Pulmonary physician at the Erasmus University Medical Centre in Rotterdam

A phase 2a/2b trial of BI 1839100, a selective oral transient receptor potential ankyrin 1 (TRPA1) antagonist, missed its week-4 primary endpoint for cough reduction in idiopathic pulmonary fibrosis (IPF) but showed a clinically meaningful effect by week 12, according to Marlies Wijsenbeek, MD, PhD, professor of interstitial lung diseases and chair of the Academic Centre of Excellence for Interstitial Lung Diseases and Sarcoidosis at Erasmus MC, University Medical Centre Rotterdam. Wijsenbeek discussed the late-breaking abstract, presented at the 

European Respiratory Society (ERS) Congress 2026

 in Barcelona, Spain, held September 5 to 9, in an interview with 

TRPA1 Antagonist Shows Delayed but Meaningful Effect on IPF Cough

Of 85 randomized patients with IPF-related chronic cough, 28 received the high dose of BI 1839100 (150 mg twice daily) and 29 received placebo, with 26 and 27, respectively, completing treatment.

 Median baseline cough burden was approximately 20 coughs per hour. The trial was designed with co-primary 24-hour cough-count endpoints at weeks 4 and 12; a prespecified interim analysis after the week-4 assessment led to termination for futility, since the high dose produced only a 5.7% relative reduction in cough count from baseline at that point. By week 12, however, the same dose showed a 45.5% reduction in 24-hour cough count relative to placebo, along with reductions in daytime cough count (48.8% vs 18.6% with placebo) and cough bouts (36.8% vs a 17.9% increase with placebo); forced vital capacity was unaffected, and the drug's safety profile was acceptable.

Wijsenbeek said the mismatch between the 2 timepoints likely reflects the drug being assessed too early rather than a lack of effect. 

“This is the first drug that is not in that category that shows something,” she said, contrasting BI 1839100 with the centrally acting, opioid-based antitussives, including morphine and nalbuphine, that have previously shown benefit in IPF cough. 

Nalbuphine extended-release, a kappa-agonist, mu-antagonist opioid, reduced objective cough frequency compared with placebo in the phase 3 CORAL trial published earlier this year.

 Wijsenbeek said she could only speculate on the mechanism behind BI 1839100's delayed onset, but noted preclinical data suggesting the drug also has antifibrotic properties, raising the possibility that its effect depends on longer-term neuroplastic or fibro-inflammatory changes rather than acute receptor blockade alone.

Mechanistically, Wijsenbeek said TRPA1 is a sensory ion channel expressed on airway afferent nerves that contributes to cough hypersensitivity and has been shown in preclinical models to be upregulated in fibrotic lung tissue; BI 1839100 works as an antagonist of that channel, a pathway she said the cough research field has considered promising for years. She said the findings support designing a new trial with a later primary endpoint to properly capture the drug's apparent delayed benefit.

Wijsenbeek M, Smith J, Adegunsoye A, et al. Selective TRPA-1 antagonist in patients with chronic cough and idiopathic pulmonary fibrosis: a phase IIa/IIb randomized, double-blind, placebo-controlled study (BI 1839100). Late-breaking abstract presented at: European Respiratory Society (ERS) Congress 2026; September 5-9, 2026; Barcelona, Spain.

Molyneaux PL, Mogulkoc N, Gunen H, et al; CORAL Study Group. Oral nalbuphine in idiopathic pulmonary fibrosis-associated cough: the CORAL randomized clinical trial. 

 2026;335(12):1050-1059. doi:10.1001/jama.2025.26179

Videos

Marlies Wijsenbeek, MD, PhD, of Erasmus MC discusses BI 1839100, a TRPA1 antagonist, which missed its week-4 endpoint in a phase 2/2b trial.

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Chelsie Derman is an associate editor for 

who covers allergy and  psychiatry. She joined MJH Life Sciences in September 2023 after graduating from The College of New Jersey with a bachelor’s degree in journalism and professional writing. In her free time, she enjoys creative writing and reading.

This summer, smoke from Canadian wildfires drifted south, casting East Coast and Midwest skies in a murky orange-yellow haze and putting millions at risk of respiratory and cardiovascular harm.¹

Numerous states experienced "very unhealthy" or "hazardous" air quality ratings.¹ The polluted air led to widespread event cancellations, including a baby parade in Michigan, a rock concert in Virginia, and the America's Mile marathon in Pittsburgh. According to CNN, Detroit, Milwaukee, Chicago, southern Ohio, and West Virginia recorded the worst air quality in the country.¹

Detroit ranked as the city with the worst air quality in the world, according to IQAir. At an air quality index (AQI) of 724, this was more than double the threshold for the "hazardous" category.

Simply standing on a front porch and inhaling minuscule smoke particles can 

trigger coughing, trouble breathing, wheezing, asthma attacks

, stinging eyes, a scratchy throat, a runny nose, irritated sinuses, headaches, fatigue, chest pain, and a rapid heartbeat.³ While these symptoms are more likely to affect people with preexisting conditions, such as asthma, chronic obstructive pulmonary disease (COPD), diabetes, chronic kidney disease, or heart disease, that doesn’t mean everyone else is in the clear, either.

Wildfire smoke may be just the thing that causes someone to develop 

“I don’t know that we really have a good handle on [the mechanism of how wildfire smoke may enhance allergic sensitization],” said Jim Blando, PhD, chair of the Department of Epidemiology, Biostatistics, and Environmental Health at Old Dominion University, in an interview with 

 “I don't think that's very well delineated. The thinking right now, without doing any kind of mechanistic studies on it, is that it simply can sensitize the immune system. That can end up resulting in [the] development of antibodies in your body that, then, when you're subsequently exposed to an allergen, you end up having a reaction to it.”

Blando compares this to poison ivy. Someone may not react the first time they brush against it, but once they've developed antibodies, later contact can trigger a reaction.

A Delayed Respiratory Effect of Wildfire Smoke

Blando and colleagues conducted a longitudinal study assessing the impact of wildfire smoke on respiratory peak flow performance in patients exposed to 2 separate wildfire events.

Participants were drawn from a single clinic in a town of < 40,000 residents, located southeast of the fire area, roughly 25 miles from its center and approximately 10 miles from the southern border of the Great Dismal Swamp National Wildlife Refuge.

At the local clinic, allergic rhinitis and asthma were the most common respiratory diagnoses during both fire events. Allergic rhinitis affected 36% of patients during the first fire and 30% during the second, while asthma diagnoses varied by age group: 8% of adults and 15% of children during the first fire, and 10% of adults and 15% of children during the second.

There was significant overlap between the 2 conditions. Roughly 80% of patients with allergic rhinitis during the first fire, and about 90% during the second, were also diagnosed with asthma. Because of this overlap, the study's subsequent analyses were limited to patients who had a diagnosis of allergic rhinitis, asthma, or both.

"We didn't see anything initially during the actual wildfire or immediately thereafter, so just kind of on a whim, being that they were allergy patients, and we figured there were probably a lot of allergens in the wildfire smoke, we thought, 'Why don't we just look and see?'” Blando said. “Lo and behold, when we did that, all of a sudden we found these statistically significant relationships, which was quite surprising to us.”

The study revealed peak flow performance declined significantly 1 year after the wildfires, with the decline most pronounced among women and Black patients, whose average measurements fell furthest below predicted levels.

Investigators also identified a direct relationship between wind exposure and lung function: for every 1% increase in the amount of time wind blew from the fire toward the clinic's community, patients' peak flow dropped by an average of 2.21 L per minute a year later. The effect held even after accounting for age, BMI, sex, and race, suggesting wildfire smoke exposure, not just these underlying demographic factors, was driving the decline.

Wildfire Smoke Is Also Showing Up on the Skin

Blando's research points to the lungs and sinuses, but allergists are seeing 

wildfire smoke's effects show up on the skin

Arianne Shadi Kourosh, a dermatologist at Massachusetts General Hospital, noticed a rise in eczema visits one summer, from under 20 patients to 160. That spike led her to review four years of summer records, where she found visit volume for these skin complaints tracked closely with air pollution severity. This pattern is consistent with other research linking wildfire pollution to increased eczema and psoriasis flares.

"Much of the atopic dermatitis... tends to be fairly immediate in terms of the exacerbations, generally the same week. [A] psoriasis… flare seems to be documented several weeks later, and that may be because that is more of a systemic inflammatory response as to more of a quick skin inflammatory response,” said Wynne Armand, MD, from Massachusetts General Hospital, in an interview with 

Armand explained that patients with atopic conditions already have a weakened skin barrier, making it easier for particles to penetrate. In her clinic, she sees the same patients report worsening seasonal allergies, sinus symptoms, and watery eyes during smoke events.

“There's a lot of direct irritation to the eyes, the nose, the airway, and if somebody [already has] underlying conditions, and that includes allergic-type conditions like allergic rhinitis, hay fever, seasonal allergies, or asthma, that is often triggered by allergens, they can then also see worsening of their disease and have exacerbations," Armand said.

What Clinicians and Patients Can Do Now About Wildfire Smoke & Allergies

Armand's guidance for patients with allergic or skin conditions centers on limiting wildfire smoke exposure before it triggers symptoms. She recommends:

Use a mineral sunscreen containing zinc or titanium

Close windows and recirculate indoor air. Keep HVAC filters clean

“Make sure that you're in an environment with healthy, clean air,” Armand said.

The Wildfire Smoke & Allergy Research Is Still Catching Up

Both physicians agree the science connecting wildfire smoke to allergic disease is still developing. Armand pointed to a specific gap: distinguishing wildfire smoke's role in triggering flares in patients who already have allergic disease from its potential role in causing these conditions to develop in the first place.

“I personally feel pretty confident that as we look into it further, we are going to find a lot of evidence supporting that wildfire smoke is very allergenic," Blando said.

Watch our accompanying dynamic video on wildfire smoke’s impact on allergies here: 

Wildfire Smoke's Hidden Toll on Patients with Allergies

Miller B. Wildfire smoke is driving terrible air quality in major cities, but relief is coming. CNN. Published July 17, 2026. Accessed September 14, 2026. 

https://www.cnn.com/2026/07/17/weather/smoke-forecast-northeast-midwest

How Wildfire Smoke Affects Your Body. CDC. Published August 24, 2026. Accessed September 14, 2026. 

https://www.cdc.gov/wildfires/risk-factors/index.html

Vawter H. Three major US cities rank among worst air quality in the world as Canadian wildfire smoke invades America. Fox News. Published July 16, 2026. Accessed September 14, 2026. 

https://www.foxweather.com/extreme-weather/3-us-cities-rank-worst-air-quality-world-canadian-wildfire-smoke

Blando J, Allen M, Galadima H, Tolson T, Akpinar-Elci M, Szklo-Coxe M. Observations of Delayed Changes in Respiratory Function among Allergy Clinic Patients Exposed to Wildfire Smoke. Int J Environ Res Public Health. 2022 Jan 22;19(3):1241. 

doi: 10.3390/ijerph19031241. PMID: 35162264; PMCID: PMC8835059

Armand W. One surprising effect of wildfires: Itchy, irritated skin. Harvard Health Publishing. Published June 24, 2024. Accessed September 14, 2026. 

https://www.health.harvard.edu/blog/one-surprising-effect-of-wildfires-itchy-irritated-skin-202406243052

Articles

Canadian wildfire smoke episodes produced hazardous AQI levels across the US, provoking acute cardiopulmonary symptoms and raising concern for allergic sensitization. A longitudinal clinic-based analysis found no immediate lung function signal but demonstrated significant peak expiratory flow decline one year post-exposure, with larger decrements in women and Black patients and a dose–response association with downwind exposure time. Clinicians are also observing pollution-linked dermatologic morbidity, with atopic dermatitis flares occurring rapidly and psoriasis exacerbations emerging weeks later. Evidence remains preliminary on causation versus flare amplification.

New research links wildfire smoke to lasting respiratory decline and skin flares, months after exposure ends.

Allergy

Allergy condition center page is a comprehensive resource for clinical news and insights on allergic and inflammatory diseases. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for food and seasonal allergies, as well as allergic asthma and related conditions.

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The HCPLive dermatology page is a resource for medical news and expert insights on skin disease. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for dermatologic conditions, and more.

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Atopic Dermatitis condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatitis research, treatment, and drug development.

Plaque Psoriasis

The HCPLive plaque psoriasis page is a resource for medical news and expert insights on psoriasis. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for psoriatic disease, and more.

Seasonal Allergy

How Wildfire Smoke Triggers Allergic Disease Long After It Clears

David Oberlin, MD, is a board-certified dermatologist practicing in Grand Rapids and Hastings, Michigan.

 approved a label update for guselkumab (Tremfya) in May 2026, crediting the phase 3b APEX trial (NCT04882098) with inhibiting radiographic joint damage in psoriatic arthritis.¹ David Oberlin, MD, dermatologist at Forefront Dermatology in Grand Rapids, Michigan, and Jesse Veenstra, MD, PhD, of Henry Ford Health, co-authored a commentary on the findings in the Journal of the American Academy of Dermatology.² The pair questioned whether APEX's enriched population reflects general dermatology patients.

"The most informative trial is not necessarily the one with the largest effect, but the one whose participants most closely resemble the patient being treated," said Oberlin. APEX enrolled biologic-naive patients with erosive disease, elevated CRP, and PsA duration beyond 6 months, criteria far more restrictive than those used in comparator trials such as DISCOVER-2 and KEEPsAKE 1.

Baseline joint damage closely tracked placebo-arm progression on radiographic Sharp scores across trials, with a near-linear correlation of 0.97.² This made a statistically significant treatment effect easier to reach in a more enriched population, regardless of drug mechanism. DISCOVER-2 carried some baseline enrichment of its own, Oberlin noted, but APEX pushed enrichment further to widen the placebo-progression gap.

This relationship helps explain why APEX reached significance on its radiographic endpoint while DISCOVER-2, also testing guselkumab, and KEEPsAKE 1, testing risankizumab (Skyrizi), did not, despite both drugs working through interleukin-23 inhibition.³ No head-to-head trial has directly compared the two drugs on joint damage outcomes, Oberlin noted. In the following interview, Oberlin discusses how trial design, rather than drug mechanism, shaped APEX's radiographic results.

: Can you walk me through the core takeaway you and your co-author wanted dermatologists to take from this commentary?

 I think the big thing Dr. Veenstra and I were looking at is, with this label update for guselkumab following the APEX trial demonstrating radiographic inhibition of joint disease in patients with PsO and PsA, what we really wanted to analyze is whether this applies to general dermatology patients. After we looked at the data and the enrichment of the baseline characteristics of these patients, we wanted to make sure we were better educating providers regarding these enrichment strategies and asking whether this particular study applies to our patients in general dermatology.

: Why does APEX's baseline erosive-disease requirement matter when comparing radiographic results across trials?

 Because of what we've seen in a regression plot with a correlation of almost 1, at 0.97, it's almost a straight line: the more baseline disease these patients have, the more placebo progression they will have over that 24-week period, with BE OPTIMAL only being a 16-week period. The higher the baseline joint disease, the more likely the placebo group is to progress in terms of Sharp scores. This allows for a statistically significant difference between baseline characteristics and the treatment arm, so by enriching for placebo progression, you're able to show statistical significance for the treatment arm.

: What does the correlation between baseline joint damage and placebo progression tell us about differing treatment effects across trials?

Not all IL-23 agents are created equally, and we know that with the IL-17 inhibitors as well; there are different nuances and different binding capacities. We don't necessarily have head-to-head data, and that's really the key for us to be able to tell these drugs apart. But what we can say is that in this specifically enriched population with APEX, they show statistical significance, whereas the other interleukin-23 agents, specifically guselkumab in DISCOVER-2 and risankizumab in KEEPsAKE, are not showing statistical significance, simply because the lack of placebo progression did not allow for that delta from the treatment arm.

Editor’s note: Oberlin disclosed having received honoraria for serving as a key opinion leader for Amgen, AbbVie, UCB, and Arcutis, and for participating on advisory boards for AbbVie, Sensus, UCB, Sanofi, Incyte, and Apogee. This transcript has been edited for grammar and clarity using artificial intelligence tools.

Johnson & Johnson. FDA approves label expansion, cementing TREMFYA as the only IL-23 inhibitor proven to help stop further joint damage. Published May 28, 2026. Accessed September 14, 2026. 

https://www.jnj.com/media-center/press-releases/fda-approves-label-expansion-cementing-tremfya-as-the-only-il-23-inhibitor-proven-to-help-stop-further-joint-damage

Oberlin D, Veenstra J. Interpreting radiographic outcomes across IL-23 inhibitor trials in psoriatic arthritis: the role of trial design. J Am Acad Dermatol. Published online July 3, 2026. doi:10.1016/j.jaad.2026.06.135.

Mease PJ, Ritchlin CT, Coates LC, et al. Inhibition of structural damage progression with the selective interleukin-23 inhibitor guselkumab in participants with active PsA: results through week 24 of the phase 3b, randomized, double-blind, placebo-controlled APEX study. Ann Rheum Dis. 2025:S0003-4967(25)04305-5. doi:10.1016/j.ard.2025.08.006.

FDA’s May 2026 label update for guselkumab in psoriatic arthritis cites APEX phase 3b evidence for inhibiting radiographic joint damage, but generalizability is debated. APEX selectively enrolled biologic-naive patients with erosive disease, elevated CRP, and longer disease duration, enriching for rapid placebo-arm progression on Sharp scores. Across trials, baseline structural damage strongly correlated with placebo progression (r=0.97), making statistical separation easier in enriched cohorts. This design effect may explain discordant radiographic outcomes versus DISCOVER-2 and KEEPsAKE 1 despite shared IL‑23 targeting.

David Oberlin, MD, explains why APEX's enriched trial population, not drug mechanism, likely drove its unique radiographic success in psoriatic arthritis.

Q&A: How Trial Enrichment Shaped APEX's Radiographic Findings in Psoriatic Disease

Michael Wechsler, MD, of National Jewish Health.

Oral STAT6 degraders represent a mechanistically distinct addition to the 

 pipeline, working further downstream than the epithelial alarmin-targeted therapies now in use, according to Michael E. Wechsler, MD, MMSc, professor of medicine and director of the Cohen Family Asthma Institute at National Jewish Health. Speaking with 

 in Barcelona, Spain, held September 5 to 9, about new data on KT-621, Kymera Therapeutics' investigational STAT6 degrader, Wechsler said the drug class acts on signaling mediated by Janus kinases and STAT6, and to some extent STAT5, in contrast to therapies like those targeting thymic stromal lymphopoietin (TSLP) or interleukin-33 (IL-33), which act further upstream at the epithelial level.

Oral STAT6 Degraders Fill Niche in Asthma Care, With Michael Wechsler, MD

Wechsler pointed to preliminary data showing KT-621 effective in atopic dermatitis as the basis for optimism that a similar effect could translate to asthma; in the phase 1b BroADen trial, the subgroup of patients with comorbid asthma had a median 56% reduction in fractional exhaled nitric oxide and a 100% Asthma Control Questionnaire-5 responder rate by day 29.

 Kymera's phase 2b BREADTH trial is now testing KT-621 specifically in moderate to severe eosinophilic asthma, with topline lung function data expected in late 2027.

 Wechsler said an oral option carries practical appeal on its own, since some patients simply prefer pills to injectable biologics, independent of any efficacy advantage.

On where the drug might fit, Wechsler said he could envision STAT6 inhibition slotting into the Global Initiative for Asthma treatment algorithm at more than one point: as an add-on to inhaled corticosteroids and long-acting beta-agonists before a patient escalates to a biologic, or as an added option for patients who remain poorly controlled despite biologic therapy, given its distinct mechanism. He was careful to note the distance still ahead. 

“Of course, there's a long way to go from being a concept in atopic dermatitis to moving past phase 3 and into the FDA and getting approval,” he said, though he added that both the mechanistic rationale and the preliminary atopic dermatitis data support pursuing it.

Wechsler framed the broader need in terms of remission: even with current biologics, he said only about 25% to 40% of patients with asthma achieve remission, underscoring that matching the right drug to the right patient at the right time still requires more tools, not fewer. “It's good to have oral options, it's good to have biologic options, and it's good to have options for our patients who continue to have significant unmet needs,” he said.

Feldman MB, Gollob J, Dey J, Shi K, Agarwal S, Graham N, Mainolfi N. KT-621, an oral STAT6 degrader, in patients with moderate-to-severe atopic dermatitis and comorbid asthma or allergic rhinitis: safety and evidence of clinical activity across type 2 inflammatory diseases in a phase 1b trial. Poster PA5913. Presented at: European Respiratory Society (ERS) Congress 2026; September 5-9, 2026; Barcelona, Spain.

Kymera Therapeutics, Inc. Kymera Therapeutics announces presentations on KT-621, a first-in-class, oral STAT6 degrader, at the European Respiratory Society and European Academy of Dermatology & Venereology congresses. Published September 1, 2026.

Oral STAT6 degraders are emerging as a downstream, mechanistically distinct approach for type 2 asthma relative to epithelial alarmin inhibitors such as anti-TSLP or anti–IL-33 therapies. Early signals with Kymera’s KT-621 in atopic dermatitis suggest potential cross-disease activity, including notable reductions in FeNO and strong ACQ-5 response rates among participants with comorbid asthma. A dedicated phase 2b program in moderate-to-severe eosinophilic asthma is underway, with key lung-function readouts anticipated in 2027. An oral alternative may also improve patient acceptance versus injectables.

Wechsler, of National Jewish Health discusses how oral STAT6 degraders like KT-621 could offer a mechanistically distinct treatment option.

Asthma

The HCPLive asthma page is a comprehensive resource for clinical news and insights on asthmatic disease. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for allergic and severe asthma, and more.

Luke Laffin, MD, is the co-director of the Center for Blood Pressure Disorders, medical director of cardiac rehabilitation, and associate professor of medicine at Cleveland Clinic.

Tonlamarsen treatment resulted in persistent and long-term reductions in angiotensin and 

 after withdrawal, according to a secondary analysis of the KARDINAL trial.

Tonlamarsen Produces Persistent, Long-Term Angiotensin and BP Improvements

European Society of Cardiology (ESC) Congress 2026

 in Munich, Germany, by Luke Laffin, MD, medical director of the Cleveland Clinic Coordinating Center for Clinical Research and lead investigator in the original KARDINAL trial.

“This is important because these are data to support that cardiovascular risk can be predicted by how high your blood pressure goes at a single time, not just on an ongoing basis,” Laffin told 

 in an exclusive interview. “What this really does is set the stage for our next trial, which is ongoing and enrolling right now – KARDINAL-ASH, which is for acute severe hypertension.”

KARDINAL was a multicenter, prospective, randomized, active run-in, double-blind, placebo-controlled phase 2 trial conducted across 39 sites in the US. Eligible patients were ≥18 years old, were receiving stable doses of 2 to 5 antihypertensive medications, and had an office systolic BP between 135 and 170 mmHg. Patients with known secondary causes of hypertension or serum potassium >5.1 mmol/L, among other criteria, were excluded.

The study’s coprimary endpoints included the percent change from baseline to week 20 in plasma angiotensin levels and the change in office systolic BP among patients receiving monthly tonlamarsen treatment, both compared with a single dose and subsequent placebo. Key secondary endpoints included the proportion of patients with systolic in-office BP <130 mmHg, change from baseline in mean self-assessed home systolic BP, and the change from baseline in mean office systolic BP, among others.

Patients were first given a single 90-mg dose of tonlamarsen subcutaneously during an active run-in period before being randomly assigned in a 1:1 ratio to 4 doses of tonlamarsen or matching placebo for the next 16 weeks. A total of 519 patients were initially screened, and 279 were administered placebo lead-in. A total of 206 received active run-in with a single dose of tonlamarsen, and a final total of 198 patients were randomized to either placebo (n = 98) or tonlamarsen (n = 100). At enrollment, 118 patients (60%) were taking a 2-drug antihypertensive regimen, while others were taking ≥3 drugs.

By week 20, the least squares mean percentage change in plasma angiotensin from baseline in patients treated with a single dose and then randomized to placebo was -23% (95% CI, -27.8% to -18.2%). Among patients treated with 20 weeks of tonlamarsen, angiotensin changed by -67.2% (95% CI, -71.9% to -62.4%). Change in office systolic BP in the single-dose arm was -6.7 mmHg (95% CI, -9.8 to -3.5 mmHg), while the change in the full treatment arm was -6.7 mmHg (97.5% CI, -51.9% to -36.4%; 

This secondary analysis extended both angiotensin and office BP measurements through 28 weeks, acting as a safety follow-up, as well as evaluating home BP time-in-target range (TTR) and incidence of markedly elevated home BP. Over this 28-week period, the placebo arm saw a reduction in angiotensin of 23.8%, while the treatment arm saw a 44% reduction. Office systolic BP also dropped by a mean of -7.1 mmHg in the placebo arm and -6.1 mmHg in the treatment arm.

Additionally, the percentage of home systolic BP TTR <140 mmHg was 75% with tonlamarsen and 67% without during this extended follow-up period (difference, -8; 95% CI, -22.9 to 7). The percent of home systolic BP TTR from 110 to 130 mmHg was 39% with tonlamarsen and 34% with placebo (difference, -4.7; 95% CI, -18.7 to 9.2).

Ultimately, Laffin and colleagues concluded that the analysis further underscores tonlamarsen’s efficacy and safety, highlighting the persistence of effect after an extended period post-treatment. Laffin also notes that these data pave the way for the next stage of trials, namely the KARDINAL-ASH trial, which is currently enrolling.

“Home blood pressure is really where we have to be able to generate evidence,” Laffin said. “We know that patients do it, and we have new technologies to measure blood pressure. Office blood pressure is a fine surrogate for cardiovascular outcomes, but we get a much higher fidelity of data, and really more informative data, if we can see home blood pressure reductions.”

Editors’ Note: Laffin reports relevant disclosures with AstraZeneca, Arrowhead, Medtronic, Eli Lilly, Mineralys, Crispr Therapeutics, Novartis, Novo Nordisk, and others.

Laffin L. Extended Follow-Up of the KARDINAL Trial Assessing the Effect of Tonlamarsen in Uncontrolled Hypertension. Presented at the European Society of Cardiology (ESC) Congress 2026, Munich, Germany. August 28-31, 2026.

Laffin, L, Wang, Q, Sarraju, A. et al. Efficacy of Tonlamarsen in Patients With Uncontrolled Hypertension: The KARDINAL Phase 2 Randomized Clinical Trial. 

https://doi.org/10.1016/j.jacc.2026.03.034

Luke Laffin, MD, discusses his secondary analysis of the phase 2 KARDINAL trial, which demonstrated substantial improvements in uncontrolled hypertension.

Cardiology

Cardiology condition center page is a comprehensive resource for clinical news and insights on cardiovascular and cardiometabolic diseases. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for heart disease and cardiovascular events, as well as associated diabetes, renal failure, and more...

Hypertension

The HCPLive hypertension page is a resource for medical news and expert insights on high blood pressure. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for hypertension, and more.

Alex Hillenbrand is an assistant editor for 

. She earned her BA in English from Lafayette College in 2023 and went on to write for pop culture, entertainment, and sports media outlets before joining MJH Life Sciences in 2025. In her free time, Alex enjoys cooking, going on walks, and meeting new people. Contact her at mjhlifesciences.com.

Martin Douglass, PhD, and Vanderbilt colleagues found a Bce module that helps C diff evade bacitracin and host iron restriction

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, IBS and IBD, Crohn's disease, and more.

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C. difficile condition center page, resources on the topics of medical news and expert insight into Clostridium difficile can be found. Content includes articles, interviews, videos, podcasts, and breaking news on C. diff research, treatment, and drug development.

C Diff Resistance to Bacitracin Reveals Potential Drug Target

Wechsler discusses why less frequent dosing matters to patients with severe asthma, plus VALIANT's safety profile and what's next for the field.

Verekitug's Quarterly Dosing Cuts Asthma Burden, With Michael Wechsler, MD

Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for 

. He is also the executive producer of two podcasts: 

. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

Ameluz is now the first FDA-approved photodynamic therapy for a skin cancer, expanding use to superficial basal cell carcinoma (sBCC) in adults.

FDA News

Ameluz Treatment Becomes First FDA-Approved PDT for Skin Cancer

Phase 3 data show zasocitinib use led to clear or almost clear skin in around 70% of patients by Week 16, setting up an FDA decision in early 2027.

FDA Priority Review Granted to Zasocitinib for Moderate to Severe Psoriasis 

Ryan Livingston joined the MJH Life Sciences team in March of 2025, shortly after graduating from TCNJ with a bachelor’s degree in English. He enjoys creative writing, reading, and scuba diving. He can be reached at rlivingston@mjhlifesciences.com.

The novel cardiac sarcomere modulator from Edgewise Therapeutics saw substantial improvements in both nonobstructive and obstructive HCM after 12 weeks.

Cardiomyopathy

CIRRUS-HCM: EDG-7500 Improves LVOT, NYHA Class in oHCM and nHCM

Beta Bionics plans to launch Mint through the pharmacy channel in the first quarter of 2027.

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This page also hosts content previously published by EndocrinologyNetwork. 


Type 1 Diabetes

FDA Clears Beta Bionics' Mint Insulin Patch Pump for Diabetes

Effective EoE care requires a treatment plan that works for both the disease and the patient. The expert faculty explore how individualized treatment selection and appropriately timed reassessment can support sustained disease control.

Video Series

Personalizing Treatment and Reassessment in EoE

Achieving remission is only one phase of EoE care. The panel explores how induction and maintenance therapies can work together to control inflammation and sustain disease control over time.

Induction and Maintenance Therapies in EoE

Guy Brusselle, MD, PhD, of Ghent University Hospital.

Guy Brusselle, MD, PhD, explains why broader cytokine blockade with dupilumab outpaced omalizumab, and why nonremitters in EVEREST still improved.

Dupilumab's IL-4/IL-13 Blockade Drives Efficacy Edge in EVEREST

Adam Friedman, MD, breaks down how to say no strategically in dermatology, from delaying an answer to sharing the decision with the requester.

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