Capmatinib instructions

1. Indications and Usage

Capmatinib is a kinase inhibitor indicated for the treatment of adult patients with metastatic non-small cell lung cancer in whom tumor mutations causing mesenchymal epithelial transition (MET) exon 14 are skipped as detected by an FDAapproved test.

2. Dosage and usage

Patients treated with capmatinib were selected based on the presence of mutations causing METexon 14 skipping.

Recommended dosage:Twice a day, 400mg twice daily, with or without food.

Three. Dosage form and strength

Tablets: 150mg and 200mg

Four. Contraindications

No.

Five. Warnings and Precautions

1.Interstitial Lung Disease(ILD)/Pneumonitis:Monitoring is indicated for new or worsening pulmonary symptoms of ILD/pneumonitis, and capmatinib should be permanently discontinued in patients with ILD/pneumonia.

2.Hepatotoxicity:Monitor liver function tests. Withhold, reduce dose, or permanently discontinue capmatinib based on severity.

3.Pancreatic Toxicity:Monitor amylase and lipase levels. Withhold, reduce dose, or permanently discontinue capmatinib based on severity.

4.Anaphylaxis:Suspend or permanently discontinue capmatinib based on severity.

5.Photosensitivity risk: may cause photosensitivity reaction, it is recommended that patients limit direct exposure to ultraviolet rays.

6.Embryo-Fetal Toxicity:Can cause fetal harm, Inform patients of the potential risks to the fetus and take effective contraceptive measures.

6. Adverse reactions

The most common adverse reactions (≥ 20%) were edema, nausea, musculoskeletal pain, fatigue, vomiting, dyspnea, cough, and decreased appetite.

7. Drug interactions

Strong and ModerateCYP3AInducers:Avoid concurrent use.

8. Use among specific groups of people

Breastfeeding:Breastfeeding is not recommended.

9. Mechanism of action

Capmatinibis a kinase inhibitor that targets MET, including mutant variants resulting from exon 14 skipping. METSkipping of exon 14 causes the protein to lose regulatory domains, thereby reducing its negative regulatory effect and resulting in increased downstream MET signaling. At clinically achievable concentrations, capmatinib inhibits the growth of cancer cells driven by mutant MET variants lacking exon 14 Pan>METexon14skipped orMETmutated human lung tumors showed antitumor activity in murine tumor xenograft models. Capmatinibinhibits METphosphorylation triggered by hepatocyte growth factor binding or METamplification, as well as MET-mediated phosphorylation of downstream signaling proteins and MET-dependent cancer cell proliferation and survival.

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