, Active, not recruiting, City of Hope Medical Center | Recruiting --> Active, not recruiting | N=70 --> 33 | Trial completion date: Jan 2026 --> Jun 2026 | Trial primary completion date: Jan 2026 --> Jun 2026

P1, N=30, Not yet recruiting, David Avigan

AML with HOXB3 hypomethylation usually has unique genetic patterns such as a normal karyotype, cytogenetic/molecular-intermediate risk, and mutations in FLT3-ITD, NPM1 and DNMT3A. Despite these associations, HOXB3 hypomethylation may serve as an independent prognostic biomarker for AML.

Five patients (8.8%) were refractory to induction therapy, and relapse occurred in 21.1% (12 patients). These findings support the effectiveness and acceptable tolerability of midostaurin in routine clinical practice for FLT3-mutated AML.

AML with KMT2A-PTD shows distinctive immunophenotypic features with increased CD123 and aberrant CD25 expression, both associated with FLT3-ITD. These markers may have diagnostic and therapeutic relevance in this AML subtype.

By targeting nucleic acids, FLT3 or CD33, several FDA-approved NPs and NPDs (i.e., cytarabine, anthracyclines, midostaurin, melphalan and calicheamicin linked to anti-CD33) are the major agents of upfront treatment of AML. This review summarizes the current state of the art, and provides a summary of selected NPs/NPDs which are either entering or have been investigated in preclinical and clinical trials, alone or in combination with current chemotherapy. With multifaceted actions, these biomolecules may target all hallmarks of AML, including multidrug resistance and deregulated metabolism.

P2, N=29, Active, not recruiting, University of Utah | Recruiting --> Active, not recruiting