OnCo

FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival. This dossier gathers the 5 products (5 approved), 3 trials, 1 pathway and 0 resistance routes in the corpus that involve it, with external identifiers so it can be joined to UniProt, ChEMBL, Open Targets and the rest of biology.

Biology

Class III receptor tyrosine kinase; ITD confers poor prognosis.

Where it is found
  • Acute myeloid leukaemia
Class: kinase · Gene: FLT3 · Facts checked 2026-09-04 · Target page
Technologies aimed at it

Elsewhere: identifiers and databases

Built from HGNC, Ensembl, UniProt and ChEMBL ids

How common it is, by cancer

Full matrix →
CancerPrevalenceSource
Acute myeloid leukaemia
25-30%
cBioPortal (TCGA)

Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.

Mutation hotspots and which drugs address them

Extracellular Ig-like domainsKinase domain1248497745993FLT3 residue (993 aa, P36888)Internal tandem dupl…D835Y/V/H (TKD)F691L (gatekeeper)
ActivatingResistanceLarger dot: a product in the corpus addresses the residue.
ResidueKindWhat it doesAddressed by
Internal tandem duplication (ITD)
572 to 603
ActivatingIn-frame duplications in the juxtamembrane domain; high allelic ratio and long insertions carry worse prognosis. Every approved FLT3 inhibitor covers ITD.
D835Y/V/H (TKD)
835
ActivatingActivation-loop mutation. Type I inhibitors (midostaurin, gilteritinib) cover it; type II quizartinib does not, and D835 emerges as resistance to quizartinib.
F691L (gatekeeper)
691
ResistanceAcquired after gilteritinib or quizartinib; reduces sensitivity to both classes.none in corpus

Frequencies are quoted from the source on each row; a blank means no figure was sourced, not that it is rare. Domain boundaries are approximate. Sources for the map: COSMIC: FLT3.

Products by modality and phase

Browse products →
TrialPhaseStatus
QuANTUM-First
NCT02668653
3Positive
ADMIRAL
NCT02421939
3Positive
RATIFY (CALGB 10603)
NCT00651261
3Positive

Resistance routes that involve this target

Unaddressed routes →

The resistance atlas has no route that names this target.

Pathways where it is a node

Pathway-to-drug matrix →
  • Menin / KMT2A (HOXA9-MEIS1 axis)
    Node: FLT3 (co-mutated; co-target) · 2 druggable nodes

    In some leukaemias a broken chromatin protein (KMT2A, once called MLL) or a mutant NPM1 keeps embryonic growth genes (HOXA9, MEIS1) switched on, so blood cells never mature. Both need a partner called menin to stay on the DNA. Menin inhibitors pull the plug and the cells mature; the first was approved in 2024.

    Which nodes have drugs →

Companion diagnostics and assays

Assay registry →
AssayPlatformCut-off
LeukoStrat CDx FLT3 Mutation Assay
Invivoscribe · FDA CDx 2017
PCRITD signal ratio at least 0.05 or TKD mutation detected (midostaurin, gilteritinib); ITD only for quizartinib

Preclinical models

All models →
Cell lineIdentifiersWhy it is used
MOLM-13CVCL_2119 · ACH-000362ITD heterozygous.
MV4-11CVCL_0064 · ACH-000045ITD homozygous.
MOLM-14CVCL_7916 · ACH-001574ITD; sister line of MOLM-13.
Ba/F3 FLT3-ITD and D835Ynot resolvedEngineered alleles including F691L gatekeeper.
Mouse models

No open questions recorded for this target yet. Suggest one.

Ideas and companies

Ideas that involve this target · 0
Companies with products against it · 4

Key papers and the live literature

Preprints →
Latest papers · live from Europe PMC
Open in Europe PMC

Query for this target: (TITLE:"FLT3" OR ABSTRACT:"FLT3") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about FLT3, not a curated reading list.

Export

The dossier as machine-readable JSON: identifiers from HGNC, Ensembl, UniProt and ChEMBL, products with status, trials, pathways, hotspots, open questions and assays. The full entity record is in the open API at /api/v1/entities/flt3.json. Licence CC BY 4.0.