Exploring Novel TYK2-Targeted Therapies for Plaque Psoriasis - Episode 1
Linda Stein Gold, MD, and Bruce Strober, MD, PhD, assess the efficacy of traditional and newer treatment options for psoriasis. They also discuss therapeutic targets and the goals of therapy.
Linda Stein Gold, MD: Hello and thank you for joining us for this Peers & Perspectives presentation entitled, “Exploring the Novel TYK2-Targeted Therapies for Plaque Psoriasis.” My name is Dr Linda Stein Gold. I’m the director of dermatology clinical research at Henry Ford Health in Detroit, Michigan. Today I’m thrilled to be joined by my friend and colleague, Dr Bruce Strober. He is a clinical professor of dermatology at Yale University School of Medicine. Today we will discuss a new class of medication for plaque psoriasis, the tyrosine kinase 2 inhibitor, it’s mechanism of action, and data on efficacy and safety. We will discuss how this therapy will impact our treatment decision-making. Thank you so much for joining us, and let’s go ahead and begin. So, Bruce, thanks. It’s really an exciting time for the treatment of psoriasis. We’ve had an explosion of new treatment options. Can you briefly tell us, for those patients with more localized and more severe disease, what are our options?
Bruce Strober, MD, PhD: For more localized disease, Linda, we are always going to rely on topical therapy. Topical therapies come in a variety of classes, mainly the topical corticosteroids, topical vitamin D analogues, some topical calcineurin inhibitors, and now a newer group of topicals that were just approved last year, an aryl hydrocarbon receptor agonist that’s called tapinarof, and a PDE4 inhibitor called roflumilast. Using all of these we’re able to control often localized disease. Now, when we get into more widespread disease or disease that affects special areas with high impact on quality of life, we may not only use the topicals but also turn to more systemic therapeutics. They can be oral therapies, or they can be injectables, and as well, we can’t forget, we can use UV phototherapy.
Linda Stein Gold, MD: Great, and we’ve seen so much in terms of research and innovation in the biologic arena. Yet in terms of oral agents, how often do you use those traditional orals at this point?
Bruce Strober, MD, PhD: The traditional orals really, there are only 3. There’s methotrexate, which is probably the most commonly used oral therapy that’s traditional, conventional; cyclosporine, the least common; and then acitretin, somewhere in between. To answer your question, I use primarily methotrexate for some patients, particularly patients who have insurance that won’t cover more expensive medications, or in some instances where I just think it might be the best drug for the condition in front of me. Acitretin is confined to male patients and maybe as an add-on to phototherapy or some systemic therapies like biologics. Cyclosporine is for emergencies, where you need to clear the patient very quickly. They can get the drug that night, but you’re ultimately going to transition them off cyclosporine to a safer long-term therapeutic.
Linda Stein Gold, MD: Then we’ve had apremilast, which has joined as a newer oral agent, much safer than the others we’ve had. The efficacy profile in terms of systemics in general is a little more modest.
Bruce Strober, MD, PhD: That’s right. Usually you have more blood test monitoring for the older systemics. With apremilast, no. Apremilast obviously is a modern therapy, twice daily, but no blood test monitoring at all for that drug, and therefore a much greater level of comfort when using it.
Linda Stein Gold, MD: I do feel this is an area of unmet need, trying to get that perfect picture of good efficacy as well as a good tolerability and safety profile. Let’s talk for a bit about what is our end goal. I know the National Psoriasis Foundation came out, as you know, with the treat to target goal. Is that something you use in practice? What does that mean to you? Or is that something you don’t necessarily use practically?
Bruce Strober, MD, PhD: Generally, I don’t look to go to targets. Targets to me have less meaning than the patients saying, “I’m happy.” Patients are usually fairly convincing in how well they feel about the therapy you’re giving them. As long as you give enough time to give the therapy its chance to work, and different therapies have different lengths of therapeutic time needed to see their full efficacy. But that said, when that’s been hit, I walk into the room, I ask the patient, “How happy are you?” I will query about symptoms like itch and pain, and as well whether the locations that are remaining are a problem for their quality of life and overall sense of well-being. If they’re happy, and they often are very clear about that, I’m not changing therapy, I’m keeping the current therapy going. If they are in any way expressing unhappiness or even on the fence, I’ll push them to do something different, which might just be adding a second therapy or changing the therapy.
Transcript edited for clarity