Victoria Johnson joined MJH Life Sciences in 2020 and has written for NeurologyLive, CGTLive, and is now an assistant managing editor for HCPLive and RheumatologyLive. She doesn’t have enough time for her various hobbies. You can reach her at vjohnson@mjhlifesciences.com.

 (PAH) and worse baseline right ventricular ejection fraction (RVEF) had greater RVEF and pulmonary vascular resistance (PVR) improvements after 24 weeks of sotatercept, according to a 20-patient analysis presented at the 

American College of Chest Physicians (CHEST) 2026 Annual Meeting

, held October 18 to 21 in Phoenix, Arizona.

Sotatercept (Winrevair), a first-in-class activin signaling inhibitor, reduced PVR and improved exercise capacity vs placebo when added to background therapy in the phase 3 STELLAR trial.

 Determinants of individual response remain incompletely defined, and the current analysis sought clinical and physiologic factors associated with benefit.

 The findings are from a conference abstract and have not yet been published in a peer-reviewed journal.

"The therapeutic effects of sotatercept appear most pronounced in patients with advanced RV dysfunction, suggesting that baseline RV phenotype may help inform treatment selection," wrote Eduardo A. Garcia Licerio, MD, and colleagues.

Sotatercept effects on RVEF and PVR by baseline right ventricular function

Investigators analyzed 20 participants with PAH from an open-label phase 2b trial evaluating sotatercept effects on exercise performance and RV function.

 RVEF and PVR were measured at baseline and 24 weeks with cardiac magnetic resonance imaging and invasive cardiopulmonary exercise testing.

 Response was defined as change above the cohort median in RVEF and PVR.

At baseline, median RVEF was 33.8% in responders and 46.5% in nonresponders.

 Median baseline PVR was 7.9 Wood units (WU; interquartile range [IQR], 4.4-9.6) in responders and 14.2 WU (IQR, 13.2-20.3) in nonresponders.

After 24 weeks, median RVEF increased by 10.7% in responders and declined by 3.2% in nonresponders.

 Median PVR fell by 6.7 WU in responders vs 1.1 WU in nonresponders.

Secondary markers of sotatercept response in PAH

Responders had larger median reductions in N-terminal pro-B-type natriuretic peptide (NT-proBNP; −388.5 vs −99 pg/mL; 

 = .049), minute ventilation to carbon dioxide output (VE/VCO2) slope (−8 vs 0; 

 = .035), and right-to-left ventricular volume ratio (−0.430 vs −0.068; 

Which patients with PAH responded best to sotatercept in this analysis?

Patients with lower baseline RVEF had greater RVEF improvement and PVR reduction after 24 weeks, along with larger declines in NT-proBNP and VE/VCO2 slope.

Did age, sex, or background therapy affect sotatercept response?

No. Response did not differ significantly after stratification by age, sex, comorbidities, or background PAH-targeted therapy in this 20-patient cohort.

Sotatercept is an activin signaling inhibitor which rebalances growth-promoting and growth-inhibiting pathways implicated in pulmonary vascular remodeling.

Changes in right ventricular mass-to-volume ratio (0.078 vs 0.019; 

 = .949) and right-to-left ventricular mass ratio (−0.166 vs −0.064; 

 No significant differences in response were observed after stratification by age, sex, comorbidities, or background PAH-targeted therapy.

The investigators concluded the magnitude of benefit was proportional to the severity of baseline RV dysfunction, suggesting response relates more closely to preexisting RV impairment than to afterload alone.

 They called for larger studies to validate predictors of response.

The analysis included 20 patients, and responder status was defined by a median split within the cohort, so half of participants were classified as responders by design. Patients with lower baseline RVEF also had more room for improvement, and the abstract did not report adjustment for multiple comparisons across the secondary measures.

The FDA updated the sotatercept label in September 2026 to include phase 3 HYPERION data in adults diagnosed with PAH within the past year.

Garcia Licerio EA, Rischard FP, Vanderpool R, et al. Identifying predictors of response to sotatercept in individuals with pulmonary arterial hypertension. 

. 2026;170(4S). doi:10.1016/j.chest.2026.07.5113

Hoeper MM, Badesch DB, Ghofrani HA, et al. Phase 3 trial of sotatercept for treatment of pulmonary arterial hypertension. 

. 2023;388(16):1478-1490. doi:10.1056/NEJMoa2213558

HCPLive. FDA updates sotatercept label with HYPERION data in early PAH. 

https://www.hcplive.com/view/fda-updates-sotatercept-label-with-hyperion-data-in-early-pah

. Published September 22, 2026. Accessed November 3, 2026.

Articles

In 20 patients with PAH, lower baseline RVEF was linked to greater RV functional recovery and PVR reduction after 24 weeks of sotatercept, per a CHEST 2026 abstract.

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Baseline RV Dysfunction May predict Sotatercept response in PAH

Katie Harris, PhD, is a senior research fellow in the professorial unit at the George Institute for Global Health.

Smaller brain volume and greater white matter hyperintensity (WMH) volumes, which indicate vascular damage, are strongly associated with poor cognitive function after 

Smaller Brain Volume, Greater WMH Lead to Cognitive Decline After Intracerebral Hemorrhage

These data, a substudy of the Triple Therapy Prevention of Recurrent Intracerebral Disease EveNts Trial (TRIDENT), were presented at the 

 in Seoul, South Korea, by Katie Harris, PhD, a senior research fellow in the professorial unit at the George Institute for Global Health.

“Of course, when someone’s survived an ICH, they have to consider physical recovery and potential disabilities, which are clearly very important, as well as the concern of a recurrent stroke,” Harris told 

 in an exclusive interview. “But now, we need to look further ahead, maybe 5, 10 years post-ICH, and see whether cognitive impairment and ultimately dementia may occur.”

The original TRIDENT study was a multinational, double-blind, randomized, placebo-controlled trial evaluating the effects of blood pressure reduction on patients with a history of intracerebral hemorrhage. Patients were eligible for inclusion if they had a systolic blood pressure (SBP) of 130-160 mmHg at baseline and were in clinically stable condition. After a 2-week active run-in phase in which patients were given a once-daily pill of 3 antihypertensive agents at low doses (namely telmisartan 20 mg, amlodipine 2.5 mg, and indapamide 1.25 mg), these patients were randomly assigned to either continue with the triple pill or move to matching placebo.

A total of 1670 patients were enrolled in the TRIDENT study, of whom 833 were assigned to the triple pill and 837 to placebo. At a median follow-up of 2.5 years, 38 patients in the treatment arm and 62 in the placebo arm saw recurrent strokes (HR, 0.61; 95% CI, 0.41-0.92; 

 = .02). Mean SBP was 127 mmHg and 138 mmHg during follow-up, respectively, and serious adverse events occurred in 23.2% of patients in the treatment arm and 26% in the placebo arm.

Harris and colleagues conducted the present substudy at either the penultimate or final study visit. Cognitive function was assessed at regular intervals in the study using the Montreal Cognitive Assessment (MoCA), and the primary MRI marker was WMH, the volume and number of whole-brain T2 lesions. The team modeled associations of WMH and whole brain volume on end of study MoCA and dementia using linear and logistic regression models, respectively, adjusted for randomized treatment, country, baseline age, baseline SBP, and follow-up duration.

A total of 714 patients participated in the MRI substudy and had good quality MRI measures and end-of-study cognitive assessment. Among these patients, Harris and colleagues saw that larger volumes of WMH were associated with poorer cognition via lower MoCA score (

 <.0001). However, the team also noted that the number of T2 lesions was not associated with cognition based on their analyses (

 = .71). Smaller brain volumes were also associated with poorer cognition (

 <.0001). For each standard deviation increase in brain volume, the team found a 51% lower risk of dementia (odds ratio, 0.49; 95% CI, 0.31-0.79; 

Ultimately, Harris and colleagues concluded that, as existing literature suggests, these results support the role of vascular pathology as a central contributor and driver of cognitive impairments following ICH.

“Blood pressure management is an important factor for stroke prevention and recurrent stroke prevention, so that’s obviously a key target,” Harris said. “But so are all of the major risk factors, such as smoking, diet, physical activity, managing diabetes and cholesterol measures. So, we need a very holistic approach, with blood pressure of course being an important primary factor as well.”

Editors’ Note: Harris reports no relevant disclosures.

Harris K. Role of Cerebral Small Vessel Disease in Cognitive Decline After Intracerebral Hemorrhage: TRIDENT MRI Substudy. Presented at the World Stroke Congress (WSC) 2026, Seoul, South Korea. October 21-23, 2026.

Anderson C, Chow C, de Silva A, et al. Three low-dose antihypertensive agents in a single pill after intracerebral hemorrhage. 

Videos

Katie Harris, PhD, discusses her MRI substudy of the TRIDENT trial, evaluating the role of T2 lesions, white matter hypersensitivity, and brain volume on dementia.

Stroke

On the HCPLive stroke page, resources on the topics of medical news and expert insight into CVA can be found. Content includes articles, interviews, videos, podcasts, and breaking news on stroke medicine, and more.

Alexa B. Kimball, MD, MPH, serves as a professor of dermatology at Harvard Medical School as well as president and CEO of Harvard Medical Faculty Physicians at Beth Israel Deaconess Medical Center. 

Tulisokibart, an investigational monoclonal antibody targeting tumor necrosis factor-like ligand 1A (TL1A), outperformed placebo on lesion response at week 16 in the phase 2b MK-7240-012 trial (NCT06956235) in adults with moderate to severe hidradenitis suppurativa (HS). Merck reported the results as a late-breaking abstract at the 

2026 European Academy of Dermatology and Venereology (EADV) Congress

“Results from the MK-7240-012 trial are promising,” said Alexa B. Kimball, MD, MPH, professor of dermatology at Harvard Medical School, president and CEO of Harvard Medical Faculty Physicians at Beth Israel Deaconess Medical Center, and lead investigator of the trial.¹

During the randomized, double-blind study, Kimball et al assigned 149 individuals to be treated with tulisokibart 480 mg every 2 weeks (n = 42), 480 mg every 4 weeks (n = 42), 240 mg every 4 weeks (n = 21), or placebo (n = 44), with a Bayesian primary analysis incorporating historical placebo data.¹ At week 16, HiSCR50 response attained 72% and 64% with the 2 higher doses vs 35% with placebo, meeting the team’s main end point. The low dose, evaluated by the investigators as an exploratory arm, saw HiSCR50 among 52%.

HiSCR75 rates followed a dose-dependent pattern at 41%, 40%, and 29% across the high, medium, and low doses, compared with 15% for placebo.¹ The high dose also produced the largest gain in Dermatology Life Quality Index (DLQI), with a mean change of -5.62 vs -2.46 with placebo.²

TL1A inhibition represents a mechanism distinct from the tumor necrosis factor and interleukin-17 pathways targeted by HS biologics approved to date, and tulisokibart is also in phase 3 development for ulcerative colitis and Crohn’s disease.¹ In the following interview, Kimball spoke with 

 at EADV 2026 in Vienna about the standout efficacy findings and the biologic rationale for targeting TL1A in HS:

: What were the key takeaways from the phase 2b MK-7240-012 trial of tulisokibart in HS, and which efficacy findings stood out most?

 First, HS has been on an incredible journey of exciting developments in terms of how we manage our patients, with really improving efficacy and safety over the past decade. It’s been amazing. This latest set of data for tulisokibart in this phase 2 program continues to show that we can reach high levels of efficacy. We were very excited because this is a new mechanism of action in the world of dermatology, which is TL1A inhibition. What we saw in this program was that, in this 3-arm dosing regimen vs placebo, HiSCR50 and HiSCR75 at week 16 showed very strong results, in the highest tier of efficacy results that we have seen to date.

: What is the biologic rationale for targeting TL1A in HS, and how might this mechanism differ from TNF and IL-17 inhibitors?

 Many people will be familiar with the use of TNF inhibitors throughout dermatology, and certainly for HS, that’s where we really started our efficacy and therapeutic journey for our patients. TL1A is actually a related cytokine to TNF. It’s in the TNF superfamily of cytokines, but it works through a different mechanism. More precisely, it’s a co-stimulatory molecule, and we were investigating a lot of co-stimulatory molecules even 20 years ago to try to break the cycle of inflammatory activation as cells talk to each other to get that cascade going.

You need a number of different things to happen. The way to think about it is like a docking mechanism. There are multiple pieces in the dock that come together to get that activity, and this is one of them. If you don’t have that docked, you have a wobbly interaction.

What’s interesting about TL1A, though, is that it interacts with something called DR3, or death receptor 3, which makes you wonder what death receptor 1 is. In any event, DR3 is found on a lot of different types of inflammatory cells, so in some ways, it has a very broad impact. What we’re trying to figure out is how this translates into the therapeutic benefits we see.

One other interesting element of the TL1A pathway is that it may have an antifibrotic effect. HS is a disease with a lot of scarring, so that would certainly be a substantial benefit to our patients if that part of the mechanism of action pans out in a way that is helpful in how scars develop and remodel over time.

Editor’s Note: This transcript has been edited for grammar and clarity using artificial intelligence tools. Kimball has disclosed her work a paid consultant for Merck.

Merck. Merck’s tulisokibart met primary and key secondary endpoints in phase 2b study in patients with moderate to severe hidradenitis suppurativa (HS). Published September 30, 2026. Accessed November 3, 2026. 

https://s2.q4cdn.com/584635680/files/doc_news/Mercks-Tulisokibart-Met-Primary-and-Key-Secondary-Endpoints-in-Phase-2b-Study-in-Patients-With-Moderate-to-Severe-Hidradenitis-Suppur-QPD75.pdf

Smith T. Tulisokibart shows phase 2b efficacy in moderate to severe HS. 

. Published September 30, 2026. Accessed November 3, 2026. 

https://www.hcplive.com/view/tulisokibart-phase-2b-efficacy-moderate-severe-hs

In this segment of her interview, Kimball discusses phase 2b tulisokibart data in hidradenitis suppurativa and the rationale for targeting TL1A.

Hidradenitis Suppurativa

Hidradenitis Suppurativa 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 dermatology research, treatment, and drug development.

Q&A: Tulisokibart Results and TL1A Inhibition in HS, With Alexa Kimball, MD, MPH

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.

At week 16, PASI 75 was reached by 51.8% and 57.4% of patients on prifemilast 10 mg and 20 mg, compared with 10.8% on placebo.

Responses separated from placebo by week 2 and were sustained through week 52.

Most adverse events were mild to moderate, with few discontinuations.

Prifemilast, an investigational oral inhibitor selective for phosphodiesterase 4B (PDE4B), produced PASI 75 response rates about 5 times higher than placebo at week 16 in adults with moderate to severe 

. The benefits appeared by week 2 and lasted through 1 year.¹ The phase 2 and 3 findings, both from trials conducted in China, were presented at the 

2026 Fall Clinical Dermatology Conference

Adverse events affecting the gastrointestinal tract and central nervous system (CNS) have long limited the tolerability of the PDE4 inhibitor class.³ Prifemilast (HPP737), developed by Newsoara Biopharma, has a molecular structure designed to limit CNS penetration and slow absorption, with the aim of reducing CNS-related adverse events.¹ A previous phase 1 study described its pharmacokinetics and tolerability in healthy participants.²

The poster was presented by Lin Cai of Peking University People’s Hospital, with co-investigators from 12 Chinese hospitals and Newsoara Biopharma.¹

What Did the Phase 2 Dose-Ranging Trial Show?

The multicenter phase 2 trial randomly assigned 123 adults 1:1:1:1 to once-daily prifemilast 6 mg, 10 mg or 20 mg (n = 31 each) or placebo (n = 30) for 12 weeks.¹ Participants had a mean age of 40.2 years, and 79.7% were male.

At week 12, all 3 prifemilast doses produced higher PASI 75 and PASI 90 response rates than placebo, and the response increased with dose. The differences were statistically significant for the 10 mg and 20 mg doses (

 < .05).¹ Of 239 adverse events reported in 84 patients, most were grade 1 or 2 and resolved by the end of the study.

The 2-part phase 3 trial randomly assigned 505 adults 1:1:1 to once-daily prifemilast 10 mg (n = 170), prifemilast 20 mg (n = 169) or placebo (n = 166) for 16 weeks.¹ All participants then received prifemilast 10 mg or 20 mg during a 36-week extension. The mean age was 46.3 years, and 79.2% of participants were male.

At week 16, PASI 75 was achieved by 51.8% (88/170) of subjects on 10 mg and 57.4% (97/169) of those on 20 mg, compared with 10.8% (18/166) of those being treated with a placebo (

 < .0001 for both doses).¹ PASI and static Physician’s Global Assessment responses were found to have separated from placebo as early as week 2.

By week 8, those evaluated also saw clinically meaningful improvements in Dermatology Life Quality Index scores, and the efficacy gains held through week 52.¹

What Is the Safety Profile of Prifemilast?

Through week 52, most adverse events were grade 1 or 2.¹ Discontinuations due to adverse events occurred at a pooled rate of 2.8 per 100 patient-years.

Both trials enrolled patients only in China, and the abstract doesn’t report rates of individual adverse events, including gastrointestinal effects. The authors concluded that the results support further development of prifemilast as an oral therapy for psoriasis, ulcerative colitis and Crohn’s disease.¹

Editor's Note: This summary has been edited for grammar and clarity using artificial intelligence tools.

Cai L, Chen K, Li L, et al. Prifemilast, an oral phosphodiesterase 4B (PDE4B)-selective inhibitor, demonstrates rapid and durable efficacy with a favorable tolerability and safety profile in moderate to severe plaque psoriasis: results from phase 2 and 3 trials. Presented at: 2026 Fall Clinical Dermatology Conference; Las Vegas, NV. 

Ye L, Wang L, Tao X, et al. Pharmacokinetics, safety and tolerability of HPP737, a novel PDE4 inhibitor, in healthy Chinese participants: phase I study. 

. 2026;20:598997. doi:10.2147/DDDT.S598997.

Rabe KF. Update on roflumilast, a phosphodiesterase 4 inhibitor for the treatment of chronic obstructive pulmonary disease. 

. 2011;163(1):53-67. doi:10.1111/j.1476-5381.2011.01218.x.

Oral prifemilast, a PDE4B-selective inhibitor, led to PASI 75 attainment in up to 57.4% of those with psoriasis at week 16 vs 10.8% with placebo.

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.

Prifemilast Achieves PASI 75 in Up to 57% of Patients With Psoriasis

Michael Wechsler, MD, of National Jewish Health.

An integrated post hoc analysis of the phase 3 SWIFT-1/-2 trials and the 52-week AGILE open-label extension, presented at the 

 in Phoenix, found patients in clinical remission with twice-yearly depemokimab (Exdensur) at the end of year 1 had fewer 

 exacerbations and greater lung function gains in year 2.¹,² Of 405 patients in the remission analysis set, 30% reached remission at the end of year 1, and 59% of these patients maintained it at the end of year 2.¹

Remission required no exacerbations across 52 weeks, no maintenance oral corticosteroids in the final 90 days, an Asthma Control Questionnaire (ACQ)-5 score < 1.5, and a forced expiratory volume in 1 second (FEV1) change from baseline of ≥ 0 mL.¹ During year 2, the annualized exacerbation rate was 0.19 (95% CI, 0.12–0.29) among patients in remission at year 1 vs. 0.69 (95% CI, 0.57–0.82) among patients not in remission.¹ From SWIFT-1/-2 baseline to the end of year 2, pre-bronchodilator FEV1 improved by 379 mL (95% CI, 301–458) vs 85 mL (95% CI, 33–137), and ACQ-5 score changed by −1.34 vs −0.71, respectively.¹

Depemokimab, an ultra-long-acting interleukin-5 (IL-5) antagonist, received FDA approval in December 2025 as add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged ≥ 12 years.

 Targeted biologics have made clinical remission a treatment goal in severe asthma, leaving clinicians to weigh how well remission holds once a patient reaches it.

In the following Q&A, Michael E. Wechsler, MD, professor of medicine and director of The Cohen Family Asthma Institute at National Jewish Health, spoke with 

at CHEST 2026 about the durability of remission, twice-yearly dosing, treatment decisions for patients who fall short of remission, and how depemokimab fits among existing biologics.

Q&A: Asthma Remission from Year 1 to Year 2 with Depemokimab

Why is clinical remission now a realistic goal in severe asthma?

Depemokimab Year 1 Remission Linked to Better Year 2 Asthma Outcomes

 We now have very effective therapies to treat patients with severe asthma. We are using targeted biologic therapies that target specific pathways involved in type 2 inflammation, and that's allowed us to get many of our patients into remission. By remission, we are talking about having no exacerbations, no oral corticosteroids, having normalized symptoms, and really achieving some improvement in FEV1 in lung function.

What does twice-yearly dosing change for patients and clinicians?

 When we offer patients twice-yearly dosing, it means that there's less of an impact on their day-to-day lives. They're not thinking about taking their medications.

If you have to take a drug every 2 weeks, every 4 weeks, even every 8 weeks, it's something you have to think about all the time. With twice-yearly dosage, it's much easier for patients to be more adherent and to potentially have better outcomes in the real world.

Why ask whether year 1 remission predicts year 2?

 It's important to ask who is most likely to stay in remission, and it’s usually people who’ve attained some degree of remission in the first year. If you analyze those people, you'll find that while about 30% of patients in the overall clinical trials achieve some degree of remission. If you take those people who've achieved remission, about 60% of those people are able to stay in remission. So, it gives you increasing confidence to continue to prescribe those therapies to those patients.

How durable was remission into the second year?

 Of the patients who attained remission in the first year, about 60% of those patients were able to continue to have remission in the second year. Those patients had no exacerbations, had stable or improved lung function, had no significant symptoms during that phase, and [had] no steroid use for their asthma.

70% didn't reach remission in year 1. Should they stay on the therapy?

 With most therapies, you want to try to find the right drug for the right patient, and remission is a pretty high bar to achieve. While our ultimate goal is remission, many patients achieve some benefits, so not everyone has complete elimination of exacerbations. But about 50% of exacerbations are reduced or eliminated with biologic therapies, like depemokimab.

We need to recognize that not everyone's going to achieve remission, but they might still have benefits, and they might have benefits in terms of reduction in steroid dose, reduction in exacerbations, improvement in lung function, [and] improvement in symptoms. They may not necessarily achieve all of those, but I think achieving even any of those outcomes might have benefits for those patients.

Is this the right definition of remission?

 There are many different definitions of remission, and they take into account different thresholds. There's a big debate among experts about what remission [is], how we define remission, [and] over what duration of time [it is]. Is it 12 months? Is it 6 months? Is it 2 years or longer?

In this study, we used a 4-component definition of remission, but a 3-component definition of remission is also good.

Sometimes people start off [with] a high lung function, and if their FEV1 is 85%, they may not necessarily improve in terms of lung function. But if they have no exacerbations, whereas they had 2 exacerbations in the year prior, that is important.

Where does depemokimab fit among existing biologics?

 The addition of depemokimab into the armamentarium of biologics has been really important for us. It offers a distinct advantage in that it has every-6-month dosing. It has benefits in terms of patients with eosinophilic asthma.

It has benefits in terms of patients with chronic rhinosinusitis with nasal polyps. It's an important addition, and it's good to have a lot of options.

The way I choose a biologic for my patients is I look at the biomarker profile. I look at the comorbidities, I look at safety, I look at dosing, and all of those are important attributes that can be benefited by utilization of a drug like depemokimab.

Wechsler ME, Tacon CE, Muccino D, et al. Attainment of clinical remission with twice-yearly depemokimab in year 1 is associated with improved clinical outcomes in year 2: SWIFT/AGILE integrated analysis. Presented at: CHEST 2026; October 20, 2026; Phoenix, AZ.

Wechsler M. Depemokimab Year 1 Remission Linked to Better Year 2 Asthma Outcomes. HCPLive. Published October 21, 2026. Accessed November 3, 2026. 

https://www.hcplive.com/view/depemokimab-year-1-remission-linked-better-year-2-asthma-outcomes

Brooks A. FDA Approves Depemokimab-ulaa (Exdensur) for Severe Asthma. HCPLive. Published December 16, 2025. Accessed November 3, 2026. 

https://www.hcplive.com/view/fda-approves-depemokimab-ulaa-exdensur-for-severe-asthma

Michael Wechsler, MD, discusses SWIFT/AGILE data showing 59% of patients in remission with depemokimab at year 1 maintained it at year 2.

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.

Q&A: Asthma Remission from Year 1 To Year 2 With Depemokimab 

Raed Joundi, MD, is an assistant professor in the department of medicine at McMaster University, a scientist in the Brain Health research program at the Population Health Research Institute (PHRI), and the Anne Marie Brune/PHRI Chair in Vascular Dementia at McMaster and PHRI.

Raed Joundi, MD, discusses the implications of his substudy of OCEANIC-STROKE and how it could change secondary prevention in ischemic stroke care.

Asundexian and the Role of Factor XIa Inhibition in Secondary Stroke Prevention

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.

October 2026 hepatology news includes FDA approval of bepirovirsen for hepatitis B, new ACLF criteria, ACG cirrhosis guidance, and MASH trial data.

Hepatology

Cholangitis

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8 Hepatology Headlines You Missed in October 2026

Raed Joundi, MD, discusses his substudy of the OCEANIC-STROKE trial, demonstrating the safety of Bayer’s investigational FXIa inhibitor across the spectrum of infarct patterns.

Asundexian Reduces Ischemic Stroke Without Increasing Bleeding Regardless of Infarct Pattern

KT-621, an oral STAT6 degrader, cut mean EASI by 62.6% after 4 weeks with no treatment-related adverse events in a phase 1b atopic dermatitis study.

Atopic Dermatitis

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.

Oral STAT6 Degrader KT-621 Reduces EASI by 62.6% in Atopic Dermatitis

Christoph Correll, MD, is a clinical professor of psychiatry at the Zucker School of Medicine at Hofstra/Northwell.

Correll discusses functional outcomes from SOLARIS and how to monitor and mitigate weight gain with once-monthly subcutaneous olanzapine.

Psychiatry

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Schizophrenia

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Olanzapine LAI: Function vs Weight Gain, With Christoph Correll, MD

Nephrology in October 2026: FDA approves ravulizumab for IgAN, plus ORIGIN 3, RAINIER, TELIGAN, and ATTACK data from Kidney Week.

Nephrology

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

Latest News

Baseline RV Dysfunction May predict Sotatercept response in PAH

Smaller Brain Volume, Greater WMH Lead to Cognitive Decline After Intracerebral Hemorrhage

Q&A: Tulisokibart Results and TL1A Inhibition in HS, With Alexa Kimball, MD, MPH

Prifemilast Achieves PASI 75 in Up to 57% of Patients With Psoriasis

Q&A: Asthma Remission from Year 1 To Year 2 With Depemokimab