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

文献中の使用例(117)

カスタマーフィードバック(13)

  • 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.

  • 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.

    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 NWTuc3E1T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NGTZTGxKdmirYnn0bY9vKG:oIHj1cYFvKEOKUD2yNVIh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{NjF3IH7NMi=> Mn7zV2FPT0WU
human H9 cell NFr6c|lIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NF7jZoRKdmirYnn0bY9vKG:oIHj1cYFvKEh7IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MkKuPFghdk1w MUnTRW5ITVJ?
human HL-60 cell NIH6cY9Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= M2C0eWlvcGmkaYTpc44hd2ZiaIXtZY4hUExvNkCgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yOE42QSCwTT6= MnPLV2FPT0WU
human A375 cells MWjQdo9tcW[ncnH0bY9vKGG|c3H5 NYnldoVsPzJiaB?= NVTOSmhDSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDBN|c2KGOnbHzzJIV5eHKnc4PpcochSlKDRjDWOlAxTSCvdYThcpQh[W[2ZYKgO|IhcHK|IHL5JGNmdGxidHn0[ZIu\2yxIHHzd4F6NCCLQ{WwQVMyKG6PLh?= MWiyN|Q4PDN6OB?=
human NOMO-1 cell M{XUcGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NEPlVm1KdmirYnn0bY9vKG:oIHj1cYFvKE6RTV:tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVMyNjl5IH7NMi=> NIGzfIJUSU6JRWK=
human DU-4475 cell MWDHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NXLwU3h3UW6qaXLpeIlwdiCxZjDoeY1idiCGVT20OFc2KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzNwNkegcm0v MknoV2FPT0WU
human M14 cell MnH3S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M2nJS2lvcGmkaYTpc44hd2ZiaIXtZY4hVTF2IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;M{[uPFkhdk1w Ml;0V2FPT0WU
human HT-144 cell MojIS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NVPGbpA6UW6qaXLpeIlwdiCxZjDoeY1idiCKVD2xOFQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF05QS5yNTDuUU4> MVvTRW5ITVJ?
human SK-N-AS cell M{XLbmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NHzPUW5KdmirYnn0bY9vKG:oIHj1cYFvKFONLV6tRXMh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF06Oi56MzDuUU4> MnvEV2FPT0WU
human LB2518-MEL cell Mn[1S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NUW2dHhkUW6qaXLpeIlwdiCxZjDoeY1idiCOQkK1NVguVUWOIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;OUOuPFIhdk1w Moe1V2FPT0WU
human C32 cell MULHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnThTY5pcWKrdHnvckBw\iCqdX3hckBEOzJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD17OD6yN{BvVS5? NFKxeYxUSU6JRWK=
human BHT-101 cell MnrKS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NVXrNVFyUW6qaXLpeIlwdiCxZjDoeY1idiCESGStNVAyKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OTB4LkmzJI5ONg>? M{K1VHNCVkeHUh?=
human KY821 cell NH\mUIpIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MV3Jcohq[mm2aX;uJI9nKGi3bXHuJGt[QDJzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MUC3MlE5KG6PLh?= M2\pXnNCVkeHUh?=
human CP50-MEL-B cell NVXLVpVyT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NEDS[4tKdmirYnn0bY9vKG:oIHj1cYFvKEOSNUCtUWVNNUJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zMkeuPVQhdk1w MUTTRW5ITVJ?
human MEL-HO cell MUjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Mkj6TY5pcWKrdHnvckBw\iCqdX3hckBOTUxvSF:gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xN|gvQDRibl2u NF7jdFdUSU6JRWK=
human MIAPaCa2 cells MWXQdo9tcW[ncnH0bY9vKGG|c3H5 NIXaUJZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3JRXBiS2F{IHPlcIx{NCCLQ{WwQVE1OiCwTT6= NGCyVFEzOzR5NEO4PC=>
human EoL-1-cell cell MojtS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M4rjVGlvcGmkaYTpc44hd2ZiaIXtZY4hTW:OLUGtZ4VtdCClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTF2ND63OkBvVS5? MWXTRW5ITVJ?
human DOK cell M4HyPWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NWDsVZp4UW6qaXLpeIlwdiCxZjDoeY1idiCGT1ugZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xOFcvODhibl2u NYL0XG5RW0GQR1XS
human SH-4 cell NGT5VHVIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MWjJcohq[mm2aX;uJI9nKGi3bXHuJHNJNTRiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zNk[uOFghdk1w M3qyR3NCVkeHUh?=
human BPH-1 cell NEDteWNIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M3G2Z2lvcGmkaYTpc44hd2ZiaIXtZY4hSlCKLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xPFIvOzFibl2u MoXPV2FPT0WU
human HuP-T4 cell NF3QWFFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NVH4enlLUW6qaXLpeIlwdiCxZjDoeY1idiCKdWCtWFQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yQTVwM{Kgcm0v M{GyTnNCVkeHUh?=
human KU812 cell MojQS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MnK3TY5pcWKrdHnvckBw\iCqdX3hckBMXThzMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUKxNU43QCCwTT6= NELveGFUSU6JRWK=
human A549 cell MWTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NXf1eJc6UW6qaXLpeIlwdiCxZjDoeY1idiCDNUS5JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlE1NjF|IH7NMi=> NUjXVXl5W0GQR1XS
human HTC-C3 cell M2rpXWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Mmm0TY5pcWKrdHnvckBw\iCqdX3hckBJXENvQ{OgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yNVQvPjFibl2u MkG2V2FPT0WU
human A101D cell MkHCS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MoDTTY5pcWKrdHnvckBw\iCqdX3hckBCOTBzRDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUK0NE4{OyCwTT6= M4\vfXNCVkeHUh?=
human ONS-76 cell NEPGNohIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MnHkTY5pcWKrdHnvckBw\iCqdX3hckBQVlNvN{[gZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yOFQvPTNibl2u MYLTRW5ITVJ?
human RKO cell MYfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M3n4WWlvcGmkaYTpc44hd2ZiaIXtZY4hWkuRIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO|YYmsJGlEPTB;MkS4MlM5KG6PLh?= MX;TRW5ITVJ?
human WM-115 cell NUPlOpFZT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NFTJTYVKdmirYnn0bY9vKG:oIHj1cYFvKFePLUGxOUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI3Py53NDDuUU4> MnnZV2FPT0WU
human HCC2998 cell MYjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MWnJcohq[mm2aX;uJI9nKGi3bXHuJGhESzJ7OUigZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yOlkvODdibl2u MYjTRW5ITVJ?
human C2BBe1 cell M4fRVWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NIXIZ|lKdmirYnn0bY9vKG:oIHj1cYFvKEN{QlLlNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI4Oi53OTDuUU4> MlfsV2FPT0WU
human RVH-421 cell NXix[GdJT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M4DXTGlvcGmkaYTpc44hd2ZiaIXtZY4hWl[KLUSyNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVI4QS5|OTDuUU4> NXn2fZM6W0GQR1XS
human H-EMC-SS cell MVvHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MYDJcohq[mm2aX;uJI9nKGi3bXHuJGguTU2FLWPTJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlkxNjl7IH7NMi=> MnH5V2FPT0WU
human ML-2 cell MoWyS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MVHJcohq[mm2aX;uJI9nKGi3bXHuJG1NNTJiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1{OUOuOlMhdk1w MofUV2FPT0WU
human SW620 cell MYXHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MmDOTY5pcWKrdHnvckBw\iCqdX3hckBUXzZ{MDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUOwNk4zKG6PLh?= M2DNbHNCVkeHUh?=
human UACC-257 cell NVPlN4Z4T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3GwfGlvcGmkaYTpc44hd2ZiaIXtZY4hXUGFQz2yOVch[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{OjFwOESgcm0v MkHUV2FPT0WU
human AsPC-1 cell M3XIS2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 MYLJcohq[mm2aX;uJI9nKGi3bXHuJGF{WENvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUOyOE4{QSCwTT6= MUHTRW5ITVJ?
human CAL-39 cell NH2xfFBIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MV\Jcohq[mm2aX;uJI9nKGi3bXHuJGNCVC1|OTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUOzNk4zPiCwTT6= NESxZZFUSU6JRWK=
human COLO-679 cell NVyxbFVyT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= M3OzZ2lvcGmkaYTpc44hd2ZiaIXtZY4hS0:OTz22O|kh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{PDFwMUmgcm0v MmfYV2FPT0WU
human NCI-H747 cell M2L3eGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NX:wZmlnUW6qaXLpeIlwdiCxZjDoeY1idiCQQ1mtTFc1PyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTN3MD65PEBvVS5? MUXTRW5ITVJ?
human NCI-H1437 cell NVXUfVRVT3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NGXoZ4ZKdmirYnn0bY9vKG:oIHj1cYFvKE6FST3INVQ{PyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTN3Mj64OUBvVS5? M2HqU3NCVkeHUh?=
human PSN1 cell MVTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NGPMe5JKdmirYnn0bY9vKG:oIHj1cYFvKFCVTkGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2zOlYvODlibl2u MYPTRW5ITVJ?
human NKM-1 cell NEmzSHBIem:5dHigbY5pcWKrdHnvckBie3OjeR?= MkXkTY5pcWKrdHnvckBw\iCqdX3hckBPU01vMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUO4OU45KG6P NIrCOmtUSU6JRWK=
human MZ2-MEL cell NFjy[GFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= Mn\VTY5pcWKrdHnvckBw\iCqdX3hckBOYjJvTVXMJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N|k1NjN5IH7NMi=> NWnaN5V1W0GQR1XS
human SK-MEL-2 cell NIWxdmFIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NVexN|FMUW6qaXLpeIlwdiCxZjDoeY1idiCVSz3NSWwuOiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTRyNT6wOkBvVS5? NY\3bGV7W0GQR1XS
human LAMA-84 cell NXvtVpV7T3Kxd4ToJIlvcGmkaYTpc44h[XO|YYm= NU\2eHJ7UW6qaXLpeIlwdiCxZjDoeY1idiCOQV3BMVg1KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PDV4LkKyJI5ONg>? NFnvOmNUSU6JRWK=
human U-266 cell MVnHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? NXTiSY9WUW6qaXLpeIlwdiCxZjDoeY1idiCXLUK2OkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ5Py55NDDuUU4> MnzYV2FPT0WU
human RCM-1 cell NIHXWm5Iem:5dHigbY5pcWKrdHnvckBie3OjeR?= NVSxTJZ{UW6qaXLpeIlwdiCxZjDoeY1idiCUQ12tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ6Oy56NTDuUU4> Ml7NV2FPT0WU

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 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:
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

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
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 --

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.

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