PDGFR

Signaling Pathway Map

Research Area

Inhibitory Selectivity
Solubility

Catalog No.	Product Name	Solubility(25°C)
Catalog No.	Product Name	Water	DMSO	Alcohol
S1040	Sorafenib Tosylate	0.01 mg/mL	127 mg/mL	<1 mg/mL
S1026	Imatinib Mesylate (STI571)	118 mg/mL	118 mg/mL	<1 mg/mL
S1042	Sunitinib Malate	<1 mg/mL	15 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
S8780	AZD3229	˂1 mg/mL	96 mg/mL	˂1 mg/mL
S8757	Ripretinib (DCC-2618)	<1 mg/mL	100 mg/mL	<1 mg/mL
S5272	Toceranib phosphate	2 mg/mL	2 mg/mL	<1 mg/mL
S5234	Nintedanib Ethanesulfonate Salt	100 mg/mL	100 mg/mL	5 mg/mL
S5077	Regorafenib Monohydrate	-1 mg/mL	100 mg/mL	-1 mg/mL
S2475	Imatinib (STI571)	<1 mg/mL	33 mg/mL	<1 mg/mL
S1010	Nintedanib (BIBF 1120)	<1 mg/mL	6 mg/mL	3 mg/mL
S1035	Pazopanib HCl (GW786034 HCl)	<1 mg/mL	17 mg/mL	<1 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
S2730	Crenolanib (CP-868596)	<1 mg/mL	88 mg/mL	7 mg/mL
S1064	Masitinib (AB1010)	<1 mg/mL	100 mg/mL	4 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
S1244	Amuvatinib (MP-470)	<1 mg/mL	32 mg/mL	<1 mg/mL
S1470	Orantinib (TSU-68, SU6668)	<1 mg/mL	62 mg/mL	<1 mg/mL
S1536	CP-673451	<1 mg/mL	28 mg/mL	4 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
S2769	Dovitinib (TKI-258) Dilactic Acid	70 mg/mL	90 mg/mL	<1 mg/mL
S2774	MK-2461	<1 mg/mL	99 mg/mL	<1 mg/mL
S8024	Tyrphostin AG 1296	<1 mg/mL	6 mg/mL	<1 mg/mL
S2895	Tyrphostin 9	<1 mg/mL	56 mg/mL	56 mg/mL
S7765	Dovitinib (TKI258) Lactate	66 mg/mL	100 mg/mL	1 mg/mL
S4018	Sennoside B	<1 mg/mL	100 mg/mL	1 mg/mL
S7781	Sunitinib	<1 mg/mL	25 mg/mL	<1 mg/mL
S8553	Avapritinib (BLU-285)	<1 mg/mL	66 mg/mL	3 mg/mL
S7003	AZD2932	<1 mg/mL	89 mg/mL	5 mg/mL
S4736	Trapidil	41 mg/mL	41 mg/mL	41 mg/mL

Isoform-specific Inhibitors

PDGFR Products

All (36) PDGFR Inhibitors (35) PDGFR Antagonists (1) New PDGFR Products

Catalog No.	Information	Product Use Citations	Product Validations
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, 2013, 122(9):1621-33 Blood, 2012, 120(19):4104-15 Hepatology, 2013, 59(4):1435-47	Western blot analysis of proteins expression levels in pericytes at 5-hour treatment with DMSO (vehicle), 10 μmol/L vemurafenib (Vemu.), 2.5 μmol/L sorafenib (Sora.), and combined therapy with 10 μmol/L vemurafenib plus 2.5 μmol/L sorafenib. These results were validated by three independent replicate measurements. Cells were grown in 0.2% FBS DMEM growth medium during treatment.
S1026	Imatinib Mesylate (STI571) Imatinib Mesylate (STI571) is an orally bioavailability mesylate salt of Imatinib, which is a multi-target inhibitor of v-Abl, c-Kit and PDGFR with IC50 of 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively.	Cell Stem Cell, 2012, 10(2):210-7 Cancer Cell, 2014, 26(6):840-50 Sci Transl Med, 2014, 6(261):261ra152	THOC5 phospho-Y225 levels were assessed in the populations shown by flow cytometry following 24 h treatment with 5 μM imatinib, 150 nM dasatinib or 5 μM nilotinib. Results are displayed as mean fluorescence intensity (n= 4) ±s.e.m.
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.
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, 2016, 534(7609):647-51 Nature, 2015, 10.1038/nature14329 Cancer Discov, 2016, 6(7):727-39	Immunoblot of H23 cells treated with trametinib (25 nM), ponatinib (750 nM), or their combination for the times shown.
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 Clin Cancer Res, 2016, 22(8):1940-50	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.
S8780^New	AZD3229 AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM), with good margin to KDR-driven effects. It also inhibits PDGFR mutants (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V).
S8757^New	Ripretinib (DCC-2618) DCC-2618 is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of the tumor-associated antigens (TAA) mast/stem cell factor receptor (SCFR) KIT and PDGFR-alpha, with IC50 values of 4 nM, 8 nM, 18 nM, 5 nM and 14 nM for WT KIT, V654A KIT, T670I KIT, D816H KIT and D816V KIT, respectively.
S5272^New	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.
S5234^New	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.
S5077^New	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.
S2475	Imatinib (STI571) Imatinib (STI571) is a multi-target inhibitor of tyrosine kinase with inhibition for v-Abl, c-Kit and PDGFR, IC50 values are 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively.	Cell Stem Cell, 2012, 10(2):210-7 Cancer Cell, 2014, 26(6):840-50 Blood, 2014, 123(21):3296-304	Ba/F3-p210T315I cells were treated with indicated concentrations of imatinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P<0.05.
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.
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.
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.	Cancer Res, 2014, 74(20):5795-807 Mol Cell Proteomics, 2012, 11(6):M112 Liver Int, 2011, 32(3):400-9	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.
S2730	Crenolanib (CP-868596) Crenolanib (CP-868596) 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.	Blood, 2018, 132(1):67-77. Blood, 2016, 10.1182/blood-2015-10-673103 Clin Cancer Res, 2018, 24(1):234-247
S1064	Masitinib (AB1010) Masitinib is a novel inhibitor for Kit and PDGFRα/β with IC50 of 200 nM and 540 nM/800 nM, weak inhibition to ABL and c-Fms. Phase 3.	Hepatology, 2016, 64(2):488-500 Biomaterials, 2013, 34(38):9737-46 Mol Syst Biol, 2015, 11(1):789	H&E stained histology slides of A), C), and E) control implants and B), D), and F) drug-loaded implants for 14, 21 and 28 day time points respectively. Location of the implants is denoted by the asterisk ‘*’. Scale bar: 200 μm.
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
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Phase 2.	Nat Genet, 2012, 44(8):852-60 Cancer Res, 2014, 74(20):5878-90 Oncogene, 2014, 33(10):1316-24	Effects of treatment for 48h with a vehicle or the indicated doses of MP-470 in parental or ER1 and ER2 cell lines in the absence and presence of erlotinib on the indicated biomarkers. Data represent 3 independent experiments.
S1470	Orantinib (TSU-68, SU6668) Orantinib (TSU-68, SU6668) has greatest potency against PDGFR autophosphorylation with K_i of 8 nM in a cell-free assay, but also strongly inhibits Flk-1 and FGFR1 trans-phosphorylation, little activity against IGF-1R, Met, Src, Lck, Zap70, Abl and CDK2; does not inhibit EGFR. Phase 3.	Proc Natl Acad Sci USA, 2014, 111(44):E4706-15 Cell Physiol Biochem, 2017, 41(6):2350-2362 Mol Cell Proteomics, 2012, 11(9):745-57	Effect of select kinase inhibitors on DF508-CFTR maturation analyzed by immunoblotting. 293MSR-GT cells stably expressing DF508-CFTR were treated with 15 uM kinase inhibitors or 0.3% DMSO (vehicle control), as indicated, grown at 37°C for 48 h, and the appearance of the mature protein, band C, monitored by immunoblotting with anti-CFTR antibodies. Band B represents the immature protein. DMSO represents vehicle- alone control, 27°C represents temperature rescue of F508-CFTR at 27°C, 37°C represents untreated DF508-CFTR control, and WT represents WT-CFTR. Top panels depict the anti-CFTR immunoblot and bottom panels depict actin (loading) control. ** represents cellular toxicity.
S1536	CP-673451 CP-673451 is a selective inhibitor of PDGFRα/β with IC50 of 10 nM/1 nM in cell-free assays, exhibits >450-fold selectivity over other angiogenic receptors, has antiangiogenic and antitumor activity.	Ann Rheum Dis, 2015, 10.1136/annrheumdis-2014-207109 Cancer Res, 2016, 76(22):6690-6700 Stem Cells, 2015, 33(2):542-56	Pharmacological inhibition of PDGFR-β by cp673451 significantly attenuated the mRNA expression of BCL2A1 (E) and SERPINE (F) in ASCs.
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 Clin Cancer Res, 2018, 24(11):2678-2687
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	PP121 induces apoptosis in ATC cells. CAL62 cells were treated with PP121 at the indicated concentrations for 48 h, followed by PI staining. The nuclei were stained with Hoechst and analyzed using a fluorescent microscope. The representative images are shown.
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, 2015, 21(5):1172-82 Clin Cancer Res, 2014, 19(9):2368-80
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 Res, 2013, 73(16):5195-205 Cancer Lett, 2016, 380(1):163-173 Br 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.
S2774	MK-2461 MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2. .	Mol Cell Biochem, 2018, 449(1-2):1-8	Both V-H cells and V-J cells are treated with MK-2461, XL-184 or ABT-869, respectively. (i-k) Western blot analysis of sFlt-1 expression after incubation with three VEGF-A receptor inhibitors or in the control.
S8024	Tyrphostin AG 1296 Tyrphostin AG 1296 is an inhibitor of PDGFR with IC50 of 0.3-0.5 μM, no activity to EGFR.	Onco Targets Ther, 2014, 7:425-32	After inoculation with KAT4 cells, administration of compounds including MK-2206 (100 mg/kg), tyrphostin AG 1296 (100 mg/kg), or a combination of MK-2206 (100 mg/kg) and tyrphostin AG 1296 (100 mg/kg) was performed. The combination of MK-2206 and tyrphostin AG 1296 induced significant apoptosis of KAT4 tumor cells in vivo measured by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay (green), and nuclei were stained with Hoechst (blue).
S2895	Tyrphostin 9 Tyrphostin 9 is firstly designed as an EGFR inhibitor with IC50 of 460 μM, but is also found to be more potent to PDGFR with IC50 of 0.5 μM.
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 Urol Oncol, 2018, 36(8):365 Eur J Haematol, 2017, 99(5):442-448	(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.
S4018	Sennoside B Sennoside B, a kind of irritant laxative isolated from rhei rhizome, inhibits PDGF-stimulated cell proliferation.
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.
S8553	Avapritinib (BLU-285) Avapritinib (BLU-285) is a small molecule kinase inhibitor that potently inhibits PDGFRα D842V mutant activity in vitro (IC50 = 0.5 nM) and PDGFRα D842V autophosphorylation in the cellular setting (IC50 = 30 nM); also a potent inhibitor of the analogous KIT mutation, D816V in KIT Exon 17 (IC50 = 0.5 nM).
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.
S4736	Trapidil Trapidil is a PDGF antagonist that can inhibit the proliferation of the PDGF-producing glioma cells.

Catalog No.	Information	Product Use Citations	Product Validations
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, 2013, 122(9):1621-33 Blood, 2012, 120(19):4104-15 Hepatology, 2013, 59(4):1435-47	Western blot analysis of proteins expression levels in pericytes at 5-hour treatment with DMSO (vehicle), 10 μmol/L vemurafenib (Vemu.), 2.5 μmol/L sorafenib (Sora.), and combined therapy with 10 μmol/L vemurafenib plus 2.5 μmol/L sorafenib. These results were validated by three independent replicate measurements. Cells were grown in 0.2% FBS DMEM growth medium during treatment.
S1026	Imatinib Mesylate (STI571) Imatinib Mesylate (STI571) is an orally bioavailability mesylate salt of Imatinib, which is a multi-target inhibitor of v-Abl, c-Kit and PDGFR with IC50 of 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively.	Cell Stem Cell, 2012, 10(2):210-7 Cancer Cell, 2014, 26(6):840-50 Sci Transl Med, 2014, 6(261):261ra152	THOC5 phospho-Y225 levels were assessed in the populations shown by flow cytometry following 24 h treatment with 5 μM imatinib, 150 nM dasatinib or 5 μM nilotinib. Results are displayed as mean fluorescence intensity (n= 4) ±s.e.m.
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.
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, 2016, 534(7609):647-51 Nature, 2015, 10.1038/nature14329 Cancer Discov, 2016, 6(7):727-39	Immunoblot of H23 cells treated with trametinib (25 nM), ponatinib (750 nM), or their combination for the times shown.
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 Clin Cancer Res, 2016, 22(8):1940-50	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.
S8780^New	AZD3229 AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM), with good margin to KDR-driven effects. It also inhibits PDGFR mutants (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V).
S8757^New	Ripretinib (DCC-2618) DCC-2618 is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of the tumor-associated antigens (TAA) mast/stem cell factor receptor (SCFR) KIT and PDGFR-alpha, with IC50 values of 4 nM, 8 nM, 18 nM, 5 nM and 14 nM for WT KIT, V654A KIT, T670I KIT, D816H KIT and D816V KIT, respectively.
S5272^New	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.
S5234^New	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.
S5077^New	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.
S2475	Imatinib (STI571) Imatinib (STI571) is a multi-target inhibitor of tyrosine kinase with inhibition for v-Abl, c-Kit and PDGFR, IC50 values are 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively.	Cell Stem Cell, 2012, 10(2):210-7 Cancer Cell, 2014, 26(6):840-50 Blood, 2014, 123(21):3296-304	Ba/F3-p210T315I cells were treated with indicated concentrations of imatinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P<0.05.
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.
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.
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.	Cancer Res, 2014, 74(20):5795-807 Mol Cell Proteomics, 2012, 11(6):M112 Liver Int, 2011, 32(3):400-9	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.
S2730	Crenolanib (CP-868596) Crenolanib (CP-868596) 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.	Blood, 2018, 132(1):67-77. Blood, 2016, 10.1182/blood-2015-10-673103 Clin Cancer Res, 2018, 24(1):234-247
S1064	Masitinib (AB1010) Masitinib is a novel inhibitor for Kit and PDGFRα/β with IC50 of 200 nM and 540 nM/800 nM, weak inhibition to ABL and c-Fms. Phase 3.	Hepatology, 2016, 64(2):488-500 Biomaterials, 2013, 34(38):9737-46 Mol Syst Biol, 2015, 11(1):789	H&E stained histology slides of A), C), and E) control implants and B), D), and F) drug-loaded implants for 14, 21 and 28 day time points respectively. Location of the implants is denoted by the asterisk ‘*’. Scale bar: 200 μm.
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
S1244	Amuvatinib (MP-470) Amuvatinib (MP-470) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. Phase 2.	Nat Genet, 2012, 44(8):852-60 Cancer Res, 2014, 74(20):5878-90 Oncogene, 2014, 33(10):1316-24	Effects of treatment for 48h with a vehicle or the indicated doses of MP-470 in parental or ER1 and ER2 cell lines in the absence and presence of erlotinib on the indicated biomarkers. Data represent 3 independent experiments.
S1470	Orantinib (TSU-68, SU6668) Orantinib (TSU-68, SU6668) has greatest potency against PDGFR autophosphorylation with K_i of 8 nM in a cell-free assay, but also strongly inhibits Flk-1 and FGFR1 trans-phosphorylation, little activity against IGF-1R, Met, Src, Lck, Zap70, Abl and CDK2; does not inhibit EGFR. Phase 3.	Proc Natl Acad Sci USA, 2014, 111(44):E4706-15 Cell Physiol Biochem, 2017, 41(6):2350-2362 Mol Cell Proteomics, 2012, 11(9):745-57	Effect of select kinase inhibitors on DF508-CFTR maturation analyzed by immunoblotting. 293MSR-GT cells stably expressing DF508-CFTR were treated with 15 uM kinase inhibitors or 0.3% DMSO (vehicle control), as indicated, grown at 37°C for 48 h, and the appearance of the mature protein, band C, monitored by immunoblotting with anti-CFTR antibodies. Band B represents the immature protein. DMSO represents vehicle- alone control, 27°C represents temperature rescue of F508-CFTR at 27°C, 37°C represents untreated DF508-CFTR control, and WT represents WT-CFTR. Top panels depict the anti-CFTR immunoblot and bottom panels depict actin (loading) control. ** represents cellular toxicity.
S1536	CP-673451 CP-673451 is a selective inhibitor of PDGFRα/β with IC50 of 10 nM/1 nM in cell-free assays, exhibits >450-fold selectivity over other angiogenic receptors, has antiangiogenic and antitumor activity.	Ann Rheum Dis, 2015, 10.1136/annrheumdis-2014-207109 Cancer Res, 2016, 76(22):6690-6700 Stem Cells, 2015, 33(2):542-56	Pharmacological inhibition of PDGFR-β by cp673451 significantly attenuated the mRNA expression of BCL2A1 (E) and SERPINE (F) in ASCs.
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 Clin Cancer Res, 2018, 24(11):2678-2687
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	PP121 induces apoptosis in ATC cells. CAL62 cells were treated with PP121 at the indicated concentrations for 48 h, followed by PI staining. The nuclei were stained with Hoechst and analyzed using a fluorescent microscope. The representative images are shown.
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, 2015, 21(5):1172-82 Clin Cancer Res, 2014, 19(9):2368-80
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 Res, 2013, 73(16):5195-205 Cancer Lett, 2016, 380(1):163-173 Br 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.
S2774	MK-2461 MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2. .	Mol Cell Biochem, 2018, 449(1-2):1-8	Both V-H cells and V-J cells are treated with MK-2461, XL-184 or ABT-869, respectively. (i-k) Western blot analysis of sFlt-1 expression after incubation with three VEGF-A receptor inhibitors or in the control.
S8024	Tyrphostin AG 1296 Tyrphostin AG 1296 is an inhibitor of PDGFR with IC50 of 0.3-0.5 μM, no activity to EGFR.	Onco Targets Ther, 2014, 7:425-32	After inoculation with KAT4 cells, administration of compounds including MK-2206 (100 mg/kg), tyrphostin AG 1296 (100 mg/kg), or a combination of MK-2206 (100 mg/kg) and tyrphostin AG 1296 (100 mg/kg) was performed. The combination of MK-2206 and tyrphostin AG 1296 induced significant apoptosis of KAT4 tumor cells in vivo measured by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay (green), and nuclei were stained with Hoechst (blue).
S2895	Tyrphostin 9 Tyrphostin 9 is firstly designed as an EGFR inhibitor with IC50 of 460 μM, but is also found to be more potent to PDGFR with IC50 of 0.5 μM.
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 Urol Oncol, 2018, 36(8):365 Eur J Haematol, 2017, 99(5):442-448	(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.
S4018	Sennoside B Sennoside B, a kind of irritant laxative isolated from rhei rhizome, inhibits PDGF-stimulated cell proliferation.
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.
S8553	Avapritinib (BLU-285) Avapritinib (BLU-285) is a small molecule kinase inhibitor that potently inhibits PDGFRα D842V mutant activity in vitro (IC50 = 0.5 nM) and PDGFRα D842V autophosphorylation in the cellular setting (IC50 = 30 nM); also a potent inhibitor of the analogous KIT mutation, D816V in KIT Exon 17 (IC50 = 0.5 nM).
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.