製品コードS7781 別名:SU11248



Sunitinibは一種の多ターゲット RTK阻害剤で、VEGFR2(Flk-1)とPDGFRβに作用する時のIC50値が80 nM 和 2 nMに分かれることです。Sunitinibはc-Kitにも抑制作用を表します。

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JPY 16102.00 あり
JPY 32702.00 あり



  • 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.




製品説明 Sunitinibは一種の多ターゲット RTK阻害剤で、VEGFR2(Flk-1)とPDGFRβに作用する時のIC50値が80 nM 和 2 nMに分かれることです。Sunitinibはc-Kitにも抑制作用を表します。
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

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SW756 cell MmL6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M4\CdGlvcGmkaYTpc44hd2ZiaIXtZY4hW1d5NU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xPU4yOzVzIN88US=> NGfTPHhUSU6JRWK=
human EoL-1-cell cell NXT6UJpCT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MkjPTY5pcWKrdHnvckBw\iCqdX3hckBGd0xvMT3j[YxtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS54NHWtNFY> NWPUR5REW0GQR1XS
human MV-4-11 cell MUHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MYjJcohq[mm2aX;uJI9nKGi3bXHuJG1XNTRvMUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlI4OiCwTR?= M1Kz[3NCVkeHUh?=
human MV411 cells M{XtTnBzd2yrZnXyZZRqd25iYYPzZZk> NEnCPZg1QCCq M2LyVmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTW[0NVEh[2WubIOgZYZ1\XJiNEigbJJ{KGK7IF3UWEBie3OjeTygbYM2OD1|IH7N NGLve2MzPDlyNEm2NS=>
3T3 cells NHrPXJpHfW6ldHnvckBie3OjeR?= M3LhPWlvcGmkaYTpc44hd2ZiUFTHSk1qdmS3Y3XkJGJz\FViaX7jc5Jxd3KjdHnvckBqdiB|VEOgZ4VtdHNid3n0bEAxNjFnIHLveolv\SC|ZYL1cUBidGK3bXnuMEBKSzVyPUegcm0> M2HDR|EzPjR4MEG5
HEK293 cells MnnmSpVv[3Srb36gZZN{[Xl? MYDCbY5lcW6pIHHm[olvcXS7IITvJGZNXDNiY3H0ZYx6fGmlIHTvcYFqdiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{KGK7IHPvcZBmfGm2aY\lJIJqdmSrbnegZZN{[XluIFvkQVAvPDdibl2= M1zEeFE6PzV2MUm5
human MDA-MB-435 cells MmT2R5l1d3SxeHnjxsBie3OjeR?= NXvmNYVrOiCq M2fNbmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSS2PQj20N|Uh[2WubIOsJGlEPTB;OT63JI5O MWGyOFg6ODZ3Mh?=
human RS4-11 cells MlTLSpVv[3Srb36gZZN{[Xl? MojrTY5pcWKrdHnvckBw\iCITGSzJIF2fG:yaH;zdIhwenmuYYTpc44hcW5iaIXtZY4hWlN2LUGxJINmdGy|IHHmeIVzKDJiaILzJIJ6KGWuZXP0do9kcGWvaXz1cYlv\XOlZX7j[UBie3OjeTygTWM2OD17Lkmgcm0> Mlq4NVk3PTR2MEi=
human Kasumi-1 cells NGfxSo5HfW6ldHnvckBie3OjeR?= M4\pZWlvcGmkaYTpc44hd2ZiYz3LbZQh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCNYYP1cYkuOSClZXzsd{BjgSCZZYP0[ZJvKGKub4SgZY5idHm|aYOsJGlEPTB;MUWgcm0> MXGyNFg{OzB|OR?=
human NOS-1 cell M1zTXWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NGj6bmhKdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= NFXYR5ZUSU6JRWK=
mouse triple negative 4T1 cells MXzDfZRwfG:6aXRCpIF{e2G7 Mn\MR5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgeJJqeGynIH7l[4F1cX[nIETUNUBk\WyuczygTWM2OD1zNjDuUS=> MoLtNlQ5QTB4NUK=
human RS4-11 cells MYHGeY5kfGmxbjDhd5NigQ>? MoXYTY5pcWKrdHnvckBw\iCITGSzJIF2fG:yaH;zdIhwenmuYYTpc44hcW5iaIXtZY4hWlN2LUGxJINmdGy|IHL5JHdme3Sncn6gZoxwfCCjbnHsfZNqeyxiSVO1NF0yPiCwTR?= MV:yNFg{OzB|OR?=
human MOLM13 cells MlrnR5l1d3SxeHnjxsBie3OjeR?= M{jQS2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1QVE1zMzDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKH[rYXLpcIl1gSCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVE4Njdibl2= NIDmUpAzPTB6OUixNC=>
human U251 cells NGG0OJhHfW6ldHnvckBie3OjeR?= NGrocmpKdmirYnn0bY9vKG:oIG\FS2ZTOiCrbjDoeY1idiCXMkWxJINmdGy|IHL5JJBpd3OyaH;0fZJwe2mwZTDFUGlUSSxiSVO1NF0yQC57IH7N MlnkNlQ6ODB6NkW=
NIH3T3 cells NVTlS|RtTnWwY4Tpc44h[XO|YYm= MmG3NUBp NIHSbItKdmirYnn0c5J6KGOxbnPlcpRz[XSrb36gZYdicW6|dDDoeY1idiCNRGKgb4lv[XOnIHX4dJJme3OnZDDpckBPUUh|VEOgZ4VtdHNid3n0bEA1KHWPIFLpc5Rqdi2DaIitRWVGTVmIRlzGRU1idWmmZTDheEBidWKrZX70JJRmdXCncnH0eZJmKG[xcjCxJIhz NUXTS|BKOTZzNkKwNFg>
MDA-MB-231 cells NYKyUVd7S3m2b4TvfIlkyqCjc4PhfS=> Mle5R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6geJJqeGynIH7l[4F1cX[nIF3ERU1OSi1{M{GgZ4VtdHNuIFnDOVA:OjJwMzDuUS=> NELDT20zPDh7ME[1Ni=>
MCF7 cells M4jNbWN6fG:2b4jpZ:Kh[XO|YYm= NF;RPHFEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBGWi2yb4PpeIl3\SCPQ1[3JINmdGy|LDDJR|UxRTJ5LkGgcm0> Mmj2NlQ5QTB4NUK=
human CGTH-W-1 cell NFW1bnJIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MmDMTY5pcWKrdHnvckBw\iCqdX3hckBET1SKLWetNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMxNjl2IH7N NYPrdY9CW0GQR1XS
human MONO-MAC-6 cell M4\TeGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NYW5Uod{UW6qaXLpeIlwdiCxZjDoeY1idiCPT17PMW1CSy14IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{OuPEBvVQ>? MUPTRW5ITVJ?
human HL60 cells NUTjfnRZS3m2b4TvfIlkyqCjc4PhfS=> Mn;SOFghcA>? M1LV[WN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhNPjBiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2zOk45KG6P NHP2WG8zPTB6OUixNC=>
human TT cells NGHpVZZRem:uaX\ldoF1cW:wIHHzd4F6 NHTsZXk4OiCq MXvBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFSWIHPlcIx{KHC{ZYTy[YF1\WRiZn;yJFczKGi{czDmc4xtd3enZDDifUBkd22yb4Xu[E14[XOqb4X0JI1m[XO3cnXkJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NECgcm0> NXLGVXhYOjR7MES5OlE>
human THP1 cells MnHRR5l1d3SxeHnjxsBie3OjeR?= MXy0PEBp NHX0Z3VEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBVUFBzIHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9OFUvPyCwTR?= M{n0b|I2ODh7OEGw
3T3 cells MXHGeY5kfGmxbjDhd5NigQ>? MkLsTY5pcWKrdHnvckBw\iCYYYPjeYxieiCnbnTveIhmdGmjbDDndo94fGhiZnHjeI9zKHKnY3XweI9zKGmwIEPUN{Bk\WyuczygTWM2OD13MDDuUS=> M3j1dlEzPjR4MEG5
human ALL-PO cell MlG4S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXjr[I04UW6qaXLpeIlwdiCxZjDoeY1idiCDTFytVG8h[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF04QS56OTDuUS=> M2X0SnNCVkeHUh?=
human SH-SY5Y cells MoToSpVv[3Srb36gZZN{[Xl? NVG5PIdwUW6qaXLpeIlwdiCxZjDQSGdHWmKndHGgbY4hcHWvYX6gV2guW1l3WTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2Eh[XO|YYmsJGlEPTB;OEOuNUBvVQ>? MVGyOFg6ODZ3Mh?=
human U251 cells NGHufo9HfW6ldHnvckBie3OjeR?= M4mwNFYxKG2rboO= MULJcohq[mm2aX;uJI9nKFCGR1\SMYJmfGFiaX6gbJVu[W5iVUK1NUBk\WyuczDjc41xd3WwZDDwdoV1emWjdHXkJIZweiB4MDDtbY4h[mWob4LlJHBFT0ZvQlKgd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME24N{4yKG6P NInmPWozPTh6MkWxPS=>
human NKM-1 cell NInNUZlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MYDJcohq[mm2aX;uJI9nKGi3bXHuJG5MVS1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;OUiuOVIhdk1? M3LHZ3NCVkeHUh?=
human HAEC cells M3f6ZXBzd2yrZnXyZZRqd25iYYPzZZk> MmqxO|IhcA>? NXvsfJZJSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIRWVEKGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygTWM2OD1yLkGg{txO MWOyNlQ1PDZ5OR?=
HUVEC cell MkS2SpVv[3Srb36gZZN{[Xl? MVSyOEBp M3foNGlvcGmkaYTpc44hd2ZiVlXHSk1CKGmwZIXj[YQhUFWYRVOgZ4VtdCC|cILveZRqdmdiYX\0[ZIhOjRiaILzJIJ6KGGwZ3nv[4Vv\XOrczDhd5NigSxiSVO1NF0xNjF{IN88US=> NUfEUY9yOjF5NEGyOFk>
human A431 cells NXLQU5l4TnWwY4Tpc44h[XO|YYm= NH7mTZI3OCCvaX7z Mn3ITY5pcWKrdHnvckBw\iCHR1\SJIlvKGi3bXHuJGE1OzFiY3XscJMh[2:vcH;1coQheHKndILlZZRm\CCob4KgOlAhdWmwIHLl[o9z\SCHR1[gd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME2xO|IvOSCwTR?= M3ryW|I2QDh{NUG5
Sf9 cells M4fuVGZ2dmO2aX;uJIF{e2G7 M{LoT2lvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDWSWdHWiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUCuNVg2KM7:TR?= NEC1UW0yQTh3NEC1NS=>
human HT-29 cells MV3Qdo9tcW[ncnH0bY9vKGG|c3H5 NELScJM4OiCq NFfT[4ZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP MU[yNlQ1PDZ5OR?=
human KM12 cell NWruNGc3T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M{PESWlvcGmkaYTpc44hd2ZiaIXtZY4hU01zMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuN|UxOTRizszN NXHFRWloW0GQR1XS
human TE-15 cell NIHqNGRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NXKye49IUW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xOUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVAvPTB5NkGg{txO M1PqRXNCVkeHUh?=
human 697 cell NHvjTWJIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NHvRW5ZKdmirYnn0bY9vKG:oIHj1cYFvKDZ7NzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOlE1OjVizszN NFSze2RUSU6JRWK=
human CAKI-1 cells MV7Qdo9tcW[ncnH0bY9vKGG|c3H5 NGTjNHZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFPBT2kuOSClZXzsd{Bi\nSncjC0PEBpenNiYomgV3JDKGG|c3H5MEBIUTVyPUCuOlMh|ryP NETkbZUzOjV4ME[yOy=>
human MOLT-16 cell NHLiVmtIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MUfJcohq[mm2aX;uJI9nKGi3bXHuJG1QVFRvMU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlY{OTN{IN88US=> MmrhV2FPT0WU
human GB-1 cell M{DpNmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mk\STY5pcWKrdHnvckBw\iCqdX3hckBISi1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD63NVAzOyEQvF2= NVnycpkzW0GQR1XS
human TE-12 cell M13IVWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mlq0TY5pcWKrdHnvckBw\iCqdX3hckBVTS1zMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuPFA1PTVizszN NVzwe3RmW0GQR1XS
human NCI-H3122 cells MWfQdo9tcW[ncnH0bY9vKGG|c3H5 MUW3NkBp Mmr6RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1mtTFMyOjJiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlg{KM7:TR?= NUnENHlsOjR7MES5OlE>
human ES6 cell MkTiS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYnuToNiUW6qaXLpeIlwdiCxZjDoeY1idiCHU{[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlk5OTB4IN88US=> MUHTRW5ITVJ?
human NCI-H526 cells MU\Qdo9tcW[ncnH0bY9vKGG|c3H5 M1zDfFczKGh? MoDFRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1mtTFUzPiClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUGuNFEh|ryP NYfNdJJZOjR7MES5OlE>
human LC-2-ad cell M4LvO2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NFewRWFKdmirYnn0bY9vKG:oIHj1cYFvKEyFLUKtZYQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yNjFzNEC3JO69VQ>? MkGzV2FPT0WU
human BL-70 cell M1T4b2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mk[1TY5pcWKrdHnvckBw\iCqdX3hckBDVC15MDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuNVE5PDZizszN M2\jPXNCVkeHUh?=
human ETK-1 cell MknvS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NWnVVZh[UW6qaXLpeIlwdiCxZjDoeY1idiCHVFutNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvOjh3ODFOwG0> NXvmeFF5W0GQR1XS
human SW620 cells Ml;jVJJwdGmoZYLheIlwdiCjc4PhfS=> NV\rZ2ZtPDhiaB?= MlTURY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCVV{[yNEBk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTFwMzFOwG0> NH3oR|IzOjV4ME[yOy=>
IM9 cells NVrPemhXS3m2b4TvfIlkyqCjc4PhfS=> M1LRSGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KEixbX:gd4FxcWWwczCobJVu[W5rIFnNPUBk\WyuczDhd5Nme3OnZDDhd{Boem:5dHigbY5pcWKrdHnvckBjgSCPVGSgZZN{[XluIFnDOVA:OS5|NTFOwG0> MV\TRW5ITVJ?
human A4-Fuk cell M3frS2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MofxTY5pcWKrdHnvckBw\iCqdX3hckBCPC2IdXugZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4Phfg+9lCCLQ{WwQVEvOzRzNEGg{txO NVLBZXE1W0GQR1XS
human SR cell NX;CZ5FJT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3\4cWlvcGmkaYTpc44hd2ZiaIXtZY4hW1JiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkW0OVczKM7:TR?= NXHwU5ZZW0GQR1XS
human A3-KAW cell MWXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M4DSZ2lvcGmkaYTpc44hd2ZiaIXtZY4hSTNvS1HXJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKGmlNUC9NU43OjV2NjFOwG0> NHHBbJdUSU6JRWK=
human KS-1 cell MV;Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MkDVTY5pcWKrdHnvckBw\iCqdX3hckBMWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62PVI1PyEQvF2= MnjlV2FPT0WU
human CTV-1 cell Mlq0S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M2nO[mlvcGmkaYTpc44hd2ZiaIXtZY4hS1SYLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlczPzVzIN88US=> NIrHVGZUSU6JRWK=
human LB1047-RCC cell NYrTe4ZlT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MlfjTY5pcWKrdHnvckBw\iCqdX3hckBNSjFyNEetVmNEKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS56MU[yOEDPxE1? M3nRUXNCVkeHUh?=
human MEG-01 cell MV;Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Mnn2TY5pcWKrdHnvckBw\iCqdX3hckBOTUdvMEGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlg{PTZ|IN88US=> NG[2dYVUSU6JRWK=
human TE-11 cell M{fC[Gdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NUO0VppwUW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvQDN7OEWg{txO M2XaTHNCVkeHUh?=
human CMK cell MmrkS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MX3Jcohq[mm2aX;uJI9nKGi3bXHuJGNOUyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOUW1NVch|ryP NYHjU4s5W0GQR1XS
human NB1 cell NYDkenlZT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M1LVVmlvcGmkaYTpc44hd2ZiaIXtZY4hVkJzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT65OlEyPyEQvF2= MWXTRW5ITVJ?
human MDA-MB-435 cells NH\wdoxRem:uaX\ldoF1cW:wIHHzd4F6 NULkSo5KPDhiaB?= MnfSRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPRFGtUWIuPDN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBUWkJiYYPzZZktKEeLPUKg{txO MYOyNlU3ODZ{Nx?=
human MCF7 cells NHTmc2hRem:uaX\ldoF1cW:wIHHzd4F6 MmrpOFghcA>? NUTx[5JPSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNR2Y4KGOnbHzzJIFnfGW{IES4JIhzeyCkeTDTVmIh[XO|YYmsJGdKPTB;MjFOwG0> MYqyNlU3ODZ{Nx?=
human A549 cells NFz0Tm1EgXSxdH;4bYPDqGG|c3H5 NGPlSZc4OiCq MkLWR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVU1QSClZXzsd{Bie3Onc4Pl[EBieyCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVIvPDRizszN NInmdnYzOzZyMkS0NS=>


体内試験 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]




+ 展開

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.


+ 展開
  • 細胞株: RS4;11, MV4;11, and OC1-AML5
  • 濃度: Dissolved in DMSO, final concentrations ~10 μM
  • 反応時間: 24 and 48 hours
  • 実験の流れ:

    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.



+ 展開
  • 動物モデル: 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
  • 製剤: Formulated as a carboxymethyl cellulose suspension or as a citrate buffered (pH 3.5) solution
  • 投薬量: ~80 mg/kg
  • 投与方法: Orally once daily

溶解度 (25°C)

体外 DMSO 25 mg/mL (62.73 mM) warming
Water Insoluble
Ethanol Insoluble
体内 順序で溶剤を入れること:
5% DMSO+corn oil

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。


分子量 398.47


CAS No. 557795-19-4
別名 SU11248





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1



  • 連続希釈剤

  • 計算結果

  • 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):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


マス 濃度 ボリューム 分子量


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



Handling Instructions


  • * 必須



Tags: Sunitinibを買う | Sunitinib ic50 | Sunitinib供給者 | Sunitinibを購入する | Sunitinib費用 | Sunitinib生産者 | オーダーSunitinib | Sunitinib化学構造 | Sunitinib分子量 | Sunitinib代理店
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID