Sunitinib

目录号:S7781 别名: SU11248

Sunitinib Chemical Structure

Molecular Weight(MW): 398.47

Sunitinib 是一种多靶点 RTK 抑制剂,以VEGFR2(Flk-1)和PDGFRβ为靶点,IC50为80 nM 和 2 nM,对c-Kit也有抑制作用。

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客户使用Selleck该产品发表文献37篇:

客户使用该产品的14个实验数据:

  • 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.

    Mice harboring PC3 prostate cancer xenograft tumors were treated with vehicle, B20-4.1.1, or sunitinib. Serial sections from tumors were immunostained to measure hypoxia (hypoxyprobe; HP-1) and PIM1 (dashed lines delineate regions of hypoxia).

    Clin Cancer Res, 2018, 24(1):169-180. Sunitinib purchased from Selleck.

  • Western blotting of Mcl-1 in HCT116 cells treated with indicated agents for 24 hours. ABT-263, 5 μmol/L; ABT-737, 5 μmol/L; SAHA, 4 μmol/L; MS-275, 5 μmol/L; regorafenib, 40 μmol/L; sorafenib, 20 μmol/L; UCN-01, 1 μmol/L; sunitinib, 15 μmol/L.

    Cancer Res, 2018, 78(16):4704-4715. 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.

产品安全说明书

PDGFR抑制剂选择性比较

生物活性

产品描述 Sunitinib 是一种多靶点 RTK 抑制剂,以VEGFR2(Flk-1)和PDGFRβ为靶点,IC50为80 nM 和 2 nM,对c-Kit也有抑制作用。
靶点
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
体外研究

Sunitinib能够有效抑制Kit 和FLT-3。[1] Sunitinib是VEGFR2 (Flk1) 和 PDGFRβ有效的ATP竞争性抑制剂,Ki分别为9 nM 和8 nM,作用于VEGFR2和 PDGFR比作用于FGFR-1,EGFR,Cdk2,Met,IGFR-1,Abl,和src选择性高10倍多。在血清饥饿的表达VEGFR2 或PDGFRβ的NIH-3T3细胞中,Sunitinib抑制VEGF依赖性VEGFR2磷酸化和PDGF依赖性PDGFRβ磷酸化,IC50分别为10 nM和10 nM。对于过表达PDGFRβ或PDGFRα的NIH-3T3细胞,Sunitinib抑制VEGF对其诱导的增殖,IC50 分别为39 nM和69 nM。[2] Sunitinib抑制野生型FLT3,FLT3-ITD,和FLT3-Asp835磷酸化,IC50分别为250 nM,50 nM,和30 nM。Sunitinib抑制MV4;11 和OC1-AML5细胞的增殖,IC50分别为8 nM和14 nM,并以剂量依赖的方式诱导细胞凋亡。[3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human SW756 cell NHLqUHlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NH[2cWNKdmirYnn0bY9vKG:oIHj1cYFvKFOZN{W2JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVkvOTN3MTFOwG0> NH[3eHpUSU6JRWK=
human EoL-1-cell cell MVXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NVH3T3B{UW6qaXLpeIlwdiCxZjDoeY1idiCHb1ytNU1k\WyuIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62OIUuODZ? MYHTRW5ITVJ?
human MV-4-11 cell M{C0[Wdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NGf4WFdKdmirYnn0bY9vKG:oIHj1cYFvKE2YLUStNVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjJ5MjDuUS=> NIfkdWVUSU6JRWK=
human MV411 cells M1PscHBzd2yrZnXyZZRqd25iYYPzZZk> MmHDOFghcA>? NWP4dI5mSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNWlQyOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBq[zVyPUOgcm0> NXrnXlB7OjR7MES5OlE>
3T3 cells NGTTVFFHfW6ldHnvckBie3OjeR?= MmLiTY5pcWKrdHnvckBw\iCSRFfGMYlv\HWlZXSgRpJlXSCrbnPvdpBwemG2aX;uJIlvKDOWMzDj[YxteyC5aYToJFAvOSViYn;2bY5mKHOncoXtJIFt[nWvaX6sJGlEPTB;NzDuUS=> MW[xNlY1PjBzOR?=
HEK293 cells M1XoXGZ2dmO2aX;uJIF{e2G7 MW\CbY5lcW6pIHHm[olvcXS7IITvJGZNXDNiY3H0ZYx6fGmlIHTvcYFqdiCneIDy[ZN{\WRiaX6gTGVMOjl|IHPlcIx{KGK7IHPvcZBmfGm2aY\lJIJqdmSrbnegZZN{[XluIFvkQVAvPDdibl2= MkXvNVk4PTRzOUm=
human MDA-MB-435 cells NX;xZ3JbS3m2b4TvfIlkyqCjc4PhfS=> NIrNbnYzKGh? MUjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNSGEuVUJvNEO1JINmdGy|LDDJR|UxRTlwNzDuUS=> MYOyOFg6ODZ3Mh?=
human RS4-11 cells NEnjSFVHfW6ldHnvckBie3OjeR?= MU\Jcohq[mm2aX;uJI9nKE[OVEOgZZV1d3Cqb4PwbI9zgWyjdHnvckBqdiCqdX3hckBTWzRvMUGgZ4VtdHNiYX\0[ZIhOiCqcoOgZpkh\WynY4Tyc4Np\W2rbIXtbY5me2OnbnPlJIF{e2G7LDDJR|UxRTlwOTDuUS=> M4KxOVE6PjV2NEC4
HUVEC NFLRO5lEgXSxdH;4bYPDqGG|c3H5 MV;DfZRwfG:6aXPpeJkh[WejaX7zeEBJXV[HQzygTWM2OD1zMT64JI5O M1j4TlI1QDlyNkWy
human Kasumi-1 cells MXLGeY5kfGmxbjDhd5NigQ>? NVfiTZA2UW6qaXLpeIlwdiCxZjDjMWtqfCCjdYTvdIhwe3Cqb4L5cIF1cW:wIHnuJIh2dWGwIFvhd5VucS1zIHPlcIx{KGK7IGfld5Rmem5iYnzveEBidmGueYPpd{whUUN3ME2xOUBvVQ>? NFjOO4UzODh|M{CzPS=>
human NOS-1 cell NVSyR|N[T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MXrJcohq[mm2aX;uJI9nKGi3bXHuJG5QWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUWuN{BvVQ>? NXvnUVZXW0GQR1XS
mouse triple negative 4T1 cells MlnBR5l1d3SxeHnjxsBie3OjeR?= MV\DfZRwfG:6aXPpeJkh[WejaX7zeEBud3W|ZTD0dolxdGVibnXnZZRqfmViNGSxJINmdGy|LDDJR|UxRTF4IH7N MkXtNlQ5QTB4NUK=
human RS4-11 cells MkHMSpVv[3Srb36gZZN{[Xl? NVTJcHA4UW6qaXLpeIlwdiCxZjDGUHQ{KGG3dH;wbI9{eGixconsZZRqd25iaX6gbJVu[W5iUmO0MVEyKGOnbHzzJIJ6KFenc4Tldo4h[myxdDDhcoFtgXOrczygTWM2OD1zNjDuUS=> MY[yNFg{OzB|OR?=
human MOLM13 cells MYnDfZRwfG:6aXRCpIF{e2G7 MUnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNU2xOOTNiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME2xO{44KG6P NFzOdGczPTB6OUixNC=>
human U251 cells Mk\mSpVv[3Srb36gZZN{[Xl? MofHTY5pcWKrdHnvckBw\iCYRVfGVlIhcW5iaIXtZY4hXTJ3MTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2EtKEmFNUC9NVgvQSCwTR?= NWjJeXBoOjR7MEC4OlU>
NIH3T3 cells NWXZeohZTnWwY4Tpc44h[XO|YYm= M3vCUFEhcA>? NWjBe|ZZUW6qaXLpeI9zgSClb37j[Y51emG2aX;uJIFo[Wmwc4SgbJVu[W5iS1TSJItqdmG|ZTDlfJBz\XO|ZXSgbY4hVkmKM2SzJINmdGy|IIfpeIghPCC3TTDCbY91cW5vQXj4MWFGTUW\Rl\MSmEu[W2rZHWgZZQh[W2kaXXueEB1\W2yZYLheJVz\SCob4KgNUBpeg>? M1jUU|E3OTZ{MEC4
MDA-MB-231 cells NEnGcIpEgXSxdH;4bYPDqGG|c3H5 MUnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjD0dolxdGVibnXnZZRqfmViTVTBMW1DNTJ|MTDj[YxteyxiSVO1NF0zOi5|IH7N M1v0e|I1QDlyNkWy
MCF7 cells M{\l[mN6fG:2b4jpZ:Kh[XO|YYm= MV7DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDFVk1xd3OrdHn2[UBOS0Z5IHPlcIx{NCCLQ{WwQVI4NjFibl2= M1fxXVI1QDlyNkWy
human CGTH-W-1 cell NV3pdYx3T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MWHJcohq[mm2aX;uJI9nKGi3bXHuJGNIXEhvVz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N|AvQTRibl2= NVraU2V1W0GQR1XS
human MONO-MAC-6 cell MUDHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NHXodmVKdmirYnn0bY9vKG:oIHj1cYFvKE2RTl:tUWFENTZiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1|Mz64JI5O NIW2PFZUSU6JRWK=
human HL60 cells NF\6V5FEgXSxdH;4bYPDqGG|c3H5 NUL3fFBuPDhiaB?= MkHUR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTGw3OCClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJZq[WKrbHn0fUBi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUO2Mlghdk1? NWe2VYNmOjVyOEm4NVA>
human TT cells MU\Qdo9tcW[ncnH0bY9vKGG|c3H5 M3zOe|czKGh? M3zEPWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iVGSgZ4VtdHNicILleJJm[XSnZDDmc5IhPzJiaILzJIZwdGyxd3XkJIJ6KGOxbYDveY5lNXejc3jveZQhdWWjc4Xy[YQh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhUUN3ME20NEBvVQ>? M2LmTVI1QTB2OU[x
human THP1 cells NWHx[YJ6S3m2b4TvfIlkyqCjc4PhfS=> NYOyNYlVPDhiaB?= MX\DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDUTHAyKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;NEWuO{BvVQ>? NHfOW4QzPTB6OUixNC=>
3T3 cells MULGeY5kfGmxbjDhd5NigQ>? MWHJcohq[mm2aX;uJI9nKF[jc3P1cIFzKGWwZH;0bIVtcWGuIHfyc5d1cCCoYXP0c5IhemWlZYD0c5IhcW5iM2SzJINmdGy|LDDJR|UxRTVyIH7N NVfUTYdWOTJ4NE[wNVk>
human ALL-PO cell NGLzZoRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MnXuTY5pcWKrdHnvckBw\iCqdX3hckBCVExvUF:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME23PU45QSCwTR?= MVrTRW5ITVJ?
human SH-SY5Y cells MUPGeY5kfGmxbjDhd5NigQ>? NX33XFNpUW6qaXLpeIlwdiCxZjDQSGdHWmKndHGgbY4hcHWvYX6gV2guW1l3WTDj[YxteyCkeTDwbI9{eGixdInyc5NqdmViRVzJV2Eh[XO|YYmsJGlEPTB;OEOuNUBvVQ>? NYPvfm55OjR6OUC2OVI>
human U251 cells Mm\aSpVv[3Srb36gZZN{[Xl? NHrVe|U3OCCvaX7z NUG1fJRLUW6qaXLpeIlwdiCxZjDQSGdHWi2kZYThJIlvKGi3bXHuJHUzPTFiY3XscJMh[2:vcH;1coQheHKndILlZZRm\CCob4KgOlAhdWmwIHLl[o9z\SCSRFfGMWJDKHO2aX31cIF1cW:wIH\vdkAyOCCvaX7zJIJ6KHCqb4PwbI91gXKxc3nu[UBGVEmVQTDjfZRw[myxdDDt[ZRpd2RuIFnDOVA:QDNwMTDuUS=> MmD1NlU5QDJ3MUm=
human NKM-1 cell Ml61S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M{jpVmlvcGmkaYTpc44hd2ZiaIXtZY4hVkuPLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME25PE42OiCwTR?= NXnDXZlPW0GQR1XS
human HAEC cells NUXqWHR[WHKxbHnm[ZJifGmxbjDhd5NigQ>? NFm5XG84OiCq NYjlbHYySW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDIRWVEKGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygTWM2OD1yLkGg{txO NH7UdpUzOjR2NE[3PS=>
HUVEC cell NETjSoRHfW6ldHnvckBie3OjeR?= Mkm0NlQhcA>? NUfXcpRrUW6qaXLpeIlwdiCxZjDWSWdHNUFiaX7keYNm\CCKVW\FR{Bk\WyuIIPwdo92fGmwZzDh[pRmeiB{NDDodpMh[nliYX7nbY9o\W6nc3nzJIF{e2G7LDDJR|UxRTBwMUKg{txO M2PmZlIyPzRzMkS5
human A431 cells NID0cHZHfW6ldHnvckBie3OjeR?= MYe2NEBucW6| MkTvTY5pcWKrdHnvckBw\iCHR1\SJIlvKGi3bXHuJGE1OzFiY3XscJMh[2:vcH;1coQheHKndILlZZRm\CCob4KgOlAhdWmwIHLl[o9z\SCHR1[gd5RqdXWuYYTpc44h\m:{IEGwJI1qdnNiYomgdIhwe3Cqb4T5do9{cW6nIFXMTXNCKGO7dH;icI91KG2ndHjv[EwhUUN3ME2xO|IvOSCwTR?= NFfTS5ozPTh6MkWxPS=>
Sf9 cells NHjYeJNHfW6ldHnvckBie3OjeR?= NWX4UpFyUW6qaXLpeIlwdiCxZjDHV3QufGGpZ3XkJHZGT0[UIHX4dJJme3OnZDDpckBU\jliY3XscJMtKEmFNUC9NE4yQDVizszN M3r6cFE6QDV2MEWx
human HT-29 cells M3rGdnBzd2yrZnXyZZRqd25iYYPzZZk> MUO3NkBp NFPqR3pCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjUMVI6KGOnbHzzJIV5eHKnc4PpcochXkWJRmKgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3Ojef-8kEBKSzVyPUCuN|Mh|ryP MnvhNlI1PDR4N{m=
human KM12 cell NWLJfldyT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MX3Jcohq[mm2aX;uJI9nKGi3bXHuJGtOOTJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1yLkO1NFE1KM7:TR?= NETuXJJUSU6JRWK=
human TE-15 cell MXHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MkXJTY5pcWKrdHnvckBw\iCqdX3hckBVTS1zNTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOVA4PjFizszN M2LwdXNCVkeHUh?=
human 697 cell MX3Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3rZRmlvcGmkaYTpc44hd2ZiaIXtZY4hPjl5IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD62NVQzPSEQvF2= M1zEfnNCVkeHUh?=
human CAKI-1 cells M2jsWXBzd2yrZnXyZZRqd25iYYPzZZk> NV7ZU4w{SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDDRWtKNTFiY3XscJMh[W[2ZYKgOFghcHK|IHL5JHNTSiCjc4PhfUwhT0l3ME2wMlY{KM7:TR?= MnmyNlI2PjB4Mke=
human MOLT-16 cell MmLFS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MXTJcohq[mm2aX;uJI9nKGi3bXHuJG1QVFRvMU[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlY{OTN{IN88US=> NVPqNJRPW0GQR1XS
human GB-1 cell MnyxS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnTQTY5pcWKrdHnvckBw\iCqdX3hckBISi1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MD63NVAzOyEQvF2= NVnCe4hvW0GQR1XS
human TE-12 cell NYLEb3ZuT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M1;MTWlvcGmkaYTpc44hd2ZiaIXtZY4hXEVvMUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlgxPDV3IN88US=> MXHTRW5ITVJ?
human NCI-H3122 cells NXjuW|lXWHKxbHnm[ZJifGmxbjDhd5NigQ>? M3zTeFczKGh? M3;Jb2FvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJMWg{OTJ{IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE45OyEQvF2= M2TlOlI1QTB2OU[x
human ES6 cell MWTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NX[wSWFuUW6qaXLpeIlwdiCxZjDoeY1idiCHU{[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2wMlk5OTB4IN88US=> NXnTT4hWW0GQR1XS
human NCI-H526 cells M{HpcnBzd2yrZnXyZZRqd25iYYPzZZk> NF;lXYE4OiCq NGCzfGdCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTU1JPTJ4IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9NU4xOSEQvF2= MlvuNlQ6ODR7NkG=
human LC-2-ad cell NYD0RnRDT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NXz6XldwUW6qaXLpeIlwdiCxZjDoeY1idiCOQz2yMYFlKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OS5zMUSwO{DPxE1? M165dXNCVkeHUh?=
human BL-70 cell NH3xNopIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MUjJcohq[mm2aX;uJI9nKGi3bXHuJGJNNTdyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT6xNVg1PiEQvF2= MoLkV2FPT0WU
human ETK-1 cell NU\JPVNNT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NEH4UI1KdmirYnn0bY9vKG:oIHj1cYFvKEWWSz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NU4zQDV6IN88US=> NHOxUWpUSU6JRWK=
human SW620 cells NIXTfHlRem:uaX\ldoF1cW:wIHHzd4F6 NIHDS4g1QCCq MXLBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFOZNkKwJINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OS5|IN88US=> MmC5NlI2PjB4Mke=
IM9 cells MWfDfZRwfG:6aXRCpIF{e2G7 NHrHSYNEgXSxdH;4bYNqfHliYXfhbY5{fCCKb33vJJNieGmnboOgLIh2dWGwKTDJUVkh[2WubIOgZZN{\XO|ZXSgZZMh\3Kxd4ToJIlvcGmkaYTpc44h[nliTWTUJIF{e2G7LDDJR|UxRTFwM{Wg{txO Mlv2V2FPT0WU
human A4-Fuk cell MnXmS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYnOOIMzUW6qaXLpeIlwdiCxZjDoeY1idiCDND3GeYsh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5Nige,:jDDJR|UxRTFwM{SxOFEh|ryP M2jTcnNCVkeHUh?=
human SR cell NYSwWnFzT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NXzvdWI{UW6qaXLpeIlwdiCxZjDoeY1idiCVUjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuOVQ2PzJizszN NFvme5RUSU6JRWK=
human A3-KAW cell NFr6NIRIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M{LEXmlvcGmkaYTpc44hd2ZiaIXtZY4hSTNvS1HXJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKGmlNUC9NU43OjV2NjFOwG0> M3rOc3NCVkeHUh?=
human KS-1 cell NHPLS3lIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MmXaTY5pcWKrdHnvckBw\iCqdX3hckBMWy1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT62PVI1PyEQvF2= NULxU5d2W0GQR1XS
human CTV-1 cell NXzNTG56T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M1zCbWlvcGmkaYTpc44hd2ZiaIXtZY4hS1SYLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlczPzVzIN88US=> MVfTRW5ITVJ?
human LB1047-RCC cell NHi5fGlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NU\wTZBjUW6qaXLpeIlwdiCxZjDoeY1idiCOQkGwOFcuWkOFIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MT64NVYzPCEQvF2= M1jQb3NCVkeHUh?=
human MEG-01 cell NHPTXnZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NHHldHpKdmirYnn0bY9vKG:oIHj1cYFvKE2HRz2wNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvQDN3NkOg{txO MV\TRW5ITVJ?
human TE-11 cell NGD4O5hIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWXtUmxOUW6qaXLpeIlwdiCxZjDoeY1idiCWRT2xNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEvQDN7OEWg{txO M2K4UXNCVkeHUh?=
human CMK cell MUTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NHX0Z2hKdmirYnn0bY9vKG:oIHj1cYFvKEOPSzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGuPVU2OTdizszN M{HUR3NCVkeHUh?=
human NB1 cell NIDySo1Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= MUXJcohq[mm2aX;uJI9nKGi3bXHuJG5DOSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTFwOU[xNVch|ryP MX\TRW5ITVJ?
human MDA-MB-435 cells NFHVVHZRem:uaX\ldoF1cW:wIHHzd4F6 MWi0PEBp MVfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2GQT3NRk01OzViY3XscJMh[W[2ZYKgOFghcHK|IHL5JHNTSiCjc4PhfUwhT0l;MjFOwG0> NWD1PIIzOjJ3NkC2Nlc>
human MCF7 cells MWrQdo9tcW[ncnH0bY9vKGG|c3H5 M3ewclQ5KGh? Mn;uRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPQ1[3JINmdGy|IHHmeIVzKDR6IHjyd{BjgSCVUlKgZZN{[XluIFfJOVA:OiEQvF2= NHPWTnUzOjV4ME[yOy=>
human A549 cells NFrCZWFEgXSxdH;4bYPDqGG|c3H5 M3rqZVczKGh? MX\DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJIF{e2W|c3XkJIF{KGe{b4f0bEBqdmirYnn0bY9vKGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEmFNUC9Nk41PCEQvF2= MW[yN|YxOjR2MR?=

... Click to View More Cell Line Experimental Data

体内研究 与实质性,选择性抑制VEGFR2 或PDGFR在体内磷酸化与信号传导一致,Sunitinib (20-80 mg/kg/day)对各种肿瘤异种移植模型,包括HT-29,A431,Colo205,H-460,SF763T,C6,A375,或MDA-MB-435表现出广泛有效的剂量依赖性抗肿瘤活性。Sunitinib以80 mg/kg/day的剂量给药21天,导致8只小鼠中6只完全的肿瘤消退,并且在治疗结束后,110天的观察期内肿瘤不会再生。第二轮使用Sunitinib治疗依然能够有效抗肿瘤,但是不能完全恢复到第一轮治疗的情况。Sunitinib治疗导致肿瘤MVD显著下降,在SF763T神经胶质瘤中减少~40%。SU11248治疗导致表达荧光素酶的PC-3M异种移植物额外的肿瘤生长被完全抑制,尽管肿瘤大小没有减少。[2] 在FLT3-ITD 骨髓移植模型中,Sunitinib治疗(20 mg/kg/day)显著抑制皮下MV4;11 (FLT3-ITD)异种移植物的生长,并延长生存。[3]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
+ 展开

生化酪氨酸激酶试验:

Sunitinib作用于VEGFR2 (Flk-1)和PDGFRβ的IC50值使用包含PKT完整胞浆区的谷胱甘肽-S-转移酶融合蛋白测定。生物化学的酪氨酸激酶试验,用来测定VEGFR2 (Flk-1)和PDGFRβ反式磷酸化活性,在多肽底物poly-Glu,Tyr (4:1)预涂层(在PBS中20 μg/well;4 °C下培养过夜)的96微孔板中进行。过量蛋白结合位点通过加入1-5% (w/v) BSA的PBS溶液阻断。纯化的GST融合蛋白在感染杆状病毒的昆虫细胞中产生。将GST-VEGFR2 和GST-PDGFRβ加入微孔板的2倍浓度激酶稀释缓冲液(由100 mM HEPES,50 mM NaCl,40 μM NaVO4,和0.02% (w/v) BSA组成)中。对GST-VEGFR2或GST-PDGFRβ的最终酶浓度为50 ng/mL。随后将25μL稀释的Sunitinib加入每个反应孔中以产生一系列适用于每个酶的抑制剂浓度。激酶反应通过加入不同浓度的ATP MnCl2溶液起始,使ATP浓度跨越酶的Km值,终MnCl2浓度为10 mM。板在室温下培养5-15分钟,然后加入EDTA停止反应。将板用TBST洗涤3次。在TBST(包含0.5% (w/v) BSA,0.025% (w/v)脱脂奶粉,和100 μM NaVO4)中以1:10,000稀释的兔子多克隆抗磷酸酪氨酸抗血清加入孔中,并在37℃下培养1小时。然后将板用TBST洗涤3次,接着加入山羊抗兔抗血清结合的辣根过氧化物酶(在TBST中以1:10,000 稀释)。板在37℃下培养1小时,然后用TBST清洗3次。加入2,2′-azino-di-[3-ethylbenzthiazoline sulfonate]作为底物后,测定每孔中的磷酸酪氨酸酶数量。
细胞实验:[3]
+ 展开
  • Cell lines: RS4;11,MV4;11,和 OC1-AML5
  • Concentrations: 溶解于DMSO,终浓度为~10 μM
  • Incubation Time: 24和48小时
  • Method: 加入Sunitinib和FL (50 ng/mL;仅FLT3-WT细胞)之前,细胞在包含0.1% FBS的培养基中饥饿过夜。培养48小时后,使用Alamar Blue法或台盼蓝细胞活性法测定增殖。加入Sunitinib 24小时后,通过蛋白免疫印迹法检测多聚(ADP-核糖)聚合酶(PARP)的裂解或caspase-3水平,以测量细胞凋亡。
    (Only for Reference)
动物实验:[2]
+ 展开
  • Animal Models: 皮下植入HT-29,A431,Colo205,H-460,SF763T,C6,A375,或MDA-MB-435的雌性nu/nu小鼠,和负荷表达荧光素酶的PC-3M肿瘤的雄性nu/nu小鼠。
  • Formulation: 以羧甲基纤维素悬浮液或柠檬酸盐缓冲溶液(pH 3.5)形成
  • Dosages: ~80 mg/kg
  • Administration: 口服,每天一次
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 25 mg/mL warmed (62.73 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
5% DMSO+corn oil
7mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 398.47
化学式

C22H27FN4O2

CAS号 557795-19-4
稳定性 powder
in solvent
别名 SU11248

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03862768 Not yet recruiting Gastrointestinal Stromal Tumors|Surgery Shanghai Zhongshan Hospital July 2019 Not Applicable
NCT03862768 Not yet recruiting Gastrointestinal Stromal Tumors|Surgery Shanghai Zhongshan Hospital July 2019 Not Applicable
NCT03878524 Not yet recruiting Breast Cancer|Prostate Cancer|Pancreatic Cancer|Acute Myelogenous Leukemia OHSU Knight Cancer Institute|Oregon Health and Science University|Prospect Creek Foundation March 14 2019 Phase 1
NCT03878524 Not yet recruiting Breast Cancer|Prostate Cancer|Pancreatic Cancer|Acute Myelogenous Leukemia OHSU Knight Cancer Institute|Oregon Health and Science University|Prospect Creek Foundation March 14 2019 Phase 1
NCT03673501 Recruiting Gastrointestinal Stromal Tumors Deciphera Pharmaceuticals LLC February 11 2019 Phase 3
NCT03641326 Recruiting Gliosarcoma|Central Nervous System Sarcoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) February 21 2019 Phase 2

技术支持

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操作手册

如果有其他问题,请给我们留言。

  • * 必填项

PDGFR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID