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
FLT3 [1]
(Cell-free assay)
c-Kit [1]
(Cell-free assay)
PDGFRβ [1]
(Cell-free assay)
VEGFR2 [1]
(Cell-free assay)
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 Mo\US5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MWTJcohq[mm2aX;uJI9nKGi3bXHuJHNYPzV4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUmuNVM2OSEQvF2= MoLMV2FPT0WU
human EoL-1-cell cell NUjENnFuT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NHfOd3hKdmirYnn0bY9vKG:oIHj1cYFvKEWxTD2xMYNmdGxiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLk[0[U0xPg>? M1rUN3NCVkeHUh?=
human MV-4-11 cell MkXES5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MUfJcohq[mm2aX;uJI9nKGi3bXHuJG1XNTRvMUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlI4OiCwTR?= NVq5NphtW0GQR1XS
human MV411 cells M3nk[XBzd2yrZnXyZZRqd25iYYPzZZk> NFr2ZmE1QCCq MV7BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2YNEGxJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCPVGSgZZN{[XluIHnjOVA:OyCwTR?= MWeyOFkxPDl4MR?=
3T3 cells NGnsNYZHfW6ldHnvckBie3OjeR?= MmT1TY5pcWKrdHnvckBw\iCSRFfGMYlv\HWlZXSgRpJlXSCrbnPvdpBwemG2aX;uJIlvKDOWMzDj[YxteyC5aYToJFAvOSViYn;2bY5mKHOncoXtJIFt[nWvaX6sJGlEPTB;NzDuUS=> NWPIfnhDOTJ4NE[wNVk>
HEK293 cells MmPXSpVv[3Srb36gZZN{[Xl? MYHCbY5lcW6pIHHm[olvcXS7IITvJGZNXDNiY3H0ZYx6fGmlIHTvcYFqdiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{KGK7IHPvcZBmfGm2aY\lJIJqdmSrbnegZZN{[XluIFvkQVAvPDdibl2= M3\ycFE6PzV2MUm5
human MDA-MB-435 cells MorLR5l1d3SxeHnjxsBie3OjeR?= M2TGVFIhcA>? NFn6XFlEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOTEFvTVKtOFM2KGOnbHzzMEBKSzVyPUmuO{BvVQ>? M4TyeVI1QDlyNkWy
human RS4-11 cells MUjGeY5kfGmxbjDhd5NigQ>? M4DKcmlvcGmkaYTpc44hd2ZiRlzUN{BifXSxcHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKFKVND2xNUBk\WyuczDh[pRmeiB{IHjyd{BjgSCnbHXjeJJw[2inbXnseY1qdmW|Y3XuZ4Uh[XO|YYmsJGlEPTB;OT65JI5O NIOzTowyQTZ3NESwPC=>
HUVEC NHvJVY9EgXSxdH;4bYPDqGG|c3H5 M1LZXWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KEiXVlXDMEBKSzVyPUGxMlghdk1? MW[yOFg6ODZ3Mh?=
human Kasumi-1 cells NGPwTplHfW6ldHnvckBie3OjeR?= NVLTVVVVUW6qaXLpeIlwdiCxZjDjMWtqfCCjdYTvdIhwe3Cqb4L5cIF1cW:wIHnuJIh2dWGwIFvhd5VucS1zIHPlcIx{KGK7IGfld5Rmem5iYnzveEBidmGueYPpd{whUUN3ME2xOUBvVQ>? Mon2NlA5OzNyM{m=
human NOS-1 cell NHTLNG5Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= M2nCfmlvcGmkaYTpc44hd2ZiaIXtZY4hVk:VLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xOU4{KG6P Mmm1V2FPT0WU
mouse triple negative 4T1 cells M333bmN6fG:2b4jpZ:Kh[XO|YYm= NVTxd2N6S3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhfHKrcHzlJI5m\2G2aY\lJFRVOSClZXzsd{whUUN3ME2xOkBvVQ>? MXmyOFg6ODZ3Mh?=
human RS4-11 cells MnXFSpVv[3Srb36gZZN{[Xl? NGX5OIpKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N M4LHPVIxQDN|MEO5
human MOLM13 cells NEnLOZREgXSxdH;4bYPDqGG|c3H5 NELNfG9EgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOV0yPMUOgZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCC4aXHibYxqfHliYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0yPy55IH7N NGC0SFIzPTB6OUixNC=>
human U251 cells MY\GeY5kfGmxbjDhd5NigQ>? M4XJOGlvcGmkaYTpc44hd2ZiVlXHSnIzKGmwIHj1cYFvKFV{NUGgZ4VtdHNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCNCCLQ{WwQVE5Njlibl2= MlvVNlQ6ODB6NkW=
NIH3T3 cells MlPNSpVv[3Srb36gZZN{[Xl? NILCOXQyKGh? NVywdIZHUW6qaXLpeI9zgSClb37j[Y51emG2aX;uJIFo[Wmwc4SgbJVu[W5iS1TSJItqdmG|ZTDlfJBz\XO|ZXSgbY4hVkmKM2SzJINmdGy|IIfpeIghPCC3TTDCbY91cW5vQXj4MWFGTUW\Rl\MSmEu[W2rZHWgZZQh[W2kaXXueEB1\W2yZYLheJVz\SCob4KgNUBpeg>? MU[xOlE3OjByOB?=
MDA-MB-231 cells MYHDfZRwfG:6aXRCpIF{e2G7 MnPRR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6geJJqeGynIH7l[4F1cX[nIF3ERU1OSi1{M{GgZ4VtdHNuIFnDOVA:OjJwMzDuUS=> NXvZdpJ5OjR6OUC2OVI>
MCF7 cells M2fCcmN6fG:2b4jpZ:Kh[XO|YYm= Mke0R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gSXIueG:|aYTpeoUhVUOINzDj[YxteyxiSVO1NF0zPy5zIH7N MWWyOFg6ODZ3Mh?=
human CGTH-W-1 cell Mnq5S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MlzhTY5pcWKrdHnvckBw\iCqdX3hckBET1SKLWetNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMxNjl2IH7N Mk[xV2FPT0WU
human MONO-MAC-6 cell MXfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NXPXOpc4UW6qaXLpeIlwdiCxZjDoeY1idiCPT17PMW1CSy14IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{OuPEBvVQ>? NWjCfXRjW0GQR1XS
human HL60 cells Mlf6R5l1d3SxeHnjxsBie3OjeR?= NGXUZWE1QCCq MXnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUFYxKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;M{[uPEBvVQ>? M4np[VI2ODh7OEGw
human TT cells M3nSUnBzd2yrZnXyZZRqd25iYYPzZZk> NEnVNI44OiCq NYPCR2p6SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDUWEBk\WyuczDwdoV1emWjdHXkJIZweiB5MjDodpMh\m:ubH;3[YQh[nliY3;tdI92dmRvd3HzbI92fCCvZXHzeZJm\CCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVQxKG6P NWfJd4VuOjR7MES5OlE>
human THP1 cells M2HGR2N6fG:2b4jpZ:Kh[XO|YYm= M1PjdlQ5KGh? MXTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDUTHAyKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NEWuO{BvVQ>? Mlq1NlUxQDl6MUC=
3T3 cells NGGw[mZHfW6ldHnvckBie3OjeR?= NUnSWIw5UW6qaXLpeIlwdiCxZjDWZZNkfWyjcjDlcoRwfGinbHnhcEBoem:5dHig[oFkfG:{IILlZ4VxfG:{IHnuJFNVOyClZXzsd{whUUN3ME21NEBvVQ>? M2DKNFEzPjR4MEG5
human ALL-PO cell NHO4bWpIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MoL5TY5pcWKrdHnvckBw\iCqdX3hckBCVExvUF:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME23PU45QSCwTR?= M4PC[HNCVkeHUh?=
human SH-SY5Y cells NGrFSmRHfW6ldHnvckBie3OjeR?= MlmwTY5pcWKrdHnvckBw\iCSRFfGVoJmfGFiaX6gbJVu[W5iU1itV3k2YSClZXzsd{BjgSCyaH;zdIhwfHm{b4PpcoUhTUyLU1GgZZN{[XluIFnDOVA:QDNwMTDuUS=> MXGyOFg6ODZ3Mh?=
human U251 cells MXTGeY5kfGmxbjDhd5NigQ>? M3fPWlYxKG2rboO= NFLJZWNKdmirYnn0bY9vKG:oIGDES2ZTNWKndHGgbY4hcHWvYX6gWVI2OSClZXzsd{Bkd22yb4Xu[EBxemW2cnXheIVlKG[xcjC2NEBucW5iYnXmc5JmKFCGR1[tRmIhe3SrbYXsZZRqd25iZn;yJFExKG2rboOgZpkheGixc4Doc5R6em:|aX7lJGVNUVODIHP5eI9jdG:2IH3leIhw\CxiSVO1NF05Oy5zIH7N MUmyOVg5OjVzOR?=
human NKM-1 cell M{jrZ2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NVfOeHdqUW6qaXLpeIlwdiCxZjDoeY1idiCQS12tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVk5NjV{IH7N NF\qUlRUSU6JRWK=
human HAEC cells NWHGTmZbWHKxbHnm[ZJifGmxbjDhd5NigQ>? NWi4dGh2PzJiaB?= MYjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiDRVOgZ4VtdHNiZYjwdoV{e2mwZzDWSWdHWiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvOSEQvF2= M3T3NlIzPDR2Nke5
HUVEC cell M3PjcmZ2dmO2aX;uJIF{e2G7 MUiyOEBp M1TaOmlvcGmkaYTpc44hd2ZiVlXHSk1CKGmwZIXj[YQhUFWYRVOgZ4VtdCC|cILveZRqdmdiYX\0[ZIhOjRiaILzJIJ6KGGwZ3nv[4Vv\XOrczDhd5NigSxiSVO1NF0xNjF{IN88US=> MkXtNlE4PDF{NEm=
human A431 cells M{L3fmZ2dmO2aX;uJIF{e2G7 MoT3OlAhdWmwcx?= M4PZWWlvcGmkaYTpc44hd2ZiRVfGVkBqdiCqdX3hckBCPDNzIHPlcIx{KGOxbYDveY5lKHC{ZYTy[YF1\WRiZn;yJFYxKG2rbjDi[YZwemViRVfGJJN1cW23bHH0bY9vKG[xcjCxNEBucW6|IHL5JJBpd3OyaH;0fZJwe2mwZTDFUGlUSSCleYTvZoxwfCCvZYToc4QtKEmFNUC9NVczNjFibl2= NF;YcoszPTh6MkWxPS=>
Sf9 cells M2\1OWZ2dmO2aX;uJIF{e2G7 NF6yOoFKdmirYnn0bY9vKG:oIFfTWE11[WepZXSgWmVITlJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{whUUN3ME2wMlE5PSEQvF2= M1HBOlE6QDV2MEWx
human HT-29 cells MVvQdo9tcW[ncnH0bY9vKGG|c3H5 NGHER|c4OiCq NHvRXlRCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP MkXvNlI1PDR4N{m=
human KM12 cell NWWzWmhuT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NEjySVRKdmirYnn0bY9vKG:oIHj1cYFvKEuPMUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlM2ODF2IN88US=> NVS1[GJoW0GQR1XS
human TE-15 cell NF;oTppIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NYHTRXd6UW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xOUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVAvPTB5NkGg{txO NUjPOXg4W0GQR1XS
human 697 cell Mn3oS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NIG0bnZKdmirYnn0bY9vKG:oIHj1cYFvKDZ7NzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOlE1OjVizszN NUjKNVRPW0GQR1XS
human CAKI-1 cells NGqxb5JRem:uaX\ldoF1cW:wIHHzd4F6 MmTIRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCFQVvJMVEh[2WubIOgZYZ1\XJiNEigbJJ{KGK7IGPSRkBie3OjeTygS2k2OD1yLk[zJO69VQ>? MojpNlI2PjB4Mke=
human MOLT-16 cell MUfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MXzJcohq[mm2aX;uJI9nKGi3bXHuJG1QVFRvMU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlY{OTN{IN88US=> MVnTRW5ITVJ?
human GB-1 cell MXLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NW\ZNXhLUW6qaXLpeIlwdiCxZjDoeY1idiCJQj2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE44OTB{MzFOwG0> MYDTRW5ITVJ?
human TE-12 cell MmHtS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? Mn\YTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuPFA1PTVizszN M{TSU3NCVkeHUh?=
human NCI-H3122 cells NGWzWYJRem:uaX\ldoF1cW:wIHHzd4F6 M1vlVlczKGh? M{flcWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg{OTJ{IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE45OyEQvF2= NYLNcFFvOjR7MES5OlE>
human ES6 cell MVLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MYrJcohq[mm2aX;uJI9nKGi3bXHuJGVUPiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTBwOUixNFYh|ryP MofQV2FPT0WU
human NCI-H526 cells NYHuNnlHWHKxbHnm[ZJifGmxbjDhd5NigQ>? NXfVd4N[PzJiaB?= M4roTGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg2OjZiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xMlAyKM7:TR?= NFi1WoczPDlyNEm2NS=>
human LC-2-ad cell NIPiWHpIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NV;KdFJPUW6qaXLpeIlwdiCxZjDoeY1idiCOQz2yMYFlKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS5zMUSwO{DPxE1? M4DYT3NCVkeHUh?=
human BL-70 cell NF3mUGlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MlzBTY5pcWKrdHnvckBw\iCqdX3hckBDVC15MDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuNVE5PDZizszN NHKzbmpUSU6JRWK=
human ETK-1 cell NV;1OoZUT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NI\hbGFKdmirYnn0bY9vKG:oIHj1cYFvKEWWSz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU4zQDV6IN88US=> MVfTRW5ITVJ?
human SW620 cells MW\Qdo9tcW[ncnH0bY9vKGG|c3H5 M4[wZlQ5KGh? MWDBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFOZNkKwJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OS5|IN88US=> NWLnRXRPOjJ3NkC2Nlc>
IM9 cells NXr1fWl6S3m2b4TvfIlkyqCjc4PhfS=> MlTWR5l1d3SxeHnjbZR6KGGpYXnud5QhUG:vbzDzZZBq\W6|IDjoeY1idiliSV25JINmdGy|IHHzd4V{e2WmIHHzJIdzd3e2aDDpcohq[mm2aX;uJIJ6KE2WVDDhd5NigSxiSVO1NF0yNjN3IN88US=> NF2xd2VUSU6JRWK=
human A4-Fuk cell NG\0bY9Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXfJcohq[mm2aX;uJI9nKGi3bXHuJGE1NU[3azDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H589yNKEmFNUC9NU4{PDF2MTFOwG0> NGXPXmtUSU6JRWK=
human SR cell MnTKS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? Mom2TY5pcWKrdHnvckBw\iCqdX3hckBUWiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwNUS1O|Ih|ryP NWnieVNVW0GQR1XS
human A3-KAW cell Mni1S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NID0e3JKdmirYnn0bY9vKG:oIHj1cYFvKEF|LVvBW{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCrY{WwQVEvPjJ3NE[g{txO M3KxUHNCVkeHUh?=
human KS-1 cell NFr4OXNIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M{i5XWlvcGmkaYTpc44hd2ZiaIXtZY4hU1NvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuOlkzPDdizszN NVLCc2VlW0GQR1XS
human CTV-1 cell M3HKVWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3;MOGlvcGmkaYTpc44hd2ZiaIXtZY4hS1SYLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlczPzVzIN88US=> MnzBV2FPT0WU
human LB1047-RCC cell Ml7TS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M3jCTGlvcGmkaYTpc44hd2ZiaIXtZY4hVEJzMES3MXJESyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOEG2NlQh|ryP NHTOU21USU6JRWK=
human MEG-01 cell NWn2Voc3T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MofvTY5pcWKrdHnvckBw\iCqdX3hckBOTUdvMEGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlg{PTZ|IN88US=> NX3zS2Z[W0GQR1XS
human TE-11 cell MlLwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnjkTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPFM6QDVizszN M1f3ZnNCVkeHUh?=
human CMK cell M3vSSWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MlXCTY5pcWKrdHnvckBw\iCqdX3hckBEVUtiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkm1OVE4KM7:TR?= NFXvOGpUSU6JRWK=
human NB1 cell MUnHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NFf0cVVKdmirYnn0bY9vKG:oIHj1cYFvKE6EMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPVYyOTdizszN M{jCb3NCVkeHUh?=
human MDA-MB-435 cells NF;FZpJRem:uaX\ldoF1cW:wIHHzd4F6 M4TLb|Q5KGh? MojpRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPRFGtUWIuPDN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBUWkJiYYPzZZktKEeLPUKg{txO MknsNlI2PjB4Mke=
human MCF7 cells M4Dac3Bzd2yrZnXyZZRqd25iYYPzZZk> M4XkN|Q5KGh? M2HmU2FvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVPGO{Bk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTJizszN MlnENlI2PjB4Mke=
human A549 cells MoHzR5l1d3SxeHnjxsBie3OjeR?= M3Li[FczKGh? NF;TZ5ZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBCPTR7IHPlcIx{KGG|c3Xzd4VlKGG|IHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:Oi52NDFOwG0> NWrR[nBqOjN4MEK0OFE>

... 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 Insoluble
Ethanol 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
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:

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*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 )

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The Serial Dilution Calculator Equation

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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