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

Evolving paradigms in targeting FLT3 for acute myeloid leukemia therapy.

Trends in pharmacological sciences - 1 Mar 2026

Thapa Rajan, Shrestha Jesus, Paudel Keshav Raj

Abstract excerpt

FLT3 mutations drive acute myeloid leukemia (AML) progression through aberrant signaling, making FLT3 inhibition a key therapeutic strategy. Current inhibitors show efficacy, yet resistance and toxicity remain challenges. Emerging approaches, including selective inhibitors, proteolysis-targeting chimeras, and protein degraders, offer enhanced potency, sustained suppression, and combinatorial potential,...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Agents
Share to Drug Resistance, Neoplasm
Share to fms-Like Tyrosine Kinase 3

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

Share to FLT3 gene

Share to Leukemia, Myeloid, Acute

Share to Molecular Targeted Therapy

Share to Mutation

Share to Protein Kinase Inhibitors

Source

Identifiers

PMID: 41735133
DOI: 10.1016/j.tips.2026.01.009

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 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

Evolving paradigms in targeting FLT3 for acute myeloid leukemia therapy.PMID 41735133Read ↗

Degrading FLT3-ITD protein by proteolysis targeting chimera (PROTAC).Semantic proximity Read ↗

Discovery of FLT3-targeting PROTACs with potent antiproliferative activity against acute myeloid leukemia cells harboring FLT3 mutations.Semantic proximity Read ↗

Discovery of LWY713 as a potent and selective FLT3 PROTAC degrader with in vivo activity against acute myeloid leukemia.Semantic proximity Read ↗

Rapid proteasomal degradation of mutant feline McDonough sarcoma-like tyrosine kinase-3 overcomes inhibitor resistance mechanisms of acute myeloid leukemia cellsSemantic proximity Read ↗

Perspectives and challenges of small molecule inhibitor therapy for FLT3-mutated acute myeloid leukemia.Semantic proximity Read ↗

Rapid proteasomal degradation of mutant feline McDonough sarcoma-like tyrosine kinase-3 overcomes tyrosine kinase inhibitor resistance of acute myeloid leukemia cellsSemantic proximity Read ↗

Modulation of FLT3-ITD and CDK9 in acute myeloid leukaemia cells by novel proteolysis targeting chimera (PROTAC).Semantic proximity Read ↗

Tyrosine kinase inhibitors targeting FLT3 in the treatment of acute myeloid leukemiaSemantic proximity Read ↗

Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challengesSemantic proximity Read ↗

Strategies targeting FLT3 beyond the kinase inhibitors.Semantic proximity Read ↗

“FLipping” the Story: FLT3-Mutated Acute Myeloid Leukemia and the Evolving Role of FLT3 InhibitorsSemantic proximity Read ↗

FLT3-ITD-Specific PROTAC: Enhanced Safety and Increased Synergy with Venetoclax in Acute Myeloid LeukemiaSemantic proximity Read ↗

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