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A MEK inhibitor is a chemical or drug that inhibits the mitogen-activated protein kinase enzymes MEK1 and/or MEK2. They can be used to affect the MAPK/ERK pathway which is often overactive in some cancers.
The most common side effects include diarrhea, rash, nausea (feeling sick), vomiting, pyrexia (fever), photosensitivity (light sensitivity) reaction, abnormal results for certain liver function tests (increased levels of alanine aminotransferase, aspartate aminotransferase) and abnormal results for an enzyme related to muscle breakdown ...
[6] [7] It is a MEK inhibitor drug with anti-cancer activity. [8] It inhibits MEK1 and MEK2. [8] It is taken by mouth. [4] [5] The most common side effects include rash, diarrhea, tiredness, peripheral edema (swelling, especially of ankles and feet), nausea and acneiform dermatitis (acne-like inflammation of the skin). [5]
Selumetinib is a kinase inhibitor, more specifically a selective inhibitor of the enzyme mitogen-activated protein kinase kinase (MAPK kinase or MEK) subtypes 1 and 2. These enzymes are part of the MAPK/ERK pathway, which regulates cell proliferation (i.e., growth and division) and is overly active in many types of cancer. [18]
Binimetinib is a selective inhibitor of MEK, a central kinase in the tumor-promoting MAPK pathway. [5] Inappropriate activation of the pathway has been shown to occur in many cancers. [ 5 ] In June 2018 it was approved by the FDA in combination with encorafenib for the treatment of patients with unresectable or metastatic BRAF V600E or V600K ...
Companies are not only focusing on improving the efficacy of BRAF inhibitors but also on reducing side effects and improving patient outcomes through combination regimens that include MEK inhibitors. The approval of combination therapies has set new standards in treatment, offering superior efficacy compared to BRAF inhibitor monotherapy.
It is a highly selective inhibitor of both MEK1 and MEK2, a type of MAPK/ERK kinase. [10] [11] U0126 was found to functionally antagonize AP-1 transcriptional activity via noncompetitive inhibition of the dual specificity kinase MEK with IC 50 of 72 nM for MEK1 and 58 nM for MEK2.
Vemurafenib interrupts the B-Raf/MEK step on the B-Raf/MEK/ERK pathway − if the B-Raf has the common V600E mutation. Vemurafenib only works in melanoma patients whose cancer has a V600E BRAF mutation (that is, at amino acid position number 600 on the B-Raf protein, the normal valine is replaced by glutamic acid). [4]