PD0325901
Pfizer辉瑞授权 目录号：S1036
Molecular Weight(MW): 482.19
PD0325901是一种选择性的，非ATP竞争性MEK抑制剂，无细胞试验中IC50为0.33 nM，对ERK1和ERK2磷酸化抑制作用比CI-1040强500倍左右。Phase 2。
客户使用该产品的19个实验数据：
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Phosphorylation of PPARg in epididymal white adipose tissue in ob/ob mice after treatment with MEK inhibitors. Gene expression in ob/ob epididymal white adipose tissue after treatment with vehicle or either of two MEK inhibitors, PD0325901 or GSK1120212 (n = 7, 7 and 8, respectively). Areas under the curve and gene expression were analysed by analysis of variance.
Nature 2015 517(7534), 391-5. PD0325901 purchased from Selleck.
Immunoblot analysis of Ser9-phosphorylated (that is, inactivated) or total GSK3β, active or total β-catenin Thr202- and Tyr204- phosphorylated or total Erk1/2, and Ser473-phosphorylated or total Akt in control; Bcl2 lymphoma cells treated with ADR for five days, together with pharmacological inhibitors targeting MAPK and PI3K kinase pathways.α -Tubulin was used as a loading control. MAPKi=PD325901.
Nature, 2018, 553(7686):96-100. PD0325901 purchased from Selleck.
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c, Examples of CDK2 activity traces aligned to the end of mitosis. Each panel shows different time windows relative to mitosis when mitogens were withdrawn (marked in grey) in d. d, Probability of proliferation (defined as CDK2 activity > 1, 10 h after mitosis) represented as a function of time when inhibitors of MEK (MEKi; 100 nM PD0325901) or of CDK4 (CDK4i; 1 μ M palbociclib) were added or when mitogens were removed, relative to mitosis. Data are mean ± s.e.m. (n = 5 biological replicates).
Nature, 2017, 549(7672):404-408. PD0325901 purchased from Selleck.
Immunoblot analysis of Ser9-phosphorylated (that is, inactivated) or total GSK3β , active or total β -catenin (as in Extended Data Fig. 5c), Thr202- and Tyr204-phosphorylated or total Erk1/2, and Ser473-phosphorylated or total Akt in control;Bcl2 lymphoma cells treated with ADR for five days, together with pharmacological inhibitors targeting MAPK and PI3K kinase pathways. α -Tubulin was used as a loading control. One out of two independent experiments shown. MPAKi:PD325901
Nature, 2017, 553(7686):96-100. PD0325901 purchased from Selleck.
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Rapamycin reduces VCAM expression in vivo. Expression of VCAM-1 mRNA (normalized to CD31) in aortas harvested from mice pretreated with vehicle, rapamycin, or rapamycin + MEK inhibitor (MEK-I; PD0325901) and then injected with TNF (n = 5 per group). Mice were treated as in D. Harvested aortas were analyzed for VCAM-1 expression via immunofluorescence.
J Exp Med 2014 211(3), 395-404. PD0325901 purchased from Selleck.
Plasma MEK inhibitor levels of PD325901 are plotted against % MEK inhibition in brain. One hundred percent pERK levels (0% MEK inhibition) were determined in vehicle-treated rats.Inhibition of pERK activity in brain, lung, and Colo205 tumor in nude xenograft mice treated with 10 mg/kg PD325901.
Cancer Res 2009 PD0325901 purchased from Selleck.
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Pharmacological inhibition of MEK (PD0325901) suppresses DR5 expression in cancer cells; this effect is reversible upon stopping of the treatment. The indicated cancer cell lines were exposed to the given concentrations of the inhibitors as indicated for 16 h. TPC-1 cells were treated with 10 uM of the indicated inhibitors for different times as labeled.
Oncogene 2015 10.1038/onc.2015.97. PD0325901 purchased from Selleck.
(B)Effect of MAPK pathway inhibition on FGF9 mediated induction of Fgf23 expression. (D) Western blot analysis of FRS2 and ERK1/2 phosphorylation in UMR 106 cells. Cells were treated for 3h (Western blot) or 24h (qPCR analysis) with FGF9 (50ng/ml), EGF (50ng/ml), PD173074 (250nM), PD0325901 (100nM) and RAF265 (500nM) as indicated. Heparin (10g/ml) was added to all treatments with FGF9. Activation of Fgf23 is shown relative to transcript levels in vehicle treated cells (relative expression of 1). Expression values were normalized to Gapdh mRNA copies and are given as average with SEM (n3). Data were compared by 1 way ANOVA; asterisk indicates p<0.05 with respect to vehicle treated cells.
J Bone Miner Res 2011 26, 2486-2497. PD0325901 purchased from Selleck.
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Assessment of in vivo toxicity to MEK inhibitor PD0325901. (A) Weight change in grams is shown for each PD0325901 (PD) treatment group in the MDA-MB-453 xenograft model. Weight change is the difference between pre- and post-treatment weight in each group. PD0325901 treatments were carried out at 5, 10, 15 and 20 mg/kg/day for 30 days, and daily gavage of carrier solution was used as control. *P < 0.01 for PD-5/PD-10 vs. control groups and PD-5/PD-10 vs. PD-15/PD-20 groups using Mann-Whitney U test. Error bars: ±2 SEM. (B) Number of days lost due to toxicity is shown for each PD0325901 treatment group in mouse xenograft model explained in Figure 5A. *P < 0.01 for PD-5/PD-10 vs. PD-15/PD-20 groups.
Breast Cancer Res 2011 13, R36. PD0325901 purchased from Selleck.
The therapeutic effect of AR and MEK inhibitors on in vivo angiogenesis. (A) Angiogenesis index for each in vivo treatment group. Angiogenesis was measured as the number of CD-31-positive blood vessels in a cross-section of each xenograft tumor. CTL: control group; FLU: flutamide; and PD: PD0325901. *P < 0.03 for PD0325901 monotherapy vs. control and **P < 0.03 for combination therapy vs. monotherapy groups using Mann-Whitney U test. Error bars: ±2 SEM. (B) Immunohistochemistry (IHC) was used to measure angiogenesis in a control xenograft tumor. Staining was performed using a CD31 rabbit polyclonal antibody. Original magnification, × 40. (C) IHC was used to measure angiogenesis in a PD0325901 monotherapy tumor. Original magnification, × 40. (D) IHC was used to measure angiogenesis in a xenograft tumor treated with combination therapy. Original magnification, × 40.
Breast Cancer Res 2011 13, R36. PD0325901 purchased from Selleck.
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Effects of the MEK inhibitor (MEKi) PD0325901 (PD) and rhBMP-2 (BMP) treatment on histology in an NF1 open fracture model. Treatment with 10 mg/kg of PD0325901 on days 22 through 10 (PD alone) slightly improved bone volume and callus size. Delivery of 10 mg of rhBMP-2 in the collagen sponge (BMP alone) resulted in a large increase in bone volume and callus size. Combination treatment with local rhBMP-2 and systemic PD0325901 (PD 1 BMP) resulted in further increases in new bone volume and total callus volume.Picro Sirius Red and Alcian Blue staining to assess fibrous tissue.
J Bone Joint Surg Am 2015 96(14), e117. PD0325901 purchased from Selleck.
Bone 2014 59, 151-61. PD0325901 purchased from Selleck.
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Characterization of rES cells. A: image of normal rES cell colonies on feeder layers. B: rES colonies were positive for AP staining. CeE: rES colonies readily expressed pluripotent markers, Sox2 (C), Oct4 (D), and SSEA-1 (E). Blue, DAPI. Scale bars: 100 um.
J Genet Genomics 2012 39, 643e651. PD0325901 purchased from Selleck.
Effect of small molecule inhibitors on reprogramming efficiency of myoblast cell derived from 5 different donors. (A) Reprogramming efficiency is shown as number of colonies from 10^5 starting cells on Y-axes. Ctrl, control condition and addition of small molecule inhibitors are marked. (B) AP staining of reprogrammed myoblast cell lines,from 5 different donors, in wells of 12-well plates at day 18. Ctrl, control condition and additions of small molecule inhibitors are marked.
Stem Cells Dev 2013 PD0325901 purchased from Selleck.
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The effects of PD0325901 on the Akt/mTOR and MAPK pathways in the two DDLS cell lines as evaluated by western blotting
Tumour Biol, 2016, 37(4):4767-76.. PD0325901 purchased from Selleck.
PD0325901 inhibited the sorafenib-induced RAS/ERK pathway activation and enhanced the cytotoxic effects of sorafenib in resistant cell lines. (A) HUH-7 hepatoma cells treated with sorafenib (5 μM) for 24 h with or without pretreatment with specific kinase inhibitors (PD0325901, 10 μM). Expressions of p-AKT and cleaved PARP were revealed by Western blotting. (B) SK-HEP-1 hepatoma cells treated with sorafenib (5 μM) for 24 h with or without pretreatment with specific kinase inhibitors (PD0325901, 10 μM). Expressions of p-AKT and cleaved PARP were revealed by Western blotting. (C) HUH-7 hepatoma cells treated with sorafenib (5 μM) with or without the kinase inhibitors for 24 h. Proportions of apoptotic cells were evaluated by annexin V labeling. (D) SK-HEP-1 hepatoma cells treated with sorafenib (5 μM) with or without the kinase inhibitors for 24 h. Proportions of apoptotic cells were evaluated by annexin V labeling. (*P<0.05, HUH- 7, SK-HEP-1 are control groups, R-HUH-7, R-SK-HEP-1 are resistant groups).
J Surg Res, 2016, 206(2):371-379. PD0325901 purchased from Selleck.
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Inhibition of anchorage-independent growth of lung tumor cell lines by selected inhibitors. Each selected cell line was treated with the indicated inhibitor at 0.1 μM and 1 μM concentrations for two weeks and cell colony size formation was scored under the Nikon inverted-phase microscope.
Int J Proteomics 2011 2011, Article ID 215496. PD0325901 purchased from Selleck.
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of PD0325901 for 24 hours.
2010 Dr Zhang of Tianjin Medical University. PD0325901 purchased from Selleck.
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Effects of PD0325901 on HT29 Xenograft tumors. PD0325901(1mg/kg carrier DMSO).Collection at 24h.
2010 Dr. Citrin, Deborah of NIH. PD0325901 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 | PD0325901是一种选择性的，非ATP竞争性MEK抑制剂，无细胞试验中IC50为0.33 nM，对ERK1和ERK2磷酸化抑制作用比CI-1040强500倍左右。Phase 2。 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| 靶点 |
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| 体外研究 |
PD0325901比另一种MEK抑制剂CI-1040具有更高的渗透率。与CI-1040相比，PD 0325901可以到达体系的更深层。[1]PD0325901是非ATP竞争性的MAPK激酶MEK抑制剂，抑制鼠类结肠26细胞的MEK时IC50为0.33nM。苏氨酸/酪氨酸激酶MEK是RAS/RAF/MEK/ERK信号通路的关键组成部分，在人类肿瘤细胞中通常是激活的。PD0325901精确有效地抑制MEK，作用于MEK1和MEK2时Ki值为1nM。PD0325901作用于细胞ERK1和ERK2的磷酸化效果比CI-1040强到大约500倍。[2] |
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| Cell Data |
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| 体内研究 | PD0325901阻止细胞黑色素瘤细胞系的生长，使异种移植鼠模型的细胞周期停止在G1期，引起细胞凋亡单独口服25 mg/kg PD032590124后，ERK的磷酸化作用被阻断达到50%以上。PD 0325901的抗癌活性已经被用于更广泛的人类移植瘤的研究中，在研究的人类肿瘤模型中,有6/7被PD 0325901明显抑制。[2] PD0325901抑制恶性黑色素瘤细胞系生长。PD0325901抑制TPC-1细胞和K2细胞生长，GI50分别为11和6.3 nM。PD0325901浓度非常低时(10 nM)也明显抑制携带BRAF突变的PTC细胞生长，且同样浓度时只稍微提高携带RET/PTC1重排的PTC细胞生长。PD0325901作用于多种PTC细胞系，有效抑制ERK1/2磷酸化。[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： |
+ 展开
体外级联实验: 在有含p44MAPK(GST-MAPK)的谷胱甘肽S-转移酶融合蛋白和含p45MEK(GST-MEK)的谷胱甘肽S-转移酶融合蛋白存在情况下，测定32P渗透到髓鞘碱性蛋白(MBP)的渗透率。实验溶液包括20 mM HEPES,pH 为7.4,10 mM MgCl2,1 mM MnCl2,1 mM EGTA,50 mM [gamma-32P]ATP,10 mg GST-MEK,0.5 mg GST-MAPK,和40 mg MBP，终体积为100 mL。实验进行20分钟后，加入三氯乙酸终止反应，然后通过GF/C过滤器过滤。使用1205 Beta板测定保留在过滤器中的32P。测定不同剂量PD0325901，绘制剂量反应曲线。 |
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| 细胞实验： |
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| 动物实验： |
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参考文献
- [1] Barrett SD, et al. Bioorg Med Chem Lett, 2008, 18(24), 6501-6504.
- [2] Judith SS, et al. Proc Amer Assoc Cancer Res.2004,45, Abstract #4003
- [3] Henderson YC, et al. Mol Cancer Ther, 2010, 9(7), 1968-1976.
- [4] Paterson A, et al. Blood, 2012, 119(7), 1726-1736.
- [5] Ricciardi MR, et al. J Mol Med (Berl), 2012, 90(10), 1133-1144.
- [6] Pratilas CA, et al. Cancer Res, 2008, 68(22), 9375-9383.
- [7] Legrier ME, et al. Cancer Res, 2007, 67(23), 11300-11308.
- [8] Barrett SD, et al. Bioorg Med Chem Lett, 2008, 18(24), 6501-6504.
溶解度 (25°C)
| 体外 | DMSO | 96 mg/mL (199.09 mM) |
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| Ethanol | 40 mg/mL (82.95 mM) | |
| Water | 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)： 30% PEG 400+5% Tween 80+ddH2O |
10mg/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 | 482.19 |
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| 化学式 | C16H14F3IN2O4 |
| CAS号 | 391210-10-9 |
| 稳定性 | powder |
| in solvent | |
| 别名 | N/A |
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
*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
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 )
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。.
分子量计算器
通过输入化合物的化学式来计算其分子量：
注：化学分子式大小写敏感。C10H16N2O2 c10h16n2o2
摩尔浓度计算器
临床试验信息
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT02510001 | Active not recruiting | Solid Tumor|Colorectal Cancer | University of Oxford|Queen''s University Belfast|Oxford University Hospitals NHS Trust|Velindre NHS Trust|University Hospital Antwerp|Hospital Vall d''Hebron|Saint Antoine University Hospital|European Georges Pompidou Hospital|Pfizer|University of Turin Italy|Belfast Health and Social Care Trust|Beaumont Hospital|European Commission|Array BioPharma|University of Paris 5 - Rene Descartes | November 2014 | Phase 1 |
| NCT02510001 | Active not recruiting | Solid Tumor|Colorectal Cancer | University of Oxford|Queen''s University Belfast|Oxford University Hospitals NHS Trust|Velindre NHS Trust|University Hospital Antwerp|Hospital Vall d''Hebron|Saint Antoine University Hospital|European Georges Pompidou Hospital|Pfizer|University of Turin Italy|Belfast Health and Social Care Trust|Beaumont Hospital|European Commission|Array BioPharma|University of Paris 5 - Rene Descartes | November 2014 | Phase 1 |
| NCT02096471 | Completed | Neurofibromatosis Type 1 and Growing or Symptomatic Inoperable PN | University of Alabama at Birmingham | June 2014 | Phase 2 |
| NCT02096471 | Completed | Neurofibromatosis Type 1 and Growing or Symptomatic Inoperable PN | University of Alabama at Birmingham | June 2014 | Phase 2 |
| NCT02039336 | Recruiting | Colorectal Cancer | The Netherlands Cancer Institute|Pfizer | January 2014 | Phase 1|Phase 2 |
| NCT02022982 | Active not recruiting | KRAS Mutant Non-Small Cell Lung Cancer|Solid Tumors | Dana-Farber Cancer Institute | January 2014 | Phase 1|Phase 2 |
技术支持
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如果有其他问题，请给我们留言。
常见问题及建议解决方法
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问题 1：
Whether the inhibitor PD0325901 interacts with other targets other than MEK?
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回答：
PD0325901 has very high selectivity to MEK. In addition, it can also inhibits VEGF activity according to the reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713590/
