Selumetinib (AZD6244)

目录号:S1008 别名: ARRY-142886

Selumetinib (AZD6244) Chemical Structure

Molecular Weight(MW): 457.68

Selumetinib (AZD6244)是一种有效,高选择性的MEK1抑制剂,无细胞试验中IC50为14 nM,也抑制ERK1/2磷酸化,IC50为10 nM,对p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf等没有抑制作用。Phase 3。

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客户购买Selleck的此次产品后发表的文献116篇:

客户使用该产品的13个实验数据:

  • Left: BRAFV600E A375 cells expressing pLKO or shMED12 vectors were cultured in the absence or presence of 2.5 μM PLX4032 or 0.5 μM AZD6244. The cells were fixed, stained, and photographed after 10 (untreated) or 28 days (treated). Right: A375 cells expressing pLKO or shMED12 vectors were grown in the absence or presence of 1 μM PLX4032 or 0.5 μM AZD6244 for 6 hr.

    Cell, 2012, 151(5): 937–950. Selumetinib (AZD6244) purchased from Selleck.

    Left: KRASV12 SKCO-1 cells expressing pLKO or shMED12 vectors were cultured in the absence or presence of 0.5 μM AZD6244. The cells were fixed, stained, and photographed after 14 (untreated) or 28 days (treated). Right: SK-CO-1 cells expressing pLKO or shMED12 vectors were grown in the absence or presence of 1 μM AZD6244 for 6 hr.

    Cell, 2012, 151(5): 937–950. Selumetinib (AZD6244) purchased from Selleck.

  • A,ERK phosphorylation in A375 expressing indicated ORFs following treatment with DMSO or 1 μM of PLX4720, RAF265, CI-1040 or AZD6244. B,ERK phosphorylation in A375 expressing indicated ORFs following treatment with DMSO, PLX4720 (1 μM) or PLX4720 in combination with CI-1040 or AZD6244 (all 1 μM).

    Nature 2010 468, 968-972. Selumetinib (AZD6244) purchased from Selleck.

    Survival curves for isogenic cell line pairs and melanoma cultures treated with the indicated AZD6244 concentration for 72 h (relative to DMSO treated controls; mean6s.e.m., n55). PLX4032 resistant cells were grown with PLX4032. Dashed line, 50% cell killing.

    Nature 2010 468, 973-977. Selumetinib (AZD6244) purchased from Selleck.

  • a-c, Inhibitors of BRAFV600E (PLX4032) and MEK1/2 (PD98059 or AZD6244) increase PGC1α and ID2 expression (a, b) and repress integrin expression and signalling (b, c). Cells were treated with indicated concentration of inhibitors for 6 h (a, b) or 24 h (c). d, e, PLX4032 increases the interaction between ID2 and TCF4 (d) and decreases the occupancy of TCF4 at the promoters of integrin genes (e). f–g, PGC1α and ID2 are partially required for PLX4032-mediated inhibition of invasion and metastasis. For in vitro assays (f), A375 cells were incubated with 1 μM PLX4032 for 10 h. Images represent one picture captured per membrane with the scale bar representing 200 μm. Values in a, b, e and f represent mean±s.d. of independent biological triplicates; *P<0.05 and **P<0.01 by Student's t-test  in a, b, e, f.

    Nature, 2016, 537(7620):422-428.. Selumetinib (AZD6244) purchased from Selleck.

    Ex vivo and functional characterization of MEK1(P124L). (A) AZD6244-mediated growth inhibition ex vivo of treatment-naïve BRAFV600E melanoma cells (black and blue) or cells cultured from an AZD6244-resistant metastatic focus (red). (B) ERK phosphorylation (p-ERK) andMEKphosphorylation (p-MEK) are shown following treatment with increasing concentrations of AZD6244 in treatment-naïve or AZD6244-resistant melanoma cells cultured ex vivo. The tubulin loading control (-tubulin) is also shown. (C) AZD6244 growth inhibition curves of parental A375 (solid black), A375 cells expressing MEK-DD (grey), wild-type MEK1 (hatched black), or MEK1(P124L) (red) are shown. In each instance n6 anderrorstandard deviation. (D) p-ERK and p-MEK are shown following treatment with increasing AZD6244 concentrations in the cell lines described in C, Above. The -tubulin control is also shown.

    Proc Natl Acad Sci USA 2009 106, 20411-20416. Selumetinib (AZD6244) purchased from Selleck.

  • AZD6244 enhanced FOXO3a expression and induced suppression of cancer cell proliferation. A, tumor volume of the HCT116 xenografts treated with Placebo or AZD6244 was measured for 21 d. The tumor sections of four individual DMSO or AZD6244-treated HCT116 xenografts were subjected to immunohistochemistry with a FOXO3a antibody. Relative percentages of nuclear FOXO3a expression of individual xenograft tumors from B were analyzed and the mean values of FOXO3a expression in Placebo or AZD6244-treated group were indicated as bars.

    Cancer Res 2010 70, 4709-4718. Selumetinib (AZD6244) purchased from Selleck.

    lysates from various cancer cell lines: breast cancer (MDA-MB-435), colon cancer (HCT116, SW620, and HT29), and melanoma (WM793) treated with DMSO or AZD6244 (10 μmol/L) for 4 h were subjected to immunoblotting with the indicated antibodies.

    Cancer Res 2010 70, 4709-4718. Selumetinib (AZD6244) purchased from Selleck.

  • A and B, clonogenic assays in 2 melanoma cell lines (YUVON and YUSIK) treated with NVPBEZ235 (BEZ) and AZD6244 (AZD) alone and in combination. Combinations were more effective in inhibiting colony formation at lower concentrations than either drug alone.

    Clin Cancer Res 2010 16, 6029-6039. Selumetinib (AZD6244) purchased from Selleck.

    Stimulation response of p37d-expressing cells. (c) Western blot of 5 min serum stimulated HEK-293 cells stably expressing p37d, p110d or control, with the presence of inhibitors as indicated at the top.

    Oncogene 2012 31, 3277–3286. Selumetinib (AZD6244) purchased from Selleck.

  • INA-6 MM cells were treated with AS703026 or AZD6244 for 2 d, followed by [3H]thymidine uptake assay. PBMCs isolated from normal donors (n = 3) were incubated with M-CSF and RANKL, in the presence or absence of AS703026 or AZD6244 for 14 d. The TRAP assay was performed to measure the formation of multinuclear osteoclast cells (OC).

    Br J Haematol 2010 149, 537–549. Selumetinib (AZD6244) purchased from Selleck.

    B-RafV600E mutated melanoma line,A375, was treated with different doses of AZD6244 for 1hour or 24 hours.Cell lysates were analyzed by Western Blotting to determine the levels of phosphorylated ERK1/2(Perk1/2)

    Dr. Jong-In Park of Medical College of Wisconsin. Selumetinib (AZD6244) purchased from Selleck.

  • Selumetinib (AZD6244) purchased from Selleck.

产品安全说明书

MEK抑制剂选择性比较

生物活性

产品描述 Selumetinib (AZD6244)是一种有效,高选择性的MEK1抑制剂,无细胞试验中IC50为14 nM,也抑制ERK1/2磷酸化,IC50为10 nM,对p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf等没有抑制作用。Phase 3。
特性 AZD6244是第一个处于随机二期研究的MEK抑制剂。
靶点
MEK1 [1]
(Cell-free assay)
14 nM
体外研究

AZD6244是ATP非竞争性的抑制剂,在IC50浓度小于40 nM时使ERK1/2的磷酸化作用失活。AZD6244也通过抑制ERK1/2和p90RSK的磷酸化抑制原代HCC细胞的生长,同时伴随着caspase-3和caspase-7分裂的加强, 及断裂的聚腺苷二磷酸核糖聚合酶的增多。AZD6244在P38,JNK,PI3K,及MEK5/ERK5通路中的作用不大。[1]AZD6244对感知乳腺癌细胞系中的raf突变和非小细胞肺癌细胞系中的ras突变很灵敏。[2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human CHP-212 cell M3LRc2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NFfHOIJKdmirYnn0bY9vKG:oIHj1cYFvKEOKUD2yNVIh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{NjF3IH7NMi=> NGTZbIpUSU6JRWK=
human H9 cell MnnHS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXHiNIVKUW6qaXLpeIlwdiCxZjDoeY1idiCKOTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUKyMlg5KG6PLh?= NHK1fmRUSU6JRWK=
human HL-60 cell M3PTRWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M2\6XmlvcGmkaYTpc44hd2ZiaIXtZY4hUExvNkCgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yOE42QSCwTT6= NHjEdXVUSU6JRWK=
human A375 cells NUjx[Gt3WHKxbHnm[ZJifGmxbjDhd5NigQ>? MYC3NkBp MoTwRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCDM{e1JINmdGy|IHX4dJJme3OrbnegRnJCTiCYNkCwSUBufXSjboSgZYZ1\XJiN{KgbJJ{KGK7IFPlcIwhfGm2ZYKt[4xwKGG|c3H5MEBKSzVyPUOxJI5ONg>? NHnIUoQzOzR5NEO4PC=>
human NOMO-1 cell MkWwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M2LvSmlvcGmkaYTpc44hd2ZiaIXtZY4hVk:PTz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N|EvQTdibl2u MYPTRW5ITVJ?
human DU-4475 cell NG\yUnpIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MV\Jcohq[mm2aX;uJI9nKGi3bXHuJGRWNTR2N{WgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2zN{43PyCwTT6= MlLFV2FPT0WU
human M14 cell NXj1V3FNT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3TGNmlvcGmkaYTpc44hd2ZiaIXtZY4hVTF2IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{[uPFkhdk1w MUPTRW5ITVJ?
human HT-144 cell MnX3S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MmCzTY5pcWKrdHnvckBw\iCqdX3hckBJXC1zNESgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME24PU4xPSCwTT6= NIH2bVJUSU6JRWK=
human SK-N-AS cell NGCxXIFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M1PtfmlvcGmkaYTpc44hd2ZiaIXtZY4hW0tvTj3BV{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVkzNjh|IH7NMi=> MYHTRW5ITVJ?
human LB2518-MEL cell M2i4emdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NX;uR3EzUW6qaXLpeIlwdiCxZjDoeY1idiCOQkK1NVguVUWOIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;OUOuPFIhdk1w MX7TRW5ITVJ?
human C32 cell NYPPeFFvT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MX7Jcohq[mm2aX;uJI9nKGi3bXHuJGM{OiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTl6LkKzJI5ONg>? NWrofndSW0GQR1XS
human BHT-101 cell MWrHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MkG2TY5pcWKrdHnvckBw\iCqdX3hckBDUFRvMUCxJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVA3Njl|IH7NMi=> MX3TRW5ITVJ?
human KY821 cell NFy5[YhIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MoLUTY5pcWKrdHnvckBw\iCqdX3hckBMYTh{MTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGwO{4yQCCwTT6= MonCV2FPT0WU
human CP50-MEL-B cell NFrQdotIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MkXNTY5pcWKrdHnvckBw\iCqdX3hckBEWDVyLV3FUE1DKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OTJ5Lkm0JI5ONg>? MWjTRW5ITVJ?
human MEL-HO cell MVnHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NIrmfm1KdmirYnn0bY9vKG:oIHj1cYFvKE2HTD3IU{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVE{QC56NDDuUU4> MVjTRW5ITVJ?
human MIAPaCa2 cells NXrJUXVDWHKxbHnm[ZJifGmxbjDhd5NigQ>? M17zcWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVnBVIFE[TJiY3XscJMtKEmFNUC9NVQzKG6PLh?= NFHoS|YzOzR5NEO4PC=>
human EoL-1-cell cell NGH4eFJIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M{[5N2lvcGmkaYTpc44hd2ZiaIXtZY4hTW:OLUGtZ4VtdCClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTF2ND63OkBvVS5? NXzFeFRJW0GQR1XS
human DOK cell MXPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3r6VmlvcGmkaYTpc44hd2ZiaIXtZY4hTE:NIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUS3MlA5KG6PLh?= NVHVTZcxW0GQR1XS
human SH-4 cell M3XMcWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MoXxTY5pcWKrdHnvckBw\iCqdX3hckBUUC12IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MU[2MlQ5KG6PLh?= M1f2bXNCVkeHUh?=
human BPH-1 cell MnLjS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MmfETY5pcWKrdHnvckBw\iCqdX3hckBDWEhvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUG4Nk4{OSCwTT6= NF74fY5USU6JRWK=
human HuP-T4 cell MV;Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MmH2TY5pcWKrdHnvckBw\iCqdX3hckBJfVBvVESgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xPVUvOzJibl2u Ml;jV2FPT0WU
human KU812 cell NVy2XVJmT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NVnNXo82UW6qaXLpeIlwdiCxZjDoeY1idiCNVUixNkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVIyOS54ODDuUU4> NHjnUYJUSU6JRWK=
human A549 cell NVnBTnNqT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NUfOfXZxUW6qaXLpeIlwdiCxZjDoeY1idiCDNUS5JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlE1NjF|IH7NMi=> MXfTRW5ITVJ?
human HTC-C3 cell MkL1S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M{HqfWlvcGmkaYTpc44hd2ZiaIXtZY4hUFSFLVOzJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlE1NjZzIH7NMi=> Mni5V2FPT0WU
human A101D cell M4KyT2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NVLwfo5HUW6qaXLpeIlwdiCxZjDoeY1idiCDMUCxSEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI1OC5|MzDuUU4> M3\VUHNCVkeHUh?=
human ONS-76 cell MljuS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NHiybXZKdmirYnn0bY9vKG:oIHj1cYFvKE:QUz23OkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI1PC53MzDuUU4> NGHPd5hUSU6JRWK=
human RKO cell NV;HXIhiT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NUnlbVA{UW6qaXLpeIlwdiCxZjDoeY1idiCUS1:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yOFgvOzhibl2u MWXTRW5ITVJ?
human WM-115 cell NX\NNGFbT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M2C0ZWlvcGmkaYTpc44hd2ZiaIXtZY4hX01vMUG1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlY4NjV2IH7NMi=> MVXTRW5ITVJ?
human HCC2998 cell NH:wPIFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MoHITY5pcWKrdHnvckBw\iCqdX3hckBJS0N{OUm4JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlY6NjB5IH7NMi=> M336[nNCVkeHUh?=
human C2BBe1 cell NXnFZ2RPT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NH;QN2RKdmirYnn0bY9vKG:oIHj1cYFvKEN{QlLlNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI4Oi53OTDuUU4> MV7TRW5ITVJ?
human RVH-421 cell Mn:4S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M2POdWlvcGmkaYTpc44hd2ZiaIXtZY4hWl[KLUSyNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI4QS5|OTDuUU4> MoPDV2FPT0WU
human H-EMC-SS cell NHj1R|lIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MY\Jcohq[mm2aX;uJI9nKGi3bXHuJGguTU2FLWPTJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlkxNjl7IH7NMi=> MVPTRW5ITVJ?
human ML-2 cell NX\QNmpqT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NEXsUYtKdmirYnn0bY9vKG:oIHj1cYFvKE2OLUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yPVMvPjNibl2u NFjXeW5USU6JRWK=
human SW620 cell NHHZUXlIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWTUOJZwUW6qaXLpeIlwdiCxZjDoeY1idiCVV{[yNEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMxOi5{IH7NMi=> MnvRV2FPT0WU
human UACC-257 cell NY\Tfo9sT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NF22V2RKdmirYnn0bY9vKG:oIHj1cYFvKFWDQ1OtNlU4KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzJzLki0JI5ONg>? MXLTRW5ITVJ?
human AsPC-1 cell M3P0U2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M{m3N2lvcGmkaYTpc44hd2ZiaIXtZY4hSXOSQz2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N|I1NjN7IH7NMi=> NVe3VWFTW0GQR1XS
human CAL-39 cell MVPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NHzoNm9KdmirYnn0bY9vKG:oIHj1cYFvKEODTD2zPUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVM{Oi5{NjDuUU4> NVvIPYZjW0GQR1XS
human COLO-679 cell NF3Xb3RIem:5dHigbY5pcWKrdHnvckBie3OjeR?= Mkf4TY5pcWKrdHnvckBw\iCqdX3hckBEV0yRLU[3PUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVM1OS5zOTDuUU4> MUnTRW5ITVJ?
human NCI-H747 cell NWfXN3h3T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NYnzdZpvUW6qaXLpeIlwdiCxZjDoeY1idiCQQ1mtTFc1PyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTN3MD65PEBvVS5? MoD5V2FPT0WU
human NCI-H1437 cell NX;KWXZ1T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= Ml;4TY5pcWKrdHnvckBw\iCqdX3hckBPS0lvSEG0N|ch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{PTJwOEWgcm0v MVjTRW5ITVJ?
human PSN1 cell NWjZe5h7T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MUTJcohq[mm2aX;uJI9nKGi3bXHuJHBUVjFiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1|Nk[uNFkhdk1w MXTTRW5ITVJ?
human NKM-1 cell M4XFTmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M{S5XGlvcGmkaYTpc44hd2ZiaIXtZY4hVkuPLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2zPFUvQCCwTR?= NHPxUJdUSU6JRWK=
human MZ2-MEL cell M1T4e2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NX3xNlVxUW6qaXLpeIlwdiCxZjDoeY1idiCPWkKtUWVNKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:Ozl2LkO3JI5ONg>? MYPTRW5ITVJ?
human SK-MEL-2 cell NXjBfI0{T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NH;Mbo9KdmirYnn0bY9vKG:oIHj1cYFvKFONLV3FUE0zKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PDB3LkC2JI5ONg>? Mni0V2FPT0WU
human LAMA-84 cell NXzmToFXT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= Mne5TY5pcWKrdHnvckBw\iCqdX3hckBNSU2DLUi0JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9OFU3NjJ{IH7NMi=> M1LxZXNCVkeHUh?=
human U-266 cell Ml;6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NXv4ToxEUW6qaXLpeIlwdiCxZjDoeY1idiCXLUK2OkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ5Py55NDDuUU4> M1r0NHNCVkeHUh?=
human RCM-1 cell M1\3TGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3ywdmlvcGmkaYTpc44hd2ZiaIXtZY4hWkOPLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME20PVMvQDVibl2u M2DOUHNCVkeHUh?=

... Click to View More Cell Line Experimental Data

体内研究 活体研究显示AZD6244在2-1318, 5-1318, 及26-1004 4-1318移植物中明显抑制ERK1/2的磷酸化,并且在原代2-1318细胞中通过激活caspase通路诱导细胞凋亡。[1]HT-29移植瘤是携带B-raf突变的直肠瘤模型,AZD6244 在100mg/kg剂量时可以抑制HT-29移植瘤中肿瘤的增长,并且AZD6244作用下的肿瘤指数比吉西他滨作用下的肿瘤指数要好[3]。另外,AZD6244可以抑制HCC移植瘤的增长,HCC移植瘤的增长与细胞凋亡的增多,及细胞周期调控的减量调节有关。包括:cyclin D1, cdc-2, CDK 2 ,CDK4, cyclin B1, 及 c-Myc。[4]

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:[3]
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激酶实验:

在杆状病毒感染的hi5昆虫细胞中表达的组成型的氮端用六聚组氨酸标记的MEK1,通过金属亲和层析、离子交换及凝胶过滤纯化。MEK1的活性评估通过测量[γ-33P]ATP 作用于ERK2的示踪[γ-33P]磷酸的渗透率。实验在96孔板中进行,保温混合物由25 mM HEPES (pH 7.4), 10 mM MgCl2, 5 mM β-甘油磷酸 100 μM 原钒酸钠, 5 mM DTT, 5 nM MEK1, 1 μM ERK2, 和AZD6244 (溶解在 1% DMSO)组成。加入10 μM ATP (0.5 μC k[γ-33P]ATP/每孔)反应开始,然后在室温下温育45分钟。加入同等量的25%的三氯乙酸反应停止,使蛋白沉淀。沉淀的蛋白加到玻璃纤维过滤板上,用0.5%的磷酸冲洗掉过量的示踪ATP,然后在液体闪烁计数管中计算放射性。通过在反应混合物中改变ATP的量来决定ATP相关性。
细胞实验:[1]
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  • Cell lines: 原代HCC细胞系包括2-1318, 4-1318和26-1004细胞
  • Concentrations: 10 μM 左右
  • Incubation Time: 24或48小时
  • Method: 肿瘤细胞按2.0×104密度接种,温育48小时,然后用培养基清洗细胞两次。用不同浓度的AZD6244处理细胞24小时或者48小时。细胞活力通过MTT实验来测定。用溴脱氧核苷尿嘧啶试剂盒测定细胞增殖。
    (Only for Reference)
动物实验:[1]
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  • Animal Models: 携带HCC移植瘤的SCID鼠
  • Formulation: 溶于水中
  • Dosages: 50或100mg/kg
  • Administration: 口服处理
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 91 mg/mL warmed (198.82 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次加入纯溶剂:
4% DMSO+30% PEG 300+5% Tween 80+ddH2O
5mg/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 457.68
化学式

C17H15BrClFN4O3

CAS号 606143-52-6
稳定性 powder
别名 ARRY-142886

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
NCT01287130 Completed Colonic Neoplasms|Cancer of the Colon|Colon Cancer|Colon Neoplasms|Colonic Cancer National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) January 7, 2011 Phase 1
NCT01134601 Terminated Non-Metastatic Adenocarcinoma of the Rectum National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) May 24, 2010 Phase 1
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
NCT03040986 Not yet recruiting KRAS NP_004976.2:p.G12R|Stage II Pancreatic Cancer|Stage IIA Pancreatic Cancer|Stage IIB Pancreatic Cancer|Stage III Pancreatic Cancer|Stage IV Pancreatic Cancer National Cancer Institute (NCI) July 2017 Phase 2
NCT03004105 Not yet recruiting Malignant Neoplasm of Respiratory and Intrathoracic Organ Carcinoma|Advanced Lung Cancer|Recurrent Nonsmall Cell Lung Cancer M.D. Anderson Cancer Center|AstraZeneca|MedImmune LLC April 2017 Phase 2
NCT02839720 Not yet recruiting Appearance Distress|Bothered by Itching Skin|Cafe Au Lait Spot|Cutaneous Neurofibroma|Disfigurement|Dysplasia|Lisch Nodule|Neurofibromatosis Type 1|NF1 Gene Mutation|Optic Nerve Glioma National Cancer Institute (NCI) January 2017 --

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操作手册

如果有其他问题,请给我们留言。

  • * 必填项

常见问题及建议解决方法

  • 问题 1:

    How about the solubility of S1008? How to prepare for the solution if I need to do the in vivo experiments?

  • 回答:

    S1008 AZD6244 in vehicle 5% DMSO+30% PEG 300+ddH2O will be a suspension for oral administration. If you want a clear solution for injection, you can dissolve it in 4% DMSO+30% PEG 300+5% Tween 80+ddH2O.

MEK Signaling Pathway Map

MEK Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID