1. MAPK/ERK Pathway
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  3. Binimetinib

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

Cat. No.: HY-15202 Purity: 99.55%
Handling Instructions

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.

Binimetinib Chemical Structure

Binimetinib Chemical Structure

CAS No. : 606143-89-9

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10 mM * 1 mL in DMSO USD 79 In-stock
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Customer Review

Based on 18 publication(s) in Google Scholar

Top Publications Citing Use of Products

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

    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.

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

    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.

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

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

    Binimetinib purchased from MCE. Usage Cited in: Sci Signal. 2018 Oct 30;11(554). pii: eaar6795. 

    MEK1 mutants with in-frame deletions of the β3-αC loop exhibit differential resistance to MEK inhibitors (GSK1120212, GDC0623, cobimetinib, AZD6244, and binimentinib).

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

    IC50 & Target[1]


    12 nM (IC50)



    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].

    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].

    Clinical Trial
    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 50 mg/mL (113.32 mM; Need ultrasonic)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    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.
    In Vivo:
    • 1.

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

      Solubility: ≥ 2.5 mg/mL (5.67 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (5.67 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (5.67 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Cell Assay

    MCF7 cells infected as indicated are seeded in 12-well plates (2×104). After 24 hours, cells are treated with BEZ235 (100 or 200 nM), BKM120 (0.75 or 1 μM), GDC-0941 (1 μM), or MK2206 (2 μM) alone or in combination with Binimetinib (MEK162) (1 μM), BI-D1870 (10 μM), or AZD6244 (1 μM), as indicated in text. Cell numbers are quantified by fixing cells with 4% glutaraldehyde or methanol, washing the cells twice in H2O, and staining the cells with 0.1% crystal violet. The dye is subsequently extracted with 10% acetic acid, and its absorbance is determined (570 nm). Growth curves are performed in triplicate. Viability assays with CellTiter-Glo are performed by plating 2,000 cells in 96-well plates, adding the drug at 24 hours, and assaying 4 to 5 days after drug addition. Cell-cycle and hypodiploid apoptotic cells are quantified by flow cytometry. Briefly, cells are washed with PBS, fixed in cold 70% ethanol, and then stained with propidium iodide while being treated with RNase. Quantitative analysis of sub-G1 cells is carried out in a FACScalibur cytometer using Cell Quest software[2].

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

    Animal Administration

    Six-week-old female athymic nude Foxn1nu mice are used. Mice are treated once daily with placebo, BEZ235, BKM120, MK-2206, or Binimetinib (MEK162) by oral gavage. BEZ235 (25-30 mg/kg, 6IW [6 days on 1 day off]) and BKM120 (30 mg/kg, 6IW) are dissolved in 10% NMP-90% PEG, freshly formulated, and administrated within 30 minutes. MK-2206 (100 mg/kg, 3IW) is formulated in 30% Captisol and Binimetinib (MEK162) (6 mg/kg, BID) in 0.5% Tween-80, 1% carboxymethyl cellulose. For tumor growth studies, mice are treated for 7-24 days, depending on the xenograft model and treatment regime. Tumor xenografts are measured with calipers 3 times a week, and tumor volume is determined using the following formula: (length×width2)×(π/6). At the end of the experiment, the animals are anesthetized with 1.5% isofluorane-air mixture and killed by cervical dislocation. Tumors are removed 2 hours following the last administration.
    Rat collagen-induced arthritis (CIA) and rat adjuvant-induced arthritis (AIA) models are used to determine efficacy in the subacute inflammation setting. In the CIA studies, rats with established disease, induced by injections of Type II collagen, are treated with 0.3, 1 or 3 mg/kg ARRY-438162 (PO, BID) with or without 30 mg/kg ibuprofen (PO, QD) for six days. Body weight and ankle diameter are used to monitor disease progression on days 0-7. The AIA model is induced by an injection of a lipoidal amine in FCA on day 0. The AIA rats are treated with 1, 3 or 10 mg/kg Binimetinib (ARRY-438162) (PO, QD) beginning on day 8 and continuing for 6 days, with or without the addition of 0.05 mg/kg CL14377 (PO, QD) which is dosed days 0-13. Disease progression is monitored on days 7-14 measuring both paw diameter and body weight.

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


    Purity: 99.55%

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    BinimetinibMEK162ARRY-162ARRY-438162MEK 162MEK-162ARRY162ARRY 162ARRY438162ARRY 438162MEKAutophagyMitogen-activated protein kinase kinaseMAPKKMAP2KInhibitorinhibitorinhibit

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