What is the data on elexacaftor/tezacaftor/ivacaftor (Trikafta) use in cystic fibrosis?

Comment by InpharmD Researcher

Elexacaftor-tezacaftor-ivacaftor (Trikafta) is a groundbreaking therapy for individuals with cystic fibrosis (CF) designed to target the underlying cause in persons with at least one F508del mutation in the CFTR gene. Key findings from pivotal clinical trials indicate substantial benefits for patients. In those homozygous for the F508del mutation, Trikafta resulted in a 10 percentage point increase in lung function (as measured by ppFEV1), reduced sweat chloride levels, and improved quality of life compared to tezacaftor-ivacaftor alone. For heterozygous patients carrying one F508del and a minimal function mutation, the combination therapy increased ppFEV1 by 13.8% compared to placebo, significantly reduced sweat chloride concentration, decreased the rate of pulmonary exacerbations by 63%, and led to improvements in BMI and quality of life. Serious adverse events were rare, but some cases required treatment adjustments. Overall, elexacaftor-tezacaftor-ivacaftor represents a significant advancement in CF treatment, broadening the reach of effective CFTR modulation therapy to approximately 90% of the CF population and offering improved outcomes in terms of lung function, quality of life, and disease management.

Background

Elexacaftor-tezacaftor-ivacaftor, a cystic fibrosis transmembrane conductance regulator (CFTR) modulating therapy for cystic fibrosis (CF), is a triple-combination therapy consists of two corrector agents (elexacaftor and tezacaftor) working at distinct binding sites to assist in the proper folding and trafficking of the CFTR protein, as well as ivacaftor, a potentiator that enhances CFTR channel function. Approval for this novel medication was spearheaded by two pivotal randomized controlled trials assessing individuals with CF aged 12 years or older who either were homozygous for the F508del mutation or carried one copy of F508del and a minimal function mutation. In those homozygous for F508del, elexacaftor-tezacaftor-ivacaftor, compared to tezacaftor-ivacaftor alone, improved lung function (10 percentage point increase in percent predicted forced expiratory volume in 1 second [ppFEV1]), reduced sweat chloride, and enhanced quality of life. Data from heterozygous patients showed a ppFEV1 increase of 13.8% vs. placebo, sustained through 24 weeks, with a 41.8 mmol/L drop in sweat chloride, a 63% reduction in pulmonary exacerbations, and improvements in BMI (improved by 1.04 kg/m²) and quality-of-life scores (improved by 20.1 points). [1]

A 2023 systematic review analyzed data from nine randomized controlled trials and 16 observational studies, encompassing individuals aged six years and older with at least one Phe508del mutation. The studies demonstrated substantial improvements in lung function, as evidenced by an increase in ppFEV1 of up to 13.8 points after treatment initiation. Additional pulmonary benefits included a significant reduction in pulmonary exacerbation rates and a notable decrease in lung clearance index, indicating improved ventilation homogeneity. Sweat chloride concentration was consistently reduced across multiple studies, frequently by more than 40 mmol/L, suggesting a robust restoration of CFTR function. Improvements in quality of life were reflected in increased scores on the Cystic Fibrosis Questionnaire-Revised Respiratory Domain, with some studies reporting enhancements exceeding 20 points. A pharmacokinetic analysis highlighted extensive metabolism via CYP3A, necessitating caution with concomitant use of CYP3A modulators. [2]

Safety analysis across multiple studies confirmed elexacaftor-tezacaftor-ivacaftor was well tolerated, reporting primarily mild to moderate adverse events, including cough, headache, and transient liver enzyme elevations. Serious adverse events were infrequent, though some cases of rash and hypertension necessitated treatment modifications. With its approval, elexacaftor-tezacaftor-ivacaftor expanded CFTR modulation therapy eligibility to approximately 90% of the CF population, marking a significant advancement in disease management. [1], [2]

More recently, a 2024 systematic review and meta-analysis of six randomized controlled trials encompassing seven reports and 1,125 CF patients evaluated the efficacy and safety elexacaftor–tezacaftor–ivacaftor (ELX-TEZ-IVA) in individuals with at least one Phe508del mutation. The primary outcomes included the ppFEV1, sweat chloride concentration, and the Cystic Fibrosis Questionnaire-Revised Respiratory Domain (CFQ-R RD). The results demonstrated that ELX-TEZ-IVA significantly improved ppFEV1 by 10.29% (95% confidence interval [CI] 6.44 to 14.14, p< 0.00001) and CFQ-R RD scores by 14.59 points (95% CI 9.25 to 19.94, p< 0.00001) compared to placebo, ivacaftor, or tezacaftor–ivacaftor. Additionally, sweat chloride concentrations were markedly reduced by 40.30 mmol/L (95% CI –49.85 to –30.74, p< 0.00001), indicating a substantial improvement in CFTR function. A safety analysis of the trials revealed that adverse events (AEs) were slightly more prevalent in the ELX-TEZ-IVA group compared to control arms; however, serious adverse events were significantly less frequent (odds ratio [OR] = 0.55, 95% CI 0.38 to 0.79, p= 0.001). While mild to moderate AEs, including oropharyngeal pain, cough, nasopharyngitis, and headache, were commonly reported, their incidence was comparable between treatment and control groups. Infective pulmonary exacerbations of CF occurred less frequently among ELX-TEZ-IVA-treated patients (OR = 0.25, 95% CI: 0.18–0.35, p <0.00001). Notably, no significant differences were observed in severe AEs or treatment discontinuations between groups, and no fatalities were reported. These findings reinforce the efficacy of ELX-TEZ-IVA in improving lung function and quality of life while maintaining an overall favorable safety profile. However, the analysis underscores the necessity for continued monitoring, particularly concerning long-term adverse effects and drug tolerability. [3]

References:

[1] Ridley K, Condren M. Elexacaftor-Tezacaftor-Ivacaftor: The First Triple-Combination Cystic Fibrosis Transmembrane Conductance Regulator Modulating Therapy. J Pediatr Pharmacol Ther. 2020;25(3):192-197. doi:10.5863/1551-6776-25.3.192
[2] Kapouni N, Moustaki M, Douros K, Loukou I. Efficacy and Safety of Elexacaftor-Tezacaftor-Ivacaftor in the Treatment of Cystic Fibrosis: A Systematic Review. Children (Basel). 2023;10(3):554. Published 2023 Mar 15. doi:10.3390/children10030554
[3] He R, Lin F, Deng Z, Yu B. Elexacaftor-tezacaftor-ivacaftor for cystic fibrosis with Phe508del mutation: Evidence from randomized controlled trials. SAGE Open Med. 2024;12:20503121231225874. Published 2024 Jan 18. doi:10.1177/20503121231225874

Literature Review

A search of the published medical literature revealed 3 studies investigating the researchable question:

What is the data on elexacaftor/tezacaftor/ivacaftor (Trikafta) use in cystic fibrosis?

Level of evidence

A - Multiple high-quality studies with consistent results  Read more→



Please see Tables 1-3 for your response.


 

Elexacaftor-Tezacaftor-Ivacaftor for Cystic Fibrosis with a Single Phe508del Allele

Design

Phase 3, randomized, double-blind, placebo-controlled trial

N= 403

Objective

To confirm the efficacy and safety of elexacaftor-tezacaftor-ivacaftor in patients 12 years of age or older with cystic fibrosis with Phe508del-minimal function genotypes

Study Groups

Elexacaftor-Tezacaftor-Ivacaftor (n= 200)

Placebo (n= 203)

Inclusion Criteria

Patients 12 years or older with cystic fibrosis and Phe508del-minimal function genotypes; percentage of predicted FEV1 of 40 to 90% at screening; stable disease during the 28-day screening period

Exclusion Criteria

History of any illness or condition that could confound the results or pose additional risk, per the investigator (e.g., transplant patients, clinically significant cirrhosis, drug abuse, cancer); acute upper or lower respiratory infection, pulmonary exacerbation, or changes in therapy (including antibiotics) for sinopulmonary disease within 28 days; lung infection with organisms associated with a more rapid decline in pulmonary status; acute illness

Methods

Patients were randomly assigned to receive elexacaftor (200 mg once daily) in combination with tezacaftor (100 mg once daily) and ivacaftor (150 mg every 12 hours) or matched placebos for 24 weeks. Randomization was stratified by percentage of predicted FEV1, age, and sex.

Duration

24-week intervention period

Outcome Measures

Primary: Absolute change from baseline in percentage of predicted FEV1 at week 4

Secondary: Absolute change in percentage of predicted FEV1 through week 24, number of pulmonary exacerbations through week 24, absolute change in sweat chloride concentration through week 24, absolute change in Cystic Fibrosis Questionnaire-Revised (CFQ-R) respiratory domain score through week 24, absolute change in BMI at week 24

Baseline Characteristics

 

Elexacaftor-Tezacaftor-Ivacaftor (n= 200)

Placebo (n= 203)

 

Age, years

25.6±9.7 26.8±11.3  
Female

48%

48.3%  

Percentage of predicted FEV1

61.6±15.0 61.3±15.5  

Body mass index, kg/m2

21.49±3.07 21.31±3.14  

Sweat chloride concentration, mmol/L

102.3±11.9 102.9±9.8  

CFQ-R respiratory domain score

68.3±16.9 70.0±17.8  

Results

Endpoint

Elexacaftor-Tezacaftor-Ivacaftor (n= 200)

Placebo (n= 203)

p-value

Absolute change in percentage of predicted FEV1 from baseline at wk 4 (95% CI)

13.6 (12.4 to 14.8) -0.2 (-1.3 to 1.0) <0.001

Pulmonary exacerbations through wk 24, no. of events (annualized estimated event rate)

41 (0.37) 113 (0.98) <0.001

Absolute change in sweat chloride concentration from baseline, mmol/L (95% CI)

-42.2 (-44.0 to -40.4) -0.4 (-2.2 to 1.4) <0.001

Absolute change in CFQ-R respiratory domain score from baseline (95% CI)

17.5 (15.6 to 19.5) -2.7 (-4.6 to -0.8) <0.001

Absolute change in body-mass index from baseline, kg/m2 (95% CI)

1.13 (0.99 to 1.26) 0.09 (−0.05 to 0.22) <0.001

Adverse Events

The percentage of patients with at least one adverse event was 93.1% in the elexacaftor-tezacaftor-ivacaftor group and 96.0% in the placebo group. Common adverse events included infective pulmonary exacerbation of cystic fibrosis, increased sputum, headache, cough, diarrhea, upper respiratory tract infection, nasopharyngitis, oropharyngeal pain, hemoptysis, and fatigue.

Serious adverse events occurred in 13.9% of the elexacaftor-tezacaftor-ivacaftor group and 20.9% of the placebo group.

Adverse events leading to discontinuation occurred in 1% of the elexacaftor-tezacaftor-ivacaftor group.

Study Author Conclusions

Elexacaftor-tezacaftor-ivacaftor was efficacious in patients with cystic fibrosis with Phe508del-minimal function genotypes, in whom previous CFTR modulator regimens were ineffective.

InpharmD Researcher Critique

The study demonstrated significant improvements in lung function and other clinical outcomes with elexacaftor-tezacaftor-ivacaftor therapy. However, the study's limitations include the short duration of 24 weeks and the lack of long-term safety data. Additionally, the study was funded by Vertex Pharmaceuticals, which may introduce potential bias.



References:

Middleton PG, Mall MA, Dřevínek P, et al. Elexacaftor-Tezacaftor-Ivacaftor for Cystic Fibrosis with a Single Phe508del Allele. N Engl J Med. 2019;381(19):1809-1819. doi:10.1056/NEJMoa1908639

 

Efficacy and Safety of the Elexacaftor/tezacaftor/ivacaftor Combination Regimen in People with Cystic Fibrosis Homozygous for the F508del Mutation: a Double-blind, Randomised, Phase 3 trial

Design

Randomized, double-blind, phase 3 trial

N= 113

Objective

To evaluate the efficacy and safety of elexacaftor in combination with tezacaftor/ivacaftor compared to tezacaftor/ivacaftor alone in people with cystic fibrosis homozygous for the F508del mutation

Study Groups

ELX/TEZ/IVA (n= 55)

TEZ/IVA (n= 52)

Inclusion Criteria

Participants aged ≥12 years with cystic fibrosis homozygous for F508del, ppFEV1 between 40 and 90, and stable disease

Exclusion Criteria

History of any illness or condition that could confound the results or pose additional risk, per the investigator (e.g., transplant patients, clinically significant cirrhosis, drug abuse, cancer); acute upper or lower respiratory infection, pulmonary exacerbation, or changes in therapy (including antibiotics) for sinopulmonary disease within 28 days; lung infection with organisms associated with a more rapid decline in pulmonary status; acute illness

Methods

Participants underwent a 4-week TEZ/IVA run-in period, followed by randomization to either ELX/TEZ/IVA or TEZ/IVA for 4 weeks. ELX was administered at 200 mg once daily, TEZ at 100 mg once daily, and IVA at 150 mg every 12 hours. All drugs were administered orally.

Duration

August 2018 to December 2018

Outcome Measures

Primary: Absolute change in ppFEV1 at week 4

Secondary: Absolute change in sweat chloride concentration, CFQ-R RD score

Baseline Characteristics  

ELX/TEZ/IVA (n= 55)

TEZ/IVA (n= 52)
Age, years 27.9 ± 10.8

28.8 ± 11.5

Female

54% 56%
ppFEV1, %

60.2 ± 14.4

61.6 ± 15.4

Body mass index, kg/m2

21.88 ± 4.12 21.75 ± 3.9

Sweat chloride concentration, mmol/L

90.0 ± 12.3 91.4 ± 11.0

Mean CFQ-R respiratory domain score

72.6 ± 17.9 70.6 ± 16.2
Results  

ELX/TEZ/IVA (n= 55)

TEZ/IVA (n= 52) p-value
ppFEV1 change, percentage points

10.4 (8.6 to 12.2)

0.4 (-1.4 to 2.3)

<0.0001
Sweat chloride change, mmol/L -43.4 (-46.9 to -40.0)

1.7 (-1.9 to 5.3)

<0.0001
CFQ-R RD score change 16.0 (12.1 to 19.9)

-1.4 (-5.4 to 2.6)

<0.0001
Adverse Events

ELX/TEZ/IVA was well tolerated with most adverse events being mild or moderate. Serious adverse events occurred in 4% of participants in the ELX/TEZ/IVA group and 2% in the TEZ/IVA group. Common adverse events included cough and pulmonary exacerbation.

Study Author Conclusions

ELX/TEZ/IVA provided clinically robust benefits compared to TEZ/IVA alone with a favorable safety profile, demonstrating potential transformative improvements for people with cystic fibrosis homozygous for F508del.

Critique

The study demonstrated significant improvements in clinical outcomes with ELX/TEZ/IVA, but the short 4-week duration may limit the understanding of long-term effects. The study was well-designed with a robust sample size. 

 

References:

Heijerman HGM, McKone EF, Downey DG, et al. Efficacy and safety of the elexacaftor plus tezacaftor plus ivacaftor combination regimen in people with cystic fibrosis homozygous for the F508del mutation: a double-blind, randomised, phase 3 trial [published correction appears in Lancet. 2020 May 30;395(10238):1694. doi: 10.1016/S0140-6736(20)31021-7.]. Lancet. 2019;394(10212):1940-1948. doi:10.1016/S0140-6736(19)32597-8

 

Triple Therapy for Cystic Fibrosis Phe508del-Gating and -Residual Function Genotypes

Design

Phase 3, double-blind, randomized, active-controlled trial

N= 258

Objective

To evaluate the magnitude of benefit of elexacaftor-tezacaftor-ivacaftor compared with ivacaftor and tezacaftor-ivacaftor in patients 12 years of age or older with Phe508del-gating and Phe508del-residual function genotypes

Study Groups

Elexacaftor-tezacaftor-ivacaftor (n= 132)

Active control: Ivacaftor or Tezacaftor-Ivacaftor (n= 126)

Inclusion Criteria

Patients 12 years of age or older with cystic fibrosis and Phe508del-gating or Phe508del-residual function genotypes

Exclusion Criteria

History of any illness or condition that could confound the results or pose additional risk, per the investigator (e.g., transplant patients, clinically significant cirrhosis, drug abuse, cancer); acute upper or lower respiratory infection, pulmonary exacerbation, or changes in therapy (including antibiotics) for sinopulmonary disease within 28 days; lung infection with organisms associated with a more rapid decline in pulmonary status; acute illness

Methods

Patients entered a 4-week run-in period with ivacaftor or tezacaftor-ivacaftor, then were randomly assigned to receive elexacaftor-tezacaftor-ivacaftor or active control for 8 weeks. The primary endpoint was the absolute change in the percentage of predicted FEV1 from baseline through week 8.

Duration

8-week treatment phase

Outcome Measures

Primary: Absolute change in percentage of predicted FEV1 from baseline through week 8

Secondary: Absolute change in sweat chloride concentration, CFQ-R respiratory domain score

Baseline Characteristics  

Elexacaftor-Tezacaftor-Ivacaftor (n=132)

Ivacaftor or Tezacaftor-Ivacaftor (n=126)

Age, years

37.7±14.7

37.7±14.7

Female

67 (50.8%) 61 (48.4%)

Percentage of predicted FEV1

67.1±15.7 68.1±16.4

Sweat chloride concentration, mmol/L

59.5±27.0 56.4±25.5

CFQ-R respiratory domain score

76.5±16.6 77.3±15.8

Body-mass index, kg/m2

24.07±4.72 24.05±4.71

Ivacaftor

Tezacaftor-Ivacaftor

---

45 (35.7%)

81 (64.3%)

Results End Point Elexacaftor-Tezacaftor-Ivacaftor (n=132)

Ivacaftor or Tezacaftor-Ivacaftor (n=126)

Percentage of predicted FEV1 - Absolute change from baseline through wk 8

3.7 (2.8 to 4.6) 0.2 (-0.7 to 1.1)

Sweat chloride concentration - Absolute change from baseline through wk 8

-22.3 (-24.5 to -20.2) 0.7 (-1.4 to 2.8)

CFQ-R respiratory domain score - Absolute change from baseline through wk 8

10.3 (8.0 to 12.7) 1.6 (-0.8 to 4.1)
Adverse Events

The incidence of adverse events was similar in the two groups; adverse events led to treatment discontinuation in one patient (elevated aminotransferase level) in the elexacaftor-tezacaftor-ivacaftor group and in two patients (anxiety or depression and pulmonary exacerbation) in the active control group.

Study Author Conclusions

Elexacaftor-tezacaftor-ivacaftor was efficacious and safe in patients with Phe508del-gating or Phe508del-residual function genotypes and conferred additional benefit relative to previous CFTR modulators.

Critique

The study was well-designed with a robust sample size and clear endpoints. The study was funded by Vertex Pharmaceuticals, which could introduce potential bias. The choice of active control agent appears to be determined by the prescribing physician, but there was no elaboration on reasoning; the active control group was not evenly distributed in terms of therapy (2:1 ratio instead of 1:1).

 

References:

Barry PJ, Mall MA, Álvarez A, et al. Triple Therapy for Cystic Fibrosis Phe508del-Gating and -Residual Function Genotypes. N Engl J Med. 2021;385(9):815-825. doi:10.1056/NEJMoa2100665