Table 2. Comparison of FLT3 inhibitors... | American Society of Hematology

Table 2.

Comparison of FLT3 inhibitors in clinical development

Drug	Type I or II inhibitor	Active as monotherapy	Cellular potency	Selectivity	Half-life	Protein binding (%)	Clinical resistance mechanisms	FDA-approved	FDA approved for AML indication
Midostaurin	I	No	++	+	19 h	>99.8	One reported case of an acquired FLT KD mutation (N676K⁴¹)	Yes, in combination with induction chemotherapy only	Yes
Sorafenib	II	Yes	++	++	25-48 h	99.5	FLT3 KD mutations (D835, F691L^13,25)	Yes	No
Quizartinib	II	Yes	+++	+++	∼1.5 d	>99	FLT3 KD mutations (D835, F691L)¹⁶	No	Development ongoing
Crenolanib	I	Yes	++	++	6-8 h	95.9	F691L, Ras pathway mutations³⁰	No	Development ongoing
Gilteritinib	I	Yes	++	++	113 h	∼94	F691L, Ras pathway mutations³¹	Yes	Yes

Drug	Type I or II inhibitor	Active as monotherapy	Cellular potency	Selectivity	Half-life	Protein binding (%)	Clinical resistance mechanisms	FDA-approved	FDA approved for AML indication
Midostaurin	I	No	++	+	19 h	>99.8	One reported case of an acquired FLT KD mutation (N676K⁴¹)	Yes, in combination with induction chemotherapy only	Yes
Sorafenib	II	Yes	++	++	25-48 h	99.5	FLT3 KD mutations (D835, F691L^13,25)	Yes	No
Quizartinib	II	Yes	+++	+++	∼1.5 d	>99	FLT3 KD mutations (D835, F691L)¹⁶	No	Development ongoing
Crenolanib	I	Yes	++	++	6-8 h	95.9	F691L, Ras pathway mutations³⁰	No	Development ongoing
Gilteritinib	I	Yes	++	++	113 h	∼94	F691L, Ras pathway mutations³¹	Yes	Yes