Indication

EGFR negative, ALK negative, non-small cell lung cancer

Epidermal growth factor receptor (EGFR)-negative, anaplastic lymphoma kinase (ALK)-negative non-small cell lung cancer denotes a molecular subset of non-small cell lung carcinoma—primarily adenocarcinoma or large cell carcinoma of the respiratory tract—whose neoplastic cells lack sensitizing mutations in the *EGFR* gene and rearrangements involving the *ALK* gene. Read more about EGFR negative, ALK negative, non-small cell lung cancer

13 drugs 10 manufacturers

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Drugs that treat it

Common EGFR negative, ALK negative, non-small cell lung cancer therapies.

Showing 1–9 of 13 drugs

YERVOY (ipilimumab)

ANTINEOPLASTIC-CYTOTOXIC T-LYMP. ANTIGEN (CTLA-4),R-MC ANTIB·METASTATIC MALIGNANT MELANOMA·+8
BMS PRIMARYCARE

OPDIVO (nivolumab)

ANTINEOPLASTIC - ANTI-PROGRAMMED DEATH-(PD-1/L1) MC ANTIBODY·MALIGNANT ESOPHAGEAL NEOPLASM·+17
BMS PRIMARYCARE

KEYTRUDA (pembrolizumab)

ANTINEOPLASTIC - ANTI-PROGRAMMED DEATH-(PD-1/L1) MC ANTIBODY·MALIGNANT MELANOMA·+36
Merck Sharp & Dohme

IMFINZI (durvalumab)

ANTINEOPLASTIC - ANTI-PROGRAMMED DEATH-(PD-1/L1) MC ANTIBODY·BILIARY TRACT MALIGNANCY·+10
AstraZeneca Pharmaceuticals

IMJUDO (tremelimumab-actl)

ANTINEOPLASTIC-CYTOTOXIC T-LYMP. ANTIGEN (CTLA-4),R-MC ANTIB·LIVER CELL CARCINOMA·+1
AstraZeneca Pharmaceuticals

PEMETREXED

FOLATE ANTAGONISTS·MALIGNANT MESOTHELIOMA OF PLEURA·+2
TEVA USA
Filter & compare in the drug finder →Opens the drug finder with EGFR negative, ALK negative, non-small cell lung cancer preselected.

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About EGFR negative, ALK negative, non-small cell lung cancer.

Epidermal growth factor receptor (EGFR)-negative, anaplastic lymphoma kinase (ALK)-negative non-small cell lung cancer denotes a molecular subset of non-small cell lung carcinoma—primarily adenocarcinoma or large cell carcinoma of the respiratory tract—whose neoplastic cells lack sensitizing mutations in the *EGFR* gene and rearrangements involving the *ALK* gene.

Affecting adult patients with primary pulmonary malignancies, this clinical state is pathologically defined by the absence of these two primary oncogenic driver alterations that typically confer sensitivity to targeted receptor tyrosine kinase inhibitors.

Consequently, tumors exhibiting this wild-type biomarker profile lack dependence on EGFR or ALK signaling cascades, distinguishing them biologically from oncogene-addicted lung cancers and determining eligibility for alternative standard systemic regimens, such as immune checkpoint inhibitors and cytotoxic chemotherapy combinations.

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