Skip to main content

Professor James Chalmers

Professor James Chalmers

Professor (Clinical), Molecular and Clinical Medicine
School of Medicine
University of Dundee School of Medicine
Dundee, Scotland, United Kingdom

Professor (Clinical), Molecular and Clinical Medicine
School of Medicine
University of Dundee School of Medicine
Dundee, Scotland, United Kingdom

Professor Chalmers, can you share your focus on new therapeutic strategies for non-CF bronchiectasis and what key topics you’ll address in the iQ&A Bronchiectasis Pulmonary Medicine Intelligence Zone?

Professor Chalmers, can you share your focus on new therapeutic strategies for non-CF bronchiectasis and what key topics you’ll address in the iQ&A Bronchiectasis Pulmonary Medicine Intelligence Zone?

Professor James Chalmers

Can you discuss the current burden of NCFBE for patients and the healthcare system, in general, especially in regions globally—U.S., Europe, and Japan—where we see high disease burden, increasing prevalence, and profoundly impaired quality of life?

Can you discuss the current burden of NCFBE for patients and the healthcare system, in general, especially in regions globally—U.S., Europe, and Japan—where we see high disease burden, increasing prevalence, and profoundly impaired quality of life?

Professor James Chalmers

Based on WILLOW results in NCFBE, which positive signals—fewer exacerbations, better quality of life, reduced antibiotic use—did you aim to further evaluate and expand upon in the Phase 3 ASPEN trial?

Based on WILLOW results in NCFBE, which positive signals—fewer exacerbations, better quality of life, reduced antibiotic use—did you aim to further evaluate and expand upon in the Phase 3 ASPEN trial?

Professor James Chalmers

Are we entering a new therapeutic era for NCFBE with agents like brensocatib, recently approved to target neutrophil-driven inflammation central to the disease’s pathobiology?

Are we entering a new therapeutic era for NCFBE with agents like brensocatib, recently approved to target neutrophil-driven inflammation central to the disease’s pathobiology?

Professor James Chalmers

Can you explain the role of neutrophil serine proteases in NCFBE inflammation and how DPP-1 inhibition with brensocatib reduces NSP activity, mitigating progressive pulmonary inflammation?

Can you explain the role of neutrophil serine proteases in NCFBE inflammation and how DPP-1 inhibition with brensocatib reduces NSP activity, mitigating progressive pulmonary inflammation?

Professor James Chalmers

Following ASPEN’s positive results and FDA approval of brensocatib, how can clinicians best identify patient populations most likely to benefit from its disease- and symptom-modifying effects?

Following ASPEN’s positive results and FDA approval of brensocatib, how can clinicians best identify patient populations most likely to benefit from its disease- and symptom-modifying effects?

Professor James Chalmers

Can you summarize the Phase 3 ASPEN trial design and findings, including insights on the two dosing regimens (10 mg vs 25 mg) and what they revealed about brensocatib’s relative efficacy and safety?

Can you summarize the Phase 3 ASPEN trial design and findings, including insights on the two dosing regimens (10 mg vs 25 mg) and what they revealed about brensocatib’s relative efficacy and safety?

Professor James Chalmers

Can you outline the Phase 2 WILLOW trial design and results for brensocatib in NCFBE, including key efficacy and safety endpoints? Did the study demonstrate improvements in quality of life for participants?

Can you outline the Phase 2 WILLOW trial design and results for brensocatib in NCFBE, including key efficacy and safety endpoints? Did the study demonstrate improvements in quality of life for participants?

Professor James Chalmers

Before discussing WILLOW and ASPEN, what clinical biomarkers and symptomatic endpoints were prioritized to fully assess brensocatib’s efficacy, disease-modifying potential, and impact on quality of life?

Before discussing WILLOW and ASPEN, what clinical biomarkers and symptomatic endpoints were prioritized to fully assess brensocatib’s efficacy, disease-modifying potential, and impact on quality of life?

Professor James Chalmers

Given ASPEN’s finding of clinically meaningful efficacy differences between 10 mg and 25 mg brensocatib, how should clinicians translate these results into frontline dosing strategies for NCFBE management?

Given ASPEN’s finding of clinically meaningful efficacy differences between 10 mg and 25 mg brensocatib, how should clinicians translate these results into frontline dosing strategies for NCFBE management?

Professor James Chalmers

Given brensocatib’s recognition as a breakthrough in NCFBE care, how do you envision its role in current management and its integration into near-future treatment strategies for this progressive condition?

Given brensocatib’s recognition as a breakthrough in NCFBE care, how do you envision its role in current management and its integration into near-future treatment strategies for this progressive condition?

Professor James Chalmers

Given NCFBE’s basis in inflammatory dysregulation, why was the prior therapeutic toolkit insufficient for meaningful outcomes, and how does brensocatib’s approval address these limitations?

Given NCFBE’s basis in inflammatory dysregulation, why was the prior therapeutic toolkit insufficient for meaningful outcomes, and how does brensocatib’s approval address these limitations?

Professor James Chalmers

Given NCFBE’s heterogeneity and global prevalence, what are its key etiologies—particularly chronic infection—and how does recognizing these factors enhance detection, treatment, and confirmation of this severe pulmonary condition?

Given NCFBE’s heterogeneity and global prevalence, what are its key etiologies—particularly chronic infection—and how does recognizing these factors enhance detection, treatment, and confirmation of this severe pulmonary condition?

Professor James Chalmers

How has our delineation of the role of the neutrophil-mediated chronic inflammation in NCFBE changed the approach to developing and validating new disease-modifying treatments?

How has our delineation of the role of the neutrophil-mediated chronic inflammation in NCFBE changed the approach to developing and validating new disease-modifying treatments?

Professor James Chalmers

Upon starting therapy with brensocatib, what are the first signs of clinical improvement that patients with NCFBE are likely to report to their treating physicians? What endpoints—symptomatic and spirometry—should be monitored?

Upon starting therapy with brensocatib, what are the first signs of clinical improvement that patients with NCFBE are likely to report to their treating physicians? What endpoints—symptomatic and spirometry—should be monitored?

Professor James Chalmers

What immune, neutrophil, serine protease, and cytokine-driven processes drive progressive lung tissue destruction underlying NCFBE’s clinical symptoms and natural history

What immune, neutrophil, serine protease, and cytokine-driven processes drive progressive lung tissue destruction underlying NCFBE’s clinical symptoms and natural history

Professor James Chalmers