Against an older diabetes drug class, yes, and against the other new class, barely. In 32,107 matched pairs of adults with type 2 diabetes and COPD, GLP-1 users had 9.89 moderate or severe exacerbations per 100 person-years against 11.49 on DPP-4 inhibitors [1]. That is a hazard ratio of 0.86 (95% CI 0.81 to 0.91). Put against SGLT2 inhibitors instead, the hazard ratio was 0.94 with an interval running to 1.00, which touches no effect. Everyone in the study had diabetes and coded COPD at a mean age near 70, which is not the population buying from a telehealth page.
Two comparisons that favor the newer drugs
The study emulated three target trials in US insurance claims, matching patients aged 40 and over who carried both diagnoses [1]. Against DPP-4 inhibitors, GLP-1 receptor agonists came in at 9.89 exacerbations per 100 person-years against 11.49 across 32,107 matched pairs. SGLT2 inhibitors against the same comparator ran 9.26 against 11.4, a hazard ratio of 0.81 (95% CI 0.76 to 0.86) across 27,991 pairs. Both results held across the sensitivity and subgroup analyses the authors report.
And one that finds almost nothing
The third comparison put the two newer classes against each other in 36,218 matched pairs, and the difference nearly vanished. It was 9.47 against 10.00 per 100 person-years, a hazard ratio of 0.94 with a 95% confidence interval of 0.89 to 1.00. The upper bound touches no effect, and the rate difference says the same thing at −0.55 per 100 person-years with an interval running to −0.01. Both classes beat an older one and neither clearly beats the other. Quoting the first two comparisons alone would imply a ranking this study does not support, which is the shape taken apart in two meta-analyses of the same six trials.
Do these drugs harm breathing in the first place
That is a separate question and it has its own answer. A systematic review screened 9,086 records and included 123 studies of respiratory adverse events on weight-loss drugs [2]. Liraglutide, semaglutide, tirzepatide and naltrexone-bupropion showed no increase against placebo, with the contributing randomized trials at low risk of bias. Of those 123 studies, 122 were in general populations and one was in people with asthma, so the reassurance mostly comes from people without a lung condition. The full reading of that gap is in the respiratory safety review.
The nearest efficacy result in another lung disease
Asthma has been measured with a tighter design. A propensity-matched cohort of 2,423 adults per group recorded an asthma exacerbation in 1.7% against 4.0% over the following year, a ratio of 0.438 (95% CI 0.306 to 0.626) [3]. Stated as a difference that is 2.2 percentage points, and the difference is the number that tells a reader what it might mean for them. Systemic glucocorticoid exposure ran 16.4% against 23.1%. COPD and asthma are different diseases, so this is a neighbor rather than a substitute. The same gap between a ratio and a difference is set out in the asthma cohort.
Who was in it, and who was not
The cohorts were old and sick by the standards of this market: a mean age near 70, type 2 diabetes, and COPD active enough to be coded as such. Median follow-up was 145 days, with an interquartile range of 61 to 355, which is short for a chronic lung condition. A person buying compounded semaglutide from a telehealth page at 45 with no lung disease sits outside the population these numbers describe. Nothing here is a reason to choose one seller over another. It is a reason to make sure whoever writes the prescription knows the rest of the history. That gap is counted in what happens outside a trial and put into questions they leave open.