Sunitinib

製品コードS7781 別名:SU11248

Sunitinib化学構造

分子量(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.

サイズ 価格(税別)  
JPY 16102.00
JPY 32702.00

文献中の使用例(33)

カスタマーフィードバック(12)

  • 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.

製品安全説明書

PDGFR阻害剤の選択性比較

生物活性

製品説明 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.
ターゲット
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
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SW756 cell NXrtXohJT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MVrJcohq[mm2aX;uJI9nKGi3bXHuJHNYPzV4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUmuNVM2OSEQvF2= MWTTRW5ITVJ?
human EoL-1-cell cell MkXIS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnH5TY5pcWKrdHnvckBw\iCqdX3hckBGd0xvMT3j[YxtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS54NHWtNFY> MnnRV2FPT0WU
human MV-4-11 cell MWHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NYO4VJVyUW6qaXLpeIlwdiCxZjDoeY1idiCPVj20MVEyKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OC5{N{Kgcm0> M4XvTHNCVkeHUh?=
human MV411 cells MlHRVJJwdGmoZYLheIlwdiCjc4PhfS=> NVH2cWFFPDhiaB?= MVLBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2YNEGxJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCPVGSgZZN{[XluIHnjOVA:OyCwTR?= M4HQTFI1QTB2OU[x
3T3 cells M1qzPGZ2dmO2aX;uJIF{e2G7 M1\WeWlvcGmkaYTpc44hd2ZiUFTHSk1qdmS3Y3XkJGJz\FViaX7jc5Jxd3KjdHnvckBqdiB|VEOgZ4VtdHNid3n0bEAxNjFnIHLveolv\SC|ZYL1cUBidGK3bXnuMEBKSzVyPUegcm0> M1HHUVEzPjR4MEG5
HEK293 cells NYTpZWZqTnWwY4Tpc44h[XO|YYm= NUS4UJJySmmwZHnu[{Bi\m[rbnn0fUB1dyCITGSzJINifGGueYTpZ{Bld22jaX6g[ZhxemW|c3XkJIlvKEiHS{K5N{Bk\WyuczDifUBkd22yZYTpeIl3\SCkaX7kbY5oKGG|c3H5MEBM\D1yLkS3JI5O Mm\6NVk4PTRzOUm=
human MDA-MB-435 cells MoDHR5l1d3SxeHnjxsBie3OjeR?= NESyOWczKGh? NVzDdGpwS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSDLV3CMVQ{PSClZXzsd{whUUN3ME25Mlchdk1? NVrXcIcyOjR6OUC2OVI>
human RS4-11 cells M1L3[mZ2dmO2aX;uJIF{e2G7 M3rRcGlvcGmkaYTpc44hd2ZiRlzUN{BifXSxcHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKFKVND2xNUBk\WyuczDh[pRmeiB{IHjyd{BjgSCnbHXjeJJw[2inbXnseY1qdmW|Y3XuZ4Uh[XO|YYmsJGlEPTB;OT65JI5O MnfCNVk3PTR2MEi=
HUVEC M4OyVGN6fG:2b4jpZ:Kh[XO|YYm= MmLxR5l1d3SxeHnjbZR6KGGpYXnud5QhUFWYRVOsJGlEPTB;MUGuPEBvVQ>? NUnDUnV4OjR6OUC2OVI>
human Kasumi-1 cells M3HzdGZ2dmO2aX;uJIF{e2G7 MoP0TY5pcWKrdHnvckBw\iClLVvpeEBifXSxcHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKEujc4XtbU0yKGOnbHzzJIJ6KFenc4Tldo4h[myxdDDhcoFtgXOrczygTWM2OD1zNTDuUS=> M2KzRlIxQDN|MEO5
human NOS-1 cell NF7YRnVIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXzJcohq[mm2aX;uJI9nKGi3bXHuJG5QWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUWuN{BvVQ>? NEXR[lZUSU6JRWK=
mouse triple negative 4T1 cells NHzhe3lEgXSxdH;4bYPDqGG|c3H5 M1;vN2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJJRzcXCuZTDu[YdifGm4ZTC0WFEh[2WubIOsJGlEPTB;MU[gcm0> MnLnNlQ5QTB4NUK=
human RS4-11 cells MVrGeY5kfGmxbjDhd5NigQ>? MmHXTY5pcWKrdHnvckBw\iCITGSzJIF2fG:yaH;zdIhwenmuYYTpc44hcW5iaIXtZY4hWlN2LUGxJINmdGy|IHL5JHdme3Sncn6gZoxwfCCjbnHsfZNqeyxiSVO1NF0yPiCwTR?= NXSxOHgzOjB6M{OwN|k>
human MOLM13 cells NITHXnBEgXSxdH;4bYPDqGG|c3H5 M2LHR2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1QVE1zMzDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKH[rYXLpcIl1gSCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVE4Njdibl2= NGSweHgzPTB6OUixNC=>
human U251 cells MkHNSpVv[3Srb36gZZN{[Xl? M3;u[2lvcGmkaYTpc44hd2ZiVlXHSnIzKGmwIHj1cYFvKFV{NUGgZ4VtdHNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCNCCLQ{WwQVE5Njlibl2= MoDCNlQ6ODB6NkW=
NIH3T3 cells NInRRldHfW6ldHnvckBie3OjeR?= MlznNUBp NHfLfWFKdmirYnn0c5J6KGOxbnPlcpRz[XSrb36gZYdicW6|dDDoeY1idiCNRGKgb4lv[XOnIHX4dJJme3OnZDDpckBPUUh|VEOgZ4VtdHNid3n0bEA1KHWPIFLpc5Rqdi2DaIitRWVGTVmIRlzGRU1idWmmZTDheEBidWKrZX70JJRmdXCncnH0eZJmKG[xcjCxJIhz NUXJ[YFvOTZzNkKwNFg>
MDA-MB-231 cells MmXER5l1d3SxeHnjxsBie3OjeR?= MULDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjD0dolxdGVibnXnZZRqfmViTVTBMW1DNTJ|MTDj[YxteyxiSVO1NF0zOi5|IH7N M17vSlI1QDlyNkWy
MCF7 cells MYHDfZRwfG:6aXRCpIF{e2G7 MUXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDFVk1xd3OrdHn2[UBOS0Z5IHPlcIx{NCCLQ{WwQVI4NjFibl2= NFHxcXYzPDh7ME[1Ni=>
human CGTH-W-1 cell NXG1RmFQT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3Xt[WlvcGmkaYTpc44hd2ZiaIXtZY4hS0eWSD3XMVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{OC57NDDuUS=> NWi3b2c5W0GQR1XS
human MONO-MAC-6 cell MnLQS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXL3R3Z7UW6qaXLpeIlwdiCxZjDoeY1idiCPT17PMW1CSy14IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{OuPEBvVQ>? NU\5VXVUW0GQR1XS
human HL60 cells M2nHRmN6fG:2b4jpZ:Kh[XO|YYm= NXPUNFd2PDhiaB?= MnHHR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTGw3OCClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJZq[WKrbHn0fUBi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUO2Mlghdk1? MoC0NlUxQDl6MUC=
human TT cells MYnQdo9tcW[ncnH0bY9vKGG|c3H5 M3yy[FczKGh? MVjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFSWIHPlcIx{KHC{ZYTy[YF1\WRiZn;yJFczKGi{czDmc4xtd3enZDDifUBkd22yb4Xu[E14[XOqb4X0JI1m[XO3cnXkJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NECgcm0> NV\ENpNDOjR7MES5OlE>
human THP1 cells M3TMZmN6fG:2b4jpZ:Kh[XO|YYm= M3\CR|Q5KGh? NVj6N4l2S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hXEiSMTDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKH[rYXLpcIl1gSCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVQ2Njdibl2= MUGyOVA5QThzMB?=
3T3 cells MX7GeY5kfGmxbjDhd5NigQ>? MXTJcohq[mm2aX;uJI9nKF[jc3P1cIFzKGWwZH;0bIVtcWGuIHfyc5d1cCCoYXP0c5IhemWlZYD0c5IhcW5iM2SzJINmdGy|LDDJR|UxRTVyIH7N NFX1XGIyOjZ2NkCxPS=>
human ALL-PO cell Mk\0S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M3HZOGlvcGmkaYTpc44hd2ZiaIXtZY4hSUyOLWDPJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9O|kvQDlibl2= NILrWHpUSU6JRWK=
human SH-SY5Y cells Mk\WSpVv[3Srb36gZZN{[Xl? NGjWUW1KdmirYnn0bY9vKG:oIGDES2ZT[mW2YTDpckBpfW2jbjDTTE1UYTW\IHPlcIx{KGK7IIDoc5NxcG:2eYLvd4lv\SCHTFnTRUBie3OjeTygTWM2OD16Mz6xJI5O M4HLXlI1QDlyNkWy
human U251 cells MX3GeY5kfGmxbjDhd5NigQ>? NFLzPZg3OCCvaX7z NInBdWVKdmirYnn0bY9vKG:oIGDES2ZTNWKndHGgbY4hcHWvYX6gWVI2OSClZXzsd{Bkd22yb4Xu[EBxemW2cnXheIVlKG[xcjC2NEBucW5iYnXmc5JmKFCGR1[tRmIhe3SrbYXsZZRqd25iZn;yJFExKG2rboOgZpkheGixc4Doc5R6em:|aX7lJGVNUVODIHP5eI9jdG:2IH3leIhw\CxiSVO1NF05Oy5zIH7N M2[xPVI2QDh{NUG5
human NKM-1 cell MkjBS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NIXU[4pKdmirYnn0bY9vKG:oIHj1cYFvKE6NTT2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVgvPTJibl2= NXO5cIZpW0GQR1XS
human HAEC cells MUDQdo9tcW[ncnH0bY9vKGG|c3H5 NVXx[IlyPzJiaB?= MW\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiDRVOgZ4VtdHNiZYjwdoV{e2mwZzDWSWdHWiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVAvOSEQvF2= M1TqclIzPDR2Nke5
HUVEC cell MnLQSpVv[3Srb36gZZN{[Xl? NX7hN2pOOjRiaB?= NFfUfHVKdmirYnn0bY9vKG:oIG\FS2YuSSCrbnT1Z4VlKEiXVlXDJINmdGxic4Dyc5V1cW6pIHHmeIVzKDJ2IHjyd{BjgSCjbnfpc4dmdmW|aYOgZZN{[XluIFnDOVA:OC5zMjFOwG0> NWT5[ldQOjF5NEGyOFk>
human A431 cells MX7GeY5kfGmxbjDhd5NigQ>? NIfERnI3OCCvaX7z MnPuTY5pcWKrdHnvckBw\iCHR1\SJIlvKGi3bXHuJGE1OzFiY3XscJMh[2:vcH;1coQheHKndILlZZRm\CCob4KgOlAhdWmwIHLl[o9z\SCHR1[gd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME2xO|IvOSCwTR?= NEHTNW8zPTh6MkWxPS=>
Sf9 cells NUfKNnRxTnWwY4Tpc44h[XO|YYm= NUnhfWtHUW6qaXLpeIlwdiCxZjDHV3QufGGpZ3XkJHZGT0[UIHX4dJJme3OnZDDpckBU\jliY3XscJMtKEmFNUC9NE4yQDVizszN NX\B[o9JOTl6NUSwOVE>
human HT-29 cells Mn7aVJJwdGmoZYLheIlwdiCjc4PhfS=> MYK3NkBp MnfCRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKVD2yPUBk\WyuczDlfJBz\XO|aX7nJHZGT0[UIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XoxvJygTWM2OD1yLkOzJO69VQ>? MX6yNlQ1PDZ5OR?=
human KM12 cell MWPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Ml:2TY5pcWKrdHnvckBw\iCqdX3hckBMVTF{IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD6zOVAyPCEQvF2= MkD0V2FPT0WU
human TE-15 cell Moj6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXPjWVlWUW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xOUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVAvPTB5NkGg{txO NXXtSlk4W0GQR1XS
human 697 cell M4CzTGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MmfOTY5pcWKrdHnvckBw\iCqdX3hckA3QTdiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1yLk[xOFI2KM7:TR?= MlvHV2FPT0WU
human CAKI-1 cells NYSxSXJIWHKxbHnm[ZJifGmxbjDhd5NigQ>? NEPnU2RCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFPBT2kuOSClZXzsd{Bi\nSncjC0PEBpenNiYomgV3JDKGG|c3H5MEBIUTVyPUCuOlMh|ryP M2TXT|IzPTZyNkK3
human MOLT-16 cell Ml;3S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXjENG5tUW6qaXLpeIlwdiCxZjDoeY1idiCPT1zUMVE3KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OC54M{GzNkDPxE1? NWXHSHpkW0GQR1XS
human GB-1 cell NGHudIVIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MmH2TY5pcWKrdHnvckBw\iCqdX3hckBISi1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD63NVAzOyEQvF2= MUjTRW5ITVJ?
human TE-12 cell M2LwOWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MWnJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTF{IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD64NFQ2PSEQvF2= NVv3Omc6W0GQR1XS
human NCI-H3122 cells MXXQdo9tcW[ncnH0bY9vKGG|c3H5 MorHO|IhcA>? MlHRRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1mtTFMyOjJiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2wMlg{KM7:TR?= MoXZNlQ6ODR7NkG=
human ES6 cell NYfF[FZ1T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M{LiTGlvcGmkaYTpc44hd2ZiaIXtZY4hTVN4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD65PFExPiEQvF2= MnHHV2FPT0WU
human NCI-H526 cells MkTBVJJwdGmoZYLheIlwdiCjc4PhfS=> M3mydlczKGh? M1;lTmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg2OjZiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xMlAyKM7:TR?= NFe1NYQzPDlyNEm2NS=>
human LC-2-ad cell MUfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NIDsOG9KdmirYnn0bY9vKG:oIHj1cYFvKEyFLUKtZYQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yNjFzNEC3JO69VQ>? M1ToeHNCVkeHUh?=
human BL-70 cell M2P4ZWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MXvJcohq[mm2aX;uJI9nKGi3bXHuJGJNNTdyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6xNVg1PiEQvF2= NIjYUJJUSU6JRWK=
human ETK-1 cell M{LzPWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mn7yTY5pcWKrdHnvckBw\iCqdX3hckBGXEtvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuNlg2QCEQvF2= NUmxTZlEW0GQR1XS
human SW620 cells MlX1VJJwdGmoZYLheIlwdiCjc4PhfS=> M2[3clQ5KGh? MXzBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFOZNkKwJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OS5|IN88US=> M3PlVlIzPTZyNkK3
IM9 cells NXnUbHloS3m2b4TvfIlkyqCjc4PhfS=> MkDUR5l1d3SxeHnjbZR6KGGpYXnud5QhUG:vbzDzZZBq\W6|IDjoeY1idiliSV25JINmdGy|IHHzd4V{e2WmIHHzJIdzd3e2aDDpcohq[mm2aX;uJIJ6KE2WVDDhd5NigSxiSVO1NF0yNjN3IN88US=> MoXrV2FPT0WU
human A4-Fuk cell NY\2WJNYT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M1XKTWlvcGmkaYTpc44hd2ZiaIXtZY4hSTRvRoXrJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZnwxIxiSVO1NF0yNjN2MUSxJO69VQ>? NGjRbJJUSU6JRWK=
human SR cell MUPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3XwWWlvcGmkaYTpc44hd2ZiaIXtZY4hW1JiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkW0OVczKM7:TR?= M1TGOXNCVkeHUh?=
human A3-KAW cell M4DqTGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NUHNPFh4UW6qaXLpeIlwdiCxZjDoeY1idiCDMz3LRXch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiaXO1NF0yNjZ{NUS2JO69VQ>? MoXNV2FPT0WU
human KS-1 cell M3vjeGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MkXVTY5pcWKrdHnvckBw\iCqdX3hckBMWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62PVI1PyEQvF2= MonGV2FPT0WU
human CTV-1 cell MVzHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MoPvTY5pcWKrdHnvckBw\iCqdX3hckBEXFZvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuO|I4PTFizszN Mn7uV2FPT0WU
human LB1047-RCC cell NFPuOmRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NF7EfmJKdmirYnn0bY9vKG:oIHj1cYFvKEyEMUC0O{1TS0NiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkixOlI1KM7:TR?= M4G4NnNCVkeHUh?=
human MEG-01 cell NEm5RVBIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MUfJcohq[mm2aX;uJI9nKGi3bXHuJG1GTy1yMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPFM2PjNizszN MXHTRW5ITVJ?
human TE-11 cell M1rMfWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MULJcohq[mm2aX;uJI9nKGi3bXHuJHRGNTFzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT64N|k5PSEQvF2= M3uzd3NCVkeHUh?=
human CMK cell NHfGSplIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M2PrWmlvcGmkaYTpc44hd2ZiaIXtZY4hS02NIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT65OVUyPyEQvF2= NX;PSIZ5W0GQR1XS
human NB1 cell MY\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3S5R2lvcGmkaYTpc44hd2ZiaIXtZY4hVkJzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT65OlEyPyEQvF2= NEnwZWZUSU6JRWK=
human MDA-MB-435 cells MkjFVJJwdGmoZYLheIlwdiCjc4PhfS=> MmOzOFghcA>? M{Xo[WFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVTBMW1DNTR|NTDj[YxteyCjZoTldkA1QCCqcoOgZpkhW1KEIHHzd4F6NCCJSU2yJO69VQ>? M2LlRlIzPTZyNkK3
human MCF7 cells NGjicWRRem:uaX\ldoF1cW:wIHHzd4F6 NUnTfXA5PDhiaB?= M2XaXmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVPGO{Bk\WyuczDh[pRmeiB2ODDodpMh[nliU2LCJIF{e2G7LDDHTVUxRTJizszN NVS0cYRQOjJ3NkC2Nlc>
human A549 cells MmPWR5l1d3SxeHnjxsBie3OjeR?= NVK5Z5hDPzJiaB?= NFP4S4VEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBCPTR7IHPlcIx{KGG|c3Xzd4VlKGG|IHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:Oi52NDFOwG0> MmXBNlM3ODJ2NEG=

多くの細胞株試験データを見る場合、クリックしてください

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]

お薦めの試験操作(参考用のみ)

キナーゼ試験:

[1]

+ 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.
細胞試験:

[3]

+ 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.


    (参考用のみ)
動物試験:

[2]

+ 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
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 25 mg/mL (62.73 mM) warming
Water Insoluble
Ethanol Insoluble
体内 左から右までの手順で、溶剤を製品に加えることです:
5% DMSO+corn oil
いい結果が出るために、混じった後、直ちに使うと推めます。
7mg/mL

* 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。

化学情報

分子量 398.47
化学式

C22H27FN4O2

CAS No. 557795-19-4
保管
別名 SU11248

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

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

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

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

希釈の計算式

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

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

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

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

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

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

Related Antibodies

PDGFRシグナル伝達経路

相関PDGFR製品

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
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