VEGFR

シグナル伝達経路

研究分野

阻害剤の選択性比較
溶解度

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 Tosylate	0.01 mg/mL	127 mg/mL	<1 mg/mL
S1042	Sunitinib Malate	<1 mg/mL	15 mg/mL	<1 mg/mL
S1119	Cabozantinib (XL184, BMS-907351)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1490	Ponatinib (AP24534)	<1 mg/mL	30 mg/mL	<1 mg/mL
S1005	Axitinib	<1 mg/mL	35 mg/mL	<1 mg/mL
S5667	Fruquintinib (HMPL-013)	<1 mg/mL	6 mg/mL	<1 mg/mL
S5272	Toceranib phosphate	2 mg/mL	2 mg/mL	<1 mg/mL
S5240	lenvatinib Mesylate	-1 mg/mL	39 mg/mL	-1 mg/mL
S5234	Nintedanib Ethanesulfonate Salt	100 mg/mL	100 mg/mL	5 mg/mL
S5242	Cediranib Maleate	<1 mg/mL	100 mg/mL	<1 mg/mL
S8726	Anlotinib (AL3818)	96 mg/mL	96 mg/mL	<1 mg/mL
S5077	Regorafenib Monohydrate	-1 mg/mL	100 mg/mL	-1 mg/mL
S8696	2-D08	<1 mg/mL	54 mg/mL	<1 mg/mL
S1111	Foretinib (GSK1363089)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1046	Vandetanib (ZD6474)	<1 mg/mL	4 mg/mL	<1 mg/mL
S1010	Nintedanib (BIBF 1120)	<1 mg/mL	6 mg/mL	3 mg/mL
S1178	Regorafenib (BAY 73-4506)	<1 mg/mL	97 mg/mL	<1 mg/mL
S1035	Pazopanib HCl (GW786034 HCl)	<1 mg/mL	17 mg/mL	<1 mg/mL
S1017	Cediranib (AZD2171)	<1 mg/mL	90 mg/mL	<1 mg/mL
S1264	PD173074	<1 mg/mL	100 mg/mL	100 mg/mL
S1018	Dovitinib (TKI-258, CHIR-258)	<1 mg/mL	30 mg/mL	<1 mg/mL
S1003	Linifanib (ABT-869)	<1 mg/mL	75 mg/mL	<1 mg/mL
S1101	Vatalanib (PTK787) 2HCl	10 mg/mL	85 mg/mL	6 mg/mL
S2161	RAF265 (CHIR-265)	<1 mg/mL	100 mg/mL	33 mg/mL
S1207	Tivozanib (AV-951)	<1 mg/mL	20 mg/mL	<1 mg/mL
S1032	Motesanib Diphosphate (AMG-706)	19 mg/mL	100 mg/mL	<1 mg/mL
S1164	Lenvatinib (E7080)	<1 mg/mL	40 mg/mL	<1 mg/mL
S1084	Brivanib (BMS-540215)	<1 mg/mL	74 mg/mL	3 mg/mL
S1361	Glesatinib (MGCD265)	<1 mg/mL	104 mg/mL	<1 mg/mL
S1486	AEE788 (NVP-AEE788)	<1 mg/mL	88 mg/mL	<1 mg/mL
S1181	ENMD-2076	1 mg/mL	105 mg/mL	<1 mg/mL
S1220	OSI-930	<1 mg/mL	89 mg/mL	3 mg/mL
S1171	CYC116	<1 mg/mL	24 mg/mL	<1 mg/mL
S1363	Ki8751	<1 mg/mL	47 mg/mL	<1 mg/mL
S2231	Telatinib	<1 mg/mL	82 mg/mL	1 mg/mL
S2622	PP121	<1 mg/mL	64 mg/mL	2 mg/mL
S3012	Pazopanib	<1 mg/mL	87 mg/mL	<1 mg/mL
S1557	KRN 633	<1 mg/mL	9 mg/mL	<1 mg/mL
S2769	Dovitinib (TKI-258) Dilactic Acid	70 mg/mL	90 mg/mL	<1 mg/mL
S2842	SAR131675	<1 mg/mL	30 mg/mL	<1 mg/mL
S2201	BMS-794833	<1 mg/mL	94 mg/mL	<1 mg/mL
S4001	Cabozantinib malate (XL184)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1138	Brivanib Alaninate (BMS-582664)	<1 mg/mL	88 mg/mL	88 mg/mL
S2859	Golvatinib (E7050)	<1 mg/mL	20 mg/mL	<1 mg/mL
S2845	Semaxanib (SU5416)	<1 mg/mL	22 mg/mL	2 mg/mL
S2897	ZM 306416	<1 mg/mL	67 mg/mL	<1 mg/mL
S2896	ZM 323881 HCl	<1 mg/mL	10 mg/mL	<1 mg/mL
S2018	ENMD-2076 L-(+)-Tartaric acid	<1 mg/mL	100 mg/mL	<1 mg/mL
S7057	LY2874455	<1 mg/mL	88 mg/mL	57 mg/mL
S8189	BAW2881 (NVP-BAW2881)	<1 mg/mL	84 mg/mL	20 mg/mL
S7667	SU5402	<1 mg/mL	59 mg/mL	<1 mg/mL
S7765	Dovitinib (TKI258) Lactate	66 mg/mL	100 mg/mL	1 mg/mL
S8188	BFH772	<1 mg/mL	87 mg/mL	87 mg/mL
S7781	Sunitinib	<1 mg/mL	25 mg/mL	<1 mg/mL
S8573	Sitravatinib (MGCD516)	<1 mg/mL	100 mg/mL	100 mg/mL
S7258	SKLB1002	<1 mg/mL	7 mg/mL	<1 mg/mL
S7003	AZD2932	<1 mg/mL	89 mg/mL	5 mg/mL
S2366	Taxifolin (Dihydroquercetin)	<1 mg/mL	60 mg/mL	60 mg/mL

亜型選択性的な製品

VEGFR阻害剤(60)
新VEGFR製品

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
A2006	Bevacizumab Bevacizumab is a humanized anti-VEGF monoclonal antibody which binds to and neutralizes all human VEGF-A isoforms and bioactive proteolytic fragments, MW:149 KD.
S1040	Sorafenib Tosylate Sorafenib Tosylate is a multikinase inhibitor of Raf-1, B-Raf and VEGFR-2 with IC50 of 6 nM, 22 nM and 90 nM in cell-free assays, respectively.	Blood, 2012, 120(19):4104-15 Blood, 2013, 122(9):1621-33 Hepatology, 2013, 59(4):1435-47	Inhibition of the MAPK signaling pathway results in downregulation of Plk-1 protein expression. (a) WB analysis for Plk-1 protein after treatment of human melanoma cell lines M14 and WM-115 with MEK 1/2 inhibitor PD98059 (10 μM), JNK inhibitor (16 μM), p38 inhibitor SB203580 (20 μM), and multikinase inhibitor sorafenib (10 μM) for 48 h showing significant reduction in the expression of Plk-1 protein after 48 hours. (b) Annexin V/PI staining of cells treated with MAPK inhibitors and induction of apoptosis. JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; MEK 1/2, mitogen-activated protein kinase kinase 1/2; Plk-1, polo-like kinase 1; WB, western blot.
S1042	Sunitinib Malate Sunitinib Malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM in cell-free assays, and also inhibits c-Kit.	Nature, 2011, 478(7369):349-55 Sci Transl Med, 2015, 7(284):284ra57 Cell Res, 2011, 21(7):1080-7	PDGF-AA induces Ezh2 expression and proliferation in juvenile islets but not in adult islets. Western immunoblots of indicated islet proteins from 3 week or 9 month-old WT islets 2 days after exposure to PDGF-AA alone, or PDGF-AA plus RTK inhibitors Sunitinib.
S1119	Cabozantinib (XL184, BMS-907351) Cabozantinib (XL184, BMS-907351) is a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret, 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.	Nature, 2017, 543(7647):728-732 Cancer Discov, 2018, 8(7):836-849 Cancer Discov, 2014, 4(7):816-27	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.
S1490	Ponatinib (AP24534) Ponatinib (AP24534) is a novel, potent multi-target inhibitor of Abl, PDGFRα, VEGFR2, FGFR1 and Src with IC50 of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM and 5.4 nM in cell-free assays, respectively.	Nature, 2015, 10.1038/nature14329 Nature, 2016, 534(7609):647-51 Cancer Discov, 2016, 6(7):727-39	RCH-ACV cells were treated with ponatinib(50 nM), PCI-32765(50 nM), or BMS-599626(500 nM) over a time course, and whole-cell extracts were subjected to immunoblot analysis for total or phospho-AKT.
S1005	Axitinib Axitinib is a multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ and c-Kit with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM in Porcine aorta endothelial cells, respectively.	Cell, 2018, 173(1):117-129 Cancer Discov, 2012, 2(4):344-55 Oncogene, 2017, 10.1038/onc.2017.132	Representative confocal image (10 x objective) of individual spheroids fixed, sectioned, and then stained for vimentin (green) and DNA (DAPI, blue). Vimentin protein expression from sections quantitated from multiple replicate spheroid treatments with U0126 and axitinib using ImageJ software.
S5667^新	Fruquintinib (HMPL-013) Fruquintinib is a small molecule inhibitor with strong potency and high selectivity against VEGFR family. It inhibits VEGFR 1, 2, 3, with IC50 values of 33 nM, 35 nM and 0.5 nM, respectively and shows only weak inhibition of RET, FGFR-1 and c-kit kinases.
S5272^新	Toceranib phosphate Toceranib phosphate, the phosphate salt of toceranib, is a selective inhibitor of the tyrosine kinase activity of several members of the split kinase RTK family, including Flk-1/KDR, PDGFR, and Kit with Ki values of 6 nM and 5 nM for Flk-1/KDR and PDGFRβ, respectively.
S5240^新	lenvatinib Mesylate Lenvatinib Mesylate is a synthetic, orally available inhibitor of VEGFR2 tyrosine kinase with potential antineoplastic activity.
S5234^新	Nintedanib Ethanesulfonate Salt Nintedanib is a small molecule tyrosine-kinase inhibitor with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β, respectively.
S5242^新	Cediranib Maleate Cediranib Maleate is the maleate salt of Cediranib, which is a potent inhibitor of VEGFR with IC50 of <1 nM and also inhibits Flt1/4 with IC50 of 5 nM/≤3 nM.
S8726^新	Anlotinib (AL3818) Anlotinib (AL3818) is a highly potent and selective VEGFR2 inhibitor with IC50 less than 1 nM. It has broad-spectrum antitumor potential in clinical trials.
S5077^新	Regorafenib Monohydrate Regorafenib is a novel oral multikinase inhibitor with IC50 values of 13, 4.2, 46, 22, 7, 1.5, 2.5, 28, 19 nM for VEGFR1, murine VEGFR2, murine VEGFR3, PDGFR-β, KIT, RET, RAF-1, B-RAF and B-RAF(V600E) respectively.
S8696^新	2-D08 2-D08 is a cell permeable, mechanistically unique inhibitor of protein sumoylation. It is also inhibits Axl, IRAK4, ROS1, MLK4, GSK3β, RET, KDR and PI3Kα with IC50 values of 0.49, 3.9, 5.3, 9.8, 11, 11, 17 and 35 nM respectively in biochemical assays.
S1111	Foretinib (GSK1363089) Foretinib (GSK1363089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for 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, PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	Nat Genet, 2012, 44(8):852-60 Clin Cancer Res, 2015, 21(10):2379-87 Leukemia, 2014, 28(3):629-41	D. Effects of erlotinib and inhibitors of PI3K, MEK, MET or IGF-1R on phosphorylation of AKT and ERK in ER3 cells.
S1046	Vandetanib (ZD6474) Vandetanib (ZD6474) is a potent inhibitor of VEGFR2 with IC50 of 40 nM in a cell-free assay. It also inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM. No activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM.	Nature, 2015, 10.1038/nature14329 Cell, 2016, 165(1):234-46 Nat Commun, 2014, 5:3116	(A) Representative in vivo bioluminescence of mice at and during time of treatment. Derived cell lines with either BCR-ABL1 WT or V299L was tail-vein injected into immunocompetent recipient mice. Initial imaging was performed at day 10 post-transplantation. Mice were subsequently treated once daily with vehicle, 10 mg/kg dasatinib, 50 mg/kg imatinib, 50 mg/kg vandetanib, or 50 mg/kg foretinib. (B) Fold change in total whole-mouse bioluminescence signal between post- and pre-treatment. Mice bearing BCR-ABL1 V299L ALLs showed significant tumor burden reduction upon treatment with foretinib or vandetanib. Statistical significance determined by Mann-Whitney test. p < 0.05, *p < 0.01.
S1010	Nintedanib (BIBF 1120) Nintedanib (BIBF 1120) is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM in cell-free assays. Phase 3.	Nature, 2011, 478(7369):349-55 Nat Neurosci, 2014, 17(1):24-6 Am J Respir Crit Care Med, 2015, 192(4):455-67	PBLs from CLL5 were treated with vehicles (0.1% ethanol and 0.005% DMSO), 106 M dexamethasone, 50 nM BIBF 1120, or both for 24 h. Cells were also treated with 0.1% ethanol or 106 M dexamethasone in the presence of either nonphosphorylated (control) EGQYEEIP or phosphorylated EGQY*EEIP H2O soluble peptides (200 nM) for 24 h.
S1178	Regorafenib (BAY 73-4506) Regorafenib (BAY 73-4506) is a multi-target inhibitor for VEGFR1, VEGFR2, VEGFR3, PDGFRβ, Kit, RET and Raf-1 with IC50 of 13 nM/4.2 nM/46 nM, 22 nM, 7 nM, 1.5 nM and 2.5 nM in cell-free assays, respectively.	Gastroenterology, 2017, 153(4):1082-1095 Clin Cancer Res, 2014, 20(22):5768-76 Proc Natl Acad Sci USA, 2015, 112(6):1839-44	Hepatoma cells 24 h after plating were treated with vehicle (DMSO), regorafenib (REGO, 0.5 µM), PDE5 inhibitor (sildenafil, 2 µM); or the drugs in combination. 24 hours after treatment cells were isolated and viability determined by trypan blue (n=3, SEM). *P 0.05
S1035	Pazopanib HCl (GW786034 HCl) Pazopanib HCl (GW786034 HCl) is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively.	Cancer Discov, 2013, 3(6):636-47 J Virol, 2011, 85(5):2296-303 J Cell Physiol, 2016, 231(10):2286-302	IC50 of Pazopanib that block ANDV-induced EC permeability. Endothelial cells were ANDV infected, and 3 days postinfection the permeability of cells in response to VEGF addition was determined in the presence or absence of increasing amounts of kinase inhibitor. (B): VEGFR2-Src inhibitors block ANDV-induced permeability. Endothelial cells were plated on vitronectin-coated Transwell inserts and infected at an MOI of 0.5 in triplicate with ANDV. Three days postinfection, the permeability of ANDV- and mock-infected endothelial cell monolayers was determined at indicated times in the presence or absence of Pazopanib.
S1017	Cediranib (AZD2171) Cediranib (AZD2171) is a highly potent VEGFR(KDR) inhibitor with IC50 of <1 nM, also inhibits Flt1/4 with IC50 of 5 nM/≤3 nM, similar activity against c-Kit and PDGFRβ, 36-, 110-fold and >1000-fold selective more for VEGFR than PDGFR-α, CSF-1R and Flt3 in HUVEC cells. Phase 3.	Clin Cancer Res, 2014, 20(14):3849-61 Neuro Oncol, 2013, 15(12):1673-83 Cancer Res, 2013, 73(16):5195-205	Western blots of EZH2 expression in A549, HCC461, and HCC4006 cells upon treatment with different doses of VEGFR-2-inhibitor AZD2171 (0, 5 and 10 nM). AZD2171 decreased the expression of EZH2 in HCC4006 and HCC461 cells expressing VEGFR-2 in a dose-dependent manner but did not do so in A549 cells lacking expression of VEGFR-2.
S1264	PD173074 PD173074 is a potent FGFR1 inhibitor with IC50 of ~25 nM and also inhibits VEGFR2 with IC50 of 100-200 nM in cell-free assays, ~1000-fold selective for FGFR1 than PDGFR and c-Src.	Science, 2011, 331(6019):912-6 Cancer Discov, 2013, 3(6):636-47 Gut, 2014, 63(12):1932-42	The inhibitor PD173074 (A) or PD184352 (B) was administered to one uterine horn of Hand2d/d mice on day 3 of pregnancy (n = 5). The other horn served as vehicle-treated control. Uterine horns were collected on the morning of day 4, and sections were subjected to IHC to detect p-FRS2, p-ERK1/2, and Ki-67. (C) IHC of pERa and Muc-1 in uterine sections of Hand2d/d mice treated with PD173074 or PD184352.
S1018	Dovitinib (TKI-258, CHIR-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, 2013, 73(16):5195-205 Haematologica, 2011, 96(6):922-6 BRIT J CANCER, 2011, 104(1):75-82	In vitro assays on CUX1-FGFR1-expressing Ba/F3 cells. a. IL-3 deprivation of Ba/F3 cells transduced with CUX1-FGFR1 resulted in transformation to growth factor independent growth. The mean growth ±SEM of three separate measurements over four consecutive days is presented. b. The dose-response curves of CUX1-FGFR1-transduced Ba/F3 cells, treated with TKI258 and PKC412 for 48 hours in the absence or presence of IL-3 (2 ng/ml) are presented. Points represent the average results of two experiments done in triplicate plotted with the curve-fitting GraphPad Prism 5 software; bars, SD. The calculated IC50 for each inhibitor is indicated. c. Western blot analyses of CUX1-FGFR1-transformed Ba/F3 cells after treatment with PKC412 and TKI258. Phosphorylation of CUX1-FGFR1 and its downstream effectors STAT5 and RPS6K decreased with increasing inhibitor concentrations. Expression of total CUX1-FGFR1, STAT5 and RPS6K remained unaffected. d. Effect of PKC412 and TKI258 on apoptosis of CUX1-FGFR1-expressing Ba/F3 cells after treatment for 48 hours. The percentage of apoptotic plus necrotic CUX1-FGFR1-transduced Ba/F3 cells is indicated.
S1003	Linifanib (ABT-869) Linifanib (ABT-869) 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). Phase 3.	Mol Cell Proteomics, 2012, 11(6):M112 Liver Int, 2011, 32(3):400-9 Int J Clin Exp Pathol, 2013, 6(10):2082-91	Effect of the anti-vascular agents Linifanib (100 nM) in the VMO(vascularized micro-organ). VMOs were exposed to the drug at day 5 and cultured for an additional 96 h.
S1101	Vatalanib (PTK787) 2HCl Vatalanib (PTK787) 2HCl is an inhibitor of VEGFR2/KDR with IC50 of 37 nM in a cell-free assay, less potent against VEGFR1/Flt-1, 18-fold against VEGFR3/Flt-4. Phase 3.	Nat Biotechnol, 2013, 31(10):898-907 Cell Res, 2011, 21(7):1080-7 Circ Res, 2011, 108(10):1190-8	Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.
S2161	RAF265 (CHIR-265) RAF265 (CHIR-265) is a potent selective inhibitor of C-Raf/B-Raf/B-Raf V600E with IC50 of 3-60 nM, and exhibits potent inhibition on VEGFR2 phosphorylation with EC50 of 30 nM in cell-free assays. Phase 2.	Hepatology, 2012, 56(6):2363-74 Pigment Cell Melanoma Res, 2014, 27(1):124-33 Mol Cell Proteomics, 2012, 11(6):M112.017764	Raf265 inhibited the kinase activity of B-Raf but not of Raf-1 in Pkd2cKO cholangiocytes. Cells were treated for 30 min with different concentrations of Raf265. B-Raf and Raf-1 were immunoprecipated as described in the methods section and a kinase assay in vitro was performed using MEK as a substrate. The kinase activity of Raf was assessed by immunoblot analysis and quantified as optical density of pMEK with respect to untreated cells. In WT cholangiocytes (A) Raf265 inhibited both B-Raf and Raf-1 kinase activity. In Pkd2cKO cholangiocytes (B), Raf265 inhibited only B-Raf while a biphasic effect was found in Raf-1 with a significant increase at doses from 0.001 to 1 uM and a significant inhibition at 10 uM. Blots are representative of four different experiments. (p<0.05 vs controls; *p<0.001 vs controls).
S1207	Tivozanib (AV-951) Tivozanib (AV-951) is a potent and selective VEGFR inhibitor for VEGFR1/2/3 with IC50 of 30 nM/6.5 nM/15 nM, and also inhibits PDGFR and c-Kit, low activity observed against FGFR-1, Flt3, c-Met, EGFR and IGF-1R. Phase 3.	J Med Chem, 2015, Cell Physiol Biochem, 2013, 32(5):1541-50 J Chem Inf Model, 2014, 54(3):881-93	After serum-starvation for 24 h, the MCF7 cells were co-treated with 10 nM TPA and the indicated doses VEGFR inhibitor, Tivozanib, for 24 h. The levels of fibronectin, p-PKC-α, p-ERK, p-AKT, t-AKT and β-actin protein expression were analyzed by western blotting. The levels of fibronectin mRNA were analyzed by real-time PCR. The results are representative of three independent experiments. The values shown are the means ±SEM. * P < 0.05, ** P < 0.01 vs. control. # P < 0.05, ## P < 0.01 vs. TPA-treated cells. Con: control. LY: LY294002, U: UO126, Go: Go6983, Akt IV: Akt IV inhibitor.
S1032	Motesanib Diphosphate (AMG-706) Motesanib Diphosphate (AMG-706) is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50 of 2 nM/3 nM/6 nM, respectively; similar activity against Kit, ~10-fold more selective for VEGFR than PDGFR and Ret. Phase 3.	Cardiovasc Res, 2011, 91(3):402-11 Int J Cardiol, 2015, 183C:221-231 Mol Cell Endocrinol, 2013, 377(1-2):1-6	(C, D, E)^VEGFCM stimulated CXCR4 expression in CSC 24 h after ^VEGFCM treatment. CSC were untreated (Control, C), or treated with ^VEGFMSC-conditioned medium (^VEGFCM, D) or ^VEGFCM and VEGFR1 inhibitor AMG(E) followed by flow cytometry. AMG inhibited the expression of ^VEGFCM-induced CXCR4. (F) Quantitative analysis of CXCR4 expression by flow cytometry. CSC were treated with ^CtrlCM or ^VEGFCM with or without VEGFR specific inhibitors for VEGFR1 (AMG), VEGFR2 (VEGFR2-I), and VEGFR3 (MAZ).P , 0.05 vs. control, AMG, VEGFR2-I. and MAZ; #P , 0.05 vs. AMG and MAZ (n = 5). (G) ^CtrlCM promoted CSC migration. P , 0.05 vs. ^CtrlCM; OP , 0.01 vs. ^CtrlCM; &P , 0.05 vs. ^CtrlCM+AMG and <sup>Ctrl</sup>CM+MAZ (n ?15); @P , 0.01 vs. ^CtrlCM; PP , 0.01 vs. ^CtrlCM; $P , 0.05 vs. ^CtrlCM+AMG and ^CtrlCM+MAZ. Note: ^CtrlCM= ^CtrlMSC< mesenchymal stem cells>-conditioned medium
S1164	Lenvatinib (E7080) Lenvatinib (E7080) is a multi-target inhibitor, mostly for VEGFR2(KDR)/VEGFR3(Flt-4) with IC50 of 4 nM/5.2 nM, less potent against VEGFR1/Flt-1, ~10-fold more selective for VEGFR2/3 against FGFR1, PDGFRα/β in cell-free assays. Phase 3.	Clin Cancer Res, 2015, 21(7):1652-64 Neoplasia, 2014, 16(11):972-81 Chin J Cancer Res, 2013, 25(5):572-84	Tetrathiomolybdate (TM) reduces anchorage-independent growth of BCPAP cells. A, % transformed growth in soft agar (mean ± SEM, triplicate samples, three experiments) normalized to vehicle control of BCPAP cells treated with increasing doses (effective concentration) of lenvatinib (blue ▲), sorafenib (■),TM (●), vemurafenib (◆), or trametinib (△).
S1084	Brivanib (BMS-540215) Brivanib is an ATP-competitive inhibitor against VEGFR2 with IC50 of 25 nM, moderate potency against VEGFR-1 and FGFR-1, but >240-fold against PDGFR-β. Phase 3.	Genome Biol, 2014, 15(8):428 Eur J Cancer, 2016, 61:20-8 Int J Oncol, 2014, 44(3):959-69	Alofanib inhibits fibroblast growth factor 2 (FGF2)-induced proliferation of human and mouse endothelial cells. Dose-response effect of alofanib was evaluated in HUVEC endothelial cells in comparison with brivanib. Cells were treated with different concentrations of alofanib, brivanib for 6 h followed by stimulation with 25 ng/ml FGF2. Cell growth inhibition were assessed.
S1361	Glesatinib (MGCD265) Glesatinib (MGCD265) is a potent, multi-target and ATP-competitive inhibitor of c-Met and VEGFR1/2/3 with IC50 of 1 nM, 3 nM/3 nM/4 nM, respectively; also inhibits Ron and Tie2. Phase 1/2.	Cancer Lett, 2013, 340(1):43-50 Int J Clin Exp Pathol, 2013, 6(10):2082-91	c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, TAE-684, and RON inhibitor I. Columns, means; bars, SEMs (n = 3). The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.
S1486	AEE788 (NVP-AEE788) AEE788 (NVP-AEE788) is a potent inhibitor of EGFR and HER2/ErbB2 with IC50 of 2 nM and 6 nM, less potent to VEGFR2/KDR, c-Abl, c-Src, and Flt-1, does not inhibit Ins-R, IGF-1R, PKCα and CDK1. Phase 1/2.	Prostate, 2013, 73(13):1453-61 PLoS One, 2015, 10(4):e0123623 Int J Clin Exp Pathol, 2013, 6(10):2082-91	EGFR-SGLT1 interaction is irresponsive to modulators of EGFR’s tyrosine kinase. A: Immunoprecipitation coupled Western blot analysis ofinteractionsbetween EGFR-HA and SGLT1-FlaginHEK293 cells treatedwith EGF or AEE788. EGFR, total EGFR; pEGFR, phosphorylated EGFR; IP, immunoprecipitation; IB, immunoblot. Input, expression levels of indicated exogenous proteinsin HEK293 whole celllysates used for the IP.
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 VEGFR2/KDR and VEGFR3, FGFR1 and FGFR2 and PDGFRα. Phase 2.	Blood, 2013, 122(7):1203-13 Cancer Res, 2013, 73(20):6310-22 PLoS One, 2014, 9(7):e102741	Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of ENMD-2076.
S1220	OSI-930 OSI-930 is a potent inhibitor of Kit, KDR and CSF-1R with IC50 of 80 nM, 9 nM and 15 nM, respectively; also potent to Flt-1, c-Raf and Lck and low activity against PDGFRα/β, Flt-3 and Abl. Phase 1.	Mol Syst Biol, 2015, 11(1):789 Biochem Pharmacol, 2012, 84(6):766-74 Int J Oncol, 2015, 47(1):122-32	RE-luc2P-HEK293 cells were pretreated with 1uM OSI-930 (green), 20uM TBB (blue), 10uM CKI-7 (purple), or 10uM H-89 (orange) for 16 h and infected with Y. enterocolitica WA or Y. pestis Ind195 at MOI 1 and 20, respectively, for 1 h. Following stimulation with 10 ng/ml TNF-α at 5 h post-infection, luciferase activity was measured 24 h post-infection. Results were determined from two independent experiments performed in triplicate. A"*" denotes that the % NF-κβ inhibition using the inhibitors was significantly different (p<0.05) compared to the no drug control (black). The relative NF-κB inhibition by Yersinia infection was determined as a percentage of luciferase activity in bacteria-infected cells relative to luciferase activity in bacteria-free control cells.
S1171	CYC116 CYC116 is a potent inhibitor of Aurora A/B with K_i of 8.0 nM/9.2 nM, is less potent to VEGFR2 (K_i of 44 nM), with 50-fold greater potency than CDKs, not active against PKA, Akt/PKB, PKC, no effect on GSK-3α/β, CK2, Plk1 and SAPK2A. Phase 1.	Cancer Res, 2013, 73(20):6310-22 PLoS One, 2014, 9(7):e102741	Breast cancer cells line MDA-MB-231 were treated with the indicated concentrations of CYC116.
S1363	Ki8751 Ki8751 is a potent and selective inhibitor of VEGFR2 with IC50 of 0.9 nM, >40-fold selective for VEGFR2 than c-Kit, PDGFRα and FGFR-2, little activity to EGFR, HGFR and InsR.	Cancer Lett, 2017, 385:12-20 Mol Cell Proteomics, 2012, 11(9):745-57 Cellular Signalling, 2016, 19;28(6):652-662	Ki8751, a VEGFR2 inhibitor, significantly mitigated the proliferation-stimulating effect of dying U87 cells on HUVEC-Fluc (one-way ANOVA, LSD, n=3).
S2231	Telatinib Telatinib is a potent inhibitor of VEGFR2/3, c-Kit and PDGFRα with IC50 of 6 nM/4 nM, 1 nM and 15 nM, respectively. Phase 2.	Biochem Pharmacol, 2014, 89(1):52-61
S2622	PP121 PP-121 is a multi-targeted inhibitor of PDGFR, Hck, mTOR, VEGFR2, Src and Abl with IC50 of 2 nM, 8 nM, 10 nM, 12 nM, 14 nM and 18 nM, also inhibits DNA-PK with IC50 of 60 nM.	Biochem Biophys Res Commun, 2015, 465(1):137-44 Int J Clin Exp Pathol, 2013, 6(10):2082-91 Tumour Biol, 2014, 35(9):8659-64	After starved in serum-free medium for 24 h,A549 cells incubated with the indicated concentrations of PP-121 for 3 h,followed by 20-minute stimolation of 100ng/ml EGF.
S3012	Pazopanib Pazopanib is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively.	Cancer Discov, 2013, 3(6):636-47 Clin Cancer Res, 2014, 19(9):2368-80 Arch Toxicol, 2018, 92(4):1435-1451
S1557	KRN 633 KRN 633 is an ATP-competitive inhibitor of VEGFR1/2/3 with IC50 of 170 nM/160 nM/125 nM, weakly inhibits PDGFR-α/β and c-Kit, does not block the phosphorylation of FGFR-1, EGFR or c-Met in cell.	Mol Cells, 2013, 36(4):347-54	Inhibited migration of hNSCs toward HeLa cells with the treatment of KRN633, a VEGFR2 inhibitor. The cultured hNSCs were treated with KRN633 for 6 h. After that, the transwell migration assay was performed as described above. The number of migrated cells was counted and the results were presented as means ± SD. Magnification,× 200. *P < 0.05 vs. KRN633 non-treated GESTECs. (A) Migrated HB1.F3.CD cells. (B) Migrated HB1.F3.CD.IFN-β cells.
S2769	Dovitinib (TKI-258) Dilactic Acid Dovitinib Dilactic acid (TKI258 Dilactic acid) is the Dilactic acid 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 Lett, 2016, 380(1):163-173 Br J Cancer, 2011, 104(1):75-82 Oral Oncol, 2012, 48(12):1242-9	In vitro assays on CUX1-FGFR1-expressing Ba/F3 cells. a. IL-3 deprivation of Ba/F3 cells transduced with CUX1-FGFR1 resulted in transformation to growth factor independent growth. The mean growth ±SEM of three separate measurements over four consecutive days is presented. b. The dose-response curves of CUX1-FGFR1-transduced Ba/F3 cells, treated with TKI258 and PKC412 for 48 hours in the absence or presence of IL-3 (2 ng/ml) are presented. Points represent the average results of two experiments done in triplicate plotted with the curve-fitting GraphPad Prism 5 software; bars, SD. The calculated IC50 for each inhibitor is indicated. c. Western blot analyses of CUX1-FGFR1-transformed Ba/F3 cells after treatment with PKC412 and TKI258. Phosphorylation of CUX1-FGFR1 and its downstream effectors STAT5 and RPS6K decreased with increasing inhibitor concentrations. Expression of total CUX1-FGFR1, STAT5 and RPS6K remained unaffected. d. Effect of PKC412 and TKI258 on apoptosis of CUX1-FGFR1-expressing Ba/F3 cells after treatment for 48 hours. The percentage of apoptotic plus necrotic CUX1-FGFR1-transduced Ba/F3 cells is indicated.
S2842	SAR131675 SAR131675 is a VEGFR3 inhibitor with IC50/K_i of 23 nM/12 nM in cell-free assays, about 50- and 10-fold more selective for VEGFR3 than VEGFR1/2, little activity against Akt1, CDKs, PLK1, EGFR, IGF-1R, c-Met, Flt2 etc.	Biomaterials, 2016, 78:115-28 Hum Mol Genet, 2015, 24(4):926-38 Cellular Signalling, 2016, 19;28(6):652-662	Blockade of IPC-induced ischemic tolerance by the VEGFR-3 inhibitor SAR131675. (A) Representative images of FJ-stained brain sections from sham + SARH (i), sham-IPC + SI + Veh (ii), IPC + SI + Veh (iii) and IPC + SI + SARH (iv) groups. Note that there were more degenerated neurons in the IPC + SI + SARH group receiving SAR131675 of 50 mg/kg as an initial dose than in the IPC + SI + Veh group. Scale bar = 50 μm. (B) The quantitative analysis shows the number of FJ-positive degenerated neurons in the CA1 subregion of the different treatment groups including the IPC + SI + SARL group receiving SAR131675 of 25 mg/kg as an initial dose. Data are presented as the mean ± SEM; # p < 0.05 compared with the sham-IPC + SI + Veh group; p < 0.05 compared with the IPC + SI + Veh group. (C) Representative images of NeuN immunofluorescence in the sham + SARH (i), sham-IPC + SI + Veh (ii), IPC + SI + Veh (iii) and IPC + SI + SARH (iv) groups. Note that NeuN-immunofluorescence in the IPC + SI + SARH group was reduced compared with the IPC + SI + Veh group. Scale bar = 50 μm. (D) The quantitative analysis shows the number of NeuN-positive intact pyramidal neurons in the CA1 subregion for the different treatment groups. Data are presented as the mean ± SEM; #p < 0.05 compared with the sham-IPC + SI + Veh group; p < 0.05 compared with the IPC + SI + Veh group.
S2201	BMS-794833 BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7 nM/15 nM, also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378. Phase 1.
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, 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.	Nature, 2017, 543(7647):728-732 Cancer Discov, 2014, 4(7):816-27 Cancer Discov, 2018, 10.1158/2159-8290.CD-18-0338	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.
S1138	Brivanib Alaninate (BMS-582664) Brivanib alaninate (BMS-582664) is the prodrug of BMS-540215, an ATP-competitive inhibitor against VEGFR2 with IC50 of 25 nM.	Int J Oncol, 2014, 44(3):959-69
S2859	Golvatinib (E7050) Golvatinib (E7050) is a dual c-Met and VEGFR-2 inhibitor with IC50 of 14 nM and 16 nM, does not inhibit bFGF-stimulated HUVEC growth (up to 1000 nM). Phase 1/2.	Cancer Sci, 2017, 108(7):1378-1385	PC-9/LMC-GR cells (2 × 105 cells/well) were incubated in 6-well plates with various concentrations of gefitinib with or without crizotinib (1 μmol/L) or golvatinib (1 μmol/L) for 1 hour. Cell lysate were obtained and subjected to immunoblotting with antibodies toward the indicated molecules.
S2845	Semaxanib (SU5416) Semaxanib (SU5416) is a potent and selective VEGFR(Flk-1/KDR) inhibitor with IC50 of 1.23 μM, 20-fold more selective for VEGFR than PDGFRβ, lack of activity against EGFR, InsR and FGFR. Phase 3.	Oncoimmunology, 2015, 10.1080/2162402X.2014.998107 PLoS One, 2016, 11(11):e0167218 Sci Rep, 2016, 6:19304	Injected tumor cells move to the tail via blood vessels. Tg (flil1:egfp) embryos at 20 hpf were treated with 2 μM SU5416 for 1 hr (+SU5416) to inhibit vasculogenesis24; the control fish were treated with 0.02% DMSO for 1 hr (-SU5416). After 1 hr, SU5416 or DMSO was washed out by changing fish media. At 48 hpf, tfRFP-B16 cells were injected into the pericardium cavity of fish. Representative images show that tumor cells moved to the tail in a drug-free larva, while no tumor cells moved to the tail in a drug-treated larva after new vessels were inhibited by SU5416. Insets are enlarged images from each corresponding tip of the tail indicated by white arrows. Dashed white lines mark extravasated tumor cells at 12 hpi. Vessels are green and tumor cells are red. –SU5416, 6 other larvae exhibit similar behaviors; +SU5416, 3 other larvae exhibit similar behaviors. Scale bars, 500 μm. Insets, 100 μm.
S2897	ZM 306416 ZM 306416 is a VEGFR (Flt and KDR) inhibitor for VEGFR1 with IC50 of 0.33 μM, but also found to inhibit EGFR with IC50 of <10 nM.	Cellular Signalling, 2016, 19;28(6):652-662 Sci Rep, 2015, 5:7890	Panels D-F show morphological changes of RBEC cells due to Sema3A treatment. RBECs were fixed after the indicated treatment and stained with phalloidin conjugated with rhodamine (red color) and counter stained with DAPI (blue color). F-actin stress fibres are very clear in untreated cells (D). Sema3A treatment caused disruption of F-actin inside the cells. Densely packed bundles of cortical actin filaments started to appear along cell membranes (arrows) over the course of treatment with Sema3A. Antibodies and inhibitors against receptors of Sema3A were pre-incubated with the cells for 15 min before the addition of Sema3A. Antibodies to VEGFR1 and NRP2 (panel E) and the inhibitor Zm 306416 (selective to VEGFR1, panel F) were effective in ameliorating the effect of Sema3A. Scale bar=20 μm.
S2896	ZM 323881 HCl ZM 323881 is a potent and selective VEGFR2 inhibitor with IC50 of <2 nM, almost no activity on VEGFR1, PDGFRβ, FGFR1, EGFR and ErbB2.	Eur J Med Chem, 2018, 160:193-206 Biochem Pharmacol, 2017, 132:29-37	(A) Fluorescence microscopic analysis of Hoechst 33342 staining of NCIH460 and NCI-H460/MX20 cells. Cells were treated as described in ‘2. Materials and Methods’. Scale bar, 10 μm. (B) Effects of ZM323881 on intracellular accumulation of [3H]-mitoxantrone in NCI-H460 and NCI-H460/MX20 cells. (C) Efflux of [3H]-mitoxantrone in the absence and presence of inhibitors in NCI-H460 cells. (D) Efflux of [3H]-mitoxantrone in the absence and presence of inhibitors in NCI-H460/MX20 cells.
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.
S7057	LY2874455 LY2874455 is a pan-FGFR inhibitor with IC50 of 2.8 nM, 2.6 nM, 6.4 nM, and 6 nM for FGFR1, FGFR2, FGFR3, and FGFR4, respectively, and also inhibits VEGFR2 activity with IC50 of 7 nM. Phase 1.	PLoS One, 2016, 11(9):e0162491	A: Overall structure of LY2874455/FGFR4 complex. B: The diagram of LY2874455. C: Fo-Fc omit map of LY2874455 in the FGFR4/LY2874455 complex. The electron density is superimposed with the final model. D: The DFG motif conformation of FGFR4. Active ApoFGFR4 DFG-in conformation is shown in blue (PDB: 4QQT); FGFR4/Ponatinib DFG-out conformation is shown in yellow (PDB: 4UXQ); FGFR4/BLU9931 DFG-in conformation is shown in pink (PDB: 4XCU); FGFR4/LY2874455 DFG-in conformation is shown in grey (this work). LY2874455 is highlighted in brown.
S8189	BAW2881 (NVP-BAW2881) BAW2881 (NVP-BAW2881) is a novel vascular endothelial growth factor (VEGF) receptor tyrosine-kinase inhibitor that potently inhibits VEGFR1-3 at 1.0-4.3 nanomolar (nM) concentrations and inhibits PDGFRβ, c-Kit, and RET at 45-72 nM concentrations.
S7667	SU5402 SU5402 is a potent multi-targeted receptor tyrosine kinase inhibitor with IC50 of 20 nM, 30 nM, and 510 nM for VEGFR2, FGFR1, and PDGF-Rβ, respectively.	Oncogene, 2016, 10.1038/onc.2016.244	Four FGFR inhibitors, namely PD-173074 (PD-74), PD-166866 (PD-66), SU5402 (SU54) and NVP-BGJ398 (BG-98), inhibit A673, SKNMC, POE, RDES and SKES Ewing cell growth in vitro in a dose-dependent manner, whereas normal cells (IMR90 fibroblasts) remained unaffected. PD-74 proved to be most effective in four out of five Ewing sarcoma cell lines tested. Cells were grown in 10% FBS conditions and cell proliferation was measured after 72 h using a Resazurin assay.
S7765	Dovitinib (TKI258) Lactate Dovitinib (TKI258) 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.	Genome Biol, 2014, 15(8):428	(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.
S8188	BFH772 BFH772 is a novel potent oral VEGFR2 inhibitor, targeting VEGFR2 kinase with IC50 of 3 nM.
S7781	Sunitinib Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit.	Nature, 2011, 478(7369):349-55 Sci Transl Med, 2015, 7(284):284ra57 Cell Res, 2011, 21(7):1080-7	PDGF-AA induces Ezh2 expression and proliferation in juvenile islets but not in adult islets. Western immunoblots of indicated islet proteins from 3 week or 9 month-old WT islets 2 days after exposure to PDGF-AA alone, or PDGF-AA plus RTK inhibitors Sunitinib.
S8573	Sitravatinib (MGCD516) Sitravatinib (MGCD516) is a novel small molecule inhibitor targeting multiple RTKs involved in driving sarcoma cell growth, including c-Kit, PDGFRβ, PDGFRα, c-Met, and Axl.
S7258	SKLB1002 SKLB1002 is a potent and ATP-competitive VEGFR2 inhibitor with IC50 of 32 nM.	BMC Cancer, 2017, 17(1):593	Protein expressions of VEGFR2, p-VEGFR2, FAK, p-FAK, ERK, p-ERK and VE-cadherin in HCT116 cells with or without SKLB1002 treatment were determined by western blotting analysis. Representative data of three experiments are shown
S4686	Vitamin E Vitamin E is a fat-soluble vitamin with potent antioxidant properties. It is a potent peroxyl radical scavenger and inhibits noncompetitively cyclooxygenase activity in many tissues, also inhibits angiogenesis and tumor dormancy through suppressing vascular endothelial growth factor (VEGF) gene transcription.
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.
S2366	Taxifolin (Dihydroquercetin) Taxifolin, type I inhibitor for VEGFR-2 kinase, is a flavonoid in many plants such as Taxus chinensis, Siberian larch, Cedrus deodara and so on.	Cytotechnology, 2016, 68(4):1633-40

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