FLT3
FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival.
FLT3-ITD and TKD mutations occur in ~30% of AML. Midostaurin, gilteritinib, and quizartinib are approved; combinations with venetoclax and menin inhibitors are being tested.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival.
- 1 · What it is
FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival.
- 2 · What goes wrong in cancer
Class III receptor tyrosine kinase; ITD confers poor prognosis.
- 3 · How drugs use it
5 products aim at FLT3: small molecules. Kinases are switched on by binding ATP inside the cell, so most drugs are small molecules shaped to plug that ATP pocket.
Biology
Class III receptor tyrosine kinase; ITD confers poor prognosis.
- Acute myeloid leukaemia
How common it is, by cancer
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Acute myeloid leukaemia | 25-30% | FLT3-ITD or TKD | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
A second JAK inhibitor for myelofibrosis that works after ruxolitinib fails; it carries a boxed warning for a rare brain toxicity (Wernicke encephalopathy) so thiamine is checked.
A single pill that beats salvage chemotherapy for relapsed FLT3-mutated AML, and the backbone of the triplets now being tested in frontline disease.
The first drug to improve survival in FLT3-mutated AML, added to standard chemotherapy: median survival went from about two years to more than six.
The JAK inhibitor for myelofibrosis patients whose platelet counts are too low for ruxolitinib.
Quizartinib is a more selective FLT3 blocker that, added to chemotherapy, roughly doubled median survival in the highest-risk FLT3 subtype.
QuANTUM-First gave FLT3-ITD AML patients a second front-line targeted option and showed that continuing a FLT3 inhibitor as long-term maintenance, including after transplant, pays off. Quizartinib was approved for this indication in 2023. Head-to-head data against midostaurin are lacking, and the design leaves open how much of the benefit came from maintenance.
ADMIRAL showed that a targeted oral drug can beat chemotherapy outright in relapsed AML, and made gilteritinib the standard bridge to transplant for FLT3-mutated relapse. Its success also underpinned FLT3 inhibitor use in first-line combinations. Resistance through FLT3-independent clones and RAS pathway mutations limits durability without transplant.
Latest papers
topQuery 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.