Besides gene therapy, we hopped over some other potentially very useful, valuable, and promising intravitreal biologic injections, going back to anti-VEGF–like approach of injecting in the office. Can you tell me, Diana, a bit about what else is out there on the horizon?


Sure. There are some exciting new agents also in late stage development. One of them is KSI-301, which is an intravitreal anti-VEGF agent built on a novel ABC platform. ABC stands for antibody biopolymer conjugate, and this medicine is designed for enhanced durability with up to 6 months of VEGF suppression via a single injection. That is also in phase 3 clinical trials right now in wet macular degeneration, diabetic macular edema, and retinal vein occlusion, and the early data have been very promising, with robust visual acuity gains, long duration of VEGF suppression with the need for very few repeat injections, and fortunately no safety signals. I think that’s a very promising program in late stage development. Carl, you’ve had some experience with that. What are your thoughts on KSI-301?



I agree. KSI is looking very promising in that category of second-generation anti-VEGF therapy with greater durability. It seems to work as well; it seems to be as safe, although that experience is still quite limited, but nonetheless looking good. Durability, boy that looks to be at least as good as faricimab. We have about 60% of patients going 6 months in the maintenance phase. That’s quite good, after the load. This ABC platform effectively doubles or more the half-life of the drug. It’s a nice way to keep it in the vitreous longer, and that’s looking like its mechanism to get that greater degree of durability. I also put that in the next-generation or second-generation anti-VEGF category.

There is another drug that is interesting. It’s not a VEGF-A blocker, but it blocks VEGF-C and VEGF-D, and is called OPT-302. That’s a fusion protein that blocks C and D. This is an add-on; it’s not a standalone drug. In phase 2 it was added to VEGF-A blocker ranibizumab and did show enhanced vision benefit. It’s aiming at getting maybe better visual acuity outcomes, not necessarily greater durability, because it has to be injected pretty frequently, either every month or every other month, that’s been tested now in phase 3. That’s the only thing on the horizon that might actually get us better acuity. We mentioned limited durability and hoping to get more durable drugs as our big unmet need, and it is. But getting some better vision outcomes of course would be welcome, and that’s working by this combo approach, VEGF-A blockade like we’ve been doing and is still coming, and then adding in a VEGF-C and VEGF-D blocker. Again, an intravitreal injection, fusion protein, and it’s combination therapy, so it’s got to show superiority in vision to what we’re using now.

Then there is this class of tyrosine kinase inhibitor [TKI] molecules, small molecules that have to be packaged in a sustained-release platform, all of which are being injected intravitreally. It’s not a surgery, and there are 4 programs. Three are intravitreal injections, either suspension of microparticles with given TKI, or maybe a biodegradable implant injected intravitreally. There is even a suspension of TKI suprachoroidal injection. They are all aiming to get an anti-VEGF–like effect over about 6 or more months, but that has yet to be demonstrated adequately. What are your thoughts about what you’re hearing about these TKIs?



I think it’s terrific to see all of this innovation continue to push the field forward for patients. It’s wonderful to think out of the box. Certainly, there is room for improvement because not all patients have an optimal response to VEGF inhibitors, and angiogenesis is complicated. There are lots of different cytokines and molecules in play. I think exploring these different inhibitors is a terrific way to try to improve the outcome for all patients. I’ll be excited to see more data as they emerge.



 In the TKI category, there are few things they have to prove. They have to prove they work as well as our anti-VEGF biologics, have to be as safe, and truly give us the durability factor, give us 6 months or more, not just 3 or 4 months, because the other medicines we’ve been talking about like faricimab and KSI are probably going to achieve that 3 or 4 or more benchmark and durability. They’ve got a hurdle there to try to stack up to what’s on the near horizon with biologics, again KSI-301, faricimab, and then we’ve got the port [Port Delivery System], all in the very near future. A lot is going to be in our hands. There will be a lot of choice for our patients, and that’s all good in terms of decreasing treatment burden with greater durability and hopefully getting better vision outcomes in practice.

Thank you for watching this 

. If you enjoyed the content please subscribe to our e-newsletter to receive upcoming Peers & Perspectives® and other great content right in your inbox.

Carl Regillo, MD and Diana Do, MD react to newer therapies being explored for wet AMD and discuss their place in future therapeutic algorithms. 

Innovative Therapies on the Horizon to Treat AMD 

Carl Regillo, MD, Thomas Jefferson University School of Medicine  

 Before we conclude, I’d like to get some final thoughts from each of you, if you have any. Let’s start with you, Dr Nordberg.

 From my perspective, treatment-resistant depression and other complex mental health challenges are systems challenges as much as they are clinical challenges. We haven’t moved the needle in treatment effectiveness in about 50 years, and in no small respect that may be because we haven’t changed our systems that provide care. I’m a big fan of looking at developing systems where we’re doing a lot more precision referral work, and to Martin’s earlier point, identifying different providers, clinics, and centers of strength, and referring to strengths. The only way to do that is to collect the data.

There are challenges around collecting the data. It creates vulnerability and a lot of visibility where there hasn’t been historically. One of the things that we’re working on at Reliant Medical Group is trying to be more precise about how and who we refer. A lot of that involves understanding the patient that we’re being presented with, and also understanding how that person matches up with what we believe is the most likely treatment to be effective for them based on data.

I’m pretty confident that if we can do that work in naturalistic settings, we’ll get past the archaic requirement of failing 2 bonafide medication interventions and get more rapidly to something that’s going to allow a care delivery organization to say, “This is a patient with treatment-resistant depression,” and a payer to say “No problem,” and then allows that care delivery organization to connect that patient with a reimbursed intervention that has a likely shot of helping them. That’s a lot of work to be done, but it starts with measurement and having the confidence to integrate that measurement into your clinical routine.

 Well said. To your original point, we haven’t moved the needle much in these past 50 years. You’re calling for improved systems, better measurement, and moving toward precision care. Hopefully that will be supported by the validation of some biomarkers that can lead to more precise and predictive treatments. Would you also agree that part of this as well is that we haven’t had very many new tools in the past 50 years, and potentially having some effective new tools in the toolbox may also help move that needle?

 It may. We also know that there’s a lot of variability between different providers and that there are different kinds of treatments that appeal more to different kinds of patients. The biomarker research is sexy and exciting because of that possibility of carving nature at its joints and being precise. It’s also a long way off. RDoC [Research Domain Criteria] didn’t deliver the promise of precision opportunities for understanding and deep learning about what drives mental health on a physiological level.

We still have a lot of opportunities with the systems and treatments that are already out there. This system still has a lot of room for optimization. It starts with having the courage to collect more data and letting those data start to tell us what kind of a patient this is and the best place for the patient to go based on what we’ve already learned about similar patients. That’s where my focus is, less so on developing novel interventions. It’s important to figure out where the patients that we’ve been discussing fit in that overall model, but we’re not going to be able to figure that out if we’re not collecting the right data.

 For those of us who deal with the fun stuff, the insurance and billing portion of things, like I’ve been saying this whole time, it’s important to make sure that you understand your payers and their guidelines and policies. You have to play that middleman role between the insurance carriers, providers, and patients. We need to make sure that we’re educating our providers so that they know if there are any changes to these policies so that they can find the right fit for patients.

It’s also important to educate the patients in regard to what qualifies them as having treatment-resistant depression and what’s available out there. Be an advocate for the patient with the payer and keep them involved in the process so that they’re not at home wondering, “What’s going on with my prior authorization? When is my treatment going to start?” Let them know everything along the way and be there for them.

 The theme that I’d leave with is the idea of “better together.” If you think about it, there are 3 participants in the goal here. Front and foremost is the patient because they want to get better. They’re suffering. There’s the provider who’s trying their best to figure out the appropriate care. There’s also the payer who wants to make sure that the patient gets access to the benefit that they deserve and that they’re able to go on and live a healthier and happier life. You have to see that triad.

There’s a likelihood that you can blame the insurer or blame someone else, but at the end of the day, it’s about figuring out how to work better together, that triad, because we have a common interest in improving the life of that patient. That’s the part that I like to focus on. What are we doing this for? Who matters the most? The other stuff can be worked out.

 Thank you. Last but not least, Dr Ares-Romero.

 I love that. I love how you ended with that. Because as somebody who treats treatment-resistant depression regularly, I’m very passionate about having my patients improve their lives. Their quality of life is what’s important, and that they get passion and fulfillment from their lives. It’s beautiful to hear that, that we can work together. That’s key, getting the payer together with a provider. It’s not about you or me. It’s about the patient and how can we come together to work together. I love that.

Despite the hurdles and challenges and everything we’ve talked about, it’s an exciting time in psychiatry. This is a time when we have new modalities, new things, all the data collection, all the systems, and the artificial intelligence that we have now that we haven’t explored. There are so many wonderful things coming that I’m excited. I’m excited for our patients. I’m excited for everything that we’re doing.

 Thank you all again. To our viewing audience, we hope you found this 

® panel discussion to be useful and informative.

An expert panel shares insight on the future treatment landscape for treatment-resistant depression. 

Optimizing the Management of TRD

Carrie Jardine

Expanding Precision Medicine in COPD With Mepolizumab, with Frank Sciurba, MD

The recent approval of mepolizumab for chronic obstructive pulmonary disease (COPD) marks another step forward for the treatment landscape, offering clinicians a biologic therapy that targets a distinct inflammatory pathway.

 Unlike traditional COPD regimens, which rely heavily on long-acting bronchodilators and inhaled corticosteroids, mepolizumab acts through IL-5 modulation to address TH2-driven inflammation, particularly in patients with elevated eosinophil counts.

Following the 2023 approval of dupilumab, which targets the IL-4/IL-13 axis, mepolizumab becomes the second biologic option for TH2-high COPD and expands the toolkit for precision medicine in a historically underserved population.

 While approximately 20–30% of patients may qualify based on eosinophil levels, the drug’s safety profile has been favorable across trials, showing no increased adverse events over placebo.

 spoke with principal investigator Frank Sciurba, MD, Associate Professor of Medicine at the University of Pittsburgh School of Medicine, and Medical Director of the Pulmonary Physiology Laboratory in the Division of Pulmonary, Allergy and Critical Care Medicine, to learn more about his reaction to mepolizumab’s approval and what it means for the COPD population.

“Just within the last couple years now, we've really now started to achieve that promise of new products for COPD with new mechanisms and indications. The first TH2 modulating drug, dupilumab, was approved last year, and it's a different mechanism of action. This is IL-5 modulation versus the IL-4a receptor, which modulates IL-13 and IL-4, and it's very likely that those differences will result in some difference in responses in individual patients," Sciurba said.

Nucala (mepolizumab) approved by US FDA for use in adults with chronic obstructive pulmonary disease (COPD). News release. GSK. May 22, 2025. https://www.gsk.com/en-gb/media/press-releases/nucala-mepolizumab-approved-by-us-fda/

Dupixent® (dupilumab) Approved in the U.S. as the First-ever Biologic Medicine for Patients with COPD. Regeneron Pharmaceuticals, Inc. September 27, 2024. https://www.globenewswire.com/news-release/2024/09/27/2954552/0/en/Dupixent-dupilumab-Approved-in-the-U-S-as-the-First-ever-Biologic-Medicine-for-Patients-with-COPD.html. Date accessed: September 27, 2024.

Sciurba shared his excitement for the recent approval of mepolizumab for people with COPD and an eosinophilic phenotype.

Frank C. Sciurba, MD

Ophthalmologist experts provide an overview of emerging treatments for dry eye disease. 

Emerging Treatments for Dry Eye Disease

I. Paul Singh, MD

 Does anything else catch your eyes, Ed or Jessica?

 I’m most excited for, at the current moment, the selective JAKs to be coming down the line, especially for Crohn disease. That’s really what I have my eye on, in addition to, as Bill just mentioned, the IL-23 inhibitors. Those are the things that are coming the soonest, and I’m excited to have more hopefully safe and efficacious options when treating Crohn disease. Those are what I have my eye on, in addition to, of course, my personal biases: the microbiome therapeutics, of which there are several under investigation. We did see some intriguing initial data from Seres Therapeutics in 1 of their agents in the treatment of ulcerative colitis, although these are still very early days. We also know there are several companies working on FMT [fecal microbiota transplantation]–like products, but really more selective microbiome therapeutics. I’m very excited for those. The positioning of microbiome therapeutics earlier or in combination with other advanced therapies is really exciting.

 Ed, do you have any final words on therapies?

 Some of the etrolizumab UC [ulcerative colitis] results were clearly mixed and somewhat disappointing, but don’t forget, we still have a Crohn [disease] trial out there. At some point, we’re going to have some anti-integrin data, and more on Crohn, so there may be something. There are a few other molecules in that realm, so who knows what will happen?

 In that same vein, there’s an orally systemically bioavailable alpha(4) beta(7) [LPAM] inhibitor that’s a small molecule. Think of it as oral vatelizumab. That’s in phase 1 testing. Then there’s another that’s a short peptide that gets down into the more distal gut, and you can think of it as inside out instead of outside in. We always knew that vatelizumab didn’t work solely the way it was proposed because, at doses and drug concentrations that are one-tenth of what’s required for clinical efficacy, you can completely saturate the alpha(4) beta(7) receptors on the appropriate lymphocytes in the periphery. If the entire mechanism of action of vatelizumab is blocking lymphocyte trafficking from the periphery to the gut, then that should be sufficient for efficacy, and it’s not. It makes you think that there’s some other mechanism beyond that, possibly with an antibody in the tissue affecting cell-cell interactions of cells that have already trafficked. With this inside-out peptide, you can see efficacy, and they saw it in a pilot study in the clinic, as well as in animal models, at concentrations where you got some into the blood but only to the point that it was 60% saturating the receptor in the periphery. You wouldn’t expect that to work, yet it did. Anyway, I’m with that. We’re going to see an evolution in anti-integrins and maybe oral therapies. Wouldn’t that be cool?

 That’s a lot to unpack and look forward to. With that, I want to thank everyone for the rich and informative discussion. Before we conclude, I’d like to get some final thoughts from each of you about what you’d like to say to our clinical colleagues. What should they be striving for in treatment and looking for the future? Jessica, why don’t we start with you?

 As we’re evolving in this space, it can potentially feel a bit overwhelming. There are almost too many potential choices coming down the line, so what I would tell my colleagues is to assess your patients. Look for prognostic factors to help you make those treatment decisions, pick targets that you’re going to follow, and do that systematically with your patients every time. It’s going to be different for every patient, but really that’s a way to keep things straight and organized. Stay attuned to the data and all these exciting developments coming down the pipeline. Remember, you can always lean on some of your colleagues at IBD [irritable bowel disease] centers if you’re unsure about therapies or want assistance. For example, I’m always happy to have discussions with my colleagues about which agent we should be choosing, why, or if they’re uncomfortable with potential therapeutic options, because until you have a lot of hands-on experience with some of these drugs, it takes a bit to get comfortable with them. That would be some of my advice to anybody out there treating IBD, but it’s starting to feel a bit overwhelming by all these new advances coming down.

 I’m going to a total side thing. We’re seeing patients with complicated diseases. One of our jobs is to stay rational but also project confidence and hope. Sometimes, we see these patients who have lost hope. Usually, for almost every patient, there’s something you can do to improve their quality of life. Just keep that in mind.

 We’re at the end of the beginning of the revolution of IBD therapy. Buckle up—a lot of new stuff will come, but we have an amazing repertoire of therapies that we can use today. Be students of the field and the craft, and learn to use those therapies and, as Ed said, improve the lives of your patients.

 I always say to the fellows here [Cumming School of Medicine at the University of Calgary], “We need to demand more.” We need to demand more of ourselves to help the patients, demand more of science to push things forward to improve the lives of the patients and to pay attention to those little things that we’ve all talked about tonight. Ed summed it up nicely, that even if you’re on your fourth biologic or advanced therapy, there’s something you can do for that patient that will make tomorrow better for them. Always look at what you can do for that individual patient. With that, to all of you, this was just fantastic stuff. I hope the audience enjoyed it.

 If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming 

 and other great content right in your in-box. I’m sure you’ll see the folks in front of you on future programs. Thank you very much.

Jessica Allegretti, MD, MPH, and Edward Loftus Jr., MD, review emerging agents in the later phases for the management of IBD.

Emerging Treatments Over the Horizon for IBD

Jessica Allegretti, MD, MPH

Joanne Nazif, MD, is an attending physician in the division of Hospital Medicine at Children's Hospital at Montefiore. She also serves as an associate professor of pediatrics at Albert Einstein College of Medicine.

RX Review: RSV Prevention Strategies and the Changing Epidemiologic Landscape

In this special report from HCP Live and Contemporary Pediatrics RX Review, Albert Rizzo, MD, moderates a discussion with Tina Tan, MD, and Joanne Nazif, MD, for an expert discussion on recent developments and persistent gaps in managing respiratory syncytial virus (RSV). 

In this clip, Tan emphasizes the major impact of RSV prevention tools in the last couple of years, including maternal immunization and monoclonal antibodies like nirsevimab, on reducing disease severity and hospitalizations, particularly in infants. Nirsevimab, sponsored by Sanofi and AstraZeneca, was FDA-approved under the name Beyfortus in July 2023.

 Tan also notes that underutilization of RSV vaccines among older adults continues to contribute to severe illness and admissions in that population.

Nazif adds that treatment for hospitalized pediatric RSV cases remains largely supportive, given the limited efficacy of pharmacologic interventions, and so prevention has become the most effective strategy. She highlights the high disease burden, citing up to 80,000 infant hospitalizations annually due to RSV-induced bronchiolitis.

The panel also addresses epidemiologic shifts post-COVID, including an initial drop in RSV hospitalizations followed by a return to baseline levels. Encouragingly, early data from the 2024–2025 season show significantly reduced hospitalization rates among infants under seven months, particularly in the youngest age group, following widespread use of maternal vaccines and nirsevimab. These trends support a promising outlook for broader prevention efforts.

Editor's note: The FDA approved Merck's clesrovimab under the name Enflonsia last month as the latest immunization strategy for infants entering their first RSV season.

is chief medical officer of the American Lung Association. Board certified in internal medicine, pulmonary, critical care and sleep medicine, Rizzo serves as the moderator for this panel discussion.

is a professor of pediatrics at the Feinberg School of Medicine at Northwestern University and an infectious disease physician. She is also medical director of the International Patient and Destination Services Program, president of the Lurie medical dental staff at Ann & Robert H. Lurie Children’s Hospital of Chicago, and president of the Infectious Disease Society of America.

is an attending physician in the division of Hospital Medicine at Children's Hospital at Montefiore. She also serves as an associate professor of pediatrics at Albert Einstein College of Medicine.

Rizzo, Tan, and Nazif report no relevant disclosures. 

FDA Approves New Drug to Prevent RSV in Babies and Toddlers. News release. FDA. July 17, 2023. Access July 16, 2025. https://www.fda.gov/news-events/press-announcements/fda-approves-new-drug-prevent-rsv-babies-and-toddlers

U.S. FDA Approves Merck’s ENFLONSIA™ (clesrovimab-cfor) for Prevention of Respiratory Syncytial Virus (RSV) Lower Respiratory Tract Disease in Infants Born During or Entering Their First RSV Season. News release. Merck. June 9, 2025. https://www.merck.com/news/u-s-fda-approves-mercks-enflonsia-clesrovimab-cfor-for-prevention-of-respiratory-syncytial-virus-rsv-lower-respiratory-tract-disease-in-infants-born-during-or-entering-their-fir/

In this video, the first in a 3-part series, panelists discuss recent advancements in RSV management.

Joanne Nazif, MD

Genetic diagnosis of inherited disease, including many X-linked diseases, has increased dramatically in recent years with more advanced genetic testing options. After a genetic diagnosis is made, family member testing may be warranted. Family member testing can identify those who are carriers of disease, those who may be affected by disease, and add insight and guidance regarding the risk of future offspring being born with the disease. While this has fostered an improved understanding of genetic drivers behind these diseases, most of the medical community has considered the carrier population as simply the messengers of the genetic information, clinically unaffected by an abnormal gene; but we’re learning this isn’t always the case.

Increasingly, research has found that there are many X-linked diseases in which carriers show signs and symptoms of the disorder, in varying degrees of severity. Historically, these symptoms have gone largely unaddressed by the medical community. Studies show that the often-overlooked symptoms in X-linked carriers may negatively impact their physical and mental health if not properly addressed. A more holistic care approach for X-linked carriers of genetic diseases requires that we look at the carrier population as potential patients, too.

Chronic Granulomatous Disease (CGD) is a good example of this. CGD is a rare, genetic immunodeficiency that increases susceptibility to severe, recurrent and life-threatening bacterial and fungal infections and can produce abscesses in internal organs like the lungs, brain and liver.

 Sophisticated diagnostic tools employed today, like the Dihydrorhodamine (DHR) assay, can accurately determine if someone has X-linked CGD, autosomal recessive CGD, or is an X-linked carrier of CGD, and also provides a prognosis for the severity of the disease. X-linked carriers of CGD can also present with recurrent skin infections and abscesses and may have DHR test values in the same range as patients with X-linked CGD. 

In an essence, they phenotypically can have CGD and the providers who care for them may need to think of them like patients. We now know that DHR values of X-linked CGD carriers may change over time with age, and as a result the risk of serious infections may increase as carriers age.

 The evolving clinical state of the X-linked CGD carriers demands that they be closely followed by medical providers, so that if and when their disease declares itself, they can be treated appropriately.

Follow-up and close monitoring are particularly important among this population, as case reports and large case series have shown that carriers of X-linked CGD may develop more symptoms as they age. Symptoms can include recurrent infections and abscesses, skin abnormalities (e.g. photosensitive rashes and discoid lupus), autoimmune thyroid disease, abdominal pain and diarrhea, and lupus-like symptoms (e.g. chronic fatigue and joint pain).

The impact of being a carrier isn’t just physical – it’s psychological, as well, and can greatly impact quality of life (QoL). In a survey of 75 X-linked CGD carriers, more than 40 percent reported experiencing moderate or higher levels of anxiety, which correlated to depression, lower self-esteem, presence of joint or bowel complications, and fatigue.

 Like in many other diseases, it is well documented that these types of QoL indicators can carry a significant impact of health and quality of life, warranting closer monitoring and care for the carrier populations.

This phenomenon is assuredly not unique to CGD, but likely a consideration across many genetic diseases. It requires a fundamental shift in thinking among not only clinicians, but the entire healthcare team, including nurses, genetic counselors and other allied professionals. Holistic care for inherited genetic disease should involve family testing, identification and proactive monitoring; and disease management guidelines for X-linked genetic diseases should clearly reflect this to improve the care we provide for both diagnosed patient populations as well as the genetic messengers, the carrier patients.

Kelli Williams, MD, MPH, is a pediatric allergist-immunologist at

South Carolina in Charleston, South Carolina, USA. She has cared for many

with Chronic Granulomatous Disease (CGD) – a rare primary immunodeficiency that

cause serious, recurrent and potentially life-threatening infections, among other symptoms.

Authors and clinicians interested in being published on HCPLive can 

1. Chronic Granulomatous Disease. AAAAI. 2021. Available at: 

https://www.aaaai.org/conditions-treatments/primary-immunodeficiency-disease/chronic-granulomatous-disease

2. Marciano B, et al. X-linked carriers of chronic granulomatous disease: Illness, lyonization, and stability. Journal of Allergy and Clinical Immunology. 2018 Jan;141(1):365-371. 

https://pubmed.ncbi.nlm.nih.gov/28528201/

https://www.researchsquare.com/article/rs-344043/v1

3. Battersby A, et al. Health-Related Quality of Life and Emotional Health in X-Linked Carriers of Chronic Granulomatous Disease in the United Kingdom. Journal of Clinical Immunology (2019) 39:195–199. 

https://doi.org/10.1007/s10875-019-00607-6

Not Just the Messengers: Carriers of X-Linked Diseases Can Be Patients Too

Kelli Williams, MD, MPH

Experts discuss strategies for making dry eye care an appealing practice option for optometry students and supporting their success in this specialized field.

Novel Treatments and Diagnostics for Dry Eye

Novel Treatment and Diagnostics for Dry Eye

Laura Periman, MD

Mack Mitchell, MD, is the vice president for medical affairs and the Nancy and Jeremy Halbreich Professor of Internal Medicine at UT Southwestern.

Reducing Alcohol Use in Patients with Liver Disease, with Mack Mitchell, MD

 remains a critical yet underutilized component of 

While significant advances have been made in addressing the complications of advanced liver disease, there is a growing recognition that early intervention is essential for preventing disease progression. However, the stigma surrounding AUD, both within the healthcare system and society at large, frequently creates barriers to effective treatment.

A 2024 study from Massachusetts General Hospital found that although practice recommendations from several medical societies advise against potentially stigmatizing language for AUD and ALD, many liver transplant centers continue to use outdated terms like “alcoholism” and “alcoholic,” potentially hindering patient care and their willingness to seek treatment.

Overcoming challenges like this will require a shift in perspective, recognizing AUD as a treatable medical condition and integrating evidence-based interventions into routine hepatology care.

, Mack Mitchell, MD, vice president for medical affairs and the Nancy and Jeremy Halbreich Professor of Internal Medicine at UT Southwestern, reviews pharmacologic treatment options for AUD in patients with ALD and looks ahead to other medications that may eventually be used in these patients.

Mitchell begins by highlighting the 3 medications that are currently approved by the FDA to reduce drinking: disulfiram, naltrexone, and acamprosate. However, he notes that disulfiram is not suitable for use in patients with liver disease due to its off-target side effects.

Of the remaining therapies, Mitchell says clinicians should consider acamprosate for their patients who have a longer drinking history and disulfiram for patients in earlier stages of AUD.

Looking ahead, Mitchell says he believes GLP-1 receptor agonists will eventually be used for patients with AUD and ALD, citing recent research demonstrating use of semaglutide led to reduced alcohol consumption. Similarly, he says he thinks resmetirom (Rezdiffra), which is currently approved by the FDA for the treatment of patients with noncirrhotic metabolic dysfunction-associated steatohepatitis (MASH), will be used for the treatment of AUD and ALD.

“I think the landscape out there is pretty exciting,” Mitchell concluded. “Hopefully, over the next 5 to 10 years, we will see a lot better outcomes in all of the patients with steatotic liver disease.”

Managing Alcohol Use Disorder in Alcohol-Associated Liver Disease, with Mack Mitchell, MD

Editors’ note: Mitchell has relevant disclosures with Durect, GlaxoSmithKline, and National Institute on Alcohol Abuse and Alcoholism.

Brooks A. The Power of Words: Liver Transplant Centers Continue to Use Stigmatizing Language. HCPLive. February 17, 2024. Accessed March 24, 2025. 

https://www.hcplive.com/view/the-power-words-liver-transplant-centers-continue-use-stigmatizing-language

Brooks A. Resmetirom (Rezdiffra) Receives Historic FDA Approval for Noncirrhotic NASH. HCPLive. March 14, 2024. Accessed March 24, 2025. 

https://www.hcplive.com/view/resmetirom-rezdiffra-receives-historic-fda-approval-for-noncirrhotic-nash

Mitchell reviews FDA-approved drugs for reducing alcohol use, which ones can be used in patients with liver disease, and other therapies on the horizon.

Mack Mitchell, MD

Sonja Ständer, MD, is a professor of dermatology and neurodermatology for the University of Münster and the head of the interdisciplinary Center for Chronic Pruritus (KCP) at the University Hospital Münster.

Discussing New Phase 3 Data on Nemolizumab for Prurigo Nodlaris, with Sonja Ständer, MD

New phase 3 findings on the pruriginous lesion types in patients with prurigo nodularis and the efficacy of nemolizumab (Nemluvio) were presented from the OLYMPIA 1 and 2 analyses at the 

American Academy of Dermatology (AAD) Annual Meeting

To discuss these data and their significance, given nemolizumab’s recent approval, Sonja Ständer, MD, spoke with the 

 Ständer—a professor of dermatology and neurodermatology and the head of the Interdisciplinary Competence Center Chronic Pruritus (KCP) at the University Hospital Münster, Germany—was asked about the OLYMPIA trials and their significance for clinicians.

“These were the phase three trials leading to approval of nemolizumab recently, and these were two independent trials with a global presentation involving like 560 patients globally,” Ständer said. “And the patients were in 2 to 1 randomization rooted in the 2 arms, either placebo or the nemolizumab. The dose given was dependent on body weight. The patients received every 4 weeks an injection of nemolizumab, and the primary endpoint was at Week 16.”

In both trials at baseline, Ständer highlighted that all participants presented with nodules, alongside papules, plaques, ulcerations, and umbilicated lesions. She and her team found that those in the nemolizumab arm of each study showed a mean reduction from baseline of 57% and 63% in their count of pruriginous lesions within representative areas. This was compared to −6% and −25% in the placebo arm of OLYMPIA 1 and 2, respectively.

“So nemolizumab acted very quick on the itch, and this is a primary aim of the patient. They want to get rid of the itching,” Ständer explained. “This was already observed after a couple of days, and it was well-tolerated, and this is also very important in the management of the patients.”

Ständer added that by the 16-week mark, 46% and 59% of individuals in OLYMPIA 1 and 2, respectively, who were given nemolizumab attained ≥75% lesion healing.

 She was also asked about which elements of her presentation she hopes that clinicians walk away knowing, and highlighted monitoring of the disease.

“There is 1 item, taking a look at the percentage of healed lesion,” Ständer said. “We nicely could see that, independent of patients’ IGA, this item performs very well, demonstrating that you really can see a very good healing of the lesions. At Week 16, the numbers were even higher than the IGA.”

For additional information on this data, view the full interview posted above. To find out more from AAD 2025, view our 

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

Ständer has reported receiving grants, personal fees, and additional compensation from Galderma, along with grants, personal fees, and additional compensation from Sanofi, Incyte, Celldex, and Amgen.

Ständer S, Legat F, Piketty C, et al. Characterization of the pruriginous lesion types in individuals with prurigo nodularis and efficacy from the randomized, placebo-controlled, Phase 3 OLYMPIA 1&2 trials. March 7, 2025. Presented at AAD 2025.

Galderma Receives U.S. FDA Approval for Nemluvio® (nemolizumab) for Adult Patients Living With Prurigo Nodularis. Galderma. August 13, 2024. 

https://www.businesswire.com/news/home/20240812791599/en/Galderma-Receives-U.S.-FDA-Approval-for-Nemluvio%C2%AE-nemolizumab-for-Adult-Patients-Living-With-Prurigo-Nodularis

This AAD 2025 interview features a discussion with Sonja Ständer, MD, new phase 3 findings from OLYMPIA 1 and 2 on nemolizumab in patients with prurigo nodularis.