Tezacaftor 100mg / Ivacaftor 150mg tablets
Requires a prescription from a doctor or prescriber
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Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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1 branded products available
MHRA licensed products
View all licensed products for Tezacaftor + Ivacaftor on the MHRA register
Symkevi 100mg/150mg tablets
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Vanzacaftor-tezacaftor-deutivacaftor for treating cystic fibrosis with 1 or more F508del mutations in the CFTR gene in people 6 years and over (TA1085)
Ivacaftor–tezacaftor–elexacaftor, tezacaftor–ivacaftor and lumacaftor–ivacaftor for treating cystic fibrosis (TA988)
Cystic fibrosis: diagnosis and management (NG78)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 13 · Randomised trials: 7 · 2012–2026
Showing the 50 most relevant studies, sorted by most relevant.
H. Heijerman, E. McKone, D. G. Downey, et al.
Lancet (London, England), 2019
Michael P Boyle, Scott C Bell, Michael W Konstan, et al.
The Lancet Respiratory Medicine, 2014
Jane Davies, Helen Sheridan, Nicholas Bell, et al.
The Lancet Respiratory Medicine, 2013
Katz T, van Dorst J, Prentice B, et al.
2026
- Cystic Fibrosis
- Aminophenols
- Pyrrolidines
Steven J Edwards, B. Farrar, Kate Ennis, et al.
Health technology assessment, 2025
Venditto L, Neece A, Forgione F, et al.
2026
- Cystic Fibrosis
- Lung Transplantation
- Aminophenols
AlMunefi F, Dyce JP, Zhao JY, et al.
2026
BackgroundElexacaftor/tezacaftor/ivacaftor (ETI) has transformed clinical outcomes in people with cystic fibrosis (PwCF), but its impact on airway and systemic inflammation is less well defined.MethodsWe systematically searched PubMed, Embase and CENTRAL (January 1, 2019-September 30, 2025) for full-text human studies of pwCF treated with ETI that reported at least one inflammatory biomarker before and after ETI initiation. Because of heterogeneity in study design, sample type, biomarker panels and assays, we did not perform a meta-analysis but instead conducted a structured narrative synthesis, grouping biomarkers by compartment (systemic vs airway); when reported, we also recorded associations between biomarker changes and clinical outcomes.ResultsThirty-two observational studies (8-272 participants) met inclusion criteria; 25 evaluated systemic and 10 airway biomarkers, with follow-up up to 30 months. ETI was associated with substantial reductions in sputum neutrophil elastase, IL-1β and IL-8, and in systemic C-reactive protein, other acute-phase reactants, circulating neutrophils and selected Th17-related cytokines, indicating an overall reduction in inflammatory burden, although residual inflammation relative to healthy controls was common. Th1-associated markers and immune-cell activation phenotypes showed heterogeneous changes, while Th2/eosinophilic markers showed less consistent modulation with ETI. Just over half of studies examined biomarker-outcome relationships; in these, reductions in neutrophil-associated markers, CRP, fibrinogen and selected cytokines were often associated with improvements in ppFEV1 or other clinical measures.ConclusionETI is associated with substantial but incomplete reductions in airway and systemic inflammation in pwCF, with the most consistent effects in neutrophil and acute-phase pathways and more variable changes across other immune markers. Persistent low-grade inflammation in many cohorts suggests that adjunctive anti-inflammatory strategies may still be relevant and that further longitudinal studies are needed to link residual biomarker abnormalities with long-term clinical and structural outcomes.
Abstract licence: CC BY
Girouard H, Jaber F, Gharib J, et al.
2026
D O, C D, DW C
2025
Rong He, Zehui Deng, Fei Lin, et al.
SAGE Publishing, 2024
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.