Peak FEV₁ response at week 24 was a prespecified co-primary endpoint.
In Trial 1, the mean improvement in peak FEV₁ between SPIRIVA Respimat and placebo Respimat was 86 mL at week 24 (95% CI 20−152; p=0.01).¹ In Trial 2, the mean improvement in peak FEV₁ between SPIRIVA Respimat and placebo Respimat was 154 mL at week 24 (95% CI 91−217; p<0.001).¹

*p<0.05; **p<0.01; ***p<0.001.

 Adapted from Kerstjens HA et al. 2012 (suppl).²

Trough FEV₁ response at week 24 was a pre-specified co-primary endpoint.

At 24 weeks, mean difference in improvement in trough FEV₁ between Spiriva Respimat and placebo Respimat was 88ml in Trial 1 (95% CI 27-149; p=0.01) and 111ml (95% CI 53-169; p<0.001) in Trial 2.¹

PrimoTinA Study Design

Two replicate randomised controlled trials (PrimoTinA-Asthma 1 and PrimoTinA-Asthma 2) compared SPIRIVA Respimat with placebo Respimat over 48 weeks as add-on controller therapy on top of usual care in adult patients with severe asthma who were symptomatic on maintenance treatment of at least ICS (≥800 μg budesonide/day or equivalent) plus LABA, had a post-bronchodilator FEV₁ of ≤80% of the predicted value and a history of ≥1 severe exacerbation in the previous year. In both the SPIRIVA Respimat and placebo Respimat groups, ICS and LABA maintenance therapy was continued. Other asthma medications were allowed if the doses remained stable for ≥4 weeks before study entry and for the duration of the trial. The co-primary endpoints were lung function measured as peak FEV1(0-3h) and trough FEV1 response at week 24, and time to first severe exacerbation (pooled data) over 48 weeks.¹

Abbreviations

CI, confidence interval; FEV₁, forced expiratory volume in 1 second; HR, hazard ratio; LABA, long-acting β2-agonist.

References: 1. Kerstjens HA et al. N Engl J Med 2012;367:1198–207. 2. Kerstjens HA et al. N Engl J Med 2012;367:1198–207, supplementary appendix.