Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The Dual PIM/FLT3 Inhibitor MEN1703 Combines Synergistically With Gilteritinib in FLT3-ITD-Mutant Acute Myeloid Leukaemia.

Journal of cellular and molecular medicine - 1 Dec 2024

Zicari Sonia, Merlino Giuseppe, Paoli Alessandro, Fiascarelli Alessio, Tunici Patrizia, Bisignano Diego, Belli Francesco, Irrissuto Clelia, Talucci Simone, Cirigliano Elena, Iannitto Maria Luisa, Bigioni Mario, Bressan Alessandro, Brzózka Krzysztof, Ghiaur Gabriel, Bellarosa Daniela, Binaschi Monica

Abstract excerpt

MEN1703 is a first-in-class, oral, Type I dual PIM/FMS-like tyrosine kinase 3 inhibitor (FLT3i) investigated in a Phase I/II DIAMOND-01 trial in patients with acute myeloid leukaemia (AML). Gilteritinib is a highly potent and selective oral FLT3i approved for the treatment of relapsed/refractory AML with FLT3 mutations. Although gilteritinib showed strong single-agent activity in FLT3-mutated AML, the development...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aniline Compounds
Share to Bridged-Ring Compounds

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Drug Synergism

Share to fms-Like Tyrosine Kinase 3

Share to Myeloid Cell Leukemia Sequence 1 Protein

Share to Pyrazines

Share to Pyrimidines

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 39653657
DOI: 10.1111/jcmm.70235
PMCID: PMC11628189

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Dual PIM/FLT3 Inhibitor MEN1703 Combines Synergistically With Gilteritinib in FLT3-ITD-Mutant Acute Myeloid Leukaemia.PMID 39653657Read ↗

Gilteritinib: An FMS-like tyrosine kinase 3/AXL tyrosine kinase inhibitor for the treatment of relapsed or refractory acute myeloid leukemia patients.Semantic proximity Read ↗

Gilteritinib: potent targeting of FLT3 mutations in AML.Semantic proximity Read ↗

Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia.Semantic proximity Read ↗

Gilteritinib in the management of acute myeloid leukemia: Current evidence and future directions.Semantic proximity Read ↗

Metformin synergizes with gilteritinib in treating FLT3-mutated leukemia via targeting PLK1 signaling.Semantic proximity Read ↗

BMX kinase mediates gilteritinib resistance in FLT3-mutated AML through microenvironmental factors.Semantic proximity Read ↗

Gilteritinib: The Story of a Proceeding Success into Hard-to-Treat FLT3 Mutated AML PatientsSemantic proximity Read ↗

Gilteritinib use in the treatment of relapsed or refractory acute myeloid leukemia with a FLT3 mutation.Semantic proximity Read ↗

Gilteritinib activity in refractory or relapsed FLT3-mutated acute myeloid leukemia patients previously treated by intensive chemotherapy and midostaurin: a study from the French AML Intergroup ALFA/FILO.Semantic proximity Read ↗

Gilteritinib monotherapy for relapsed/refractory FLT3 mutated acute myeloid leukemia: a real-world, multi-center, matched analysis.Semantic proximity Read ↗

A potential therapeutic target for FLT3-ITD AML: PIM1 kinase.Semantic proximity Read ↗

Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.