Selumetinib (AZD6244)

製品コードS1008 別名:ARRY-142886

Selumetinib (AZD6244)化学構造

分子量(MW):457.68

Selumetinib (AZD6244) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Phase 3.

サイズ 価格(税別)  
JPY 19422.00
JPY 14940.00
JPY 21580.00
JPY 28220.00
JPY 61420.00

文献中Selleckの製品使用例(118)

カスタマーフィードバック(14)

  • 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.

    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.

  • Parental murine KRasG12V;p53-/- lung cancer cells or the same cell lines stably expressing exogenous KRASWT or KRASD154Q were injected intravenously into nude mice. After one week, animals were treated with selumetinib (50 mg/kg daily) and sacrificed at the indicated time points. Lungs were lysed and analyzed by western blot with the indicated antibodies.

    Cell, 2018, 172(4):857-868. 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.

  • 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.

    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.

  • Concentration equilibrium transport assays (CETAs) for selumetinib using parental and (murine) Mdr1a or (human) MDR1 overexpressing LLC cells. Zosuquidar (5 μM) was used to specifically inhibit P-gp mediated transport. Data are means ± SD; n = 6; ** p < 0.01, *** p < 0.001.

    Int J Cancer, 2018, 142(2):381-391. 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.

製品安全説明書

MEK阻害剤の選択性比較

生物活性

製品説明 Selumetinib (AZD6244) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Phase 3.
特性 First MEK inhibitor being tested in Phase II clinical trials.
ターゲット
MEK1 [1]
(Cell-free assay)
MEK1 [13]
(Cell-free assay)
MEK2 [13]
(Cell-free assay)
14 nM 99 nM(Kd) 530 nM(Kd)
体外試験

AZD6244 is not competitive with ATP and inactivates the ERK1/2 phosphorylation with IC50 concentrations below 40 nM. AZD6244 also inhibits the growth of primary HCC cells through inhibition of ERK1/2 and p90RSK phosphorylation, accompanied with elevation of the cleavage of caspase-3 and caspase-7, and cleaved poly(ADP)ribose polymerase. AZD6244 has little effects on the p38, c-Jun-NH2-kinase, phosphatidylinositol 3-kinase, and MEK5/ERK5 pathways. [1] AZD6244 is sensitive to Raf mutations in breast cancer cell lines and Ras mutations in NSCLC cell lines. [2]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human CHP-212 cell MnXJS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYTjbJBFUW6qaXLpeIlwdiCxZjDoeY1idiCFSGCtNlEzKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:Oy5zNTDuUU4> NH\nTVBUSU6JRWK=
human H9 cell M17PbGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NFXzSW1KdmirYnn0bY9vKG:oIHj1cYFvKEh7IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MkKuPFghdk1w MXHTRW5ITVJ?
human HL-60 cell NW\mVXlvT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MV3Jcohq[mm2aX;uJI9nKGi3bXHuJGhNNTZyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MkSuOVkhdk1w MmnMV2FPT0WU
human A375 cells NITjPGdRem:uaX\ldoF1cW:wIHHzd4F6 M3jvXFczKGh? MXfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEF|N{WgZ4VtdHNiZYjwdoV{e2mwZzDCVmFHKFZ4MEDFJI12fGGwdDDh[pRmeiB5MjDodpMh[nliQ3XscEB1cXSncj3ncI8h[XO|YYmsJGlEPTB;M{Ggcm0v NIGzUFIzOzR5NEO4PC=>
human NOMO-1 cell M2G5bWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NVzsV2ZGUW6qaXLpeIlwdiCxZjDoeY1idiCQT13PMVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{OS57NzDuUU4> M{L1UXNCVkeHUh?=
human DU-4475 cell NGLKTHBIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M3P4fmlvcGmkaYTpc44hd2ZiaIXtZY4hTFVvNES3OUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVM{NjZ5IH7NMi=> M4jQfHNCVkeHUh?=
human M14 cell M2[0SWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MUTJcohq[mm2aX;uJI9nKGi3bXHuJG0yPCClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTN4Lki5JI5ONg>? NG\3V2pUSU6JRWK=
human HT-144 cell MX\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NF;FNYtKdmirYnn0bY9vKG:oIHj1cYFvKEiWLUG0OEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVg6NjB3IH7NMi=> NEG2[nBUSU6JRWK=
human SK-N-AS cell NUXoTJlPT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MonYTY5pcWKrdHnvckBw\iCqdX3hckBUUy2QLVHTJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVIvQDNibl2u MVfTRW5ITVJ?
human LB2518-MEL cell M{P0Z2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3vDcGlvcGmkaYTpc44hd2ZiaIXtZY4hVEJ{NUG4MW1GVCClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTl|LkiyJI5ONg>? NYXLelRGW0GQR1XS
human C32 cell NIj2[XJIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXPJcohq[mm2aX;uJI9nKGi3bXHuJGM{OiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTl6LkKzJI5ONg>? Mlq2V2FPT0WU
human BHT-101 cell M4\kXmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MYHJcohq[mm2aX;uJI9nKGi3bXHuJGJJXC1zMEGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xNFYvQTNibl2u MXjTRW5ITVJ?
human KY821 cell M{Dsdmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MnjRTY5pcWKrdHnvckBw\iCqdX3hckBMYTh{MTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUGwO{4yQCCwTT6= NWLWSpNQW0GQR1XS
human CP50-MEL-B cell MoHSS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MkLaTY5pcWKrdHnvckBw\iCqdX3hckBEWDVyLV3FUE1DKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OTJ5Lkm0JI5ONg>? NIS4OG5USU6JRWK=
human MEL-HO cell NGrJWIZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NH75TGJKdmirYnn0bY9vKG:oIHj1cYFvKE2HTD3IU{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVE{QC56NDDuUU4> Mm\rV2FPT0WU
human MIAPaCa2 cells NEDJRlRRem:uaX\ldoF1cW:wIHHzd4F6 M3facmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTVnBVIFE[TJiY3XscJMtKEmFNUC9NVQzKG6PLh?= MorxNlM1PzR|OEi=
human EoL-1-cell cell MW\Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Mnv5TY5pcWKrdHnvckBw\iCqdX3hckBGd0xvMT3j[YxtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OTR2Lke2JI5ONg>? MmrDV2FPT0WU
human DOK cell MkXQS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M17FVWlvcGmkaYTpc44hd2ZiaIXtZY4hTE:NIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUS3MlA5KG6PLh?= NEO2W2pUSU6JRWK=
human SH-4 cell NULM[VVMT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NUfqR|hGUW6qaXLpeIlwdiCxZjDoeY1idiCVSD20JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVY3NjR6IH7NMi=> NHzsOmZUSU6JRWK=
human BPH-1 cell MonHS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MWXJcohq[mm2aX;uJI9nKGi3bXHuJGJRUC1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUiyMlMyKG6PLh?= MWXTRW5ITVJ?
human HuP-T4 cell NIGzR4JIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXnJcohq[mm2aX;uJI9nKGi3bXHuJGh2WC2WNDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUG5OU4{OiCwTT6= MYTTRW5ITVJ?
human KU812 cell MkHwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NVixdFdIUW6qaXLpeIlwdiCxZjDoeY1idiCNVUixNkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVIyOS54ODDuUU4> MU\TRW5ITVJ?
human A549 cell NIDVTWNIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NFG3fmVKdmirYnn0bY9vKG:oIHj1cYFvKEF3NEmgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yNVQvOTNibl2u MmnMV2FPT0WU
human HTC-C3 cell M1nLWWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MYPJcohq[mm2aX;uJI9nKGi3bXHuJGhVSy2FMzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUKxOE43OSCwTT6= NEnOUXpUSU6JRWK=
human A101D cell MUjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MlvFTY5pcWKrdHnvckBw\iCqdX3hckBCOTBzRDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUK0NE4{OyCwTT6= MYLTRW5ITVJ?
human ONS-76 cell MmPqS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NFLDWGVKdmirYnn0bY9vKG:oIHj1cYFvKE:QUz23OkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI1PC53MzDuUU4> NFHuVYRUSU6JRWK=
human RKO cell MX;Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M1e4bWlvcGmkaYTpc44hd2ZiaIXtZY4hWkuRIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MkS4MlM5KG6PLh?= NVTIc5VLW0GQR1XS
human WM-115 cell M{XKeGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M1XOemlvcGmkaYTpc44hd2ZiaIXtZY4hX01vMUG1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlY4NjV2IH7NMi=> NVnrdWd7W0GQR1XS
human HCC2998 cell MkjQS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? Mn7BTY5pcWKrdHnvckBw\iCqdX3hckBJS0N{OUm4JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlY6NjB5IH7NMi=> MWjTRW5ITVJ?
human C2BBe1 cell M1;ZTWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M4D2UGlvcGmkaYTpc44hd2ZiaIXtZY4hSzKEQnWxJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlczNjV7IH7NMi=> M2nJfXNCVkeHUh?=
human RVH-421 cell NIDyeFFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWC1OWE6UW6qaXLpeIlwdiCxZjDoeY1idiCUVlitOFIyKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:Ojd7LkO5JI5ONg>? NFP0O|JUSU6JRWK=
human H-EMC-SS cell M37wU2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MU\Jcohq[mm2aX;uJI9nKGi3bXHuJGguTU2FLWPTJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlkxNjl7IH7NMi=> MWHTRW5ITVJ?
human ML-2 cell MULHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MWPJcohq[mm2aX;uJI9nKGi3bXHuJG1NNTJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1{OUOuOlMhdk1w NVPKN49RW0GQR1XS
human SW620 cell NGnCVWtIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MXzJcohq[mm2aX;uJI9nKGi3bXHuJHNYPjJyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{CyMlIhdk1w MomwV2FPT0WU
human UACC-257 cell M33tW2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M3\qeGlvcGmkaYTpc44hd2ZiaIXtZY4hXUGFQz2yOVch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{OjFwOESgcm0v MVnTRW5ITVJ?
human AsPC-1 cell MVrHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MX7Jcohq[mm2aX;uJI9nKGi3bXHuJGF{WENvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUOyOE4{QSCwTT6= M1;wNHNCVkeHUh?=
human CAL-39 cell NXjCfVZ7T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= MY\Jcohq[mm2aX;uJI9nKGi3bXHuJGNCVC1|OTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUOzNk4zPiCwTT6= MUXTRW5ITVJ?
human COLO-679 cell MmOzS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NWryS3U5UW6qaXLpeIlwdiCxZjDoeY1idiCFT1zPMVY4QSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTN2MT6xPUBvVS5? M4O0RXNCVkeHUh?=
human NCI-H747 cell MmX1S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MlfuTY5pcWKrdHnvckBw\iCqdX3hckBPS0lvSEe0O{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVM2OC57ODDuUU4> MnfkV2FPT0WU
human NCI-H1437 cell M{fPemdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M4G0cGlvcGmkaYTpc44hd2ZiaIXtZY4hVkOLLVixOFM4KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzV{Lki1JI5ONg>? MofEV2FPT0WU
human PSN1 cell MoPzS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MkXaTY5pcWKrdHnvckBw\iCqdX3hckBRW05zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{[2MlA6KG6PLh?= NHrzVGdUSU6JRWK=
human NKM-1 cell Ml7yS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NITyOpVKdmirYnn0bY9vKG:oIHj1cYFvKE6NTT2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N|g2Njhibl2= NHvGXZlUSU6JRWK=
human MZ2-MEL cell MXLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M1\FN2lvcGmkaYTpc44hd2ZiaIXtZY4hVVp{LV3FUEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVM6PC5|NzDuUU4> M1XyfnNCVkeHUh?=
human SK-MEL-2 cell Mn\tS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M1PU[WlvcGmkaYTpc44hd2ZiaIXtZY4hW0tvTVXMMVIh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF01ODVwME[gcm0v NHLSUVhUSU6JRWK=
human LAMA-84 cell MVjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NFHKO21KdmirYnn0bY9vKG:oIHj1cYFvKEyDTVGtPFQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF01PTZwMkKgcm0v MUnTRW5ITVJ?
human U-266 cell M4Dl[2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MVXJcohq[mm2aX;uJI9nKGi3bXHuJHUuOjZ4IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;NEi3Mlc1KG6PLh?= NEHl[JVUSU6JRWK=
human RCM-1 cell MlfNS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NWfmVY5yUW6qaXLpeIlwdiCxZjDoeY1idiCUQ12tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ6Oy56NTDuUU4> Mkf5V2FPT0WU

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

体内試験 AZD6244 significantly inhibits phosphorylation of ERK1/2 in 2-1318, 5-1318, 26-1004 and 4-1318 xenografts and induces apoptosis in primary 2-1318 cells by activating the caspase pathway. [1] AZD6244 could inhibit the tumor growth in HT-29 xenograft, which is a colorectal tumor model carrying a B-Raf mutation, at a dose of 100 mg/kg and the tumor growth inhibition of AZD6244 is better than it of Gemcitabine. [3] Otherwise AZD6244 could inhibit HCC xenografts tumor growth, which associated with increased apoptosis and down-regulation of cell cycle regulators, including cyclin D1, Cdc-2, CDK2 and 4, cyclin B1, and c-Myc. [4]

お薦めの試験操作(参考用のみ)

キナーゼ試験:

[1]

+ 展開

Assay of MEK Kinase Activity:

Anti-MEK1 antibody is used to immunoprecipitate MEK1 molecules. MEK kinase activity is measured as the ability of immuno-isolated MEK1 to activate recombinant ERK1 in a coupled assay using MBP as the end point of the assay. Phosphorylated MBP is resolved on a 14% SDS-PAGE gel and vacuum-dried before exposure to X-ray film.
細胞試験:

[1]

+ 展開
  • 細胞株: Primary HCC cell lines including 2-1318, 4-1318 and 26-1004 cells
  • 濃度: ~ 10 μM
  • 反応時間: 24 or 48 hours
  • 実験の流れ:

    Cells are seeded at a density of 2.0 × 104. After 48 hours incubation, the cells are rinsed twice with culture media. Cells are treated with various concentrations of AZD6244 for 24 or 48 hours. Cell viability is determined by the 3-(4,5-dimethylthiazol-2y1)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation is assayed using a bromodeoxyuridine kit.


    (参考用のみ)
動物試験:

[1]

+ 展開
  • 動物モデル: HCC xenografts in mice homozygous for the SCID (severe combined immunodeficiency) mutation
  • 製剤: In water
  • 投薬量: 50 or 100mg/kg
  • 投与方法: Administered via p.o.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 91 mg/mL (198.82 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(文献ではなく、Selleckの実験によるデータ):
4% DMSO+30% PEG 300+5% Tween 80+ddH2O
混合させたのち直ちに使用することを推奨します。
5mg/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 457.68
化学式

C17H15BrClFN4O3

CAS No. 606143-52-6
保管
in solvent
別名 ARRY-142886

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    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

貯蔵液を準備するために必要な希釈率を計算してください。Selleck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 ( 入力 出力 )

  • 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

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03095248 Recruiting Neurofibromatosis 2|Vestibular Schwannoma|Meningioma|Ependymoma|Glioma Children''s Hospital Medical Center Cincinnati|AstraZeneca May 8 2017 Phase 2
NCT00463814 Active not recruiting Tumor|Cancer AstraZeneca March 8 2007 Phase 1
NCT02299999 Recruiting Metastatic Breast Cancer UNICANCER|Fondation ARC|AstraZeneca April 7 2014 Phase 2
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
NCT02337530 Active not recruiting Non-Small Cell Lung Cancer Canadian Cancer Trials Group|AstraZeneca February 5 2015 Phase 2
NCT02188264 Active not recruiting Recurrent Colorectal Carcinoma|Solid Neoplasm|Stage IIIA Colorectal Cancer AJCC v7|Stage IIIB Colorectal Cancer AJCC v7|Stage IIIC Colorectal Cancer AJCC v7|Stage IVA Colorectal Cancer AJCC v7|Stage IVB Colorectal Cancer AJCC v7 National Cancer Institute (NCI) August 5 2014 Phase 1

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

よくある質問(FAQ)

  • 質問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シグナル伝達経路

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