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FLT3-F691L is a gatekeeper mutation arising under FLT3-TKI selective pressure (gilteritin...

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IDBMA-FLT3-F691L-AML
TypePertinence thérapeutique
Étatreviewed 2026-04-27 | pending_clinical_signoff | actionability review required
MaladiesDIS-AML
SourcesSRC-ADMIRAL-PERL-2019 SRC-CIVIC SRC-ELN-AML-2022

Faits relatifs à l ' action en justice

BiomarqueurBIO-FLT3-D835
VarianteMutation de résistance du gardien de porte F691L (post-FLT3i)
MaladieDIS-AML
Niveau ESCATIIA
Combinaisons recommandéessalvage chemo + allo-SCT (preferred when fit), clinical trial (next-gen FLT3i, crenolanib, FF-10101), venetoclax + azacitidine (off-label salvage)
Contre-indiqué en monothérapiegilteritinib (résistance croisée F691L), quizartinib(résistance traversée F 691L)
Résumé des faitsFLT3-F691L is a gatekeeper mutation arising under FLT3-TKI selective pressure (gilteritinib, quizartinib). Confers cross-resistance to most current FLT3i. Crenolanib (investigational type-I) and next-gen FLT3i retain partial activity. No approved targeted option — clinical trial enrollment or salvage chemo + allo-SCT.

Notes

ESCAT IIA (resistance biomarker — guides what NOT to use). OncoKB Level R1. Cell intentionally uses BIO-FLT3-D835 as biomarker_id because F691L is a TKD/kinase-domain mutation captured under the FLT3-D835 / TKD entity per the cherry-picked BIO file (no separate F691L biomarker). variant_qualifier disambiguates. Clinical use: trigger ctDNA / BM rebiopsy at gilteritinib failure to detect F691L vs D835 emergence.

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Pertinence thérapeutique