Lung Cancer Treatments

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Lung cancer treatments that exploit specific abnormalities in cancer cells are known as targeted therapies. These drugs are different from chemotherapy in the way they work. Unlike chemo, targeted therapy recognizes cancer cells based on mutations, or changes, in their DNA or proteins that are not seen elsewhere in the body. It specifically attacks the cancer cells, not healthy cells.

Typically, targeted medicines don’t cause as many side effects as chemo, but you could experience a rash, diarrhea, fatigue, nausea, high blood pressure, liver function issues, and heart, vision, or lung problems.

Most targeted drugs work only if you have certain gene mutations, which your doctor can test you for, says Dr. Gheeya. If there are no mutations present, that’s when a person would receive chemo or immunotherapy, he adds. Here are the common mutations that may be treated with targeted therapies for lung cancer.

EGFR Mutations

Epidermal growth factor receptor (EGFR) is a protein found on the surface of cells, and a mutation in the cancer gene can lead to an abnormal protein, causing lung cancer. Some mutations in the EGFR gene can be treated with drugs, such as:

  • afatinib (Gilotrif)
  • amivantamab (Rybrevant), amivantamab and hyaluronidase-lpuj (Rybrevant-faspro)

  • dacomitinib (Vizimpro)
  • erlotinib (Tarceva)
  • gefitinib (Iressa)
  • osimertinib (Tagrisso)
  • lazertinib (Lazcluze)

HER2 Mutations

HER2 (human epidermal growth factor receptor 2), also known as ERBB2, is another protein found on the surface of cells. A mutation in this gene or an overly gene causes abnormal cell growth, leading to cancer. If testing shows that your lung cancer is HER2-positive, it means your cancer cells display a greater amount of HER2 on their surface. Certain medications can use these proteins as targets to find and destroy those cancer cells.

About 1 to 4 percent of NSCLCs are HER2-mutated, and many more are HER2-positive.

There are three U.S. Food and Drug Administration (FDA)–approved medications for locally advanced or metastatic HER2-mutated or HER2-positive lung cancer:

  • trastuzumab deruxtecan (Enhertu) for HER2-positive lung cancer, which is also a type of drug called an antibody-drug conjugate, discussed below
  • sevabertinib (Hyrnuo) for HER2-mutated
  • zongertinib (Hernexeos) for HER2-mutated

ALK Fusion

About 5 percent of NSCLCs have an alteration in the anaplastic lymphoma kinase (ALK) gene. When mutated, it can cause abnormal cell growth and spread. Drugs that target ALK changes include:

  • alectinib (Alecensa)
  • brigatinib (Alunbrig)
  • ceritinib (Zykadia)
  • crizotinib (Xalkori)
  • lorlatinib (Lorbrena)

ROS1 Fusions

The ROS1 gene arrangement is related to the ALK gene, and some drugs that work for one also work for the other.

In July 2026, the FDA approved a new second-line ROS1 treatment, zidesamtinib, for those with locally advanced or metastatic ROS1 NSCLC who have received a prior ROS1 treatment.

  • ceritinib (Zykadia)
  • crizotinib (Xalkori)
  • entrectinib (Rozlytrek)
  • lorlatinib (Lorbrena)
  • repotrectinib (Augtyro)
  • taletrectinib (Ibtrozi)
  • zidesamtinib (Jideytro)

BRAF Mutations

The BRAF gene helps manage important cell functions related to growth. When mutated, it signals cells to divide uncontrollably.

Two drug combinations are approved by the FDA to target changes in the BRAF V600E gene:

  • dabrafenib (Tafinlar) and trametinib (Mekinist)
  • encorafenib (Braftovi) and binimetinib (Mektovi)

KRAS Mutations

The KRAS gene helps regulate cell growth, serving as an on-off switch. Similar to the BRAF mutations, when mutated, KRAS allows cells to grow uncontrollably. KRAS mutations are one of the most common mutations linked to cancer, driving 32 percent of lung cancers. There are several types of KRAS mutations. KRAS G12C can be targeted by FDA-approved agents.

 Examples include:

  • adagrasib (Krazati)
  • sotorasib (Lumakras)

MET Alterations

Only around 5 percent of patients who have lung cancer have this gene mutation. For those who do, targeted therapy MET inhibitor drugs, such as capmatinib (Tabrecta) or tepotinib (Tepmetko) may be recommended treatments.

Sometimes even if there is no MET mutation, an overly active MET gene can cause excessive protein production, causing cancer. If your cancer is tested MET-positive, it can be treated with a type of therapy called an antibody-drug conjugate, discussed below.

RET Mutations

An error in the RET gene, sometimes called a rearrangement, can cause lung cancer, although it appears in only 1 to 2 percent of patients. Patients who have this mutation are often younger and have never smoked. The two FDA-approved RET inhibitors are selpercatinib (Retevmo) and pralsetinib (Gavreto).