MEK 162

Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor with an IC50 of 12 nM.
Binimetinib is a member of the class of benzimidazoles that is 1-methyl-1H-benzimidazole which is substituted at positions 4, 5, and 6 by fluorine, (4-bromo-2-fluorophenyl)nitrilo, and N-(2-hydroxyethoxy)aminocarbonyl groups, respectively. It is a MEK1 and MEK2 inhibitor (IC50= 12 nM). Approved by the FDA for the treatment of patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation in combination with encorafenib. It has a role as an EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor, an antineoplastic agent and an apoptosis inducer. It is a member of benzimidazoles, a member of bromobenzenes, a member of monofluorobenzenes, a hydroxamic acid ester and a secondary amino compound.|Binimetinib, also known as Mektovi, is a potent is a potent and selective oral mitogen-activated protein kinase 1/2 (MEK 1/2) inhibitor which is combined with [Encorafenib],. On June 27, 2018, the Food and Drug Administration approved the combination of [Encorafenib] and binimetinib (BRAFTOVI and MEKTOVI, from Array BioPharma Inc.) in combination for patients with unresectable or metastatic melanoma with the BRAF V600E or V600K mutations, as detected by an FDA-approved test.|Encorafenib is a selective inhibitor of BRAF kinase that is used in combination with binimetinib, an inhibitor of MEK, in the therapy of metastatic and advanced malignant melanoma. Encorafenib-binimetinib combination therapy is commonly associated with transient elevations in serum aminotransferase levels during therapy, but has yet to be linked to instances of clinically apparent acute liver injury.|Binimetinib is an orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2 dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.