FLT3

シグナル伝達経路

研究分野

阻害剤の選択性比較

カタログ番号	製品カタログ	溶解度(25°C)
カタログ番号	製品カタログ	水	DMSO	アルコール
S1040	Sorafenib (BAY 43-9006) tosylate	0.01 mg/mL	127 mg/mL	'<1 mg/mL
S1048	Tozasertib (VX-680, MK-0457)	<1 mg/mL	93 mg/mL	'<1 mg/mL
S1460	SP600125	<1 mg/mL	44 mg/mL	<1 mg/mL
S1111	Foretinib (GSK1363089)	<1 mg/mL	100 mg/mL	''<1 mg/mL
S2194	R406	<1 mg/mL	100 mg/mL	0 mg/mL
S6839	MRX-2843	<1 mg/mL	98 mg/mL	'25 mg/mL
S9662	UNC2025	<1 mg/mL	100 mg/mL	''60 mg/mL
S1526	Quizartinib (AC220)	<1 mg/mL	33 mg/mL	<1 mg/mL
S1018	Dovitinib (TKI-258)	<1 mg/mL	30 mg/mL	<1 mg/mL
S2736	Fedratinib (TG101348)	<1 mg/mL	100 mg/mL	'<1 mg/mL
S1003	Linifanib (ABT-869)	<1 mg/mL	75 mg/mL	<1 mg/mL
S2730	Crenolanib (CP-868596)	<1 mg/mL	88 mg/mL	7 mg/mL
S2198	SGI-1776 free base	<1 mg/mL	81 mg/mL	'81 mg/mL
S1533	R406 (free base)	<1 mg/mL	21 mg/mL	<1 mg/mL
S1244	Amuvatinib (MP-470)	<1 mg/mL	32 mg/mL	<1 mg/mL
S1043	Tandutinib (MLN518)	<1 mg/mL	5 mg/mL	6 mg/mL
S2692	TG101209	<1 mg/mL	102 mg/mL	'<1 mg/mL
S2158	KW-2449	<1 mg/mL	67 mg/mL	67 mg/mL
S1181	ENMD-2076	1 mg/mL	105 mg/mL	<1 mg/mL
S7083	Ceritinib (LDK378)	<1 mg/mL	20 mg/mL	3 mg/mL
S8032	PRT062607 (P505-15) HCl	86 mg/mL	86 mg/mL	'<1 mg/mL
S7397	Sorafenib (BAY 43-9006)	<1 mg/mL	63 mg/mL	''<1 mg/mL
S8057	Pacritinib (SB1518)	<1 mg/mL	11 mg/mL	<1 mg/mL
S4001	Cabozantinib malate (XL184)	<1 mg/mL	100 mg/mL	'<1 mg/mL
S8023	TCS 359	<1 mg/mL	15 mg/mL	<1 mg/mL
S2018	ENMD-2076 L-(+)-Tartaric acid	<1 mg/mL	100 mg/mL	<1 mg/mL
S7765	Dovitinib (TKI258) Lactate	66 mg/mL	100 mg/mL	'1 mg/mL
S7576	UNC2025 HCl	100 mg/mL	25 mg/mL	8 mg/mL
S0278	SU5614	<1 mg/mL	10 mg/mL	<1 mg/mL
S7014	Merestinib (LY2801653)	<1 mg/mL	100 mg/mL	'100 mg/mL
S6662	AST-487 (NVP-AST487)	<1 mg/mL	100 mg/mL	''33 mg/mL
S9275	Isoguanosine	-1 mg/mL	57 mg/mL	-1 mg/mL
S8442	TAK-659	4 mg/mL	<1 mg/mL	<1 mg/mL
S8229	Brigatinib (AP26113)	<1 mg/mL	1 mg/mL	43 mg/mL
S7545	G-749	<1 mg/mL	24 mg/mL	<1 mg/mL
S1099	SKLB4771 (FLT3-IN-1)	<1 mg/mL	50 mg/mL	<1 mg/mL
S7754	Gilteritinib (ASP2215)	<1 mg/mL	100 mg/mL	'85 mg/mL
S7003	AZD2932	<1 mg/mL	89 mg/mL	5 mg/mL
S7818	Pexidartinib (PLX3397)	<1 mg/mL	83 mg/mL	'''''<1 mg/mL
S7119	Go6976	<1 mg/mL	18 mg/mL	<1 mg/mL
S7533	AMG 925	<1 mg/mL	0.01 mg/mL	<1 mg/mL

FLT3製品

All (41) FLT3阻害剤(41)

製品コード	製品説明	文献中Selleckの製品使用例	お客様のフィードバック
S1040	Sorafenib (BAY 43-9006) tosylate Sorafenib (BAY 43-9006) tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib Tosylate inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib Tosylate induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Theranostics, 2021, 11(12):5650-5674 J Clin Med, 2021, 10(9)1889 Cell Biol Toxicol, 2021, 10.1007/s10565-021-09607-y	Inhibition of breast cancer cell growth using sorafenib. MCF-7 breast cancer cells were treated with increasing concentrations of sorafenib for 5 days. Cell number was measured using a colorimetric growth assay (crystal violet stain) and expressed relative to DMSO treated control cells.
S1048	Tozasertib (VX-680, MK-0457) Tozasertib (VX-680, MK-0457) is a pan-Aurora inhibitor, mostly against Aurora A with K_i_app of 0.6 nM in a cell-free assay, less potent towards Aurora B/Aurora C and 100-fold more selective for Aurora A than 55 other kinases. The only exceptions are Fms-related tyrosine kinase-3 (FLT-3) and BCR-ABL tyrosine kinase, which are inhibited by the Tozasertib with both Ki of 30 nM. Tozasertib induces apoptosis and autophagy. Phase 2.	J Cell Biol, 2021, 220(2)e202008029 PLoS Biol, 2021, 19(1):e3001029 Breast Cancer, 2021, 10.1007/s12282-021-01242-z	Senescence induction upon PKCι depletion combined with aurora kinase inhibition. ( a) MCF7 cells were transfected as above to deplete PKCι . Two days after transfection, cells were treated for the indicated time period with 400 n M VX-680. Medium with VX-680 was then removed and fresh medium was added. Cells were stained for SA-b -gal activity 5 days after the start of transfection.* indicates a P value <0.05. ( b) MCF7 cells were treated as above. Five days after transfection, cells were fixed and assessed for the presence of gH2AX foci by immunofluorescence microscopy. (c, d) MCF7 cells were treated with dimethyl sulfoxide (DMSO) control or 400 n M VX-680 for the indicated time periods. Total cell lysates were then analyzed by western blotting for levels of p21 and GAPDH (as loading control). A representative blot is shown in panel c. Quantitation of changes in p21 levels (normalized to vehicle-treated controls) is shown in panel d. The data shown are the means ±s.e. of three independent experiments.
S1460	SP600125 SP600125 (Nsc75890) is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. SP600125 is also a broad‐spectrum inhibitor of serine/threonine kinases including Aurora kinase A，FLT3 and TRKA with of IC50 of 60 nM, 90 nM and 70 nM. SP600125 inhibits autophagy and activates apoptosis.	Theranostics, 2021, 11(9):4335-4350 EBioMedicine, 2021, 66:103290 Cancer Lett, 2021, 509:13-25	Loss of DUSP4 function upregulates IL-6 and IL-8 and enhances mammosphere growth. Immunoblot analysis of MDA-231 cells after treatment of 24 hours with 1 umol/L selumetinib (MEKi) or 10 umol/L SP600125 (JNKi). I, MDA-231 mammosphere formation quantitated by GelCount software 7 days after siRNA transfection. Where indicated, selumetinib (MEKi) or SP600125 (JNK1) or the combination was added to the mammosphere cultures.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089, EXEL-2880, XL-880, GSK089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-Met) and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Cancers (Basel), 2021, 13(3)E372 Angiogenesis, 2021, 10.1007/s10456-021-09771-z Sci Adv, 2020, 22;6(21):eaaz8521	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. Cell growth was determined using the sulforhodamine B assay. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, and TAE-684I. The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
S2194	R406 R406 is a potent Syk inhibitor with IC50 of 41 nM in cell-free assays, strongly inhibits Syk but not Lyn, 5-fold less potent to Flt3. R406 induces apoptosis. Phase 1.	Cell Rep, 2021, 34(11):108870 J Leukoc Biol, 2021, 10.1002/JLB.2A0520-334R J Biol Chem, 2021, S0021-9258(21)00238-6	Platelets (3 x 10⁸/mL) were preincubated with Y27632 (10 uM), R406 (1 uM), or a combination of Y27632 and R406 for 20 minutes followed by stimulation with oxLDL (50 ug/mL) for 15 seconds and lysis. Samples were then separated by SDS-PAGE and were immunoblotted for phospho-MLCSer19, followed by reprobing for β-tubulin. (Fi) Representative blots. (Fii) Densitometric analysis of 3 independent experiments. *P < .05. Data are presented as mean ± SEM. Experiments were carried out in the presence of apyrase (2 U/mL), indomethacin (10 uM), and EGTA (1 mM).
S6839^新	MRX-2843 MRX-2843 (UNC2371) is an orally active dual inhibitor of tyrosine kinases MERTK and FLT3 with IC50 of 1.3 nM and 0.64 nM, respectively.
S9662^新	UNC2025 UNC2025 is a potent and orally active dual inhibitor of FLT3 and MER with IC50 of 0.35 nM and 0.46 nM, respectively. UNC2025 also inhibits AXL, TRKA, TRKC, QIK, TYRO3, SLK, NuaK1, Kit (c-Kit) and Met (c-Met) with IC50 of 1.65 nM, 1.67 nM, 4.38 nM, 5.75 nM, 5.83 nM, 6.14 nM, 7.97 nM, 8.18 nM and 364 nM, respectively.	Front Immunol, 2020, 11:564133
S1526	Quizartinib (AC220) Quizartinib (AC220) is a second-generation FLT3 inhibitor for Flt3(ITD/WT) with IC50 of 1.1 nM/4.2 nM in MV4-11 and RS4;11 cells, respectively, 10-fold more selective for Flt3 than KIT, PDGFRα, PDGFRβ, RET, and CSF-1R. Quizartinib (AC220) induces apoptosis of tumor cells. Phase 3.	Autophagy, 2021, 1-10 Blood Cancer J, 2021, 11(3):57 Cancer Discov, 2021, candisc.0738.2020	Cotreatment with JQ1 and AC220 synergistically induces apoptosis of FLT3-ITD–expressing AML cells. MV4-11 cells were treated with the indicated concentrations of AC220 and/or JQ1 for 24 hours. At the end of treatment, immunoblot analyses were conducted as indicated. The numbers beneath the blots represent densitometry analysis conducted on representative blots.
S1018	Dovitinib (TKI-258) Dovitinib (TKI258, CHIR258) is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGF-1R and HER2 in cell-free assays. Phase 4.	Cancer Res, 2021, canres.1780.2020 Nat Protoc, 2020, 10.1038/s41596-020-00412-1 Genome Med, 2020, 18;12(1):17	Orthotopic xenografts of HNSCC cell lines (A) SCC-1 and (B) OSC-19 were treated with dovitinib (20 mg/kg/day). In addition, the OSC-19 xenografts were treated with +/ radiation therapy. Marker, mean for triplicate; bars, SE. Statistical significance by unpaired t-test, p < 0.05.
S2736	Fedratinib (TG101348) Fedratinib (SAR302503, TG101348) is a selective inhibitor of JAK2 with IC50 of 3 nM in cell-free assays, 35- and 334-fold more selective for JAK2 versus JAK1 and JAK3. Fedratinib also inhibits FMS-like tyrosine kinase 3 (FLT3) and RET (c-RET) with IC50 of 15 nM and 48 nM, respectively. Fedratinib has potential antineoplastic activity. Fedratinib inhibits proliferation and induces apoptosis. Phase 2.	Cell, 2021, 184(2):334-351.e20 Int J Biol Macromol, 2021, 173:379-398 Cancer Biol Ther, 2021, 22(1):66-78	Colony-forming assay results showing that the Jak2 inhibitor TG101348 reduces CFU-GM colonies generated from mutant fetal liver R2 cells. Results from 4 independent control or mutant fetal livers treated with TG101348 or dimethylsulfoxide (DMSO) are shown (mean ?SD). ***P < .001.
S1003	Linifanib (ABT-869) Linifanib (ABT-869, AL39324, RG3635) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). Linifanib (ABT-869) induces autophagy and apoptosis. Phase 3.	Cancer Lett, 2021, 507:80-88 Cancer Lett, 2020, S0304-3835(20)30497-3 Cancers (Basel), 2020, 27;12(5)pii: E1087	(B and C) KMCH-1 cells were plated alone (monoculture) or together with PDGF-BB-secreting LX-2 cells (co-culture) in a transwell insert co-culture system (KMCH-1 cells in the bottom wells and LX-2 cells in the inserts; 1:1 ratio) for 2 days. Cells were treated as indicated with vehicle, rhTRAIL (10 ng/ml for 6 h on day 2), rhTRAIL plus imatinib [rhTRAIL:10 ng/ml for 6 h on day 2; Imatinib: 5 μmol/L for 24 h (day2)], or rhTRAIL plus linifanib [rhTRAIL: 10 ng/ml for 6 h on day 2; Linifanib:0.5 μmol/L for 24 h (day2)]. After rhTRAIL treatment for 6 h,KMCH-1 cells were analysed for apoptotic nuclear morphology by DAPI-staining (B) and for DNA fragmentation by transferasemediated dUTP nick end labelling assay (C) with quantification of apoptotic nuclei by fluorescence microscopy.
S2730	Crenolanib (CP-868596) Crenolanib (CP-868596, ARO 002) is a potent and selective inhibitor of PDGFRα/β with K_d of 2.1 nM/3.2 nM in CHO cells, also potently inhibits FLT3, sensitive to D842V mutation not V561D mutation, >100-fold more selective for PDGFR than c-Kit, VEGFR-2, TIE-2, FGFR-2, EGFR, erbB2, and Src. Crenolanib helps to induce mitophagy.	Cells, 2021, 10(4)804 Stem Cell Rev Rep, 2021, 10.1007/s12015-021-10156-4 Nature, 2020, 584(7822):608-613	Western blot analysis using 4G10 and anti-FLT3 antibody after immunoprecipitation with anti-FLT3 antibody and Western blot analysis of phospho-ERK (pERK) and ERK performed on whole cell lysates from HB119 and Molm14 cells. Cells were exposed to 100 nM crenolanib for 60 min.
S2198	SGI-1776 free base SGI-1776 free base is a novel ATP competitive inhibitor of Pim1 with IC50 of 7 nM in a cell-free assay, 50- and 10-fold selective versus Pim2 and Pim3, also potent to Flt3 and haspin. SGI-1776 induces apoptosis and autophagy. Phase 1.	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Haematologica, 2020, 28;haematol.2019.223529	VCaP cells were steroid starved overnight then treated with 10nM R1881 and PIM kinase inhibitor SGI-1776 as indicated for 4 hours. Total protein lysates were analyzed by Western blot with antibodies against P-AR S213, AR (total), P-4EBP1 Thr 37/46, and tubulin.
S1533	R406 (free base) R406 (free base) is a potent Syk inhibitor with IC50 of 41 nM in a cell-free assay, strongly inhibits Syk but not Lyn, 5-fold less potent to Flt3. R406 (free base) triggers apoptosis. Phase 1.	Nat Genet, 2021, 53(4):500-510 Cell Rep, 2021, 34(3):108627 Cell Rep, 2020, 5;31(5):107585	(C) Z-138 and JEKO-1 cells were simultaneously exposed to sorafenib and R406 at the indicated doses, and cell viability was determined at 48 hours by annexin V/PI staining. Bars represent the mean ± SD of 3 independent experiments. CI value is indicated for each combination. (D) Primary MCL cells from 7 patients were simultaneously exposed to sorafenib and R406 at the indicated doses for 48 hours, and cell viability was determined as above. Bars represent the mean ± SEM of all the samples analyzed. CI value is indicated for each combination.
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Amuvatinib suppresses c-MET and c-RET. Amuvatinib is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Hum Cell, 2020, 10.1007/s13577-020-00420-z PLoS Genet, 2016, 12(9):e1006279 Oncotarget, 2016, 7(15):19620-30	Inactivation of AXL by MP470 reverses epithelial to mesenchymal transition. Immunoblot analyses of lysates from TGFβ/TNFα- treated MCF10A cells treated with varying amounts of MP470 for 72 hours.
S1043	Tandutinib (MLN518) Tandutinib (MLN518, CT53518, NSC726292) is a potent FLT3 antagonist with IC50 of 0.22 μM, also inhibits PDGFR and c-Kit, 15 to 20-fold higher potency for FLT3 versus CSF-1R and >100-fold selectivity for the same target versus FGFR, EGFR and KDR. Phase 2.	Drug Metab Dispos, 2021, 49(1):53-61 Genome Med, 2020, 18;12(1):17 Cell Rep, 2019, 28(9):2331-2344
S2692	TG101209 TG101209 is a selective JAK2 inhibitor with IC50 of 6 nM, less potent to Flt3 and RET (c-RET) with IC50 of 25 nM and 17 nM in cell-free assays, ~30-fold selective for JAK2 than JAK3, sensitive to JAK2V617F and MPLW515L/K mutations.	Carcinogenesis, 2020, 41(7):993-1004 Cancer Sci, 2020, 112(1):133-143 Exp Neurol, 2020, S0014-4886(20)30337-X	EGFR-ERCC1 effect on survival. QGP1 cells were transfected with Scrambled, ERCC1, EGFR, or EGFR-ERCC1 siRNA. Following 48 hours of siRNA transfection, Scrambled siRNA and ERCC1 siRNA-transfected cells were treated with 1 umol/L gefitinib or 125 nmol/L NU7026 (DNAPK inhibitor), or both, while EGFR siRNA and EGFR-ERCC1 siRNA-transfected cells were treated with 125 nmol/L of NU7026 1 hour prior 4 Gy IR treatment. Survival of these cells was then assessed 72 hours following IR treatment via MTT assay. The graphs show percentage of survival from 3 independent experiments as compared with untreated control. Bars show SD. Asterisks show statistical significance (,P < 0.05; , P < 0.01; **, P < 0.001; NS, nonsignificant).
S2158	KW-2449 KW-2449 is a multiple-targeted inhibitor, mostly for Flt3 with IC50 of 6.6 nM, modestly potent to FGFR1, Bcr-Abl and Aurora A; little effect on PDGFRβ, IGF-1R, EGFR. Phase 1.	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Molecules, 2020, 8;25(9) pii: E2220	Western blot analysis of p-histone and histone. 0-10μM KW2449 was added.
S1181	ENMD-2076 ENMD-2076 has selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold selective for Aurora A than over Aurora B and less potent to RET, SRC, NTRK1/TRKA, CSF1R/FMS, VEGFR2/KDR, FGFR and PDGFRα. ENMD-2076 inhibits the growth of a wide range of human solid tumor and hematopoietic cancer cell lines with IC50 from 0.025 to 0.7 μM, which induces apoptosis and G2/M phase arrest. Phase 2.	Cell, 2021, 184(2):334-351.e20 Sci Adv, 2021, 7(4)eabd7851 J Pediatr Hematol Oncol, 2019, 41(6):e359-e370	Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of ENMD-2076.
S7083	Ceritinib (LDK378) Ceritinib (LDK378) is potent inhibitor against ALK with IC50 of 0.2 nM in cell-free assays. Ceritinib (LDK378) also inhibits IGF-1R, InsR, STK22D and FLT3 with IC50 of 8 nM, 7 nM, 23 nM and 60 nM, respectively. Phase 3.	Cereb Cortex, 2021, bhab058 Sci Rep, 2021, 11(1):9011 Jpn J Clin Oncol, 2021, hyab048	Quantitation of crystal violet uptake by ORF-expressing cells exposed to crizotinib (CRZ) or ceritinib (CER) normalized to Lac Z. Mean and SE are shown for six (CRZ) or four (CER) independent experiments of three replicates each.
S8032	PRT062607 (P505-15) HCl PRT062607 (P505-15, BIIB057, PRT-2607) is a novel, highly selective Syk inhibitor with IC50 of 1 nM in cell-free assays, >80-fold selective for Syk than Fgr, PAK5, Lyn, FAK, Pyk2, FLT3, MLK1 and Zap70.	Mol Cell, 2021, S1097-2765(21)00264-1 Biochem Pharmacol, 2021, S0006-2952(21)00185-4 Nat Neurosci, 2020, 8	Dectin-1 is involved in activation of NLRP3-inflammasome by Malassezia spp. IL-1b secretion from mature human mono-DCs incubated with Syk-inhibitors (piceatannol, R406 or P505), 1 h prior to exposure to medium, MSU, b-glucan, nigericin or live M. furfur (MOI = 10) was determined after 6 h by ELISA.
S7397	Sorafenib (BAY 43-9006) Sorafenib (BAY 43-9006, NSC-724772) is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Genome Biol, 2021, 22(1):41 Nat Chem Biol, 2021, 10.1038/s41589-021-00751-4 Theranostics, 2021, 11(12):5650-5674	Involvement of EV linc-VLDLR in tumor cell responses to chemotherapy. Cells were incubated with sorafenib, camptothecin, or doxorubicin. EVs were obtained after 24 hours, and qRT-PCR was performed for linc-VLDLR. The bars represent the mean ?SEM of the increase in cell viability from 3 independent studies. *, P < 0.05.
S8057	Pacritinib (SB1518) Pacritinib (SB1518) is a potent and selective inhibitor of Janus Kinase 2 (JAK2) and Fms-Like Tyrosine Kinase-3 (FLT3) with IC50s of 23 and 22 nM in cell-free assays, respectively. Phase 3.	Cancer Res, 2021, canres.2125.2020 Leukemia, 2020, 10.1038/s41375-020-01077-1 Am J Transplant, 2020, 10.1111/ajt.16071	Phosphorylation of the CSF-1R targets indicated was examined by immunoblotting
S4001	Cabozantinib malate (XL184) Cabozantinib malate (XL184) is the malate of Cabozantinib, a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret (c-Ret), Kit (c-Kit), Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively. Cabozantinib malate (XL184) induces apoptosis.	J Clin Endocrinol Metab, 2021, dgab020 Front Oncol, 2021, 11:663517 Cancer Gene Ther, 2021, 10.1038/s41417-021-00329-1	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive control.
S8023	TCS 359 TCS 359 is a potent FLT3 inhibitor with IC50 of 42 nM.	Nat Commun, 2021, 12(1):2148 Blood, 2016, 127(23):2890-90
S2018	ENMD-2076 L-(+)-Tartaric acid ENMD-2076 L-(+)-Tartaric acid is the tartaric acid of ENMD-2076, selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold more selective for Aurora A than Aurora B and less potent to VEGFR2/KDR and VEGFR3, FGFR1 and FGFR2 and PDGFRα. Phase 2.		Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of ENMD-2076.
S7765	Dovitinib (TKI258) Lactate Dovitinib (TKI258, CHIR258) Lactate is the Lactate of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.	Cancer Res, 2021, canres.1780.2020 Genome Med, 2020, 18;12(1):17 Cell Oncol (Dordr), 2020, 10.1007/s13402-020-00562-0	(c) Percent survival for the AGS cancer cell line is shown with FGFR2 inhibitors of varying specificity. (d) The KatoIII diffuse gastric cancer cell line was treated with FGFR2 inhibitors of varying specificity. The Y-axis depicts percent survival versus the X-axis with log concentrations. In all panels, error bars represent standard error of the mean. The difference in percent cell survival between KatoIII and AGS cells was statistically significant (P <0.05) at the three highest concentrations of all drugs, except Brivanib which was only significant at the highest concentration.
S7576	UNC2025 HCl UNC-2025 HCl is a potent and orally bioavailable dual MER/FLT3 inhibitor with IC50 of 0.74 nM and 0.8 nM, respectively, about 20-fold selectivity over Axl and Tyro3.	Front Immunol, 2020, 11:564133 Nat Commun, 2020, 11(1):3521 Nat Biomed Eng, 2018, 2(8):578-588
S0278	SU5614 SU5614 (Chloro-SU5416, Chloro-Semaxanib) is a small molecule receptor tyrosine kinases (RTK) inhibitor of VEGFR-2, c-kit, and both wild-type and mutant FLT3. SU5614 reduces cell proliferation and induces apoptosis.
S7014	Merestinib (LY2801653) Merestinib (LY2801653) is a type-II ATP competitive, slow-off inhibitor of Met (c-Met) tyrosine kinase with a dissociation constant (Ki) of 2 nM, a pharmacodynamic residence time (Koff) of 0.00132 min(-1) and t1/2 of 525 min. Merestinib (LY2801653) also inhibits MST1R, AXL, ROS1, MKNK1/2, FLT3, MERTK, DDR1 and DDR2 with IC50 of 11 nM, 2 nM, 23 nM, 7 nM, 7 nM, 10 nM, 0.1 nM and 7 nM, respectively.	Front Oncol, 2020, 12;10:700 Cancer Commun (Lond), 2020, 11 J Thorac Oncol, 2019, 14(10):1753-1765
S6662	AST-487 (NVP-AST487) AST-487 (NVP-AST487), a N,N'-diphenyl urea,is an ATP competitive inhibitor of Flt3 with ki of 0.12 μM.Besides FLT3, AST487 also inhibits RET,KDR,c-KIT,and c-ABL kinase with IC50 values below 1 μM.	Nat Commun, 2020, 21;11(1):1924
S9275	Isoguanosine Isoguanosine (Crotonoside) inhibits FLT3 and HDAC3/6 for the treatment of AML.Isoguanosine is a naturally occurring active isomer of guanosine that is found in the seeds of Croton tiglium.
S8442	TAK-659 TAK-659 is a potent and selective inhibitor of spleen tyrosine kinase (SYK) with an IC50 value of 3.2 nM. It is selective against most other kinases, but potent toward both SYK and FLT3.	[email protected], 2020, 51
S8229	Brigatinib (AP26113) Brigatinib (AP26113) is a potent and selective ALK (IC50, 0.6 nM) and ROS1 (IC50, 0.9 nM) inhibitor. It also inhibits IGF-1R, FLT3, and mutant variants of FLT3 (D835Y) and EGFR with lower potentcy.	EMBO J, 2021, e105784 Sci Signal, 2020, 26;13(633):eaba3176 Oncol Rep, 2020, 44(6):2581-2594	Immunoblotting analysis of H3122 and H3122-CER cells showing that brigatinib did not inhibit EGFR phosphorylation (p-EGFR). Total EGFR (t-EGFR) is also shown. Actin was used as a loading control. The cells were treated with brigatinib for 2 hours.
S7545	G-749 G-749 is a novel and potent FLT3 inhibitor with IC50 of 0.4 nM, 0.6 nM and 1 nM for FLT3 (WT), FLT3 (D835Y), and Mer, respectively, showing lower potency against other tyrosine kinases.
S1099	SKLB4771 (FLT3-IN-1) SKLB4771 is a potent and selective inhibitor of human receptor-type tyrosine-protein kinase FLT3 with IC50 of 10 nM.
S7754	Gilteritinib (ASP2215) Gilteritinib (ASP2215) is a small-molecule FLT3/AXL inhibitor with IC50 values of 0.29 nM and 0.73 nM for FLT3 and AXL, respectively. It inhibits FLT3 at an IC50 value that was approximately 800-fold more potent than the concentration required to inhibit c-KIT (230 nM).	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Sci Adv, 2020, 22;6(21):eaaz8521
S7003	AZD2932 AZD2932 is a potent and mutil-targeted protein tyrosine kinase inhibitor with IC50 of 8 nM, 4 nM, 7 nM, and 9 nM for VEGFR-2, PDGFRβ, Flt-3, and c-Kit, respectively.	Cancer Res, 2020, canres.1992.2020 Molecules, 2020, 8;25(9) pii: E2220 Development, 2016, 143(23):4394-4404
S7818	Pexidartinib (PLX3397) Pexidartinib (PLX3397) is an oral, potent mutil-targeted receptor tyrosine kinase inhibitor of CSF-1R, Kit (c-Kit), and FLT3 with IC50 of 20 nM, 10 nM and 160 nM, respectively. Pexidartinib (PLX3397) induces apoptosis and necrosis with antitumor activity. Phase 3.	Brain, 2021, awab122 J Neuroinflammation, 2021, 18(1):4 J Inflamm Res, 2021, 14:1341-1356	(a) Reduced tumour burden in PLX3397 (PLX) treated mice relative to untreated (NT) (n=6, P=.015; unpaired t-test). Bars represent total tumour volume with number of identified tumours indicated above each bar.
S7119	Go6976 Go6976 (PD406976) is a potent PKC inhibitor with IC50 of 7.9 nM, 2.3 nM, and 6.2 nM for PKC (Rat brain), PKCα, and PKCβ1, respectively. Also a potent inhibitor of JAK2 and Flt3.	Biochimie, 2021, 184:8-17 J Cell Physiol, 2020, 10.1002/jcp.30207 Front Pharmacol, 2020, 10:1589	Erk5 activation depends on Mek5, classical PKC and Mek1/2. MOVAS cells were serum-starved overnight and then treated for 1 h if not indicated otherwise with inhibitors targeting Jnk (SP600125, 10 μM), p38 (SB203580, 10 μM), Mek1/2 (CI-1040, 3 μM), Jak2 (AG490, 10 μM), Src (SU6656, 0.5 μM), Go6983 (PKC, 1 μM), Gö6976 (classical PKC, 1 μM), proteasomes (MG132, 25 μM), TPA (100 ng/ml for 15 min to activate PKCs or overnight to inhibit) and Mek5 (BIX02189, 1 μM), as well as Ca2 + chelators (EDTA, 2 mM; BAPTA-AM, 10 μM; both with 30 min preincubation), followed by stimulation with 20 ng/ml PDGF-BB for 10 min. Total cell lysates (TCL) were prepared and subjected to SDS-PAGE. Erk5 and PDGFRβ activities were measured by band shift and Tyr857 phosphorylation, respectively, using immunoblotting. Panel E and G show representative immunoblots.
S7533	AMG 925 AMG 925 is a potent and orally bioavailable dual FLT3/CDK4 inhibitor with IC50 of 1 nM and 3 nM, respectively.	Molecules, 2020, 8;25(9) pii: E2220

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S1040	Sorafenib (BAY 43-9006) tosylate Sorafenib (BAY 43-9006) tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib Tosylate inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib Tosylate induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Theranostics, 2021, 11(12):5650-5674 J Clin Med, 2021, 10(9)1889 Cell Biol Toxicol, 2021, 10.1007/s10565-021-09607-y	Inhibition of breast cancer cell growth using sorafenib. MCF-7 breast cancer cells were treated with increasing concentrations of sorafenib for 5 days. Cell number was measured using a colorimetric growth assay (crystal violet stain) and expressed relative to DMSO treated control cells.
S1048	Tozasertib (VX-680, MK-0457) Tozasertib (VX-680, MK-0457) is a pan-Aurora inhibitor, mostly against Aurora A with K_i_app of 0.6 nM in a cell-free assay, less potent towards Aurora B/Aurora C and 100-fold more selective for Aurora A than 55 other kinases. The only exceptions are Fms-related tyrosine kinase-3 (FLT-3) and BCR-ABL tyrosine kinase, which are inhibited by the Tozasertib with both Ki of 30 nM. Tozasertib induces apoptosis and autophagy. Phase 2.	J Cell Biol, 2021, 220(2)e202008029 PLoS Biol, 2021, 19(1):e3001029 Breast Cancer, 2021, 10.1007/s12282-021-01242-z	Senescence induction upon PKCι depletion combined with aurora kinase inhibition. ( a) MCF7 cells were transfected as above to deplete PKCι . Two days after transfection, cells were treated for the indicated time period with 400 n M VX-680. Medium with VX-680 was then removed and fresh medium was added. Cells were stained for SA-b -gal activity 5 days after the start of transfection.* indicates a P value <0.05. ( b) MCF7 cells were treated as above. Five days after transfection, cells were fixed and assessed for the presence of gH2AX foci by immunofluorescence microscopy. (c, d) MCF7 cells were treated with dimethyl sulfoxide (DMSO) control or 400 n M VX-680 for the indicated time periods. Total cell lysates were then analyzed by western blotting for levels of p21 and GAPDH (as loading control). A representative blot is shown in panel c. Quantitation of changes in p21 levels (normalized to vehicle-treated controls) is shown in panel d. The data shown are the means ±s.e. of three independent experiments.
S1460	SP600125 SP600125 (Nsc75890) is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. SP600125 is also a broad‐spectrum inhibitor of serine/threonine kinases including Aurora kinase A，FLT3 and TRKA with of IC50 of 60 nM, 90 nM and 70 nM. SP600125 inhibits autophagy and activates apoptosis.	Theranostics, 2021, 11(9):4335-4350 EBioMedicine, 2021, 66:103290 Cancer Lett, 2021, 509:13-25	Loss of DUSP4 function upregulates IL-6 and IL-8 and enhances mammosphere growth. Immunoblot analysis of MDA-231 cells after treatment of 24 hours with 1 umol/L selumetinib (MEKi) or 10 umol/L SP600125 (JNKi). I, MDA-231 mammosphere formation quantitated by GelCount software 7 days after siRNA transfection. Where indicated, selumetinib (MEKi) or SP600125 (JNK1) or the combination was added to the mammosphere cultures.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089, EXEL-2880, XL-880, GSK089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-Met) and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Cancers (Basel), 2021, 13(3)E372 Angiogenesis, 2021, 10.1007/s10456-021-09771-z Sci Adv, 2020, 22;6(21):eaaz8521	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. Cell growth was determined using the sulforhodamine B assay. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, and TAE-684I. The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
S2194	R406 R406 is a potent Syk inhibitor with IC50 of 41 nM in cell-free assays, strongly inhibits Syk but not Lyn, 5-fold less potent to Flt3. R406 induces apoptosis. Phase 1.	Cell Rep, 2021, 34(11):108870 J Leukoc Biol, 2021, 10.1002/JLB.2A0520-334R J Biol Chem, 2021, S0021-9258(21)00238-6	Platelets (3 x 10⁸/mL) were preincubated with Y27632 (10 uM), R406 (1 uM), or a combination of Y27632 and R406 for 20 minutes followed by stimulation with oxLDL (50 ug/mL) for 15 seconds and lysis. Samples were then separated by SDS-PAGE and were immunoblotted for phospho-MLCSer19, followed by reprobing for β-tubulin. (Fi) Representative blots. (Fii) Densitometric analysis of 3 independent experiments. *P < .05. Data are presented as mean ± SEM. Experiments were carried out in the presence of apyrase (2 U/mL), indomethacin (10 uM), and EGTA (1 mM).
S6839^新	MRX-2843 MRX-2843 (UNC2371) is an orally active dual inhibitor of tyrosine kinases MERTK and FLT3 with IC50 of 1.3 nM and 0.64 nM, respectively.
S9662^新	UNC2025 UNC2025 is a potent and orally active dual inhibitor of FLT3 and MER with IC50 of 0.35 nM and 0.46 nM, respectively. UNC2025 also inhibits AXL, TRKA, TRKC, QIK, TYRO3, SLK, NuaK1, Kit (c-Kit) and Met (c-Met) with IC50 of 1.65 nM, 1.67 nM, 4.38 nM, 5.75 nM, 5.83 nM, 6.14 nM, 7.97 nM, 8.18 nM and 364 nM, respectively.	Front Immunol, 2020, 11:564133
S1526	Quizartinib (AC220) Quizartinib (AC220) is a second-generation FLT3 inhibitor for Flt3(ITD/WT) with IC50 of 1.1 nM/4.2 nM in MV4-11 and RS4;11 cells, respectively, 10-fold more selective for Flt3 than KIT, PDGFRα, PDGFRβ, RET, and CSF-1R. Quizartinib (AC220) induces apoptosis of tumor cells. Phase 3.	Autophagy, 2021, 1-10 Blood Cancer J, 2021, 11(3):57 Cancer Discov, 2021, candisc.0738.2020	Cotreatment with JQ1 and AC220 synergistically induces apoptosis of FLT3-ITD–expressing AML cells. MV4-11 cells were treated with the indicated concentrations of AC220 and/or JQ1 for 24 hours. At the end of treatment, immunoblot analyses were conducted as indicated. The numbers beneath the blots represent densitometry analysis conducted on representative blots.
S1018	Dovitinib (TKI-258) Dovitinib (TKI258, CHIR258) is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGF-1R and HER2 in cell-free assays. Phase 4.	Cancer Res, 2021, canres.1780.2020 Nat Protoc, 2020, 10.1038/s41596-020-00412-1 Genome Med, 2020, 18;12(1):17	Orthotopic xenografts of HNSCC cell lines (A) SCC-1 and (B) OSC-19 were treated with dovitinib (20 mg/kg/day). In addition, the OSC-19 xenografts were treated with +/ radiation therapy. Marker, mean for triplicate; bars, SE. Statistical significance by unpaired t-test, p < 0.05.
S2736	Fedratinib (TG101348) Fedratinib (SAR302503, TG101348) is a selective inhibitor of JAK2 with IC50 of 3 nM in cell-free assays, 35- and 334-fold more selective for JAK2 versus JAK1 and JAK3. Fedratinib also inhibits FMS-like tyrosine kinase 3 (FLT3) and RET (c-RET) with IC50 of 15 nM and 48 nM, respectively. Fedratinib has potential antineoplastic activity. Fedratinib inhibits proliferation and induces apoptosis. Phase 2.	Cell, 2021, 184(2):334-351.e20 Int J Biol Macromol, 2021, 173:379-398 Cancer Biol Ther, 2021, 22(1):66-78	Colony-forming assay results showing that the Jak2 inhibitor TG101348 reduces CFU-GM colonies generated from mutant fetal liver R2 cells. Results from 4 independent control or mutant fetal livers treated with TG101348 or dimethylsulfoxide (DMSO) are shown (mean ?SD). ***P < .001.
S1003	Linifanib (ABT-869) Linifanib (ABT-869, AL39324, RG3635) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). Linifanib (ABT-869) induces autophagy and apoptosis. Phase 3.	Cancer Lett, 2021, 507:80-88 Cancer Lett, 2020, S0304-3835(20)30497-3 Cancers (Basel), 2020, 27;12(5)pii: E1087	(B and C) KMCH-1 cells were plated alone (monoculture) or together with PDGF-BB-secreting LX-2 cells (co-culture) in a transwell insert co-culture system (KMCH-1 cells in the bottom wells and LX-2 cells in the inserts; 1:1 ratio) for 2 days. Cells were treated as indicated with vehicle, rhTRAIL (10 ng/ml for 6 h on day 2), rhTRAIL plus imatinib [rhTRAIL:10 ng/ml for 6 h on day 2; Imatinib: 5 μmol/L for 24 h (day2)], or rhTRAIL plus linifanib [rhTRAIL: 10 ng/ml for 6 h on day 2; Linifanib:0.5 μmol/L for 24 h (day2)]. After rhTRAIL treatment for 6 h,KMCH-1 cells were analysed for apoptotic nuclear morphology by DAPI-staining (B) and for DNA fragmentation by transferasemediated dUTP nick end labelling assay (C) with quantification of apoptotic nuclei by fluorescence microscopy.
S2730	Crenolanib (CP-868596) Crenolanib (CP-868596, ARO 002) is a potent and selective inhibitor of PDGFRα/β with K_d of 2.1 nM/3.2 nM in CHO cells, also potently inhibits FLT3, sensitive to D842V mutation not V561D mutation, >100-fold more selective for PDGFR than c-Kit, VEGFR-2, TIE-2, FGFR-2, EGFR, erbB2, and Src. Crenolanib helps to induce mitophagy.	Cells, 2021, 10(4)804 Stem Cell Rev Rep, 2021, 10.1007/s12015-021-10156-4 Nature, 2020, 584(7822):608-613	Western blot analysis using 4G10 and anti-FLT3 antibody after immunoprecipitation with anti-FLT3 antibody and Western blot analysis of phospho-ERK (pERK) and ERK performed on whole cell lysates from HB119 and Molm14 cells. Cells were exposed to 100 nM crenolanib for 60 min.
S2198	SGI-1776 free base SGI-1776 free base is a novel ATP competitive inhibitor of Pim1 with IC50 of 7 nM in a cell-free assay, 50- and 10-fold selective versus Pim2 and Pim3, also potent to Flt3 and haspin. SGI-1776 induces apoptosis and autophagy. Phase 1.	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Haematologica, 2020, 28;haematol.2019.223529	VCaP cells were steroid starved overnight then treated with 10nM R1881 and PIM kinase inhibitor SGI-1776 as indicated for 4 hours. Total protein lysates were analyzed by Western blot with antibodies against P-AR S213, AR (total), P-4EBP1 Thr 37/46, and tubulin.
S1533	R406 (free base) R406 (free base) is a potent Syk inhibitor with IC50 of 41 nM in a cell-free assay, strongly inhibits Syk but not Lyn, 5-fold less potent to Flt3. R406 (free base) triggers apoptosis. Phase 1.	Nat Genet, 2021, 53(4):500-510 Cell Rep, 2021, 34(3):108627 Cell Rep, 2020, 5;31(5):107585	(C) Z-138 and JEKO-1 cells were simultaneously exposed to sorafenib and R406 at the indicated doses, and cell viability was determined at 48 hours by annexin V/PI staining. Bars represent the mean ± SD of 3 independent experiments. CI value is indicated for each combination. (D) Primary MCL cells from 7 patients were simultaneously exposed to sorafenib and R406 at the indicated doses for 48 hours, and cell viability was determined as above. Bars represent the mean ± SEM of all the samples analyzed. CI value is indicated for each combination.
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Amuvatinib suppresses c-MET and c-RET. Amuvatinib is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Hum Cell, 2020, 10.1007/s13577-020-00420-z PLoS Genet, 2016, 12(9):e1006279 Oncotarget, 2016, 7(15):19620-30	Inactivation of AXL by MP470 reverses epithelial to mesenchymal transition. Immunoblot analyses of lysates from TGFβ/TNFα- treated MCF10A cells treated with varying amounts of MP470 for 72 hours.
S1043	Tandutinib (MLN518) Tandutinib (MLN518, CT53518, NSC726292) is a potent FLT3 antagonist with IC50 of 0.22 μM, also inhibits PDGFR and c-Kit, 15 to 20-fold higher potency for FLT3 versus CSF-1R and >100-fold selectivity for the same target versus FGFR, EGFR and KDR. Phase 2.	Drug Metab Dispos, 2021, 49(1):53-61 Genome Med, 2020, 18;12(1):17 Cell Rep, 2019, 28(9):2331-2344
S2692	TG101209 TG101209 is a selective JAK2 inhibitor with IC50 of 6 nM, less potent to Flt3 and RET (c-RET) with IC50 of 25 nM and 17 nM in cell-free assays, ~30-fold selective for JAK2 than JAK3, sensitive to JAK2V617F and MPLW515L/K mutations.	Carcinogenesis, 2020, 41(7):993-1004 Cancer Sci, 2020, 112(1):133-143 Exp Neurol, 2020, S0014-4886(20)30337-X	EGFR-ERCC1 effect on survival. QGP1 cells were transfected with Scrambled, ERCC1, EGFR, or EGFR-ERCC1 siRNA. Following 48 hours of siRNA transfection, Scrambled siRNA and ERCC1 siRNA-transfected cells were treated with 1 umol/L gefitinib or 125 nmol/L NU7026 (DNAPK inhibitor), or both, while EGFR siRNA and EGFR-ERCC1 siRNA-transfected cells were treated with 125 nmol/L of NU7026 1 hour prior 4 Gy IR treatment. Survival of these cells was then assessed 72 hours following IR treatment via MTT assay. The graphs show percentage of survival from 3 independent experiments as compared with untreated control. Bars show SD. Asterisks show statistical significance (,P < 0.05; , P < 0.01; **, P < 0.001; NS, nonsignificant).
S2158	KW-2449 KW-2449 is a multiple-targeted inhibitor, mostly for Flt3 with IC50 of 6.6 nM, modestly potent to FGFR1, Bcr-Abl and Aurora A; little effect on PDGFRβ, IGF-1R, EGFR. Phase 1.	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Molecules, 2020, 8;25(9) pii: E2220	Western blot analysis of p-histone and histone. 0-10μM KW2449 was added.
S1181	ENMD-2076 ENMD-2076 has selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold selective for Aurora A than over Aurora B and less potent to RET, SRC, NTRK1/TRKA, CSF1R/FMS, VEGFR2/KDR, FGFR and PDGFRα. ENMD-2076 inhibits the growth of a wide range of human solid tumor and hematopoietic cancer cell lines with IC50 from 0.025 to 0.7 μM, which induces apoptosis and G2/M phase arrest. Phase 2.	Cell, 2021, 184(2):334-351.e20 Sci Adv, 2021, 7(4)eabd7851 J Pediatr Hematol Oncol, 2019, 41(6):e359-e370	Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of ENMD-2076.
S7083	Ceritinib (LDK378) Ceritinib (LDK378) is potent inhibitor against ALK with IC50 of 0.2 nM in cell-free assays. Ceritinib (LDK378) also inhibits IGF-1R, InsR, STK22D and FLT3 with IC50 of 8 nM, 7 nM, 23 nM and 60 nM, respectively. Phase 3.	Cereb Cortex, 2021, bhab058 Sci Rep, 2021, 11(1):9011 Jpn J Clin Oncol, 2021, hyab048	Quantitation of crystal violet uptake by ORF-expressing cells exposed to crizotinib (CRZ) or ceritinib (CER) normalized to Lac Z. Mean and SE are shown for six (CRZ) or four (CER) independent experiments of three replicates each.
S8032	PRT062607 (P505-15) HCl PRT062607 (P505-15, BIIB057, PRT-2607) is a novel, highly selective Syk inhibitor with IC50 of 1 nM in cell-free assays, >80-fold selective for Syk than Fgr, PAK5, Lyn, FAK, Pyk2, FLT3, MLK1 and Zap70.	Mol Cell, 2021, S1097-2765(21)00264-1 Biochem Pharmacol, 2021, S0006-2952(21)00185-4 Nat Neurosci, 2020, 8	Dectin-1 is involved in activation of NLRP3-inflammasome by Malassezia spp. IL-1b secretion from mature human mono-DCs incubated with Syk-inhibitors (piceatannol, R406 or P505), 1 h prior to exposure to medium, MSU, b-glucan, nigericin or live M. furfur (MOI = 10) was determined after 6 h by ELISA.
S7397	Sorafenib (BAY 43-9006) Sorafenib (BAY 43-9006, NSC-724772) is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Genome Biol, 2021, 22(1):41 Nat Chem Biol, 2021, 10.1038/s41589-021-00751-4 Theranostics, 2021, 11(12):5650-5674	Involvement of EV linc-VLDLR in tumor cell responses to chemotherapy. Cells were incubated with sorafenib, camptothecin, or doxorubicin. EVs were obtained after 24 hours, and qRT-PCR was performed for linc-VLDLR. The bars represent the mean ?SEM of the increase in cell viability from 3 independent studies. *, P < 0.05.
S8057	Pacritinib (SB1518) Pacritinib (SB1518) is a potent and selective inhibitor of Janus Kinase 2 (JAK2) and Fms-Like Tyrosine Kinase-3 (FLT3) with IC50s of 23 and 22 nM in cell-free assays, respectively. Phase 3.	Cancer Res, 2021, canres.2125.2020 Leukemia, 2020, 10.1038/s41375-020-01077-1 Am J Transplant, 2020, 10.1111/ajt.16071	Phosphorylation of the CSF-1R targets indicated was examined by immunoblotting
S4001	Cabozantinib malate (XL184) Cabozantinib malate (XL184) is the malate of Cabozantinib, a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret (c-Ret), Kit (c-Kit), Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively. Cabozantinib malate (XL184) induces apoptosis.	J Clin Endocrinol Metab, 2021, dgab020 Front Oncol, 2021, 11:663517 Cancer Gene Ther, 2021, 10.1038/s41417-021-00329-1	Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive control.
S8023	TCS 359 TCS 359 is a potent FLT3 inhibitor with IC50 of 42 nM.	Nat Commun, 2021, 12(1):2148 Blood, 2016, 127(23):2890-90
S2018	ENMD-2076 L-(+)-Tartaric acid ENMD-2076 L-(+)-Tartaric acid is the tartaric acid of ENMD-2076, selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold more selective for Aurora A than Aurora B and less potent to VEGFR2/KDR and VEGFR3, FGFR1 and FGFR2 and PDGFRα. Phase 2.		Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of ENMD-2076.
S7765	Dovitinib (TKI258) Lactate Dovitinib (TKI258, CHIR258) Lactate is the Lactate of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.	Cancer Res, 2021, canres.1780.2020 Genome Med, 2020, 18;12(1):17 Cell Oncol (Dordr), 2020, 10.1007/s13402-020-00562-0	(c) Percent survival for the AGS cancer cell line is shown with FGFR2 inhibitors of varying specificity. (d) The KatoIII diffuse gastric cancer cell line was treated with FGFR2 inhibitors of varying specificity. The Y-axis depicts percent survival versus the X-axis with log concentrations. In all panels, error bars represent standard error of the mean. The difference in percent cell survival between KatoIII and AGS cells was statistically significant (P <0.05) at the three highest concentrations of all drugs, except Brivanib which was only significant at the highest concentration.
S7576	UNC2025 HCl UNC-2025 HCl is a potent and orally bioavailable dual MER/FLT3 inhibitor with IC50 of 0.74 nM and 0.8 nM, respectively, about 20-fold selectivity over Axl and Tyro3.	Front Immunol, 2020, 11:564133 Nat Commun, 2020, 11(1):3521 Nat Biomed Eng, 2018, 2(8):578-588
S0278	SU5614 SU5614 (Chloro-SU5416, Chloro-Semaxanib) is a small molecule receptor tyrosine kinases (RTK) inhibitor of VEGFR-2, c-kit, and both wild-type and mutant FLT3. SU5614 reduces cell proliferation and induces apoptosis.
S7014	Merestinib (LY2801653) Merestinib (LY2801653) is a type-II ATP competitive, slow-off inhibitor of Met (c-Met) tyrosine kinase with a dissociation constant (Ki) of 2 nM, a pharmacodynamic residence time (Koff) of 0.00132 min(-1) and t1/2 of 525 min. Merestinib (LY2801653) also inhibits MST1R, AXL, ROS1, MKNK1/2, FLT3, MERTK, DDR1 and DDR2 with IC50 of 11 nM, 2 nM, 23 nM, 7 nM, 7 nM, 10 nM, 0.1 nM and 7 nM, respectively.	Front Oncol, 2020, 12;10:700 Cancer Commun (Lond), 2020, 11 J Thorac Oncol, 2019, 14(10):1753-1765
S6662	AST-487 (NVP-AST487) AST-487 (NVP-AST487), a N,N'-diphenyl urea,is an ATP competitive inhibitor of Flt3 with ki of 0.12 μM.Besides FLT3, AST487 also inhibits RET,KDR,c-KIT,and c-ABL kinase with IC50 values below 1 μM.	Nat Commun, 2020, 21;11(1):1924
S9275	Isoguanosine Isoguanosine (Crotonoside) inhibits FLT3 and HDAC3/6 for the treatment of AML.Isoguanosine is a naturally occurring active isomer of guanosine that is found in the seeds of Croton tiglium.
S8442	TAK-659 TAK-659 is a potent and selective inhibitor of spleen tyrosine kinase (SYK) with an IC50 value of 3.2 nM. It is selective against most other kinases, but potent toward both SYK and FLT3.	[email protected], 2020, 51
S8229	Brigatinib (AP26113) Brigatinib (AP26113) is a potent and selective ALK (IC50, 0.6 nM) and ROS1 (IC50, 0.9 nM) inhibitor. It also inhibits IGF-1R, FLT3, and mutant variants of FLT3 (D835Y) and EGFR with lower potentcy.	EMBO J, 2021, e105784 Sci Signal, 2020, 26;13(633):eaba3176 Oncol Rep, 2020, 44(6):2581-2594	Immunoblotting analysis of H3122 and H3122-CER cells showing that brigatinib did not inhibit EGFR phosphorylation (p-EGFR). Total EGFR (t-EGFR) is also shown. Actin was used as a loading control. The cells were treated with brigatinib for 2 hours.
S7545	G-749 G-749 is a novel and potent FLT3 inhibitor with IC50 of 0.4 nM, 0.6 nM and 1 nM for FLT3 (WT), FLT3 (D835Y), and Mer, respectively, showing lower potency against other tyrosine kinases.
S1099	SKLB4771 (FLT3-IN-1) SKLB4771 is a potent and selective inhibitor of human receptor-type tyrosine-protein kinase FLT3 with IC50 of 10 nM.
S7754	Gilteritinib (ASP2215) Gilteritinib (ASP2215) is a small-molecule FLT3/AXL inhibitor with IC50 values of 0.29 nM and 0.73 nM for FLT3 and AXL, respectively. It inhibits FLT3 at an IC50 value that was approximately 800-fold more potent than the concentration required to inhibit c-KIT (230 nM).	Cell, 2020, 182(3):685-712.e19 Cell, 2020, 182(3):685-712.e19 Sci Adv, 2020, 22;6(21):eaaz8521
S7003	AZD2932 AZD2932 is a potent and mutil-targeted protein tyrosine kinase inhibitor with IC50 of 8 nM, 4 nM, 7 nM, and 9 nM for VEGFR-2, PDGFRβ, Flt-3, and c-Kit, respectively.	Cancer Res, 2020, canres.1992.2020 Molecules, 2020, 8;25(9) pii: E2220 Development, 2016, 143(23):4394-4404
S7818	Pexidartinib (PLX3397) Pexidartinib (PLX3397) is an oral, potent mutil-targeted receptor tyrosine kinase inhibitor of CSF-1R, Kit (c-Kit), and FLT3 with IC50 of 20 nM, 10 nM and 160 nM, respectively. Pexidartinib (PLX3397) induces apoptosis and necrosis with antitumor activity. Phase 3.	Brain, 2021, awab122 J Neuroinflammation, 2021, 18(1):4 J Inflamm Res, 2021, 14:1341-1356	(a) Reduced tumour burden in PLX3397 (PLX) treated mice relative to untreated (NT) (n=6, P=.015; unpaired t-test). Bars represent total tumour volume with number of identified tumours indicated above each bar.
S7119	Go6976 Go6976 (PD406976) is a potent PKC inhibitor with IC50 of 7.9 nM, 2.3 nM, and 6.2 nM for PKC (Rat brain), PKCα, and PKCβ1, respectively. Also a potent inhibitor of JAK2 and Flt3.	Biochimie, 2021, 184:8-17 J Cell Physiol, 2020, 10.1002/jcp.30207 Front Pharmacol, 2020, 10:1589	Erk5 activation depends on Mek5, classical PKC and Mek1/2. MOVAS cells were serum-starved overnight and then treated for 1 h if not indicated otherwise with inhibitors targeting Jnk (SP600125, 10 μM), p38 (SB203580, 10 μM), Mek1/2 (CI-1040, 3 μM), Jak2 (AG490, 10 μM), Src (SU6656, 0.5 μM), Go6983 (PKC, 1 μM), Gö6976 (classical PKC, 1 μM), proteasomes (MG132, 25 μM), TPA (100 ng/ml for 15 min to activate PKCs or overnight to inhibit) and Mek5 (BIX02189, 1 μM), as well as Ca2 + chelators (EDTA, 2 mM; BAPTA-AM, 10 μM; both with 30 min preincubation), followed by stimulation with 20 ng/ml PDGF-BB for 10 min. Total cell lysates (TCL) were prepared and subjected to SDS-PAGE. Erk5 and PDGFRβ activities were measured by band shift and Tyr857 phosphorylation, respectively, using immunoblotting. Panel E and G show representative immunoblots.
S7533	AMG 925 AMG 925 is a potent and orally bioavailable dual FLT3/CDK4 inhibitor with IC50 of 1 nM and 3 nM, respectively.	Molecules, 2020, 8;25(9) pii: E2220

研究分野別

製品類型

FLT3

シグナル伝達経路

研究分野

阻害剤の選択性比較

FLT3製品