PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
22875628-3	2013	Ruxolitinib-treated Ba/F3 cells transformed to IL3 independence by ETV6-JAK2 showed reduced proliferation and survival (IC(50) = 370 nM) compared with KG1A or Ba/F3 cells transformed by BCR-ABL1, SPBN1-FLT3 and ZMYM2-FGFR1 (IC(50) > 10 muM for all).	ruxolitinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	202-206
23638177-4	2013	MLN0518 (tandutinib) is a potent inhibitor of type III receptor tyrosine kinases that demonstrates activity against PDGFRalpha/beta, FLT3 and c-KIT.	mln0518	0-7	FMS-like tyrosine kinase 3	Mus musculus	133-137
23638177-4	2013	MLN0518 (tandutinib) is a potent inhibitor of type III receptor tyrosine kinases that demonstrates activity against PDGFRalpha/beta, FLT3 and c-KIT.	tandutinib	9-19	FMS-like tyrosine kinase 3	Mus musculus	133-137
23127761-6	2013	The transforming potential of the CBL mutant was completely abolished by the mutation of the CBL PTB domain and was decreased by the mutation of tyrosines 589 and 591 in the juxtamembrane domain of FLT3.	Tyrosine	145-154	FMS-like tyrosine kinase 3	Mus musculus	198-202
22820730-0	2013	Structure-based design of nitrogen-linked macrocyclic kinase inhibitors leading to the clinical candidate SB1317/TG02, a potent inhibitor of cyclin dependant kinases (CDKs), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase-3 (FLT3).	14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene	106-112	FMS-like tyrosine kinase 3	Mus musculus	201-227
22820730-0	2013	Structure-based design of nitrogen-linked macrocyclic kinase inhibitors leading to the clinical candidate SB1317/TG02, a potent inhibitor of cyclin dependant kinases (CDKs), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase-3 (FLT3).	Nitrogen	26-34	FMS-like tyrosine kinase 3	Mus musculus	201-227
22820730-0	2013	Structure-based design of nitrogen-linked macrocyclic kinase inhibitors leading to the clinical candidate SB1317/TG02, a potent inhibitor of cyclin dependant kinases (CDKs), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase-3 (FLT3).	Nitrogen	26-34	FMS-like tyrosine kinase 3	Mus musculus	229-233
22820730-0	2013	Structure-based design of nitrogen-linked macrocyclic kinase inhibitors leading to the clinical candidate SB1317/TG02, a potent inhibitor of cyclin dependant kinases (CDKs), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase-3 (FLT3).	14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene	106-112	FMS-like tyrosine kinase 3	Mus musculus	229-233
22820730-7	2013	Macrocycles with a basic nitrogen in the linker form a salt bridge with Asp86 in CDK2 and Asp698 in FLT3.	Nitrogen	25-33	FMS-like tyrosine kinase 3	Mus musculus	100-104
22820730-11	2013	Compound 5 (SB1317/TG02), a pan-CDK/FLT3/JAK2 inhibitor, was selected for preclinical development, and is now in phase 1 clinical trials.	14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene	12-18	FMS-like tyrosine kinase 3	Mus musculus	36-40
22927251-5	2012	Growth inhibition studies indicate that FLT3/ITD-expressing cells were killed with an IC(50) within a range of 0.2-2muM fluvastatin.	Fluvastatin	120-131	FMS-like tyrosine kinase 3	Mus musculus	40-44
22962687-0	2012	SB1578, a novel inhibitor of JAK2, FLT3, and c-Fms for the treatment of rheumatoid arthritis.	15-(2-(pyrrolidin-1-yl)ethoxy)-7,12,25-trioxa-19,21,24-triazatetracyclo(18.3.1.1(2,5).1(14,18))hexacosa-1(24),2,4,9,14(26),15,17,20,22-nonaene	0-6	FMS-like tyrosine kinase 3	Mus musculus	35-39
22962687-1	2012	SB1578 is a novel, orally bioavailable JAK2 inhibitor with specificity for JAK2 within the JAK family and also potent activity against FLT3 and c-Fms.	15-(2-(pyrrolidin-1-yl)ethoxy)-7,12,25-trioxa-19,21,24-triazatetracyclo(18.3.1.1(2,5).1(14,18))hexacosa-1(24),2,4,9,14(26),15,17,20,22-nonaene	0-6	FMS-like tyrosine kinase 3	Mus musculus	135-139
22858906-6	2013	Balb/c mice transplanted with the FLT3/ITD Y842C mutation confirmed resistance to sorafenib in vivo but not to lestaurtinib.	Sorafenib	82-91	FMS-like tyrosine kinase 3	Mus musculus	34-38
22990016-0	2012	Flt3 inhibitor AC220 is a potent therapy in a mouse model of myeloproliferative disease driven by enhanced wild-type Flt3 signaling.	quizartinib	15-20	FMS-like tyrosine kinase 3	Mus musculus	0-4
22990016-0	2012	Flt3 inhibitor AC220 is a potent therapy in a mouse model of myeloproliferative disease driven by enhanced wild-type Flt3 signaling.	quizartinib	15-20	FMS-like tyrosine kinase 3	Mus musculus	117-121
22942183-5	2012	We have identified the tyrosine residues 572, 591, and 919 of FLT3 as phosphorylation sites involved in direct binding to Lnk.	Tyrosine	23-31	FMS-like tyrosine kinase 3	Mus musculus	62-66
22942183-6	2012	Lnk itself was tyrosine phosphorylated by both FLT3 ligand (FL)-activated FLT3-WT and constitutively activated FLT3-ITD.	Tyrosine	15-23	FMS-like tyrosine kinase 3	Mus musculus	74-81
22942183-6	2012	Lnk itself was tyrosine phosphorylated by both FLT3 ligand (FL)-activated FLT3-WT and constitutively activated FLT3-ITD.	Tyrosine	15-23	FMS-like tyrosine kinase 3	Mus musculus	47-51
22927251-7	2012	An increase in the IC(50) for inhibition of phosphorylated FLT3/ITD by lestaurtinib caused by exogenous FLT3 ligand, resistance to sorafenib caused by the D835Y or FLT3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastatin treatment.	lestaurtinib	71-83	FMS-like tyrosine kinase 3	Mus musculus	59-63
22927251-7	2012	An increase in the IC(50) for inhibition of phosphorylated FLT3/ITD by lestaurtinib caused by exogenous FLT3 ligand, resistance to sorafenib caused by the D835Y or FLT3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastatin treatment.	lestaurtinib	71-83	FMS-like tyrosine kinase 3	Mus musculus	104-108
22927251-7	2012	An increase in the IC(50) for inhibition of phosphorylated FLT3/ITD by lestaurtinib caused by exogenous FLT3 ligand, resistance to sorafenib caused by the D835Y or FLT3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastatin treatment.	Fluvastatin	258-269	FMS-like tyrosine kinase 3	Mus musculus	59-63
22927251-8	2012	Finally, fluvastatin treatment in vivo reduced engraftment of BaF3 FLT3/ITD cells in Balb/c mice.	Fluvastatin	9-20	FMS-like tyrosine kinase 3	Mus musculus	67-71
22958289-2	2012	Fms-like tyrosine kinase 3 (FLT3) signaling represents a highly specific pathway for the manipulation of cDCs in vivo.	Chenodeoxycholate 3-sulphate	105-109	FMS-like tyrosine kinase 3	Mus musculus	0-26
22958289-2	2012	Fms-like tyrosine kinase 3 (FLT3) signaling represents a highly specific pathway for the manipulation of cDCs in vivo.	Chenodeoxycholate 3-sulphate	105-109	FMS-like tyrosine kinase 3	Mus musculus	28-32
22187040-0	2012	BPR1J-097, a novel FLT3 kinase inhibitor, exerts potent inhibitory activity against AML.	N1-(3-3-((phenylsulphonyl)amino)phenyl-1H-5-pyrazolyl)-4-(4-methylpiperazino) benzamide	0-9	FMS-like tyrosine kinase 3	Mus musculus	19-23
23264850-0	2012	The STAT5 Inhibitor Pimozide Displays Efficacy in Models of Acute Myelogenous Leukemia Driven by FLT3 Mutations.	Pimozide	20-28	FMS-like tyrosine kinase 3	Mus musculus	97-101
23264850-7	2012	Significantly, pimozide reduces the tumor burden in a mouse model of FLT3-driven AML.	Pimozide	15-23	FMS-like tyrosine kinase 3	Mus musculus	69-73
21360050-8	2012	The observed efficacy that was displayed by LY2457546 in the AML FLT3-ITD mutant tumor model was superior to sunitinib when both were evaluated using equivalent doses normalized to in vivo inhibition of pKDR in mouse lung.	LY2457546	44-53	FMS-like tyrosine kinase 3	Mus musculus	65-69
22438257-7	2012	DEP-1 reactivation was also achieved by counteracting the high levels of reactive oxygen species (ROS) production detected in FLT3 ITD-expressing cell lines by inhibition of reduced NAD phosphate (NADPH)-oxidases, or by overexpression of catalase or peroxiredoxin-1 (Prx-1).	Reactive Oxygen Species	73-96	FMS-like tyrosine kinase 3	Mus musculus	126-130
22438257-7	2012	DEP-1 reactivation was also achieved by counteracting the high levels of reactive oxygen species (ROS) production detected in FLT3 ITD-expressing cell lines by inhibition of reduced NAD phosphate (NADPH)-oxidases, or by overexpression of catalase or peroxiredoxin-1 (Prx-1).	Reactive Oxygen Species	98-101	FMS-like tyrosine kinase 3	Mus musculus	126-130
22438257-7	2012	DEP-1 reactivation was also achieved by counteracting the high levels of reactive oxygen species (ROS) production detected in FLT3 ITD-expressing cell lines by inhibition of reduced NAD phosphate (NADPH)-oxidases, or by overexpression of catalase or peroxiredoxin-1 (Prx-1).	NADP	182-195	FMS-like tyrosine kinase 3	Mus musculus	126-130
22438257-8	2012	Interference with ROS production in 32D cells inhibited cell transformation by FLT3 ITD in a DEP-1-dependent manner, because RNAi-mediated depletion of DEP-1 partially abrogated the inhibitory effect of ROS quenching.	Reactive Oxygen Species	18-21	FMS-like tyrosine kinase 3	Mus musculus	79-83
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	67-71
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	137-141
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	137-141
22514634-7	2012	Blocking N-CoR loss with Genistein; an inhibitor of N-CoR misfolding, significantly down-regulated Flt3 levels regardless of the Flt3 receptor mutational status and promoted the differentiation of AML-M5 cells.	Genistein	25-34	FMS-like tyrosine kinase 3	Mus musculus	99-103
23300935-8	2012	Depletion of SLAP expression by shRNA in Flt3-transfected Ba/F3 cells resulted in a weaker activation of FL-induced PI3K-Akt and MAPK signaling.	fl	105-107	FMS-like tyrosine kinase 3	Mus musculus	41-45
22514634-7	2012	Blocking N-CoR loss with Genistein; an inhibitor of N-CoR misfolding, significantly down-regulated Flt3 levels regardless of the Flt3 receptor mutational status and promoted the differentiation of AML-M5 cells.	Genistein	25-34	FMS-like tyrosine kinase 3	Mus musculus	129-133
22829080-4	2011	Oral administration of pacritinib in murine models of FLT3-ITD-driven AML led to significant inhibition of primary tumor growth and lung metastasis.	11-(2-pyrrolidin-1-ylethoxy)-14,19-dioxa-5,7,26-triazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8,10,12(27),16,21,23-decaene	23-33	FMS-like tyrosine kinase 3	Mus musculus	54-58
21775820-1	2011	Antitumor imidazoacridinone C-1311 is a DNA-reactive topoisomerase II and FLT3 receptor tyrosine kinase inhibitor.	imidazoacridinone c-1311	10-34	FMS-like tyrosine kinase 3	Mus musculus	74-78
21848891-0	2011	Irreversible pan-ERBB inhibitor canertinib elicits anti-leukaemic effects and induces the regression of FLT3-ITD transformed cells in mice.	Canertinib	32-42	FMS-like tyrosine kinase 3	Mus musculus	104-108
21683111-0	2011	Mucosal immune features to phosphorylcholine by nasal Flt3 ligand cDNA-based vaccination.	Phosphorylcholine	27-44	FMS-like tyrosine kinase 3	Mus musculus	54-58
21768087-4	2011	The Hsp90 inhibitor 17-allylaminodemethoxygeldanamycin (17-AAG) preferentially induced the polyubiquitination and proteasomal degradation of Flt3-ITD autophosphorylated on Tyr-591 in these cells.	17-allylaminodemethoxygeldanamycin	20-54	FMS-like tyrosine kinase 3	Mus musculus	141-145
21768087-4	2011	The Hsp90 inhibitor 17-allylaminodemethoxygeldanamycin (17-AAG) preferentially induced the polyubiquitination and proteasomal degradation of Flt3-ITD autophosphorylated on Tyr-591 in these cells.	tanespimycin	56-62	FMS-like tyrosine kinase 3	Mus musculus	141-145
21768087-4	2011	The Hsp90 inhibitor 17-allylaminodemethoxygeldanamycin (17-AAG) preferentially induced the polyubiquitination and proteasomal degradation of Flt3-ITD autophosphorylated on Tyr-591 in these cells.	Tyrosine	172-175	FMS-like tyrosine kinase 3	Mus musculus	141-145
21768087-5	2011	The E3 ubiquitin ligases c-Cbl and to a lesser extent Cbl-b facilitated at least partly Lys-48-linked polyubiquitination of autophosphorylated Flt3-ITD when coexpressed in 293T cells.	Lysine	88-91	FMS-like tyrosine kinase 3	Mus musculus	143-147
21768087-6	2011	Moreover, c-Cbl and Cbl-b facilitated degradation of Flt3-ITD in 293T cells and significantly enhanced the 17-AAG-induced decline in autophosphorylated Flt3-ITD.	tanespimycin	107-113	FMS-like tyrosine kinase 3	Mus musculus	152-156
21683111-8	2011	Nasal administration of Flt3 ligand cDNA with PC may contribute to the development of nasal vaccination for prevention of S. pneumoniae infection.	Phosphorylcholine	46-48	FMS-like tyrosine kinase 3	Mus musculus	24-28
21288478-3	2011	MATERIALS AND METHODS: A genetically defined mouse model of AML was used to examine the effects of the Flt3-ITD on response to cytarabine and doxorubicin in vitro and in vivo.	Cytarabine	127-137	FMS-like tyrosine kinase 3	Mus musculus	103-107
21604762-2	2011	Herein, we describe the design and synthesis of a series of small molecule 4-aryl-2-aminopyrimidine macrocycles and their biological evaluation against the JAK family of kinase enzymes and FLT3.	4-aryl-2-aminopyrimidine	75-99	FMS-like tyrosine kinase 3	Mus musculus	189-193
21237204-7	2011	FLT3-ITD and a constitutively active form of Ras (CA-N-Ras) yielded more FL-DCs than the control, whereas the other class I mutations tested yielded less FL-DCs.	fl-dcs	73-79	FMS-like tyrosine kinase 3	Mus musculus	0-4
21237204-7	2011	FLT3-ITD and a constitutively active form of Ras (CA-N-Ras) yielded more FL-DCs than the control, whereas the other class I mutations tested yielded less FL-DCs.	fl-dcs	154-160	FMS-like tyrosine kinase 3	Mus musculus	0-4
21262971-12	2011	Furthermore, FL-stimulated colony formation of 32D cells expressing FLT3 in methylcellulose was induced in response to shRNA-mediated DEP-1 knockdown.	Methylcellulose	76-91	FMS-like tyrosine kinase 3	Mus musculus	68-72
21131587-3	2011	Mice treated with bisphosphonates exhibited a decrease in proportion and absolute number of Lin(-)cKit(+)Sca1(+) Flk2(-) (LKS Flk2(-)) and long-term culture-initiating cells in bone marrow (BM).	Diphosphonates	18-33	FMS-like tyrosine kinase 3	Mus musculus	113-120
21262971-6	2011	In particular, the sites pTyr-589, pTyr-591, and pTyr-842 involved in the FLT3 ligand (FL)-mediated activation of FLT3 were hyperphosphorylated the most.	Phosphotyrosine	25-29	FMS-like tyrosine kinase 3	Mus musculus	74-78
21262971-6	2011	In particular, the sites pTyr-589, pTyr-591, and pTyr-842 involved in the FLT3 ligand (FL)-mediated activation of FLT3 were hyperphosphorylated the most.	Phosphotyrosine	35-39	FMS-like tyrosine kinase 3	Mus musculus	74-78
21262971-6	2011	In particular, the sites pTyr-589, pTyr-591, and pTyr-842 involved in the FLT3 ligand (FL)-mediated activation of FLT3 were hyperphosphorylated the most.	Phosphotyrosine	35-39	FMS-like tyrosine kinase 3	Mus musculus	74-78
21131587-3	2011	Mice treated with bisphosphonates exhibited a decrease in proportion and absolute number of Lin(-)cKit(+)Sca1(+) Flk2(-) (LKS Flk2(-)) and long-term culture-initiating cells in bone marrow (BM).	Diphosphonates	18-33	FMS-like tyrosine kinase 3	Mus musculus	113-117
20705060-2	2010	We here present a novel low molecular weight kinase inhibitor, AKN-032, targeting the FMS-like tyrosine kinase 3 (FLT3) and discovered in a new type of screening funnel combining the target therapy approach with sequential cellular screens.	AKN 032	63-70	FMS-like tyrosine kinase 3	Mus musculus	86-112
21272320-9	2011	Lestaurtinib, a small molecule FLT3 inhibitor, significantly inhibited the growth of GL-1 cells, while not affecting the growth of two other canine lymphoid cell lines without the FLT3 mutation.	lestaurtinib	0-12	FMS-like tyrosine kinase 3	Mus musculus	31-35
20705060-2	2010	We here present a novel low molecular weight kinase inhibitor, AKN-032, targeting the FMS-like tyrosine kinase 3 (FLT3) and discovered in a new type of screening funnel combining the target therapy approach with sequential cellular screens.	AKN 032	63-70	FMS-like tyrosine kinase 3	Mus musculus	114-118
20197394-4	2010	ABT-869 is a multitargeted small-molecule inhibitor that targets Fms-like tyrosine kinase-3, c-KIT, vascular endothelial growth receptors, and PDGFRs.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-7	FMS-like tyrosine kinase 3	Mus musculus	65-91
20138114-9	2010	Whereas expression of the cyclin-dependent kinase inhibitor genes p21(cip1), p27(Kip1), and p57(Kip2) increased in LSK cells by hypoxia, only p21(cip1) was upregulated in FLT3(-)CD34(-)LSK cells.	lsk	115-118	FMS-like tyrosine kinase 3	Mus musculus	171-175
20393130-3	2010	Alternatively, FLT3 might be expressed at the earliest stages of GM development.	gm	65-67	FMS-like tyrosine kinase 3	Mus musculus	15-19
20393130-6	2010	A higher expression of FLT3 was found in preGMP compared with GMP, and preGMPs were more responsive to stimulation with FLT3 ligand (FL).	guanosine 5'-monophosphorothioate	44-47	FMS-like tyrosine kinase 3	Mus musculus	23-27
19958352-8	2010	Rapamycin, an inhibitor of mTOR involved in CEBPB translation, completely blocked the increase in LIP in FL-stimulated FLT3-WT- but not FLT3-ITD-positive cells.	Sirolimus	0-9	FMS-like tyrosine kinase 3	Mus musculus	119-123
19438505-3	2009	In this study, we identified tyrosines 768, 955 and 969 of Flt3 as phosphorylation sites and mediators of growth factor receptor binding protein 2 (Grb2) interaction, leading to the association of Grb2 associated binder 2 (Gab2) and contributing to proliferation and survival.	Tyrosine	29-38	FMS-like tyrosine kinase 3	Mus musculus	59-63
17182033-7	2007	In addition, treatment of the animals with Flt3 ligand attenuated airway hyperresponsiveness to methacholine in OVA-sensitized and challenged mice.	Methacholine Chloride	96-108	FMS-like tyrosine kinase 3	Mus musculus	43-47
18617424-7	2008	Our work shows that Wnt4 overexpression has a unique ability to expand Flt3(+) LSKs in adults and demonstrates that noncanonical Wnt signaling regulates thymopoiesis.	lsks	79-83	FMS-like tyrosine kinase 3	Mus musculus	71-75
18293383-1	2008	BACKGROUND: Sunitinib is an orally bioavailable, multi-targeted tyrosine kinase inhibitor with selectivity for PDGF receptors, VEGF receptors, FLT3, and KIT.	Sunitinib	12-21	FMS-like tyrosine kinase 3	Mus musculus	143-147
18178810-6	2008	Conversely, in Flt3 ligand-supplemented cultures initiated from the same MP, estradiol inhibited cell survival in a dose-dependent manner, thereby decreasing the yield of plasmacytoid and conventional myeloid and lymphoid DC.	Estradiol	77-86	FMS-like tyrosine kinase 3	Mus musculus	15-19
18835166-0	2008	Novel and orally active 5-(1,3,4-oxadiazol-2-yl)pyrimidine derivatives as selective FLT3 inhibitors.	ODZ101408	24-58	FMS-like tyrosine kinase 3	Mus musculus	84-88
18835166-1	2008	5-(1,3,4-Oxadiazol-2-yl)pyrimidine derivative 1 was identified as a new class of FLT3 inhibitor from our compound library.	ODZ101408	0-34	FMS-like tyrosine kinase 3	Mus musculus	81-85
18230792-0	2008	Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.	Sorafenib	32-41	FMS-like tyrosine kinase 3	Mus musculus	7-11
18230792-2	2008	The kinase inhibitor sorafenib induces growth arrest and apoptosis at much lower concentrations in AML cell lines that harbor FLT3-ITD mutations than in AML cell lines with wild-type FLT3.	Sorafenib	21-30	FMS-like tyrosine kinase 3	Mus musculus	126-130
18230792-2	2008	The kinase inhibitor sorafenib induces growth arrest and apoptosis at much lower concentrations in AML cell lines that harbor FLT3-ITD mutations than in AML cell lines with wild-type FLT3.	Sorafenib	21-30	FMS-like tyrosine kinase 3	Mus musculus	183-187
18230792-8	2008	RESULTS: Sorafenib was 1000- to 3000-fold more effective in inducing growth arrest and apoptosis in Ba/F3 cells with FLT3-ITD or D835G mutations than in Ba/F3 cells with FLT3-D835Y mutant or wild-type FLT3 and inhibited the phosphorylation of tyrosine residues in ITD mutant but not wild-type FLT3 protein.	Sorafenib	9-18	FMS-like tyrosine kinase 3	Mus musculus	117-121
18230792-8	2008	RESULTS: Sorafenib was 1000- to 3000-fold more effective in inducing growth arrest and apoptosis in Ba/F3 cells with FLT3-ITD or D835G mutations than in Ba/F3 cells with FLT3-D835Y mutant or wild-type FLT3 and inhibited the phosphorylation of tyrosine residues in ITD mutant but not wild-type FLT3 protein.	Sorafenib	9-18	FMS-like tyrosine kinase 3	Mus musculus	170-174
18230792-8	2008	RESULTS: Sorafenib was 1000- to 3000-fold more effective in inducing growth arrest and apoptosis in Ba/F3 cells with FLT3-ITD or D835G mutations than in Ba/F3 cells with FLT3-D835Y mutant or wild-type FLT3 and inhibited the phosphorylation of tyrosine residues in ITD mutant but not wild-type FLT3 protein.	Sorafenib	9-18	FMS-like tyrosine kinase 3	Mus musculus	170-174
18230792-8	2008	RESULTS: Sorafenib was 1000- to 3000-fold more effective in inducing growth arrest and apoptosis in Ba/F3 cells with FLT3-ITD or D835G mutations than in Ba/F3 cells with FLT3-D835Y mutant or wild-type FLT3 and inhibited the phosphorylation of tyrosine residues in ITD mutant but not wild-type FLT3 protein.	Sorafenib	9-18	FMS-like tyrosine kinase 3	Mus musculus	170-174
17827387-0	2007	Uniform sensitivity of FLT3 activation loop mutants to the tyrosine kinase inhibitor midostaurin.	midostaurin	85-96	FMS-like tyrosine kinase 3	Mus musculus	23-27
17827387-3	2007	We therefore tested the sensitivity of 8 FLT3 activation loop mutants to midostaurin.	midostaurin	73-84	FMS-like tyrosine kinase 3	Mus musculus	41-45
17827387-5	2007	For each mutant tested, midostaurin inhibited cell growth and phosphorylation of FLT3, STAT5, and ERK.	midostaurin	24-35	FMS-like tyrosine kinase 3	Mus musculus	81-85
17541402-2	2007	We developed TG101209, an orally bioavailable small molecule that potently inhibits JAK2 (IC(50)=6 nM), FLT3 (IC(50)=25 nM) and RET (IC(50)=17 nM) kinases, with significantly less activity against other tyrosine kinases including JAK3 (IC(50)=169 nM).	TG101209	13-21	FMS-like tyrosine kinase 3	Mus musculus	104-108
17671144-0	2007	A novel FLT3 inhibitor FI-700 selectively suppresses the growth of leukemia cells with FLT3 mutations.	FI-700	23-29	FMS-like tyrosine kinase 3	Mus musculus	8-12
17671144-0	2007	A novel FLT3 inhibitor FI-700 selectively suppresses the growth of leukemia cells with FLT3 mutations.	FI-700	23-29	FMS-like tyrosine kinase 3	Mus musculus	87-91
17339451-5	2007	Lineage(-)sca-1(+)c-kit(+)flt3(+) lymphoid progenitor cell numbers were significantly increased in bone marrow of FL-treated mice before recovery of thymopoiesis.	fl	114-116	FMS-like tyrosine kinase 3	Mus musculus	26-30
17184839-0	2007	Dual treatment with FLT3 inhibitor SU11657 and doxorubicin increases survival of leukemic mice.	SU 11657	35-42	FMS-like tyrosine kinase 3	Mus musculus	20-24
17184839-2	2007	We used our model of APL with activated FLT3 to assess the effectiveness of chemotherapy in combination with SU11657, an inhibitor of FLT3.	SU 11657	109-116	FMS-like tyrosine kinase 3	Mus musculus	134-138
16627759-0	2006	Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITD.	Tyrosine	9-17	FMS-like tyrosine kinase 3	Mus musculus	81-85
16956345-0	2006	Go6976 is a potent inhibitor of the JAK 2 and FLT3 tyrosine kinases with significant activity in primary acute myeloid leukaemia cells.	Go 6976	0-6	FMS-like tyrosine kinase 3	Mus musculus	46-50
16956345-7	2006	Expression of FLT3-WT, ITD and D835Y in 32D cells showed that Go6976 is also a potent inhibitor of WT and mutant FLT3.	Go 6976	62-68	FMS-like tyrosine kinase 3	Mus musculus	14-18
16956345-7	2006	Expression of FLT3-WT, ITD and D835Y in 32D cells showed that Go6976 is also a potent inhibitor of WT and mutant FLT3.	Go 6976	62-68	FMS-like tyrosine kinase 3	Mus musculus	113-117
16956345-8	2006	In AML cells, Go6976 reduced the survival to 55 +/- 5% of control in FLT3-ITD cases and to 69 +/- 5% in FLT3-WT samples.	Go 6976	14-20	FMS-like tyrosine kinase 3	Mus musculus	69-73
16990784-0	2006	FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248).	Sunitinib	114-123	FMS-like tyrosine kinase 3	Mus musculus	0-4
16990784-0	2006	FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248).	Sunitinib	125-132	FMS-like tyrosine kinase 3	Mus musculus	0-4
16990784-8	2006	Of note, this mutation was potently inhibited by Sunitinib (SU11248), a previously described FLT3 kinase inhibitor.	Sunitinib	49-58	FMS-like tyrosine kinase 3	Mus musculus	93-97
16990784-8	2006	Of note, this mutation was potently inhibited by Sunitinib (SU11248), a previously described FLT3 kinase inhibitor.	Sunitinib	60-67	FMS-like tyrosine kinase 3	Mus musculus	93-97
16990784-9	2006	Sunitinib reduced the proliferation and induced apoptosis of transformed Ba/F3 cells expressing FLT3 K663Q.	Sunitinib	0-9	FMS-like tyrosine kinase 3	Mus musculus	96-100
16990784-10	2006	The potency of Sunitinib against FLT3 K663Q was similar to its potency against FLT3 ITD mutations.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	33-37
16990784-10	2006	The potency of Sunitinib against FLT3 K663Q was similar to its potency against FLT3 ITD mutations.	k663q	38-43	FMS-like tyrosine kinase 3	Mus musculus	33-37
16869825-3	2006	Both Ser-112 and Ser-136 of BAD are rapidly dephosphorylated after treatment with the FLT3 inhibitor CEP-701 in BaF3/ITD and MV4-11 cells.	Serine	5-8	FMS-like tyrosine kinase 3	Mus musculus	86-90
16869825-3	2006	Both Ser-112 and Ser-136 of BAD are rapidly dephosphorylated after treatment with the FLT3 inhibitor CEP-701 in BaF3/ITD and MV4-11 cells.	Serine	17-20	FMS-like tyrosine kinase 3	Mus musculus	86-90
17230226-5	2007	We also demonstrated that FLT3/ITD receptors displayed a higher affinity to bind to Lyn than wild-type FLT3 receptors in vitro and that this affinity was relative to the intensity of tyrosil phosphorylation of the receptor.	tyrosil	183-190	FMS-like tyrosine kinase 3	Mus musculus	26-30
17230226-5	2007	We also demonstrated that FLT3/ITD receptors displayed a higher affinity to bind to Lyn than wild-type FLT3 receptors in vitro and that this affinity was relative to the intensity of tyrosil phosphorylation of the receptor.	tyrosil	183-190	FMS-like tyrosine kinase 3	Mus musculus	103-107
16956345-8	2006	In AML cells, Go6976 reduced the survival to 55 +/- 5% of control in FLT3-ITD cases and to 69 +/- 5% in FLT3-WT samples.	Go 6976	14-20	FMS-like tyrosine kinase 3	Mus musculus	104-108
16627759-5	2006	In vitro mapping of tyrosine phosphorylation sites in FLT3-ITD identified 2 candidate STAT5 docking sites within the juxtamembrane domain that are disrupted by the ITD.	Tyrosine	20-28	FMS-like tyrosine kinase 3	Mus musculus	54-58
16627759-6	2006	Tyrosine to phenylalanine substitution of residues 589 and 591 in the context of the FLT3-ITD did not affect tyrosine kinase activity, but abrogated STAT5 activation.	Tyrosine	0-8	FMS-like tyrosine kinase 3	Mus musculus	85-89
16627759-6	2006	Tyrosine to phenylalanine substitution of residues 589 and 591 in the context of the FLT3-ITD did not affect tyrosine kinase activity, but abrogated STAT5 activation.	Phenylalanine	12-25	FMS-like tyrosine kinase 3	Mus musculus	85-89
15797998-6	2005	As a final test of the importance of FLT3/ITD signaling in this engraftment model, we used a small molecule FLT3 inhibitor, CEP-701, to inhibit engraftment of FLT3/ITD stem cells.	lestaurtinib	124-131	FMS-like tyrosine kinase 3	Mus musculus	108-112
16091740-2	2005	To explore activation mechanism of FLT3 TKD mutation, we analysed critical tyrosine residues for the constitutive activation and downstream signaling of the mutant by generating a series of single Tyr --> Phe substitution mutant of all 22 cytoplasmic tyrosine residues of murine FLT3 TKD-mutant (mFLT3Asp838Val).	Phenylalanine	208-211	FMS-like tyrosine kinase 3	Mus musculus	35-39
16103085-0	2005	The FLT3 internal tandem duplication mutation prevents apoptosis in interleukin-3-deprived BaF3 cells due to protein kinase A and ribosomal S6 kinase 1-mediated BAD phosphorylation at serine 112.	Serine	184-190	FMS-like tyrosine kinase 3	Mus musculus	4-8
16103085-6	2005	Inhibiting both MAPK kinase (MEK)/ERK and PKA pathways by a combination of U0126 (10 micromol/L) and H-89 (5 micromol/L) reduced most of BAD phosphorylation at Ser112 and induced apoptosis to a level comparable with that induced by FLT3 inhibitor AG1296 (5 micromol/L) in BaF3/FLT3/ITD cells.	U 0126	75-80	FMS-like tyrosine kinase 3	Mus musculus	232-236
16103085-6	2005	Inhibiting both MAPK kinase (MEK)/ERK and PKA pathways by a combination of U0126 (10 micromol/L) and H-89 (5 micromol/L) reduced most of BAD phosphorylation at Ser112 and induced apoptosis to a level comparable with that induced by FLT3 inhibitor AG1296 (5 micromol/L) in BaF3/FLT3/ITD cells.	U 0126	75-80	FMS-like tyrosine kinase 3	Mus musculus	277-281
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	U 0126	18-23	FMS-like tyrosine kinase 3	Mus musculus	91-95
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	U 0126	18-23	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	U 0126	18-23	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	U 0126	18-23	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	49-53	FMS-like tyrosine kinase 3	Mus musculus	91-95
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	49-53	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	49-53	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	49-53	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	6,7-dimethoxy-3-phenylquinoxaline	106-112	FMS-like tyrosine kinase 3	Mus musculus	91-95
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	6,7-dimethoxy-3-phenylquinoxaline	106-112	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	6,7-dimethoxy-3-phenylquinoxaline	106-112	FMS-like tyrosine kinase 3	Mus musculus	140-144
16103085-8	2005	The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the FLT3 inhibitor AG1296, suggesting that combining FLT3/ITD downstream pathway inhibition with FLT3 inhibitors may be a viable therapeutic strategy for AML caused by a FLT3/ITD mutation.	6,7-dimethoxy-3-phenylquinoxaline	106-112	FMS-like tyrosine kinase 3	Mus musculus	140-144
16091740-0	2005	Roles of tyrosine residues 845, 892 and 922 in constitutive activation of murine FLT3 kinase domain mutant.	Tyrosine	9-17	FMS-like tyrosine kinase 3	Mus musculus	81-85
16091740-2	2005	To explore activation mechanism of FLT3 TKD mutation, we analysed critical tyrosine residues for the constitutive activation and downstream signaling of the mutant by generating a series of single Tyr --> Phe substitution mutant of all 22 cytoplasmic tyrosine residues of murine FLT3 TKD-mutant (mFLT3Asp838Val).	Tyrosine	75-83	FMS-like tyrosine kinase 3	Mus musculus	35-39
16091740-4	2005	In contrast, these three Tyr --> Phe mutations partially suppressed but maintained the ligand-dependent activation and anti-apoptotic activity of wild-type FLT3, suggesting that these tyrosine residues were more critical for the constitutive activation and signaling of mFLT3Asp838Val.	Tyrosine	25-28	FMS-like tyrosine kinase 3	Mus musculus	159-163
16091740-4	2005	In contrast, these three Tyr --> Phe mutations partially suppressed but maintained the ligand-dependent activation and anti-apoptotic activity of wild-type FLT3, suggesting that these tyrosine residues were more critical for the constitutive activation and signaling of mFLT3Asp838Val.	Phenylalanine	36-39	FMS-like tyrosine kinase 3	Mus musculus	159-163
16091740-4	2005	In contrast, these three Tyr --> Phe mutations partially suppressed but maintained the ligand-dependent activation and anti-apoptotic activity of wild-type FLT3, suggesting that these tyrosine residues were more critical for the constitutive activation and signaling of mFLT3Asp838Val.	Tyrosine	187-195	FMS-like tyrosine kinase 3	Mus musculus	159-163
16091740-5	2005	These three Tyr --> Phe mutations also inhibited the constitutive activation of other FLT3 mutants bearing internal tandem duplication, Asp838Tyr or Ile839del.	Tyrosine	12-15	FMS-like tyrosine kinase 3	Mus musculus	89-93
16091740-5	2005	These three Tyr --> Phe mutations also inhibited the constitutive activation of other FLT3 mutants bearing internal tandem duplication, Asp838Tyr or Ile839del.	Phenylalanine	23-26	FMS-like tyrosine kinase 3	Mus musculus	89-93
16091740-5	2005	These three Tyr --> Phe mutations also inhibited the constitutive activation of other FLT3 mutants bearing internal tandem duplication, Asp838Tyr or Ile839del.	ile839del	152-161	FMS-like tyrosine kinase 3	Mus musculus	89-93
16148112-3	2005	In the present study, we show that SU11657, a small multitargeted receptor tyrosine kinase inhibitor with Flt3 affinity, suppressed in vitro natural IFN-producing and DC development in Flt3L-supplemented mouse whole bone marrow cell cultures in a dose-dependant manner, while DC development in GM-CSF-supplemented cultures was not affected.	SU 11657	35-42	FMS-like tyrosine kinase 3	Mus musculus	106-110
15797998-6	2005	As a final test of the importance of FLT3/ITD signaling in this engraftment model, we used a small molecule FLT3 inhibitor, CEP-701, to inhibit engraftment of FLT3/ITD stem cells.	lestaurtinib	124-131	FMS-like tyrosine kinase 3	Mus musculus	108-112
15256420-0	2004	Variable sensitivity of FLT3 activation loop mutations to the small molecule tyrosine kinase inhibitor MLN518.	tandutinib	103-109	FMS-like tyrosine kinase 3	Mus musculus	24-28
15345593-4	2005	FLT3-Y842C-transfected 32D cells showed constitutive FLT3 tyrosine phosphorylation and interleukin 3 (IL-3)-independent growth.	Tyrosine	58-66	FMS-like tyrosine kinase 3	Mus musculus	0-4
15345593-4	2005	FLT3-Y842C-transfected 32D cells showed constitutive FLT3 tyrosine phosphorylation and interleukin 3 (IL-3)-independent growth.	Tyrosine	58-66	FMS-like tyrosine kinase 3	Mus musculus	53-57
15242881-3	2004	MLN518 (formerly CT53518) is a small molecule inhibitor of the FLT3, KIT, and platelet-derived growth-factor receptor (PDGFR) tyrosine kinases with significant activity in murine models of FLT3 ITD-positive leukemia.	tandutinib	0-6	FMS-like tyrosine kinase 3	Mus musculus	63-67
15256420-2	2004	We tested the sensitivity of 8 activation loop mutations to the small molecule FLT3 inhibitor, MLN518.	tandutinib	95-101	FMS-like tyrosine kinase 3	Mus musculus	79-83
15242881-3	2004	MLN518 (formerly CT53518) is a small molecule inhibitor of the FLT3, KIT, and platelet-derived growth-factor receptor (PDGFR) tyrosine kinases with significant activity in murine models of FLT3 ITD-positive leukemia.	tandutinib	17-24	FMS-like tyrosine kinase 3	Mus musculus	63-67
15256420-4	2004	MLN518 inhibited FLT3 autophosphorylation and phosphorylation of STAT5 and ERK in FLT3-ITD-transformed Ba/F3 cells with an IC(50) (50% inhibition of cell viability) of approximately 500 nM.	tandutinib	0-6	FMS-like tyrosine kinase 3	Mus musculus	17-21
15256420-4	2004	MLN518 inhibited FLT3 autophosphorylation and phosphorylation of STAT5 and ERK in FLT3-ITD-transformed Ba/F3 cells with an IC(50) (50% inhibition of cell viability) of approximately 500 nM.	tandutinib	0-6	FMS-like tyrosine kinase 3	Mus musculus	82-86
15044254-2	2004	SU11657 is a multitargeted selective inhibitor of class III/V receptor tyrosine kinases, including the platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptors KIT and FLT3.	SU 11657	0-7	FMS-like tyrosine kinase 3	Mus musculus	205-209
12842996-11	2003	FLT3 kinase inhibitor, AG1296, alone not only dephosphorylated Bad but also down-regulated Bcl-XL, leading FLT3/ITD-32D cells into apoptosis.	6,7-dimethoxy-3-phenylquinoxaline	23-29	FMS-like tyrosine kinase 3	Mus musculus	0-4
15067010-5	2004	In culture with stem cell factor, FLT3 ligand, and IL-6, a 4-hydroxytamoxifen-inducible form of c-Myc (Myc/ERT) enabled murine Lin(-)Sca-1(+) HSCs to proliferate with the surface phenotype compatible with HSCs for more than 28 days.	hydroxytamoxifen	59-77	FMS-like tyrosine kinase 3	Mus musculus	34-38
12842996-11	2003	FLT3 kinase inhibitor, AG1296, alone not only dephosphorylated Bad but also down-regulated Bcl-XL, leading FLT3/ITD-32D cells into apoptosis.	6,7-dimethoxy-3-phenylquinoxaline	23-29	FMS-like tyrosine kinase 3	Mus musculus	107-111
12384447-4	2002	In functional analyses we could show that this mutant is hyperphosphorylated on tyrosine and confers interleukin 3-independent growth to Ba/F3 cells, which can be inhibited by a specific FLT3 protein tyrosine kinase (PTK) inhibitor.	Tyrosine	80-88	FMS-like tyrosine kinase 3	Mus musculus	187-191
12406902-5	2003	The PTK inhibitor SU5614 has inhibitory activity for FLT3 and selectively induces growth arrest, apoptosis, and cell cycle arrest in Ba/F3 and AML cell lines expressing a constitutively activated FLT3.	SU 5614	18-24	FMS-like tyrosine kinase 3	Mus musculus	196-200
12406902-8	2003	At the biochemical level, SU5614 down-regulated the activity of the hyperphosphorylated FLT3 receptor and its downstream targets, signal transducer and activator of (STAT) 3, STAT5, and mitogen-activated protein kinase (MAPK), and the STAT5 target genes BCL-X(L) and p21.	SU 5614	26-32	FMS-like tyrosine kinase 3	Mus musculus	88-92
12406902-9	2003	Our results show that SU5614 is a PTK inhibitor of FLT3 and has antiproliferative and proapoptotic activity in AML-derived cell lines that endogenously express an activated FLT3 receptor.	SU 5614	22-28	FMS-like tyrosine kinase 3	Mus musculus	51-55
12531798-7	2003	These novel findings have implications for RAPA-based therapy of chronic DC-triggered autoimmune diseases, transplant rejection, and hematologic malignancies with activating Flt3 mutations.	Sirolimus	43-47	FMS-like tyrosine kinase 3	Mus musculus	174-178
12406902-0	2003	The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.	SU 5614	38-44	FMS-like tyrosine kinase 3	Mus musculus	54-58
12406902-0	2003	The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.	SU 5614	38-44	FMS-like tyrosine kinase 3	Mus musculus	163-167
12406902-5	2003	The PTK inhibitor SU5614 has inhibitory activity for FLT3 and selectively induces growth arrest, apoptosis, and cell cycle arrest in Ba/F3 and AML cell lines expressing a constitutively activated FLT3.	SU 5614	18-24	FMS-like tyrosine kinase 3	Mus musculus	53-57
12393674-7	2002	CEP-701, a potent FLT3 tyrosine kinase inhibitor, overcame the morphologic block in differentiation caused by FLT3/ITD expression and allowed G-CSF induction of myeloid maturation markers.	lestaurtinib	0-7	FMS-like tyrosine kinase 3	Mus musculus	18-22
12393674-7	2002	CEP-701, a potent FLT3 tyrosine kinase inhibitor, overcame the morphologic block in differentiation caused by FLT3/ITD expression and allowed G-CSF induction of myeloid maturation markers.	lestaurtinib	0-7	FMS-like tyrosine kinase 3	Mus musculus	110-114
12145694-0	2002	Bis(1H-2-indolyl)-1-methanones as inhibitors of the hematopoietic tyrosine kinase Flt3.	bis(1h-2-indolyl)-1-methanones	0-30	FMS-like tyrosine kinase 3	Mus musculus	82-86
12145694-4	2002	Several bis(1H-2-indolyl)-1-methanone derivatives, represented by the compounds D-64406 and D-65476, are also potent inhibitors of Flt3.	bis(1h-2-indolyl)-1-methanone	8-37	FMS-like tyrosine kinase 3	Mus musculus	131-135
12145694-4	2002	Several bis(1H-2-indolyl)-1-methanone derivatives, represented by the compounds D-64406 and D-65476, are also potent inhibitors of Flt3.	D-64406	80-87	FMS-like tyrosine kinase 3	Mus musculus	131-135
12145694-4	2002	Several bis(1H-2-indolyl)-1-methanone derivatives, represented by the compounds D-64406 and D-65476, are also potent inhibitors of Flt3.	D-65476	92-99	FMS-like tyrosine kinase 3	Mus musculus	131-135
12145694-8	2002	32D cells, expressing a constitutively active Flt3 variant with internal tandem duplication are greatly sensitized to radiation-induced apoptosis in the presence of D-64406 or D-65476 in the absence but not in the presence of IL-3.	Deuterium	2-3	FMS-like tyrosine kinase 3	Mus musculus	46-50
12145694-9	2002	Thus, bis(1H-2-indolyl)-1-methanones are potential candidates for the treatment of Flt3-driven leukemias.	bis(1h-2-indolyl)-1-methanones	6-36	FMS-like tyrosine kinase 3	Mus musculus	83-87
12145695-2	2002	As a therapeutic approach, we previously reported that herbimycin A (HA) inhibited the growth of tandemly duplicated FLT3 (TDFLT3)-transformed cells (Leukemia 2000; 14: 374).	herbimycin	55-67	FMS-like tyrosine kinase 3	Mus musculus	117-121
12145695-5	2002	The tyrosine-phosphorylation of TDFLT3 was inhibited by HA, whereas FLT3 ligand-induced phosphorylation of wild-type FLT3 (WtFLT3) was not.	Tyrosine	4-12	FMS-like tyrosine kinase 3	Mus musculus	34-38
11455967-11	2001	In transfected Ba/F3 cells, AG1296 selectively and potently inhibited autophosphorylation of FL-stimulated wild-type and constitutively activated FLT3.	6,7-dimethoxy-3-phenylquinoxaline	28-34	FMS-like tyrosine kinase 3	Mus musculus	146-150
12124172-0	2002	CT53518, a novel selective FLT3 antagonist for the treatment of acute myelogenous leukemia (AML).	tandutinib	0-7	FMS-like tyrosine kinase 3	Mus musculus	27-31
12124172-2	2002	For this purpose we have developed CT53518, a potent antagonist that inhibits FLT3, platelet-derived growth factor receptor (PDGFR), and c-Kit (IC(50) approximately 200 nM), while other tyrosine or serine/threonine kinases were not significantly inhibited.	tandutinib	35-42	FMS-like tyrosine kinase 3	Mus musculus	78-82
11971190-2	2002	Previously we reported that FLT3 with ITD (FLT3/ITD) formed a homodimer and was autophosphorylated on tyrosine residues, while the mechanism remains unclear.	Tyrosine	102-110	FMS-like tyrosine kinase 3	Mus musculus	28-32
11971190-2	2002	Previously we reported that FLT3 with ITD (FLT3/ITD) formed a homodimer and was autophosphorylated on tyrosine residues, while the mechanism remains unclear.	Tyrosine	102-110	FMS-like tyrosine kinase 3	Mus musculus	43-51
11971190-4	2002	Mutant FLT3 with not only ITD but also an elongating or shortening JM domain transformed murine IL3-dependent myeloid progenitor cell line 32D regardless of the tyrosine residues in the JM domain.	Tyrosine	161-169	FMS-like tyrosine kinase 3	Mus musculus	7-11
11971190-5	2002	These mutant FLT3s were constitutively tyrosine phosphorylated and activated signal-transduction molecules such as SHC, MAP kinase and STAT5a.	Tyrosine	39-47	FMS-like tyrosine kinase 3	Mus musculus	13-17
11971190-7	2002	In these cells, truncated FLT3/ITD generated a hetero-complex with Wt-FLT3 and Wt-FLT3 was constitutively tyrosine phosphorylated.	Tyrosine	106-114	FMS-like tyrosine kinase 3	Mus musculus	26-30
11587362-6	2001	It suppressed the constitutive tyrosine phosphorylation of the mutant FLT3, but not the phosphorylation of the ligand-stimulated wild-type FLT3.	Tyrosine	31-39	FMS-like tyrosine kinase 3	Mus musculus	70-74
11369667-6	2001	A second type of CID, rapamycin, brings together one FKBP12 domain and one FRB domain, resulting in heterodimerization of the c-Kit(FKBP12) and Flt-3(FRB) fusions.	Sirolimus	22-31	FMS-like tyrosine kinase 3	Mus musculus	144-149
11369667-7	2001	Ba/F3 cell growth was promoted not only by FK1012- or AP1510-induced homodimerization of the c-Kit(FKBP12) fusion (as reported previously), but also by rapamycin-induced c-Kit(FKBP12)-Flt-3(FRB) heterodimerization.	FK 1012	43-49	FMS-like tyrosine kinase 3	Mus musculus	184-189
11369667-7	2001	Ba/F3 cell growth was promoted not only by FK1012- or AP1510-induced homodimerization of the c-Kit(FKBP12) fusion (as reported previously), but also by rapamycin-induced c-Kit(FKBP12)-Flt-3(FRB) heterodimerization.	AP 1510	54-60	FMS-like tyrosine kinase 3	Mus musculus	184-189
11369667-7	2001	Ba/F3 cell growth was promoted not only by FK1012- or AP1510-induced homodimerization of the c-Kit(FKBP12) fusion (as reported previously), but also by rapamycin-induced c-Kit(FKBP12)-Flt-3(FRB) heterodimerization.	Sirolimus	152-161	FMS-like tyrosine kinase 3	Mus musculus	184-189
11290608-9	2001	All D835-mutant FLT3 were constitutively tyrosine-phosphorylated and transformed 32D cells, suggesting these mutations were constitutively active.	Tyrosine	41-49	FMS-like tyrosine kinase 3	Mus musculus	16-20
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	Imatinib Mesylate	24-30	FMS-like tyrosine kinase 3	Mus musculus	186-190
10080542-0	1999	Flt3 signaling involves tyrosyl-phosphorylation of SHP-2 and SHIP and their association with Grb2 and Shc in Baf3/Flt3 cells.	cyclo(tyrosyl-tyrosyl)	24-31	FMS-like tyrosine kinase 3	Mus musculus	0-4
11021752-6	2000	Immunoblot analyses showed that JAK 2, STAT 3, STAT 5a, STAT 5b and CBL were tyrosine-phosphorylated in TEL-FLT3 expressing Ba/F3 cells in the absence of IL-3.	Tyrosine	77-85	FMS-like tyrosine kinase 3	Mus musculus	108-112
10482988-3	1999	Intracellular FLT3 signaling involves tyrosine phosphorylation of several cytoplasmic proteins including SHC.	Tyrosine	38-46	FMS-like tyrosine kinase 3	Mus musculus	14-18
10482988-4	1999	We have found that upon FLT3 activation SHC phosphorylation occurs at tyrosine 239/240 and 313.	Tyrosine	70-78	FMS-like tyrosine kinase 3	Mus musculus	24-28
10482988-7	1999	Overexpression of SHC increases the level of SHIP phosphorylation on tyrosines in response to FLT3 activation, suggesting that SHC availability is a limiting step for SHIP phosphorylation.	Tyrosine	69-78	FMS-like tyrosine kinase 3	Mus musculus	94-98
10482988-9	1999	Interestingly, SHC overexpression in FLT3-activatable Ba/F3 cells limits FLT3-dependent cell growth and this effect requires tyrosine 313.	Tyrosine	125-133	FMS-like tyrosine kinase 3	Mus musculus	37-41
10720129-6	2000	Herbimycin A suppressed the constitutive tyrosine phosphorylation of the mutant FLT3 but not the phosphorylation of the ligand-stimulated wild-type FLT3.	herbimycin	0-12	FMS-like tyrosine kinase 3	Mus musculus	80-84
10720129-6	2000	Herbimycin A suppressed the constitutive tyrosine phosphorylation of the mutant FLT3 but not the phosphorylation of the ligand-stimulated wild-type FLT3.	Tyrosine	41-49	FMS-like tyrosine kinase 3	Mus musculus	80-84
10089915-0	1999	Marrow sensitization to 5-fluorouracil using the ligands for Flt-3 and c-Kit.	Fluorouracil	24-38	FMS-like tyrosine kinase 3	Mus musculus	61-66
10089915-2	1999	Studies were performed to determine whether the in vivo administration of Flk-2/Flt-3 ligand (FL) is also capable of sensitizing progenitors to 5-FU.	Fluorouracil	144-148	FMS-like tyrosine kinase 3	Mus musculus	74-79
10080542-0	1999	Flt3 signaling involves tyrosyl-phosphorylation of SHP-2 and SHIP and their association with Grb2 and Shc in Baf3/Flt3 cells.	cyclo(tyrosyl-tyrosyl)	24-31	FMS-like tyrosine kinase 3	Mus musculus	114-118
10080542-7	1999	Like the chimeric murine Flt3, human Flt3 undergoes autophosphorylation, associates with Grb2, and leads to tyrosine phosphorylation of Shc on ligand binding.	Tyrosine	108-116	FMS-like tyrosine kinase 3	Mus musculus	25-29
9918857-2	1999	Like other members of type III receptor tyrosine kinases, murine Flt3 induces tyrosine phosphorylation of p85 and subsequently activation of PI3 kinase upon FL binding.	Tyrosine	40-48	FMS-like tyrosine kinase 3	Mus musculus	65-69
9918857-2	1999	Like other members of type III receptor tyrosine kinases, murine Flt3 induces tyrosine phosphorylation of p85 and subsequently activation of PI3 kinase upon FL binding.	fl	157-159	FMS-like tyrosine kinase 3	Mus musculus	65-69
33761599-0	2021	Studies on the anti-psoriasis effects and its mechanism of a dual JAK2/FLT3 inhibitor flonoltinib maleate.	flonoltinib maleate	86-105	FMS-like tyrosine kinase 3	Mus musculus	71-75
33761599-5	2021	Flonoltinib maleate (FM), a high selectivity dual JAK2/FLT3 inhibitor with IC50 values of 0.8 nM and 15 nM for JAK2 and FLT3, respectively, was developed by our laboratory.	flonoltinib maleate	0-19	FMS-like tyrosine kinase 3	Mus musculus	55-59
33761599-5	2021	Flonoltinib maleate (FM), a high selectivity dual JAK2/FLT3 inhibitor with IC50 values of 0.8 nM and 15 nM for JAK2 and FLT3, respectively, was developed by our laboratory.	flonoltinib maleate	0-19	FMS-like tyrosine kinase 3	Mus musculus	120-124
33761599-5	2021	Flonoltinib maleate (FM), a high selectivity dual JAK2/FLT3 inhibitor with IC50 values of 0.8 nM and 15 nM for JAK2 and FLT3, respectively, was developed by our laboratory.	Fermium	21-23	FMS-like tyrosine kinase 3	Mus musculus	55-59
33761599-5	2021	Flonoltinib maleate (FM), a high selectivity dual JAK2/FLT3 inhibitor with IC50 values of 0.8 nM and 15 nM for JAK2 and FLT3, respectively, was developed by our laboratory.	Fermium	21-23	FMS-like tyrosine kinase 3	Mus musculus	120-124
34468904-2	2021	In this work, we identified that anisomycin is a potential selective anti-AML candidate, particularly for those with FLT3-ITD mutation.	Anisomycin	33-43	FMS-like tyrosine kinase 3	Mus musculus	117-121
34710737-7	2022	HQP1351 monotherapy also significantly suppressed growth of FLT3-ITD mutant AML xenograft tumors and prolonged survival of tumor-bearing mice.	olverembatinib	0-7	FMS-like tyrosine kinase 3	Mus musculus	60-64
34468904-7	2021	In addition, FLT3-ITD cells were more sensitive to anisomycin than FLT3 WT cells.	Anisomycin	51-61	FMS-like tyrosine kinase 3	Mus musculus	13-17
34468904-11	2021	Finally, we showed that mitochondrial biogenesis contributes to differential sensitivity of FLT3-ITD and FLT3 WT cells to anisomycin.	Anisomycin	122-132	FMS-like tyrosine kinase 3	Mus musculus	92-96
34468904-11	2021	Finally, we showed that mitochondrial biogenesis contributes to differential sensitivity of FLT3-ITD and FLT3 WT cells to anisomycin.	Anisomycin	122-132	FMS-like tyrosine kinase 3	Mus musculus	105-109
34768286-10	2022	Consequently, concomitant inhibition of FLT3 and downregulation of MYC by momelotinib treatment showed better efficacy in suppressing the leukemia in a preclinical murine model of AML.	N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide	74-85	FMS-like tyrosine kinase 3	Mus musculus	40-44
34159458-7	2021	Mechanistic studies revealed that PGE2 increases expression of the tyrosine kinase receptor Flt3 on MDP and increases the DC-lineage-related transcription factor PU.1, while reducing expression of M-CSFR and the MO-lineage-related transcription factor MafB.	Dinoprostone	34-38	FMS-like tyrosine kinase 3	Mus musculus	92-96
34768286-11	2022	Altogether, these data provide evidence that momelotinib is an effective type-1 dual JAK2/FLT3 inhibitor and may offer an alternative to gilteritinib.	N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide	45-56	FMS-like tyrosine kinase 3	Mus musculus	90-94
34750506-7	2022	FLT3-ITD-dependent CSF2RB phosphorylation required phosphorylation of the FLT3 juxtamembrane domain at tyrosines 589 or 591, whereas the ITD insertion site and sequence were of no relevance.	Tyrosine	103-112	FMS-like tyrosine kinase 3	Mus musculus	0-4
34750506-7	2022	FLT3-ITD-dependent CSF2RB phosphorylation required phosphorylation of the FLT3 juxtamembrane domain at tyrosines 589 or 591, whereas the ITD insertion site and sequence were of no relevance.	Tyrosine	103-112	FMS-like tyrosine kinase 3	Mus musculus	74-78
34831215-4	2021	AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity.	Tunicamycin	96-107	FMS-like tyrosine kinase 3	Mus musculus	190-194
34732043-2	2021	The specific Anexelekto/MER Tyrosine Kinase (AXL) inhibitor ONO-7475 kills FLT3-mutant acute myeloid leukemia cells with targets including Extracellular-signal Regulated Kinase (ERK) and Myeloid Cell Leukemia 1 (MCL1).	ONO-7475	60-68	FMS-like tyrosine kinase 3	Mus musculus	75-79
34732043-4	2021	ONO-7475 synergizes with ABT-199 to potently kill FLT3-mutant acute myeloid leukemia cell lines and primary cells.	ONO-7475	0-8	FMS-like tyrosine kinase 3	Mus musculus	50-54
34732043-4	2021	ONO-7475 synergizes with ABT-199 to potently kill FLT3-mutant acute myeloid leukemia cell lines and primary cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	25-28	FMS-like tyrosine kinase 3	Mus musculus	50-54
34831215-11	2021	Importantly, in Ba/F3 cells that were stably expressing distinct FLT3-ITD variants that were located either in the juxtamembrane domain (JMD) or in the tyrosine kinase 1 domain (TKD1), response to the sequential treatments with tunicamycin and 17-AAG varied between individual FLT3-ITD motifs without dependence on the localization of the ITD.	Tunicamycin	228-239	FMS-like tyrosine kinase 3	Mus musculus	65-69
34831215-4	2021	AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity.	Glucose	121-128	FMS-like tyrosine kinase 3	Mus musculus	190-194
34831215-12	2021	In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation.	Tunicamycin	74-85	FMS-like tyrosine kinase 3	Mus musculus	14-18
34831215-12	2021	In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation.	Tunicamycin	74-85	FMS-like tyrosine kinase 3	Mus musculus	132-136
34831215-13	2021	In contrast, treatment of Ba/F3-FLT3-ITD cells with VPA was associated with a significant increase of FLT3-ITD surface expression depending on FLT3 protein synthesis.	Valproic Acid	52-55	FMS-like tyrosine kinase 3	Mus musculus	32-36
34831215-4	2021	AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity.	Valproic Acid	167-180	FMS-like tyrosine kinase 3	Mus musculus	190-194
34831215-13	2021	In contrast, treatment of Ba/F3-FLT3-ITD cells with VPA was associated with a significant increase of FLT3-ITD surface expression depending on FLT3 protein synthesis.	Valproic Acid	52-55	FMS-like tyrosine kinase 3	Mus musculus	102-106
34732858-8	2022	Carfilzomib strongly enhanced the activity of targeting AXL (upstream of FLT3) against murine and human leukemic cells.	carfilzomib	0-11	FMS-like tyrosine kinase 3	Mus musculus	73-77
34831215-13	2021	In contrast, treatment of Ba/F3-FLT3-ITD cells with VPA was associated with a significant increase of FLT3-ITD surface expression depending on FLT3 protein synthesis.	Valproic Acid	52-55	FMS-like tyrosine kinase 3	Mus musculus	143-147
34831215-4	2021	AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity.	Valproic Acid	182-185	FMS-like tyrosine kinase 3	Mus musculus	190-194
34831215-14	2021	The allocation of FLT3 to different cellular compartments that was induced by tunicamycin, 2-deoxy-D-glucose, or VPA resulted in the activation of distinct downstream signaling pathways.	Tunicamycin	78-89	FMS-like tyrosine kinase 3	Mus musculus	18-22
34831215-5	2021	We sought to determine the potential differences between the distinct FLT3-ITD variants, particularly concerning their susceptibility towards combined treatment by addressing either N-glycosylation and the heat shock protein 90 (HSP90) by 17-AAG, or by targeting the PI3K/AKT/mTOR pathway by rapamycin after treatment with VPA.	Nitrogen	182-183	FMS-like tyrosine kinase 3	Mus musculus	70-74
34831215-14	2021	The allocation of FLT3 to different cellular compartments that was induced by tunicamycin, 2-deoxy-D-glucose, or VPA resulted in the activation of distinct downstream signaling pathways.	Glucose	101-108	FMS-like tyrosine kinase 3	Mus musculus	18-22
34831215-14	2021	The allocation of FLT3 to different cellular compartments that was induced by tunicamycin, 2-deoxy-D-glucose, or VPA resulted in the activation of distinct downstream signaling pathways.	Valproic Acid	113-116	FMS-like tyrosine kinase 3	Mus musculus	18-22
34831215-16	2021	CONCLUSION: The allocation of FLT3-ITD to different cellular compartments and targeting distinct downstream signaling pathways by combined treatment with N-glycosylation and HSP90 inhibitors or VPA and rapamycin might represent new therapeutic strategies to overcome resistance towards tyrosine kinase inhibitors in FLT3-ITD-positive AML.	Nitrogen	154-155	FMS-like tyrosine kinase 3	Mus musculus	30-34
34831215-16	2021	CONCLUSION: The allocation of FLT3-ITD to different cellular compartments and targeting distinct downstream signaling pathways by combined treatment with N-glycosylation and HSP90 inhibitors or VPA and rapamycin might represent new therapeutic strategies to overcome resistance towards tyrosine kinase inhibitors in FLT3-ITD-positive AML.	Valproic Acid	194-197	FMS-like tyrosine kinase 3	Mus musculus	30-34
34831215-16	2021	CONCLUSION: The allocation of FLT3-ITD to different cellular compartments and targeting distinct downstream signaling pathways by combined treatment with N-glycosylation and HSP90 inhibitors or VPA and rapamycin might represent new therapeutic strategies to overcome resistance towards tyrosine kinase inhibitors in FLT3-ITD-positive AML.	Sirolimus	202-211	FMS-like tyrosine kinase 3	Mus musculus	30-34
34831215-17	2021	The treatment approaches addressing N-glycosylation of FLT3-ITD appear to depend on patient-specific FLT3-ITD sequences, potentially affecting the efficacy of such pharmacological strategies.	Nitrogen	36-37	FMS-like tyrosine kinase 3	Mus musculus	55-59
34831215-17	2021	The treatment approaches addressing N-glycosylation of FLT3-ITD appear to depend on patient-specific FLT3-ITD sequences, potentially affecting the efficacy of such pharmacological strategies.	Nitrogen	36-37	FMS-like tyrosine kinase 3	Mus musculus	101-105
34217323-7	2021	Orally administered KX2-391 significantly prolonged the survival of a murine leukemia model induced by FLT3-ITD-F691L.	kx2-391	20-27	FMS-like tyrosine kinase 3	Mus musculus	103-107
34400415-7	2021	CONCLUSIONS: Overall, these findings suggest that Gilteritinib as a single agent, compared with Quizartinib, is more likely to reach leukemic cells in their protective microenvironment, particularly AML clones highly dependent on FLT3-ITD signaling.	gilteritinib	50-62	FMS-like tyrosine kinase 3	Mus musculus	230-234
34324343-0	2021	Identification of Thieno(3,2-d)pyrimidine Derivatives as Dual Inhibitors of Focal Adhesion Kinase and FMS-like Tyrosine Kinase 3.	thienopyrimidine	18-41	FMS-like tyrosine kinase 3	Mus musculus	102-128
34362479-7	2021	Under the exposure of FLT3 inhibitor AC220, the IC50 values was 0.183, 0.446 and 0.836 nmol/L, and apoptosis rates was 88.6%, 34.2% and 16.1%, respectively.	quizartinib	37-42	FMS-like tyrosine kinase 3	Mus musculus	22-26
34362479-8	2021	CONCLUSION: FLT3-ITD mutant expressed cell strains with longer ITD show higher capacity of proliferation and higher tolerance to AC220 treatment.	quizartinib	129-134	FMS-like tyrosine kinase 3	Mus musculus	12-16
34721022-1	2021	G-749 is an FLT3 kinase inhibitor that was originally developed as a treatment for acute myeloid leukemia.	G-749	0-5	FMS-like tyrosine kinase 3	Mus musculus	12-16
34288692-4	2021	Docking studies with the FLT3 kinase showed a type I binding mode, where the 3H-pyrazolo group interacts with Cys694 in the hinge region.	Tritium	77-80	FMS-like tyrosine kinase 3	Mus musculus	25-29
34288692-4	2021	Docking studies with the FLT3 kinase showed a type I binding mode, where the 3H-pyrazolo group interacts with Cys694 in the hinge region.	pyrazolo	80-88	FMS-like tyrosine kinase 3	Mus musculus	25-29
34288692-5	2021	The compounds blocked the proliferation of AML cell lines harboring oncogenic FLT3-ITD mutations with remarkable IC50 values, which were comparable to the approved FLT3 inhibitor quizartinib.	quizartinib	179-190	FMS-like tyrosine kinase 3	Mus musculus	78-82
34288692-5	2021	The compounds blocked the proliferation of AML cell lines harboring oncogenic FLT3-ITD mutations with remarkable IC50 values, which were comparable to the approved FLT3 inhibitor quizartinib.	quizartinib	179-190	FMS-like tyrosine kinase 3	Mus musculus	164-168
34365291-0	2021	Development, validation, and application of an LC-MS/MS method for the determination of the AXL/FLT3 inhibitor gilteritinib in mouse plasma.	gilteritinib	111-123	FMS-like tyrosine kinase 3	Mus musculus	96-100
35489222-4	2022	Through structure-activity relationship studies, the most optimized compound 13a was developed as a potent inhibitor at FLT3 and FLT3/D835Y with IC50 values of 0.26 nM and 0.18 nM, respectively, which also displayed remarkably strong in vitro anticancer activities, with single-digit nanomolar GI50 values for several AML (MV4-11 and MOLM14) and Ba/F3 cell lines expressed with secondary TKD mutated FLT3 kinases as well as FLT3-ITD.	13a	77-80	FMS-like tyrosine kinase 3	Mus musculus	400-404
34249005-0	2021	Regulatory Dendritic Cells Induced by Bendamustine Are Associated With Enhanced Flt3 Expression and Alloreactive T-Cell Death.	Bendamustine Hydrochloride	38-50	FMS-like tyrosine kinase 3	Mus musculus	80-84
34249005-5	2021	Here, we demonstrate that exposure to BEN increases Flt3 expression on both murine bone marrow-derived DCs (BMDCs) and human monocyte-derived DCs (moDCs).	Bendamustine Hydrochloride	38-41	FMS-like tyrosine kinase 3	Mus musculus	52-56
35489222-4	2022	Through structure-activity relationship studies, the most optimized compound 13a was developed as a potent inhibitor at FLT3 and FLT3/D835Y with IC50 values of 0.26 nM and 0.18 nM, respectively, which also displayed remarkably strong in vitro anticancer activities, with single-digit nanomolar GI50 values for several AML (MV4-11 and MOLM14) and Ba/F3 cell lines expressed with secondary TKD mutated FLT3 kinases as well as FLT3-ITD.	13a	77-80	FMS-like tyrosine kinase 3	Mus musculus	424-428
35246156-11	2022	The FLT3 inhibitor gilteritinib can synergistically improve this effect by upregulating NF-kappaB2-dependent NKG2DL expression in AML cells.	gilteritinib	19-31	FMS-like tyrosine kinase 3	Mus musculus	4-8
35311954-6	2022	Mechanistically, SHP2 inhibition induced tyrosine phosphorylation and feedback-driven activation of the FLT3 receptor, which in turn phosphorylated SHP2 on tyrosine 62.	Tyrosine	156-164	FMS-like tyrosine kinase 3	Mus musculus	104-108
35228711-2	2022	A recent study showed that sorafenib, a first generation FLT3 and multikinase inhibitor, enhanced graft-versus-leukemia (GVL) effects against FLT3-ITD+ leukemia via interleukin-15 (IL-15) production.	Sorafenib	27-36	FMS-like tyrosine kinase 3	Mus musculus	57-61
35228711-4	2022	We investigated whether gilteritinib, a selective FLT3 inhibitor, could enhance GVL effects against FLT3-ITD transfected Ba/F3 leukemia (Ba/F3-FLT3-ITD) in mice.	gilteritinib	24-36	FMS-like tyrosine kinase 3	Mus musculus	50-54
35114569-5	2022	However, a type I TKI, gilteritinib, inhibited the expression of BCL2A1 through inactivation of STAT5 and alleviated TKI resistance of FLT3-ITD/D835.	gilteritinib	23-35	FMS-like tyrosine kinase 3	Mus musculus	135-139
35114569-6	2022	The combination of gilteritinib and venetoclax showed synergistic effects in the FLT3-ITD/D835 positive AML cells.	gilteritinib	19-31	FMS-like tyrosine kinase 3	Mus musculus	81-85
35114569-6	2022	The combination of gilteritinib and venetoclax showed synergistic effects in the FLT3-ITD/D835 positive AML cells.	venetoclax	36-46	FMS-like tyrosine kinase 3	Mus musculus	81-85
35114569-8	2022	Thus, the blockade of BRD4 with a BET inhibitor (CPI-0610) downregulated BCL2A1 in FLT3-mutated AML cells and extended profound suppression of FLT3-ITD/D835 mutant cells.	CPI-0610	49-57	FMS-like tyrosine kinase 3	Mus musculus	83-87
6242871-3	1984	The Ly-7.2 antigen also had an unusual distribution on cells responding to mitogens: leucoagglutinin-responsive cells were Ly-7.2-, concanavalin A Ly-7.2+, pokeweed mitogen Ly-7.2+/-, and lipopolysaccharide Ly-7.2-, i.e., Ly-7 can distinguish between subpopulations of T cells which respond to mitogens (phytohaemagglutinin and concanavalin A).	Lysine	4-6	FMS-like tyrosine kinase 3	Mus musculus	123-129
35068331-16	2022	Moreover, miR-223 inhibitor or FLT3 overexpression partially annulled the effect of 2-ME + AA on CML cells.	2-Methoxyestradiol	84-88	FMS-like tyrosine kinase 3	Mus musculus	31-35
35068331-17	2022	2-ME + AA inhibited the PI3K/AKT pathway via the miR-223/FLT3 axis.	2-Methoxyestradiol	0-4	FMS-like tyrosine kinase 3	Mus musculus	57-61
35068331-19	2022	Collectively, 2-ME + AA promoted miR-223 expression and suppressed FLT3 and the PI3K/AKT pathway, thereby facilitating the apoptosis of CML cells and inhibiting CML xenograft growth in mice.	2-Methoxyestradiol	14-20	FMS-like tyrosine kinase 3	Mus musculus	67-71
35138851-0	2022	Identification of 2-Aminopyrimidine Derivatives as FLT3 Kinase Inhibitors with High Selectivity over c-KIT.	2-aminopyrimidine	18-35	FMS-like tyrosine kinase 3	Mus musculus	51-55
35148084-6	2022	Treatment with HP1328 significantly reduced the leukemia burden and prolonged the survival of mice with FLT3/ITD leukemia.	HP1328	15-21	FMS-like tyrosine kinase 3	Mus musculus	104-108
6242871-3	1984	The Ly-7.2 antigen also had an unusual distribution on cells responding to mitogens: leucoagglutinin-responsive cells were Ly-7.2-, concanavalin A Ly-7.2+, pokeweed mitogen Ly-7.2+/-, and lipopolysaccharide Ly-7.2-, i.e., Ly-7 can distinguish between subpopulations of T cells which respond to mitogens (phytohaemagglutinin and concanavalin A).	Lysine	4-6	FMS-like tyrosine kinase 3	Mus musculus	123-129
6242871-3	1984	The Ly-7.2 antigen also had an unusual distribution on cells responding to mitogens: leucoagglutinin-responsive cells were Ly-7.2-, concanavalin A Ly-7.2+, pokeweed mitogen Ly-7.2+/-, and lipopolysaccharide Ly-7.2-, i.e., Ly-7 can distinguish between subpopulations of T cells which respond to mitogens (phytohaemagglutinin and concanavalin A).	Lysine	4-6	FMS-like tyrosine kinase 3	Mus musculus	123-129
6242871-3	1984	The Ly-7.2 antigen also had an unusual distribution on cells responding to mitogens: leucoagglutinin-responsive cells were Ly-7.2-, concanavalin A Ly-7.2+, pokeweed mitogen Ly-7.2+/-, and lipopolysaccharide Ly-7.2-, i.e., Ly-7 can distinguish between subpopulations of T cells which respond to mitogens (phytohaemagglutinin and concanavalin A).	Lysine	4-6	FMS-like tyrosine kinase 3	Mus musculus	123-129
33390479-2	2021	Preclinical studies demonstrated that gilteritinib inhibited FLT3 and showed antiproliferative activity against Ba/F3 cells expressing mutated FLT3.	gilteritinib	38-50	FMS-like tyrosine kinase 3	Mus musculus	61-65
33436370-3	2021	Using human and murine models of FLT3-ITD-driven AML, we demonstrate that FLT3-ITD promotes serine synthesis and uptake via ATF4-dependent transcriptional regulation of genes in the de novo serine biosynthesis pathway and neutral amino acid transport.	Serine	92-98	FMS-like tyrosine kinase 3	Mus musculus	33-37
33436370-3	2021	Using human and murine models of FLT3-ITD-driven AML, we demonstrate that FLT3-ITD promotes serine synthesis and uptake via ATF4-dependent transcriptional regulation of genes in the de novo serine biosynthesis pathway and neutral amino acid transport.	Serine	92-98	FMS-like tyrosine kinase 3	Mus musculus	74-78
33436370-3	2021	Using human and murine models of FLT3-ITD-driven AML, we demonstrate that FLT3-ITD promotes serine synthesis and uptake via ATF4-dependent transcriptional regulation of genes in the de novo serine biosynthesis pathway and neutral amino acid transport.	Serine	190-196	FMS-like tyrosine kinase 3	Mus musculus	33-37
33436370-3	2021	Using human and murine models of FLT3-ITD-driven AML, we demonstrate that FLT3-ITD promotes serine synthesis and uptake via ATF4-dependent transcriptional regulation of genes in the de novo serine biosynthesis pathway and neutral amino acid transport.	Serine	190-196	FMS-like tyrosine kinase 3	Mus musculus	74-78
33254022-6	2021	In vivo, triptonide treatment markedly suppressed lethal FLT3-ITD-driven AML with good tolerance and prolonged survival time in orthotopic mouse model.	triptonide	9-19	FMS-like tyrosine kinase 3	Mus musculus	57-61
33254022-7	2021	Our studies identify Hedgehog/FLT3 axis as a novel target for treating FLT3-ITD-driven leukemia and demonstrate that triptonide is an active lead compound that can kill FLT3-ITD-driven leukemia cells.	triptonide	117-127	FMS-like tyrosine kinase 3	Mus musculus	30-34
33254022-7	2021	Our studies identify Hedgehog/FLT3 axis as a novel target for treating FLT3-ITD-driven leukemia and demonstrate that triptonide is an active lead compound that can kill FLT3-ITD-driven leukemia cells.	triptonide	117-127	FMS-like tyrosine kinase 3	Mus musculus	71-75
33254022-7	2021	Our studies identify Hedgehog/FLT3 axis as a novel target for treating FLT3-ITD-driven leukemia and demonstrate that triptonide is an active lead compound that can kill FLT3-ITD-driven leukemia cells.	triptonide	117-127	FMS-like tyrosine kinase 3	Mus musculus	71-75
33831397-5	2021	Here, we showed that HHT synergizes with a selective next-generation FLT3 inhibitor, quizartinib, to inhibit cell growth/viability and induce cell-cycle arrest and apoptosis in FLT3-ITD AML cells in vitro, significantly inhibit acute myeloid leukemia progression in vivo, and substantially prolong survival of mice-bearing human FLT3-ITD AML.	quizartinib	85-96	FMS-like tyrosine kinase 3	Mus musculus	69-73
33373830-11	2021	In NOD-SCID mice engrafted with MOLM13-LUC cells, the FLT3 inhibitor midostaurin and LIMKi delayed MOLM13-LUC engraftment as detected by in vivo bioluminescence imaging and the LIMKi and midostaurin combination prolonged significantly survival of leukemic mice.	midostaurin	69-80	FMS-like tyrosine kinase 3	Mus musculus	54-58
33373830-11	2021	In NOD-SCID mice engrafted with MOLM13-LUC cells, the FLT3 inhibitor midostaurin and LIMKi delayed MOLM13-LUC engraftment as detected by in vivo bioluminescence imaging and the LIMKi and midostaurin combination prolonged significantly survival of leukemic mice.	midostaurin	187-198	FMS-like tyrosine kinase 3	Mus musculus	54-58
33390479-2	2021	Preclinical studies demonstrated that gilteritinib inhibited FLT3 and showed antiproliferative activity against Ba/F3 cells expressing mutated FLT3.	gilteritinib	38-50	FMS-like tyrosine kinase 3	Mus musculus	143-147
33391463-9	2021	We also showed that LT-171-861 had an inhibitory effect on FLT3 mutants in cellular assays.	lt-171-861	20-30	FMS-like tyrosine kinase 3	Mus musculus	59-63
33327561-4	2020	In addition, bone marrow-derived dendritic cells (BMDCs) from Flt3 KO mice directed Th2 immune responses in vitro, and the adoptive transfer of these BMDCs exacerbated allergic asthma with more marked Th2 responses than that of BMDCs from wild-type (WT) mice.	th2	84-87	FMS-like tyrosine kinase 3	Mus musculus	62-66
33327561-6	2020	In conclusion, we revealed that Flt3-independent CD11b+ DCs direct Th2 responses with the elevated OX40L and are the primary cause of allergic asthma.	th2	67-70	FMS-like tyrosine kinase 3	Mus musculus	32-36
32543003-4	2020	In vivo, oral administration of erlotinib at 100 mg/kg/day induced rapid MV4-11 tumor regression and significantly prolonged the survival time of bone marrow engraftment AML mice via inhibiting the FLT3 signal.	Erlotinib Hydrochloride	32-41	FMS-like tyrosine kinase 3	Mus musculus	198-202
32480429-8	2020	These pathological alterations in Ang II-treated mice were significantly ameliorated by Flt3 activation with FL administration.	fl	109-111	FMS-like tyrosine kinase 3	Mus musculus	88-92
32999332-3	2020	Treatment of mice on a HFD with Quizartinib, a potent inhibitor of FLT3 phosphorylation, inhibits the JAK3/STAT3, signaling and finally antagonizes the accelerated development of AML that occurred following the HFD regimen.	quizartinib	32-43	FMS-like tyrosine kinase 3	Mus musculus	67-71
33256378-11	2020	Our results demonstrate that in a subgroup of FLT3/ITD AML (4 out of 9) dasatinib significantly inhibits LSC engraftment.	Dasatinib	72-81	FMS-like tyrosine kinase 3	Mus musculus	46-50
32543003-5	2020	Thus, the therapeutic benefits of erlotinib on AML are due to its ability to target FLT3.	Erlotinib Hydrochloride	34-43	FMS-like tyrosine kinase 3	Mus musculus	84-88
32543003-6	2020	FLT3-ITD mutation is an effective biomarker for erlotinib during AML treatment.	Erlotinib Hydrochloride	48-57	FMS-like tyrosine kinase 3	Mus musculus	0-4
32543003-7	2020	In addition, we also demonstrate that erlotinib inhibits the activity of AML cell KG-1 (no FLT3 expression) by targeting Lyn.	Erlotinib Hydrochloride	38-47	FMS-like tyrosine kinase 3	Mus musculus	91-95
32765499-10	2020	Additionally, we observed that BEN treatment results in greater expression of Flt3 receptor (CD135) on host DCs compared to CY, potentially contributing to the skewing of host DCs toward cDC1s.	NSC281612	31-34	FMS-like tyrosine kinase 3	Mus musculus	93-98
32343677-6	2020	Transcriptional profiling revealed that ginsenoside Rd is functionally related to FLT3 signaling, while fenofibrate is linked to TGF-beta signaling.	Ginsenosides	40-51	FMS-like tyrosine kinase 3	Mus musculus	82-86
32629802-2	2020	Quizartinib, a potent FLT3 inhibitor, induced apoptosis in FLT3-ITD-AML, while LY2510924 blocked surface CXCR4 without inducing apoptosis.	quizartinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	22-26
32565734-4	2020	Results: Combination of Gilteritinib with ATO showed synergistic effects on inhibiting proliferation, increasing apoptosis and attenuating invasive ability in FLT3-ITD-mutated cells and reducing tumor growth in nude mice.	gilteritinib	24-36	FMS-like tyrosine kinase 3	Mus musculus	159-163
32565734-4	2020	Results: Combination of Gilteritinib with ATO showed synergistic effects on inhibiting proliferation, increasing apoptosis and attenuating invasive ability in FLT3-ITD-mutated cells and reducing tumor growth in nude mice.	ato	42-45	FMS-like tyrosine kinase 3	Mus musculus	159-163
32565734-5	2020	Results of western blot indicated that Gilteritinib increased a 160KD form of FLT3 protein on the surface of cell membrane.	gilteritinib	39-51	FMS-like tyrosine kinase 3	Mus musculus	78-82
32565734-6	2020	Detection of endoplasmic reticulum stress marker protein revealed that IRE1a and its downstream signal phosphorylated JNK were suppressed in Gilteritinib-treated FLT3-ITD positive cells.	gilteritinib	141-153	FMS-like tyrosine kinase 3	Mus musculus	162-166
32565734-9	2020	Conclusions: Thus, ATO at low concentration potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK signal pathway, targeting IRE1a to cooperate with Gilteritinib may serve as a new theoretical basis on FLT3-ITD mutant AML treatment.	ato	19-22	FMS-like tyrosine kinase 3	Mus musculus	90-94
32565734-9	2020	Conclusions: Thus, ATO at low concentration potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK signal pathway, targeting IRE1a to cooperate with Gilteritinib may serve as a new theoretical basis on FLT3-ITD mutant AML treatment.	ato	19-22	FMS-like tyrosine kinase 3	Mus musculus	240-244
32565734-9	2020	Conclusions: Thus, ATO at low concentration potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK signal pathway, targeting IRE1a to cooperate with Gilteritinib may serve as a new theoretical basis on FLT3-ITD mutant AML treatment.	gilteritinib	56-68	FMS-like tyrosine kinase 3	Mus musculus	90-94
32565734-9	2020	Conclusions: Thus, ATO at low concentration potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK signal pathway, targeting IRE1a to cooperate with Gilteritinib may serve as a new theoretical basis on FLT3-ITD mutant AML treatment.	gilteritinib	56-68	FMS-like tyrosine kinase 3	Mus musculus	240-244
32215183-5	2020	When quizartinib was administered to mice bearing FLT3-ITD mutated tumors, AC886 was rapidly detected and tumor regression was observed at doses of >=1 mg/kg without severe body weight loss.	quizartinib	5-16	FMS-like tyrosine kinase 3	Mus musculus	50-54
32272419-3	2020	Herein, we describe the discovery of novel orally available type 1 FLT3 inhibitors from structure-activity relationship (SAR) studies for the optimization of indirubin derivatives with biological and pharmacokinetic profiles as potential therapeutic agents for AML.	indirubin	158-167	FMS-like tyrosine kinase 3	Mus musculus	67-71
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	1,3-Diphenylguanidine	63-66	FMS-like tyrosine kinase 3	Mus musculus	86-90
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	1,3-Diphenylguanidine	63-66	FMS-like tyrosine kinase 3	Mus musculus	178-182
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	crenolanib	194-204	FMS-like tyrosine kinase 3	Mus musculus	86-90
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	crenolanib	194-204	FMS-like tyrosine kinase 3	Mus musculus	178-182
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	gilteritinib	209-221	FMS-like tyrosine kinase 3	Mus musculus	86-90
32272419-7	2020	The molecular docking study of 36 in the homology model of the DFG-in conformation of FLT3 resulted in a reasonable binding mode in type 1 kinases similar to the reported type 1 FLT3 inhibitors Crenolanib and Gilteritinib.	gilteritinib	209-221	FMS-like tyrosine kinase 3	Mus musculus	178-182
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	MK-8776	97-103	FMS-like tyrosine kinase 3	Mus musculus	30-34
31992353-9	2020	RESULTS: Our data demonstrate that ARQ 531 treatment has anti-proliferative activity in vitro and impairs colony formation in AML cell lines and primary AML cells independent of the presence of a FLT3 ITD mutation.	ARQ 531	35-42	FMS-like tyrosine kinase 3	Mus musculus	196-200
31943762-4	2020	We show that FLT3 inhibitors ranging from promiscuous to highly targeted are potent inhibitors of growth of leukaemia cells expressing mutant CBL in vitro, and we demonstrate in vivo efficacy of midostaurin using mouse models of mutant CBL.	midostaurin	195-206	FMS-like tyrosine kinase 3	Mus musculus	13-17
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	106-116	FMS-like tyrosine kinase 3	Mus musculus	30-34
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	140-150	FMS-like tyrosine kinase 3	Mus musculus	30-34
31692922-0	2019	Effect of Fms-like tyrosine kinase 3 (FLT3) ligand (FL) on antitumor activity of gilteritinib, a FLT3 inhibitor, in mice xenografted with FL-overexpressing cells.	gilteritinib	81-93	FMS-like tyrosine kinase 3	Mus musculus	10-36
30590794-4	2019	Methods: To test the effect on CD103+ DCs and kidney injury of inhibition of Flt3, we used a selective Flt3 inhibitor (AC220) to treat mice with AN.	quizartinib	119-124	FMS-like tyrosine kinase 3	Mus musculus	77-81
30590794-4	2019	Methods: To test the effect on CD103+ DCs and kidney injury of inhibition of Flt3, we used a selective Flt3 inhibitor (AC220) to treat mice with AN.	quizartinib	119-124	FMS-like tyrosine kinase 3	Mus musculus	103-107
30590794-10	2019	Conclusion: Flt3 inhibitor AC220 effectively reduced kidney injury in AN mice, suggesting that this inhibitor might be a useful pharmaceutical agent to treat CKD.	quizartinib	27-32	FMS-like tyrosine kinase 3	Mus musculus	12-16
31692922-4	2019	Here, we investigated the effect of FL on the efficacy of gilteritinib, a FLT3 inhibitor, in AML-derived cells in vitro and in mice.	gilteritinib	58-70	FMS-like tyrosine kinase 3	Mus musculus	74-78
31692922-7	2019	In the FLT3 signaling analyses, gilteritinib inhibited FLT3wt and FLT3-ITD to a similar degree in HEK293 and Ba/F3 cells, and similarly suppressed FLT3 downstream signaling molecules (including ERK1/2 and STAT5) in both the presence and absence of FL in MOLM-13 cells.	gilteritinib	32-44	FMS-like tyrosine kinase 3	Mus musculus	55-59
31692922-0	2019	Effect of Fms-like tyrosine kinase 3 (FLT3) ligand (FL) on antitumor activity of gilteritinib, a FLT3 inhibitor, in mice xenografted with FL-overexpressing cells.	gilteritinib	81-93	FMS-like tyrosine kinase 3	Mus musculus	38-42
31692922-0	2019	Effect of Fms-like tyrosine kinase 3 (FLT3) ligand (FL) on antitumor activity of gilteritinib, a FLT3 inhibitor, in mice xenografted with FL-overexpressing cells.	gilteritinib	81-93	FMS-like tyrosine kinase 3	Mus musculus	97-101
30947742-5	2019	METHODS: We established two sorafenib-resistant cell lines carrying FLT3/ITD mutations, namely the murine BaF3/ITD-R and the human MV4-11-R cell lines.	Sorafenib	28-37	FMS-like tyrosine kinase 3	Mus musculus	68-72
30923103-3	2019	Here, we investigated mechanisms dampening the response to the FLT3 inhibitor quizartinib, which is specific to the hematopoietic niche.	quizartinib	78-89	FMS-like tyrosine kinase 3	Mus musculus	63-67
30923103-4	2019	Using AML primary samples and cell lines, we demonstrate that convergent signals from the hematopoietic microenvironment drive FLT3-ITD cell resistance to quizartinib through the expression and activation of the tyrosine kinase receptor AXL.	quizartinib	155-166	FMS-like tyrosine kinase 3	Mus musculus	127-131
30923103-7	2019	Finally, in a xenograft mouse model, inhibition of AXL significantly increased the response of FLT3-ITD cells to quizartinib exclusively within a bone marrow environment.	quizartinib	113-124	FMS-like tyrosine kinase 3	Mus musculus	95-99
31281512-7	2019	Importantly, combination of melatonin and sorafenib exhibited highly synergistic therapeutic activity in MV4-11 xenografts and a murine model bearing FLT3/ITD leukemia.	Melatonin	28-37	FMS-like tyrosine kinase 3	Mus musculus	150-154
31281512-7	2019	Importantly, combination of melatonin and sorafenib exhibited highly synergistic therapeutic activity in MV4-11 xenografts and a murine model bearing FLT3/ITD leukemia.	Sorafenib	42-51	FMS-like tyrosine kinase 3	Mus musculus	150-154
31103903-3	2019	Herein, a series of new compounds with pyrazole amine scaffold was discovered, which showed potent inhibitory activity against FLT3-ITD and significant selectivity against both FLT3-ITD and AML cells expressing FLT3-ITD.	pyrazole amine	39-53	FMS-like tyrosine kinase 3	Mus musculus	127-131
31103903-3	2019	Herein, a series of new compounds with pyrazole amine scaffold was discovered, which showed potent inhibitory activity against FLT3-ITD and significant selectivity against both FLT3-ITD and AML cells expressing FLT3-ITD.	pyrazole amine	39-53	FMS-like tyrosine kinase 3	Mus musculus	177-181
31103903-3	2019	Herein, a series of new compounds with pyrazole amine scaffold was discovered, which showed potent inhibitory activity against FLT3-ITD and significant selectivity against both FLT3-ITD and AML cells expressing FLT3-ITD.	pyrazole amine	39-53	FMS-like tyrosine kinase 3	Mus musculus	177-181
31217189-7	2019	Mechanistically, PRMT1 catalyzed FLT3-ITD protein methylation at arginine 972/973, and PRMT1 promoted leukemia cell growth in an FLT3 methylation-dependent manner.	Arginine	65-73	FMS-like tyrosine kinase 3	Mus musculus	33-37
31217189-7	2019	Mechanistically, PRMT1 catalyzed FLT3-ITD protein methylation at arginine 972/973, and PRMT1 promoted leukemia cell growth in an FLT3 methylation-dependent manner.	Arginine	65-73	FMS-like tyrosine kinase 3	Mus musculus	129-133
31217189-8	2019	Moreover, the effects of FLT3-ITD methylation in AML cells were partially due to cross talk with FLT3-ITD phosphorylation at tyrosine 969.	Tyrosine	125-133	FMS-like tyrosine kinase 3	Mus musculus	25-29
31217189-8	2019	Moreover, the effects of FLT3-ITD methylation in AML cells were partially due to cross talk with FLT3-ITD phosphorylation at tyrosine 969.	Tyrosine	125-133	FMS-like tyrosine kinase 3	Mus musculus	97-101
31286998-4	2019	METHODS: We generated a triple transgenic mouse model, in which tamoxifen-inducible Cre-recombinase targets expression of a constitutively nuclear transcription factor NFATC1 to FLT3ITD positive HSC.	Tamoxifen	64-73	FMS-like tyrosine kinase 3	Mus musculus	178-182
30953928-2	2019	In the present study, we found that homoharringtonine (HHT), a protein translation inhibitor of plant alkaloid in China, exhibited potent cytotoxic effect against FLT3-ITD (+) cell lines and primary leukemia cells, and a remarkable synergistic anti-leukemia action was demonstrated in vitro and in vivo in xenograft mouse models when co-treated with the heat shock protein 90 inhibitor IPI504.	Homoharringtonine	36-53	FMS-like tyrosine kinase 3	Mus musculus	163-167
30947742-11	2019	In addition, we observed that chronic treatment with sorafenib resulted in an increased oxidative stress in FLT3/ITD-positive leukemia cells, which was accompanied by decreased cell proliferation and an enhanced antioxidant response.	Sorafenib	53-62	FMS-like tyrosine kinase 3	Mus musculus	108-112
30947742-12	2019	CONCLUSIONS: Our data regarding comparative metabolomics characterized a distinct metabolic and redox adaptation that may contribute to sorafenib resistance in FLT3/ITD-mutated leukemia cells.	Sorafenib	136-145	FMS-like tyrosine kinase 3	Mus musculus	160-164
30862120-9	2019	The multi-kinase inhibitor cabozantinib inhibited FLT3-ITD signaling in MV4-11-R cells and MV4-11-R-derived tumors in mice.	cabozantinib	27-39	FMS-like tyrosine kinase 3	Mus musculus	50-54
30674471-0	2019	FLT3-ITD impedes retinoic acid, but not arsenic, responses in murine acute promyelocytic leukemias.	Tretinoin	17-30	FMS-like tyrosine kinase 3	Mus musculus	0-4
30674471-6	2019	Using mouse APL models, we unexpectedly demonstrate that FLT3-ITD severely blunts ATRA response.	Tretinoin	82-86	FMS-like tyrosine kinase 3	Mus musculus	57-61
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Tretinoin	31-35	FMS-like tyrosine kinase 3	Mus musculus	86-90
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	FMS-like tyrosine kinase 3	Mus musculus	86-90
30674471-10	2019	These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination.	Tretinoin	175-179	FMS-like tyrosine kinase 3	Mus musculus	63-67
30674471-10	2019	These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination.	Arsenic	180-187	FMS-like tyrosine kinase 3	Mus musculus	63-67
30862120-9	2019	The multi-kinase inhibitor cabozantinib inhibited FLT3-ITD signaling in MV4-11-R cells and MV4-11-R-derived tumors in mice.	mv4-11-r	72-80	FMS-like tyrosine kinase 3	Mus musculus	50-54
30862120-11	2019	Together, our findings suggest that Mcl-1 and Akt phosphorylation are potential therapeutic targets for p53 mutants and that cabozantinib is an effective treatment in cytarabine-resistant FLT3-ITD-positive AML.	cabozantinib	125-137	FMS-like tyrosine kinase 3	Mus musculus	188-192
30862120-11	2019	Together, our findings suggest that Mcl-1 and Akt phosphorylation are potential therapeutic targets for p53 mutants and that cabozantinib is an effective treatment in cytarabine-resistant FLT3-ITD-positive AML.	Cytarabine	167-177	FMS-like tyrosine kinase 3	Mus musculus	188-192
30553002-0	2019	P-glycoprotein (MDR1/ABCB1) and Breast Cancer Resistance Protein (BCRP/ABCG2) limit brain accumulation of the FLT3 inhibitor quizartinib in mice.	quizartinib	125-136	FMS-like tyrosine kinase 3	Mus musculus	110-114
30770553-9	2019	Finally, we determined that combined treatment of NSG mice engrafted with FLT3-ITD + MV4-11 AML cells with 8-Cl-Ado and the FLT3 inhibitor AC220 (quizartinib) synergistically enhanced survival, compared with that of mice treated with the individual drugs, suggesting a potentially effective approach for FLT3-ITD AML patients.	mv4-11	85-91	FMS-like tyrosine kinase 3	Mus musculus	74-78
30770553-9	2019	Finally, we determined that combined treatment of NSG mice engrafted with FLT3-ITD + MV4-11 AML cells with 8-Cl-Ado and the FLT3 inhibitor AC220 (quizartinib) synergistically enhanced survival, compared with that of mice treated with the individual drugs, suggesting a potentially effective approach for FLT3-ITD AML patients.	8-chloroadenosine	107-115	FMS-like tyrosine kinase 3	Mus musculus	74-78
30770553-9	2019	Finally, we determined that combined treatment of NSG mice engrafted with FLT3-ITD + MV4-11 AML cells with 8-Cl-Ado and the FLT3 inhibitor AC220 (quizartinib) synergistically enhanced survival, compared with that of mice treated with the individual drugs, suggesting a potentially effective approach for FLT3-ITD AML patients.	quizartinib	146-157	FMS-like tyrosine kinase 3	Mus musculus	74-78
30553002-1	2019	Quizartinib, a second-generation FLT3 inhibitor, is in clinical development for the treatment of acute myeloid leukemia.	quizartinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	33-37
30206099-9	2018	TCS 359, an FLT3 inhibitor, significantly increased PLP production independently of FLT3 or AhR.	Technetium	0-3	FMS-like tyrosine kinase 3	Mus musculus	12-16
30262727-8	2018	By doing so, STAT5 activation promotes an overall elevation of ROS level, which acts as a feed-forward loop, especially in high risk Fms-related tyrosine kinase 3 (FLT3) mutant leukemia.	Reactive Oxygen Species	63-66	FMS-like tyrosine kinase 3	Mus musculus	133-162
30262727-8	2018	By doing so, STAT5 activation promotes an overall elevation of ROS level, which acts as a feed-forward loop, especially in high risk Fms-related tyrosine kinase 3 (FLT3) mutant leukemia.	Reactive Oxygen Species	63-66	FMS-like tyrosine kinase 3	Mus musculus	164-168
29471895-7	2018	The association between ETV6/FLT3 fusion protein and Hsp90 was impaired after treating ETV6/FLT3 transient transfection cos7 cells with 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	136-174	FMS-like tyrosine kinase 3	Mus musculus	29-33
29471895-7	2018	The association between ETV6/FLT3 fusion protein and Hsp90 was impaired after treating ETV6/FLT3 transient transfection cos7 cells with 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	136-174	FMS-like tyrosine kinase 3	Mus musculus	92-96
29471895-7	2018	The association between ETV6/FLT3 fusion protein and Hsp90 was impaired after treating ETV6/FLT3 transient transfection cos7 cells with 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	176-182	FMS-like tyrosine kinase 3	Mus musculus	29-33
29471895-7	2018	The association between ETV6/FLT3 fusion protein and Hsp90 was impaired after treating ETV6/FLT3 transient transfection cos7 cells with 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	176-182	FMS-like tyrosine kinase 3	Mus musculus	92-96
29471895-8	2018	17-AAG induced a time- and dose-dependent downregulation of ectopically expressed ETV6/FLT3 protein in cos7 and HeLa-transfected cells.	tanespimycin	0-6	FMS-like tyrosine kinase 3	Mus musculus	87-91
29471895-8	2018	17-AAG induced a time- and dose-dependent downregulation of ectopically expressed ETV6/FLT3 protein in cos7 and HeLa-transfected cells.	cos7	103-107	FMS-like tyrosine kinase 3	Mus musculus	87-91
29471895-9	2018	By using cycloheximide to block new protein translation, we found that 17-AAG accelerated the decay of ETV6/FLT3.	Cycloheximide	9-22	FMS-like tyrosine kinase 3	Mus musculus	108-112
29471895-9	2018	By using cycloheximide to block new protein translation, we found that 17-AAG accelerated the decay of ETV6/FLT3.	tanespimycin	71-77	FMS-like tyrosine kinase 3	Mus musculus	108-112
30004616-10	2018	Flt3-L treatment significantly expanded Treg, and restored their facilitating function.	treg	40-44	FMS-like tyrosine kinase 3	Mus musculus	0-4
29227282-4	2018	This upregulation was recapitulated in an in vivo murine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.	Sorafenib	96-105	FMS-like tyrosine kinase 3	Mus musculus	57-61
29959200-8	2018	Mice xenografted with FLT3-ITD MOLM13 cell line treated with the Sorafenib/ATO combination have significantly improved survival.	Sorafenib	65-74	FMS-like tyrosine kinase 3	Mus musculus	22-26
29959200-8	2018	Mice xenografted with FLT3-ITD MOLM13 cell line treated with the Sorafenib/ATO combination have significantly improved survival.	Arsenic Trioxide	75-78	FMS-like tyrosine kinase 3	Mus musculus	22-26
29857559-0	2018	The Cellular p53 Inhibitor MDM2 and the Growth Factor Receptor FLT3 as Biomarkers for Treatment Responses to the MDM2-Inhibitor Idasanutlin and the MEK1 Inhibitor Cobimetinib in Acute Myeloid Leukemia.	RG7388	128-139	FMS-like tyrosine kinase 3	Mus musculus	63-67
29857559-9	2018	Our data indicate that AML cells with normal karyotype (NK) and wild-type status of TP53 with elevated FLT3 and MDM2 expression emerge to be most sensitive to the combined treatment with cobimetinib and idasanutlin.	cobimetinib	187-198	FMS-like tyrosine kinase 3	Mus musculus	103-107
29857559-9	2018	Our data indicate that AML cells with normal karyotype (NK) and wild-type status of TP53 with elevated FLT3 and MDM2 expression emerge to be most sensitive to the combined treatment with cobimetinib and idasanutlin.	RG7388	203-214	FMS-like tyrosine kinase 3	Mus musculus	103-107
29857559-10	2018	FLT3 and MDM2 are biomarkers for treatment response to idasanutlin and cobimetinib in AML.	RG7388	55-66	FMS-like tyrosine kinase 3	Mus musculus	0-4
29857559-10	2018	FLT3 and MDM2 are biomarkers for treatment response to idasanutlin and cobimetinib in AML.	cobimetinib	71-82	FMS-like tyrosine kinase 3	Mus musculus	0-4
29672049-5	2018	Additionally, a single dose of 7d in mice with subcutaneous MV4-11 xenografts caused sustained inhibition of FLT3 and STAT5 phosphorylation over 48 h, in contrast to the shorter effect observed after administration of the reference FLT3 inhibitor quizartinib.	mv4-11	60-66	FMS-like tyrosine kinase 3	Mus musculus	109-113
29672049-5	2018	Additionally, a single dose of 7d in mice with subcutaneous MV4-11 xenografts caused sustained inhibition of FLT3 and STAT5 phosphorylation over 48 h, in contrast to the shorter effect observed after administration of the reference FLT3 inhibitor quizartinib.	mv4-11	60-66	FMS-like tyrosine kinase 3	Mus musculus	232-236
29854425-3	2018	We found that mice deficient in Flt3 or mice that received an Flt3 inhibitor (AC220) showed significantly reduced areas of ischemia-induced retinal neovascularization (RNV) and laser-induced choroidal NV (CNV) (P < 0.05).	quizartinib	78-83	FMS-like tyrosine kinase 3	Mus musculus	62-66
29854425-4	2018	Increased Flt3 expression at the protein level was detected in retinas of oxygen-induced retinopathy (OIR) mice at P15 and P18 during retinal NV (RNV) progression.	Oxygen	74-80	FMS-like tyrosine kinase 3	Mus musculus	10-14
29187377-3	2018	Recently, a selective FLT3 inhibitor, quizartinib, demonstrated favorable outcomes in clinical studies.	quizartinib	38-49	FMS-like tyrosine kinase 3	Mus musculus	22-26
29187377-6	2018	The co-crystal structure of FLT3 protein bound to FF-10101 revealed the formation of a covalent bond between FF-10101 and the cysteine residue at 695 of FLT3.	Cysteine	126-134	FMS-like tyrosine kinase 3	Mus musculus	28-32
29187377-6	2018	The co-crystal structure of FLT3 protein bound to FF-10101 revealed the formation of a covalent bond between FF-10101 and the cysteine residue at 695 of FLT3.	Cysteine	126-134	FMS-like tyrosine kinase 3	Mus musculus	153-157
29187377-9	2018	In mouse subcutaneous implantation models, orally administered FF-10101 showed significant growth inhibitory effect on FLT3-ITD-D835Y- and FLT3-ITD-F691L-expressing 32D cells.	FF-10101	63-71	FMS-like tyrosine kinase 3	Mus musculus	119-123
29187377-9	2018	In mouse subcutaneous implantation models, orally administered FF-10101 showed significant growth inhibitory effect on FLT3-ITD-D835Y- and FLT3-ITD-F691L-expressing 32D cells.	FF-10101	63-71	FMS-like tyrosine kinase 3	Mus musculus	139-143
29187377-10	2018	Furthermore, FF-10101 potently inhibited growth of primary AML cells harboring either FLT3-ITD or FLT3-D835 mutation in vitro and in vivo.	FF-10101	13-21	FMS-like tyrosine kinase 3	Mus musculus	86-90
29187377-10	2018	Furthermore, FF-10101 potently inhibited growth of primary AML cells harboring either FLT3-ITD or FLT3-D835 mutation in vitro and in vivo.	FF-10101	13-21	FMS-like tyrosine kinase 3	Mus musculus	98-102
29357250-0	2018	Discovery of 4-((7H-Pyrrolo[2,3-d]pyrimidin-4-yl)amino)-N-(4-((4-methylpiperazin-1-yl)methyl)phenyl)-1H-pyrazole-3-carboxamide (FN-1501), an FLT3- and CDK-Kinase Inhibitor with Potentially High Efficiency against Acute Myelocytic Leukemia.	FN-1501	128-135	FMS-like tyrosine kinase 3	Mus musculus	141-145
29357250-1	2018	A series of 1-H-pyrazole-3-carboxamide derivatives have been designed and synthesized that exhibit excellent FLT3 and CDK inhibition and antiproliferative activities.	1-h-pyrazole-3-carboxamide	12-38	FMS-like tyrosine kinase 3	Mus musculus	109-113
29357250-2	2018	A structure-activity-relationship study illustrates that the incorporation of a pyrimidine-fused heterocycle at position 4 of the pyrazole is critical for FLT3 and CDK inhibition.	pyrimidine	80-90	FMS-like tyrosine kinase 3	Mus musculus	155-159
29357250-2	2018	A structure-activity-relationship study illustrates that the incorporation of a pyrimidine-fused heterocycle at position 4 of the pyrazole is critical for FLT3 and CDK inhibition.	pyrazole	130-138	FMS-like tyrosine kinase 3	Mus musculus	155-159
29227282-4	2018	This upregulation was recapitulated in an in vivo murine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.	Sorafenib	96-105	FMS-like tyrosine kinase 3	Mus musculus	76-80
29074603-5	2018	Concurrent treatment with AZD1208 and the FLT3 inhibitor quizartinib decreased growth of MV4-11 cells, with FLT3-ITD, in mouse xenografts, and prolonged survival, enhanced apoptosis of FLT3-ITD primary AML blasts, but not FLT3-WT blasts or remission marrow cells, and decreased FLT3-ITD AML blast colony formation.	AZD1208	26-33	FMS-like tyrosine kinase 3	Mus musculus	108-112
29074603-5	2018	Concurrent treatment with AZD1208 and the FLT3 inhibitor quizartinib decreased growth of MV4-11 cells, with FLT3-ITD, in mouse xenografts, and prolonged survival, enhanced apoptosis of FLT3-ITD primary AML blasts, but not FLT3-WT blasts or remission marrow cells, and decreased FLT3-ITD AML blast colony formation.	quizartinib	57-68	FMS-like tyrosine kinase 3	Mus musculus	108-112
28516360-0	2017	Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia.	gilteritinib	0-12	FMS-like tyrosine kinase 3	Mus musculus	16-20
29416774-9	2018	These leukemic cells were selectively killed by the FLT3 inhibitors crenolanib and midostaurin in vitro.	crenolanib	68-78	FMS-like tyrosine kinase 3	Mus musculus	52-56
29416774-9	2018	These leukemic cells were selectively killed by the FLT3 inhibitors crenolanib and midostaurin in vitro.	midostaurin	83-94	FMS-like tyrosine kinase 3	Mus musculus	52-56
28516360-4	2017	The studies reported here evaluated the ability of a novel FLT3/AXL inhibitor, gilteritinib, to block mutated FLT3 in cellular and animal models of AML.	gilteritinib	79-91	FMS-like tyrosine kinase 3	Mus musculus	110-114
28516360-5	2017	Initial kinase studies showed that gilteritinib, a type I tyrosine kinase inhibitor, was highly selective for both FLT3 and AXL while having weak activity against c-KIT.	gilteritinib	35-47	FMS-like tyrosine kinase 3	Mus musculus	115-119
29507660-8	2018	Finally, AZD1208 and GDC-0941 cooperatively inhibited the mTORC1/Mcl-1 pathway and reduced viable cell numbers of primary AML cells from some FLT3-ITD positive cases.	AZD1208	9-16	FMS-like tyrosine kinase 3	Mus musculus	142-146
29507660-8	2018	Finally, AZD1208 and GDC-0941 cooperatively inhibited the mTORC1/Mcl-1 pathway and reduced viable cell numbers of primary AML cells from some FLT3-ITD positive cases.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	21-29	FMS-like tyrosine kinase 3	Mus musculus	142-146
28516360-6	2017	Gilteritinib demonstrated potent inhibitory activity against the internal tandem duplication (FLT3-ITD) and FLT3-D835Y point mutations in cellular assays using MV4-11 and MOLM-13 cells as well as Ba/F3 cells expressing mutated FLT3.	gilteritinib	0-12	FMS-like tyrosine kinase 3	Mus musculus	108-112
28516360-0	2017	Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia.	gilteritinib	0-12	FMS-like tyrosine kinase 3	Mus musculus	83-87
28516360-7	2017	Gilteritinib also inhibited FLT3-F691 mutations, although to a lesser degree, in these assays.	gilteritinib	0-12	FMS-like tyrosine kinase 3	Mus musculus	28-32
28516360-4	2017	The studies reported here evaluated the ability of a novel FLT3/AXL inhibitor, gilteritinib, to block mutated FLT3 in cellular and animal models of AML.	gilteritinib	79-91	FMS-like tyrosine kinase 3	Mus musculus	59-63
28516360-8	2017	Furthermore, gilteritinib decreased the phosphorylation levels of FLT3 and its downstream targets in both cellular and animal models.	gilteritinib	13-25	FMS-like tyrosine kinase 3	Mus musculus	66-70
29209657-0	2017	Hitting the snooze button: Inducing quiescence with the FLT3 inhibitor quizartinib protects hematopoietic progenitors from chemotherapy.	quizartinib	71-82	FMS-like tyrosine kinase 3	Mus musculus	56-60
28516360-10	2017	The decreased FLT3 activity and high intratumor distribution of gilteritinib translated to tumor regression and improved survival in xenograft and intra-bone marrow transplantation models of FLT3-driven AML.	gilteritinib	64-76	FMS-like tyrosine kinase 3	Mus musculus	191-195
28516360-12	2017	These results indicate that gilteritinib may be an important next-generation FLT3 inhibitor for use in the treatment of FLT3 mutation-positive AML.	gilteritinib	28-40	FMS-like tyrosine kinase 3	Mus musculus	77-81
28516360-12	2017	These results indicate that gilteritinib may be an important next-generation FLT3 inhibitor for use in the treatment of FLT3 mutation-positive AML.	gilteritinib	28-40	FMS-like tyrosine kinase 3	Mus musculus	120-124
28825709-6	2017	Ascorbate depletion cooperated with Flt3 internal tandem duplication (Flt3ITD) leukaemic mutations to accelerate leukaemogenesis, through cell-autonomous and possibly non-cell-autonomous mechanisms, in a manner that was reversed by dietary ascorbate.	Ascorbic Acid	0-9	FMS-like tyrosine kinase 3	Mus musculus	36-40
28825709-6	2017	Ascorbate depletion cooperated with Flt3 internal tandem duplication (Flt3ITD) leukaemic mutations to accelerate leukaemogenesis, through cell-autonomous and possibly non-cell-autonomous mechanisms, in a manner that was reversed by dietary ascorbate.	Ascorbic Acid	240-249	FMS-like tyrosine kinase 3	Mus musculus	36-40
28194038-6	2017	Glycolytic inhibitors significantly enhances the cytotoxicity induced by FLT3 tyrosine kinase inhibitor sorafenib.	Sorafenib	104-113	FMS-like tyrosine kinase 3	Mus musculus	73-77
29209657-2	2017	Our recent work outlines a strategy to prevent chemotherapy-induced myelosuppression by administering a priming dose of the FMS-Like Tyrosine kinase 3 (FLT3) inhibitor quizartinib.	quizartinib	168-179	FMS-like tyrosine kinase 3	Mus musculus	124-150
29209657-2	2017	Our recent work outlines a strategy to prevent chemotherapy-induced myelosuppression by administering a priming dose of the FMS-Like Tyrosine kinase 3 (FLT3) inhibitor quizartinib.	quizartinib	168-179	FMS-like tyrosine kinase 3	Mus musculus	152-156
29212189-2	2017	Quizartinib (AC220), a potent class III receptor tyrosine kinase inhibitor (TKI), was synthesized to selectively inhibit FMS-like tyrosine kinase-3 (FLT3), a target in the treatment of acute myeloid leukemia (AML).	quizartinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	121-147
29212189-2	2017	Quizartinib (AC220), a potent class III receptor tyrosine kinase inhibitor (TKI), was synthesized to selectively inhibit FMS-like tyrosine kinase-3 (FLT3), a target in the treatment of acute myeloid leukemia (AML).	quizartinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	149-153
29212189-2	2017	Quizartinib (AC220), a potent class III receptor tyrosine kinase inhibitor (TKI), was synthesized to selectively inhibit FMS-like tyrosine kinase-3 (FLT3), a target in the treatment of acute myeloid leukemia (AML).	quizartinib	13-18	FMS-like tyrosine kinase 3	Mus musculus	121-147
29212189-2	2017	Quizartinib (AC220), a potent class III receptor tyrosine kinase inhibitor (TKI), was synthesized to selectively inhibit FMS-like tyrosine kinase-3 (FLT3), a target in the treatment of acute myeloid leukemia (AML).	quizartinib	13-18	FMS-like tyrosine kinase 3	Mus musculus	149-153
29212189-3	2017	Quizartinib is currently under clinical trials for FLT3 ITD and wild-type AML and is tested in combination with chemotherapy.	quizartinib	0-11	FMS-like tyrosine kinase 3	Mus musculus	51-55
28772226-1	2017	A bioanalytical assay for quizartinib -a potent, and selective FLT3 tyrosine kinase inhibitor- in mouse plasma was developed and validated.	quizartinib -a	26-40	FMS-like tyrosine kinase 3	Mus musculus	63-67
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	FMS-like tyrosine kinase 3	Mus musculus	122-126
28794285-0	2017	Preventing chemotherapy-induced myelosuppression by repurposing the FLT3 inhibitor quizartinib.	quizartinib	83-94	FMS-like tyrosine kinase 3	Mus musculus	68-72
28794285-2	2017	We found that short-term exposure of mice to the FLT3 inhibitor quizartinib induced the transient quiescence of multipotent progenitors (MPPs).	quizartinib	64-75	FMS-like tyrosine kinase 3	Mus musculus	49-53
28271164-0	2017	Tyrosine 842 in the activation loop is required for full transformation by the oncogenic mutant FLT3-ITD.	Tyrosine	0-8	FMS-like tyrosine kinase 3	Mus musculus	96-100
28271164-3	2017	Phosphorylation on several critical tyrosine residues is known to be essential for FLT3 signaling.	Tyrosine	36-44	FMS-like tyrosine kinase 3	Mus musculus	83-87
28418873-6	2017	Besides, combined treatment with sunitinib, PF-04691502 and GANT61 significantly prolonged the survival of mice transplanted with FLT3-mutated MV4-11 cells compared to the single agent treatments.	Sunitinib	33-42	FMS-like tyrosine kinase 3	Mus musculus	130-134
28418873-6	2017	Besides, combined treatment with sunitinib, PF-04691502 and GANT61 significantly prolonged the survival of mice transplanted with FLT3-mutated MV4-11 cells compared to the single agent treatments.	pyrazofurin	44-46	FMS-like tyrosine kinase 3	Mus musculus	130-134
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sorafenib	14-23	FMS-like tyrosine kinase 3	Mus musculus	122-126
27132990-2	2016	We established two sorafenib-resistant cell lines carrying FLT3/ITD mutations, including the murine BaF3/ITD-R and human MV4-11-R cell lines.	Sorafenib	19-28	FMS-like tyrosine kinase 3	Mus musculus	59-63
27535613-0	2016	Drug Discovery against Psoriasis: Identification of a New Potent FMS-like Tyrosine Kinase 3 (FLT3) Inhibitor, 1-(4-((1H-Pyrazolo[3,4-d]pyrimidin-4-yl)oxy)-3-fluorophenyl)-3-(5-(tert-butyl)isoxazol-3-yl)urea, That Showed Potent Activity in a Psoriatic Animal Model.	1-(4-(1H-pyrazolo(3,4-d)pyrimidin-4-yloxy)-3-fluorophenyl)-3-(5-tert-butylisoxazol-3-yl)urea	110-206	FMS-like tyrosine kinase 3	Mus musculus	65-91
27535613-0	2016	Drug Discovery against Psoriasis: Identification of a New Potent FMS-like Tyrosine Kinase 3 (FLT3) Inhibitor, 1-(4-((1H-Pyrazolo[3,4-d]pyrimidin-4-yl)oxy)-3-fluorophenyl)-3-(5-(tert-butyl)isoxazol-3-yl)urea, That Showed Potent Activity in a Psoriatic Animal Model.	1-(4-(1H-pyrazolo(3,4-d)pyrimidin-4-yloxy)-3-fluorophenyl)-3-(5-tert-butylisoxazol-3-yl)urea	110-206	FMS-like tyrosine kinase 3	Mus musculus	93-97
27535613-2	2016	In this investigation, structural optimization was performed on a lead compound, 1-(4-(1H-pyrazolo[3,4-d]pyrimidin-4-yloxy)phenyl)-3-(4-chloro-3-(trifluoromethyl)phenyl)urea (1), which showed a moderate inhibitory activity againt FLT3.	1-(4-(1H-pyrazolo(3,4-d)pyrimidin-4-yloxy)phenyl)-3-(4-chloro-3-(trifluoromethyl)phenyl)urea	81-173	FMS-like tyrosine kinase 3	Mus musculus	230-234
27535613-3	2016	A series of pyrazolo[3,4-d]pyrimidine derivatives were synthesized, and structure-activity relationship analysis led to the discovery of a number of potent FLT3 inhibitors.	pyrazolo(3,4-d)pyrimidine	12-37	FMS-like tyrosine kinase 3	Mus musculus	156-160
26891877-7	2016	Importantly, leukemic cells carrying the FLT3-N676K mutant in the absence of an ITD mutation were highly sensitive to FLT3 inhibitors AC220 and crenolanib, and crenolanib even retained activity against the AC220-resistant FLT3-ITD-N676K mutant.	crenolanib	144-154	FMS-like tyrosine kinase 3	Mus musculus	41-45
27387666-0	2016	Internal Tandem Duplication in FLT3 Attenuates Proliferation and Regulates Resistance to the FLT3 Inhibitor AC220 by Modulating p21Cdkn1a and Pbx1 in Hematopoietic Cells.	quizartinib	108-113	FMS-like tyrosine kinase 3	Mus musculus	31-35
27387666-0	2016	Internal Tandem Duplication in FLT3 Attenuates Proliferation and Regulates Resistance to the FLT3 Inhibitor AC220 by Modulating p21Cdkn1a and Pbx1 in Hematopoietic Cells.	quizartinib	108-113	FMS-like tyrosine kinase 3	Mus musculus	93-97
27387666-5	2016	The loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of concomitantly enriching the S+G2/M phase population and significantly increasing the expression of Pbx1, but not Evi-1, in FLT3-ITD+ cells.	Cytarabine	95-105	FMS-like tyrosine kinase 3	Mus musculus	249-253
27387666-7	2016	When FLT3-ITD was antagonized with AC220, a selective inhibitor of FLT3-ITD, p21 expression was decreased coincident with Pbx1 mRNA up-regulation and a rapid decline in the number of viable FLT3-ITD+ Ba/F3 cells; however, the cells eventually became refractory to AC220.	quizartinib	35-40	FMS-like tyrosine kinase 3	Mus musculus	5-9
27387666-7	2016	When FLT3-ITD was antagonized with AC220, a selective inhibitor of FLT3-ITD, p21 expression was decreased coincident with Pbx1 mRNA up-regulation and a rapid decline in the number of viable FLT3-ITD+ Ba/F3 cells; however, the cells eventually became refractory to AC220.	quizartinib	35-40	FMS-like tyrosine kinase 3	Mus musculus	67-71
27387666-7	2016	When FLT3-ITD was antagonized with AC220, a selective inhibitor of FLT3-ITD, p21 expression was decreased coincident with Pbx1 mRNA up-regulation and a rapid decline in the number of viable FLT3-ITD+ Ba/F3 cells; however, the cells eventually became refractory to AC220.	quizartinib	35-40	FMS-like tyrosine kinase 3	Mus musculus	67-71
26896780-3	2016	In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunitinib, imatinib and dasatinib) were obtained through homology modelling and molecular docking.	Sunitinib	95-104	FMS-like tyrosine kinase 3	Mus musculus	51-55
26896780-3	2016	In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunitinib, imatinib and dasatinib) were obtained through homology modelling and molecular docking.	Imatinib Mesylate	106-114	FMS-like tyrosine kinase 3	Mus musculus	51-55
26896780-3	2016	In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunitinib, imatinib and dasatinib) were obtained through homology modelling and molecular docking.	Dasatinib	119-128	FMS-like tyrosine kinase 3	Mus musculus	51-55
26896780-6	2016	CEP701, PKC412 and sunitinib interacted with the ATP-binding pocket of FLT3, forming H-bonds with Cys694 and Glu692.	Sunitinib	19-28	FMS-like tyrosine kinase 3	Mus musculus	71-75
26896780-6	2016	CEP701, PKC412 and sunitinib interacted with the ATP-binding pocket of FLT3, forming H-bonds with Cys694 and Glu692.	Adenosine Triphosphate	49-52	FMS-like tyrosine kinase 3	Mus musculus	71-75
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	72-76
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	177-181
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	lestaurtinib	48-54	FMS-like tyrosine kinase 3	Mus musculus	72-76
27186148-4	2016	In preclinical studies, midostaurin exhibited broad-spectrum antitumor activity toward a wide range of tumor xenografts, as well as an FLT3-ITD-driven mouse model of myelodysplastic syndrome (MDS).	midostaurin	24-35	FMS-like tyrosine kinase 3	Mus musculus	135-139
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	lestaurtinib	48-54	FMS-like tyrosine kinase 3	Mus musculus	177-181
26891877-7	2016	Importantly, leukemic cells carrying the FLT3-N676K mutant in the absence of an ITD mutation were highly sensitive to FLT3 inhibitors AC220 and crenolanib, and crenolanib even retained activity against the AC220-resistant FLT3-ITD-N676K mutant.	crenolanib	144-154	FMS-like tyrosine kinase 3	Mus musculus	118-122
26891877-7	2016	Importantly, leukemic cells carrying the FLT3-N676K mutant in the absence of an ITD mutation were highly sensitive to FLT3 inhibitors AC220 and crenolanib, and crenolanib even retained activity against the AC220-resistant FLT3-ITD-N676K mutant.	crenolanib	144-154	FMS-like tyrosine kinase 3	Mus musculus	118-122
26891877-7	2016	Importantly, leukemic cells carrying the FLT3-N676K mutant in the absence of an ITD mutation were highly sensitive to FLT3 inhibitors AC220 and crenolanib, and crenolanib even retained activity against the AC220-resistant FLT3-ITD-N676K mutant.	crenolanib	160-170	FMS-like tyrosine kinase 3	Mus musculus	41-45
26308771-0	2016	NOX4-driven ROS formation mediates PTP inactivation and cell transformation in FLT3ITD-positive AML cells.	Reactive Oxygen Species	12-15	FMS-like tyrosine kinase 3	Mus musculus	79-83
26308771-2	2016	Transforming FLT3ITD signal transduction causes formation of reactive oxygen species (ROS) and inactivation of the protein-tyrosine phosphatase (PTP) DEP-1/PTPRJ, a negative regulator of FLT3 signaling.	Reactive Oxygen Species	61-84	FMS-like tyrosine kinase 3	Mus musculus	13-17
26308771-2	2016	Transforming FLT3ITD signal transduction causes formation of reactive oxygen species (ROS) and inactivation of the protein-tyrosine phosphatase (PTP) DEP-1/PTPRJ, a negative regulator of FLT3 signaling.	Reactive Oxygen Species	61-84	FMS-like tyrosine kinase 3	Mus musculus	187-191
26308771-2	2016	Transforming FLT3ITD signal transduction causes formation of reactive oxygen species (ROS) and inactivation of the protein-tyrosine phosphatase (PTP) DEP-1/PTPRJ, a negative regulator of FLT3 signaling.	Reactive Oxygen Species	86-89	FMS-like tyrosine kinase 3	Mus musculus	13-17
26308771-2	2016	Transforming FLT3ITD signal transduction causes formation of reactive oxygen species (ROS) and inactivation of the protein-tyrosine phosphatase (PTP) DEP-1/PTPRJ, a negative regulator of FLT3 signaling.	Reactive Oxygen Species	86-89	FMS-like tyrosine kinase 3	Mus musculus	187-191
24619500-5	2014	RESULTS: We identified several acquired point mutations in the tyrosine kinase domains (TKD) of the FLT3 gene in sorafenib-resistant murine leukemia cell line carrying human FLT3-ITD mutations, which were also detected in two of four sorafenib-resistant patient samples.	Sorafenib	113-122	FMS-like tyrosine kinase 3	Mus musculus	100-104
26870340-0	2016	Internal tandem duplication and tyrosine kinase domain mutations in FLT3 alter the response to daunorubicin in Ba/F3 cells.	Daunorubicin	95-107	FMS-like tyrosine kinase 3	Mus musculus	68-72
26870340-4	2016	As a result, the 50% effective dose for daunorubicin was significantly higher in both Ba/F3-FLT3-ITD clones, and also in one of the two Ba/F3-FLT3-TKD clones when cells were cultured without IL-3.	Daunorubicin	40-52	FMS-like tyrosine kinase 3	Mus musculus	92-96
26870340-4	2016	As a result, the 50% effective dose for daunorubicin was significantly higher in both Ba/F3-FLT3-ITD clones, and also in one of the two Ba/F3-FLT3-TKD clones when cells were cultured without IL-3.	Daunorubicin	40-52	FMS-like tyrosine kinase 3	Mus musculus	142-146
26870340-6	2016	Collectively, these results indicate that ITD and TKD mutations in FLT3 may confer daunorubicin resistance in Ba/F3 cells.	Daunorubicin	83-95	FMS-like tyrosine kinase 3	Mus musculus	67-71
24895100-4	2014	SKLB4771, a potent and selective FLT3 inhibitor that we designed and synthesised, was used to treat cutaneous inflammation and psoriasis-like symptoms of disease in mice and almost completely cured the psoriasis-like disease without obvious toxicity.	1-(5-(7-(3-morpholinopropoxy)quinazolin-4-ylthio)-(1,3,4)thiadiazol-2-yl)-3-p-tolylurea	0-8	FMS-like tyrosine kinase 3	Mus musculus	33-37
25482131-8	2015	Co-treatment with the pan-histone deacetylase inhibitor panobinostat and BC synergistically induced apoptosis of cultured and primary AML BPCs, including those expressing FLT3-ITD, as well as further significantly improved the survival of immune-depleted mice engrafted with primary AML BPCs.	Panobinostat	56-68	FMS-like tyrosine kinase 3	Mus musculus	171-175
25826077-2	2015	Here, we show that the PI3K inhibitor GDC-0941 or the Akt inhibitor MK-2206 induced apoptosis through the mitochondria-mediated intrinsic pathway more efficiently in hematopoietic 32D cells driven by FLT3-TKD (32D/TKD) than FLT3-ITD (32D/ITD), which robustly activated STAT5.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	38-46	FMS-like tyrosine kinase 3	Mus musculus	200-204
25826077-2	2015	Here, we show that the PI3K inhibitor GDC-0941 or the Akt inhibitor MK-2206 induced apoptosis through the mitochondria-mediated intrinsic pathway more efficiently in hematopoietic 32D cells driven by FLT3-TKD (32D/TKD) than FLT3-ITD (32D/ITD), which robustly activated STAT5.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	38-46	FMS-like tyrosine kinase 3	Mus musculus	224-228
25826077-2	2015	Here, we show that the PI3K inhibitor GDC-0941 or the Akt inhibitor MK-2206 induced apoptosis through the mitochondria-mediated intrinsic pathway more efficiently in hematopoietic 32D cells driven by FLT3-TKD (32D/TKD) than FLT3-ITD (32D/ITD), which robustly activated STAT5.	MK 2206	68-75	FMS-like tyrosine kinase 3	Mus musculus	200-204
25826077-2	2015	Here, we show that the PI3K inhibitor GDC-0941 or the Akt inhibitor MK-2206 induced apoptosis through the mitochondria-mediated intrinsic pathway more efficiently in hematopoietic 32D cells driven by FLT3-TKD (32D/TKD) than FLT3-ITD (32D/ITD), which robustly activated STAT5.	MK 2206	68-75	FMS-like tyrosine kinase 3	Mus musculus	224-228
25826077-3	2015	The resistance to GDC-0941 and MK-2206 was gained by expression of the constitutively activated STAT5 mutant STAT5A1*6 in 32D/TKD cells, while it was abrogated by the STAT5 inhibitor pimozide in 32D/ITD cells or FLT3-ITD-expressing human leukemic MV4-11 cells.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	18-26	FMS-like tyrosine kinase 3	Mus musculus	212-216
25826077-3	2015	The resistance to GDC-0941 and MK-2206 was gained by expression of the constitutively activated STAT5 mutant STAT5A1*6 in 32D/TKD cells, while it was abrogated by the STAT5 inhibitor pimozide in 32D/ITD cells or FLT3-ITD-expressing human leukemic MV4-11 cells.	MK 2206	31-38	FMS-like tyrosine kinase 3	Mus musculus	212-216
25826077-6	2015	Finally, it was confirmed in primary AML cells with FLT3-ITD that pimozide enhanced 4EBP1 dephosphorylation and Mcl-1 downregulation to augment cytotoxicity of GDC-0941.	Pimozide	66-74	FMS-like tyrosine kinase 3	Mus musculus	52-56
25697362-0	2015	NADPH oxidase-generated hydrogen peroxide induces DNA damage in mutant FLT3-expressing leukemia cells.	Hydrogen Peroxide	24-41	FMS-like tyrosine kinase 3	Mus musculus	71-75
25697362-2	2015	FLT3-ITD expressing cell lines have been shown to generate increased levels of reactive oxygen species (ROS) and DNA double strand breaks (DSBs).	Reactive Oxygen Species	79-102	FMS-like tyrosine kinase 3	Mus musculus	0-4
25697362-2	2015	FLT3-ITD expressing cell lines have been shown to generate increased levels of reactive oxygen species (ROS) and DNA double strand breaks (DSBs).	Reactive Oxygen Species	104-107	FMS-like tyrosine kinase 3	Mus musculus	0-4
25697362-2	2015	FLT3-ITD expressing cell lines have been shown to generate increased levels of reactive oxygen species (ROS) and DNA double strand breaks (DSBs).	dsbs	139-143	FMS-like tyrosine kinase 3	Mus musculus	0-4
25697362-3	2015	However, the molecular basis of how FLT3-ITD-driven ROS leads to the aggressive form of AML is not clearly understood.	Reactive Oxygen Species	52-55	FMS-like tyrosine kinase 3	Mus musculus	36-40
25697362-10	2015	Taken together these data indicate that NOX and p22(phox) mediate the ROS production from FLT3-ITD that signal to the nucleus causing genomic instability.	Reactive Oxygen Species	70-73	FMS-like tyrosine kinase 3	Mus musculus	90-94
24619500-5	2014	RESULTS: We identified several acquired point mutations in the tyrosine kinase domains (TKD) of the FLT3 gene in sorafenib-resistant murine leukemia cell line carrying human FLT3-ITD mutations, which were also detected in two of four sorafenib-resistant patient samples.	Sorafenib	234-243	FMS-like tyrosine kinase 3	Mus musculus	100-104
24416160-7	2014	The combination treatment of the HDAC inhibitor vorinostat (SAHA) with BPR1J-340 synergistically induced apoptosis via Mcl-1 down-regulation in MOLM-13 AML cells, indicating that the combination of selective FLT3 kinase inhibitors and HDAC inhibitors could exhibit clinical benefit in AML therapy.	Vorinostat	60-64	FMS-like tyrosine kinase 3	Mus musculus	208-212
24408321-8	2014	Survival and tumor burden of mice in several FLT3/ITD transplantation models is significantly improved by administration of TTT-3002 via oral dosing.	TTT-3002	124-132	FMS-like tyrosine kinase 3	Mus musculus	45-49
24772390-10	2014	Further in vivo studies employing injected and ingested 5-Bromodeoxyuridine (BrdU), showed that the G0 Lin-Sca-1, c-kit+ Flt3- cell was rapidly passing through cell cycle.	Bromodeoxyuridine	56-75	FMS-like tyrosine kinase 3	Mus musculus	121-125
24772390-10	2014	Further in vivo studies employing injected and ingested 5-Bromodeoxyuridine (BrdU), showed that the G0 Lin-Sca-1, c-kit+ Flt3- cell was rapidly passing through cell cycle.	Bromodeoxyuridine	77-81	FMS-like tyrosine kinase 3	Mus musculus	121-125
24416160-7	2014	The combination treatment of the HDAC inhibitor vorinostat (SAHA) with BPR1J-340 synergistically induced apoptosis via Mcl-1 down-regulation in MOLM-13 AML cells, indicating that the combination of selective FLT3 kinase inhibitors and HDAC inhibitors could exhibit clinical benefit in AML therapy.	Vorinostat	48-58	FMS-like tyrosine kinase 3	Mus musculus	208-212
24085765-6	2013	Taken together, these data support that liposomal bortezomib, as a single agent, eradicates Mll(PTD/wt):Flt3(ITD/wt) AML in mouse and may represent a powerful and potentially curative approach to high-risk human disease.	Bortezomib	50-60	FMS-like tyrosine kinase 3	Mus musculus	104-108
24046014-6	2013	Crenolanib was active against Ba/F3 cells harboring FLT3-ITD and secondary KD mutations and sorafenib-resistant MOLM-13 cells containing FLT3-ITD/D835Y both in vitro and in vivo.	crenolanib	0-10	FMS-like tyrosine kinase 3	Mus musculus	52-56
23275061-7	2013	In subsequent nonclinical characterization, LY2801653 was found to have potent activity against several other receptor tyrosine oncokinases including MST1R, FLT3, AXL, MERTK, TEK, ROS1, DDR1/2 and against the serine/threonine kinases MKNK1/2.	merestinib	44-53	FMS-like tyrosine kinase 3	Mus musculus	157-161