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所有产品 PDGFR抑制剂(35) PDGFR拮抗剂(1) 新PDGFR产品

产品目录	产品描述	文献引用	实验数据
S1040	Sorafenib Tosylate Sorafenib Tosylate是一种酪氨酸激酶(VEGFR和PDGFR)和RAF/MEK/ERK级联抑制剂，同时作用于Raf-1，^wtBRAF和^V599EBRAF，IC50分别为6 nM， 22 nM和38 nM。	Blood, 2012, 120(19):4104-15 Blood, 2013, 122(9):1621-33 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)是一种口服生物有效的Imatinib甲磺酸盐，是一种多靶点抑制剂，作用于v-Abl，c-Kit和PDGFR，在无细胞和细胞试验中，IC50分别为0.6 μM，0.1 μM 和0.1 μM。	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是一种多靶点RTK抑制剂，作用于VEGFR2 (Flk-1)和 PDGFRβ，在无细胞试验中IC50分别为80 nM 和2 nM，也会抑制c-Kit的活性。	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)是一种新型有效的多靶点抑制剂，在无细胞试验中作用于Abl，PDGFRα，VEGFR2，FGFR1和Src，IC50分别为0.37 nM，1.1 nM，1.5 nM，2.2 nM和5.4 nM。	Nature, 2015, 10.1038/nature14329 Nature, 2016, 534(7609):647-51 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是一种多靶点抑制剂，作用于 VEGFR1，VEGFR2，VEGFR3，PDGFRβ和c-Kit，在猪主动脉内皮细胞中IC50分别为0.1 nM，0.2 nM，0.1-0.3 nM，1.6 nM和1.7 nM。	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是一种有效的泛KIT mutant抑制剂，在KIT突变体所驱动的Ba/F3细胞系中，GI50为1-50 nM。它还能抑制PDGFR突变体 (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V)。
S8757^New	Ripretinib (DCC-2618) DCC-2618是一种具有口服活性的KIT和PDGFR-alpha抑制剂，对WT KIT、V654A KIT、T670I KIT、D816H KIT和D816V KIT的IC50分别为4 nM、8 nM、18 nM、5 nM和14 nM。
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 瑞戈非尼是一种新型口服的多重激酶抑制剂，对VEGFR1、小鼠VEGFR2、小鼠VEGFR3、PDGFR-β、KIT、RET、RAF-1、B-RAF和B-RAF(V600E)的IC50分别为13, 4.2, 46, 22, 7, 1.5, 2.5, 28, 19 nM。
S2475	Imatinib (STI571) Imatinib (STI571)是一种多靶点酪氨酸激酶抑制剂，抑制v-Abl、c-Kit和PDGFR的IC50分别为0.6，0.1和0.1 μM。	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) 尼达尼布是一种有效的三重血管激酶抑制剂，作用于VEGFR1/2/3， FGFR1/2/3和PDGFRα/β，在无细胞试验中IC50分别为34 nM/13 nM/13 nM， 69 nM/37 nM/108 nM和59 nM/65 nM。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)是一种新型多靶点抑制剂，作用于VEGFR1，VEGFR2，VEGFR3，PDGFR，FGFR，c-Kit和c-fms，在无细胞试验中IC50分别是10 nM，30 nM，47 nM，84 nM，74 nM，140 nM和146 nM。	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 (TKI-258, CHIR-258)是一种多靶点的RTK抑制剂，在无细胞试验中对III型(FLT3/c-Kit)作用最强，IC50为1 nM/2 nM，同时也作用于IV类(FGFR1/3)和V类(VEGFR1-4) RTKs，IC50为8-13 nM，但对InsR，EGFR，c-Met，EphA2，Tie2，IGF-1R和HER2作用较弱。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)是一种新型有效的ATP竞争性VEGFR/PDGFR抑制剂，作用于KDR，CSF-1R，Flt-1/3和PDGFRβ，其IC50分别为4 nM，3 nM，3 nM/4 nM和66 nM，对突变激酶依赖性癌细胞（即FLT3）最有效。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)是一种有效的，选择性PDGFRα/β抑制剂，在CHO细胞中K_d为2.1 nM/3.2 nM，也能有效抑制FLT3，对D842V突变型敏感对V561D突变型不敏感，作用于PDGFR比作用于c-Kit，VEGFR-2，TIE-2，FGFR-2，EGFR，erbB2，和Src的选择性高100倍以上。	Blood, 2018, 132(1):67-77. Blood, 2016, 10.1182/blood-2015-10-673103 Clin Cancer Res, 2013, 19(24):6935-42	Combined treatment with Pim and FLT3 inhibitors abrogates growth of Ba/F3-ITD cells. Ba/F3-ITD cells were cultured at 1 × 105/mL with the Pim kinase inhibitor AZD1208 at 1 μmol/L and/or the FLT3 inhibitors quizartinib at 1 nmol/L, sorafenib at 2.5 nmol/L, crenolanib at 20 nmol/L or gilteritinib at 15 nmol/L, or DMSO control. Cell counts measured at 24, 48, and 72 hours were normalized to 0-hour control. Line graphs represent means ± SEM of triplicate values.
S1064	Masitinib (AB1010) Masitinib (AB1010)是一种新型的Kit和PDGFRα/β抑制剂，IC50分别为200 nM和540 nM/800 nM，但对ABL和c-Fms抑制作用较弱。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)是一种有效的，选择性VEGFR抑制剂，作用于VEGFR1/2/3时，IC50分别为0.21 nM/0.16 nM/0.24 nM，也抑制PDGFR和c-Kit，作用于FGFR-1， Flt3， c-Met EGFR和IGF-1R活性较弱。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)是一种有效的ATP竞争性的VEGFR1/2/3抑制剂，IC50分别为2 nM/3 nM/6 nM；对Kit具有相似的抑制活性，对VEGFR选择性比PDGFR和Ret高10倍。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)是一种有效的，作用于c-Kit， PDGFα和Flt3的多靶点抑制剂，IC50分别为10 nM， 40 nM和81 nM。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)有效作用于PDGFR自磷酸化，无细胞试验中K_i为8 nM，也强效抑制Flk-1和FGFR1反式磷酸化，对IGF-1R，Met， Src，Lck，Zap70，Abl和CDK2几乎没有抑制活性；对EGFR没有抑制作用。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是一种选择性的PDGFRα/β抑制剂，无细胞试验中IC50为10 nM/1 nM，比作用于其他血管生成受体选择性高450倍以上，具有抗血管生成和抗肿瘤活性。	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是一种有效的，选择性的VEGFR2抑制剂，IC50为0.9 nM，作用于VEGFR2比作用于c-Kit， PDGFRα和FGFR-2选择性高40倍以上，对EGFR， HGFR和InsR没有抑制活性。	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是一种有效的VEGFR2/3， c-Kit和PDGFRα抑制剂，IC50分别为6 nM/4 nM， 1 nM和15 nM。Phase 2。	Biochem Pharmacol, 2014, 89(1):52-61 Clin Cancer Res, 2018, 24(11):2678-2687	Serum starved and stimulated HUVECs overexpressing truncated FOSB were harvested 5 and 10 minutes after addition of serum. The cells were treated with telatinib at the indicated concentrations for 6 hours prior to addition of serum. At 100 nmol/L most phosphorylated VEGFR2 (KDR) is absent, whereas at 2 μmol/L it is completely absent.
S2622	PP121 PP121是一种作用于PDGFR， Hck， mTOR， VEGFR2， Src和Abl的多靶点抑制剂，IC50分别为2 nM， 8 nM， 10 nM， 12 nM， 14 nM和18 nM，也抑制DNA-PK，IC50为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是一种新型多靶点的VEGFR1，VEGFR2，VEGFR3，PDGFR，FGFR，c-Kit 和 c-Fms抑制剂，无细胞试验中IC50分别为10 nM，30 nM，47 nM，84 nM，74 nM，140 nM 和 146 nM。	Cancer Discov, 2013, 3(6):636-47 Clin Cancer Res, 2014, 19(9):2368-80 Clin Cancer Res, 2015, 21(5):1172-82
S2769	Dovitinib (TKI-258) Dilactic Acid Dovitinib (TKI-258) Dilactic Acid 是一种多靶点的RTK抑制剂，作用于III型(FLT3/c-Kit)最有效，IC50为1 nM/2 nM，也有效作用于IV型(FGFR1/3)和V型(VEGFR1-4)RTKs，IC50为8-13 nM，对InsR， EGFR， c-Met， EphA2， Tie2， IGFR1和HER2作用效果稍弱。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是一种有效的，多靶点抑制剂，作用于c-Met(WT/mutants)，IC50为0.4-2.5 nM，对Ron，和Flt1作用效果稍弱；作用于c-Met比作用于FGFR1， FGFR2， FGFR3， PDGFRβ， KDR， Flt3， Flt4， TrkA和TrkB选择性高8到30倍。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是一种PDGFR抑制剂，IC50为0.3-0.5 μM，对EGFR没有抑制活性。	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 是第一个EGFR抑制剂，IC50为460 μM，作用于PDGFR更有效，IC50为0.5μM。
S7765	Dovitinib (TKI258) Lactate Dovitinib (TKI258) Lactate是Dovitinib的乳酸盐，Dovitinib是一种多靶点的PTK抑制剂，主要对第III类(FLT3/c-Kit)发挥作用，IC50为1 nM/2 nM，对第IV 类(FGFR1/3)和第V 类(VEGFR1-4) RTKs也有效，IC50为8-13 nM，对InsR，EGFR，c-Met，EphA2，Tie2，IGFR1 和HER2作用较差。Phase 4。	Genome Biol, 2014, 15(8):428 Amino Acids, 2016, 48(7):1591-9 Neoplasia, 2013, 15(8):975-88	(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，一种从大黄根茎中分离得到的刺激性泻药，抑制PDGF刺激的细胞增殖。
S7781	Sunitinib Sunitinib 是一种多靶点 RTK 抑制剂，以VEGFR2(Flk-1)和PDGFRβ为靶点，IC50为80 nM 和 2 nM，对c-Kit也有抑制作用。	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)是一种小分子激酶抑制剂，可有效抑制PDGFRα D842V突变体的活性、在细胞背景下抑制PDGFRα D842V自我磷酸化（IC50=30 nM）；同时也是KIT突变（KIT D816V）的抑制剂（IC50=0.5 nM）。
S7003	AZD2932 AZD2932 是一种有效的多靶点蛋白酪氨酸激酶抑制剂，对VEGFR-2，PDGFRβ，Flt-3，和 c-Kit 的 IC50 分别为 8 nM，4 nM，7 nM，和 9 nM。
S4736	Trapidil Trapidil是PDGF的拮抗剂，可以抑制生成PDGF的神经胶质瘤细胞的增殖。

产品目录	产品描述	文献引用	实验数据
S1040	Sorafenib Tosylate Sorafenib Tosylate是一种酪氨酸激酶(VEGFR和PDGFR)和RAF/MEK/ERK级联抑制剂，同时作用于Raf-1，^wtBRAF和^V599EBRAF，IC50分别为6 nM， 22 nM和38 nM。	Blood, 2012, 120(19):4104-15 Blood, 2013, 122(9):1621-33 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)是一种口服生物有效的Imatinib甲磺酸盐，是一种多靶点抑制剂，作用于v-Abl，c-Kit和PDGFR，在无细胞和细胞试验中，IC50分别为0.6 μM，0.1 μM 和0.1 μM。	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是一种多靶点RTK抑制剂，作用于VEGFR2 (Flk-1)和 PDGFRβ，在无细胞试验中IC50分别为80 nM 和2 nM，也会抑制c-Kit的活性。	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)是一种新型有效的多靶点抑制剂，在无细胞试验中作用于Abl，PDGFRα，VEGFR2，FGFR1和Src，IC50分别为0.37 nM，1.1 nM，1.5 nM，2.2 nM和5.4 nM。	Nature, 2015, 10.1038/nature14329 Nature, 2016, 534(7609):647-51 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是一种多靶点抑制剂，作用于 VEGFR1，VEGFR2，VEGFR3，PDGFRβ和c-Kit，在猪主动脉内皮细胞中IC50分别为0.1 nM，0.2 nM，0.1-0.3 nM，1.6 nM和1.7 nM。	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是一种有效的泛KIT mutant抑制剂，在KIT突变体所驱动的Ba/F3细胞系中，GI50为1-50 nM。它还能抑制PDGFR突变体 (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V)。
S8757^New	Ripretinib (DCC-2618) DCC-2618是一种具有口服活性的KIT和PDGFR-alpha抑制剂，对WT KIT、V654A KIT、T670I KIT、D816H KIT和D816V KIT的IC50分别为4 nM、8 nM、18 nM、5 nM和14 nM。
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 瑞戈非尼是一种新型口服的多重激酶抑制剂，对VEGFR1、小鼠VEGFR2、小鼠VEGFR3、PDGFR-β、KIT、RET、RAF-1、B-RAF和B-RAF(V600E)的IC50分别为13, 4.2, 46, 22, 7, 1.5, 2.5, 28, 19 nM。
S2475	Imatinib (STI571) Imatinib (STI571)是一种多靶点酪氨酸激酶抑制剂，抑制v-Abl、c-Kit和PDGFR的IC50分别为0.6，0.1和0.1 μM。	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) 尼达尼布是一种有效的三重血管激酶抑制剂，作用于VEGFR1/2/3， FGFR1/2/3和PDGFRα/β，在无细胞试验中IC50分别为34 nM/13 nM/13 nM， 69 nM/37 nM/108 nM和59 nM/65 nM。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)是一种新型多靶点抑制剂，作用于VEGFR1，VEGFR2，VEGFR3，PDGFR，FGFR，c-Kit和c-fms，在无细胞试验中IC50分别是10 nM，30 nM，47 nM，84 nM，74 nM，140 nM和146 nM。	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 (TKI-258, CHIR-258)是一种多靶点的RTK抑制剂，在无细胞试验中对III型(FLT3/c-Kit)作用最强，IC50为1 nM/2 nM，同时也作用于IV类(FGFR1/3)和V类(VEGFR1-4) RTKs，IC50为8-13 nM，但对InsR，EGFR，c-Met，EphA2，Tie2，IGF-1R和HER2作用较弱。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)是一种新型有效的ATP竞争性VEGFR/PDGFR抑制剂，作用于KDR，CSF-1R，Flt-1/3和PDGFRβ，其IC50分别为4 nM，3 nM，3 nM/4 nM和66 nM，对突变激酶依赖性癌细胞（即FLT3）最有效。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)是一种有效的，选择性PDGFRα/β抑制剂，在CHO细胞中K_d为2.1 nM/3.2 nM，也能有效抑制FLT3，对D842V突变型敏感对V561D突变型不敏感，作用于PDGFR比作用于c-Kit，VEGFR-2，TIE-2，FGFR-2，EGFR，erbB2，和Src的选择性高100倍以上。	Blood, 2018, 132(1):67-77. Blood, 2016, 10.1182/blood-2015-10-673103 Clin Cancer Res, 2013, 19(24):6935-42	Combined treatment with Pim and FLT3 inhibitors abrogates growth of Ba/F3-ITD cells. Ba/F3-ITD cells were cultured at 1 × 105/mL with the Pim kinase inhibitor AZD1208 at 1 μmol/L and/or the FLT3 inhibitors quizartinib at 1 nmol/L, sorafenib at 2.5 nmol/L, crenolanib at 20 nmol/L or gilteritinib at 15 nmol/L, or DMSO control. Cell counts measured at 24, 48, and 72 hours were normalized to 0-hour control. Line graphs represent means ± SEM of triplicate values.
S1064	Masitinib (AB1010) Masitinib (AB1010)是一种新型的Kit和PDGFRα/β抑制剂，IC50分别为200 nM和540 nM/800 nM，但对ABL和c-Fms抑制作用较弱。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)是一种有效的，选择性VEGFR抑制剂，作用于VEGFR1/2/3时，IC50分别为0.21 nM/0.16 nM/0.24 nM，也抑制PDGFR和c-Kit，作用于FGFR-1， Flt3， c-Met EGFR和IGF-1R活性较弱。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)是一种有效的ATP竞争性的VEGFR1/2/3抑制剂，IC50分别为2 nM/3 nM/6 nM；对Kit具有相似的抑制活性，对VEGFR选择性比PDGFR和Ret高10倍。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)是一种有效的，作用于c-Kit， PDGFα和Flt3的多靶点抑制剂，IC50分别为10 nM， 40 nM和81 nM。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)有效作用于PDGFR自磷酸化，无细胞试验中K_i为8 nM，也强效抑制Flk-1和FGFR1反式磷酸化，对IGF-1R，Met， Src，Lck，Zap70，Abl和CDK2几乎没有抑制活性；对EGFR没有抑制作用。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是一种选择性的PDGFRα/β抑制剂，无细胞试验中IC50为10 nM/1 nM，比作用于其他血管生成受体选择性高450倍以上，具有抗血管生成和抗肿瘤活性。	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是一种有效的，选择性的VEGFR2抑制剂，IC50为0.9 nM，作用于VEGFR2比作用于c-Kit， PDGFRα和FGFR-2选择性高40倍以上，对EGFR， HGFR和InsR没有抑制活性。	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是一种有效的VEGFR2/3， c-Kit和PDGFRα抑制剂，IC50分别为6 nM/4 nM， 1 nM和15 nM。Phase 2。	Biochem Pharmacol, 2014, 89(1):52-61 Clin Cancer Res, 2018, 24(11):2678-2687	Serum starved and stimulated HUVECs overexpressing truncated FOSB were harvested 5 and 10 minutes after addition of serum. The cells were treated with telatinib at the indicated concentrations for 6 hours prior to addition of serum. At 100 nmol/L most phosphorylated VEGFR2 (KDR) is absent, whereas at 2 μmol/L it is completely absent.
S2622	PP121 PP121是一种作用于PDGFR， Hck， mTOR， VEGFR2， Src和Abl的多靶点抑制剂，IC50分别为2 nM， 8 nM， 10 nM， 12 nM， 14 nM和18 nM，也抑制DNA-PK，IC50为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是一种新型多靶点的VEGFR1，VEGFR2，VEGFR3，PDGFR，FGFR，c-Kit 和 c-Fms抑制剂，无细胞试验中IC50分别为10 nM，30 nM，47 nM，84 nM，74 nM，140 nM 和 146 nM。	Cancer Discov, 2013, 3(6):636-47 Clin Cancer Res, 2014, 19(9):2368-80 Clin Cancer Res, 2015, 21(5):1172-82
S2769	Dovitinib (TKI-258) Dilactic Acid Dovitinib (TKI-258) Dilactic Acid 是一种多靶点的RTK抑制剂，作用于III型(FLT3/c-Kit)最有效，IC50为1 nM/2 nM，也有效作用于IV型(FGFR1/3)和V型(VEGFR1-4)RTKs，IC50为8-13 nM，对InsR， EGFR， c-Met， EphA2， Tie2， IGFR1和HER2作用效果稍弱。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是一种有效的，多靶点抑制剂，作用于c-Met(WT/mutants)，IC50为0.4-2.5 nM，对Ron，和Flt1作用效果稍弱；作用于c-Met比作用于FGFR1， FGFR2， FGFR3， PDGFRβ， KDR， Flt3， Flt4， TrkA和TrkB选择性高8到30倍。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是一种PDGFR抑制剂，IC50为0.3-0.5 μM，对EGFR没有抑制活性。	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 是第一个EGFR抑制剂，IC50为460 μM，作用于PDGFR更有效，IC50为0.5μM。
S7765	Dovitinib (TKI258) Lactate Dovitinib (TKI258) Lactate是Dovitinib的乳酸盐，Dovitinib是一种多靶点的PTK抑制剂，主要对第III类(FLT3/c-Kit)发挥作用，IC50为1 nM/2 nM，对第IV 类(FGFR1/3)和第V 类(VEGFR1-4) RTKs也有效，IC50为8-13 nM，对InsR，EGFR，c-Met，EphA2，Tie2，IGFR1 和HER2作用较差。Phase 4。	Genome Biol, 2014, 15(8):428 Amino Acids, 2016, 48(7):1591-9 Neoplasia, 2013, 15(8):975-88	(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，一种从大黄根茎中分离得到的刺激性泻药，抑制PDGF刺激的细胞增殖。
S7781	Sunitinib Sunitinib 是一种多靶点 RTK 抑制剂，以VEGFR2(Flk-1)和PDGFRβ为靶点，IC50为80 nM 和 2 nM，对c-Kit也有抑制作用。	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)是一种小分子激酶抑制剂，可有效抑制PDGFRα D842V突变体的活性、在细胞背景下抑制PDGFRα D842V自我磷酸化（IC50=30 nM）；同时也是KIT突变（KIT D816V）的抑制剂（IC50=0.5 nM）。
S7003	AZD2932 AZD2932 是一种有效的多靶点蛋白酪氨酸激酶抑制剂，对VEGFR-2，PDGFRβ，Flt-3，和 c-Kit 的 IC50 分别为 8 nM，4 nM，7 nM，和 9 nM。