Phase Ib/IIa data show an experimental antibody cutting severe COPD flare-ups by up to 100% at the highest dose, a signal for aging lungs.
Chronic obstructive pulmonary disease doesn’t come up much in longevity conversations. It probably should. It’s largely a disease of decades, cumulative lung damage, often from years of smoking, that catches up with people later in life and steadily narrows what their bodies can do. Every flare-up chips away at lung function that doesn’t come back. Fewer flare-ups is a healthspan story as much as it’s a respiratory one, even if nobody frames it that way.
That’s roughly the backdrop for new data out of Mabwell, a Shanghai-listed biopharmaceutical company. The company shared Phase Ib/IIa results for its antibody 9MW1911 in patients with moderate-to-severe COPD, results that were also presented as a poster at the European Respiratory Society International Congress 2026 [1].
The antibody blocks a protein called ST2, part of a signaling pathway involved in the kind of inflammation that drives a COPD flare-up. Mabwell built it on its own high-efficiency B lymphocyte screening platform, and it’s now the first homegrown antibody targeting ST2 to reach clinical testing in China.
The trial, known as 9MW1911-C03, enrolled 80 former smokers with moderate-to-severe COPD. Randomized, double-blind and placebo-controlled. Four doses were tested, 100mg, 300mg, 600mg and 900mg, given by IV infusion every four weeks. Safety, tolerability and pharmacokinetics were the primary goals; efficacy and immunogenicity were assessed as secondary measures.
Compared with placebo, the annualized rate of moderate-to-severe exacerbations dropped 24% in the 600mg group and 81% in the 900mg group. Severe exacerbations fell further still, 47% at 600mg, 100% at 900mg. This is an 80-person study, still early phase, so those numbers are promising rather than proven. However, a dose-response curve that clean, in a disease with genuinely limited treatment options, is hard to wave off.
Drug exposure rose roughly in proportion to dose across the range tested, and blood concentrations reached a steady state by around week 12. Most participants had relatively low blood eosinophil counts, a detail worth sitting with. Some existing COPD therapies tend to work best in patients with higher eosinophil levels, so 9MW1911 may be working through a different piece of the inflammatory puzzle altogether.
Mabwell isn’t treating this as a one-off readout. Enrollment has already wrapped for a larger Phase IIb study, and the company expects to start Phase III around the end of 2026. The FDA has also cleared an IND application for a separate Phase IIa trial in moderate-to-severe COPD patients in the United States, so this isn’t strictly a China story anymore.
COPD remains one of the leading causes of death worldwide, and older adults bear the brunt of it. Aging lungs simply have less reserve capacity to absorb repeated inflammatory hits. Treatments that meaningfully cut exacerbation frequency don’t just help in the moment; they slow how fast lung function erodes over the years that follow, which is the kind of thing that stretches functional years rather than just chronological ones.
Longevity science tends to get associated with senescent cells, NAD+, that whole vocabulary. A lot of the actual progress against age-related decline looks more like this instead: a targeted antibody, an inflammatory pathway most people have never heard of and a disease that quietly takes independence away from older adults one flare-up at a time. If Phase III holds up anywhere close to what’s shown here, 9MW1911 could become one of those unglamorous but genuinely useful additions to how we treat aging lungs.
