Abebaw Yohannes, MSc, PhD, is a professor of physical therapy at the University of Alabama at Birmingham School of Health Professions.

Duloxetine for Patients with COPD Suffering from Comorbid Depression

chronic obstructive pulmonary disease (COPD)

 who also suffer from comorbid depression may be 3 times more likely to be admitted to a hospital compared to non-depressed individuals with COPD. Given that over 15 million people suffer from physician-diagnosed COPD and given the likelihood of such comorbidities, addressing depression has become a significant concern for some in the world of health care providers.

Abebaw Yohannes, MSc, PhD, a professor of physical therapy at the University of Alabama at Birmingham School of Health Professions, is working with a team of investigators on a study assessing the feasibility of duloxetine as a treatment for depression among patients suffering from COPD. Yohannes spoke in the latest issue of 

, the quarterly pulmonology research newsletter powered by the American Lung Association Research Foundation, about his team’s work.

“We may ask why this study is needed,” Yohannes said. “We know from the literature that pharmacological interventions have been employed with the comorbidity of depression for moderate to severe COPD. However, they have been inconclusive. We're especially looking at using…selective norepinephrine reuptake inhibitors, sNRIs, as the first line of treatment for major depression in the general population, because of their efficacy and their safety, compared to tricyclic antidepressants.”

Yohannes highlighted the pilot study’s examination of duloxetine as a newer sNRI and its potential for patients with depression and COPD.

“The overall aim, for one, is to examine attitudes, perceptions, and beliefs of patients…living with depression,” Yohannes said. “So we are hoping to conduct a semi-structured qualitative interview. Patients will be recruited from the outpatient clinic here at the University of Alabama healthcare system as well as Baylor College of Medicine. We’ll try, first, to elucidate the acceptability and attitudes of patients about antidepressant drug therapy, and also probe any fears and misconceptions as well as barriers and facilitators about the treatment.”

To learn more about Yohannes’s research, view the interview above or read his contribution to the second issue of The Respiratory Report here:

Exploring Duloxetine for Depression in COPD: A Pilot Study

Abebaw Yohannes, MSc, PhD, speaks about his team’s pilot study designed to assess the use of duloxetine for patients with COPD and comorbid depression.

Abebaw Yohannes, MSc, PhD

Brian LaMoreaux, MD, MS, is a rheumatologist and Senior Medical Director at Horizon Therapeutics. 

If I told you that people who have been living with urate crystal deposition disease for less than 10 years have twice the risk of death compared to the general population,

 you’d want to know more, right? The disease’s prevalence and severity, which are only increasing, command our attention.

Around 9.2 million people in the United States. are living with this form of arthritis caused by the buildup of uric acid crystals in the body. The disease can cause acute inflammation of joints, hard, lumpy deposits in the skin, called tophi, and permanent joint damage.

 About 100,000 Americans suffer from uncontrolled urate crystal deposition disease, meaning they experience ongoing pain and high uric acid levels even while taking medication.

 All-cause hospitalizations from this disease have increased more than 400% in the last 2 decades,

 likely influenced by the fact that people who live with it are undertreated

 and more likely to have other serious health conditions such as obesity, hypertension, type 2 diabetes, chronic kidney disease, and cardiovascular disease.

At this point, you might be thinking, “If urate crystal deposition disease is so serious, why haven’t I ever heard of it?” The reality is that you have, but you’ve likely never heard it discussed with this name. This disease, experienced by about 4% of the U.S. population, is known much more commonly as 

Despite its severity, gout is often misdiagnosed or left untreated altogether. In fact, only 33% of people who live with gout report using urate-lowering therapies.

Many people have heard of gout, but that name recognition isn’t helping in terms of understanding and treatment. It’s what people 

 they know aboutthe disease that results in and continues to fuel the false narrative that gout is the product of an unhealthy lifestyle. Further complicating matters is the fact that gout often appears as a punchline in popular culture—it’s depicted as humorous, embarrassing and a consequence of overindulgence in food and alcohol.

This stereotype doesn’t just exist among the general public; even rheumatologists, despite their advanced training, often perceive gout as a lifestyle disease and consider patients more responsible for their condition than patients with rheumatoid arthritis. As a result, rheumatologists might believe people who live with gout are less likely to adhere to treatment protocols, and these physicians are, therefore, less likely to think patients would benefit from biological and/or pharmacological interventions.

 Even when they see patients experiencing gout symptoms, physicians may not dig deep enough to diagnose it because they might not consider it as serious as other ailments.

As an industry and a society, we must take gout more seriously. That effort begins with the physicians who diagnose and treat it. It’s essential to recognize that the prevailing stigma and absence of urgency around gout are simply the result of a lack of awareness. Doctors, naturally, are not willfully ignorant, but nearly all are overburdened with disease information and need educational materials along with the time to review them. Physicians should try to stay aware of their potential biases to limit how these beliefs may impact their clinical decision-making and understand how to overcome them to optimize diagnoses and clinical care for all their patients.

Provider burnout plays a role as well; primary care physicians are already screening for a variety of conditions when they see patients, and gout is nowhere near the top of their list. Our primary care colleagues need guidance better to understand the severity of gout and uncontrolled gout so that they can appropriately screen for it and, when indicated, refer patients to specialists and ensure they receive the treatment they need.

The good news is that the technology to detect gout exists. The gold standard for diagnosing gout is still the detection of negatively birefringent monosodium urate crystals from the synovial fluid.

 Additionally, ultrasound has emerged somewhat recently as a promising modality for gout diagnosis.

 Imaging technologies allow us to detect and quantify the overall urate burden and measure the body’s response to treatments in real time by showing urate depletion.

Gout isn’t a punchline. It’s an unfortunate daily reality for millions of people in our country, whether they realize it or not. It’s time to take this severe disease seriously. As a medical community, we need to prioritize provider education to increase screenings, specialist referrals and usage of treatments for gout and uncontrolled gout. We can detect, diagnose and diminish urate deposits in patients, but these technologies only work if we put them to use. And when we do that, when we commit ourselves to improve the quality of care we’re providing people who live with gout and uncontrolled gout, and we also work to improve their quality of life.

Brian LaMoreaux, MD, MS, is a rheumatologist and Senior Medical Director at Horizon Therapeutics.

Vincent ZL, Gamble G, House M, et al. Predictors of mortality in people with recent-onset gout: a prospective observational study. J Rheumatol. 2017;44(3):368-373. doi: 10.3899/jrheum.160596

Kevin Yip MD. Patient information: Gout. JAMA. https://jamanetwork.com/journals/jama/fullarticle/2787544#:~:text=Gout%20affects%20approximately%209.2%20million,in%20men%20and%20older%20people. Published December 28, 2021.

What is gout? - Horizon Therapeutics. https://www.horizontherapeutics.com/PDFs/Uncontrolled-Gout-Facts.pdf. Published May 19, 2019.

Chen-Xu M;Yokose C;Rai SK;Pillinger MH;Choi HK; Contemporary prevalence of gout and hyperuricemia in the United States and decadal trends: The National Health and Nutrition Examination Survey, 2007-2016. Arthritis &amp; rheumatology (Hoboken, N.J.). https://pubmed.ncbi.nlm.nih.gov/30618180/. Published April 15, 2019.

PT; SLKC. Gout and its comorbidities: Implications for therapy. Rheumatology (Oxford, England). https://pubmed.ncbi.nlm.nih.gov/22949727/#:~:text=Gout%20is%20a%20common%20form,known%20as%20the%20metabolic%20syndrome. Published September 3, 2012.

Chen-Xu M, Yokose C, Rai SK, Pillinger MH, Choi HK. Contemporary prevalence of gout and hyperuricemia in the United States and decadal trends: The national health and nutrition examination survey, 2007-2016. Arthritis Rheumatol. 2019;71(6):991-999.

Derksen C, Murdoch R, Petrie KJ, Dalbeth N. "An apple pie a day does not keep the doctor away": Fictional depictions of gout in contemporary film and television. BMC rheumatology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812654/. Published January 18, 2021.

Lopez MA. Perception of gout as a lifestyle disease reinforces stigma. Rheumatology Advisor. https://www.rheumatologyadvisor.com/home/conference-highlights/eular-2022-coverage/perception-of-gout-as-a-lifestyle-disease-reinforces-stigma/. Published June 8, 2022. Accessed August 31, 2022.

Doherty TS, Carroll AE. Believing in Overcoming Cognitive Biases. IUPUI. https://scholarworks.iupui.edu/handle/1805/27596. Published September 1, 2020.

Park S; Lee LE; Kim H; Kim JE; Lee SJ; Yoon S; Shin S; Kang H; Park Y; Song JJ; Lee S; Detection of intracellular monosodium urate crystals in gout synovial fluid using optical diffraction tomography. Scientific reports. https://pubmed.ncbi.nlm.nih.gov/33976275/. Published May 11, 2021.

Thiele RG, Schlesinger N. Diagnosis of gout by ultrasound. OUP Academic. https://academic.oup.com/rheumatology/article/46/7/1116/2899456. Published April 27, 2007.

As an industry and a society, we must take gout more seriously. That effort begins with the physicians who diagnose and treat it. 

Gout Isn’t a Punchline. It’s Time to Stop Treating it Like One. 

Brian LaMoreaux, MD, MS

On September 26, 2024, the US Food and Drug Administration (FDA) approved xanomeline and trospium chloride capsules (Cobenfy), a muscarinic agent, for 

10 months later, the future of muscarinic agents was discussed at the 2025 Southern California Psychiatry Conference (So Cal Psych) in Huntington Beach, CA, from July 11 – 12, 2025.

In this interview at So Cal Psych, Chelsie Monroe, APN, PMHNP-BC, a psychiatric nurse practitioner and founder of a group private practice, Balanced Mental Wellness in Colorado, talked about muscarinic agents—why they are exciting, their robust efficacy data, and when to consider xanomeline trospium chloride (Cobenfy) over clozapine.

 What is exciting about muscarinic agents?

This is really exciting because it's a whole new mechanism of action to use in treating schizophrenia. We're really working off of a whole new pathway, so this is cholinergic pathways to modulate dopamine, which doesn't have the same baggage as our D2 antagonists.

If a clinician is considering trying this with a patient, what should they be thinking about?

We should be thinking about a whole conglomerate of symptoms that we're wanting to improve, and so this particular medication has the opportunity to change both positive, negative, and cognitive symptoms in schizophrenia. We want to be mindful, though, that if they're on current medications for antipsychotics with their schizophrenia, that if there is an anticholinergic on board…combining that with this muscarinic agonist [can lead to] some potential changes that you need to be aware of in the muscarinic system. It's a little bit different, as this medication is typically used as monotherapy, but in reality, we're all trying to figure out how to treat schizophrenia really well, and so we need to be mindful of what other medications are on board.

What does the data show that really makes people think this is what we want to be trying?

The effect sizes of the first 3 trials that were done for Cobenfy, for this muscarinic agonist…are pretty robust. We're looking at in comparison to other antipsychotics; we see that the effect sizes are pretty up there, point 5, 6. If you look at other antipsychotics, the only outlier that's much higher than that is clozapine, which we know is really used well for treatment-resistant schizophrenia, but this has the efficacy that we're looking for in a robust antipsychotic without the baggage of metabolic syndrome, tardive dyskinesia, motor movements.

You mentioned treatment-resistant schizophrenia. What are the thoughts on using Cobenfy treatment?

I have some mixed thoughts. We always think as clinicians, ‘Oh, a new drug is out there. I'm going to use this for my most difficult client, that nothing will work for them, and now this is a new thing, let me try it.’

I want to provide some caution around that we know that about 30% of clients with schizophrenia may be treatment resistant, and that may not be solely due to a dopaminergic problem. So, there is a dopaminergic dysfunction in most patients with schizophrenia, but in those treatment-resistant cases, it may not just be dopamine; it may also be other things like glutamate. And so, there is a reason why we should provide some caution for something like clozapine.

I would definitely not rip clozapine off and try this new medication, because those folks who have met the criteria for clozapine generally can be destabilized very easily. We want to exercise some caution if you're going to use it… with clozapine…. because clozapine is highly anticholinergic, and if you're adding in an anticholinergic with this medication, you want to be really cautious that we're not causing more anticholinergic effects for the client.

Persistently around Clozapine. I'm worried about constipation and ileus, those sorts of things. And so, there's a way to potentially manage both, but I would not switch one for the other.

What advice would you give a clinician to talk to their patient who is nervous about adverse events?

I would give them reassurance that we actually have been managing schizophrenia all along with all this baggage of side effects that you have to follow for that patient's life, right? Every 6 months to a year, we're really managing metabolics. We're constantly looking for tardive dyskinesia. The long haul of this medication, you don't have some of those same concerns that I've been dealing with for the entirety of schizophrenia in my career. All I have to worry about is the first 2 weeks to a month, and that's just getting past the hump of someone potentially having cholinergic side effects that's very different than what they're used to for other antipsychotics.

I would encourage the clinician to actually have some hope and excitement and encourage the client, the patient, that this is a whole new mechanism of action. This is not your typical antipsychotic. It's not just another med that I'm giving you, that you have some predictive value of what you've been experiencing in the past. It's a whole new mechanism. Now, there may be some side effects early on, but if we can mitigate those and get you through the first couple of weeks, we may be in the clear and have the efficacy that we've been looking for all along without all the downsides.

Any other thoughts or tips that you want to share with people?

I would say have openness. You know that you really have to think critically when using these new muscarinic agonists, and it's not necessarily just an easy drug to throw at your patient. You have to think through a little bit in the beginning how to start them on the medication…our patients really do deserve the highest level of care, and getting past some of these residual positive symptoms that many of them experience, let alone the cognitive and the negative symptoms, I think that this really has the opportunity to change psychiatry, and this is the first of several that will be in the line thereafter. We really need to challenge ourselves to get used to using these agents and learning about the muscarinic system.

What else is in the pipeline, and what we might be can you talk about that?

They're looking at really isolating the different muscarinic receptors. Right now, we have an M1 M4 agonist, but there's some things in the pipeline where they're really looking at M1 specifically, M4 specifically, positive allosteric modulators…and so really there's an expansion around muscarinics right now.

There may be several molecules out there in the future that can modulate these muscarinics and dopamine pre-synaptically. That's really what we're getting to; instead of blocking everything after the fact, like a leaky basement, you've got this flood going on in your basement with dopamine. Instead of taking a bucket and throwing out that water 1 by 1 with our normal antipsychotics, we now can shut the water off at the faucet. It's exciting times be looking out there for all of the other muscarinic agents that should be coming in the future.

Derman, C. FDA Approves Xanomeline and Trospium Chloride (Cobenfy) for Schizophrenia. HCPLive. September 26, 2024. 

https://www.hcplive.com/view/fda-approves-xanomeline-and-trospium-chloride-cobenfy-for-schizophrenia

The FDA approved xanomeline and trospium chloride (Cobenfy) for schizophrenia, marking a significant advancement in treatment options. Muscarinic agents offer a novel mechanism by modulating cholinergic pathways to influence dopamine, potentially improving positive, negative, and cognitive symptoms without the side effects associated with traditional antipsychotics. While promising, caution is advised when considering Cobenfy for treatment-resistant schizophrenia, especially in patients on clozapine due to potential anticholinergic interactions. Future developments in muscarinic agents focus on targeting specific receptors, offering hope for more precise and effective treatments.

At So Cal Psych 2025, Monroe discusses the promise of xanomeline-trospium (Cobenfy) and its novel mechanism.

When to Use Cobenfy Over Clozapine, With Chelsie Monroe, APN

Chelsie Monroe, APN

Lam discussed a retrospective cohort analysis he presented at the 2025 ACP IM meeting and its findings.

Confirming the Benefit of SGLT2 Inhibitors in People With ATTR Amyloidosis, with Justin Riley Lam, MD

Although SGLT2 inhibitors have become standard in the management of heart failure with preserved and reduced ejection fraction, their use in patients with ATTR amyloidosis with cardiac disease remains largely unstudied. Most major trials have excluded this population, and current guidelines do not address it.

A retrospective cohort analysis, presented at the 

American College of Physicians (ACP) Internal Medicine (IM) Meeting 2025

, held April 3-5, in New Orleans, Louisiana, by Justin Riley Lam, MD, medical resident at Albert Einstein Medical Center in Philadelphia, Pennsylvania, evaluated the impact of SGLT2 inhibitors in patients with ATTR amyloidosis compared to those who were not using SGLT2 inhibitors.

spoke with Lam to learn more about the analysis and its findings. Among these findings, investigators found that those on SGLT2 inhibitors had a lower mortality rate compared to those not on it. These participants also had a lower rate of using intravenous diuretics, which Lam and colleagues used as a surrogate marker for hospitalizations, because they could not use hospitalizations as an outcome in their database.

“Most people who have ATTR amyloidosis already have heart failure, so they are already usually on it, which is a good thing. And you know, with the recent studies pushing for either preserved ejection fraction or reduced ejection fraction, this gives us a better shot at treating this condition,” Lam told 

Lam has no relevant disclosures to report.

Lam JRY. Impact of SGLT2 Inhibitors on Survival and Cardiac Outcomes in Wild-Type ATTR Amyloidosis: A Retrospective Cohort Analysis. Presented at: ACP IM Meeting 2025; April 3-5; New Orleans, Louisiana.

Justin Riley Lam, MD

Michael Schilsky, MD, is a professor of medicine and medical director of adult liver transplant at Yale-New Haven Transplantation Center.

Challenges and Innovations in Wilson Disease, with Michael Schilsky, MD

, also known as hepatolenticular degeneration, is a genetic disorder of copper metabolism that leads to the accumulation of copper in the liver and other tissues, including the brain.

With an estimated prevalence of 1 case per 30,000 live births in most populations, Wilson disease is rare but serious, with gradual damage from copper accumulation resulting in hepatic, neurologic, and 

 manifestations. With the availability of effective treatment options, early detection and intervention are critical for preventing disease progression, mitigating symptoms, and maintaining quality of life.

, Michael Schilsky, MD, a professor of medicine and medical director of adult liver transplant at Yale-New Haven Transplantation Center, discusses the biggest challenges in Wilson disease and recent innovations that have helped to address some of the field’s largest unmet needs.

Schilsky begins by highlighting the need for tools to effectively monitor patients, citing shortcomings in the historical approach of examining urinary copper excretion. He references novel approaches with better sensitivity, also describing advances in diagnostics that have the potential to be implemented universally and catch the disease during infancy.

However, Schilsky notes that detecting Wilson disease so early introduces questions about when to start treatment. He says the current understanding is that it is relatively safe to wait 2 to 3 years while monitoring copper and diet before slowly initiating therapy.

“Whenever you deal with a rare disorder, and Wilson's disease is typically present in about 1 in 30,000 individuals, the key is really recognizing the disease,” Schilsky said. “If we can have newborn screening, we’ll capture a lot and that would be wonderful. If we don't, we have to continue to raise awareness so that we can identify patients at a younger age before they develop more severe symptoms.”

Schilsky goes on to commend his colleagues working in pediatrics for moving the needle and helping identify more patients at a younger age. He additionally recognizes the work being done by patient organizations that are providing advocacy and support for patients and families.

Considerations for Effectively Managing Wilson Disease, with Michael Schilsky, MD

Editors’ note: Schilsky has relevant disclosures with Vivet Therapeutics, Orphalan, Alexion, Wilson Disease Association, National Institute of Health, DepYmed, and Arbomed.

UpToDate. Wilson disease: Epidemiology and pathogenesis. Jun 19, 2024. Accessed March 24, 2025. 

https://www.uptodate.com/contents/wilson-disease-epidemiology-and-pathogenesis

Schilsky describes lingering challenges and unmet needs in Wilson disease and highlights recent innovations in monitoring and diagnosis.

Michael Schilsky, MD

FCS Patient Case study

Familial chylomicronemia syndrome (FCS) is a rare genetic disorder characterized by extremely high triglyceride levels, leading to recurrent pancreatitis and other complications. Delayed diagnosis and treatment can exacerbate cardiovascular and metabolic consequences, including increased risk of atherosclerosis, cardiovascular disease, and metabolic syndrome. Long-term health risks involve persistent hypertriglyceridemia, which can cause chronic pancreatitis, diabetes, and liver disease. Early intervention is crucial to mitigate these risks, improve patient outcomes, and enhance quality of life by managing triglyceride levels and preventing severe complications.

Panelists walk through a patient case scenario involving Maria, a 29-year-old woman diagnosed with familial chylomicronemia syndrome (FCS), offering recommendations from each of their specialty perspectives, including dietary modifications, triglyceride-lowering medications, and patient education on managing the condition to prevent recurrent pancreatitis and improve overall quality of life.

FCS Patient Case study 

Peter Toth, MD, PhD, FCCP, FESC, FAHA, FACC 

Pranav Garimella, MBBS, MPH, is chief medical officer of the American Kidney Fund.

Crisis Point: Curbing the Chronic Kidney Disease Epidemic

Our mini-docuseries has returned, taking a comprehensive look at public health crises affecting the United States today, with global implications tomorrow. If the crisis point is the moment where a crisis will worsen or begin to get better, the question remains: where are we now?

CKD’s Emergence As A Public Health Crisis: Next Steps for Halting the Silent Spread

In recognition of National Kidney Month, this episode addresses the growing burden of 

 and its emergence as the biggest public health crisis of our time.

CKD is estimated to affect 35 million adults in the US alone, but despite its widespread impact, it often flies under the radar. In many patients, the disease progresses silently and goes undetected until it reaches advanced stages when symptoms appear but treatment options are limited. While there has been no single cause of the CKD crisis, the growing prevalence of risk factors like diabetes, hypertension, and obesity has intensified the threat posed by CKD, setting the stage for a surge in cases that could overwhelm healthcare systems and disrupt countless lives.

Current estimates suggest 9 out of 10 people with kidney disease are unaware they have it, and 1 in 3 of those with severely reduced kidney function but who are not yet on dialysis are unaware they have kidney disease.

In addition to the need for better public awareness to facilitate early detection and treatment of CKD, patient-focused multidisciplinary care is also essential for improving outcomes. The burden of CKD cannot fall on nephrologists alone. Addressing this crisis requires a collaborative effort across the entire health care system but must be tailored in a way that ensures complete, equitable care for the patient.

Be sure to check out part 1 of this episode, which delves into the complex challenges surrounding CKD, exploring the various factors contributing to its growth, the importance of early detection and intervention, and the need for heightened public awareness.

In part 2, the conversation shifts to the importance of collaborative, multidisciplinary care that maintains a focus on patients’ wants and needs as well as the future of CKD care.

Brief descriptions of the speakers featured in this project are provided below:

, chief medical officer of the American Kidney Fund

, associate clinical professor of medicine in the division of nephrology at Icahn School of Medicine at Mount Sinai and chief medical officer of the National Kidney Foundation

, chief executive officer of Carna Health

, a patient advocate who was diagnosed with CKD during pregnancy, eventually requiring dialysis and a kidney transplant

 to see other episodes on improving health equity in eye care, disparities in cardiovascular health, insulin access in the United States, physician burnout across healthcare, and the ongoing obesity crisis.

American Kidney Fund. Quick kidney disease facts and stats. Accessed March 5, 2025. 

https://www.kidneyfund.org/all-about-kidneys/quick-kidney-disease-facts-and-stats

In part 2 of this episode of Crisis Point, 3 nephrology experts and a patient advocate discuss strategies to address the CKD crisis.

Pranav Garimella, MBBS, MPH

Shauna Applin, ARNP, provides clinical insights on treatment options and best practices for restarting therapy.

Restarting Therapy in Patients with HIV

Video content above is prompted by the following question:

What treatment regimens do you consider in patients with HIV who have fallen out of care?

Addressing patients with HIV who have fallen out of care, Shauna Applin, ARNP, provides clinical insights on treatment options and best practices for restarting therapy.

Shauna Applin, ARNP

Key Takeaways for Improving CKD Diagnosis and Treatment in Patients With Type 2 Diabetes

In closing, what are the key takeaways for improving CKD diagnosis and treatment in patients with type 2 diabetes?

Now that we have many options in CKD, how should we think about sequencing these products in different patient types, for instance, to address CV and renal risk, in patients with earlier, less advanced disease as well those with later, advanced stages?

Chronic kidney disease (CKD) in Type 2 Diabetes patients necessitates early detection to prevent progression and associated complications. Identifying at-risk patients involves considering factors such as hypertension, family history of kidney disease, and elevated blood glucose levels. Screening tests include estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR). Early detection is crucial as it allows timely intervention, potentially slowing disease progression and reducing cardiovascular risks. CKD is a significant risk factor for heart failure, making early detection vital for comprehensive cardiovascular risk management.

Panelists discuss the key takeaways for improving chronic kidney disease (CKD) diagnosis and treatment in patients with type 2 diabetes, emphasizing how to effectively sequence treatment options based on patient types to address cardiovascular and renal risks in both early and advanced stages of the disease.

Susanne B. Nicholas, MD, MPH, PhD

American Thoracic Society (ATS) International Conference

, discussing the phase 3 FIBRONEER-IPF and FIBRONEER-ILD studies, Toby Maher, MD, PhD, described nerandomilast’s success in achieving its primary endpoint in both trials on patients with idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF).

After discussing some of the most notable findings in these late-breaking data on the investigational oral phosphodiesterase 4B (PDE4B) inhibitor, the FIBRONEER trial investigator and professor of Clinical Medicine at USC’s Keck School of Medicine spoke with 

 about nerandomilast’s safety findings in the analyses.

Safety Findings on Nerandomilast for Pulmonary Fibrosis, with Toby Maher, MD, PhD

In addition to nerandomilast’s efficacy demonstrated by the reduction of forced vital capacity (FVC) in those with IPF and PPF over 52 weeks of medication use, discontinuation rates due to adverse events were also noted as having been comparable between nerandomilast and placebo cohorts in both of trials.

“I think it is an important observation that the discontinuation rates are similar across all 3 arms, including the placebo arm,” Maher said. “We know that IPF trials are difficult for patients. They're committing to over a year of being in the study. Life events come up, and disease related events come up. So we always expect some patients to discontinue. In the past, when we've used difficult to tolerate drugs, we've seen a very clear increase in discontinuations in the active treatment arm. The fact that we're not seeing that in this study, to me, reinforces the idea that nerandomilast is a much easier drug for patients to tolerate. I'm hoping that that is going to make life a lot easier in clinical practice.”

Maher was also asked about the future of nerandomilast for IPF and PPF, given the positive findings in the FIBRONEER trial program presented at ATS.

“Hopefully the regulatory bodies, the FDA, will look very favorably upon this data,” Maher said. “I'm very optimistic that the drug will hopefully be approved in the near future for use in clinical practice. You know, this trial was designed to test the effect of nerandomilast in an environment where we have anti-fibrotic drugs. We know that it slows disease progression, and we know that it can be used safely in combination with existing treatments.”

Maher added that what is not yet present is evidence on is whether clinicians should be thinking about upfront combinations of drugs.

“I think that is something that we need to look at in the future,” Maher said. “Similarly, we don't have data on when it is a new drug should be added on, so I think there are things for us to still tease out and understand about the position of nerandomilast within treatment and how we now think about treating IPF and PPF when we have drugs that can be used in combination.”

To find out any additional information on recent data presented at ATS, view our 

The quotes used in this summary were edited for the purposes of clarity.

Maher previously reported receiving personal fees from Boehringer Ingelheim, Galapagos, Roche/Genentech, Pfizer, BMS, GSK, Sanofi-Aventis, Pliant, Trevi, Galecto, Merck, Astra Zeneca, CSL Behring, Vicore, Scleroderma Research Foundation, Qureight, and Veracyte.

Global phase III trials demonstrate that nerandomilast slowed lung function decline in IPF and PPF, with similar discontinuation rates to placebo. Boehringer Ingelheim. May 19, 2025. Accessed May 23, 2025. 

https://www.boehringer-ingelheim.com/human-health/lung-diseases/pulmonary-fibrosis/phase-3-trials-nerandomilast-slowed-lung-function-decline-ipf-and-ppf.

In this interview, nerandomilast’s safety profile in idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF) is highlighted.

Authors