Cat. No.: HY-15202

Binimetinib

(Synonyms: MEK162; ARRY-162; ARRY-438162)

52 Cited Publications

Customer Review

Based on 52 publication(s) in Google Scholar

Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

For research use only. We do not sell to patients.

Purity: 99.92%
CAS No.: 606143-89-9
Formula: C₁₇H₁₅BrF₂N₄O₃
Molecular Weight:441.23

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months

Binimetinib Chemical Structure

CAS No.: 606143-89-9

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (52)
Solvent & Solubility
- In Vitro
- In Vivo
Protocol
Purity & Documentation
References
Help & FAQs
Bioz

Biological Activity

Description

Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

IC₅₀ & Target^[1]

MEK

12 nM (IC₅₀)

Autophagy

All MEK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	IC₅₀	1.997 μM Compound: Binimetinib	Antiproliferative activity against human HCT-116 cells harboring KRAS G13D mutant incubated for 72 hrs by CCK8 assay Antiproliferative activity against human HCT-116 cells harboring KRAS G13D mutant incubated for 72 hrs by CCK8 assay	[PMID: 39166848]
MIA PaCa-2	IC₅₀	0.182 μM Compound: Binimetinib	Antiproliferative activity against human MIA PaCa-2 cells harboring KRAS G12C mutant incubated for 72 hrs by CCK8 assay Antiproliferative activity against human MIA PaCa-2 cells harboring KRAS G12C mutant incubated for 72 hrs by CCK8 assay	[PMID: 39166848]
SK-MEL-2	IC₅₀	1 μM Compound: MEK-162	Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of MK2206 by MTT assay Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of MK2206 by MTT assay	[PMID: 36961300]
SK-MEL-2	IC₅₀	1 μM Compound: MEK-162	Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of Rapamycin by MTT assay Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of Rapamycin by MTT assay	[PMID: 36961300]

In Vitro

In MCF7 cells, RSK3 or RSK4 expression decreases response to treatment with any of the PI3K inhibitors alone. However, the combination of PI3K inhibition with Binimetinib (MEK162) or BI-D1870 completely reverses the resistance of RSK-expressing cells^[2]. Binimetinib (MEK162) blocks basal ERK phosphorylation in all HRAS mutant cell lines. The combination of RAD001 and AZD6244/MEK162 causes a stronger inhibition of S6 kinase than single use of RAD001 on Western blot. The combination of RAD001 and AZD6244/MEK162 also translated in a stronger blockade of cell growth in HRAS mutant cells than single use. Binimetinib (MEK162) shows stronger synergism with RAD001 than AZD6244^[3].

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

In Vivo

Treatment with Binimetinib (ARRY-438162) reduces disease severity in a dose-related manner in both animal models. ARRY-438162 in the CIA model inhibits increases in ankle diameter by 27% and 50% at 1 and 3 mg/kg, while Ibuprofen has 46% inhibition. When combined with Ibuprofen, these same two doses result in 74% and 72% inhibition, respectively. Microscopic examination of the ankle joints show Binimetinib (ARRY-438162) significantly inhibits lesions (inflammation, cartilage damage, pannus formation and bone resorption) by 32% and 60% at 1 and 3 mg/kg, while treatment with Ibuprofen alone results in 17% inhibition, which is not significantly different from the controls. When these two doses of Binimetinib (ARRY-438162) are combined with ibuprofen, the result is 54% and 77% inhibition of joint destruction. In AIA, 3 and 10 mg/kg of Binimetinib (ARRY-438162) inhibit AIA ankle diameter 11% and 34%, while MTX has 33% inhibition. When combined with MTX, 3 and 10 mg/kg of Binimetinib (ARRY-438162) result in 55% and 71% inhibition. Microscopic examination of ankle joints for inflammation and bone resorption also shows improved efficacy versus either compound alone^[1]. When Binimetinib (MEK162) is combined with BEZ235, a significant reduction of tumor growth is observed (P=0.01). This increase in antitumor activity is accompanied by a decrease in phospho-ERK and phospho-S6 staining. No significant changes are observed in phospho-4EBP1 staining, a direct target of mTOR activity^[2].

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

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 606143-89-9
Appearance Solid
Molecular Weight 441.23
Formula C₁₇H₁₅BrF₂N₄O₃
Color White to off-white
SMILES

BrC1=CC=C(C(F)=C1)NC2=C(C3=C(C=C2C(NOCCO)=O)N(C=N3)C)F
Synonyms

MEK162; ARRY-162; ARRY-438162
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	1 year
	-20°C	6 months

Publications (52)

All WB

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Journal Impact Factor

Cancer Cell

Neurofibromin Is an Estrogen Receptor-α Transcriptional Co-repressor in Breast Cancer. [Abstract]

2020 Mar 16;37(3):387-402.e7. PMID: 32142667
Cell Stem Cell

Leukemic stem cell subtypes determine venetoclax resistance and therapeutic vulnerabilities in AML. [Abstract]

2026 Jun 4;33(6):982-999.e8. PMID: 42102807
Cancer Res

Activity and Resistance of a Brain-Permeable Paradox Breaker BRAF Inhibitor in Melanoma Brain Metastasis. [Abstract]

2022 Jul 18;82(14):2552-2564. PMID: 35584009
Bone Res

The HOXC10/NOD1/ERK axis drives osteolytic bone metastasis of pan-KRAS-mutant lung cancer. [Abstract]

2024 Aug 27;12(1):47. PMID: 39191757
Sci Transl Med

PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]

2018 Jul 18;10(450):eaaq1093. PMID: 30021885
Adv Sci (Weinh)

EGR Proteins Mediate Interferon-Independent Anti-HSV-1 Responses Through Viral and Host Targets. [Abstract]

2026 Mar;13(13):e15546. PMID: 41486724
Adv Sci (Weinh)

Lactylation of HDAC1 Confers Resistance to Ferroptosis in Colorectal Cancer. [Abstract]

2025 Jan 31:e2408845. PMID: 39888307
Adv Sci (Weinh)

Microfluidic Organoid Cultures Derived from Pancreatic Cancer Biopsies for Personalized Testing of Chemotherapy and Immunotherapy. [Abstract]

2024 Feb;11(5):e2303088. PMID: 38018486
Nat Chem Biol

MEK interactions tune RAF kinase sensitivity to conformation-selective inhibition. [Abstract]

2026 May 12:10.1038/s41589-026-02212-2. PMID: 42120500
Neuro Oncol

Preclinical assessment of MEK1/2 inhibitors for neurofibromatosis type 2-associated schwannomas reveals differences in efficacy and drug resistance development. [Abstract]

2019 Mar 18;21(4):486-497. PMID: 30615146
Sci Adv

Gain-of-function mutations in the catalytic domain of DOT1L promote lung cancer malignant phenotypes via the MAPK/ERK signaling pathway. [Abstract]

2023 Jun 2;9(22):eadc9273. PMID: 37256945
J Immunother Cancer

Tempered signal strength via low-dose MEK inhibition optimizes therapeutic performance of engineered T cells. [Abstract]

2025 Dec 1;13(12):e012800. PMID: 41330614
Clin Cancer Res

Triple Combination of MEK, BET, and CDK Inhibitors Significantly Reduces Human Malignant Peripheral Nerve Sheath Tumors in Mouse Models. [Abstract]

2025 Mar 3;31(5):907-920. PMID: 39786423
Clin Cancer Res

Precision Oncology and Systemic Targeted Therapy in Pseudomyxoma Peritonei. [Abstract]

2024 Sep 13;30(18):4082-4099. PMID: 39018564
Cancer Lett

Targeting the EphB4 receptor tyrosine kinase sensitizes HER2-positive breast cancer cells to Lapatinib. [Abstract]

2020 Apr 10;475:53-64. PMID: 32006616
Cell Syst

Receptor-Driven ERK Pulses Reconfigure MAPK Signaling and Enable Persistence of Drug-Adapted BRAF-Mutant Melanoma Cells. [Abstract]

2020 Nov 18;11(5):478-494.e9. PMID: 33113355
J Transl Med

Personalized medicine strategy for MPNSTs: using precision oncology on PDOX models to inform tumor boards. [Abstract]

2026 Feb 4;24(1):385. PMID: 41639724
Oncogene

PIK3CA(H1047R)- and Her2-initiated mammary tumors escape PI3K dependency by compensatory activation of MEK-ERK signaling. [Abstract]

2016 Jun 9;35(23):2961-70. PMID: 26640141

Binimetinib purchased from MedChemExpress. Usage Cited in: Oncogene. 2016 Jun 9;35(23):2961-70. [Abstract]

The combined use of MEK162 with HER kinase inhibitor GW572016, almost completely abolishes MAPK signaling as evidenced by diminished phospho-Erk levels. Western blot analyses of ERK signaling in tumor transplants from mice treated as indicated. Three hours after their dose on day four of treatment, the mice are sacrificed for analysis. Vinculin is used as a loading control.
Cell Rep

Biased signaling by mutant EGFR underlies dependence on PKCα in lung adenocarcinoma. [Abstract]

2024 Dec 3;43(12):115026. PMID: 39630579
Sci Data

High-throughput drug screening identifies novel therapeutics for Low Grade Serous Ovarian Carcinoma. [Abstract]

2024 Sep 19;11(1):1024. PMID: 39300112
Sci Signal

Activating mutations in MEK1 enhance homodimerization and promote tumorigenesis. [Abstract]

2018 Oct 30;11(554):eaar6795. PMID: 30377225
Mol Cancer Ther

Concurrent inhibition of ICMT and RAF/MEK suppresses RAC1P29S-driven MAPK-pathway-inhibitor resistance in BRAFV600E melanoma by regulating TAZ activity. [Abstract]

2026 Jun 24. PMID: 42338299
Mol Cancer Ther

Mosperafenib, a novel paradox breaker BRAF inhibitor with potent preclinical activity in BRAF mutated colorectal cancer. [Abstract]

2025 Dec 4. PMID: 41340484
Pharmaceutics

A Dual-Payload Bispecific ADC Improved Potency and Efficacy over Single-Payload Bispecific ADCs. [Abstract]

2025 Jul 25;17(8):967. PMID: 40870990
Commun Biol

The identification of functional regions of MEK1 using CRISPR tiling screens. [Abstract]

2025 Apr 24;8(1):656. PMID: 40274952
Cancer Immunol Immunother

Antitumor effects of immunotherapy combined with BRAF and MEK inhibitors in BRAF V600E metastatic colorectal cancer. [Abstract]

2025 Mar 19;74(5):154. PMID: 40105971
Int J Mol Sci

Triple Blockade of Oncogenic RAS Signaling Using KRAS and MEK Inhibitors in Combination with Irradiation in Pancreatic Cancer. [Abstract]

2024 Jun 6;25(11):6249. PMID: 38892436
Eur J Pharm Sci

Biophysical and docking study on the interaction of anticancer drugs encorafenib and binimetinib with human serum albumin. [Abstract]

2023 Oct 1:189:106550. PMID: 37527692
Molecules

A Rapid and Sensitive Liquid Chromatography-Tandem Mass Spectrometry Bioanalytical Method for the Quantification of Encorafenib and Binimetinib as a First-Line Treatment for Advanced (Unresectable or Metastatic) Melanoma-Application to a Pharmacokinetic Study. [Abstract]

2022 Dec 22;28(1):79. PMID: 36615272
Molecules

A Validated LC-MS/MS Assay for the Simultaneous Quantification of the FDA-Approved Anticancer Mixture (Encorafenib and Binimetinib): Metabolic Stability Estimation. [Abstract]

2021 May 5;26(9):2717. PMID: 34063139
Cell Rep Methods

Tumor immune microenvironment reconstitution in patient-derived organoids enables therapy modeling for NSCLC. [Abstract]

2026 Jun 15;6(6):101339. PMID: 42134319
iScience

Possible involvement of a MEG3-miR-21-SPRY1-NF-κB feedback loop in spermatogenic cells proliferation, autophagy, and apoptosis. [Abstract]

2024 Sep 10;27(10):110904. PMID: 39398251
Comput Struct Biotechnol J

Unveiling the Kinomes of Leishmania infantum and L. braziliensis Empowers the Discovery of New Kinase Targets and Antileishmanial Compounds. [Abstract]

2019 Feb 8:17:352-361. PMID: 30949306
Chem Res Toxicol

Binimetinib Is a Potent Reversible and Time-Dependent Inhibitor of Cytochrome P450 1A2. [Abstract]

2021 Apr 19;34(4):1169-1174. PMID: 33728909
Mol Pharmacol

Influence of Tyrosine Kinase Inhibition on Organic Anion Transporting Polypeptide 1B3-Mediated Uptake. [Abstract]

2022 Jun;101(6):381-389. PMID: 35383108
Pigment Cell Melanoma Res

Immunoregulatory protein B7-H3 promotes growth and decreases sensitivity to therapy in metastatic melanoma cells. [Abstract]

2017 Sep;30(5):467-476. PMID: 28513992
Bioanalysis

LC-MS/MS bioanalytical method for quantification of binimetinib and venetoclax, and their pharmacokinetic interaction. [Abstract]

2022 Jan;14(2):75-86. PMID: 34841894
Charles University

2026.
University of Pennsylvania

2025.
State University of New York at Stony Brook

2025.
Patent

US20250161243A1.
Hong Kong Polytechnic University

2025.
bioRxiv

Capacity for compensatory cyclin D2 response confers trametinib resistance in canine mucosal melanoma. [Abstract]

2025 Apr 26:2025.04.24.650512. PMID: 40568110
Patent

US20240366605A1
Patent

US20240366605A1.
bioRxiv

2024 September 19.
McGill University

2023 Dec.
bioRxiv

2019 Sep.
Patent

US20180263995A1.
Oncotarget

ERK inhibition sensitizes CZ415-induced anti-osteosarcoma activity in vitro and in vivo. [Abstract]

2017 May 30;8(47):82027-82036. PMID: 29137241

Binimetinib purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 May 30;8(47):82027-82036. [Abstract]

U0126 and MEK162 block ERK activation (p-ERK1/2) in CZ415-treated U2OS cells.
Oncotarget

MEK inhibition is a promising therapeutic strategy for MLL-rearranged infant acute lymphoblastic leukemia patients carrying RAS mutations. [Abstract]

2017 Feb 28;8(9):14835-14846. PMID: 27588400

Binimetinib purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Feb 28;8(9):14835-14846. [Abstract]

MEK inhibition results in reduced ERK phosphorylation.A. Western blot analysis of SEM and KOPN8 exposed to 500 nM of MEK inhibitor or vehicle control (DMSO) for 6, 24 and 48 hours. Both cell lines almost completely lose ERK phosphorylation (p-ERK), while total ERK (t-ERK) levels remain unaffected. B. Analysis of MEK phosphorylation (p-MEK) suggests exposure to MEK162 and Selumetinib results in enhanced MEK phosphorylation in both cell lines, whereas total MEK (t-MEK) levels remain constant.
Oncotarget

Fibroblast-induced switching to the mesenchymal-like phenotype and PI3K/mTOR signaling protects melanoma cells from BRAF inhibitors. [Abstract]

2016 Apr 12;7(15):19997-20015. PMID: 26918352

Solvent & Solubility

In Vitro:

DMSO : 50 mg/mL (113.32 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.2664 mL

11.3320 mL

22.6639 mL

5 mM

0.4533 mL

2.2664 mL

4.5328 mL

10 mM

0.2266 mL

1.1332 mL

2.2664 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Molarity Calculator

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

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Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline