2. PROTAC MAPK/ERK Pathway Cell Cycle/DNA Damage GPCR/G Protein Apoptosis
  3. Molecular Glues MEK Raf PERK Ras p38 MAPK Apoptosis
  4. MEK-IN-10

MEK-IN-10 是一种具有口服活性的泛 MEK/RAF 非降解分子胶 (molecular glue)，对人源 MEK1 的 IC50 为 782 nM。MEK-IN-10 可阻断 MEK 和 ERK 的磷酸化，诱导并稳定 MEK1-RAF 复合物，同时破坏 RAS-MAPK 信号通路。MEK-IN-10 诱导癌细胞发生凋亡 (apoptosis)，将细胞阻滞于 G0/G1 期。MEK-IN-10 在小鼠异种移植模型中可诱导肿瘤生长抑制。MEK-IN-10 可用于 RAS 驱动型癌症，如结直肠癌、胰腺癌的研究。

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MEK-IN-10

MEK-IN-10 Chemical Structure

CAS No. : 3096958-11-8

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MEK-IN-10 相关抗体

Top Publications Citing Use of Products

查看 MEK 亚型特异性产品:

查看所有亚型
MEK1 MEK2 MEK5 MEK MAP2K4/MEK4

查看 Raf 亚型特异性产品:

查看所有亚型
B-Raf C-Raf Raf

查看 Ras 亚型特异性产品:

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K-Ras H-Ras N-Ras Ras

查看 p38 MAPK 亚型特异性产品:

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

MEK-IN-10 is an orally active pan-MEK/RAF non-degrading molecular glue with an IC50 of 782 nM against human MEK1. MEK-IN-10 blocks the phosphorylation of MEK and ERK, induces and stabilizes the MEK1-RAF complex, and disrupts the RAS-MAPK signaling pathway. MEK-IN-10 induces apoptosis in cancer cells and arrests cells at the G0/G1 phase. MEK-IN-10 induces tumor growth inhibition in mouse xenograft models. MEK-IN-10 can be used in the research of RAS-driven cancers, such as colorectal cancer and pancreatic cancer[1].

IC50 & Target[1]

MEK1

782 nM (IC50)

体外研究
(In Vitro)

MEK-IN-10 (D56) 可强效抑制 AsPC-1、MIA PaCa-2、HCT116、OCI-AML-3 和 HT-29 细胞的增殖，IC50 分别为 0.42、3.48、2.27、0.23、2.63 nM[1]。
MEK-IN-10 (0-100 nM; 0-96 h) 可强效且持久地抑制 AsPC-1 细胞中的 p-MEK (IC50 = 0.379 nM) 与 p-ERK (IC50 = 0.015 nM)[1]。
MEK-IN-10 (0.01-10000 nM，60 min) 可作为分子胶水，在无细胞 TR-FRET 实验中强效稳定 MEK1-BRAF 复合物 (EC50 = 2.37 nM) 和 MEK1-CRAF 复合物 (EC50 = 11.95 nM)[1]。
MEK-IN-10 (10 nM; 4 h) 可增强 HCT116 细胞中 MEK-BRAF 复合物的形成[1]。
MEK-IN-10 (1-100 nM，10 天) 可呈剂量依赖性抑制 HCT116 和 AsPC-1 细胞的长期集落形成[1]。
MEK-IN-10 (0-100 nM; 48 h) 诱导 AsPC-1、HCT116 和 OCI-AML-3 细胞发生凋亡，将细胞阻滞于 G0/G1 期[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

MEK-IN-10 相关抗体:

Apoptosis Analysis[1]

Cell Line: AsPC-1, HCT116 and OCI-AML-3 cells
Concentration: 0-100 nM
Incubation Time: 48 h
Result: Induced a dose-dependent increase in apoptotic cells: in AsPC-1 cells, the apoptotic population rose from 7.01% to 17.02%; in HCT116 cells, it rose from 17.08% to 76.0%.
Induced apoptosis in OCI-AML-3 cells.

Cell Cycle Analysis[1]

Cell Line: AsPC-1, HCT116 and OCI-AML-3 cells
Concentration: 0-100 nM
Incubation Time: 48 h
Result: Induced dose-dependent accumulation of cells in the G0/G1 phase: in AsPC-1 cells, the G0/G1 population rose from 60.81% to 88.15%; in HCT116 cells, it rose from 42.42% to 75.2%.
Induced G0/G1 phase arrest in OCI-AML-3 cells.

Western Blot Analysis[1]

Cell Line: AsPC-1 cells
Concentration: 0, 0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30, 100 nM
Incubation Time: 4 h
Result: Inhibited p-MEK (IC50 = 0.379 nM) and p-ERK (IC50 = 0.015 nM).

Western Blot Analysis[1]

Cell Line: AsPC-1 cells
Concentration: 3 nM
Incubation Time: 0, 0.25, 1, 4, 8, 24, 48, 72, 96 h
Result: Sustained suppression of both
p-MEK and p-ERK for over 96 h.
药代动力学
(Parmacokinetics)
Species Dose Route AUC0-t MRT0-t T1/2 CL Vss Cmax Tmax
Mice[1] 5 mg/kg p.o. 417.294 μg/L·h 1.668 h 1.731 h 12.228 L/h/kg 33.921 L/kg 238.628 μg/L 0.333 h
体内研究
(In Vivo)

MEK-IN-10 (1-10 mg/kg，口服，隔日 1 次×21-28 天) 可抑制 AsPC-1 (KRASG12D) 和 HCT116 (KRASG13D) 模型小鼠的肿瘤体积增长[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: AsPC-1 (KRASG12D) model mice[1]
Dosage: 1, 3, 10 mg/kg
Administration: p.o., QOD×28
Result: Inhibited tumor volume growth in a dose-dependent manne.
Exhibited obvious antitumor effects and the TGI rate was
79% at 10 mg/kg.
Significantly suppressed p-
ERK expression.
Animal Model: HCT116 (KRASG13D) model mice[1]
Dosage: 1, 3 mg/kg
Administration: p.o., QOD×21
Result: Significantly inhibited tumor growth with TGI rates of 78% and 86%, respectively at 1 and 3 mg/kg.
Significantly suppressed p-
ERK expression.
分子量

521.95

Formula

C22H21ClFN5O5S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

MEK-IN-10 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
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Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

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浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

MEK-IN-103096958-11-8Molecular GluesMEKRafPERKRasp38 MAPKApoptosisMitogen-activated protein kinase kinaseMAPKKMAP2KRaf kinasesProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinasemouse xenograft modelsRAS-MAPK signaling pathwayHCT116ERKBRAFAsPC-1MEK1OCI-AML-3MIA PaCa-2ras-driven cancersInhibitorinhibitorinhibit

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