PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19754199-0	2009	Identification of N-(5-tert-butyl-isoxazol-3-yl)-N"-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo[2,1-b][1,3]benzothiazol-2-yl]phenyl}urea dihydrochloride (AC220), a uniquely potent, selective, and efficacious FMS-like tyrosine kinase-3 (FLT3) inhibitor.	quizartinib	149-154	fms related receptor tyrosine kinase 3	Homo sapiens	203-229
19754199-0	2009	Identification of N-(5-tert-butyl-isoxazol-3-yl)-N"-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo[2,1-b][1,3]benzothiazol-2-yl]phenyl}urea dihydrochloride (AC220), a uniquely potent, selective, and efficacious FMS-like tyrosine kinase-3 (FLT3) inhibitor.	quizartinib	149-154	fms related receptor tyrosine kinase 3	Homo sapiens	231-235
19654408-0	2009	AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML).	quizartinib	0-5	fms related receptor tyrosine kinase 3	Homo sapiens	54-58
33777220-8	2021	Combinations of AXL-targeted agents with AC220 exerted synergistic cytotoxic effects and induced apoptosis in MV4-11/AC220 cells and FLT3 inhibitor-resistant blast cells.	quizartinib	41-46	fms related receptor tyrosine kinase 3	Homo sapiens	133-137
34555701-6	2021	Here, we report on the preclinical activity of the combination of the FLT3 inhibitor quizartinib with the dual PI3K/mTOR inhibitor PF-04691502 in FLT3-ITD cells.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
33799721-5	2021	Using RNAseq data from AML cells with an internal tandem duplication FLT3 mutation (FLT3-ITD) under six drug treatment conditions including quizartinib and dexamethasone, we identified seven distinct gene programs representing diverse biological processes involved in AML drug-induced changes.	quizartinib	140-151	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
33799721-5	2021	Using RNAseq data from AML cells with an internal tandem duplication FLT3 mutation (FLT3-ITD) under six drug treatment conditions including quizartinib and dexamethasone, we identified seven distinct gene programs representing diverse biological processes involved in AML drug-induced changes.	quizartinib	140-151	fms related receptor tyrosine kinase 3	Homo sapiens	84-88
34665271-4	2022	Low nanomolar doses of the FLT3 inhibitor (FLT3i) AC220 and an inhibition of class I HDACs with nanomolar concentrations of FK228 or micromolar doses of the HDAC3 specific agent RGFP966 synergistically induce apoptosis of AML cells that carry hyperactive FLT3 with an internal tandem duplication (FLT3-ITD).	quizartinib	50-55	fms related receptor tyrosine kinase 3	Homo sapiens	27-31
34665271-4	2022	Low nanomolar doses of the FLT3 inhibitor (FLT3i) AC220 and an inhibition of class I HDACs with nanomolar concentrations of FK228 or micromolar doses of the HDAC3 specific agent RGFP966 synergistically induce apoptosis of AML cells that carry hyperactive FLT3 with an internal tandem duplication (FLT3-ITD).	quizartinib	50-55	fms related receptor tyrosine kinase 3	Homo sapiens	255-259
34665271-4	2022	Low nanomolar doses of the FLT3 inhibitor (FLT3i) AC220 and an inhibition of class I HDACs with nanomolar concentrations of FK228 or micromolar doses of the HDAC3 specific agent RGFP966 synergistically induce apoptosis of AML cells that carry hyperactive FLT3 with an internal tandem duplication (FLT3-ITD).	quizartinib	50-55	fms related receptor tyrosine kinase 3	Homo sapiens	297-301
34665271-10	2022	While HDACi induce p21, AC220 suppresses the expression of p53 and p21.	quizartinib	24-29	tumor protein p53	Homo sapiens	59-62
34665271-10	2022	While HDACi induce p21, AC220 suppresses the expression of p53 and p21.	quizartinib	24-29	cyclin dependent kinase inhibitor 1A	Homo sapiens	67-70
34597366-3	2021	Quizartinib is an oral Fms-like tyrosine kinase 3 (FLT3) inhibitor with reported activity in wild type patients.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	23-49
34597366-3	2021	Quizartinib is an oral Fms-like tyrosine kinase 3 (FLT3) inhibitor with reported activity in wild type patients.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	51-55
34597366-6	2021	Overall survival (OS) in these FLT3-ITD positive patients was also significantly improved at 2 years for quizartinib + LDAC; hazard ratio 0.36 (95% confidence intervals 0.16, 0.85), (p=0.04).	quizartinib	105-116	fms related receptor tyrosine kinase 3	Homo sapiens	31-35
34555701-6	2021	Here, we report on the preclinical activity of the combination of the FLT3 inhibitor quizartinib with the dual PI3K/mTOR inhibitor PF-04691502 in FLT3-ITD cells.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	146-150
34424108-4	2021	First-generation multi-kinase inhibitors (midostaurin, sorafenib, lestaurtinib) target multiple proteins, whereas second-generation inhibitors (crenolanib, quizartinib, gilteritinib) are more specific and potent inhibitors of FLT3, so they are associated with less off-target toxic effects.	quizartinib	156-167	fms related receptor tyrosine kinase 3	Homo sapiens	226-230
34835225-7	2021	Finally, we show that activated CD8+ T cells express FLT3 from day two post activation, and FLT3 inhibition with AC220 (quizartinib) or siRNA-mediated knockdown affects cell cycle kinetics.	quizartinib	113-118	CD8a molecule	Homo sapiens	32-35
34835225-7	2021	Finally, we show that activated CD8+ T cells express FLT3 from day two post activation, and FLT3 inhibition with AC220 (quizartinib) or siRNA-mediated knockdown affects cell cycle kinetics.	quizartinib	113-118	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
34835225-7	2021	Finally, we show that activated CD8+ T cells express FLT3 from day two post activation, and FLT3 inhibition with AC220 (quizartinib) or siRNA-mediated knockdown affects cell cycle kinetics.	quizartinib	120-131	CD8a molecule	Homo sapiens	32-35
34835225-7	2021	Finally, we show that activated CD8+ T cells express FLT3 from day two post activation, and FLT3 inhibition with AC220 (quizartinib) or siRNA-mediated knockdown affects cell cycle kinetics.	quizartinib	120-131	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
34583130-4	2021	Especially, compounds 17 and 19 inhibited the quizartinib resistance- conferring mutations, FLT3D835Y, both with IC50 values of 0.3 nM.	quizartinib	46-57	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
34268710-0	2021	A critical appraisal of Japan"s new drug approval process: a case study of FLT3-ITD inhibitor quizartinib.	quizartinib	94-105	fms related receptor tyrosine kinase 3	Homo sapiens	75-79
34400415-3	2021	RESULTS: We observed that Gilteritinib maintained a stronger pro-apoptotic effect in hypoxia and coculture with bone marrow stromal cells compared with Quizartinib, linked to a dose-dependent inhibition of AXL phosphorylation.	quizartinib	152-163	AXL receptor tyrosine kinase	Homo sapiens	206-209
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
34490088-0	2021	The Combined Treatment With the FLT3-Inhibitor AC220 and the Complex I Inhibitor IACS-010759 Synergistically Depletes Wt- and FLT3-Mutated Acute Myeloid Leukemia Cells.	quizartinib	47-52	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
34490088-0	2021	The Combined Treatment With the FLT3-Inhibitor AC220 and the Complex I Inhibitor IACS-010759 Synergistically Depletes Wt- and FLT3-Mutated Acute Myeloid Leukemia Cells.	quizartinib	47-52	fms related receptor tyrosine kinase 3	Homo sapiens	126-130
34490088-4	2021	A novel synergy between the oxidative phosphorylation inhibitor IACS-010759 and the FMS-like tyrosine kinase 3 (FLT3) inhibitor AC220 (quizartinib) was discovered in AML and then validated by ATP bioluminescence and apoptosis assays.	quizartinib	128-133	fms related receptor tyrosine kinase 3	Homo sapiens	84-110
34490088-4	2021	A novel synergy between the oxidative phosphorylation inhibitor IACS-010759 and the FMS-like tyrosine kinase 3 (FLT3) inhibitor AC220 (quizartinib) was discovered in AML and then validated by ATP bioluminescence and apoptosis assays.	quizartinib	128-133	fms related receptor tyrosine kinase 3	Homo sapiens	112-116
34490088-4	2021	A novel synergy between the oxidative phosphorylation inhibitor IACS-010759 and the FMS-like tyrosine kinase 3 (FLT3) inhibitor AC220 (quizartinib) was discovered in AML and then validated by ATP bioluminescence and apoptosis assays.	quizartinib	135-146	fms related receptor tyrosine kinase 3	Homo sapiens	84-110
34490088-4	2021	A novel synergy between the oxidative phosphorylation inhibitor IACS-010759 and the FMS-like tyrosine kinase 3 (FLT3) inhibitor AC220 (quizartinib) was discovered in AML and then validated by ATP bioluminescence and apoptosis assays.	quizartinib	135-146	fms related receptor tyrosine kinase 3	Homo sapiens	112-116
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
35532877-3	2022	First-generation inhibitors, including midostaurin and sorafenib, lack specificity for FLT3 and act on multiple kinases, whereas second-generation inhibitors, including gilteritinib, and quizartinib, are highly specific to FLT3 and are more potent than first-generation inhibitors.	quizartinib	187-198	fms related receptor tyrosine kinase 3	Homo sapiens	223-227
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
34298678-8	2021	Accordingly, the ABL inhibitor imatinib and the FLT3 inhibitor quizartinib sensitize leukemic cells to pro-apoptotic effects of hydroxyurea.	quizartinib	63-74	fms related receptor tyrosine kinase 3	Homo sapiens	48-52
34298678-9	2021	Moreover, hydroxyurea and navitoclax kill leukemic cells with mutant FLT3 that are resistant to quizartinib.	quizartinib	96-107	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
33945602-6	2021	Combination of histone deacetylase 1/2 inhibitor Romidepsin with FLT3 tyrosine kinase inhibitor AC220 or bromodomain inhibitor JQ1 exert synergistic anti-leukemic effects on FLT3-ITD+ and MLL-AF9+ AML, respectively, by dually activating GADD45g.	quizartinib	96-101	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
35259456-7	2022	In case of BCR-ABL-positive B-ALL cells we used a combination with the classic inhibitor Imatinib and in case of MLL-AF4-positive B-ALL cells we used a combination with Quizartinib (directed against FLT3).	quizartinib	169-180	AF4/FMR2 family member 1	Homo sapiens	117-120
35259456-7	2022	In case of BCR-ABL-positive B-ALL cells we used a combination with the classic inhibitor Imatinib and in case of MLL-AF4-positive B-ALL cells we used a combination with Quizartinib (directed against FLT3).	quizartinib	169-180	fms related receptor tyrosine kinase 3	Homo sapiens	199-203
35453402-6	2022	Transient knockdown or inhibitor-based suppression of HO-1 enhances vulnerability to the TKI, quizartinib, in both TKI-resistant and sensitive primary AML and cell line models.	quizartinib	94-105	heme oxygenase 1	Homo sapiens	54-58
35140970-2	2022	We report the first case of successful bridge therapy of novel FLT3 inhibitor, quizartinib, to umbilical cord blood stem cell transplantation for FLT3-ITD-positive AML-primary induction failure patients with central nervous system involvement.	quizartinib	79-90	fms related receptor tyrosine kinase 3	Homo sapiens	63-67
33831397-0	2021	Homoharringtonine synergizes with quizartinib in FLT3-ITD acute myeloid leukemia by targeting FLT3-AKT-c-Myc pathway.	quizartinib	34-45	fms related receptor tyrosine kinase 3	Homo sapiens	49-53
33831397-0	2021	Homoharringtonine synergizes with quizartinib in FLT3-ITD acute myeloid leukemia by targeting FLT3-AKT-c-Myc pathway.	quizartinib	34-45	AKT serine/threonine kinase 1	Homo sapiens	99-102
33831397-0	2021	Homoharringtonine synergizes with quizartinib in FLT3-ITD acute myeloid leukemia by targeting FLT3-AKT-c-Myc pathway.	quizartinib	34-45	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	103-108
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
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	AKT serine/threonine kinase 1	Homo sapiens	64-67
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	glycogen synthase kinase 3 alpha	Homo sapiens	95-103
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	105-110
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	cyclin D1	Homo sapiens	116-125
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	BCL2 like 11	Homo sapiens	180-183
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	BCL2 associated X, apoptosis regulator	Homo sapiens	188-191
33831397-6	2021	Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1.	quizartinib	25-36	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	238-242
35114569-4	2022	Overexpression of BCL2A1 attenuated the sensitivity to quizartinib, a type II TKI, and venetoclax, a selective BCL2 inhibitor, in AML cell lines.	quizartinib	55-66	B cell leukemia/lymphoma 2 related protein A1a	Mus musculus	18-24
35033885-4	2022	Guided by ligand-based design and structure simplification of the FLT3 inhibitor, quizartinib, we developed a benzimidazole-based small molecule, 4ACP, that exhibited nanomolar activity against wild-type FLT3, FLT3-Internal tandem duplications (FLT3-ITD), and FLT3-D835Y (FLT3-TKD) mutation (IC50 = 43.8, 97.2, and 92.5 nM respectively).	quizartinib	82-93	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
35033885-4	2022	Guided by ligand-based design and structure simplification of the FLT3 inhibitor, quizartinib, we developed a benzimidazole-based small molecule, 4ACP, that exhibited nanomolar activity against wild-type FLT3, FLT3-Internal tandem duplications (FLT3-ITD), and FLT3-D835Y (FLT3-TKD) mutation (IC50 = 43.8, 97.2, and 92.5 nM respectively).	quizartinib	82-93	fms related receptor tyrosine kinase 3	Homo sapiens	204-208
33945602-6	2021	Combination of histone deacetylase 1/2 inhibitor Romidepsin with FLT3 tyrosine kinase inhibitor AC220 or bromodomain inhibitor JQ1 exert synergistic anti-leukemic effects on FLT3-ITD+ and MLL-AF9+ AML, respectively, by dually activating GADD45g.	quizartinib	96-101	fms related receptor tyrosine kinase 3	Homo sapiens	174-178
33945602-6	2021	Combination of histone deacetylase 1/2 inhibitor Romidepsin with FLT3 tyrosine kinase inhibitor AC220 or bromodomain inhibitor JQ1 exert synergistic anti-leukemic effects on FLT3-ITD+ and MLL-AF9+ AML, respectively, by dually activating GADD45g.	quizartinib	96-101	lysine methyltransferase 2A	Homo sapiens	188-191
33945602-6	2021	Combination of histone deacetylase 1/2 inhibitor Romidepsin with FLT3 tyrosine kinase inhibitor AC220 or bromodomain inhibitor JQ1 exert synergistic anti-leukemic effects on FLT3-ITD+ and MLL-AF9+ AML, respectively, by dually activating GADD45g.	quizartinib	96-101	MLLT3 super elongation complex subunit	Homo sapiens	192-195
33945602-6	2021	Combination of histone deacetylase 1/2 inhibitor Romidepsin with FLT3 tyrosine kinase inhibitor AC220 or bromodomain inhibitor JQ1 exert synergistic anti-leukemic effects on FLT3-ITD+ and MLL-AF9+ AML, respectively, by dually activating GADD45g.	quizartinib	96-101	growth arrest and DNA damage inducible gamma	Homo sapiens	237-244
33853292-2	2021	We hypothesized that quizartinib, a selective and potent FLT3 inhibitor, with azacitidine (AZA) or low-dose cytarabine (LDAC) might improve the outcomes in patients with FLT3-ITD-mutated AML.	quizartinib	21-32	fms related receptor tyrosine kinase 3	Homo sapiens	57-61
33853292-2	2021	We hypothesized that quizartinib, a selective and potent FLT3 inhibitor, with azacitidine (AZA) or low-dose cytarabine (LDAC) might improve the outcomes in patients with FLT3-ITD-mutated AML.	quizartinib	21-32	fms related receptor tyrosine kinase 3	Homo sapiens	170-174
33853292-5	2021	Among previously untreated patients, composite response (CRc) was achieved in 13/15 (87%, 8 CR, 4 Cri, 1 CRp) treated with quizartinib/AZA and 14/19 (74%, 1 CR, 8 CRi, 5 CRp) in quizartinib/LDAC.	quizartinib	123-134	C-reactive protein	Homo sapiens	57-59
33853292-10	2021	Quizartinib-based combinations, particularly with AZA, appear effective in both frontline and first-salvage for patients with FLT3-ITD-mutated AML and are well tolerated.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	126-130
32414851-5	2021	In vivo, venetoclax combined with quizartinib, a potent FLT3 inhibitor, showed greater anti-tumor efficacy and prolonged survival compared to monotherapies.	quizartinib	34-45	fms related receptor tyrosine kinase 3	Homo sapiens	56-60
33832508-6	2021	The gatekeeper mutation F691L confers resistance to specific FLT3 inhibitors such as quizartinib, but pexidartinib is much less resistance to this mutation.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	61-65
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-45
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-52
33415416-10	2021	Because concomitant strong cytochrome P450 3A (CYP3A) inhibitor use significantly increases quizartinib concentration, these results support the clinical recommendation of quizartinib dose reduction in patients concurrently receiving a strong CYP3A inhibitor.	quizartinib	172-183	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-52
32414851-6	2021	In a patient-derived FLT3-ITD+ xenograft model, cotreatment with venetoclax and quizartinib at clinically relevant doses had greater anti-tumor activity in the tumor microenvironment compared to quizartinib or venetoclax alone.	quizartinib	80-91	fms related receptor tyrosine kinase 3	Homo sapiens	21-25
33781547-0	2021	Quizartinib for Relapsed/Refractory FLT3-Mutated Acute Myeloid Leukemia: More Patients Make It to Transplant, but Are There Any Other Benefits?	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	36-40
33017662-0	2021	Clinical Outcomes in Patients With FLT3-ITD-Mutated Relapsed/Refractory Acute Myeloid Leukemia Undergoing Hematopoietic Stem Cell Transplant After Quizartinib or Salvage Chemotherapy in the QuANTUM-R Trial.	quizartinib	147-158	fms related receptor tyrosine kinase 3	Homo sapiens	35-39
33017662-13	2021	Additionally, post-HSCT quizartinib was found to be tolerable and may be associated with prolonged survival in some patients, highlighting its potential value in the management of patients with FLT3-ITD R/R AML.	quizartinib	24-35	fms related receptor tyrosine kinase 3	Homo sapiens	194-198
32513964-0	2021	Notch blockade overcomes endothelial cell-mediated resistance of FLT3/ITD-positive AML progenitors to AC220 treatment.	quizartinib	102-107	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
33242449-7	2021	Midostaurin and quizartinib are tyrosine kinase inhibitors (TKIs) with inhibitory efficacy against FLT3-ITD, but exhibit limited clinical impact.	quizartinib	16-27	fms related receptor tyrosine kinase 3	Homo sapiens	99-103
33189657-0	2021	Corrigendum to "AC220 and AraC cause differential inhibitory dynamics in patient-derived M5-AML with FLT3-ITD and, thus, ultimately distinct therapeutic outcomes" [Experimental Hematology 2017;45:36-44].	quizartinib	16-21	fms related receptor tyrosine kinase 3	Homo sapiens	101-105
33375770-5	2022	Importantly, MAPK and/or MTOR complex1 (MTORC1) activity were upregulated in AML cells made resistant to several FLT3 inhibitors, including crenolanib, quizartinib, or sorafenib.	quizartinib	152-163	origin recognition complex subunit 1	Homo sapiens	40-46
32772726-6	2020	This article reviews the mechanism of action, pharmacology, clinical efficacy, and safety of quizartinib, a FLT3 inhibitor, for the treatment of acute myeloid leukemia.	quizartinib	93-104	fms related receptor tyrosine kinase 3	Homo sapiens	108-112
32772726-8	2020	Quizartinib yielded an improvement in OS and complete remission (CR) rates in a phase 3 trial for relapsed/refractory FLT3-mutated AML.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	118-122
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	quizartinib	185-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
32598495-1	2020	Quizartinib is an FMS-like tyrosine kinase 3 (FLT3) inhibitor that has shown robust clinical activity in patients with FLT3-internal tandem duplication-mutated relapsed/refractory acute myeloid leukemia (AML).	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	18-44
32598495-1	2020	Quizartinib is an FMS-like tyrosine kinase 3 (FLT3) inhibitor that has shown robust clinical activity in patients with FLT3-internal tandem duplication-mutated relapsed/refractory acute myeloid leukemia (AML).	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	46-50
32598495-1	2020	Quizartinib is an FMS-like tyrosine kinase 3 (FLT3) inhibitor that has shown robust clinical activity in patients with FLT3-internal tandem duplication-mutated relapsed/refractory acute myeloid leukemia (AML).	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	119-123
32598495-4	2020	Strong CYP3A inhibitor use resulted in an 82% increase in the area under the curve (AUC) and a 72% increase in the maximum concentration (Cmax ) of quizartinib.	quizartinib	148-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	7-12
32598495-10	2020	Only concomitant use of strong CYP3A inhibitors had a clinically meaningful effect on quizartinib and AC886 PK exposure.	quizartinib	86-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-36
32409689-0	2020	Dasatinib overcomes stroma-based resistance to the FLT3 inhibitor quizartinib using multiple mechanisms.	quizartinib	66-77	fms related receptor tyrosine kinase 3	Homo sapiens	51-55
32409689-4	2020	We demonstrate that human bone marrow derived conditioned medium (CM) protects FLT3-ITD+ AML cells from the 2nd generation FLT3 TKI quizartinib and activates STAT3 and STAT5 in leukemia cells.	quizartinib	132-143	fms related receptor tyrosine kinase 3	Homo sapiens	123-127
32409689-6	2020	Combination treatment with quizartinib and dasatinib abolishes STAT5 activation and significantly reduces the IC50 of quizartinib in FLT3-ITD+ AML cells cultured in CM.	quizartinib	27-38	signal transducer and activator of transcription 5A	Homo sapiens	63-68
32409689-6	2020	Combination treatment with quizartinib and dasatinib abolishes STAT5 activation and significantly reduces the IC50 of quizartinib in FLT3-ITD+ AML cells cultured in CM.	quizartinib	27-38	fms related receptor tyrosine kinase 3	Homo sapiens	133-137
32409689-6	2020	Combination treatment with quizartinib and dasatinib abolishes STAT5 activation and significantly reduces the IC50 of quizartinib in FLT3-ITD+ AML cells cultured in CM.	quizartinib	118-129	fms related receptor tyrosine kinase 3	Homo sapiens	133-137
32409689-7	2020	We demonstrate that CM protects FLT3-ITD+ AML cells from the inhibitory effects of quizartinib on glycolysis and that this is partially reversed by treating cells with the combination of quizartinib and dasatinib.	quizartinib	83-94	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
32409689-7	2020	We demonstrate that CM protects FLT3-ITD+ AML cells from the inhibitory effects of quizartinib on glycolysis and that this is partially reversed by treating cells with the combination of quizartinib and dasatinib.	quizartinib	187-198	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
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
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	Janus kinase 3	Mus musculus	102-106
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	signal transducer and activator of transcription 3	Mus musculus	107-112
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	quizartinib	185-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
32748108-15	2020	CONCLUSION: Simultaneous administration of quizartinib and CYT every other day is a promising combination regimen for AML patients with FLT3 mutations.	quizartinib	43-54	fms related receptor tyrosine kinase 3	Homo sapiens	136-140
32629802-7	2020	Disruption of the CXCL12/CXCR4 axis in FLT3-ITD-AML by LY2510924 and its negligible effects on normal immunocytes could safely enhance the potency of quizartinib, which may be further improved by blockade of TGF-b signaling.	quizartinib	150-161	chemokine (C-X-C motif) ligand 12	Mus musculus	18-24
32396937-5	2020	Using RNA-sequencing and drug-screening, here we report that treatment of FLT3-ITD AML cells with quizartinib, a selective FLT3 inhibitor, up-regulates inflammatory genes in DTPs and thereby confers susceptibility to anti-inflammatory glucocorticoids.	quizartinib	98-109	fms related receptor tyrosine kinase 3	Homo sapiens	74-78
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
32629802-5	2020	Sequencing of the transcriptome of the leukemic cells surviving in vivo treatment with quizartinib and LY2510924 revealed that genes related to TGF-b signaling may confer resistance against the drug combination.	quizartinib	87-98	transforming growth factor, beta 1	Mus musculus	144-149
32722211-1	2020	Two recent phase 3 trials showed that outcomes for relapsed/refractory (R/R) FLT3-mutated acute myeloid leukemia (AML) patients may be improved by a single-agent tyrosine kinase inhibitor (TKI) (i.e., quizartinib or gilteritinib).	quizartinib	201-212	fms related receptor tyrosine kinase 3	Homo sapiens	77-81
32722298-2	2020	FLT3 inhibitors such as midostaurin, gilteritinib and quizartinib show excellent response rates in patients with FLT3-mutated AML, but its duration of response may not be sufficient yet.	quizartinib	54-65	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
32722298-2	2020	FLT3 inhibitors such as midostaurin, gilteritinib and quizartinib show excellent response rates in patients with FLT3-mutated AML, but its duration of response may not be sufficient yet.	quizartinib	54-65	fms related receptor tyrosine kinase 3	Homo sapiens	113-117
32722298-4	2020	On-target mutations (i.e., FLT3-TKD) such as D835Y keep the TK domain in its active form, abrogating pharmacodynamics of type II FLT3 inhibitors (e.g., midostaurin and quizartinib).	quizartinib	168-179	fms related receptor tyrosine kinase 3	Homo sapiens	27-31
32722298-4	2020	On-target mutations (i.e., FLT3-TKD) such as D835Y keep the TK domain in its active form, abrogating pharmacodynamics of type II FLT3 inhibitors (e.g., midostaurin and quizartinib).	quizartinib	168-179	fms related receptor tyrosine kinase 3	Homo sapiens	129-133
32629802-7	2020	Disruption of the CXCL12/CXCR4 axis in FLT3-ITD-AML by LY2510924 and its negligible effects on normal immunocytes could safely enhance the potency of quizartinib, which may be further improved by blockade of TGF-b signaling.	quizartinib	150-161	chemokine (C-X-C motif) receptor 4	Mus musculus	25-30
32629802-7	2020	Disruption of the CXCL12/CXCR4 axis in FLT3-ITD-AML by LY2510924 and its negligible effects on normal immunocytes could safely enhance the potency of quizartinib, which may be further improved by blockade of TGF-b signaling.	quizartinib	150-161	transforming growth factor, beta 1	Mus musculus	208-213
32199135-9	2020	Models indicate corresponding interactions of 16 and quizartinib with FLT3.	quizartinib	53-64	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
31912423-1	2020	Quizartinib is a tyrosine kinase inhibitor selectively targeting the FMS-like tyrosine kinase 3 (FLT3) receptor that has been developed for the treatment of acute myeloid leukaemia (AML).	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	69-95
32109580-13	2020	Quizartinib is a Flt3 multikinase inhibitor that was approved by the Ministry of Health, Labor and Welfare (MHLW) of Japan for the treatment of adult patients with relapsed/refractory Flt3-positive acute myelogenous leukemias.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	17-21
32109580-13	2020	Quizartinib is a Flt3 multikinase inhibitor that was approved by the Ministry of Health, Labor and Welfare (MHLW) of Japan for the treatment of adult patients with relapsed/refractory Flt3-positive acute myelogenous leukemias.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	184-188
32109580-14	2020	Gilteritinib and quizartinib bind to Flt3 with the inactive DFG-Dout structure and are classified as type II inhibitors.	quizartinib	17-28	fms related receptor tyrosine kinase 3	Homo sapiens	37-41
32134197-8	2020	In FLT3/ITD AML patients treated with FLT3 inhibitor quizartinib, serum FST levels correlated with clinical response.	quizartinib	53-64	fms related receptor tyrosine kinase 3	Homo sapiens	3-7
32134197-8	2020	In FLT3/ITD AML patients treated with FLT3 inhibitor quizartinib, serum FST levels correlated with clinical response.	quizartinib	53-64	fms related receptor tyrosine kinase 3	Homo sapiens	38-42
32215183-0	2020	Quizartinib, a selective FLT3 inhibitor, maintains antileukemic activity in preclinical models of RAS-mediated midostaurin-resistant acute myeloid leukemia cells.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	25-29
32215183-2	2020	In this preclinical study, we characterized the binding affinity and selectivity of quizartinib, a small-molecule inhibitor of FLT3, and AC886, the active metabolite of quizartinib, compared with those of other FLT3 inhibitors.	quizartinib	84-95	fms related receptor tyrosine kinase 3	Homo sapiens	127-131
32215183-3	2020	Selectivity profiling against >400 kinases showed that quizartinib and AC886 were highly selective against FLT3.	quizartinib	55-66	fms related receptor tyrosine kinase 3	Homo sapiens	107-111
32215183-4	2020	Quizartinib and AC886 inhibited FLT3 signaling pathways in FLT3-ITD-mutated AML cells, leading to potent growth inhibition with IC50 values of <1 nM.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
32215183-4	2020	Quizartinib and AC886 inhibited FLT3 signaling pathways in FLT3-ITD-mutated AML cells, leading to potent growth inhibition with IC50 values of <1 nM.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
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
32215183-8	2020	Preclinical antileukemic activity in midostaurin-resistant FLT3-ITD-mutated AML cells suggests the potential value of quizartinib following midostaurin failure in patients with FLT3-ITD mutated AML.	quizartinib	118-129	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
32215183-8	2020	Preclinical antileukemic activity in midostaurin-resistant FLT3-ITD-mutated AML cells suggests the potential value of quizartinib following midostaurin failure in patients with FLT3-ITD mutated AML.	quizartinib	118-129	fms related receptor tyrosine kinase 3	Homo sapiens	177-181
31912423-1	2020	Quizartinib is a tyrosine kinase inhibitor selectively targeting the FMS-like tyrosine kinase 3 (FLT3) receptor that has been developed for the treatment of acute myeloid leukaemia (AML).	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	97-101
31912423-2	2020	The Phase 3 QuANTUM-R study investigated the efficacy of quizartinib monotherapy in patients with relapsed/refractory FLT3-ITD mutation-positive AML.	quizartinib	57-68	fms related receptor tyrosine kinase 3	Homo sapiens	118-122
32021432-8	2020	This review focuses on quizartinib, a potent second-generation FLT3 inhibitor.	quizartinib	23-34	fms related receptor tyrosine kinase 3	Homo sapiens	63-67
31919472-4	2020	FLT3 inhibitors are divided into first generation multi-kinase inhibitors (such as sorafenib, lestaurtinib, midostaurin) and next generation inhibitors (such as quizartinib, crenolanib, gilteritinib) based on their potency and specificity of FLT3 inhibition.	quizartinib	161-172	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
32021432-0	2020	Profile of Quizartinib for the Treatment of Adult Patients with Relapsed/Refractory FLT3-ITD-Positive Acute Myeloid Leukemia: Evidence to Date.	quizartinib	11-22	fms related receptor tyrosine kinase 3	Homo sapiens	84-88
31385001-1	2019	PURPOSE: Quizartinib, a potent, selective FMS-like tyrosine kinase 3 (FLT3) inhibitor, is currently in phase 3 development for patients with FLT3-internal tandem duplication-mutated acute myeloid leukemia (AML).	quizartinib	9-20	fms related receptor tyrosine kinase 3	Homo sapiens	42-68
30931863-4	2020	METHODS: The crystallographic structures of two inhibitors complexed within Flt3, namely, quizartinib and F6M, were used to guide the synthesis of new sulfonamide-based Flt3 inhibitors.	quizartinib	90-101	fms related receptor tyrosine kinase 3	Homo sapiens	76-80
30931863-4	2020	METHODS: The crystallographic structures of two inhibitors complexed within Flt3, namely, quizartinib and F6M, were used to guide the synthesis of new sulfonamide-based Flt3 inhibitors.	quizartinib	90-101	fms related receptor tyrosine kinase 3	Homo sapiens	169-173
31778791-1	2020	Treatment of pediatric acute leukemia might involve combined therapies targeting the FMS-like tyrosine kinase 3 (FLT3) receptor (i.e. quizartinib - AC220) and nucleotide metabolism (cytarabine - AraC).	quizartinib	134-145	fms related receptor tyrosine kinase 3	Homo sapiens	85-111
31778791-1	2020	Treatment of pediatric acute leukemia might involve combined therapies targeting the FMS-like tyrosine kinase 3 (FLT3) receptor (i.e. quizartinib - AC220) and nucleotide metabolism (cytarabine - AraC).	quizartinib	134-145	fms related receptor tyrosine kinase 3	Homo sapiens	113-117
32378580-4	2020	In addition, second-generation FLT3 inhibitors, gilteritinib and quizartinib, were developed in Japan, and the treatment outcome of AML has been improved.	quizartinib	65-76	fms related receptor tyrosine kinase 3	Homo sapiens	31-35
31559849-0	2019	Quizartinib in the treatment of FLT3-internal-tandem duplication-positive acute myeloid leukemia.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
31559849-4	2019	This review focuses on quizartinib, a second-generation FLT3 inhibitor that has demonstrated efficacy and safety as a single agent and in combination with chemotherapy.	quizartinib	23-34	fms related receptor tyrosine kinase 3	Homo sapiens	56-60
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
30590794-9	2019	The protective effect of AC220 was associated with its suppression of CD103+ DCs-mediated CD8 T cell proliferation and activation in AN mice.	quizartinib	25-30	integrin alpha E, epithelial-associated	Mus musculus	70-75
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
31692922-3	2019	FLT3 ligand (FL) represents a mechanism of resistance to FLT3 inhibitors, including quizartinib, midostaurin, and sorafenib, in AML cells harboring both wild-type and mutant FLT3 (FLT3 wt/FLT3 mut).	quizartinib	84-95	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	0-11
31692922-3	2019	FLT3 ligand (FL) represents a mechanism of resistance to FLT3 inhibitors, including quizartinib, midostaurin, and sorafenib, in AML cells harboring both wild-type and mutant FLT3 (FLT3 wt/FLT3 mut).	quizartinib	84-95	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	0-2
31692922-3	2019	FLT3 ligand (FL) represents a mechanism of resistance to FLT3 inhibitors, including quizartinib, midostaurin, and sorafenib, in AML cells harboring both wild-type and mutant FLT3 (FLT3 wt/FLT3 mut).	quizartinib	84-95	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
33162511-4	2020	In addition, the second-generation FLT3 inhibitors, gilteritinib and quizartinib, were developed in Japan, which significantly improved the treatment outcome of AML.	quizartinib	69-80	fms related receptor tyrosine kinase 3	Homo sapiens	35-39
31359361-2	2019	The present phase 1, multicenter, open-label, dose-escalation and dose-expansion study was conducted to assess the safety, pharmacokinetics, and efficacy of multiple-dose monotherapy of the FLT3 inhibitor, quizartinib, in Japanese patients with R/R AML.	quizartinib	206-217	fms related receptor tyrosine kinase 3	Homo sapiens	190-194
31473943-0	2019	Efficacy and safety of quizartinib in Japanese patients with FLT3-ITD positive relapsed or refractory acute myeloid leukemia in an open-label, phase 2 study.	quizartinib	23-34	fms related receptor tyrosine kinase 3	Homo sapiens	61-65
31473943-10	2019	Quizartinib monotherapy was well tolerated and resulted in clinically meaningful reductions in blast count in Japanese patients with FLT3-ITD R/R AML.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	133-137
31385001-1	2019	PURPOSE: Quizartinib, a potent, selective FMS-like tyrosine kinase 3 (FLT3) inhibitor, is currently in phase 3 development for patients with FLT3-internal tandem duplication-mutated acute myeloid leukemia (AML).	quizartinib	9-20	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
31385001-1	2019	PURPOSE: Quizartinib, a potent, selective FMS-like tyrosine kinase 3 (FLT3) inhibitor, is currently in phase 3 development for patients with FLT3-internal tandem duplication-mutated acute myeloid leukemia (AML).	quizartinib	9-20	fms related receptor tyrosine kinase 3	Homo sapiens	141-145
30923103-0	2019	Hematopoietic niche drives FLT3-ITD acute myeloid leukemia resistance to quizartinib via STAT5-and hypoxia-dependent upregulation of AXL.	quizartinib	73-84	signal transducer and activator of transcription 5A	Mus musculus	89-94
30923103-0	2019	Hematopoietic niche drives FLT3-ITD acute myeloid leukemia resistance to quizartinib via STAT5-and hypoxia-dependent upregulation of AXL.	quizartinib	73-84	AXL receptor tyrosine kinase	Mus musculus	133-136
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
30923103-4	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	AXL receptor tyrosine kinase	Mus musculus	237-240
30923103-5	2019	Indeed, cytokines sustained phosphorylation of the transcription factor STAT5 in quizartinib-treated cells, which enhanced AXL expression by direct binding of a conserved motif in its genomic sequence.	quizartinib	81-92	signal transducer and activator of transcription 5A	Mus musculus	72-77
30923103-5	2019	Indeed, cytokines sustained phosphorylation of the transcription factor STAT5 in quizartinib-treated cells, which enhanced AXL expression by direct binding of a conserved motif in its genomic sequence.	quizartinib	81-92	AXL receptor tyrosine kinase	Mus musculus	123-126
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	AXL receptor tyrosine kinase	Mus musculus	51-54
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
30923103-8	2019	These data highlight a new bypass mechanism specific to the hematopoietic niche that hampers the response to quizartinib through combined upregulation of AXL activity.	quizartinib	109-120	AXL receptor tyrosine kinase	Mus musculus	154-157
31528345-3	2019	Multiple FLT3 inhibitors are in clinical development, including lestaurtinib, tandutinib, quizartinib, midostaurin, gilteritinib, and crenolanib.	quizartinib	90-101	fms related receptor tyrosine kinase 3	Homo sapiens	9-13
31286998-8	2019	FLT3ITD/NFATC1-AML is re-transplantable in secondary recipients and shows primary resistance to the FLT3ITD-kinase inhibitor quizartinib.	quizartinib	125-136	nuclear factor of activated T cells 1	Homo sapiens	8-14
30997851-0	2019	FLT3 inhibitor quizartinib (AC220).	quizartinib	15-26	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
30997851-0	2019	FLT3 inhibitor quizartinib (AC220).	quizartinib	28-33	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
30997851-5	2019	Quizartinib is the first drug developed specifically as a FLT3 inhibitor.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	58-62
31173645-0	2019	Effects of CYP3A inhibitors on the pharmacokinetics of quizartinib, a potent and selective FLT3 inhibitor, and its active metabolite.	quizartinib	55-66	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	11-16
31173645-0	2019	Effects of CYP3A inhibitors on the pharmacokinetics of quizartinib, a potent and selective FLT3 inhibitor, and its active metabolite.	quizartinib	55-66	fms related receptor tyrosine kinase 3	Homo sapiens	91-95
31173645-1	2019	AIMS: Quizartinib is an oral, highly potent and selective next-generation FMS-like tyrosine kinase 3 (FLT3) inhibitor under investigation in patients with FLT3-internal tandem duplication-mutated acute myeloid leukaemia.	quizartinib	6-17	fms related receptor tyrosine kinase 3	Homo sapiens	74-100
31173645-1	2019	AIMS: Quizartinib is an oral, highly potent and selective next-generation FMS-like tyrosine kinase 3 (FLT3) inhibitor under investigation in patients with FLT3-internal tandem duplication-mutated acute myeloid leukaemia.	quizartinib	6-17	fms related receptor tyrosine kinase 3	Homo sapiens	102-106
31173645-1	2019	AIMS: Quizartinib is an oral, highly potent and selective next-generation FMS-like tyrosine kinase 3 (FLT3) inhibitor under investigation in patients with FLT3-internal tandem duplication-mutated acute myeloid leukaemia.	quizartinib	6-17	fms related receptor tyrosine kinase 3	Homo sapiens	155-159
31173645-11	2019	CONCLUSIONS: These results suggest reducing the dose of quizartinib when coadministered with a strong CYP3A inhibitor, but not with a moderate or weak CYP3A inhibitor.	quizartinib	56-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	102-107
31243041-2	2019	Recently reported, positive randomized trials of the drugs gilteritinib, quizartinib, and sorafenib predict even wider use of FLT3 inhibitors going forward.	quizartinib	73-84	fms related receptor tyrosine kinase 3	Homo sapiens	126-130
31286998-11	2019	CONCLUSIONS: NFATC1 expression causes FLT3ITD-induced transcriptome changes, which are associated with HSC transformation, quizartinib resistance, and a poor prognosis in AML.	quizartinib	123-134	nuclear factor of activated T cells 1	Homo sapiens	13-19
30939008-3	2019	It also showed excellent inhibitory activities in FLT3-ITD-D835V and FLT3-ITD-F691L cells which were resistant to quizartinib.	quizartinib	114-125	fms related receptor tyrosine kinase 3	Homo sapiens	50-54
31175001-2	2019	We aimed to assess whether single-agent quizartinib, an oral, highly potent and selective type II FLT3 inhibitor, improves overall survival versus salvage chemotherapy.	quizartinib	40-51	fms related receptor tyrosine kinase 3	Homo sapiens	98-102
31203997-5	2019	However, emerging data on new highly potent and specific FLT3 inhibitors such as quizartinib, gilteritinib, and crenolanib suggest that these agents may soon supplant midostaurin and sorafenib in the upfront setting.	quizartinib	81-92	fms related receptor tyrosine kinase 3	Homo sapiens	57-61
30939008-3	2019	It also showed excellent inhibitory activities in FLT3-ITD-D835V and FLT3-ITD-F691L cells which were resistant to quizartinib.	quizartinib	114-125	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
31114157-1	2019	Quizartinib is an effective therapy for patients with FLT3-ITD acute myeloid leukemia (AML) by continuing to inhibit the activity of FLT3 gene, leading to apoptosis of tumor cells.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	54-58
31114157-5	2019	Quizartinib presents its advantages as a very promising agent in the treatment of AML, especially in patients with FLT3-ITD mutations.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
31114157-6	2019	FLT3/ITD mutation can lead to constitutive autophosphorylation of FLT3 and activation of its downstream effectors including RAS/RAF/MEK, MAPK/ERK, PI3K/AKT/mTOR and JAK/STAT5 signal pathways, while Quizartinib can inhibit these downstream pathways through specific FLT3 inhibition.	quizartinib	198-209	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
31114157-6	2019	FLT3/ITD mutation can lead to constitutive autophosphorylation of FLT3 and activation of its downstream effectors including RAS/RAF/MEK, MAPK/ERK, PI3K/AKT/mTOR and JAK/STAT5 signal pathways, while Quizartinib can inhibit these downstream pathways through specific FLT3 inhibition.	quizartinib	198-209	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
31114157-6	2019	FLT3/ITD mutation can lead to constitutive autophosphorylation of FLT3 and activation of its downstream effectors including RAS/RAF/MEK, MAPK/ERK, PI3K/AKT/mTOR and JAK/STAT5 signal pathways, while Quizartinib can inhibit these downstream pathways through specific FLT3 inhibition.	quizartinib	198-209	signal transducer and activator of transcription 5A	Homo sapiens	169-174
31114157-6	2019	FLT3/ITD mutation can lead to constitutive autophosphorylation of FLT3 and activation of its downstream effectors including RAS/RAF/MEK, MAPK/ERK, PI3K/AKT/mTOR and JAK/STAT5 signal pathways, while Quizartinib can inhibit these downstream pathways through specific FLT3 inhibition.	quizartinib	198-209	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
30553232-2	2019	FLT3 activation can be blocked by inhibition of its phosphorylation using the nontoxic and selective inhibitor, quizartinib.	quizartinib	112-123	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
30898762-6	2019	We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML).	quizartinib	121-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
30898762-6	2019	We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML).	quizartinib	121-132	fms related receptor tyrosine kinase 3	Homo sapiens	99-103
30898762-6	2019	We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML).	quizartinib	121-132	fms related receptor tyrosine kinase 3	Homo sapiens	160-164
30681373-4	2019	The failure of these agents to induce durable responses led to the development of second generation FLT3 tyrosine kinase inhibitors (quizartinib, crenolinib, gilteritinib) exhibiting high potency and specificity for mutant FLT3 kinases and sustained in vivo FLT3 inhibition.	quizartinib	133-144	fms related receptor tyrosine kinase 3	Homo sapiens	223-227
30681373-4	2019	The failure of these agents to induce durable responses led to the development of second generation FLT3 tyrosine kinase inhibitors (quizartinib, crenolinib, gilteritinib) exhibiting high potency and specificity for mutant FLT3 kinases and sustained in vivo FLT3 inhibition.	quizartinib	133-144	fms related receptor tyrosine kinase 3	Homo sapiens	223-227
30681373-4	2019	The failure of these agents to induce durable responses led to the development of second generation FLT3 tyrosine kinase inhibitors (quizartinib, crenolinib, gilteritinib) exhibiting high potency and specificity for mutant FLT3 kinases and sustained in vivo FLT3 inhibition.	quizartinib	133-144	fms related receptor tyrosine kinase 3	Homo sapiens	100-104
30553232-6	2019	While the level of FLT3 was unaffected, the levels of phospho-FLT3 were significantly altered in spermatozoa by quizartinib.	quizartinib	112-123	fms related receptor tyrosine kinase 3	Homo sapiens	62-66
30553232-10	2019	The inhibition of FLT3 by quizartinib may affect the fertilization and embryonic development by reducing tyrosine phosphorylation through a PKA-dependent pathway.	quizartinib	26-37	fms related receptor tyrosine kinase 3	Homo sapiens	18-22
30559310-4	2018	Notably, we observed that samples from both patients demonstrated FLT3 inhibitor (quizartinib and sorafenib) sensitivity in ex vivo drug screening assay.	quizartinib	82-93	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
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	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	16-20
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	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	21-26
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	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	66-70
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	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	71-76
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
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
30553002-3	2019	Quizartinib was transported by human ABCB1 in vitro, and by mouse (m)Abcb1 and mAbcg2 in vivo.	quizartinib	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	37-42
30553002-3	2019	Quizartinib was transported by human ABCB1 in vitro, and by mouse (m)Abcb1 and mAbcg2 in vivo.	quizartinib	0-11	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	69-74
30553002-3	2019	Quizartinib was transported by human ABCB1 in vitro, and by mouse (m)Abcb1 and mAbcg2 in vivo.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	79-85
30553002-4	2019	Upon oral administration, the brain accumulation of quizartinib was 6-fold decreased by mAbcb1 and 2-fold by mAbcg2 (together: 12-fold).	quizartinib	52-63	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	88-94
30553002-4	2019	Upon oral administration, the brain accumulation of quizartinib was 6-fold decreased by mAbcb1 and 2-fold by mAbcg2 (together: 12-fold).	quizartinib	52-63	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	109-115
30553002-5	2019	Unexpectedly, the absence of mAbcb1 resulted in a ~2-fold lower plasma exposure in Abcb1a/1b-/- and Abcb1a/1b;Abcg2-/- mice, suggesting that loss of mAbcb1 causes compensatory alterations in alternative quizartinib elimination or uptake systems.	quizartinib	203-214	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	29-35
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	139-144	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
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
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 related receptor tyrosine kinase 3	Homo sapiens	124-128
30427680-2	2018	Conversion of a FLT-3 inhibitor (quizartinib) into a proteolysis targeting chimera (PROTAC) results in a compound that induces degradation of FLT-3 ITD mutant at low nanomolar concentrations.	quizartinib	33-44	fms related receptor tyrosine kinase 3	Homo sapiens	16-21
30344940-2	2018	Quizartinib, gilteritinib, and midostaurin are inhibitors against FLT3-ITD that have good efficacy for FLT3-ITD-positive AML patients.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
30427680-2	2018	Conversion of a FLT-3 inhibitor (quizartinib) into a proteolysis targeting chimera (PROTAC) results in a compound that induces degradation of FLT-3 ITD mutant at low nanomolar concentrations.	quizartinib	33-44	fms related receptor tyrosine kinase 3	Homo sapiens	142-147
30344940-2	2018	Quizartinib, gilteritinib, and midostaurin are inhibitors against FLT3-ITD that have good efficacy for FLT3-ITD-positive AML patients.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	103-107
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	42-53	NAD(P)H quinone dehydrogenase 1	Homo sapiens	78-81
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	42-53	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	86-89
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	42-53	fms related receptor tyrosine kinase 3	Homo sapiens	177-181
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	42-53	fms related receptor tyrosine kinase 3	Homo sapiens	196-200
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	152-163	NAD(P)H quinone dehydrogenase 1	Homo sapiens	78-81
30344940-9	2018	Similar results were also observed in the quizartinib-resistant MV4-11 cells, QR1 and QR2, which were established by culturing cells in the presence of quizartinib and harbored FLT3-ITD+D835H and FLT3-ITD+D835V, respectively, in a single allele.	quizartinib	152-163	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	86-89
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 &lt; 0.05).	quizartinib	78-83	FMS-like tyrosine kinase 3	Mus musculus	62-66
30081867-0	2018	Safety and tolerability of quizartinib, a FLT3 inhibitor, in advanced solid tumors: a phase 1 dose-escalation trial.	quizartinib	27-38	fms related receptor tyrosine kinase 3	Homo sapiens	42-46
30081867-1	2018	BACKGROUND: Quizartinib, an inhibitor of class III receptor tyrosine kinases (RTKs), is currently in phase 3 development for the treatment of acute myeloid leukemia (AML) bearing internal tandem duplications in the FLT3 gene.	quizartinib	12-23	fms related receptor tyrosine kinase 3	Homo sapiens	215-219
29875101-0	2018	Phase 2b study of 2 dosing regimens of quizartinib monotherapy in FLT3-ITD-mutated, relapsed or refractory AML.	quizartinib	39-50	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
29986851-0	2018	Quizartinib Bests Chemo for FLT3-Mutant AML.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	28-32
29986851-1	2018	The FLT3 inhibitor quizartinib provided a survival benefit over chemotherapy in a phase III trial of patients with relapsed or refractory FLT3-mutant acute myeloid leukemia.	quizartinib	19-30	fms related receptor tyrosine kinase 3	Homo sapiens	4-8
29986851-1	2018	The FLT3 inhibitor quizartinib provided a survival benefit over chemotherapy in a phase III trial of patients with relapsed or refractory FLT3-mutant acute myeloid leukemia.	quizartinib	19-30	fms related receptor tyrosine kinase 3	Homo sapiens	138-142
29894944-3	2018	Among them, compound 50 was identified as a highly potent and selective FLT3 inhibitor (IC50 = 0.213 nM), which showed equal activities against various mutants of FLT3 including FLT3 (ITD)-D835V and FLT3 (ITD)-F691L that is resistant to quizartinib.	quizartinib	237-248	fms related receptor tyrosine kinase 3	Homo sapiens	72-76
29859851-0	2018	Quizartinib, an FLT3 inhibitor, as monotherapy in patients with relapsed or refractory acute myeloid leukaemia: an open-label, multicentre, single-arm, phase 2 trial.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	16-20
29859851-2	2018	Quizartinib is an oral, highly potent, and selective next-generation FLT3 inhibitor with clinical antileukaemic activity in relapsed or refractory acute myeloid leukaemia.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
29859851-21	2018	INTERPRETATION: Single-agent quizartinib was shown to be highly active and generally well tolerated in patients with relapsed or refractory acute myeloid leukaemia, particularly those with FLT3-ITD mutations.	quizartinib	29-40	fms related receptor tyrosine kinase 3	Homo sapiens	189-193
29463558-5	2018	We investigated the antileukemia activity of combined Wnt/beta-catenin and FLT3 inhibition in FLT3-mutant AML.Experimental Design: Wnt/beta-catenin signaling was inhibited by the beta-catenin/CBP antagonist C-82/PRI-724 or siRNAs, and FLT3 signaling by sorafenib or quizartinib.	quizartinib	266-277	catenin beta 1	Homo sapiens	135-147
29463558-5	2018	We investigated the antileukemia activity of combined Wnt/beta-catenin and FLT3 inhibition in FLT3-mutant AML.Experimental Design: Wnt/beta-catenin signaling was inhibited by the beta-catenin/CBP antagonist C-82/PRI-724 or siRNAs, and FLT3 signaling by sorafenib or quizartinib.	quizartinib	266-277	catenin beta 1	Homo sapiens	135-147
29139135-2	2018	Quizartinib is a selective and highly potent FLT3 inhibitor that has shown strong single-agent activity in relapsed or refractory (R/R) AML.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	45-49
29336115-3	2018	FLT3 kinase domain mutation F691L is one of the common causes of acquired resistance to the FLT3 inhibitors including quizartinib.	quizartinib	118-129	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
29336115-3	2018	FLT3 kinase domain mutation F691L is one of the common causes of acquired resistance to the FLT3 inhibitors including quizartinib.	quizartinib	118-129	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
29336115-8	2018	Further free energy landscape analysis revealed that FLT3 F691L bound to MZH29 and crenolanib was more stable as compared to quizartinib.	quizartinib	125-136	fms related receptor tyrosine kinase 3	Homo sapiens	53-57
29139135-12	2018	The phase 3 QuANTUM-First trial (NCT02668653) is further evaluating the effect of quizartinib plus SOC chemotherapy in ndAML FLT3-ITD mutated patients.	quizartinib	82-93	fms related receptor tyrosine kinase 3	Homo sapiens	125-129
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
28947392-7	2018	We found that the FLT3 inhibitor AC220 inhibited glutamine flux into the antioxidant factor glutathione profoundly due to defective glutamine import.	quizartinib	33-38	fms related receptor tyrosine kinase 3	Homo sapiens	18-22
29142066-8	2018	When combined with a FLT3 inhibitor quizartinib, SGN-CD123A enhanced the activity of quizartinib against two FLT3-mutated xenograft models.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	21-25
29142066-8	2018	When combined with a FLT3 inhibitor quizartinib, SGN-CD123A enhanced the activity of quizartinib against two FLT3-mutated xenograft models.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	109-113
29374185-3	2018	AC220 (Quizartinib), an FLT3 receptor tyrosine kinase inhibitor, developed for the treatment of AML, has been tested in phase II human clinical trials.	quizartinib	0-5	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
29374185-3	2018	AC220 (Quizartinib), an FLT3 receptor tyrosine kinase inhibitor, developed for the treatment of AML, has been tested in phase II human clinical trials.	quizartinib	7-18	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
29074603-6	2018	Mechanistically, AZD1208 and quizartinib cotreatment decreased expression of the antiapoptotic protein Mcl-1.	quizartinib	29-40	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	103-108
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 related receptor tyrosine kinase 3	Homo sapiens	42-46
27460866-0	2017	An open-label, single-dose, phase 1 study of the absorption, metabolism and excretion of quizartinib, a highly selective and potent FLT3 tyrosine kinase inhibitor, in healthy male subjects, for the treatment of acute myeloid leukemia.	quizartinib	89-100	fms related receptor tyrosine kinase 3	Homo sapiens	132-136
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 related receptor tyrosine kinase 3	Homo sapiens	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
28799176-0	2017	The molecular mechanism behind resistance of the kinase FLT3 to the inhibitor quizartinib.	quizartinib	78-89	fms related receptor tyrosine kinase 3	Homo sapiens	56-60
28799176-5	2017	Extensive fully atomistic molecular dynamics (MD) simulations of FLT3 were carried out with an inhibited form (FLT-quizartinib complex), a free (apo) form, and an active conformation.	quizartinib	115-126	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
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
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
27671675-1	2016	Potent FLT3 inhibitors, such as quizartinib (AC220), have shown promise in treating acute myeloid leukemia (AML) containing FLT3 internal tandem duplication (ITD) mutations.	quizartinib	32-43	fms related receptor tyrosine kinase 3	Homo sapiens	7-11
29212189-0	2017	Quizartinib (AC220) reverses ABCG2-mediated multidrug resistance: In vitro and in vivo studies.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	29-34
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
29212189-4	2017	While non-toxic to cell lines, quizartinib at 3 muM showed significant reversal effect on wild-type and mutant ABCG2 (R482T)-mediated MDR, and only a moderate reversal effect on mutant ABCG2 (R482G)-mediated MDR.	quizartinib	31-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	111-116
29212189-4	2017	While non-toxic to cell lines, quizartinib at 3 muM showed significant reversal effect on wild-type and mutant ABCG2 (R482T)-mediated MDR, and only a moderate reversal effect on mutant ABCG2 (R482G)-mediated MDR.	quizartinib	31-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	185-190
29212189-5	2017	Results also showed that quizartinib reversed MDR not by reducing the expression of ABCG2 protein, but by antagonizing the drug efflux function and increasing the intracellular accumulation of substrate anticancer drugs in ABCG2-overexpressing cells.	quizartinib	25-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	84-89
29212189-5	2017	Results also showed that quizartinib reversed MDR not by reducing the expression of ABCG2 protein, but by antagonizing the drug efflux function and increasing the intracellular accumulation of substrate anticancer drugs in ABCG2-overexpressing cells.	quizartinib	25-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	223-228
29212189-6	2017	Importantly, quizartinib at 30 mg/kg strongly enhanced the effect of topotecan (3 mg/kg) in ABCG2-overexpressing (H460/MX20) xenografts in athymic nude mice.	quizartinib	13-24	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	92-97
29212189-7	2017	These results demonstrated that quizartinib potentiates the antineoplastic activity of wild-type and R482T mutant ABCG2 substrates.	quizartinib	32-43	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	114-119
28625976-4	2017	Quizartinib (AC220) is a potent and selective second-generation inhibitor of FLT3.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	77-81
28625976-4	2017	Quizartinib (AC220) is a potent and selective second-generation inhibitor of FLT3.	quizartinib	13-18	fms related receptor tyrosine kinase 3	Homo sapiens	77-81
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
28522571-6	2017	Inhibition of FLT3 kinase activity with AC220 significantly reduced p27 tyrosine 88 phosphorylation in cells isolated from FLT3 wild type expressing acute myeloid leukemia (AML) patients.	quizartinib	40-45	fms related receptor tyrosine kinase 3	Homo sapiens	14-18
28522571-6	2017	Inhibition of FLT3 kinase activity with AC220 significantly reduced p27 tyrosine 88 phosphorylation in cells isolated from FLT3 wild type expressing acute myeloid leukemia (AML) patients.	quizartinib	40-45	zinc ribbon domain containing 2	Homo sapiens	68-71
28522571-6	2017	Inhibition of FLT3 kinase activity with AC220 significantly reduced p27 tyrosine 88 phosphorylation in cells isolated from FLT3 wild type expressing acute myeloid leukemia (AML) patients.	quizartinib	40-45	fms related receptor tyrosine kinase 3	Homo sapiens	123-127
28978059-7	2017	Importantly, stromal cell-mediated resistance to targeted inhibition of oncogenic FLT3 kinase activity by quizartinib was circumvented by 6PGD knockdown.	quizartinib	106-117	fms related receptor tyrosine kinase 3	Homo sapiens	82-86
28490572-3	2017	Using targeted sequencing from single cells and colonies from patient samples, we demonstrate tremendous clonal diversity in the majority of acute myeloid leukemia (AML) patients with activating FLT3 internal tandem duplication mutations at the time of acquired resistance to the FLT3 inhibitor quizartinib.	quizartinib	295-306	fms related receptor tyrosine kinase 3	Homo sapiens	195-199
28000291-2	2017	Several FLT3 inhibitors have been used in clinical trials, and these include midostaurin, sorafenib, quizartinib, crenolanib, and gilteritinib.	quizartinib	101-112	fms related receptor tyrosine kinase 3	Homo sapiens	8-12
27671675-1	2016	Potent FLT3 inhibitors, such as quizartinib (AC220), have shown promise in treating acute myeloid leukemia (AML) containing FLT3 internal tandem duplication (ITD) mutations.	quizartinib	32-43	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
26920889-1	2016	PURPOSE: To determine a safe and biologically active dose of quizartinib (AC220), a potent and selective class III receptor tyrosine kinase (RTK) FLT3 inhibitor, in combination with salvage chemotherapy in children with relapsed acute leukemia.	quizartinib	61-72	fms related receptor tyrosine kinase 3	Homo sapiens	146-150
26920889-2	2016	EXPERIMENTAL DESIGN: Quizartinib was administered orally to children with relapsed AML or MLL-rearranged ALL following 5 days of high-dose cytarabine and etoposide (AE).	quizartinib	21-32	lysine methyltransferase 2A	Homo sapiens	90-93
26920889-9	2016	FLT3-ITD patients, but not FLT3 wild-type (WT) patients, had significantly lower blast counts post-quizartinib.	quizartinib	99-110	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
26920889-11	2016	CONCLUSIONS: Quizartinib plus intensive chemotherapy is well tolerated at 60 mg/m(2)/day with near complete inhibition of FLT3 phosphorylation in all patients.	quizartinib	13-24	fms related receptor tyrosine kinase 3	Homo sapiens	122-126
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
27387666-0	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	pre B cell leukemia homeobox 1	Mus musculus	142-146
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	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	77-80
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	pre B cell leukemia homeobox 1	Mus musculus	122-126
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
27190596-2	2016	The development of drug resistance due to mutation is a growing concern for mutant FLT3 inhibitors, such as PKC412, Quizartinib, PLX3397, and Crenolanib.	quizartinib	116-127	fms related receptor tyrosine kinase 3	Homo sapiens	83-87
27158668-7	2016	Additionally, MRX-2843 retained activity against quizartinib-resistant FLT3-ITD-mutant proteins with clinically relevant alterations at the D835 or F691 loci and prolonged survival in xenograft models of quizartinib-resistant AML.	quizartinib	49-60	discs large MAGUK scaffold protein 3	Homo sapiens	14-17
27158668-7	2016	Additionally, MRX-2843 retained activity against quizartinib-resistant FLT3-ITD-mutant proteins with clinically relevant alterations at the D835 or F691 loci and prolonged survival in xenograft models of quizartinib-resistant AML.	quizartinib	49-60	fms related receptor tyrosine kinase 3	Homo sapiens	71-75
27158668-7	2016	Additionally, MRX-2843 retained activity against quizartinib-resistant FLT3-ITD-mutant proteins with clinically relevant alterations at the D835 or F691 loci and prolonged survival in xenograft models of quizartinib-resistant AML.	quizartinib	204-215	discs large MAGUK scaffold protein 3	Homo sapiens	14-17
27158668-7	2016	Additionally, MRX-2843 retained activity against quizartinib-resistant FLT3-ITD-mutant proteins with clinically relevant alterations at the D835 or F691 loci and prolonged survival in xenograft models of quizartinib-resistant AML.	quizartinib	204-215	fms related receptor tyrosine kinase 3	Homo sapiens	71-75
26286850-6	2016	Moreover, proteasome inhibitors overcome resistance to quizartinib induced by mutations in the kinase domain of FLT3, suggesting that these compounds may prevent the emergence of mutant clones arising from tyrosine kinase inhibitor treatments.	quizartinib	55-66	fms related receptor tyrosine kinase 3	Homo sapiens	112-116
26491063-3	2016	We here show that a metalloprotease present in the culture supernatant of cerebellar granular neurons (CGN) cleaves Reelin between Ala2688 and Asp2689.	quizartinib	143-150	reelin	Mus musculus	116-122
25797966-7	2015	Recently developed AC220 is a highly selective and sensitive FLT3 inhibitor.	quizartinib	19-24	fms related receptor tyrosine kinase 3	Homo sapiens	61-65
26208887-1	2015	Based on a putative binding mode of quizartinib (AC220, 1), a potent FMS-like tyrosine kinase 3 (FLT3) inhibitor in Phase III clinical development, we have designed de novo a simpler aminopyridine-based hinge binding motif.	quizartinib	36-47	fms related receptor tyrosine kinase 3	Homo sapiens	69-95
26208887-1	2015	Based on a putative binding mode of quizartinib (AC220, 1), a potent FMS-like tyrosine kinase 3 (FLT3) inhibitor in Phase III clinical development, we have designed de novo a simpler aminopyridine-based hinge binding motif.	quizartinib	36-47	fms related receptor tyrosine kinase 3	Homo sapiens	97-101
25487917-7	2015	In contrast, selection with the FLT3 inhibitors sorafenib or AC220 (Quizartinib), led to a resistance and the appearance of a number of mutations in FLT3 kinase domains, including the known hot spot sites D835 and F691.	quizartinib	61-66	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
25487917-7	2015	In contrast, selection with the FLT3 inhibitors sorafenib or AC220 (Quizartinib), led to a resistance and the appearance of a number of mutations in FLT3 kinase domains, including the known hot spot sites D835 and F691.	quizartinib	61-66	fms related receptor tyrosine kinase 3	Homo sapiens	149-153
25487917-7	2015	In contrast, selection with the FLT3 inhibitors sorafenib or AC220 (Quizartinib), led to a resistance and the appearance of a number of mutations in FLT3 kinase domains, including the known hot spot sites D835 and F691.	quizartinib	68-79	fms related receptor tyrosine kinase 3	Homo sapiens	32-36
25487917-7	2015	In contrast, selection with the FLT3 inhibitors sorafenib or AC220 (Quizartinib), led to a resistance and the appearance of a number of mutations in FLT3 kinase domains, including the known hot spot sites D835 and F691.	quizartinib	68-79	fms related receptor tyrosine kinase 3	Homo sapiens	149-153
25487917-8	2015	However, when AC220 was combined with the CDK4 inhibitor PD0332991 (palbociclib) at 0.1 mumol/L or higher, no resistance mutations were obtained, indicating that the CDK4-inhibiting activity of AMG 925 contributed to the failure to develop drug resistance.	quizartinib	14-19	cyclin dependent kinase 4	Homo sapiens	166-170
26172401-7	2015	We also found that resistance of AML cells against the FLT3 inhibitor PKC412 and AC220 was substantially diminished by the inhibition of Axl via a small-molecule inhibitor TP-0903, a soluble receptor Axl fusion protein Axl-Fc or knockdown of Axl gene expression by shRNA.	quizartinib	81-86	AXL receptor tyrosine kinase	Homo sapiens	137-140
26172401-7	2015	We also found that resistance of AML cells against the FLT3 inhibitor PKC412 and AC220 was substantially diminished by the inhibition of Axl via a small-molecule inhibitor TP-0903, a soluble receptor Axl fusion protein Axl-Fc or knockdown of Axl gene expression by shRNA.	quizartinib	81-86	AXL receptor tyrosine kinase	Homo sapiens	200-203
26172401-7	2015	We also found that resistance of AML cells against the FLT3 inhibitor PKC412 and AC220 was substantially diminished by the inhibition of Axl via a small-molecule inhibitor TP-0903, a soluble receptor Axl fusion protein Axl-Fc or knockdown of Axl gene expression by shRNA.	quizartinib	81-86	AXL receptor tyrosine kinase	Homo sapiens	200-203
26172401-7	2015	We also found that resistance of AML cells against the FLT3 inhibitor PKC412 and AC220 was substantially diminished by the inhibition of Axl via a small-molecule inhibitor TP-0903, a soluble receptor Axl fusion protein Axl-Fc or knockdown of Axl gene expression by shRNA.	quizartinib	81-86	AXL receptor tyrosine kinase	Homo sapiens	200-203
26625890-4	2015	Lestaurtinib, midostaurin, sorafenib, and quizartinib were selected among the FLT3 inhibitor drugs that are currently used in clinics for the treatment of acute myeloid leukemia.	quizartinib	42-53	fms related receptor tyrosine kinase 3	Homo sapiens	78-82
25837374-0	2015	Crystal structure of the FLT3 kinase domain bound to the inhibitor Quizartinib (AC220).	quizartinib	67-78	fms related receptor tyrosine kinase 3	Homo sapiens	25-29
25837374-0	2015	Crystal structure of the FLT3 kinase domain bound to the inhibitor Quizartinib (AC220).	quizartinib	80-85	fms related receptor tyrosine kinase 3	Homo sapiens	25-29
25837374-2	2015	A small-molecule inhibitor of FLT3 (known as quizartinib or AC220) that is currently in clinical trials appears promising for the treatment of AML.	quizartinib	45-56	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
25837374-2	2015	A small-molecule inhibitor of FLT3 (known as quizartinib or AC220) that is currently in clinical trials appears promising for the treatment of AML.	quizartinib	60-65	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
25837374-3	2015	Here, we report the co-crystal structure of the kinase domain of FLT3 in complex with quizartinib.	quizartinib	86-97	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
25837374-4	2015	FLT3 with quizartinib bound adopts an "Abl-like" inactive conformation with the activation loop stabilized in the "DFG-out" orientation and folded back onto the kinase domain.	quizartinib	10-21	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
25837374-6	2015	The co-crystal structure reveals the interactions between quizartinib and the active site of FLT3 that are key for achieving its high potency against both wild-type FLT3 as well as a FLT3 variant observed in many AML patients.	quizartinib	58-69	fms related receptor tyrosine kinase 3	Homo sapiens	93-97
25837374-6	2015	The co-crystal structure reveals the interactions between quizartinib and the active site of FLT3 that are key for achieving its high potency against both wild-type FLT3 as well as a FLT3 variant observed in many AML patients.	quizartinib	58-69	fms related receptor tyrosine kinase 3	Homo sapiens	165-169
25837374-6	2015	The co-crystal structure reveals the interactions between quizartinib and the active site of FLT3 that are key for achieving its high potency against both wild-type FLT3 as well as a FLT3 variant observed in many AML patients.	quizartinib	58-69	fms related receptor tyrosine kinase 3	Homo sapiens	165-169
25775444-0	2015	Catastrophic eruptive keratoacanthomas and squamous cell cancers after treatment with an FLT3 inhibitor quizartinib (AC220).	quizartinib	104-115	fms related receptor tyrosine kinase 3	Homo sapiens	89-93
25775444-0	2015	Catastrophic eruptive keratoacanthomas and squamous cell cancers after treatment with an FLT3 inhibitor quizartinib (AC220).	quizartinib	117-122	fms related receptor tyrosine kinase 3	Homo sapiens	89-93
24623852-5	2014	Here we demonstrate that the investigational type I TKI crenolanib is a potent inhibitor of Fms tyrosine kinase-3 (FLT3) internal tandem duplication, a validated therapeutic target in human acute myeloid leukemia (AML), as well as all secondary KD mutants previously shown to confer resistance to the first highly active FLT3 TKI quizartinib.	quizartinib	330-341	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
24310825-3	2014	METHODS: We report four pediatric patients with various malignancies (chronic myelogenous leukemia, acute lymphoblastic leukemia, and glioma/renal cell carcinoma) who developed nephrotic syndrome during treatment with TK inhibitors (imatinib, sunitinib, dasatinib, and quizartinib).	quizartinib	269-280	TXK tyrosine kinase	Homo sapiens	218-220
25053825-2	2014	Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primary CD34(+) human AML blast progenitor cells (BPC) expressing FLT3-ITD.	quizartinib	105-110	CD34 molecule	Homo sapiens	168-172
25053825-2	2014	Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primary CD34(+) human AML blast progenitor cells (BPC) expressing FLT3-ITD.	quizartinib	105-110	fms related receptor tyrosine kinase 3	Homo sapiens	226-230
24633870-0	2014	Clinically relevant doses of FLT3-kinase inhibitors quizartinib and midostaurin do not impair T-cell reactivity and function.	quizartinib	52-63	fms related receptor tyrosine kinase 3	Homo sapiens	29-33
24883179-0	2014	The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.	quizartinib	64-75	fms related receptor tyrosine kinase 3	Homo sapiens	21-25
24883179-6	2014	These results have prompted the development of second-generation FLT3 inhibitors, epitomized by the novel agent quizartinib.	quizartinib	112-123	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
24582753-4	2014	Changes in FoxM1 expression were detected after MV4-11 cells, which have an internal tandem duplication (ITD) of the fms-like tyrosine kinase 3 gene (FLT3-ITD), and control THP1 cells (encoding wild-type FLT3) were treated with the FLT3 receptor tyrosine kinase inhibitor AC220 (quizartinib) or FLT3 ligand (FL).	quizartinib	272-277	forkhead box M1	Homo sapiens	11-16
24582753-4	2014	Changes in FoxM1 expression were detected after MV4-11 cells, which have an internal tandem duplication (ITD) of the fms-like tyrosine kinase 3 gene (FLT3-ITD), and control THP1 cells (encoding wild-type FLT3) were treated with the FLT3 receptor tyrosine kinase inhibitor AC220 (quizartinib) or FLT3 ligand (FL).	quizartinib	279-290	forkhead box M1	Homo sapiens	11-16
24070241-4	2013	Quizartinib (AC220) is a second-generation FLT3 inhibitor that has shown promising activity in AML in Phase II clinical trials.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	43-47
25145428-0	2014	Quizartinib for the treatment of FLT3/ITD acute myeloid leukemia.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	33-37
25145428-3	2014	Quizartinib is the first small molecule FLT3 tyrosine kinase inhibitor expressly developed as a FLT3 inhibitor.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	40-44
25145428-3	2014	Quizartinib is the first small molecule FLT3 tyrosine kinase inhibitor expressly developed as a FLT3 inhibitor.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	96-100
24070241-4	2013	Quizartinib (AC220) is a second-generation FLT3 inhibitor that has shown promising activity in AML in Phase II clinical trials.	quizartinib	13-18	fms related receptor tyrosine kinase 3	Homo sapiens	43-47
24070241-6	2013	EXPERT OPINION: Quizartinib is potent and selective FLT3 tyrosine kinase inhibitor with significant activity in both FLT3-mutant and wild-type AML.	quizartinib	16-27	fms related receptor tyrosine kinase 3	Homo sapiens	52-56
24070241-6	2013	EXPERT OPINION: Quizartinib is potent and selective FLT3 tyrosine kinase inhibitor with significant activity in both FLT3-mutant and wild-type AML.	quizartinib	16-27	fms related receptor tyrosine kinase 3	Homo sapiens	117-121
24070241-9	2013	In addition, quizartinib in combination with other agents tackling the bone marrow microenvironment and FLT3 cooperative pathways may enhance response to quizartinib.	quizartinib	154-165	fms related receptor tyrosine kinase 3	Homo sapiens	104-108
23998902-6	2013	Co-treatment of FLT3-ITD-positive cells with the specific FLT3 inhibitor AC220 was able to overcome TNF-alpha resistance.	quizartinib	73-78	fms related receptor tyrosine kinase 3	Homo sapiens	16-20
23998902-6	2013	Co-treatment of FLT3-ITD-positive cells with the specific FLT3 inhibitor AC220 was able to overcome TNF-alpha resistance.	quizartinib	73-78	fms related receptor tyrosine kinase 3	Homo sapiens	58-62
23998902-6	2013	Co-treatment of FLT3-ITD-positive cells with the specific FLT3 inhibitor AC220 was able to overcome TNF-alpha resistance.	quizartinib	73-78	tumor necrosis factor	Homo sapiens	100-109
23967177-0	2013	The FLT3 inhibitor quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug interactions.	quizartinib	19-30	fms related receptor tyrosine kinase 3	Homo sapiens	4-8
24002496-10	2013	CONCLUSION: Quizartinib has clinical activity in patients with relapsed/refractory AML, particularly those with FLT3-ITD, and is associated with an acceptable toxicity profile.	quizartinib	12-23	fms related receptor tyrosine kinase 3	Homo sapiens	112-116
24002496-2	2013	Quizartinib potently and selectively inhibits FLT3 kinase activity in preclinical AML models.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	46-50
23967177-0	2013	The FLT3 inhibitor quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug interactions.	quizartinib	19-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	40-45
23967177-1	2013	The oral second-generation bis-aryl urea fms-like tyrosine kinase 3 (FLT3) inhibitor quizartinib (AC220) has favorable kinase selectivity and pharmacokinetics.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	41-67
23967177-1	2013	The oral second-generation bis-aryl urea fms-like tyrosine kinase 3 (FLT3) inhibitor quizartinib (AC220) has favorable kinase selectivity and pharmacokinetics.	quizartinib	85-96	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
23967177-1	2013	The oral second-generation bis-aryl urea fms-like tyrosine kinase 3 (FLT3) inhibitor quizartinib (AC220) has favorable kinase selectivity and pharmacokinetics.	quizartinib	98-103	fms related receptor tyrosine kinase 3	Homo sapiens	41-67
23967177-1	2013	The oral second-generation bis-aryl urea fms-like tyrosine kinase 3 (FLT3) inhibitor quizartinib (AC220) has favorable kinase selectivity and pharmacokinetics.	quizartinib	98-103	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
23967177-4	2013	We characterized interactions of quizartinib with the ATP-binding cassette (ABC) proteins ABCB1 (P-glycoprotein) and ABCG2 (breast cancer resistance protein).	quizartinib	33-44	ATP binding cassette subfamily B member 1	Homo sapiens	90-95
23967177-4	2013	We characterized interactions of quizartinib with the ATP-binding cassette (ABC) proteins ABCB1 (P-glycoprotein) and ABCG2 (breast cancer resistance protein).	quizartinib	33-44	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	117-122
23967177-4	2013	We characterized interactions of quizartinib with the ATP-binding cassette (ABC) proteins ABCB1 (P-glycoprotein) and ABCG2 (breast cancer resistance protein).	quizartinib	33-44	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	124-156
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	57-62
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	77-82
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	88-93
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	77-82
23967177-6	2013	Quizartinib inhibited transport of fluorescent ABCG2 and ABCB1 substrates in ABCG2- and ABCB1-overexpressing cells in a concentration-dependent manner, from 0.1 to 5 microM and from 0.5 to 10 microM, respectively, and inhibited [125I]-IAAP photolabeling of ABCG2 and ABCB1 with IC50 values of 0.07 and 3.3 microM, respectively.	quizartinib	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	88-93
23967177-7	2013	Quizartinib at higher concentrations decreased ABCG2, but not ABCB1, ATPase activity.	quizartinib	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
23967177-7	2013	Quizartinib at higher concentrations decreased ABCG2, but not ABCB1, ATPase activity.	quizartinib	0-11	dynein axonemal heavy chain 8	Homo sapiens	69-75
23967177-8	2013	Co-incubation with quizartinib at 0.1 to 1 microM sensitized ABCG2-overexpressing K562/ABCG2 and 8226/MR20 cells to ABCG2 substrate chemotherapy drugs in a concentration-dependent manner in cell viability and apoptosis assays.	quizartinib	19-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	61-66
23967177-8	2013	Co-incubation with quizartinib at 0.1 to 1 microM sensitized ABCG2-overexpressing K562/ABCG2 and 8226/MR20 cells to ABCG2 substrate chemotherapy drugs in a concentration-dependent manner in cell viability and apoptosis assays.	quizartinib	19-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	87-92
23967177-8	2013	Co-incubation with quizartinib at 0.1 to 1 microM sensitized ABCG2-overexpressing K562/ABCG2 and 8226/MR20 cells to ABCG2 substrate chemotherapy drugs in a concentration-dependent manner in cell viability and apoptosis assays.	quizartinib	19-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	87-92
23967177-9	2013	Additionally, quizartinib increased cellular uptake of the ABCG2 substrate fluoroquinolone antibiotic ciprofloxacin, which also prolongs the QT interval, in a concentration-dependent manner, predicting altered ciprofloxacin pharmacokinetics and pharmacodynamics when co-administered with quizartinib.	quizartinib	14-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	59-64
23967177-9	2013	Additionally, quizartinib increased cellular uptake of the ABCG2 substrate fluoroquinolone antibiotic ciprofloxacin, which also prolongs the QT interval, in a concentration-dependent manner, predicting altered ciprofloxacin pharmacokinetics and pharmacodynamics when co-administered with quizartinib.	quizartinib	288-299	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	59-64
23967177-10	2013	Thus quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug interactions.	quizartinib	5-16	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	26-31
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	fms related receptor tyrosine kinase 3	Homo sapiens	77-85
23012328-4	2012	Quizartinib is a novel potent and selective FLT3 inhibitor currently being studied in clinical trials.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	44-48
23012328-5	2012	In 13 of 14 FLT3/ITD AML patients with normal karyotype treated with quizartinib, we observed terminal myeloid differentiation of BM blasts in association with a clinical differentiation syndrome.	quizartinib	69-80	fms related receptor tyrosine kinase 3	Homo sapiens	12-16
23012328-7	2012	In vitro, in primary blasts cocultured with human BM stroma, FLT3 inhibition with quizartinib induced cell-cycle arrest and differentiation rather than apoptosis.	quizartinib	82-93	fms related receptor tyrosine kinase 3	Homo sapiens	61-65
22875611-0	2012	The N676D and G697R mutations in the kinase domain of FLT3 confer resistance to the inhibitor AC220.	quizartinib	94-99	fms related receptor tyrosine kinase 3	Homo sapiens	54-58
23430109-1	2013	Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the FLT3 inhibitors AC220 (quizartinib) and sorafenib.	quizartinib	175-186	fms related receptor tyrosine kinase 3	Homo sapiens	33-59
23430109-1	2013	Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the FLT3 inhibitors AC220 (quizartinib) and sorafenib.	quizartinib	175-186	fms related receptor tyrosine kinase 3	Homo sapiens	61-65
23430109-1	2013	Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the FLT3 inhibitors AC220 (quizartinib) and sorafenib.	quizartinib	175-186	fms related receptor tyrosine kinase 3	Homo sapiens	152-156
23412931-0	2013	Transient exposure to quizartinib mediates sustained inhibition of FLT3 signaling while specifically inducing apoptosis in FLT3-activated leukemia cells.	quizartinib	22-33	fms related receptor tyrosine kinase 3	Homo sapiens	67-71
23412931-0	2013	Transient exposure to quizartinib mediates sustained inhibition of FLT3 signaling while specifically inducing apoptosis in FLT3-activated leukemia cells.	quizartinib	22-33	fms related receptor tyrosine kinase 3	Homo sapiens	123-127
23412931-3	2013	Quizartinib (AC220) has previously been shown to be a potent and selective FLT3 inhibitor.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	75-79
23412931-3	2013	Quizartinib (AC220) has previously been shown to be a potent and selective FLT3 inhibitor.	quizartinib	13-18	fms related receptor tyrosine kinase 3	Homo sapiens	75-79
23412931-4	2013	In the current study, we expand on previous observations by showing that quizartinib potently inhibits the phosphorylation of FLT3 and downstream signaling molecules independent of FLT3 genotype, yet induces loss of viability only in cells expressing constitutively activated FLT3.	quizartinib	73-84	fms related receptor tyrosine kinase 3	Homo sapiens	126-130
23412931-5	2013	We further show that transient exposure to quizartinib, whether in vitro or in vivo, leads to prolonged inhibition of FLT3 signaling, induction of apoptosis, and drastic reductions in tumor volume and pharmacodynamic endpoints.	quizartinib	43-54	fms related receptor tyrosine kinase 3	Homo sapiens	118-122
23412931-7	2013	Together these data suggest quizartinib, with its unique combination of selectivity and potent/sustained inhibition of FLT3, may provide a safe and effective treatment against FLT3-driven leukemia.	quizartinib	28-39	fms related receptor tyrosine kinase 3	Homo sapiens	119-123
23412931-7	2013	Together these data suggest quizartinib, with its unique combination of selectivity and potent/sustained inhibition of FLT3, may provide a safe and effective treatment against FLT3-driven leukemia.	quizartinib	28-39	fms related receptor tyrosine kinase 3	Homo sapiens	176-180
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	0-11	fms related receptor tyrosine kinase 3	Homo sapiens	145-149
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	0-11	platelet derived growth factor receptor alpha	Homo sapiens	152-158
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	0-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	13-18	fms related receptor tyrosine kinase 3	Homo sapiens	145-149
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	13-18	platelet derived growth factor receptor alpha	Homo sapiens	152-158
23497317-0	2013	Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.	quizartinib	13-18	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
23497317-3	2013	However, the expanding spectrum of TK-mutations, bioavailability issues and the emerging problem of primary or secondary TKI-therapy resistance have lead to the search for novel second generation TKIs to improve target potency and to overcome resistant clones.Quizartinib was recently demonstrated to be a selective FLT3 inhibitor with excellent pharmacokinetics and promising in vivo activity in a phase II study for FLT3 ITD + AML patients.	quizartinib	260-271	fms related receptor tyrosine kinase 3	Homo sapiens	316-320
23497317-3	2013	However, the expanding spectrum of TK-mutations, bioavailability issues and the emerging problem of primary or secondary TKI-therapy resistance have lead to the search for novel second generation TKIs to improve target potency and to overcome resistant clones.Quizartinib was recently demonstrated to be a selective FLT3 inhibitor with excellent pharmacokinetics and promising in vivo activity in a phase II study for FLT3 ITD + AML patients.	quizartinib	260-271	fms related receptor tyrosine kinase 3	Homo sapiens	418-422
23497317-7	2013	Using immunoblotting, we examined the effects of quizartinib on activation of mutant KIT or FLT3 isoforms.	quizartinib	49-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-88
23497317-7	2013	Using immunoblotting, we examined the effects of quizartinib on activation of mutant KIT or FLT3 isoforms.	quizartinib	49-60	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
23497317-8	2013	RESULTS: Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.	quizartinib	71-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
23497317-8	2013	RESULTS: Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.	quizartinib	71-82	platelet derived growth factor receptor beta	Homo sapiens	44-49
23497317-8	2013	RESULTS: Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.	quizartinib	71-82	fms related receptor tyrosine kinase 3	Homo sapiens	54-58
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	55-60	fms related receptor tyrosine kinase 3	Homo sapiens	31-35
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	55-60	fms related receptor tyrosine kinase 3	Homo sapiens	134-138
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	55-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	258-261
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	55-60	Janus kinase 2	Homo sapiens	266-270
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	62-73	fms related receptor tyrosine kinase 3	Homo sapiens	31-35
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	62-73	fms related receptor tyrosine kinase 3	Homo sapiens	134-138
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	62-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	258-261
23714533-2	2013	Recently, selective and potent FLT3 inhibitors such as AC220 (quizartinib) have proven clinically effective in patients with AML with FLT3 internal tandem duplication (ITD) mutations, but inhibitors of other pathologically activated kinases in AML such as c-KIT and JAK2 have achieved less clinical success.	quizartinib	62-73	Janus kinase 2	Homo sapiens	266-270
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
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	fms related receptor tyrosine kinase 3	Homo sapiens	77-81
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	199-202
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	platelet derived growth factor receptor beta	Homo sapiens	212-218
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	ret proto-oncogene	Homo sapiens	223-226
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	fms related receptor tyrosine kinase 3	Homo sapiens	193-197
21895538-7	2011	Newer, more potent FLT3 inhibitors such as sorafenib and AC220 possess the ability to achieve more sustained in vivo inhibition of FLT3 and have shown highly promising activity in early clinical studies.	quizartinib	57-62	fms related receptor tyrosine kinase 3	Homo sapiens	19-23
21895538-7	2011	Newer, more potent FLT3 inhibitors such as sorafenib and AC220 possess the ability to achieve more sustained in vivo inhibition of FLT3 and have shown highly promising activity in early clinical studies.	quizartinib	57-62	fms related receptor tyrosine kinase 3	Homo sapiens	131-135
21263155-5	2011	In vitro, exogenous FL at concentrations similar to those observed in patients mitigated FLT3 inhibition and cytotoxicity for each of 5 different FLT3 inhibitors (lestaurtinib, midostaurin, sorafenib, KW-2449, and AC220).	quizartinib	214-219	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	20-22