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Discover how precision medicine reshapes COPD treatment, focusing on inflammation and patient-specific traits for improved outcomes in airway diseases.
Over the past several years, pulmonology has been undergoing a profound transformation. What was once a field dominated by incremental adjustments to inhaled bronchodilators and corticosteroids is now moving toward a more individualized, precision-medicine model.
Despite previous setbacks in the field such as with benralizumab (Fasenra), that shift has accelerated in 2025, driven not only by expanding biomarker research but also by the long-awaited arrival of biologic therapies for chronic obstructive pulmonary disease (COPD).1
With the US Food and Drug Administration (FDA) approvals of dupilumab (Dupixent) for eosinophilic COPD in 2024 and mepolizumab in 2025, clinicians finally have targeted options and an expanded toolbox that reflect an increasingly nuanced understanding of disease endotypes beyond traditional silos of “asthma” and “COPD.”2,3
“At least in certain patients, there are mechanisms across the traditional disease categories, which, which may be flawed. It may be that our traditional names for these diseases are even fundamentally flawed. You know, there are some experts in the field who are discussing that more and more… There’s definitely food for thought in what they say,” Linda Rogers, MD, associate professor in the Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Mount Sinai, told HCPLive.
In this installment of HCPLive’s This Year in Medicine series, HCPLive spoke with Rogers along with Gerard Criner, MD, and Andrew (Troung-An) Ho, MD, from Temple University, to explore how biologics, biomarker-guided decision making, and new conceptual frameworks for airway disease are reshaping care today—and where the next decade of precision pulmonology may be headed.
Criner, Ho, and Rogers concur that clinicians have been moving away from rigid disease categories and lean instead into a “treatable traits” philosophy that prioritizes inflammatory patterns, biomarker profiles, exacerbation behavior, patient history, and longitudinal outcome tracking. This evolution is still in its early phases, and the field continues to grapple with operational challenges such as incomplete data sharing, fragmented care, and the wide variability in patient expectations for what optimized control looks like. But the shift is undeniable, and for many specialists, it represents the most exciting era in respiratory medicine in decades.
For much of modern respiratory medicine, asthma and COPD have been treated as distinct, siloed conditions defined primarily by symptoms, spirometry thresholds, and smoking history. Yet clinicians increasingly recognize these categorical labels often oversimplify a highly heterogeneous set of airway diseases. This is particularly true in COPD, where the past decade has revealed substantial variation in inflammatory profiles, exacerbation patterns, airway remodeling, and longitudinal progression.
All 3 experts emphasized that Type 2 (T2) inflammation—long associated with asthma—has a meaningful footprint in COPD as well. Its presence has diagnostic, prognostic, and therapeutic implications, especially now that multiple biologics are proving active across both disease spaces. The idea that a COPD patient can meaningfully respond to therapies historically approved for severe asthma has forced the field to re-examine earlier assumptions about what defines each disorder.
“This is what a clinician is going to have to decide when they see a patient, you know, is this asthma? Is this COPD? Is a COPD with overlap? And I guess the question is, does it really matter if they've they're phenotypically behaving more like COPD,” Ho, a Pulmonary and Critical Care Fellow at the Temple Lung Center, said.
Clinicians have moved away from the concept of “asthma-COPD overlap” which implies 2 fixed diseases coexisting in the same patient, in favor of viewing airway disease as a spectrum. In that model, features such as eosinophilia, fixed airflow limitation, hyperreactivity, and exacerbation susceptibility can present in various combinations, independent of which diagnostic label a patient initially receives.
This spectrum-based framing aligns with the emerging “treatable traits” strategy clinicians have adopted: identifying which traits drive morbidity in their patients, including T2 inflammation, chronic bronchitis, emphysema distribution, exacerbation frequency, and treating them directly.
“We used to kind of think about these as 2 really separate baskets. And the more we learn, the less separate they are. There are definitely gray areas in between… The therapies that are effective in patients with asthma with eosinophils and type 2 inflammation seem to also be effective in COPD with that type of inflammation. And so, the therapies are crossing boundaries, and that is going to add a lot of value for high-risk COPD patients. We're pretty excited about that,” Rogers said.
As both asthma and COPD shift toward biological phenotyping, blood eosinophil counts have become indispensable to patient selection, risk stratification, and monitoring, especially in patients without clear separating features between asthma and COPD.
Eosinophil counts have long been considered more traditionally associated with asthma, but in practice they have become one of the most clinically actionable measures for COPD as well. However, they do not provide a full picture alone, and they can be influenced by infection, steroids, and comorbidities. Additionally, not all patients with elevated eosinophils respond to biologics, and some patients with lower counts can still exhibit T2-driven disease.
The diagnostic boundary between asthma and COPD has always been porous, but biological insights and therapeutic advances are prompting clinicians to question whether traditional labels remain fit for purpose, especially when they may fail to predict response to key therapies.
Yet moving beyond categorical diagnoses is not trivial. It impacts trial design, regulatory structures, payer policies, and the logistics of real-world practice. Even so, 2025 appears to be a tipping point: a year when novel biologic options for COPD have enabled trait-based thinking to align with therapeutic reality.
“The lines between the 2 diagnoses are getting blurrier as more data comes out. I think there may be changes in these diagnostic boxes. It's a complicated issue because it impacts sort of how the criteria for designing clinical trials and drug approval. So, it's not an easy issue to really shift on, but there's definitely movement in those spaces,” Rogers said.
The approval of dupilumab in late 2024 as the first biologic for eosinophilic COPD marked a watershed moment in respiratory care. For more than a decade, pulmonologists had seen targeted biologics transform outcomes in severe asthma, with patients who needed chronic prednisone, or had multiple annual exacerbations, suddenly able to dramatically reduce flares, improve symptoms, and in some cases even achieve clinical remission.
COPD clinicians, dealing with a condition historically defined by slow decline and limited therapeutic innovation, lacked equivalent tools. The arrival of dupilumab—and soon after, mepolizumab—changed that calculus as the first targeted biologic option for COPD, one that offered hope to a subset of patients who had exhausted traditional inhaled regimens.
Although the experts note that biologics do not work for everyone, there is consensus that when they work, the responses can be striking. Patients long accustomed to multiple exacerbations per year, chronic systemic steroid use, or prolonged symptom burden may see substantial improvement once T2 inflammation is addressed directly.
Even more strikingly, subsets of patients have begun to achieve clinical remission using reasonable definitions of “no systemic steroids, no exacerbations, and good symptom control.” While remission terminology is not yet widely applied in COPD, the idea is beginning to permeate discussions—especially since the same medications are now approved in both diseases. Clinicians are beginning to wonder: if remission is possible in asthma, might it be achievable for a biologic-eligible COPD subset as well?
That question remains open, but the shift in mindset is meaningful. Many pulmonologists are moving from managing deterioration to aiming for measurable stability, flare prevention, and long-term maintenance.
Ho, Criner, and Rogers agreed that remission criteria will increasingly shape real-world care and clinical trials, particularly as more therapies targeting different inflammatory pathways enter evaluation. Biomarkers, trait-based diagnostics, early intervention, and better patient education will all be necessary to operationalize remission as a standard clinical goal.
“We'll still need some kind of bedside tool biomarker that everyone can use to define the patients better moving forward. So, I think it's still early days on patient selection, at least for COPD,” Ho said.
In practice, most clinicians already treat based primarily on traits rather than labels—particularly when faced with a patient who has a significant smoking history, fixed obstruction, and elevated eosinophils. Furthermore, what clinicians historically considered overlap may simply reflect flawed disease constructs. If T2 inflammation is driving exacerbations regardless of whether spirometry meets classic asthma criteria, does labeling meaningfully change management? Our experts think not.
“Whether they have asthma or COPD, if they have [T2 inflammation], then we're going to treat that patient with those agents that treat [T2 inflammation]. Similarly, if we have a patient with type 1 inflammation, we're going to identify and treat the patient with that… I think a lot of the classifications that have been used for disease categories in the past, they're going to become less important in the biologic pathway that needs to be treated that's causing the patient's symptoms. That's what's going to be treated,” Criner, chair and professor of thoracic medicine and surgery at Lewis Katz School of Medicine at Temple University and director of the Temple Lung Center, said.
Other hurdles include clinical trial design, which will evolve to allow inclusion of patients with mixed or ambiguous phenotypes in the near future, and regulatory frameworks, which may need to consider approvals based on trait profiles rather than diseases.
But for now, the practical takeaway is clear: clinicians cannot rely on historical categories to guide every therapeutic decision. Biologics and biomarkers are forcing the field to accept that asthma and COPD share more pathobiology than once thought and that patient outcomes improve when therapies target what is driving disease rather than what diagnosis the chart says.
Despite growing enthusiasm for biologics and precision medicine, major barriers still limit optimal airway disease care. Many patients underreport or forget exacerbations—especially those treated outside pulmonology—which leaves clinicians without full visibility into disease activity. At the same time, long-standing expectations that flare-ups are inevitable prevent some patients from recognizing that zero exacerbations may now be attainable with advanced therapies. Compounding these issues, many individuals reach specialty care only after years of progressive damage, underscoring the need for earlier identification of high-risk patients through better education, improved data integration, and proactive biomarker- or risk-based screening.
Our conversations with Criner, Ho, and Rogers reveal a specialty in transition. COPD is no longer managed solely through bronchodilation, smoking cessation, and palliative stabilization. With biologics now entering the treatment armamentarium, clinicians are beginning to treat COPD in a manner more akin to modern asthma care, in which inflammatory pathways dictate therapy, biomarkers guide decisions, and remission becomes an attainable target rather than an abstract ideal.
“The data we have in clinical trials [support] that there is a role for biologics in patients with COPD and [T2 inflammation]. I think the big kind of hurdle to cross is patient selection and how to really define these in the clinical setting, and which treatments to use for patients. I don't think we know that yet, and it's a little bit too early,” Ho cautioned.
This transformation requires more than new drugs. It demands broader adoption of trait-based diagnostic models, better integration between primary care and specialty care, and a concerted effort to define what good control looks like. The historical silos separating asthma and COPD management are becoming increasingly artificial, and collapsing those silos may be essential for maximizing the benefits of precision medicine.
As 2025 continues to unfold, pulmonology finds itself in a moment of convergence: biologics that transcend traditional categories, biomarkers that illuminate new pathways of risk, and clinicians who are rapidly evolving their definitions of success. The task now is to ensure that these scientific gains translate into practical, equitable, and forward-looking care for every patient with chronic airway disease.
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