MEK Inhibitors

April 27, 2026

This page was reviewed under our medical and editorial policy by Gaurav Singh, M.D., M.P.H., F.A.C.M.S., Mohs Micrographic Surgeon and Dermatologist, City of Hope^® Chicago Cancer Center.

Considered among the most promising areas in cancer research, mitogen-activated protein kinase kinase (MEK) inhibitors are a type of targeted therapy used to treat certain cancers, most notably melanoma. As its name suggests, targeted therapy works by targeting specific features, changes (mutations) or substances in or on cancer cells to stop them from growing uncontrollably.

What Is a MEK Inhibitor?

As a class of targeted therapy, MEK inhibitors do precisely that — inhibit or block proteins called MEK1 and MEK2, which play a significant role in cell growth and survival. By blocking these proteins, MEK inhibitors may help stunt the growth of cancer cells or destroy them.

While MEK inhibitors are mainly used to treat cancers with mutations in the BRAF gene, such as melanoma, they’ve also proven effective in other cancers, including colorectal cancer, non-small cell lung cancer (NSCLC) and certain types of thyroid cancer.

Are MEK Inhibitors Chemotherapy?

MEK inhibitors are not chemotherapy. There’s a key difference in the way they work.

Standard chemotherapy drugs attack any rapidly dividing cells. In contrast, MEK inhibitors precisely target parts of the cancer cells that make them different from normal cells. The goal: Kill cancer cells, without harming healthy ones.

MEK Inhibitor Drugs

The following Food and Drug Administration-approved MEK inhibitor drugs are regularly used in combination with other targeted therapies like BRAF inhibitors to strengthen their effectiveness and fight resistance.

Binimetinib: This drug is used to treat metastatic melanoma with specific mutations.

Cobimetinib: This is used to treat inoperable or metastatic melanoma.

Mirdametinib: This is used to treat neurofibromatosis type 1 (NF1) in children and adults.

Selumetinib: This is used to treat NF1 in children, accompanied by symptomatic, inoperable plexiform neurofibromas (PN, or tumors involving the coating around nerve fibers.

Trametinib: This is used alone or in combination with dabrafenib to treat cancers with specific BRAF mutations, including melanoma and non-small cell lung cancer.

How Are MEK Inhibitor Drugs Administered?

MEK inhibitors are taken orally (pills) once or twice a day, offering patients more convenience than intravenous options. Doctors determine dosing schedules based on cancer type and individual patient needs.

Side Effects

As with any treatment decision, it’s important to understand the benefits and risks of taking these medications. MEK inhibitor toxicity, or the harmful effects of treatment, may vary from mild to severe.

With MEK inhibitors specifically, common side effects include:

• Rash, including itch
• Nausea and diarrhea
• Sensitivity to sunlight
• Swelling
• Mouth and tongue sores
• Fatigue
• Loss of appetite
• Elevated liver enzymes

Rare but serious side effects include:

• Bleeding
• Blood clots
• Heart, lung or liver damage
• Muscle issues
• Vision problems
• Skin infections

In some cases, trametinib raises the risk for developing new skin cancers and other cancers and decreases fertility in women. Cobimetinib may decrease fertility in women and men.

Combining a MEK inhibitor with a BRAF inhibitor is common. Notably, the combination also lessens the likelihood of certain side effects, for example, developing other skin cancers.

Regular monitoring is key to side effect management, allowing doctors to appropriately modify drug dosage.

MEK Inhibitor Resistance

When cancers that once responded to a drug or therapy start to grow again, it’s called resistance. In other words, the drug loses its effectiveness. For some patients, resistance develops quickly, within a matter of weeks of beginning treatment. For others, it develops over time, possibly months or even years later.

MEK inhibitor resistance is a concern for patients, clinicians and researchers. Specifically, BRAF gene mutations can promote resistance, allowing cancer cells to grow despite MEK inhibitors.

Researchers continue to study combination therapies to delay or overcome MEK inhibitor resistance.