Catalog No.S7781 Synonyms: SU11248

Sunitinib Chemical Structure

Molecular Weight(MW): 398.47

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.

Size Price Stock Quantity  
USD 97 In stock
USD 197 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Cited by 32 Publications

11 Customer Reviews

  • 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.

    Nature 2011 478(7369):349-55. Sunitinib purchased from Selleck.

    Assessment of effects on human juvenile or adult islets after exposure to PDGF-AA (50 ng/ml) for 2 days, with or without Sunitinib (2 uM) or U0126 (10 uM)co-treatment. Average percentage of BrdU+ insulin+ cells was morphometry from sectioned islets immunostained for insulin (green), glucagon (white) and BrdU (red). n = 3-6 independent experiments.

    Nature 2011 478(7369):349-55. Sunitinib purchased from Selleck.

  • 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.

    Cell Res 2011 21, 1080-1087. Sunitinib purchased from Selleck.

    Sunitinib decreases FLT-3 and RET phosphor ylation but increases ERK phosphorylation in a time-dependent manner. H295R and SW13 cells were treated with sunitinib (10 nM) for various time points as indi-cated. Cell lysates were prepared and phospho-FLT-3, RET, and ERK levels were monitored by Western Blot-ting. Re-probing against FLT-3, RET, and ERK was done to ensure equal protein loading.

    Surgery 2012 152, 1045-50. Sunitinib purchased from Selleck.

  • Sunitinib or PD98059 decreases cell proliferation in a dose-dependent manner. H295R and SW13 cells were treated with various concentration of sunitinib or PD98059 for 48 hours as indicated. Treated cells were subjected to the MTS proliferation assay. Similar experiments were repeated 3 times. Histograms represent relative % of OD490 nm absorbance (* P < .05). All data are relative multiples of expression compared with untreated cells. The data are representative of three experiments and are expressed as the mean ?SE.

    Surgery 2012 152, 1045-50. Sunitinib purchased from Selleck.

    Autophagic activation in sunitinib- and sorafenib- but not AZD6244-treated cells. Medullary thyroid cancer-1.1 (MTC-1.1; A) and TT ( B) cells were treated with dimethyl sulfoxide (DMSO), sunitinib (50 nM), sorafenib (10 nM), AZD6244 (30 nM), or everolimus (20 nM) for 48 hours. Cell lysates were prepared, and light chain 3 (LC3)-I and -II cleaved caspase-3 protein levels were monitored by Western blotting. Reprobing against actin was per formed to ensure equal protein loading. ( C ) MTC-1.1 and TT cells were transiently transfected with autophagy protein 5 (Atg-5) small inter fering RNA. Transfection with scrambled small inter fering RNA was used as a control. After transfection, cells with and without Atg-5 knockdown were exposed to DMSO or 20 nM of everolimus for 48 hours. Cell lysates were pre- pared and LC3-I and -II protein expression levels were monitored by Western blotting. Reprobing against Atg-5 was per formed to monitor Atg-5 knockdown efficiency. Reprobing against actin was per formed to ensure equal protein.

    Surgery 2012 152, 1142-9. Sunitinib purchased from Selleck.

  • Autophagy inhibition blocks the antiproliferative effects of sunitinib and sorafenib but not AZD6244. Medullary thyroid cancer–1.1 (MTC-1.1) and TT cells were transfected transiently with scrambled or autophagy protein 5 (Atg-5) small inter fering RNA. After transfection, cells with and without Atg-5 knockdown were exposed to sunitinib (50 nM), sorafenib (10 nM), and AZD6244 (30 nM) for 48 hours. Treated cells were subjected to a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium proliferation assay. Similar experiments were repeated 3 times. Histograms represent the relative percent of OD490 nM absorbance. The asterisk indicates significance versus scrambled small inter fering RNA–treated control ( P < .05). All data are relative multiples of expression compared to untreated cells. The data are representative of 3 experiments and are expressed as the mean ± the standard error.

    Surgery 2012 152, 1142-9. Sunitinib purchased from Selleck.

    Sunitinib limits the colonial growth of HT-29 by downregulating HIF-1a. (A) The number and size of colonies formed in soft agar. The numbers of small colonies (<50 μm diameter) were not different among conditions of a serial concentration of sunitinib. On the contrary, large colonies (>50 μm diameter) disappeared after incubation with sunitinib. Each point represents the mean and SD from four separate experiments. (B) HIF-1a expression and hypoxia within HT-29 colony. After colonies grew for 4 weeks, HIF-1a and hypoxia were visualized by immunofluoroscence staining. Bar = 20 μm.

    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

  • 2. Sunitinib downregulates HIF-1a. (A) Dose-dependent repression of HIF-1a protein level by sunitinib in HT-29. HT-29 cells were incubated under normoxic (N) or hypoxic (H) conditions in the presence of sunitinib for 24 h. HIF-1a and ARNT proteins in total cell lysates were analyzed by Western blotting. (B) Sunitinib attenuates the hypoxic induction of HIF-1 target genes. RNAs were isolated from HT-29 cells subjected to normoxia (N) or hypoxia (H) in the presence of sunitinib for 16 h. The mRNAs of HIF-1a and its target genes were analyzed by RT-PCR and autoradiography. PGK1 indicates phosphoglycerate kinase 1; PDK1, pyruvate dyhydrogenase kinase 1; CAIX, carbonic anhydrase IX. (C) Sunitinib-induced HIF-1 inhibition. Epo-enhancer and b- galactosidase reporter plasmids were co-transfected into HEK293 cells. After 16 h incubation, luciferase and b-galactosidase activities were measured. *P < .05 versus the hypoxic control.



    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

    Sunitinib inhibits 50-UTR-dependent translation of HIF-1a. (A) 50 cap-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the tk promoter and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 lg per 100-mm dish) and the b-gal plasmid (4 μg). After 16 h incubation under normoxic or hypoxic conditions with sunitinib, cells were lysed and subjected to luciferase assay. *P < .05 versus the hypoxic control. (B) IRES-dependent translational activity of HIF-1a. The luciferase reporter plasmid contains the HIF-1a 50-UTR segment between the GFP gene and the luciferase gene. HT-29 cells were co-transfected with the reporter plasmid (8 μg) and the b-gal plasmid (4 μg). *P < .05 versus the hypoxic control. (C) Sunitinib inhibits phosphorylation of Akt. After 8 h incubation under hypoxic condition with sunitinib, HT-29 cells were lysed and subjected to Western blotting. (D) Sunitinib suppresses HIF-1a in VHL-null RCC4 cells. VHL (-/-) RCC4 cells were incubated under normoxic conditions sunitinib for 8 h, and HIF-1a in total cell lysates was analyzed by Western blotting.



    Biochem Bioph Res Co 2010 398, 205-211. Sunitinib purchased from Selleck.

  • Experimental layout for VEGF signaling blocking and LCMV infection in WT mice. Mice received two injections on day 0 and 3 p.i. of Abs as described in Material and Methods, or daily gavage of the VEGFR/PDGFR-inhibitor sunitinib. Inguinal LN volume on day 0 (D0) or day 8 (D8) p.i. after treatment of mice with control Ig or anti-VEGFR2, anti-VEGF-A Abs or sunitinib. Pooled from 1-2 independent experiments with 3-5 mice per treatment. D. Total HEV length on day 0 (D0) or day 8 (D8) p.i. as in C. No significant difference was found in C and D between day 8 control Ig and Ab- or inhibitor-treated values (One-way ANOVA).

    AACR Sunitinib purchased from Selleck.

Purity & Quality Control

Choose Selective PDGFR Inhibitors

Biological Activity

Description 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.
Kit [1] FLT3 [1] c-Kit [1] PDGFRβ [1] VEGFR2 [1]
2 nM 80 nM
In vitro

Sunitinib also potently inhibits Kit and FLT-3. [1] Sunitinib is a potent ATP-competitive inhibitor of VEGFR2 (Flk1) and PDGFRβ with Ki of 9 nM and 8 nM, respectively, displaying >10-fold higher selectivity for VEGFR2 and PDGFR than FGFR-1, EGFR, Cdk2, Met, IGFR-1, Abl, and src. In serum-starved NIH-3T3 cells expressing VEGFR2 or PDGFRβ, Sunitinib inhibits VEGF-dependent VEGFR2 phosphorylation and PDGF-dependent PDGFRβ phosphorylation with IC50 of 10 nM and 10 nM, respectively. Sunitinib inhibits VEGF-induced proliferation of serum-starved HUVECs with IC50 of 40 nM, and inhibits PDGF-induced proliferation of NIH-3T3 cells overexpressing PDGFRβ or PDGFRα with IC50 of 39 nM and 69 nM, respectively. [2] Sunitinib inhibits phosphorylation of wild-type FLT3, FLT3-ITD, and FLT3-Asp835 with IC50 of 250 nM, 50 nM, and 30 nM, respectively. Sunitinib inhibits the proliferation of MV4;11 and OC1-AML5 cells with IC50 of 8 nM and 14 nM, respectively, and induces apoptosis in a dose-dependent manner. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SW756 cell M3[wb2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M{HKTWlvcGmkaYTpc44hd2ZiaIXtZY4hW1d5NU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xPU4yOzVzIN88US=> NWHuOpZtW0GQR1XS
human EoL-1-cell cell MmDyS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NUfNcpNRUW6qaXLpeIlwdiCxZjDoeY1idiCHb1ytNU1k\WyuIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62OIUuODZ? NGDTb2pUSU6JRWK=
human MV-4-11 cell MUXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MUXJcohq[mm2aX;uJI9nKGi3bXHuJG1XNTRvMUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlI4OiCwTR?= MljpV2FPT0WU
human MV411 cells M1LTZnBzd2yrZnXyZZRqd25iYYPzZZk> NVvD[VE{PDhiaB?= MWPBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2YNEGxJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCPVGSgZZN{[XluIHnjOVA:OyCwTR?= Mn7SNlQ6ODR7NkG=
3T3 cells NF3DSVdHfW6ldHnvckBie3OjeR?= MkT4TY5pcWKrdHnvckBw\iCSRFfGMYlv\HWlZXSgRpJlXSCrbnPvdpBwemG2aX;uJIlvKDOWMzDj[YxteyC5aYToJFAvOSViYn;2bY5mKHOncoXtJIFt[nWvaX6sJGlEPTB;NzDuUS=> NFzx[|kyOjZ2NkCxPS=>
HEK293 cells M3zGVGZ2dmO2aX;uJIF{e2G7 NX\oRlFjSmmwZHnu[{Bi\m[rbnn0fUB1dyCITGSzJINifGGueYTpZ{Bld22jaX6g[ZhxemW|c3XkJIlvKEiHS{K5N{Bk\WyuczDifUBkd22yZYTpeIl3\SCkaX7kbY5oKGG|c3H5MEBM\D1yLkS3JI5O MYWxPVc2PDF7OR?=
human MDA-MB-435 cells MUnDfZRwfG:6aXRCpIF{e2G7 NGDaW2YzKGh? NUfHeVhbS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSDLV3CMVQ{PSClZXzsd{whUUN3ME25Mlchdk1? M2KzXlI1QDlyNkWy
human RS4-11 cells NF\aUpBHfW6ldHnvckBie3OjeR?= NWfkR3FRUW6qaXLpeIlwdiCxZjDGUHQ{KGG3dH;wbI9{eGixconsZZRqd25iaX6gbJVu[W5iUmO0MVEyKGOnbHzzJIFnfGW{IEKgbJJ{KGK7IHXs[YN1em:laHXtbYx2dWmwZYPj[Y5k\SCjc4PhfUwhUUN3ME25Mlkhdk1? MlrwNVk3PTR2MEi=
HUVEC NYTZVJNkS3m2b4TvfIlkyqCjc4PhfS=> NEK1[XBEgXSxdH;4bYNqfHliYXfhbY5{fCCKVW\FR{whUUN3ME2xNU45KG6P NH:1bFEzPDh7ME[1Ni=>
human Kasumi-1 cells Mnj5SpVv[3Srb36gZZN{[Xl? NInvWmlKdmirYnn0bY9vKG:oIHOtT4l1KGG3dH;wbI9{eGixconsZZRqd25iaX6gbJVu[W5iS3HzeY1qNTFiY3XscJMh[nliV3XzeIVzdiCkbH;0JIFv[Wy7c3nzMEBKSzVyPUG1JI5O NHq5TZozODh|M{CzPS=>
human NOS-1 cell M3HIWGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NHSzNI1KdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= Ml7sV2FPT0WU
mouse triple negative 4T1 cells MmK3R5l1d3SxeHnjxsBie3OjeR?= NEm4VZJEgXSxdH;4bYNqfHliYXfhbY5{fCCvb4Xz[UB1emmybHWgcoVo[XSrdnWgOHQyKGOnbHzzMEBKSzVyPUG2JI5O Ml;KNlQ5QTB4NUK=
human RS4-11 cells MoXnSpVv[3Srb36gZZN{[Xl? NHnhbZJKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N MmX5NlA5OzNyM{m=
human MOLM13 cells MmHMR5l1d3SxeHnjxsBie3OjeR?= NIfKflZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOV0yPMUOgZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCC4aXHibYxqfHliYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0yPy55IH7N MXSyOVA5QThzMB?=
human U251 cells M1PwZWZ2dmO2aX;uJIF{e2G7 NYKye4RjUW6qaXLpeIlwdiCxZjDWSWdHWjJiaX6gbJVu[W5iVUK1NUBk\WyuczDifUBxcG:|cHjveJlzd3OrbnWgSWxKW0FuIFnDOVA:OThwOTDuUS=> NXnyWYg2OjR7MEC4OlU>
NIH3T3 cells MorlSpVv[3Srb36gZZN{[Xl? NUjJeZB5OSCq MXrJcohq[mm2b4L5JINwdmOnboTyZZRqd25iYXfhbY5{fCCqdX3hckBMTFJia3nuZZNmKGW6cILld5Nm\CCrbjDOTWg{XDNiY3XscJMhf2m2aDC0JJVOKEKrb4Tpck1CcHhvQVXFSXlHTkyIQT3hcYll\SCjdDDhcYJq\W62IITlcZBmemG2dYLlJIZweiBzIHjy MVKxOlE3OjByOB?=
MDA-MB-231 cells MUTDfZRwfG:6aXRCpIF{e2G7 NWrJN|lVS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hfHKrcHzlJI5m\2G2aY\lJG1FSS2PQj2yN|Eh[2WubIOsJGlEPTB;MkKuN{BvVQ>? MX:yOFg6ODZ3Mh?=
MCF7 cells MmXZR5l1d3SxeHnjxsBie3OjeR?= MXvDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDFVk1xd3OrdHn2[UBOS0Z5IHPlcIx{NCCLQ{WwQVI4NjFibl2= NH;jTY0zPDh7ME[1Ni=>
human CGTH-W-1 cell NY[2Xow2T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MlvRTY5pcWKrdHnvckBw\iCqdX3hckBET1SKLWetNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMxNjl2IH7N MXPTRW5ITVJ?
human MONO-MAC-6 cell NGrsN2FIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MW\Jcohq[mm2aX;uJI9nKGi3bXHuJG1QVk9vTVHDMVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{Oy56IH7N NInhNYtUSU6JRWK=
human HL60 cells NVP2S|Y6S3m2b4TvfIlkyqCjc4PhfS=> MWS0PEBp MUfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUFYxKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;M{[uPEBvVQ>? MYGyOVA5QThzMB?=
human TT cells NHXCNJpRem:uaX\ldoF1cW:wIHHzd4F6 NUjjfHp3PzJiaB?= NFe4d4RCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGTUJINmdGy|IIDy[ZRz\WG2ZXSg[o9zKDd{IHjyd{Bnd2yub4fl[EBjgSClb33wc5Vv\C25YYPoc5V1KG2nYYP1doVlKGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9OFAhdk1? NGjKVnYzPDlyNEm2NS=>
human THP1 cells M3rIb2N6fG:2b4jpZ:Kh[XO|YYm= NYPFb2V6PDhiaB?= M4HwW2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHRJWDFiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME20OU44KG6P MoXvNlUxQDl6MUC=
3T3 cells M13Eb2Z2dmO2aX;uJIF{e2G7 NXHocZJzUW6qaXLpeIlwdiCxZjDWZZNkfWyjcjDlcoRwfGinbHnhcEBoem:5dHig[oFkfG:{IILlZ4VxfG:{IHnuJFNVOyClZXzsd{whUUN3ME21NEBvVQ>? NXHXS3I3OTJ4NE[wNVk>
human ALL-PO cell NF:4UVlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NILnT21KdmirYnn0bY9vKG:oIHj1cYFvKEGOTD3QU{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVc6Njh7IH7N Mnq4V2FPT0WU
human SH-SY5Y cells MmrESpVv[3Srb36gZZN{[Xl? NF64[HdKdmirYnn0bY9vKG:oIGDES2ZT[mW2YTDpckBpfW2jbjDTTE1UYTW\IHPlcIx{KGK7IIDoc5NxcG:2eYLvd4lv\SCHTFnTRUBie3OjeTygTWM2OD16Mz6xJI5O M4X6V|I1QDlyNkWy
human U251 cells M3rTcmZ2dmO2aX;uJIF{e2G7 NGL4Wpg3OCCvaX7z MWfJcohq[mm2aX;uJI9nKFCGR1\SMYJmfGFiaX6gbJVu[W5iVUK1NUBk\WyuczDjc41xd3WwZDDwdoV1emWjdHXkJIZweiB4MDDtbY4h[mWob4LlJHBFT0ZvQlKgd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME24N{4yKG6P NXrUcHE6OjV6OEK1NVk>
human NKM-1 cell NVfKc2EzT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MVjJcohq[mm2aX;uJI9nKGi3bXHuJG5MVS1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;OUiuOVIhdk1? MXnTRW5ITVJ?
human HAEC cells NVm1OnlXWHKxbHnm[ZJifGmxbjDhd5NigQ>? MWG3NkBp NHjMUWpCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjBSWMh[2WubIOg[ZhxemW|c3nu[{BXTUeIUjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTBwMTFOwG0> NF6yTIwzOjR2NE[3PS=>
HUVEC cell M4ry[mZ2dmO2aX;uJIF{e2G7 MWWyOEBp NVzkVWtnUW6qaXLpeIlwdiCxZjDWSWdHNUFiaX7keYNm\CCKVW\FR{Bk\WyuIIPwdo92fGmwZzDh[pRmeiB{NDDodpMh[nliYX7nbY9o\W6nc3nzJIF{e2G7LDDJR|UxRTBwMUKg{txO MXiyNVc1OTJ2OR?=
human A431 cells M3T4bGZ2dmO2aX;uJIF{e2G7 NI\sS|Y3OCCvaX7z NFvHO3lKdmirYnn0bY9vKG:oIFXHSnIhcW5iaIXtZY4hSTR|MTDj[YxteyClb33wc5Vv\CCycnX0doVifGWmIH\vdkA3OCCvaX6gZoVnd3KnIFXHSkB{fGmvdXzheIlwdiCob4KgNVAhdWmwczDifUBxcG:|cHjveJlzd3OrbnWgSWxKW0FiY4n0c4Jtd3RibXX0bI9lNCCLQ{WwQVE4Oi5zIH7N M{jCTlI2QDh{NUG5
Sf9 cells MlzOSpVv[3Srb36gZZN{[Xl? M1HGd2lvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDWSWdHWiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUCuNVg2KM7:TR?= NYjyOplUOTl6NUSwOVE>
human HT-29 cells MnXZVJJwdGmoZYLheIlwdiCjc4PhfS=> NWH4ZlFPPzJiaB?= M2Xae2FvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSGStNlkh[2WubIOg[ZhxemW|c3nu[{BXTUeIUjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G778{MJGlEPTB;MD6zN{DPxE1? M1[2RVIzPDR2Nke5
human KM12 cell MlPTS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NVf2dIlTUW6qaXLpeIlwdiCxZjDoeY1idiCNTUGyJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE4{PTBzNDFOwG0> MYXTRW5ITVJ?
human TE-15 cell MlvlS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NX;qZXV2UW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xOUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVAvPTB5NkGg{txO M2\6T3NCVkeHUh?=
human 697 cell NGT1NolIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NEHzV3ZKdmirYnn0bY9vKG:oIHj1cYFvKDZ7NzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOlE1OjVizszN MnPkV2FPT0WU
human CAKI-1 cells NUjiepEzWHKxbHnm[ZJifGmxbjDhd5NigQ>? MWHBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEODS1mtNUBk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTBwNkOg{txO NYrUTmVZOjJ3NkC2Nlc>
human MOLT-16 cell MYrHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MWHJcohq[mm2aX;uJI9nKGi3bXHuJG1QVFRvMU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlY{OTN{IN88US=> NHWzWWtUSU6JRWK=
human GB-1 cell MYTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NW\uOGRzUW6qaXLpeIlwdiCxZjDoeY1idiCJQj2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE44OTB{MzFOwG0> NUDQZlh4W0GQR1XS
human TE-12 cell NI\ySWRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M3;QW2lvcGmkaYTpc44hd2ZiaIXtZY4hXEVvMUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlgxPDV3IN88US=> NF\Gc2RUSU6JRWK=
human NCI-H3122 cells NWnCN29FWHKxbHnm[ZJifGmxbjDhd5NigQ>? MUK3NkBp NHzaTmVCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTU1JOzF{MjDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvQDNizszN NIj3N4szPDlyNEm2NS=>
human ES6 cell Mme3S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M{LwR2lvcGmkaYTpc44hd2ZiaIXtZY4hTVN4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD65PFExPiEQvF2= MVrTRW5ITVJ?
human NCI-H526 cells NHGxcJVRem:uaX\ldoF1cW:wIHHzd4F6 M2DlflczKGh? MkjzRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1mtTFUzPiClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUGuNFEh|ryP MUeyOFkxPDl4MR?=
human LC-2-ad cell MYDHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M4DrTGlvcGmkaYTpc44hd2ZiaIXtZY4hVENvMj3h[EBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvOTF2MEeg{txO MnLzV2FPT0WU
human BL-70 cell Mn6xS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXqyPYx5UW6qaXLpeIlwdiCxZjDoeY1idiCETD23NEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvOTF6NE[g{txO MUTTRW5ITVJ?
human ETK-1 cell M1Pjb2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MmK1TY5pcWKrdHnvckBw\iCqdX3hckBGXEtvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuNlg2QCEQvF2= NWO1bXFSW0GQR1XS
human SW620 cells MlyzVJJwdGmoZYLheIlwdiCjc4PhfS=> MUG0PEBp MknZRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCVV{[yNEBk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTFwMzFOwG0> MWeyNlU3ODZ{Nx?=
IM9 cells NWDkd3N5S3m2b4TvfIlkyqCjc4PhfS=> MU\DfZRwfG:6aXPpeJkh[WejaX7zeEBJd22xIIPhdIlmdnNiKHj1cYFvMSCLTUmgZ4VtdHNiYYPz[ZN{\WRiYYOg[5Jwf3SqIHnubIljcXSrb36gZpkhVVSWIHHzd4F6NCCLQ{WwQVEvOzVizszN MmPBV2FPT0WU
human A4-Fuk cell M1ThUmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M37YOmlvcGmkaYTpc44hd2ZiaIXtZY4hSTRvRoXrJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZnwxIxiSVO1NF0yNjN2MUSxJO69VQ>? NVTJSpBoW0GQR1XS
human SR cell NW\TRmtWT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MWHJcohq[mm2aX;uJI9nKGi3bXHuJHNTKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS53NEW3NkDPxE1? MVnTRW5ITVJ?
human A3-KAW cell MmnBS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M{LsOWlvcGmkaYTpc44hd2ZiaIXtZY4hSTNvS1HXJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKGmlNUC9NU43OjV2NjFOwG0> MlHqV2FPT0WU
human KS-1 cell M2m2fWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MnuyTY5pcWKrdHnvckBw\iCqdX3hckBMWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62PVI1PyEQvF2= M4nKZnNCVkeHUh?=
human CTV-1 cell M2X2U2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NHewd|JKdmirYnn0bY9vKG:oIHj1cYFvKEOWVj2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU44Ojd3MTFOwG0> NGPrSJJUSU6JRWK=
human LB1047-RCC cell MUPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NGPIfpNKdmirYnn0bY9vKG:oIHj1cYFvKEyEMUC0O{1TS0NiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkixOlI1KM7:TR?= MVnTRW5ITVJ?
human MEG-01 cell M1\3VGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MWnJcohq[mm2aX;uJI9nKGi3bXHuJG1GTy1yMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPFM2PjNizszN MV7TRW5ITVJ?
human TE-11 cell NXrJT|ZjT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M{WwTmlvcGmkaYTpc44hd2ZiaIXtZY4hXEVvMUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlg{QTh3IN88US=> MUDTRW5ITVJ?
human CMK cell MoK4S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MYTJcohq[mm2aX;uJI9nKGi3bXHuJGNOUyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOUW1NVch|ryP M1rpdnNCVkeHUh?=
human NB1 cell M3ft[2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NV3FTotlUW6qaXLpeIlwdiCxZjDoeY1idiCQQkGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlk3OTF5IN88US=> MojnV2FPT0WU
human MDA-MB-435 cells MnXnVJJwdGmoZYLheIlwdiCjc4PhfS=> Mon5OFghcA>? NYLMXFM{SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNSGEuVUJvNEO1JINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJQVIh|ryP MViyNlU3ODZ{Nx?=
human MCF7 cells MX;Qdo9tcW[ncnH0bY9vKGG|c3H5 M2e0e|Q5KGh? NESyNppCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3DSlch[2WubIOgZYZ1\XJiNEigbJJ{KGK7IGPSRkBie3OjeTygS2k2OD1{IN88US=> NVTkeoxlOjJ3NkC2Nlc>
human A549 cells MULDfZRwfG:6aXRCpIF{e2G7 M{HWe|czKGh? NVnZTm1CS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTV2OTDj[YxteyCjc4Pld5Nm\CCjczDndo94fGhiaX7obYJqfGmxbjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTJwNESg{txO MVSyN|YxOjR2MR?=

... Click to View More Cell Line Experimental Data

In vivo Consistent with the substantial and selective inhibition of VEGFR2 or PDGFR phosphorylation and signaling in vivo, Sunitinib (20-80 mg/kg/day) exhibits broad and potent dose-dependent anti-tumor activity against a variety of tumor xenograft models including HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435. Sunitinib dosing at 80 mg/kg/day for 21 days leads to complete tumor regression in six of eight mice, without tumor re-growing during a 110-day observation period after the end of treatment. Second round of treatment with Sunitinib remains efficacious against tumors that are not fully regressed during the first round of treatment. Sunitinib treatment results in significant decrease in tumor MVD, with ~40% reduction in SF763T glioma tumors. SU11248 treatment results in a complete inhibition of additional tumor growth of luciferase-expressing PC-3M xenografts, despite no reduction in tumor size. [2] Sunitinib treatment (20 mg/kg/day) dramatically suppresses the growth subcutaneous MV4;11 (FLT3-ITD) xenografts and prolongs survival in the FLT3-ITD bone marrow engraftment model. [3]


Kinase Assay:


+ Expand

Biochemical Tyrosine Kinase Assays:

IC50 values for Sunitinib against VEGFR2 (Flk-1) and PDGFRβ are determined using glutathione S-transferase fusion proteins containing the complete cytoplasmic domain of the RTK. Biochemical tyrosine kinase assays to quantitate the trans-phosphorylation activity of VEGFR2 (Flk-1) and PDGFRβ are performed in 96-well microtiter plates precoated (20 μg/well in PBS; incubated overnight at 4 °C) with the peptide substrate poly-Glu,Tyr (4:1). Excess protein binding sites are blocked with the addition of 1-5% (w/v) BSA in PBS. Purified GST-fusion proteins are produced in baculovirus-infected insect cells. GST-VEGFR2 and GST-PDGFRβ are then added to the microtiter wells in 2 × concentration kinase dilution buffer consisting of 100 mM HEPES, 50 mM NaCl, 40 μM NaVO4, and 0.02% (w/v) BSA. The final enzyme concentration for GST-VEGFR2 or GST-PDGFRβ is 50 ng/mL. Twenty-five μL of diluted Sunitinib are subsequently added to each reaction well to produce a range of inhibitor concentrations appropriate for each enzyme. The kinase reaction is initiated by the addition of different concentrations of ATP in a solution of MnCl2 so that the final ATP concentrations spanned the Km for the enzyme, and the final concentration of MnCl2 is 10 mM. The plates are incubated for 5-15 minutes at room temperature before stopping the reaction with the addition of EDTA. The plates are then washed three times with TBST. Rabbit polyclonal antiphosphotyrosine antisera are added to the wells at a 1:10,000 dilution in TBST containing 0.5% (w/v) BSA, 0.025% (w/v) nonfat dry milk, and 100 μM NaVO4 and incubated for 1 hour at 37 °C. The plates are then washed three times with TBST, followed by the addition of goat antirabbit antisera conjugated with horseradish peroxidase (1:10,000 dilution in TBST). The plates are incubated for 1 hour at 37 °C and then washed three times with TBST. The amount of phosphotyrosine in each well is quantitated after the addition of 2,2′-azino-di-[3-ethylbenzthiazoline sulfonate] as substrate.
Cell Research:


+ Expand
  • Cell lines: RS4;11, MV4;11, and OC1-AML5
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 24 and 48 hours
  • Method:

    Cells are starved overnight in medium containing 0.1% FBS prior to addition of Sunitinib and FL (50 ng/mL; FLT3-WT cells only). Proliferation is measured after 48 hours of culture using the Alamar Blue assay or trypan blue cell viability assays. Apoptosis is measured 24 hours after Sunitinib addition by Western blotting to detect cleavage of poly (ADP-ribose) polymerase (PARP) or levels of caspase-3.

    (Only for Reference)
Animal Research:


+ Expand
  • Animal Models: Female nu/nu mice implanted s.c. with HT-29, A431, Colo205, H-460, SF763T, C6, A375, or MDA-MB-435, and male nu/nu mice bearing luciferase-expressing PC-3M tumors
  • Formulation: Formulated as a carboxymethyl cellulose suspension or as a citrate buffered (pH 3.5) solution
  • Dosages: ~80 mg/kg
  • Administration: Orally once daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 25 mg/mL warmed (62.73 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 5% DMSO+corn oil 7mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 398.47


CAS No. 557795-19-4
Storage powder
in solvent
Synonyms SU11248

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01731925 Active, not recruiting Carcinoid Tumors Groupe Cooperateur Multidisciplinaire en Oncologie (GERCOR)|Pfizer|Ipsen January 7, 2013 Phase 2
NCT02315625 Recruiting Neuroendocrine Tumors National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 5, 2014 Phase 2
NCT01306045 Recruiting Carcinoma, Non-Small-Cell Lung|Carcinoma, Small Cell Lung|Carcinoma, Thymic National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) January 21, 2011 Phase 2
NCT03025893 Not yet recruiting Glioblastoma Multiforme|Glioblastoma, Adult|Glioblastoma|Recurrent Brain Tumor|GBM VU University Medical Center March 2017 Phase 2|Phase 3
NCT03035630 Not yet recruiting Clear-cell Renal Cell Carcinoma|RCC|Kidney Cancer|Clear-cell Kidney Carcinoma Guru Sonpavde|Hoosier Cancer Research Network|Pfizer February 2017 Phase 2
NCT02959554 Recruiting Metastatic Renal Cell Carcinoma AIO-Studien-gGmbH|Bristol-Myers Squibb November 2016 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

PDGFR Signaling Pathway Map

Related PDGFR Products

Tags: buy Sunitinib | Sunitinib supplier | purchase Sunitinib | Sunitinib cost | Sunitinib manufacturer | order Sunitinib | Sunitinib distributor
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID