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Mirdametinib

Mirdametinib

产品编号 T6189   CAS 391210-10-9
别名: PD325901, PD0325901

Mirdametinib (PD325901) 是一种 MEK 抑制剂 (IC50=0.33 nM),具有选择性、非 ATP 竞争性和口服活性。Mirdametinib 具有抗肿瘤活性,可以抑制 p-ERK1/2 的表达并诱导细胞凋亡

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Mirdametinib Chemical Structure
Mirdametinib, CAS 391210-10-9
规格 价格/CNY 货期 数量
1 mg ¥ 189 现货
5 mg ¥ 428 现货
10 mg ¥ 738 现货
25 mg ¥ 1,420 现货
50 mg ¥ 2,190 现货
100 mg ¥ 3,590 现货
200 mg ¥ 4,880 现货
1 g ¥ 6,590 现货
1 mL * 10 mM (in DMSO) ¥ 461 现货
千万补贴 助力科研
BCA蛋白浓度测定试剂盒限时半价
Venetoclax限时半价
MG-132限时半价
产品目录号及名称: Mirdametinib (T6189)
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选择批次  
纯度: 99.91%
纯度: 99.5%
纯度: 99.18%
更多批次查询请联系客服
生物活性
化学信息
存储 & 溶解度
参考文献
产品描述 Mirdametinib (PD325901) is an MEK inhibitor (IC50=0.33 nM) with selective, non-ATP-competitive, and oral activity. Mirdametinib exhibits antitumor activity by inhibiting p-ERK1/2 expression and inducing apoptosis.
靶点活性 MEK:0.33 nM (cell free)
体外活性 方法:11 种人黑色素瘤细胞系上用 Mirdametinib (0.1-1000 nM) 处理 72 h,使用 trypan blue exclusion test 检测细胞数。
结果:Mirdametinib (IC50=20-50 nM) 有效抑制具有 BRAF 突变 (M14/A375P/A375M/A375SM/ME10538/ME4686/JR8) 或不具有 BRAF 突变 (ME4405/ME13923) 的人黑色素瘤细胞系的生长。ME1007 和 ME8959均具有野生型 BRAF,对 Mirdametinib介导的生长抑制的抗性略高 (IC50≥100 nM)。[1]
方法:乳头状甲状腺癌 (PTC) 细胞系 K2 和 TPC-1 用 Mirdametinib (0.1-1000 nmol/L) 处理 1-96 h,使用 Western Blot 检测靶点蛋白表达水平。
结果:Mirdametinib 可以有效抑制多种 PTC 细胞系中 ERK1/2 的磷酸化。[2]
体内活性 方法:为检测体内抗肿瘤活性,将 Mirdametinib (20-25 mg/kg,80 mmol/L citric buffer (pH 7)) 灌胃给药给携带 PTC 肿瘤 K2 或 TPC-1 的 Athymic Ncr-nu/nu 小鼠,每周五次,持续三周。
结果:Mirdametinib 在接种携带 BRAF 突变的 PTC 细胞 K2 的小鼠中完全抑制肿瘤生长,并且在接种携带 RET/PTC1 重排的 PTC 细胞 TPC-1 的小鼠中显着降低肿瘤生长。[2]
方法:为检测体内抗肿瘤活性,将 Mirdametinib (1.6-25 mg/kg,0.5% hydroxypropylmethylcellulose+0.2% Tween 80 in water) 口服给药给携带小鼠结直肠癌肿瘤 CT26 的小鼠,每天一次,持续十四天。
结果:Mirdametinib 显著抑制肿瘤中的 pERK 水平。[3]
激酶实验 Incorporation of 32P into myelin basic protein (MBP) is assayed in the presence of a glutathione S-transferase fusion protein containing p44MAP kinase (GST-MAPK) and a glutathione S-transferase protein containing p45MEK (GST-MEK). The assay solution contained 20 mM HEPES, pH 7.4, 10 mM MgCl2, 1 mM MnCl2, 1 mM EGTA, 50 mM [γ-32P]ATP, 10 mg GST-MEK, 0.5 mg GST-MAPK and 40 mg MBP in a final volume of 100 mL. Reactions are stopped after 20 minutes by addition of trichloroacetic acid and filtered through a GF/C filter mat. 32P retained on the filter mat is determined using a 1205 Betaplate [1].
细胞实验 A cell death detection enzyme-linked immunosorbent assay was used per the manufacturer's instructions. Briefly, 4 × 10^4 cells were plated in 24-well plates in triplicate the day before treatment. PTC cells were treated with 0.1 μmol/L PD0325901 for 96 hours. Cells treated with 1 μmol/L staurosporine served as positive controls for apoptosis. At the end of treatment, cells were lysed using the lysis buffer provided in the kit for 30 minutes at room temperature and then centrifuged in 24-well plates. Lysates (20 μL of supernatant) were transferred to streptavidin-coated wells and incubated for 2 hours at room temperature with two antibodies (biotin-labeled anti-histone antibody and peroxidase-conjugated anti-DNA antibody). After the wells were washed three times, the samples were incubated with peroxidase substrate (ABTS) and the amount of colored product was determined spectrophotometrically at 405 nm. The background was measured at 490 nm [2].
动物实验 Athymic Ncr-nu/nu mice were obtained from the National Cancer Institute at ages 6 to 8 weeks and housed for at least 1 week after arrival. Mice (10–14 per group) were anesthetized s.c. with a cocktail (100 μL/10 g body weight of 10 mg/mL ketamine and 1 mg/mL xylazine). K2 and TPC-1 cells stably infected with a retrovirus expressing luciferase (5 × 105 cells in 5 μL RPMI1640 medium) were inoculated into the thyroid gland, and the mice were monitored weekly for tumor growth by Xenogen (IVIS 200 imaging system) using Living Image 3.0 software. One week after inoculation, PD0325901 was dissolved in 80 mmol/L citric buffer (pH 7) by sonication and given to mice daily by oral gavage (20–25 mg/kg) for 3 weeks (5 consecutive days/week). Mice were sacrificed only due to tumor burden or loss of 20% of body weight. Tumor sizes were measured with calipers and tumor volume (V) was calculated by the formula (V = length × width × depth). Control mice were given 80 mmol/L citric buffer (pH 7) alone. All in vivo experiments were done at least twice [2].
别名 PD325901, PD0325901
分子量 482.19
分子式 C16H14F3IN2O4
CAS No. 391210-10-9

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

H2O: Insoluble

DMSO: 50 mg/mL (103.69 mM)

溶液配制表

可选溶剂 浓度 体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 2.0739 mL 10.3694 mL 20.7387 mL 51.8468 mL
5 mM 0.4148 mL 2.0739 mL 4.1477 mL 10.3694 mL
10 mM 0.2074 mL 1.0369 mL 2.0739 mL 5.1847 mL
20 mM 0.1037 mL 0.5185 mL 1.0369 mL 2.5923 mL
50 mM 0.0415 mL 0.2074 mL 0.4148 mL 1.0369 mL
100 mM 0.0207 mL 0.1037 mL 0.2074 mL 0.5185 mL

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TargetMol Library Books参考文献

1. Ciuffreda L, et al. Growth-inhibitory and antiangiogenic activity of the MEK inhibitor PD0325901 in malignant melanoma with or without BRAF mutations. Neoplasia. 2009 Aug;11(8):720-31. 2. Henderson YC, et al. MEK inhibitor PD0325901 significantly reduces the growth of papillary thyroid carcinoma cells in vitro and in vivo. Mol Cancer Ther. 2010 Jul;9(7):1968-76. 3. Barrett SD, et al. The discovery of the benzhydroxamate MEK inhibitors CI-1040 and PD 0325901. Bioorg Med Chem Lett. 2008 Dec 15;18(24):6501-4. 4. Lin T, et al. A chemical platform for improved induction of human iPSCs. Nat Methods. 2009 Nov;6(11):805-8. 5. Li Y, He Y, Peng J, et al. Mutant Kras co-opts a proto-oncogenic enhancer network in inflammation-induced metaplastic progenitor cells to initiate pancreatic cancer[J]. Nature Cancer. 2020: 1-17. 6. Chen F, Zhang M, Feng X, et al. Discovery of a Novel Long Noncoding RNA Lx8-SINE B2 as a Marker of Pluripotency[J]. Stem Cells International. 2021, 2021. 7. Guo Z, Kang S, Sun D, et al. MAPK-dependent hormonal signaling plasticity contributes to overcoming Bacillus thuringiensis toxin action in an insect host[J]. Nature Communications. 2020, 11(1): 1-14.

TargetMol Library Books文献引用

1. Guo Z, Guo L, Qin J, et al. A single transcription factor facilitates an insect host combating Bacillus thuringiensis infection while maintaining fitness. Nature Communications. 2022, 13(1): 1-15. 2. Guo Z, Kang S, Sun D, et al. MAPK-dependent hormonal signaling plasticity contributes to overcoming Bacillus thuringiensis toxin action in an insect host. Nature Communications. 2020 Jun 12;11(1):3003. doi: 10.1038/s41467-020-16608-8. 3. Kuang, Junqi, et al. SS18 regulates pluripotent-somatic transition through phase separation.. Nature Communications. 2021 Jul 2;12(1):4090. doi: 10.1038/s41467-021-24373-5. 4. Wang W, Ren S, Lu Y, et al. Inhibition of Syk promotes chemical reprogramming of fibroblasts via metabolic rewiring and H2S production. The EMBO Journal. 2021 Jun 1;40(11):e106771. doi: 10.15252/embj.2020106771. Epub 2021 Apr 28. 5. Lin R, Zhai Z, Kuang J, et al. H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition. Cell & Bioscience. 2022, 12(1): 1-14 6. Guo Z, Kang S, Wu Q, et al. The regulation landscape of MAPK signaling cascade for thwarting Bacillus thuringiensis infection in an insect host. PLoS pathogens. 2021, 17(9): e1009917. 7. Chen F, Zhang M, Feng X, et al. Discovery of a Novel Long Noncoding RNA Lx8-SINE B2 as a Marker of Pluripotency. Stem Cells International. 2021 Feb 6;2021:6657597. doi: 10.1155/2021/6657597. eCollection 2021. 8. Yu Y, Li X, Jiao R, et al.H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.Cell & Bioscience.2023, 13(1): 1-20. 9. Yang Y, Xiao L, Xue Y, et al.ZBTB7A regulates primed‐to‐naïve transition of pluripotent stem cells via recognition of the PNT‐associated sequence by Zinc Fingers 1–2 and recognition of γ‐globin− 200 gene element by Zinc Fingers 1–4.The FEBS Journal.2023
NS3694 Ac-IETD-CHO TFA Epothilone A Solasodine Oxibendazole SRT 2183 AES-350 Fangchinoline

相关化合物库

该产品包含在如下化合物库中:
抗癌活性化合物库 激酶抑制剂库 抗癌临床化合物库 药物功能重定位化合物库 高选择性抑制剂库 抗癌药物库 抑制剂库 酪氨酸激酶分子库 口服活性化合物库 ReFRAME 相关化合物库

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Keywords

Mirdametinib 391210-10-9 Apoptosis Autophagy MAPK MEK PD325901 PD 0325901 MAPKK Mitogen-activated protein kinase kinase PD-0325901 PD0325901 inhibit MAP2K PD-325901 Inhibitor PD 325901 inhibitor

 

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