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 M1\LfGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MYfJcohq[mm2aX;uJI9nKGi3bXHuJHNYPzV4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUmuNVM2OSEQvF2= MUnTRW5ITVJ?
human EoL-1-cell cell MofwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? Ml7ITY5pcWKrdHnvckBw\iCqdX3hckBGd0xvMT3j[YxtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS54NHWtNFY> NU\ifpJ[W0GQR1XS
human MV-4-11 cell NIHlXY1Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= NGXmWohKdmirYnn0bY9vKG:oIHj1cYFvKE2YLUStNVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjJ5MjDuUS=> NXG3epo{W0GQR1XS
human MV411 cells MVrQdo9tcW[ncnH0bY9vKGG|c3H5 NYPqUohbPDhiaB?= M2rnbmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTW[0NVEh[2WubIOgZYZ1\XJiNEigbJJ{KGK7IF3UWEBie3OjeTygbYM2OD1|IH7N NVfNW2J3OjR7MES5OlE>
3T3 cells NYLPUWR5TnWwY4Tpc44h[XO|YYm= NXXYSHNWUW6qaXLpeIlwdiCxZjDQSGdHNWmwZIXj[YQhSnKmVTDpcoNwenCxcnH0bY9vKGmwIEPUN{Bk\WyuczD3bZRpKDBwMTWgZo93cW6nIIPldpVuKGGuYoXtbY4tKEmFNUC9O{BvVQ>? NG\4ZVAyOjZ2NkCxPS=>
HEK293 cells MUPGeY5kfGmxbjDhd5NigQ>? MXzCbY5lcW6pIHHm[olvcXS7IITvJGZNXDNiY3H0ZYx6fGmlIHTvcYFqdiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{KGK7IHPvcZBmfGm2aY\lJIJqdmSrbnegZZN{[XluIFvkQVAvPDdibl2= NGPrTJgyQTd3NEG5PS=>
human MDA-MB-435 cells NXfDRZRRS3m2b4TvfIlkyqCjc4PhfS=> M2LVNlIhcA>? NWXHZm5zS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSDLV3CMVQ{PSClZXzsd{whUUN3ME25Mlchdk1? M1LtbVI1QDlyNkWy
human RS4-11 cells NV\PW2MxTnWwY4Tpc44h[XO|YYm= NGi3foNKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZYZ1\XJiMjDodpMh[nliZXzlZ5Rzd2OqZX3pcJVucW6nc3PlcoNmKGG|c3H5MEBKSzVyPUmuPUBvVQ>? MkjoNVk3PTR2MEi=
HUVEC MXLDfZRwfG:6aXRCpIF{e2G7 MX7DfZRwfG:6aXPpeJkh[WejaX7zeEBJXV[HQzygTWM2OD1zMT64JI5O NY[1dmFDOjR6OUC2OVI>
human Kasumi-1 cells NG\hNFlHfW6ldHnvckBie3OjeR?= M2jvRWlvcGmkaYTpc44hd2ZiYz3LbZQh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCNYYP1cYkuOSClZXzsd{BjgSCZZYP0[ZJvKGKub4SgZY5idHm|aYOsJGlEPTB;MUWgcm0> M1fDcVIxQDN|MEO5
human NOS-1 cell NIXwfIlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NH74VpRKdmirYnn0bY9vKG:oIHj1cYFvKE6RUz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOyCwTR?= NV7XXXlCW0GQR1XS
mouse triple negative 4T1 cells M3LJfGN6fG:2b4jpZ:Kh[XO|YYm= MXHDfZRwfG:6aXPpeJkh[WejaX7zeEBud3W|ZTD0dolxdGVibnXnZZRqfmViNGSxJINmdGy|LDDJR|UxRTF4IH7N MW[yOFg6ODZ3Mh?=
human RS4-11 cells MkLsSpVv[3Srb36gZZN{[Xl? NEX4WJBKdmirYnn0bY9vKG:oIF\MWFMh[XW2b4Doc5NxcG:{eXzheIlwdiCrbjDoeY1idiCUU{StNVEh[2WubIOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m|LDDJR|UxRTF4IH7N M4LaclIxQDN|MEO5
human MOLM13 cells NUX3Uok6S3m2b4TvfIlkyqCjc4PhfS=> MVfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNU2xOOTNiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xO{44KG6P NUjYSI41OjVyOEm4NVA>
human U251 cells NUXlU|M2TnWwY4Tpc44h[XO|YYm= MlnyTY5pcWKrdHnvckBw\iCYRVfGVlIhcW5iaIXtZY4hXTJ3MTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2EtKEmFNUC9NVgvQSCwTR?= NYW0fZNlOjR7MEC4OlU>
NIH3T3 cells M2D5SGZ2dmO2aX;uJIF{e2G7 M4DiXlEhcA>? Ml7QTY5pcWKrdH;yfUBkd26lZX70doF1cW:wIHHnZYlve3RiaIXtZY4hU0SUIHvpcoF{\SCneIDy[ZN{\WRiaX6gUmlJO1R|IHPlcIx{KHerdHigOEB2VSCEaX;0bY4uSWi6LVHFSWV[Tk[ORlGtZY1q\GViYYSgZY1jcWWwdDD0[Y1x\XKjdIXy[UBnd3JiMTDodi=> MV6xOlE3OjByOB?=
MDA-MB-231 cells Moe3R5l1d3SxeHnjxsBie3OjeR?= MVXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjD0dolxdGVibnXnZZRqfmViTVTBMW1DNTJ|MTDj[YxteyxiSVO1NF0zOi5|IH7N M3\tVVI1QDlyNkWy
MCF7 cells NXHq[2F7S3m2b4TvfIlkyqCjc4PhfS=> Mk\mR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gSXIueG:|aYTpeoUhVUOINzDj[YxteyxiSVO1NF0zPy5zIH7N MUeyOFg6ODZ3Mh?=
human CGTH-W-1 cell NEXFd|ZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MojJTY5pcWKrdHnvckBw\iCqdX3hckBET1SKLWetNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMxNjl2IH7N NX\BcWRlW0GQR1XS
human MONO-MAC-6 cell M3eyR2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MoTUTY5pcWKrdHnvckBw\iCqdX3hckBOV06RLV3BR{03KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzNwODDuUS=> M4TsTXNCVkeHUh?=
human HL60 cells MoKwR5l1d3SxeHnjxsBie3OjeR?= MlnOOFghcA>? NHLQfHREgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVDZyIHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwhfmmjYnnsbZR6KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9N|YvQCCwTR?= MoHNNlUxQDl6MUC=
human TT cells M33TcnBzd2yrZnXyZZRqd25iYYPzZZk> MknDO|IhcA>? M4XWcGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iVGSgZ4VtdHNicILleJJm[XSnZDDmc5IhPzJiaILzJIZwdGyxd3XkJIJ6KGOxbYDveY5lNXejc3jveZQhdWWjc4Xy[YQh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME20NEBvVQ>? M2XSflI1QTB2OU[x
human THP1 cells M{XlcmN6fG:2b4jpZ:Kh[XO|YYm= M4fndlQ5KGh? MX\DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDUTHAyKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NEWuO{BvVQ>? NGrVSJgzPTB6OUixNC=>
3T3 cells NXm4UJJUTnWwY4Tpc44h[XO|YYm= NYC1e|BwUW6qaXLpeIlwdiCxZjDWZZNkfWyjcjDlcoRwfGinbHnhcEBoem:5dHig[oFkfG:{IILlZ4VxfG:{IHnuJFNVOyClZXzsd{whUUN3ME21NEBvVQ>? NFu5O4wyOjZ2NkCxPS=>
human ALL-PO cell NWTXNYl5T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MlrzTY5pcWKrdHnvckBw\iCqdX3hckBCVExvUF:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME23PU45QSCwTR?= MWfTRW5ITVJ?
human SH-SY5Y cells M1nJUWZ2dmO2aX;uJIF{e2G7 M2e1SWlvcGmkaYTpc44hd2ZiUFTHSnJj\XSjIHnuJIh2dWGwIGPIMXN[PVliY3XscJMh[nlicHjvd5Bpd3S7cn;zbY5mKEWOSWPBJIF{e2G7LDDJR|UxRTh|LkGgcm0> NEXpcJIzPDh7ME[1Ni=>
human U251 cells MUHGeY5kfGmxbjDhd5NigQ>? MlLJOlAhdWmwcx?= MXzJcohq[mm2aX;uJI9nKFCGR1\SMYJmfGFiaX6gbJVu[W5iVUK1NUBk\WyuczDjc41xd3WwZDDwdoV1emWjdHXkJIZweiB4MDDtbY4h[mWob4LlJHBFT0ZvQlKgd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME24N{4yKG6P MXmyOVg5OjVzOR?=
human NKM-1 cell NX\qZmxtT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NWPUXHJMUW6qaXLpeIlwdiCxZjDoeY1idiCQS12tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVk5NjV{IH7N NF;CZ|dUSU6JRWK=
human HAEC cells NIHy[|VRem:uaX\ldoF1cW:wIHHzd4F6 NGHLOGw4OiCq MkXERY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKQVXDJINmdGy|IHX4dJJme3OrbnegWmVITlJiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiSVO1NF0xNjFizszN NUTaPGdIOjJ2NES2O|k>
HUVEC cell NFjveHpHfW6ldHnvckBie3OjeR?= MYmyOEBp NX7RRpIzUW6qaXLpeIlwdiCxZjDWSWdHNUFiaX7keYNm\CCKVW\FR{Bk\WyuIIPwdo92fGmwZzDh[pRmeiB{NDDodpMh[nliYX7nbY9o\W6nc3nzJIF{e2G7LDDJR|UxRTBwMUKg{txO MnO1NlE4PDF{NEm=
human A431 cells M1uxT2Z2dmO2aX;uJIF{e2G7 MmDZOlAhdWmwcx?= MY\Jcohq[mm2aX;uJI9nKEWJRmKgbY4hcHWvYX6gRVQ{OSClZXzsd{Bkd22yb4Xu[EBxemW2cnXheIVlKG[xcjC2NEBucW5iYnXmc5JmKEWJRjDzeIlufWyjdHnvckBnd3JiMUCgcYlveyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2Eh[3m2b3Lsc5QhdWW2aH;kMEBKSzVyPUG3Nk4yKG6P NHTBO2czPTh6MkWxPS=>
Sf9 cells Ml\qSpVv[3Srb36gZZN{[Xl? M3f2Z2lvcGmkaYTpc44hd2ZiR2PUMZRi\2enZDDWSWdHWiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUCuNVg2KM7:TR?= MkT5NVk5PTRyNUG=
human HT-29 cells NFfZZ|NRem:uaX\ldoF1cW:wIHHzd4F6 MkfLO|IhcA>? NGjpV|RCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP M2i0TlIzPDR2Nke5
human KM12 cell NEjvZ2FIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MVfJcohq[mm2aX;uJI9nKGi3bXHuJGtOOTJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1yLkO1NFE1KM7:TR?= NWjqZYJHW0GQR1XS
human TE-15 cell MW\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NEjz[YFKdmirYnn0bY9vKG:oIHj1cYFvKFSHLUG1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NE42ODd4MTFOwG0> MkjiV2FPT0WU
human 697 cell NIP1dZpIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWflUoljUW6qaXLpeIlwdiCxZjDoeY1idiB4OUegZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlYyPDJ3IN88US=> MX;TRW5ITVJ?
human CAKI-1 cells MnfSVJJwdGmoZYLheIlwdiCjc4PhfS=> NVu5OnBHSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDDRWtKNTFiY3XscJMh[W[2ZYKgOFghcHK|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlY{KM7:TR?= NIrOeI0zOjV4ME[yOy=>
human MOLT-16 cell NV\ZWItpT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NYDHO|Z3UW6qaXLpeIlwdiCxZjDoeY1idiCPT1zUMVE3KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OC54M{GzNkDPxE1? NFPtZlZUSU6JRWK=
human GB-1 cell MVXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MV;Jcohq[mm2aX;uJI9nKGi3bXHuJGdDNTFiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1yLkexNFI{KM7:TR?= NF3VcnhUSU6JRWK=
human TE-12 cell M17EcGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MonVTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuPFA1PTVizszN MXrTRW5ITVJ?
human NCI-H3122 cells NUHv[|hpWHKxbHnm[ZJifGmxbjDhd5NigQ>? NXnOV4tRPzJiaB?= M1Tye2FvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg{OTJ{IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE45OyEQvF2= MmG4NlQ6ODR7NkG=
human ES6 cell NWn0[lEyT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MXzJcohq[mm2aX;uJI9nKGi3bXHuJGVUPiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTBwOUixNFYh|ryP NX7aR5dDW0GQR1XS
human NCI-H526 cells NFPMVnZRem:uaX\ldoF1cW:wIHHzd4F6 MlHtO|IhcA>? NI\zSVBCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTU1JPTJ4IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NU4xOSEQvF2= M1HINlI1QTB2OU[x
human LC-2-ad cell M2HPb2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MWrJcohq[mm2aX;uJI9nKGi3bXHuJGxENTJvYXSgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlEyPDB5IN88US=> MUPTRW5ITVJ?
human BL-70 cell M3LjVWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MX7Jcohq[mm2aX;uJI9nKGi3bXHuJGJNNTdyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6xNVg1PiEQvF2= MWjTRW5ITVJ?
human ETK-1 cell M1jiZmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NU\wSmZOUW6qaXLpeIlwdiCxZjDoeY1idiCHVFutNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvOjh3ODFOwG0> M12ybHNCVkeHUh?=
human SW620 cells MXPQdo9tcW[ncnH0bY9vKGG|c3H5 M3j0d|Q5KGh? M3XUbWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iU2e2NlAh[2WubIOgZYZ1\XJiNEigbJJ{KGK7IGPSRkBie3OjeTygS2k2OD1zLkOg{txO Mly1NlI2PjB4Mke=
IM9 cells M13SWmN6fG:2b4jpZ:Kh[XO|YYm= MWjDfZRwfG:6aXPpeJkh[WejaX7zeEBJd22xIIPhdIlmdnNiKHj1cYFvMSCLTUmgZ4VtdHNiYYPz[ZN{\WRiYYOg[5Jwf3SqIHnubIljcXSrb36gZpkhVVSWIHHzd4F6NCCLQ{WwQVEvOzVizszN NFPKNY9USU6JRWK=
human A4-Fuk cell NI[zTHRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NYDIcYllUW6qaXLpeIlwdiCxZjDoeY1idiCDND3GeYsh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5Nige,:jDDJR|UxRTFwM{SxOFEh|ryP NYnXSIdkW0GQR1XS
human SR cell NIXvc5NIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXLJcohq[mm2aX;uJI9nKGi3bXHuJHNTKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS53NEW3NkDPxE1? NWrrc3VYW0GQR1XS
human A3-KAW cell MXHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3zhd2lvcGmkaYTpc44hd2ZiaIXtZY4hSTNvS1HXJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKGmlNUC9NU43OjV2NjFOwG0> MX;TRW5ITVJ?
human KS-1 cell MY\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnW5TY5pcWKrdHnvckBw\iCqdX3hckBMWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62PVI1PyEQvF2= MlPqV2FPT0WU
human CTV-1 cell M3;KOGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MnXKTY5pcWKrdHnvckBw\iCqdX3hckBEXFZvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuO|I4PTFizszN M4nPVnNCVkeHUh?=
human LB1047-RCC cell MlPMS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M4HZWWlvcGmkaYTpc44hd2ZiaIXtZY4hVEJzMES3MXJESyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOEG2NlQh|ryP NWTjPVhrW0GQR1XS
human MEG-01 cell M2H0T2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M4ficmlvcGmkaYTpc44hd2ZiaIXtZY4hVUWJLUCxJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU45OzV4MzFOwG0> MmTwV2FPT0WU
human TE-11 cell NF7CcWtIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NI[0[YRKdmirYnn0bY9vKG:oIHj1cYFvKFSHLUGxJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU45Ozl6NTFOwG0> M1zqbnNCVkeHUh?=
human CMK cell MkDPS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NWfQblNtUW6qaXLpeIlwdiCxZjDoeY1idiCFTVugZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlk2PTF5IN88US=> NETyW5VUSU6JRWK=
human NB1 cell NWrn[|lDT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MmjSTY5pcWKrdHnvckBw\iCqdX3hckBPSjFiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zLkm2NVE4KM7:TR?= MnjkV2FPT0WU
human MDA-MB-435 cells M4XabXBzd2yrZnXyZZRqd25iYYPzZZk> NVroW2JOPDhiaB?= MlfXRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPRFGtUWIuPDN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBUWkJiYYPzZZktKEeLPUKg{txO MnTpNlI2PjB4Mke=
human MCF7 cells Mn3rVJJwdGmoZYLheIlwdiCjc4PhfS=> MlnkOFghcA>? NWnjfGpXSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNR2Y4KGOnbHzzJIFnfGW{IES4JIhzeyCkeTDTVmIh[XO|YYmsJGdKPTB;MjFOwG0> MnzaNlI2PjB4Mke=
human A549 cells M{PPS2N6fG:2b4jpZ:Kh[XO|YYm= MU[3NkBp MoS3R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVU1QSClZXzsd{Bie3Onc4Pl[EBieyCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCLQ{WwQVIvPDRizszN M4\ZdVI{PjB{NESx

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(NMPから)右の順に溶剤を製品に加えます:
5% DMSO+corn oil
混合させたのち直ちに使用することを推奨します。
7mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程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、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

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
×
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID