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 33 Publications

12 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.

    A, Tumour growth curves from the initial sunitinib drug trials, with endpoint set at 1300 mm3 (mean ± SEM ). Measurements begin one week after tumour inoculation and on the day sunitinib treatment began. Subsequent experimental endpoints were set based on these growth curves and their intersections with this data are shown. B, histogram plot showing the distribution of tumour sizes at day 8 of treatment. Sunitinib treated tumours exceeding 250 mm3 in size were identified as falling into the non-responsive cohort. Sunitinib treatment significantly retards growth of responsive tumours.

    Cancer Res, 2017, 77(4):1008-1020. 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.
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 Mm[0S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NH3DZWtKdmirYnn0bY9vKG:oIHj1cYFvKFOZN{W2JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVkvOTN3MTFOwG0> MXjTRW5ITVJ?
human EoL-1-cell cell NGTCT3BIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NInJNlNKdmirYnn0bY9vKG:oIHj1cYFvKEWxTD2xMYNmdGxiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLk[0[U0xPg>? M4HhV3NCVkeHUh?=
human MV-4-11 cell M4TvcGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NVTvR4s3UW6qaXLpeIlwdiCxZjDoeY1idiCPVj20MVEyKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OC5{N{Kgcm0> MYjTRW5ITVJ?
human MV411 cells M1O1VHBzd2yrZnXyZZRqd25iYYPzZZk> NXHYUGpsPDhiaB?= MkjhRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPVkSxNUBk\WyuczDh[pRmeiB2ODDodpMh[nliTWTUJIF{e2G7LDDpZ|UxRTNibl2= Mn\LNlQ6ODR7NkG=
3T3 cells NW\jVpFCTnWwY4Tpc44h[XO|YYm= M2T2TWlvcGmkaYTpc44hd2ZiUFTHSk1qdmS3Y3XkJGJz\FViaX7jc5Jxd3KjdHnvckBqdiB|VEOgZ4VtdHNid3n0bEAxNjFnIHLveolv\SC|ZYL1cUBidGK3bXnuMEBKSzVyPUegcm0> MV6xNlY1PjBzOR?=
HEK293 cells MWLGeY5kfGmxbjDhd5NigQ>? MUXCbY5lcW6pIHHm[olvcXS7IITvJGZNXDNiY3H0ZYx6fGmlIHTvcYFqdiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{KGK7IHPvcZBmfGm2aY\lJIJqdmSrbnegZZN{[XluIFvkQVAvPDdibl2= M2\BZVE6PzV2MUm5
human MDA-MB-435 cells MoTnR5l1d3SxeHnjxsBie3OjeR?= MmC2NkBp MUTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNSGEuVUJvNEO1JINmdGy|LDDJR|UxRTlwNzDuUS=> MX:yOFg6ODZ3Mh?=
human RS4-11 cells NW\OW3BTTnWwY4Tpc44h[XO|YYm= MXvJcohq[mm2aX;uJI9nKE[OVEOgZZV1d3Cqb4PwbI9zgWyjdHnvckBqdiCqdX3hckBTWzRvMUGgZ4VtdHNiYX\0[ZIhOiCqcoOgZpkh\WynY4Tyc4Np\W2rbIXtbY5me2OnbnPlJIF{e2G7LDDJR|UxRTlwOTDuUS=> NWHjVFB1OTl4NUS0NFg>
HUVEC MnLER5l1d3SxeHnjxsBie3OjeR?= MXvDfZRwfG:6aXPpeJkh[WejaX7zeEBJXV[HQzygTWM2OD1zMT64JI5O NGfpZpEzPDh7ME[1Ni=>
human Kasumi-1 cells MUDGeY5kfGmxbjDhd5NigQ>? NITIeINKdmirYnn0bY9vKG:oIHOtT4l1KGG3dH;wbI9{eGixconsZZRqd25iaX6gbJVu[W5iS3HzeY1qNTFiY3XscJMh[nliV3XzeIVzdiCkbH;0JIFv[Wy7c3nzMEBKSzVyPUG1JI5O NEHBNWIzODh|M{CzPS=>
human NOS-1 cell NWCzendXT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NIHNeIpKdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= MUPTRW5ITVJ?
mouse triple negative 4T1 cells M1\I[GN6fG:2b4jpZ:Kh[XO|YYm= MXvDfZRwfG:6aXPpeJkh[WejaX7zeEBud3W|ZTD0dolxdGVibnXnZZRqfmViNGSxJINmdGy|LDDJR|UxRTF4IH7N Mm\PNlQ5QTB4NUK=
human RS4-11 cells NF7FeXpHfW6ldHnvckBie3OjeR?= NH7FRldKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N MUiyNFg{OzB|OR?=
human MOLM13 cells MmjGR5l1d3SxeHnjxsBie3OjeR?= Mmq4R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUW9NVTF|IHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9NVcvPyCwTR?= Mn\6NlUxQDl6MUC=
human U251 cells MkHRSpVv[3Srb36gZZN{[Xl? M{TZemlvcGmkaYTpc44hd2ZiVlXHSnIzKGmwIHj1cYFvKFV{NUGgZ4VtdHNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCNCCLQ{WwQVE5Njlibl2= NWLvNFhiOjR7MEC4OlU>
NIH3T3 cells NVf1bVFSTnWwY4Tpc44h[XO|YYm= M2nPclEhcA>? MmnDTY5pcWKrdH;yfUBkd26lZX70doF1cW:wIHHnZYlve3RiaIXtZY4hU0SUIHvpcoF{\SCneIDy[ZN{\WRiaX6gUmlJO1R|IHPlcIx{KHerdHigOEB2VSCEaX;0bY4uSWi6LVHFSWV[Tk[ORlGtZY1q\GViYYSgZY1jcWWwdDD0[Y1x\XKjdIXy[UBnd3JiMTDodi=> MX[xOlE3OjByOB?=
MDA-MB-231 cells M1ruXmN6fG:2b4jpZ:Kh[XO|YYm= M2DLOWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJJRzcXCuZTDu[YdifGm4ZTDNSGEuVUJvMkOxJINmdGy|LDDJR|UxRTJ{LkOgcm0> NInQNHEzPDh7ME[1Ni=>
MCF7 cells NXfWbXpQS3m2b4TvfIlkyqCjc4PhfS=> M{LMVWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGVTNXCxc3n0bZZmKE2FRkegZ4VtdHNuIFnDOVA:OjdwMTDuUS=> MYiyOFg6ODZ3Mh?=
human CGTH-W-1 cell M3L0Zmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NUXOSI9GUW6qaXLpeIlwdiCxZjDoeY1idiCFR2TIMXcuOSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTNyLkm0JI5O MXHTRW5ITVJ?
human MONO-MAC-6 cell NIjDNYFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MVTJcohq[mm2aX;uJI9nKGi3bXHuJG1QVk9vTVHDMVYh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{Oy56IH7N MWHTRW5ITVJ?
human HL60 cells MmPrR5l1d3SxeHnjxsBie3OjeR?= NFTTeVA1QCCq NUT1[oczS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUEx4MDDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKH[rYXLpcIl1gSCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVM3Njhibl2= MWCyOVA5QThzMB?=
human TT cells Mlm1VJJwdGmoZYLheIlwdiCjc4PhfS=> M1[1blczKGh? MXvBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFSWIHPlcIx{KHC{ZYTy[YF1\WRiZn;yJFczKGi{czDmc4xtd3enZDDifUBkd22yb4Xu[E14[XOqb4X0JI1m[XO3cnXkJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NECgcm0> NGnqeZUzPDlyNEm2NS=>
human THP1 cells MknGR5l1d3SxeHnjxsBie3OjeR?= MYG0PEBp NGL1UpVEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBVUFBzIHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9OFUvPyCwTR?= M1q4clI2ODh7OEGw
3T3 cells MnHuSpVv[3Srb36gZZN{[Xl? NUfLXWIxUW6qaXLpeIlwdiCxZjDWZZNkfWyjcjDlcoRwfGinbHnhcEBoem:5dHig[oFkfG:{IILlZ4VxfG:{IHnuJFNVOyClZXzsd{whUUN3ME21NEBvVQ>? MXWxNlY1PjBzOR?=
human ALL-PO cell M4nzdGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M2q0OGlvcGmkaYTpc44hd2ZiaIXtZY4hSUyOLWDPJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9O|kvQDlibl2= NEPhZohUSU6JRWK=
human SH-SY5Y cells MWDGeY5kfGmxbjDhd5NigQ>? NWfsPZhnUW6qaXLpeIlwdiCxZjDQSGdHWmKndHGgbY4hcHWvYX6gV2guW1l3WTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2Eh[XO|YYmsJGlEPTB;OEOuNUBvVQ>? NIe1ZmQzPDh7ME[1Ni=>
human U251 cells NFHBfVlHfW6ldHnvckBie3OjeR?= NFW2S5o3OCCvaX7z MkPlTY5pcWKrdHnvckBw\iCSRFfGVk1j\XSjIHnuJIh2dWGwIGWyOVEh[2WubIOgZ49ueG:3bnSgdJJmfHKnYYTl[EBnd3JiNkCgcYlvKGKnZn;y[UBRTEeILVLCJJN1cW23bHH0bY9vKG[xcjCxNEBucW6|IHL5JJBpd3OyaH;0fZJwe2mwZTDFUGlUSSCleYTvZoxwfCCvZYToc4QtKEmFNUC9PFMvOSCwTR?= M1zoWlI2QDh{NUG5
human NKM-1 cell MUDHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MkK4TY5pcWKrdHnvckBw\iCqdX3hckBPU01vMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUm4MlUzKG6P M3HjR3NCVkeHUh?=
human HAEC cells NI\DfmZRem:uaX\ldoF1cW:wIHHzd4F6 M3\2dVczKGh? M3;ORWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFHFR{Bk\WyuczDlfJBz\XO|aX7nJHZGT0[UIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:OC5zIN88US=> MVSyNlQ1PDZ5OR?=
HUVEC cell M2fvcmZ2dmO2aX;uJIF{e2G7 MkPENlQhcA>? NGPkXYdKdmirYnn0bY9vKG:oIG\FS2YuSSCrbnT1Z4VlKEiXVlXDJINmdGxic4Dyc5V1cW6pIHHmeIVzKDJ2IHjyd{BjgSCjbnfpc4dmdmW|aYOgZZN{[XluIFnDOVA:OC5zMjFOwG0> M3HUOlIyPzRzMkS5
human A431 cells NV\RdmhXTnWwY4Tpc44h[XO|YYm= M3vONFYxKG2rboO= NF3KPFVKdmirYnn0bY9vKG:oIFXHSnIhcW5iaIXtZY4hSTR|MTDj[YxteyClb33wc5Vv\CCycnX0doVifGWmIH\vdkA3OCCvaX6gZoVnd3KnIFXHSkB{fGmvdXzheIlwdiCob4KgNVAhdWmwczDifUBxcG:|cHjveJlzd3OrbnWgSWxKW0FiY4n0c4Jtd3RibXX0bI9lNCCLQ{WwQVE4Oi5zIH7N NV;WU5lNOjV6OEK1NVk>
Sf9 cells MXHGeY5kfGmxbjDhd5NigQ>? NV34OGpwUW6qaXLpeIlwdiCxZjDHV3QufGGpZ3XkJHZGT0[UIHX4dJJme3OnZDDpckBU\jliY3XscJMtKEmFNUC9NE4yQDVizszN MUSxPVg2PDB3MR?=
human HT-29 cells MX\Qdo9tcW[ncnH0bY9vKGG|c3H5 NGG0c4Y4OiCq NGjwRZJCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP M1X2cVIzPDR2Nke5
human KM12 cell MYjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NETHfpBKdmirYnn0bY9vKG:oIHj1cYFvKEuPMUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlM2ODF2IN88US=> MWfTRW5ITVJ?
human TE-15 cell MkjrS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NHnWb4RKdmirYnn0bY9vKG:oIHj1cYFvKFSHLUG1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE42ODd4MTFOwG0> MlnNV2FPT0WU
human 697 cell M4W0RWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NUC5VlE5UW6qaXLpeIlwdiCxZjDoeY1idiB4OUegZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlYyPDJ3IN88US=> MlHPV2FPT0WU
human CAKI-1 cells M1rKPHBzd2yrZnXyZZRqd25iYYPzZZk> MonoRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCFQVvJMVEh[2WubIOgZYZ1\XJiNEigbJJ{KGK7IGPSRkBie3OjeTygS2k2OD1yLk[zJO69VQ>? MkToNlI2PjB4Mke=
human MOLT-16 cell NVT6dmVCT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M{fTVmlvcGmkaYTpc44hd2ZiaIXtZY4hVU:OVD2xOkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVAvPjNzM{Kg{txO M3v1ZXNCVkeHUh?=
human GB-1 cell NYe0WnFPT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M{TNVmlvcGmkaYTpc44hd2ZiaIXtZY4hT0JvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuO|ExOjNizszN M3TRc3NCVkeHUh?=
human TE-12 cell MVvHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MYXJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTF{IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD64NFQ2PSEQvF2= M1zLSXNCVkeHUh?=
human NCI-H3122 cells MkC4VJJwdGmoZYLheIlwdiCjc4PhfS=> MmK0O|IhcA>? M2K2TWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg{OTJ{IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE45OyEQvF2= M{LFT|I1QTB2OU[x
human ES6 cell MVHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NVW3bnhEUW6qaXLpeIlwdiCxZjDoeY1idiCHU{[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlk5OTB4IN88US=> NELkT2pUSU6JRWK=
human NCI-H526 cells M2DienBzd2yrZnXyZZRqd25iYYPzZZk> M3H0VFczKGh? M4jtSWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg2OjZiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xMlAyKM7:TR?= M3GwRlI1QTB2OU[x
human LC-2-ad cell NHS0cVNIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NGHqUHJKdmirYnn0bY9vKG:oIHj1cYFvKEyFLUKtZYQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yNjFzNEC3JO69VQ>? NHH6bGJUSU6JRWK=
human BL-70 cell NHPHRoZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXLJcohq[mm2aX;uJI9nKGi3bXHuJGJNNTdyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6xNVg1PiEQvF2= MlL4V2FPT0WU
human ETK-1 cell MYLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnHjTY5pcWKrdHnvckBw\iCqdX3hckBGXEtvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuNlg2QCEQvF2= M2rDbXNCVkeHUh?=
human SW620 cells MVzQdo9tcW[ncnH0bY9vKGG|c3H5 MnL3OFghcA>? MUjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFOZNkKwJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OS5|IN88US=> Ml\0NlI2PjB4Mke=
IM9 cells MUTDfZRwfG:6aXRCpIF{e2G7 NFHlcI1EgXSxdH;4bYNqfHliYXfhbY5{fCCKb33vJJNieGmnboOgLIh2dWGwKTDJUVkh[2WubIOgZZN{\XO|ZXSgZZMh\3Kxd4ToJIlvcGmkaYTpc44h[nliTWTUJIF{e2G7LDDJR|UxRTFwM{Wg{txO NHzsfJpUSU6JRWK=
human A4-Fuk cell MULHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NX7VWGxLUW6qaXLpeIlwdiCxZjDoeY1idiCDND3GeYsh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5Nige,:jDDJR|UxRTFwM{SxOFEh|ryP MWfTRW5ITVJ?
human SR cell NVjWeJo2T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MmrLTY5pcWKrdHnvckBw\iCqdX3hckBUWiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwNUS1O|Ih|ryP MoX1V2FPT0WU
human A3-KAW cell MV3Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NV6yXmZ3UW6qaXLpeIlwdiCxZjDoeY1idiCDMz3LRXch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiaXO1NF0yNjZ{NUS2JO69VQ>? MlzwV2FPT0WU
human KS-1 cell M2H1eGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NEXjUGZKdmirYnn0bY9vKG:oIHj1cYFvKEuVLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlY6OjR5IN88US=> M{HEc3NCVkeHUh?=
human CTV-1 cell NV7WWJhuT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NYPK[YlzUW6qaXLpeIlwdiCxZjDoeY1idiCFVG[tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvPzJ5NUGg{txO MW\TRW5ITVJ?
human LB1047-RCC cell MkfBS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NFPlZYVKdmirYnn0bY9vKG:oIHj1cYFvKEyEMUC0O{1TS0NiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkixOlI1KM7:TR?= MX3TRW5ITVJ?
human MEG-01 cell NX7lZYI6T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NGW5doJKdmirYnn0bY9vKG:oIHj1cYFvKE2HRz2wNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvQDN3NkOg{txO MkCzV2FPT0WU
human TE-11 cell NE\xNZFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MWDJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTFzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT64N|k5PSEQvF2= MWrTRW5ITVJ?
human CMK cell NVntO|VWT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NEnXPG1KdmirYnn0bY9vKG:oIHj1cYFvKEOPSzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPVU2OTdizszN NGnrb3BUSU6JRWK=
human NB1 cell NWOy[HpYT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MUjJcohq[mm2aX;uJI9nKGi3bXHuJG5DOSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOU[xNVch|ryP NFnJ[nVUSU6JRWK=
human MDA-MB-435 cells NFXLd4ZRem:uaX\ldoF1cW:wIHHzd4F6 M2O5[lQ5KGh? M{n0OGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVTBMW1DNTR|NTDj[YxteyCjZoTldkA1QCCqcoOgZpkhW1KEIHHzd4F6NCCJSU2yJO69VQ>? NWr5OplJOjJ3NkC2Nlc>
human MCF7 cells NHXvRZlRem:uaX\ldoF1cW:wIHHzd4F6 NFLQXZE1QCCq NIDqSIVCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3DSlch[2WubIOgZYZ1\XJiNEigbJJ{KGK7IGPSRkBie3OjeTygS2k2OD1{IN88US=> M4LLW|IzPTZyNkK3
human A549 cells M1PSTmN6fG:2b4jpZ:Kh[XO|YYm= MW[3NkBp MmjyR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVU1QSClZXzsd{Bie3Onc4Pl[EBieyCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVIvPDRizszN M2rJNlI{PjB{NESx

... 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 slightly soluble or insoluble
Ethanol slightly soluble or insoluble
In vivo Add solvents individually and in order:
5% DMSO+corn oil
7mg/mL

* 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.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID