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细胞生物学 肿瘤
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MAPK/ERK Pathway 肿瘤生长增殖和凋亡 乳腺癌 前列腺癌 肝癌 胰腺癌 结直肠癌
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MEK
/ Mirdametinib

Mirdametinib {[allProObj[0].p_purity_real_show]}

货号：A370482 同义名： PD0325901; PD325901

Mirdametinib是一种选择性且非ATP竞争性的MEK抑制剂，IC50为0.33 nM。

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There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.

Type HazMat fee for 500 gram (Estimated)
Excepted Quantity USD 0.00
Limited Quantity USD 15-60
Inaccessible (Haz class 6.1), Domestic USD 80+
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Accessible (Haz class 3, 4, 5 or 8), Domestic USD 100+
Accessible (Haz class 3, 4, 5 or 8), International USD 200+
Mirdametinib 化学结构 CAS号：391210-10-9
Mirdametinib 化学结构
CAS号：391210-10-9
Mirdametinib 3D分子结构
CAS号：391210-10-9
Mirdametinib 化学结构 CAS号：391210-10-9
Mirdametinib 3D分子结构 CAS号：391210-10-9
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Mirdametinib 纯度/质量文件 产品仅供科研

货号：A370482 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

全球学术期刊中引用的产品

• Nature, 2025, 645, 793-800. Ambeed. [ A201204 , A444152 , A344107 , A952055 ]
• Cell, 2025. Ambeed. [ A122167 ]
• Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]
• Sig. Transduct. Target. Ther., 2025, 10, 257. Ambeed. [ A104916 ]
• Nat. Nanotechnol., 2025. Ambeed. [ A243018 , A1216705 , A522597 , A125401 , A1355641 ]
更多 >
产品名称 MEK ↓ MEK1 ↓ MEK1/2 ↓ MEK2 ↓ MEK5 ↓ 其他靶点 纯度
Honokiol ✔ 98%
Mirdametinib ++++

MEK, IC50: 0.33 nM

 		99%+
Binimetinib +++

MEK, IC50: 12 nM

 		99%+
BI-847325 ++

MEK1, IC50: 25 nM

 		+++

MEK2, IC50: 4 nM

 		99%+
U0126-EtOH +

MEK1, IC50: 0.07 μM

 		++

MEK2, IC50: 0.06 μM

 		98%
GDC-0623 ++++

MEK1, IC50: 0.13 nM

 		99%+
TAK-733 ++++

MEK1, IC50: 3.2 nM

 		99%+
Trametinib ++++

MEK1, IC50: 0.92 nM

 		++++

MEK2, IC50: 1.8 nM

 		99%+
Selumetinib +++

MEK1, Kd: 99 nM

MEK1, IC50: 14 nM

 		+

MEK2, Kd: 530 nM

 		99%+
CI-1040 ++

MEK1, IC50: 17 nM

 		++

MEK2, IC50: 17 nM

 		99%+
Myricetin ✔ 98%
Refametinib ++

MEK1, IC50: 19 nM

 		++

MEK2, IC50: 47 nM

 		99%+
Cobimetinib +++

MEK1, IC50: 4.2 nM

 		99%+
PD98059 +

MEK1, IC50: 2 μM

 		99%+
SL327 +

MEK1, IC50: 0.18 μM

 		+

MEK2, IC50: 0.22 μM

 		AP-1 98+%
PD318088 ✔ 99%
AZD8330 +++

MEK1/2, IC50: 7 nM

 		99%+
Pimasertib 98%
(E/Z)-BIX02189 ++++

MEK5, IC50: 1.5 nM

 		99%+
(E/Z)-BIX02188 +++

MEK5, IC50: 4.3 nM

 		99%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

Mirdametinib 生物活性

靶点

  • MEK

    MEK, IC50:0.33 nM
描述 MEKs, which are members of the MAPKK family, can activate both ERK1 and ERK2 by catalyzing the phosphorylation on T202/Y204. Also MEK itself can be phosphorylated and activated through Ras when the upstream signaling is activated by extracellular stimuli, including growth factors, hormones etc.. PD0325901 is a MEK1/2 with IC50 value of 0.33nM[1]. PD0325901 showed more potency to cell lines harboring BRAF-mutation , including SKMEL28, SKMEL3, SKMEL19, SKMEL1, MALME3M, Colo205 and DU4475, with IC50 values below 10nM, compared with RAS/BRAF-WT cells with IC50>100nM. Meanwhile, dose-dependent decreased p-ERK and Cyclin D1 by PD0325901 can also be observed in these BRAF-mutant cells at concentration>10nM. These suggested that the BRAF mutation may confer the preferential sensitivity of cell lines to MEK inhibition by PD0325901. Consistent with the cellular studies, oral administration with PD0325901 suppressed the tumor growth in mice xenograft SKMEL28 harboring BRAF-V600E mutation at both dose of 5mg/kg and 25mg/kg, accompanied with decrease of p-ERK, Cyclin D1, RB and increased p27. In contrast, treatment with PD0325901 suppressed tumor growth in SKMEL31 (RAS/RAF-WT) xenografts only at high dose (25mg/kg) or even showed no effect in BT-474 (RAS/RAF-WT) xenografts at both dose, regardless the decreased p-ERK by PD0325901[2]. Also it is found that PD0325901 can enhance generation of iPSCs[3].
作用机制 PD0325901 is a derivative of CI-1040, which is a non-competitive inhibitor of MEK1/2.[2]

Mirdametinib 细胞实验

Cell Line
Concentration Treated Time Description References
WU-225 10 µM 2 h Evaluate the inhibitory effect of Mirdametinib on WU-225 microtissues, results showed that Mirdametinib significantly inhibited the growth of WU-225 microtissues. Neuro Oncol. 2023 Nov 2;25(11):2044-2057.
JH-2-079-c 10 µM 2 h Evaluate the inhibitory effect of Mirdametinib on JH-2-079-c microtissues, results showed that Mirdametinib significantly inhibited the growth of JH-2-079-c microtissues. Neuro Oncol. 2023 Nov 2;25(11):2044-2057.
JH-2-002 10 µM 2 h Evaluate the inhibitory effect of Mirdametinib on JH-2-002 microtissues, results showed that Mirdametinib significantly inhibited the growth of JH-2-002 microtissues. Neuro Oncol. 2023 Nov 2;25(11):2044-2057.
MN-2 10 µM 2 h Evaluate the inhibitory effect of Mirdametinib on MN-2 microtissues, results showed that Mirdametinib significantly inhibited the growth of MN-2 microtissues. Neuro Oncol. 2023 Nov 2;25(11):2044-2057.
K562-R cells 0.5 μM 3 h Mirdametinib significantly increased ATO-induced cell death in TKI-resistant primary blasts derived from patients with CML or ALL. Leukemia. 2023 Aug;37(8):1671-1685.
Ba/F3p210T315I cells 0.5 μM 3 h The combination of Mirdametinib and ATO synergistically induced apoptosis in all tested cell lines, regardless of their sensitivity to TKIs. Leukemia. 2023 Aug;37(8):1671-1685.
JHH-136 10 nM 72 h To evaluate the effect of Mirdametinib combined with radiation, results showed that combined therapy significantly inhibited cell growth and sphere formation in NF1-deficient neurospheres. Mol Cancer Ther. 2024 Sep 4;23(9):1261-1272.
HSR-GBM1 10 nM 72 h To evaluate the effect of Mirdametinib combined with radiation, results showed that combined therapy significantly inhibited cell growth and sphere formation in NF1-deficient neurospheres. Mol Cancer Ther. 2024 Sep 4;23(9):1261-1272.
Calu-6 3 µM BGB-283 significantly enhanced the antiproliferative activity of PD-0325901, with a 59-fold decrease in EC50. Mol Oncol. 2020 Aug;14(8):1833-1849.

Mirdametinib 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Mice NRG mice Oral 1.5 mg/kg Daily for 5-6 weeks Evaluate the inhibitory effect of Mirdametinib on MPNST tumor growth in NRG mice, results showed that Mirdametinib significantly inhibited tumor growth. Neuro Oncol. 2023 Nov 2;25(11):2044-2057.
Mice BCR::ABL1-T315I-induced leukemia model Oral 10 mg/kg Continued for 3 weeks The combination of Mirdametinib and ATO significantly prolonged the survival of mice bearing BCR::ABL1-T315I-induced leukemia and reduced tumor cell infiltration. Leukemia. 2023 Aug;37(8):1671-1685.
Mice BTBR mice Intraperitoneal injection 1 mg/kg, 10 mg/kg, 25 mg/kg Once daily for 11 days To evaluate the effects of Mirdametinib on core symptoms of autism. Results showed that Mirdametinib dose-dependently reduced social deficits, vocalization abnormalities, and repetitive behaviors in BTBR mice, and reversed abnormal EEG signals. EBioMedicine. 2023 May;91:104565
NSG mice Heterotopic xenograft models Oral gavage 1.5 mg/kg Twice daily for 4 weeks To evaluate the effect of Mirdametinib combined with radiation, results showed that combined therapy significantly inhibited tumor growth in NF1-deficient heterotopic xenograft models. Mol Cancer Ther. 2024 Sep 4;23(9):1261-1272.
Mice Calu-6 NSCLC xenograft model Oral 25 mg/kg Twice daily for 28 days The combination of BGB-283 and selumetinib showed enhanced antitumor efficacy in suppressing tumor growth and resulted in partial and complete tumor regression. Mol Oncol. 2020 Aug;14(8):1833-1849.

Mirdametinib 动物研究

Dose Pig: 0.79 mg/kg[4] (p.o.)
Mice: 0.5 mg/kg, 1 mg/kg[5] (i.p.), 1.5 mg/kg - 10 mg/kg[6] (p.o.), 25 mg/kg[7] (p.o.)
Rat: 10 mg/kg - 100 mg/kg[8] (i.v., p.o.)
Administration p.o., i.p., i.v.
Pharmacokinetics
Animal Rats[8]
Dose 30 mg/kg (i.v. or p.o.)
Administration i.v.
p.o.
Cmax 129 µg/ml (i.v.)
16.9 µg/ml (p.o.)
Tmax 1 h (p.o.)
AUC0→24h 148 µg·h/ml (i.v..)
82.7 µg·h/ml (p.o.)

Mirdametinib 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT03170206 Lung Cancer Phase 1 Phase 2 Recruiting March 31, 2024 United States, Massachusetts ... 展开 >> Dana Farber Cancer Institute Recruiting Boston, Massachusetts, United States, 02215 Contact: Geoffrey Shapiro, MD, PhD    617-632-4942       Principal Investigator: Geoffrey Shapiro, MD          Massachusetts General Hospital Not yet recruiting Boston, Massachusetts, United States, 02215 Contact: Rebecca Heist, MD    617-726-1838       Principal Investigator: Rebecca Heist, MD 收起 <<
NCT02510001 Solid Tumor C... 展开 >>olorectal Cancer 收起 << Phase 1 Active, not recruiting September 2019 United Kingdom ... 展开 >> Oxford University Hospital NHS Trust Oxford, United Kingdom, OX3 7LE 收起 <<
NCT01347866 - Terminated(Refer to Detailed D... 展开 >>escription for documentaion of Termination Statement.) 收起 << - -

Mirdametinib 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.07mL

0.41mL

0.21mL

10.37mL

2.07mL

1.04mL

20.74mL

4.15mL

2.07mL

Mirdametinib 技术信息

CAS号391210-10-9
分子式C16H14F3IN2O4
分子量 482.19
SMILES Code O=C(C1=CC=C(C(F)=C1NC2=CC=C(I)C=C2F)F)NOC[C@H](O)CO
MDL No. MFCD08435926
别名 PD0325901; PD325901
运输蓝冰
InChI Key SUDAHWBOROXANE-SECBINFHSA-N
Pubchem ID 9826528
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, 2-8°C
溶解方案

DMSO: 55 mg/mL(114.06 mM)，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议现用现配，当天使用； 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶
方案 一
方案 二
方案 三

Tags: Mirdametinib | 391210-10-9 | PD0325901 | PD325901 | PD 0325901 | PD-0325901 | PD325901 | PD 325901 | PD-325901 | MEK Inhibitor | MAPK/ERK Pathway | MEK | 仅供科研使用 | AmBeed-信号通路专用抑制剂 | Mirdametinib 纯度/质量文件 | Mirdametinib 亚型比较 | Mirdametinib 生物活性 | Mirdametinib 动物研究 | Mirdametinib 临床数据 | Mirdametinib 实验方案 | Mirdametinib 技术信息

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