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Molecular Profile FLT3 exon 14 ins FLT3 F691L
Therapy Quizartinib
Indication/Tumor Type hematologic cancer
Response Type resistant

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Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
FLT3 exon 14 ins FLT3 F691L hematologic cancer resistant Quizartinib Preclinical - Cell culture Actionable In a preclinical study, transformed hematologic cells expressing FLT3-ITD and FLT3 F691L demonstrated resistance to treatment with Vanflyta (quizartinib) in culture (PMID: 33780043). 33780043
FLT3 exon 14 ins FLT3 F691L hematologic cancer resistant Quizartinib Preclinical - Cell culture Actionable In a preclinical study, transformed hematologic cells expressing FLT3-ITD and FLT3 F691L were resistant to Vanflyta (quizartinib) treatment in culture (PMID: 35395091). 35395091
FLT3 exon 14 ins FLT3 F691L hematologic cancer resistant Quizartinib Preclinical - Cell line xenograft Actionable In a preclinical study, cells expressing FLT3-ITD and FLT3 F691L were resistant to treatment with Vanflyta (quizartinib) in culture and in a cell line xenograft model (PMID: 38231480). 38231480
FLT3 exon 14 ins FLT3 F691L hematologic cancer resistant Quizartinib Preclinical - Cell culture Actionable In a preclinical study, transformed hematologic cells expressing both FLT3 exon 14 insertions (ITD) and FLT3 F691L were less sensitive to Vanflyta (quizartinib)-induced growth inhibition compared to cells expressing FLT3 ITD in culture (PMID: 31309543). 31309543
PubMed Id Reference Title Details
(31309543) Comparison of effects of midostaurin, crenolanib, quizartinib, gilteritinib, sorafenib and BLU-285 on oncogenic mutants of KIT, CBL and FLT3 in haematological malignancies. Full reference...
(33780043) A noncanonical FLT3 gatekeeper mutation disrupts gilteritinib binding and confers resistance. Full reference...
(35395091) The Irreversible FLT3 Inhibitor FF-10101 Is Active Against a Diversity of FLT3 Inhibitor Resistance Mechanisms. Full reference...
(38231480) Foretinib is effective in acute myeloid leukemia by inhibiting FLT3 and overcoming secondary mutations that drive resistance to quizartinib and gilteritinib. Full reference...