Brensocatib: The First Pill Approved for Bronchiectasis

Table of Contents

1. Why the Drug Targets Neutrophils
2. How It Lowers Neutrophil Enzyme Activity
3. The Phase 2 WILLOW Trial
4. The Phase 3 ASPEN Trial
5. Lung Function and Symptoms in ASPEN
6. Subgroups and Pooled Analysis
7. Skin, Gum and Tooth Findings
8. Other Label Warnings and Findings
9. Approval Dates in the United States and Europe
10. How the Body Handles the Drug
11. Results in Other Diseases
12. Who Was Not Studied
13. What Remains Unknown
14. Key Research Papers
15. Connections
16. Featured Videos

Why the Drug Targets Neutrophils

In bronchiectasis the airways are permanently widened and scarred, mucus collects, and infection and inflammation keep returning. A 2025 review describes this as a "vicious vortex" of chronic inflammation, recurring infection, poor mucus clearance and progressive lung damage. Neutrophils sit at the center of that inflammation.

Neutrophils carry three tissue-digesting enzymes called neutrophil serine proteases: neutrophil elastase, cathepsin G and proteinase 3. These enzymes help the cell's work against microbes, and they also damage tissue when released in excess. Reviews of the disease report that when free enzyme activity outruns the body's protective enzyme blockers, the result can be structural lung destruction, defects in the airway lining, further infection and worse outcomes. High airway levels of these enzymes are linked to more severe disease.

Earlier attempts included blocking neutrophil elastase directly, and a 2025 review states that those approaches were not successful. Brensocatib takes a different route. It acts one step earlier on the enzyme that switches on all three proteases, so it is not limited to elastase. The same reviews, written just before approval, state that no drug was yet licensed to treat bronchiectasis.

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How It Lowers Neutrophil Enzyme Activity

Dipeptidyl peptidase-1, also called cathepsin C, is the activating enzyme. According to the label, it switches on neutrophil serine proteases while neutrophils are still maturing in the bone marrow. Brensocatib is a competitive, reversible blocker of this enzyme. The result is less active protease in neutrophils.

The effect has been measured in people. In an exploratory analysis of the WILLOW trial, activity of all three proteases fell in sputum, and neutrophil elastase activity fell in white blood cell extracts. The fall was dose-dependent and was visible after four weeks of treatment. Cathepsin G fell the most, then neutrophil elastase, then proteinase 3. Activity returned to baseline four weeks after treatment ended, which fits a reversible drug.

A second WILLOW analysis looked further down the inflammatory chain in sputum:

• Rose with the drug: two natural antimicrobial proteins, secretory leukoproteinase inhibitor and alpha-defensin-3, rose compared with placebo at weeks 4 and 24.
• Fell with the drug: the mucus protein mucin-5AC fell, mainly among patients who began with high neutrophil elastase.
• Did not change: myeloperoxidase, another neutrophil enzyme, did not change.
• Mixed picture: fifteen cytokines and chemokines, which are chemical signals between immune cells, rose compared with placebo at week 4 or week 28. These included interleukin-6.

The authors read this as a broad anti-inflammatory effect beyond the proteases themselves. The analysis does not settle why signaling molecules rose while protease activity fell, or what that means over years.

A modeling study of phase 1 and phase 2 data found a threshold: above a certain drug exposure, sputum neutrophil elastase tended to fall below the level that could be measured, and that outcome was strongly related to fewer flare-ups. The same analysis found no noticeable trend between drug exposure and the safety events of special interest, which were periodontal disease, skin thickening and infections outside the lungs. These results led to the 10 mg and 25 mg doses used in phase 3.

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The Phase 2 WILLOW Trial

WILLOW was a randomized, double-blind, placebo-controlled trial published in 2020 and funded by the drug's manufacturer. It enrolled 256 adults with bronchiectasis who had at least two flare-ups in the previous year, at 116 sites in 14 countries. The trial gave 10 mg of brensocatib (82 people), 25 mg (87 people) or placebo (87 people) once a day for 24 weeks.

The main measure was the time until the first flare-up. The report gives the point at which the first quarter of each group had flared up:

• Placebo: 67 days
• 10 mg: 134 days
• 25 mg: 96 days

The adjusted hazard ratio, a measure of the risk of a flare-up at any given moment, was 0.58 at 10 mg (95% confidence interval 0.35 to 0.95) and 0.62 at 25 mg (0.38 to 0.99), each compared with placebo. Numbers below 1 favor the drug.

The overall flare-up rate was a secondary measure, and the two doses did not behave alike. The rate ratio was 0.64 at 10 mg (0.42 to 0.98), a statistically significant result, and 0.75 at 25 mg (0.50 to 1.13), which was not. Sputum neutrophil elastase activity fell at both doses. Dental adverse events of special interest were more common at 10 mg than with placebo, and skin adverse events of special interest were more common at 25 mg than with placebo.

A later post hoc analysis split WILLOW by disease severity, flare-up history, blood eosinophil count, long-term macrolide antibiotic use and Pseudomonas aeruginosa infection. Results pointed in the drug's favor across these groups, though many of the groups were small and their confidence intervals crossed 1. For example, the hazard ratio was 0.60 (0.25 to 1.45) in people on long-term macrolides and 0.60 (0.38 to 0.94) in people not on them.

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The Phase 3 ASPEN Trial

ASPEN was the larger, year-long test, published in 2025 and funded by the drug's manufacturer. This double-blind trial randomized 1,721 people: 1,680 adults and 41 adolescents. Adults were assigned in equal thirds to 10 mg, 25 mg or placebo once a day for 52 weeks. Adolescents were assigned in a 2:2:1 ratio, so more of them received the drug than placebo.

Adults had to have at least two flare-ups in the previous 12 months, and adolescents at least one. The published design paper for the adults reports 35 countries, a mean age of 61.3 years and 64.7% women. About 70% had moderate-to-severe disease on the Bronchiectasis Severity Index, and 35.7% tested positive for Pseudomonas aeruginosa. No cause was found for the disease in 58.4%.

The label defines a flare-up, called a pulmonary exacerbation in the trial, as a worsening of three or more major symptoms over 48 hours that led a clinician to prescribe antibiotics by mouth or vein. The symptoms are cough, sputum volume or consistency, pus in the sputum, breathlessness, exercise tolerance, fatigue and coughing up blood. A flare-up counted as severe if it needed intravenous antibiotics or a hospital stay.

In percentage terms the flare-up rate was about 21% lower at 10 mg and 19% lower at 25 mg. In absolute terms the gap is about 0.25 to 0.27 flare-ups per person per year, which by simple arithmetic is about one fewer flare-up for every four years of treatment. This figure is an average across the whole group, not a forecast for one person.

The severe flare-up rate was lower on the drug, but the confidence intervals for both doses cross 1, so the trial did not establish a reduction in severe flare-ups.

The 41 adolescents

Adolescents aged 12 to under 18 made up 41 of the 1,721 participants, or about 2.4%. The label says use in this age group is supported by ASPEN, which enrolled these 41 participants, and by additional drug-level data in people aged 12 to 17. The label states that common side effects in these patients were consistent with those in adults. The trial abstract and the label do not give separate flare-up numbers for adolescents, and a group this small could not produce a precise estimate. A 2026 modeling analysis pooling 11 clinical trials supported the same two doses for people aged 12 and older without adjustment.

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Lung Function and Symptoms in ASPEN

Lung function was measured with forced expiratory volume in 1 second, the amount of air a person can blow out in the first second after taking a full breath and using a bronchodilator. All three groups declined over the year:

• Placebo: a decline of 62 mL
• 10 mg: a decline of 50 mL, a difference of 11 mL from placebo (95% confidence interval −14 to 37), not statistically significant
• 25 mg: a decline of 24 mL, a difference of 38 mL from placebo (11 to 65), statistically significant

So the lung-function signal appeared only at the higher dose, and it amounts to a slower decline, not a gain in lung function. For scale, 38 mL is about two and a half tablespoons. Whether it adds up to a larger difference over many years is unknown, since the trial lasted one year.

Symptoms were measured in adults with the respiratory symptoms score of the Quality of Life-Bronchiectasis questionnaire. The trial registry lists these results for week 52:

• Placebo: a 4.8-point improvement
• 10 mg: a 6.8-point improvement, a difference of 2.0 points from placebo (−0.1 to 4.1)
• 25 mg: an 8.6-point improvement, a difference of 3.8 points from placebo (1.7 to 5.9)

A later ASPEN report describes the 25 mg symptom result as "nominally" significant. The trial's order of testing placed symptoms after severe flare-ups, which had not reached significance. For scale, a 2015 validation study set the minimal important difference on this scale at 8.0 points. The trial result is a difference between group averages, so the two figures are not a direct comparison.

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Subgroups and Pooled Analysis

Two ASPEN subgroup reports came out in 2026. Among 191 participants of Asian race, both doses lowered the flare-up rate by about 60% compared with placebo. At 25 mg the difference in forced expiratory volume in 1 second was 69 mL (24 to 114), and the symptom score difference was 7.49 points (2.48 to 12.50). Among 87 Japanese patients, the rate ratios were 0.37 at 10 mg (0.16 to 0.87) and 0.32 at 25 mg (0.14 to 0.75). At 25 mg the difference in forced expiratory volume in 1 second was 97 mL (32 to 162). The first report states that ASPEN was not powered to detect treatment differences in these subgroups, so these larger numbers come with wide uncertainty.

A 2025 meta-analysis pooled four randomized trials of this drug family, with 2,523 patients in total. It covers the drug family as a whole, not brensocatib alone. It reports fewer patients with at least one flare-up (risk ratio 0.64, 0.52 to 0.78), fewer with severe flare-ups (0.44, 0.21 to 0.92), more who stayed free of flare-ups (1.33, 1.13 to 1.57), and a modest gain in symptom scores (2.80 points, 1.10 to 4.50). It found no difference in post-bronchodilator forced expiratory volume in 1 second, which differs from the ASPEN 25 mg result.

The severe flare-up figure in this pooled analysis also goes further than ASPEN's own result, where the intervals crossed 1. A second drug of the same family, tested in the phase 2 AIRLEAF trial of 322 adults, showed a dose-dependent benefit on time to first flare-up. Its individual doses did not reach significance (hazard ratio 0.71, 0.48 to 1.05, at the highest dose, and 0.66, 0.40 to 1.08, at the middle dose).

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Skin, Gum and Tooth Findings

Skin and gum effects are two of the three warnings on the label, and they have a biological backstory. People born with two broken copies of the cathepsin C gene have a rare inherited disease called Papillon-Lefèvre syndrome. It causes thickened skin on the palms and soles and severe early gum disease that costs them both their baby teeth and adult teeth. A 2004 study found that these patients have a severe reduction in the activity of neutrophil serine proteases. Their neutrophils were not uniformly defective at killing two common bacteria, however.

Brensocatib blocks the same enzyme, but temporarily and in adults and adolescents who were born with it working. The syndrome is a lifelong, complete genetic loss, and the sources read for this page do not show that the drug reproduces it. The trials monitored skin and periodontal events specifically, and WILLOW's independent safety committee included experts in both fields.

Skin findings in ASPEN

All three were most frequent at 25 mg. The ASPEN report singles out hyperkeratosis as the one adverse event with a higher incidence on the drug. A phase 1 study in healthy Japanese and White adults had already listed skin exfoliation among its most frequent side effects. The label directs prescribers to watch for new rashes and skin conditions and to refer patients to a dermatologist for evaluation.

Gum and tooth findings

The findings on gums are not uniform across sources, and both sides of the record are reported here:

• Label, WILLOW: gingival and periodontal adverse reactions occurred in 9.9% at 10 mg and 10.1% at 25 mg, compared with 2.4% on placebo. The label states this was higher than in ASPEN and carries gum and periodontal reactions as a named warning.
• Examination data, WILLOW: a prespecified dental analysis measured the depth of the pockets around teeth at screening, week 8 and week 24. At week 24, the changes were similar in all groups (−0.07, −0.06 and −0.15 mm at 10 mg, 25 mg and placebo). Gum inflammation scores were also similar. The authors report no changes in periodontal status over 24 weeks and note that oral health improved in all groups, possibly from regular dental care during the trial.

So reported gum events were more frequent on the drug in WILLOW, while measured pocket depth over six months did not separate the groups. Six months of measurement cannot speak to years of use. The label directs prescribers to send patients for regular dental checkups and routine dental hygiene during treatment. The patient leaflet lists new gum or tooth symptoms among the problems to report.

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Other Label Warnings and Findings

The current label on DailyMed, a version effective in March 2026, lists no contraindications. It gives three warnings: skin reactions, gum and periodontal reactions, and live attenuated vaccines. These are its other findings:

• Live attenuated vaccines: combined use has not been evaluated, and whether such a vaccine stays safe and effective during treatment is unknown. The label's instruction is against using them during treatment.
• Upper respiratory infections: 25% on placebo, 27% at 10 mg, 29% at 25 mg. This category includes COVID-19 and influenza.
• Headache: 7%, 7% and 9%.
• High blood pressure: 3% on placebo, 5% at 10 mg and 2% at 25 mg, with no rise at the higher dose.
• Liver enzymes: average alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase rose from baseline more on the drug from week 4 through week 56. Alanine aminotransferase above three times the upper limit of normal occurred in 0% on placebo, 1.2% at 10 mg and 0.9% at 25 mg. Aspartate aminotransferase above three times that limit occurred in 0.2%, 0.3% and 0.5%. Alkaline phosphatase above 1.5 times its limit occurred in 2.5%, 4.1% and 4.0%.
• Skin cancers: 1.1% on placebo, 0.5% at 10 mg and 1.9% at 25 mg, with no consistent direction across the doses. A two-year study in rats and a six-month study in transgenic mice found no evidence of tumors.
• Hair loss: 0.4% on placebo, 1.5% at 10 mg and 1.6% at 25 mg.
• Pregnancy: the label reports no available data in pregnant women. In pregnant rats, a bent shoulder blade malformation appeared at maternal exposure 128 times the top human dose, with no adverse findings at 42 times. Rabbits showed no adverse fetal effects up to 20 times.
• Breastfeeding: no data exist on the drug in human milk, on a breastfed infant, or on milk production.

For serious adverse events in ASPEN, the trial registry lists 101 of 582 people at 10 mg, 97 of 574 at 25 mg and 108 of 563 on placebo. Serious events coded as "bronchiectasis" affected 47, 48 and 67 people. Deaths numbered 2, 4 and 8 respectively, but death was not among the trial's listed efficacy measures. Overall, adverse events of any kind were reported by 452, 440 and 448 people. The published report calls the incidence similar across groups except for hyperkeratosis.

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Approval Dates in the United States and Europe

The Food and Drug Administration's drug approvals database records the original approval of this application on 12 August 2025, under priority review. That date matches the one on this site's Bronchiectasis page and the 2026 "First Approval" drug profile. The approved use covers non-cystic fibrosis bronchiectasis in adults and in children 12 years and older.

The same profile reports a positive opinion in the European Union on 17 October 2025. The European Medicines Agency's public record lists the marketing authorization as issued on 18 November 2025.

ASPEN gave 10 mg or 25 mg once a day, and the label lists these same two tablet strengths, with or without food. Its dosing section gives no rule for choosing between them. As the numbers above show, the flare-up reduction was close at the two doses, while the lung-function difference appeared only at 25 mg and skin findings were more frequent at 25 mg.

Two guidelines were published after the approval. The European Respiratory Society's 2025 guideline strongly recommends long-term macrolide treatment for adults at high risk of flare-ups, airway clearance for most patients, and long-term inhaled antibiotics for those with chronic Pseudomonas aeruginosa infection at high risk. The American College of Chest Physicians' 2026 guideline reports 13 conditional recommendations, mostly on low-certainty evidence. Neither guideline's abstract names brensocatib, and the full recommendation texts were not available for this page. In ASPEN, 19% of participants were already on long-term macrolides.

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How the Body Handles the Drug

According to the label, the drug peaks in the blood within about 1 to 1.4 hours and is more than 80% absorbed, and a high-fat meal made no clinically relevant difference. Its half-life in healthy people ranged from 25 to 39 hours, which fits once-daily use. After a single radiolabeled dose, 54.2% was recovered in urine and 28.3% in stool.

The liver breaks it down mainly through the cytochrome P450 3A enzyme, and less through two others. One main breakdown product is thiocyanate. The label states that plasma thiocyanate did not change in a clinically meaningful way at the approved doses.

Drug interaction studies listed on the label measured these changes in blood levels:

• Clarithromycin (a macrolide antibiotic that strongly blocks the enzyme): peak up 68%, total exposure up 55%.
• Verapamil (a moderate blocker): peak up 53%, total exposure up 32%.
• Rifampin (a strong inducer of the enzyme): peak down 15%, total exposure down 33%.
• Esomeprazole (an acid reducer): no change.

The clarithromycin figure matters to this disease because long-term macrolides are common in it. The label reports no study with azithromycin. The 2026 modeling analysis found no factor it judged clinically relevant enough to change the dose.

Single-dose studies found little effect from impaired organs. In 28 people with normal or impaired kidney function, drug levels did not differ significantly. In 27 people with normal or impaired liver function, exposure differed by 20% or less. Those were single doses, so they do not describe long-term use in these groups.

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Results in Other Diseases

Because neutrophils play a part in many illnesses, the drug has been tried elsewhere, and the results so far do not match the bronchiectasis results:

• COVID-19 in hospital: a randomized trial at 14 UK hospitals gave 25 mg or placebo for 28 days to 406 patients. Those on brensocatib had worse clinical status at day 29 (adjusted odds ratio 0.72, 0.57 to 0.92). The authors concluded that it did not improve clinical status.
• Hidradenitis suppurativa: the phase 2b CEDAR trial is listed on the trial registry as terminated, with the stated reason "Lack of Efficacy".
• Chronic rhinosinusitis without nasal polyps: the phase 2b BiRCh trial is listed as completed in October 2025. The registry record showed no posted results when read for this page, and no published report of its results was found.
• Cystic fibrosis: a 28-day phase 2a study in 29 adults measured drug levels and safety, not flare-ups. Blood and sputum protease levels fell, and no new safety signals appeared. The approved use excludes bronchiectasis due to cystic fibrosis, which ASPEN also excluded.

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Who Was Not Studied

The ASPEN registry entry lists who could not enroll, and the trial results apply most directly to the people who did. The exclusions and entry limits included:

• People with bronchiectasis due to cystic fibrosis.
• People whose main diagnosis was chronic obstructive pulmonary disease or asthma.
• Current smokers.
• People with known or suspected immune deficiency, including human immunodeficiency virus infection or a history of invasive opportunistic infections.
• People under treatment for nontuberculous mycobacterial lung infection, allergic bronchopulmonary aspergillosis or tuberculosis.
• People with active symptomatic COVID-19, or a flare-up within 4 weeks before screening.
• People given a live attenuated vaccine within the previous 4 weeks.
• Adults with fewer than two flare-ups in the past year, and adolescents with none.
• Children under 12. The label states safety and effectiveness are not established in this age group.

Pregnancy was not studied, and participants of childbearing potential had to use highly effective contraception. The label's table of participants also shows how few people were enrolled from some groups: 10 Black or African American participants of 1,721 in ASPEN (1%), and 4 of 256 in WILLOW (2%). On the other side, age was well represented, with 51% of drug-treated patients aged 65 or older and 15% aged 75 or older, and the label reports no observed differences in safety or effectiveness for them.

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What Remains Unknown

• Long-term effects: the published randomized results stop at 52 weeks of treatment. This disease lasts decades, and no results were found on whether skin, gum or lung effects change with many years of use.
• Lung damage itself: the sources read here report flare-ups, breathing tests and symptoms. They do not show whether the drug slows the structural airway damage seen on scans.
• Survival: no trial here was designed to test whether the drug extends life.
• Severe flare-ups: ASPEN's result fell short of statistical significance, and only a pooled analysis of the drug family found a reduction.
• Which dose suits whom: the label lists two doses without a rule, and the sources read here do not identify a group that does better on either.
• Adolescents: 41 participants cannot give a precise estimate of benefit or of rarer harms.
• Immune defense: people with immune deficiency were excluded, and the COVID-19 trial's abstract does not explain the worse outcome.
• Who gains most: a 2025 review names finding biomarkers to guide treatment as a future direction.

Most of the trial evidence also comes from one funder. ASPEN and WILLOW were funded by the manufacturer, and several analyses on this page have company employees as authors. The COVID-19 trial was sponsored by a university with support from the same company.

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Key Research Papers

1. Chalmers JD, Burgel PR, Daley CL, De Soyza A, Haworth CS, Mauger D, Loebinger MR, McShane PJ, Ringshausen FC, Blasi F, Shteinberg M, Mange K, Teper A, Fernandez C, Zambrano M, Fan C, Zhang X, Metersky ML; ASPEN Investigators. Phase 3 Trial of the DPP-1 Inhibitor Brensocatib in Bronchiectasis. N Engl J Med. 2025;392(16):1569-1581. PubMed PMID: 40267423
2. Chalmers JD, Haworth CS, Metersky ML, Loebinger MR, Blasi F, Sibila O, O'Donnell AE, Sullivan EJ, Mange KC, Fernandez C, Zou J, Daley CL; WILLOW Investigators. Phase 2 Trial of the DPP-1 Inhibitor Brensocatib in Bronchiectasis. N Engl J Med. 2020;383(22):2127-2137. PubMed PMID: 32897034
3. Chalmers JD, Burgel PR, Daley CL, De Soyza A, Haworth CS, Mauger D, Mange K, Teper A, Fernandez C, Conroy D, Metersky M. Brensocatib in non-cystic fibrosis bronchiectasis: ASPEN protocol and baseline characteristics. ERJ Open Res. 2024;10(4):00151-2024. PubMed PMID: 39040578
4. Cipolla D, Zhang J, Korkmaz B, Chalmers JD, Basso J, Lasala D, Fernandez C, Teper A, Mange KC, Perkins WR, Sullivan EJ. Dipeptidyl peptidase-1 inhibition with brensocatib reduces the activity of all major neutrophil serine proteases in patients with bronchiectasis: results from the WILLOW trial. Respir Res. 2023;24(1):133. PubMed PMID: 37198686
5. Johnson ED, Long MB, Perea L, Shih VH, Fernandez C, Teper A, Cipolla D, McIntosh E, Galloway R, Eke Z, Shuttleworth M, Hull R, Spinou A, De Soyza A, Ringshausen FC, Goeminne P, Lorent N, Haworth C, Loebinger MR, Blasi F, Shteinberg M, Aliberti S, Polverino E, Sibila O, Shoemark A, Mange K, Huang JTJ, Stobo J, Chalmers JD. Broad Immunomodulatory Effects of the Dipeptidyl Peptidase-1 Inhibitor Brensocatib in Bronchiectasis: Data from the Phase 2, Double-Blind, Placebo-controlled WILLOW Trial. Am J Respir Crit Care Med. 2025;211(5):770-778. PubMed PMID: 39938076
6. Chalmers JD, Usansky H, Rubino CM, Teper A, Fernandez C, Zou J, Mange KC. Pharmacokinetic/Pharmacodynamic Evaluation of the Dipeptidyl Peptidase 1 Inhibitor Brensocatib for Non-cystic Fibrosis Bronchiectasis. Clin Pharmacokinet. 2022;61(10):1457-1469. PubMed PMID: 35976570
7. Chalmers JD, Loebinger MR, Teper A, McShane PJ, Fernandez C, Fucile S, Haworth CS, Lauterio M, van der Laan R, Shih VH, Metersky ML. Brensocatib in patients with bronchiectasis: subgroup analyses from the WILLOW trial. ERJ Open Res. 2025;11(1):00505-2024. PubMed PMID: 39872387
8. Gunsolley JC, Chalmers JD, Sibila O, Fernandez C, Scannapieco FA. Periodontal Effects of the Reversible Dipeptidyl Peptidase 1 Inhibitor Brensocatib in Bronchiectasis. JDR Clin Trans Res. 2024;9(3):277-285. PubMed PMID: 37746735
9. Addrizzo-Harris D, Chalmers JD, Aliberti S, Burgel PR, Morrissey BM, Zhang X, Fan C, Lauterio M, Fucile S, Griffis D, Teper A. Efficacy and Safety of Brensocatib in Participants of Asian Race with Non-cystic Fibrosis Bronchiectasis: A Subgroup Analysis of the ASPEN Trial. Pulm Ther. 2026;12(3):917-936. PubMed PMID: 42461571
10. Morimoto K, Chalmers JD, Burgel PR, Daley CL, De Soyza A, Mauger D, Metersky ML, Zhang X, Li S, Goto Y, Teper A, Fernandez C, Hasegawa N. Efficacy and safety of brensocatib in Japanese patients with non-cystic fibrosis bronchiectasis: Analysis of the ASPEN trial. Respir Investig. 2026;64(2):101357. PubMed PMID: 41519018
11. Emara A, Awashra A, Ellebedy M, Abbas OF, Diaa A, Elgendy MS, Emara M, Shubietah A, Abdeen AMZ, Safi F. Efficacy and safety of DPP-1 inhibitors in bronchiectasis: a GRADE-assessed meta-analysis of randomized controlled trials. Respir Res. 2025;26(1):332. PubMed PMID: 41299471
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16. Usansky H, Yoon E, Teper A, Zou J, Fernandez C. Safety, Tolerability, and Pharmacokinetic Evaluation of Single and Multiple Doses of the Dipeptidyl Peptidase 1 Inhibitor Brensocatib in Healthy Japanese and White Adults. Clin Pharmacol Drug Dev. 2022;11(7):832-842. PubMed PMID: 35411669
17. Yeung SA, Stein DS, Marbury TC, Usansky H. The pharmacokinetics of brensocatib in participants with renal impairment following a single oral administration. Br J Clin Pharmacol. 2025;91(4):1191-1197. PubMed PMID: 39574348
18. Usansky H, Au Yeung S, Li S, Marbury T, Lawitz E, Kayali Z, Stein DS. Pharmacokinetics and Safety of a Single Dose of Brensocatib in Participants with Hepatic Impairment and Matched Participants with Normal Hepatic Functions. Clin Pharmacokinet. 2026;65(3):441-452. PubMed PMID: 41586857
19. Usansky H, Cammarata A, Li C, Au Yeung S, Rubino CM, Wang L, Teper A, Fernandez C, Mange K. Population Pharmacokinetic Analysis of Brensocatib in Adult and Adolescent Patients With Non-Cystic Fibrosis Bronchiectasis. CPT Pharmacometrics Syst Pharmacol. 2026;15(9):e70340. PubMed PMID: 42712175
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24. Chalmers JD, Metersky M, Aliberti S, Morgan L, Fucile S, Lauterio M, McDonald PP. Neutrophilic inflammation in bronchiectasis. Eur Respir Rev. 2025;34(176):240179. PubMed PMID: 40174958
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26. Chalmers JD, Haworth CS, Flume P, Long MB, Burgel PR, Dimakou K, Blasi F, Herrero-Cortina B, Dhar R, Chotirmall SH, Ringshausen FC, Altenburg J, Morgan L, Nigro M, Crichton ML, Van Meel C, Sibila O, Timothy A, Kompatsiari E, Hedberg T, Vandendriessche T, McShane PJ, Tonia T, Winthrop K, Loebinger MR, Lorent N, Goeminne P, Shteinberg M, Polverino E, Aliberti S. European Respiratory Society clinical practice guideline for the management of adult bronchiectasis. Eur Respir J. 2025;66(6):2501126. PubMed PMID: 41016738
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PubMed Topic Searches

1. PubMed: brensocatib
2. PubMed: dipeptidyl peptidase-1 inhibitors in bronchiectasis
3. PubMed: neutrophil serine proteases in bronchiectasis
4. PubMed: Papillon-Lefèvre syndrome and cathepsin C

Label and Registry Records

1. DailyMed: current US prescribing information for brensocatib tablets
2. Food and Drug Administration, Drugs@FDA: application 217673, approved 12 August 2025
3. ClinicalTrials.gov NCT04594369: ASPEN, eligibility and posted results
4. ClinicalTrials.gov NCT03218917: WILLOW
5. ClinicalTrials.gov NCT06685835: CEDAR, hidradenitis suppurativa
6. ClinicalTrials.gov NCT06013241: BiRCh, chronic rhinosinusitis without nasal polyps
7. European Medicines Agency, public medicine record for brensocatib: marketing authorization issued 18 November 2025.

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Connections

• Drugs — the parent section for drug pages
• Bronchiectasis — the disease this drug is approved for
• Pulmonology — the lung disease section
• Cystic Fibrosis — the form of bronchiectasis left out of the approval
• Chronic Obstructive Pulmonary Disease — a main diagnosis excluded from ASPEN
• Pseudomonas Aeruginosa — the airway bacterium in about a third of ASPEN participants
• Periodontitis (Gum Disease) — the background for the label's gum warning
• Hidradenitis Suppurativa — where a phase 2b trial of this drug was stopped

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