At the 2026 European Respiratory Society (ERS) International Congress, Boehringer Ingelheim (BI) presented results from the Phase IIa/IIb trial of BI 1839100, an investigational asset for chronic cough in idiopathic pulmonary fibrosis (IPF). BI terminated the trial in 2025, citing a sponsor decision ahead of planned completion, and also terminated a separate Phase I mass-balance/ADME study at the same time. The presentation matters because chronic cough in IPF remains a persistent unmet need, and full data readouts from terminated assets are rare, according to GlobalData, a leading intelligence and productivity platform.
BI 1839100 is an oral, selective small molecule antagonist of TRPA-1, a sensory ion channel implicated in cough hypersensitivity in fibrotic disease. A Phase I trial confirmed its safety, tolerability, and pharmacokinetics in healthy male subjects, supporting progression to Phase IIa/IIb.
Connor Daniels, Healthcare Analyst at GlobalData, comments: “The ERS 2026 poster provides the first insight into the reasons behind the termination and what it means for the TRPA-1 class in IPF.”
The Phase IIa/IIb trial was a global, randomized, double-blind, placebo-controlled study in 85 patients with IPF and PPF who had clinically meaningful cough, across four arms: 50mg, 100mg or 150mg BI 1839100 twice daily, or placebo. Treatment ran for up to 12 weeks; after four weeks, cough in the 150mg arm was assessed via a portable monitoring device to gauge efficacy. The primary endpoint was the change from baseline in 24-hour cough frequency at week 4 (Phase IIa) and week 12 (Phase IIb).
Although well tolerated, none of the dose groups showed a statistically significant reduction versus placebo at four weeks, so the prespecified interim continuation criteria were not met, and the trial was terminated. However, 97.6% of patients completed the full 12-week observational period, and the results showed a numerical reduction in cough frequency across all dose groups, with the 150mg arm demonstrating a statistically significant, placebo-corrected relative change of -45.5% in 24-hour cough frequency.
Daniels adds: “This suggests that the treatment effect of TRPA-1 inhibition may take longer to emerge clinically, though this should be treated cautiously given the small sample size.”
Directionally favorable findings were also observed in the daytime cough frequency endpoint, with the 150mg group demonstrating a 48.8% decrease in cough frequency compared to 18.6% in the placebo group.
Chronic cough in IPF remains a crowded but clinically unproven space. Merck’s gefapixant (P2X3 antagonist) failed to significantly reduce cough frequency versus its primary endpoint in IPF, and GSK’s camlipixant and Shionogi’s sivopixant have also reported setbacks in refractory chronic cough more broadly. However, in the same ERS 2026 session, Trevi Therapeutics’ nalbuphine (a kappa opioid receptor agonist) reported positive Phase IIb CORAL trial results in IPF cough, with the highest dose (108mg twice daily) showing a -60.2% reduction in objective cough count at week 6 versus -16.9% for placebo.
Daniels concludes: “BI 1839100’s outcome adds to a pattern in which cough mechanisms validated in broader refractory cough populations have struggled to translate into IPF, where cough is thought to be entangled with fibrotic remodelling rather than purely neurogenic hypersensitivity. BI must now decide whether to continue investing in TRPA-1 antagonism, given the week 12 signal at 150mg, or redirect resources to its antifibrotic portfolio.”