The mean effective half-life of elexacaftor, tezacaftor, and ivacaftor is 27.4 hours, 25.1 hours, and 15 hours, respectively. It is excreted as metabolites or unchanged mainly through feces and to a smaller extent urine. This medication should be taken with a high fat meal to improve absorption through the gut. Two combination Elexacaftor, Tezacaftor, Ivacaftor tablets and one ivacaftor tablet Pharmacokinetics Įlexacaftor/tezacaftor/ivacaftor is primarily metabolized by CYP3A4 /5. Mechanism of action Įlexacaftor/tezacaftor/ivacaftor is a tridrug treatment in which the medications work together to increase the transport of chloride and sodium ions, and reducing thick mucus production. The thickened mucus can lead to inflammation, respiratory infections, and clogged ducts. CFTR has a role in the production of mucus, sweat, and digestive fluids. The CFTR protein is found in epithelial cells of the lung, liver, pancreas, digestive tract, and reproductive tracts. Pharmacology Cystic fibrosis and CFTR Ĭystic fibrosis is an autosomal recessive genetic disorder of the CFTR protein which reduces chloride and sodium ion transport through the cell membrane, causing thicker than normal mucus secretions. Other drugs with the potential for interaction include: warfarin, digoxin, statins, glyburide, nateglinide, repaglinide. Dosage must be adjusted with moderate or strong CYP3A inhibitors. Interactions Ĭoncomitant use with CYP3A inducers is not recommended. The most common side effects affecting more than 5% of patients are headache, upper respiratory tract infection, abdominal pain, diarrhea, rash, alanine aminotransferase increased, nasal congestion, blood creatine phosphokinase increased, aspartate aminotransferase increased, rhinorrhea, rhinitis, influenza, sinusitis and blood bilirubin increased. The combination is indicated for the treatment of people aged six years and older who have cystic fibrosis with a F508del mutation or other mutations in the CFTR gene.
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