Sunitinib

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.

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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

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

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.
Targets
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 MoHsS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M1n5bmlvcGmkaYTpc44hd2ZiaIXtZY4hW1d5NU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xPU4yOzVzIN88US=> MojoV2FPT0WU
human EoL-1-cell cell MmDKS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? Mm\jTY5pcWKrdHnvckBw\iCqdX3hckBGd0xvMT3j[YxtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS54NHWtNFY> MXPTRW5ITVJ?
human MV-4-11 cell MmDPS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NHu4WoRKdmirYnn0bY9vKG:oIHj1cYFvKE2YLUStNVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjJ5MjDuUS=> Mnq3V2FPT0WU
human MV411 cells MVjQdo9tcW[ncnH0bY9vKGG|c3H5 MlixOFghcA>? MUnBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2YNEGxJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCPVGSgZZN{[XluIHnjOVA:OyCwTR?= M3\IWlI1QTB2OU[x
3T3 cells MVvGeY5kfGmxbjDhd5NigQ>? MnTmTY5pcWKrdHnvckBw\iCSRFfGMYlv\HWlZXSgRpJlXSCrbnPvdpBwemG2aX;uJIlvKDOWMzDj[YxteyC5aYToJFAvOSViYn;2bY5mKHOncoXtJIFt[nWvaX6sJGlEPTB;NzDuUS=> M4DXV|EzPjR4MEG5
HEK293 cells Mmm3SpVv[3Srb36gZZN{[Xl? MmPHRolv\GmwZzDh[oZqdmm2eTD0c{BHVFR|IHPheIFtgXSrYzDkc41icW5iZYjwdoV{e2WmIHnuJGhGUzJ7MzDj[YxteyCkeTDjc41x\XSrdHn2[UBjcW6maX7nJIF{e2G7LDDL[F0xNjR5IH7N MVyxPVc2PDF7OR?=
human MDA-MB-435 cells NUnYdFhsS3m2b4TvfIlkyqCjc4PhfS=> MmjuNkBp Ml72R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCNU2ELUSzOUBk\WyuczygTWM2OD17Lkegcm0> NX3SPXNzOjR6OUC2OVI>
human RS4-11 cells MoDJSpVv[3Srb36gZZN{[Xl? NELkUHBKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZYZ1\XJiMjDodpMh[nliZXzlZ5Rzd2OqZX3pcJVucW6nc3PlcoNmKGG|c3H5MEBKSzVyPUmuPUBvVQ>? NXm3PWhKOTl4NUS0NFg>
HUVEC NV:0XFBYS3m2b4TvfIlkyqCjc4PhfS=> MkfoR5l1d3SxeHnjbZR6KGGpYXnud5QhUFWYRVOsJGlEPTB;MUGuPEBvVQ>? NG\RfVczPDh7ME[1Ni=>
human Kasumi-1 cells M1PkWmZ2dmO2aX;uJIF{e2G7 Mn2yTY5pcWKrdHnvckBw\iClLVvpeEBifXSxcHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKEujc4XtbU0yKGOnbHzzJIJ6KFenc4Tldo4h[myxdDDhcoFtgXOrczygTWM2OD1zNTDuUS=> MoLwNlA5OzNyM{m=
human NOS-1 cell NH\2S29Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= NF7YclFKdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= MXTTRW5ITVJ?
mouse triple negative 4T1 cells MWPDfZRwfG:6aXRCpIF{e2G7 MYPDfZRwfG:6aXPpeJkh[WejaX7zeEBud3W|ZTD0dolxdGVibnXnZZRqfmViNGSxJINmdGy|LDDJR|UxRTF4IH7N MlrPNlQ5QTB4NUK=
human RS4-11 cells NF23TYNHfW6ldHnvckBie3OjeR?= NIrzVIhKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N M1PFcFIxQDN|MEO5
human MOLM13 cells NF71PJNEgXSxdH;4bYPDqGG|c3H5 MmfrR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUW9NVTF|IHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9NVcvPyCwTR?= Ml3UNlUxQDl6MUC=
human U251 cells NXLPZVg{TnWwY4Tpc44h[XO|YYm= MYXJcohq[mm2aX;uJI9nKF[HR1\SNkBqdiCqdX3hckBWOjVzIHPlcIx{KGK7IIDoc5NxcG:2eYLvd4lv\SCHTFnTRUwhUUN3ME2xPE46KG6P M{T3XlI1QTByOE[1
NIH3T3 cells M{LMTGZ2dmO2aX;uJIF{e2G7 M3jMcFEhcA>? NWDoTmNjUW6qaXLpeI9zgSClb37j[Y51emG2aX;uJIFo[Wmwc4SgbJVu[W5iS1TSJItqdmG|ZTDlfJBz\XO|ZXSgbY4hVkmKM2SzJINmdGy|IIfpeIghPCC3TTDCbY91cW5vQXj4MWFGTUW\Rl\MSmEu[W2rZHWgZZQh[W2kaXXueEB1\W2yZYLheJVz\SCob4KgNUBpeg>? M3TBWVE3OTZ{MEC4
MDA-MB-231 cells NU\mflh1S3m2b4TvfIlkyqCjc4PhfS=> NGHvNHNEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckB1emmybHWgcoVo[XSrdnWgUWRCNU2ELUKzNUBk\WyuczygTWM2OD1{Mj6zJI5O NF\BVIIzPDh7ME[1Ni=>
MCF7 cells NVzUXFFJS3m2b4TvfIlkyqCjc4PhfS=> NFHododEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBGWi2yb4PpeIl3\SCPQ1[3JINmdGy|LDDJR|UxRTJ5LkGgcm0> MXKyOFg6ODZ3Mh?=
human CGTH-W-1 cell NEHFWYdIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NFuyd3hKdmirYnn0bY9vKG:oIHj1cYFvKEOJVFitW{0yKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzBwOUSgcm0> NYXYflVpW0GQR1XS
human MONO-MAC-6 cell NXO1dHZRT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MWnJcohq[mm2aX;uJI9nKGi3bXHuJG1QVk9vTVHDMVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{Oy56IH7N MXzTRW5ITVJ?
human HL60 cells NGrwR|FEgXSxdH;4bYPDqGG|c3H5 NV\aeIx{PDhiaB?= Mnu1R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTGw3OCClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJZq[WKrbHn0fUBi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUO2Mlghdk1? NEPDepQzPTB6OUixNC=>
human TT cells NGLkbGZRem:uaX\ldoF1cW:wIHHzd4F6 M2DibFczKGh? NHnvfGNCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGTUJINmdGy|IIDy[ZRz\WG2ZXSg[o9zKDd{IHjyd{Bnd2yub4fl[EBjgSClb33wc5Vv\C25YYPoc5V1KG2nYYP1doVlKGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9OFAhdk1? Ml;MNlQ6ODR7NkG=
human THP1 cells NHSyRWVEgXSxdH;4bYPDqGG|c3H5 MlXSOFghcA>? NVfRNXA{S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hXEiSMTDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKH[rYXLpcIl1gSCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVQ2Njdibl2= Mn;tNlUxQDl6MUC=
3T3 cells NVeycXhWTnWwY4Tpc44h[XO|YYm= M2TYSmlvcGmkaYTpc44hd2ZiVnHzZ5Vt[XJiZX7kc5Rp\WyrYXyg[5Jwf3SqIH\hZ5RweiC{ZXPldJRweiCrbjCzWFMh[2WubIOsJGlEPTB;NUCgcm0> MXixNlY1PjBzOR?=
human ALL-PO cell MXHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MVTJcohq[mm2aX;uJI9nKGi3bXHuJGFNVC2STzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUe5Mlg6KG6P M1zwV3NCVkeHUh?=
human SH-SY5Y cells NGrZSI9HfW6ldHnvckBie3OjeR?= NGLMcIRKdmirYnn0bY9vKG:oIGDES2ZT[mW2YTDpckBpfW2jbjDTTE1UYTW\IHPlcIx{KGK7IIDoc5NxcG:2eYLvd4lv\SCHTFnTRUBie3OjeTygTWM2OD16Mz6xJI5O Mne4NlQ5QTB4NUK=
human U251 cells M2rueGZ2dmO2aX;uJIF{e2G7 NW\jdppyPjBibXnudy=> NITiTpRKdmirYnn0bY9vKG:oIGDES2ZTNWKndHGgbY4hcHWvYX6gWVI2OSClZXzsd{Bkd22yb4Xu[EBxemW2cnXheIVlKG[xcjC2NEBucW5iYnXmc5JmKFCGR1[tRmIhe3SrbYXsZZRqd25iZn;yJFExKG2rboOgZpkheGixc4Doc5R6em:|aX7lJGVNUVODIHP5eI9jdG:2IH3leIhw\CxiSVO1NF05Oy5zIH7N M{HwdFI2QDh{NUG5
human NKM-1 cell MUXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NEDuNoNKdmirYnn0bY9vKG:oIHj1cYFvKE6NTT2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVgvPTJibl2= NGPKUnFUSU6JRWK=
human HAEC cells NFmwdoRRem:uaX\ldoF1cW:wIHHzd4F6 NHe2SYg4OiCq NXrIdnBHSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIRWVEKGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygTWM2OD1yLkGg{txO MVmyNlQ1PDZ5OR?=
HUVEC cell NGS1O4dHfW6ldHnvckBie3OjeR?= M2S5b|I1KGh? MWHJcohq[mm2aX;uJI9nKF[HR1[tRUBqdmS3Y3XkJGhWXkWFIHPlcIwhe3C{b4X0bY5oKGGodHXyJFI1KGi{czDifUBidmerb3flcoV{cXNiYYPzZZktKEmFNUC9NE4yOiEQvF2= NWL2[odDOjF5NEGyOFk>
human A431 cells MlTPSpVv[3Srb36gZZN{[Xl? NXLFfVBvPjBibXnudy=> M3rqfmlvcGmkaYTpc44hd2ZiRVfGVkBqdiCqdX3hckBCPDNzIHPlcIx{KGOxbYDveY5lKHC{ZYTy[YF1\WRiZn;yJFYxKG2rbjDi[YZwemViRVfGJJN1cW23bHH0bY9vKG[xcjCxNEBucW6|IHL5JJBpd3OyaH;0fZJwe2mwZTDFUGlUSSCleYTvZoxwfCCvZYToc4QtKEmFNUC9NVczNjFibl2= M4[0OlI2QDh{NUG5
Sf9 cells NXrISW95TnWwY4Tpc44h[XO|YYm= MkfiTY5pcWKrdHnvckBw\iCJU2SteIFo\2WmIG\FS2ZTKGW6cILld5Nm\CCrbjDT[lkh[2WubIOsJGlEPTB;MD6xPFUh|ryP MVSxPVg2PDB3MR?=
human HT-29 cells NYLvfHBEWHKxbHnm[ZJifGmxbjDhd5NigQ>? M1HjO|czKGh? M2D2eWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSGStNlkh[2WubIOg[ZhxemW|c3nu[{BXTUeIUjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G778{MJGlEPTB;MD6zN{DPxE1? NGqyXI0zOjR2NE[3PS=>
human KM12 cell M1S1XWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NYnvUnF7UW6qaXLpeIlwdiCxZjDoeY1idiCNTUGyJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE4{PTBzNDFOwG0> M37DfHNCVkeHUh?=
human TE-15 cell NFLaeVRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MWXJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTF3IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD61NFc3OSEQvF2= MX;TRW5ITVJ?
human 697 cell NUDMW5g{T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M4m2[mlvcGmkaYTpc44hd2ZiaIXtZY4hPjl5IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD62NVQzPSEQvF2= MX3TRW5ITVJ?
human CAKI-1 cells MUDQdo9tcW[ncnH0bY9vKGG|c3H5 MXfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEODS1mtNUBk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTBwNkOg{txO NXnld29iOjJ3NkC2Nlc>
human MOLT-16 cell MmLuS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NF;wUmtKdmirYnn0bY9vKG:oIHj1cYFvKE2RTGStNVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjZ|MUOyJO69VQ>? NIXpTItUSU6JRWK=
human GB-1 cell MXXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnO1TY5pcWKrdHnvckBw\iCqdX3hckBISi1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD63NVAzOyEQvF2= M3L1dnNCVkeHUh?=
human TE-12 cell NGPPfppIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NEXvfGhKdmirYnn0bY9vKG:oIHj1cYFvKFSHLUGyJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE45ODR3NTFOwG0> NG\yfnVUSU6JRWK=
human NCI-H3122 cells Mn\QVJJwdGmoZYLheIlwdiCjc4PhfS=> NYDQN|lrPzJiaB?= NHXWRY9CdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTU1JOzF{MjDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvQDNizszN NFPHOIMzPDlyNEm2NS=>
human ES6 cell NWPjUGZiT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3PnfmlvcGmkaYTpc44hd2ZiaIXtZY4hTVN4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD65PFExPiEQvF2= M3W4cXNCVkeHUh?=
human NCI-H526 cells NGXGNW9Rem:uaX\ldoF1cW:wIHHzd4F6 NFXNZZA4OiCq M3y1PWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg2OjZiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xMlAyKM7:TR?= NY\Jco1{OjR7MES5OlE>
human LC-2-ad cell NHf2fmxIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MmjTTY5pcWKrdHnvckBw\iCqdX3hckBNSy1{LXHkJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU4yOTRyNzFOwG0> M1O3N3NCVkeHUh?=
human BL-70 cell M4fqV2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NF\CN2tKdmirYnn0bY9vKG:oIHj1cYFvKEKOLUewJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU4yOTh2NjFOwG0> M3rTbHNCVkeHUh?=
human ETK-1 cell MY\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MVTJcohq[mm2aX;uJI9nKGi3bXHuJGVVUy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6yPFU5KM7:TR?= MkWwV2FPT0WU
human SW620 cells NWfnW4JuWHKxbHnm[ZJifGmxbjDhd5NigQ>? NF\o[lY1QCCq NHTN[FFCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGPXOlIxKGOnbHzzJIFnfGW{IES4JIhzeyCkeTDTVmIh[XO|YYmsJGdKPTB;MT6zJO69VQ>? MoXnNlI2PjB4Mke=
IM9 cells MWXDfZRwfG:6aXRCpIF{e2G7 M1;nTmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KEixbX:gd4FxcWWwczCobJVu[W5rIFnNPUBk\WyuczDhd5Nme3OnZDDhd{Boem:5dHigbY5pcWKrdHnvckBjgSCPVGSgZZN{[XluIFnDOVA:OS5|NTFOwG0> NEj6e5JUSU6JRWK=
human A4-Fuk cell NWnxTGdQT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MmDyTY5pcWKrdHnvckBw\iCqdX3hckBCPC2IdXugZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4Phfg+9lCCLQ{WwQVEvOzRzNEGg{txO MVjTRW5ITVJ?
human SR cell MXTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M4G5O2lvcGmkaYTpc44hd2ZiaIXtZY4hW1JiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkW0OVczKM7:TR?= M3\2WXNCVkeHUh?=
human A3-KAW cell NU\1TY5uT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= Mm\DTY5pcWKrdHnvckBw\iCqdX3hckBCOy2NQWegZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhcWN3ME2xMlYzPTR4IN88US=> NGm4TWtUSU6JRWK=
human KS-1 cell MmPoS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NWrEO3RxUW6qaXLpeIlwdiCxZjDoeY1idiCNUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU43QTJ2NzFOwG0> NEX3dVdUSU6JRWK=
human CTV-1 cell M1K3bGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MmPETY5pcWKrdHnvckBw\iCqdX3hckBEXFZvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuO|I4PTFizszN MkHCV2FPT0WU
human LB1047-RCC cell NEi4bIxIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWPHRoV4UW6qaXLpeIlwdiCxZjDoeY1idiCOQkGwOFcuWkOFIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT64NVYzPCEQvF2= MUfTRW5ITVJ?
human MEG-01 cell M1\TWmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NXzSeIYxUW6qaXLpeIlwdiCxZjDoeY1idiCPRVetNFEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yNjh|NU[zJO69VQ>? NEDWO2NUSU6JRWK=
human TE-11 cell Mn7SS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MYLJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTFzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT64N|k5PSEQvF2= MmDOV2FPT0WU
human CMK cell NWXrTIY4T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MYnJcohq[mm2aX;uJI9nKGi3bXHuJGNOUyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOUW1NVch|ryP Mmn6V2FPT0WU
human NB1 cell NWLB[HdLT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M2H4UGlvcGmkaYTpc44hd2ZiaIXtZY4hVkJzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT65OlEyPyEQvF2= NXf6[GhWW0GQR1XS
human MDA-MB-435 cells NFfCdJdRem:uaX\ldoF1cW:wIHHzd4F6 M2LVdlQ5KGh? NIfjOHpCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3ERU1OSi12M{WgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KFOUQjDhd5NigSxiR1m9NkDPxE1? M{LiWVIzPTZyNkK3
human MCF7 cells NFKxVWpRem:uaX\ldoF1cW:wIHHzd4F6 NVTGXnBVPDhiaB?= MkDTRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPQ1[3JINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OiEQvF2= M3njW|IzPTZyNkK3
human A549 cells NWXaO|dTS3m2b4TvfIlkyqCjc4PhfS=> NHvlSpo4OiCq M3Oz[2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[XO|ZYPz[YQh[XNiZ4Lve5RpKGmwaHnibZRqd25iYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0zNjR2IN88US=> NYnJd5NyOjN4MEK0OFE>

... 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]

Protocol

Kinase Assay:

[1]

+ 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:

[3]

+ 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:

[2]

+ 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
Formula

C22H27FN4O2

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

Bio Calculators

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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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID