Binimetinib (MEK162)

For research use only.

Catalog No.S7007 Synonyms: ARRY-162,ARRY-438162

62 publications

Binimetinib (MEK162) Chemical Structure

CAS No. 606143-89-9

Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Binimetinib induces G1 cell cycle arrest and apoptosis in human NSCLC cell lines and induces autophagy. Phase 3.

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Selleck's Binimetinib (MEK162) has been cited by 62 publications

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Description Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Binimetinib induces G1 cell cycle arrest and apoptosis in human NSCLC cell lines and induces autophagy. Phase 3.
MEK [1]
(Cell-free assay)
12 nM
In vitro

ARRY-438162 (625 nM) inhibits in vitro osteoclast differentiation with IC50 of 39 nM. ARRY-438162 (10 μM) inhibits in vitro osteoclast resorption with IC50 of 625 nM. ARRY-438162 (2 μM) weakly affects osteoblast differentiation. [2] ARRY-438162 is a recently disclosed potent and selective ATP non-competitive MEK1/2 inhibitor, inhibits pERK in cells with an IC50 of11 nM. [3] MEK162 (1 μM) combined with MK-2206 (2 μM) completely reverses the resistance of RSK-expressing MCF7 cells. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NCI-H727 NInPXZFHfW6ldHnvckBie3OjeR?= M3exSWlEPTB;MUG1JI5O M1LjSFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyM{WyOVY2Lz5|MEO1NlU3PTxxYU6=
Mel IL NVP2[XNsS3m2b4TvfIlkcXS7IHHzd4F6 NUTkb|lEUUN3ME2zMlchyrFiMD6yJO69VQ>? MnvyQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzB3NUG1NVUoRjNyNUWxOVE2RC:jPh?=
Mel IL/R MXvDfZRwfG:6aXPpeJkh[XO|YYm= NGftOYFKSzVyPUKuO{DDuSByLkOg{txO NVOwOnh5RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{C1OVE2OTVpPkOwOVUyPTF3PD;hQi=>
Mel Z M2rleWN6fG:2b4jpZ4l1gSCjc4PhfS=> M3W2e2lEPTB;Mz64JOKyKDBwMjFOwG0> MX68ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8{ODV3MUWxOUc,OzB3NUG1NVU9N2F-
A375 Ml\DR5l1d3SxeHnjbZR6KGG|c3H5 NVTJe2NiUUN3ME25MlghyrFiMD6xJO69VQ>? M1zSUlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyNUWxOVE2Lz5|MEW1NVUyPTxxYU6=
Mel Me M1WwN2N6fG:2b4jpZ4l1gSCjc4PhfS=> NGX3RnRKSzVyPUGzMlMhyrFiMD6zJO69VQ>? MUK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8{ODV3MUWxOUc,OzB3NUG1NVU9N2F-
Mel MTP NI\GenBEgXSxdH;4bYNqfHliYYPzZZk> MVzJR|UxRTFyLkKgxtEhOC52IN88US=> MWq8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8{ODV3MUWxOUc,OzB3NUG1NVU9N2F-
U2OS cells NWjHW5ZETnWwY4Tpc44h[XO|YYm= M3m4bVEh|ryP NY\X[IVKVUWNMU[yJIJtd2OtZXSgSXJMKGGldHn2ZZRqd25iKICtSXJMOS9{KTDpckBEYjRzNT30doVifGWmIGWyU3Mh[2WubIO= M2njNVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7MUO3NlQyLz5{OUGzO|I1OTxxYU6=
CHP-212 MXzD[YxtKH[rYXLpcIl1gSCjc4PhfS=> NV\NUJp7OTJywrDo Ml\DTWM2OD1yLkCwPFMh|ryP MmqzQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
SK-N-AS MV;D[YxtKH[rYXLpcIl1gSCjc4PhfS=> NFe3VncyOjEEoHi= MojzTWM2OD1yLkC2O{DPxE1? NHXWXVY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkmyOVg1OSd-Mk[5NlU5PDF:L3G+
SK-N-BE(2) NH\CUmdE\WyuII\pZYJqdGm2eTDhd5NigQ>? M{W4dFEzOMLiaB?= Moe3TWM2OD1yLkK4JO69VQ>? NYTNSnlMRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[5NlU5PDFpPkK2PVI2QDRzPD;hQi=>
SJ-NB-10 MWLD[YxtKH[rYXLpcIl1gSCjc4PhfS=> MYKxNlDDqGh? MUnJR|UxRTFwMU[g{txO MmfVQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
CHP-134 MU\D[YxtKH[rYXLpcIl1gSCjc4PhfS=> M{XDZlEzOMLiaB?= NUTjOG57UUN3ME6xOUDPxE1? NX;pVHFvRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[5NlU5PDFpPkK2PVI2QDRzPD;hQi=>
Kelly MUTD[YxtKH[rYXLpcIl1gSCjc4PhfS=> NX23OFRbOTJywrDo NYDibok1UUN3ME6xOUDPxE1? Mm\5QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
LAN-5 M4G2UmNmdGxidnnhZoltcXS7IHHzd4F6 MYixNlDDqGh? MoXCTWM2OD5zNTFOwG0> MkTQQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
NGP MUXD[YxtKH[rYXLpcIl1gSCjc4PhfS=> M2LiVlEzOMLiaB?= NVLqSYpjUUN3ME6xOUDPxE1? MnjWQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
SK-N-DZ M2nr[WNmdGxidnnhZoltcXS7IHHzd4F6 M3\wfVEzOMLiaB?= MlHSTWM2OD5zNTFOwG0> MoDVQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ7MkW4OFEoRjJ4OUK1PFQyRC:jPh?=
A549 NX\oToJKS2WubDDjfYNt\SCjc4PhfS=> NWrGTFloOCxiMD61MEAyKM7:TR?= NFr1RWs1QGh? M3O0fYF1KHKnbHH0bZZmdHlibH;3JINwdmOnboTyZZRqd25icnHu[4V{KOLLpDCxJO69VSBqZT7nMkwhOC53IHHu[EAyKM7:TTmgbY5lfWOnZDDHNUBienKnc4S= NX3PVmE{RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkW5N|czQTlpPkK1PVM4Ojl7PD;hQi=>
H157 Mmf5R4VtdCCleXPs[UBie3OjeR?= MlviNEwhOC53LDCxJO69VQ>? NUHrSlh6PDiq MV\heEBz\WyjdHn2[Yx6KGyxdzDjc45k\W62cnH0bY9vKHKjbnfld{DjkaRiMTFOwG0hMGVwZz6sJFAvPSCjbnSgNUDPxE1rIHnu[JVk\WRiR{GgZZJz\XO2 NFvl[mU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NUmzO|I6QSd-MkW5N|czQTl:L3G+
H522 NF20fJVE\WyuIHP5Z4xmKGG|c3H5 MoTUNEwhOC53LDCxJO69VQ>? NV7nVXJPPDiq M3PGeIF1KHKnbHH0bZZmdHlibH;3JINwdmOnboTyZZRqd25icnHu[4V{KOLLpDCxJO69VSBqZT7nMkwhOC53IHHu[EAyKM7:TTmgbY5lfWOnZDDHNUBienKnc4S= M2fDZ|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ3OUO3Nlk6Lz5{NUmzO|I6QTxxYU6=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
MEK / p-MEK / ERK / p-ERK ; 

PubMed: 26925841     

Binimetinib inhibits RAS/MAPK pathway activity. Neuroblastoma cells were treated with 1 μM binimetinib for 1 h and then lysed and Western blots for total MEK, phospho-MEK (p-MEK), total ERK, and phospho-ERK (p-ERK) were performed. Actin was used as a loading control.

p-KIT / KIT / ETV1 ; 

PubMed: 25572173     

Immunoblot of ETV1, pKIT and pERK levels in GIST882 and GIST-T1 cells treated with Imatinib (500 nM) or MEK162 (1 μM) for the indicated time points.

26925841 25572173
Growth inhibition assay
Cell viability; 

PubMed: 26925841     

e CHP-134, Kelly, LAN-5, NGP, and SK-N-DZ cells maintain resistance to binimetinib treatment after 120 h of drug exposure. f IC50 values (μM) were calculated for cells treated with binimetinib for 120 h.

In vivo ARRY-438162 (10 mg/kg, po, bid) reduces disease severity in a dose-related manner in rat collagen-induced arthritis (CIA) and rat adjuvant-induced arthritis (AIA) models. ARRY-438162 (po, bid) inhibits increases in ankle diameter by 27% and 50% at 1 mg/kg and 3 mg/kg in the rat collagen-induced arthritis (CIA) model, while ibuprofen has 46% inhibition. ARRY-438162 (10 mg/kg, po, bid) significantly inhibits lesions (inflammation, cartilage damage, pannus formation and bone resorption) by 32% and 60% at 1 mg/kg and 3 mg/kg in the rat collagen-induced arthritis (CIA) model. ARRY-438162 inhibits AIA ankle diameter 11% and 34% at 3 mg/kg and 10 mg/kg in rat adjuvant-induced arthritis (AIA) models. [1] ARRY-438162 demonstrates dose-related inhibition of ankle swelling in rat adjuvant-induced arthritis (AIA) models, significant at 10 mg/kg and 30 mg/kg when compared to vehicle control. ARRY-438162 demonstrates dose-related inhibition of serum IL-6 concentration in rat adjuvant-induced arthritis (AIA) models, with complete inhibition at 10 mg/kg when compared to vehicle control. ARRY-438162 (30 mg/kg) demonstrates dose-related inhibition of relative spleen weights in rat adjuvant-induced arthritis (AIA) models. ARRY-438162 (30 mg/kg) significantly inhibits bone resorption and inflammation with delayed dosing when compared to vehicle in rat adjuvant-induced arthritis (AIA) models. [2] MEK162 (6 mg/kg, BID) combined with BEZ235 results in a significant reduction of tumor growth in immunodeficient mice injected with MCF7 cells. [4]


Animal Research:[4]
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  • Animal Models: immunodeficient mice injected with MCF7-RSK4 cells.
  • Dosages: 6 mg/kg
  • Administration: oral
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 88 mg/mL warmed (199.44 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% CMC+0.5% Tween-80
For best results, use promptly after mixing.
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 441.23


CAS No. 606143-89-9
Storage powder
in solvent
Synonyms ARRY-162,ARRY-438162
Smiles CN1C=NC2=C1C=C(C(=C2F)NC3=C(C=C(C=C3)Br)F)C(=O)NOCCO

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04657991 Recruiting Drug: Encorafenib|Drug: Binimetinib|Drug: Pembrolizumab Melanoma Pfizer|Merck Sharp & Dohme Corp. January 15 2021 Phase 3
NCT03878719 Recruiting Drug: binimetinib|Drug: encorafenib Melanoma Pfizer|Pierre Fabre Laboratories August 13 2020 Phase 1
NCT04720768 Recruiting Drug: Binimetinib|Drug: Encorafenib|Drug: Palbociclib Melanoma|Metastasis Peter MacCallum Cancer Centre Australia June 4 2020 Phase 1|Phase 2
NCT04045691 Recruiting Drug: Encorafenib|Drug: Binimetinib Melanoma Stage IV|Melanoma Stage III Pierre Fabre Pharma GmbH|Pierre Fabre Pharma Austria|Pierre Fabre Pharma AG October 17 2019 --
NCT03839342 Recruiting Drug: Binimetinib|Drug: Encorafenib Solid Tumor University Health Network Toronto June 7 2019 Phase 2

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  • Question 1:

    Could please clarify the formulation in vivo for S7007 is clear or not?

  • Answer:

    S7007 can be dissolved in 5% DMSO+45% PEG 300+ddH2O at 5 mg/ml clearly for injection.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID