Video
Emerging Systemic Therapy for Atopic Dermatitis
Author(s):
Expert panelists share excitement for novel therapies in the pipeline for the management of atopic dermatitis.
Transcript:
Peter A. Lio, MD: Could we move into some of the treatments that are being developed? Because I often say this is the tip of the spear. We have some amazing new treatments, but my goodness, there is a real pipeline that has not been there. For the entire first part of my career, we had nothing in the pipeline, and now we have a whole bunch of medicines. Some are going to be systemic agents, biologic agents, another IL-13 [interleukin-13] inhibitor, lebrikizumab. Also, for IL-31, the master itch cytokine, there is nemolizumab; I’m very excited about that one.
That could be really different and presumably will not have too much of a dampening effect on the immune system. It might be a little more of a pure anti-itch [medication], although we know it has an effect in some of the earlier trials we’ve seen on the lesions themselves. Because that’s another thought. Would you just see the itch go down, but the skin looks the same? No, it really does seem to help. And then, of course, there are other things, some topical agents like tapinarof, which is fascinating, an aryl hydrocarbon modulator. It works a little like coal tar, the old tars we used to use, which I think are fascinating. And roflumilast, which is another phosphodiesterase inhibitor. So, some really neat stuff.
What are your thoughts on these? Or which ones are you keying into? Are there ones that you’ve been following with interest?
Neal Jain, MD: With [roflumilast], it’ll be interesting to see if that has similar efficacy to crisaborole, perhaps without some of the irritability that we see with that, the irritation, and the burning that we see. I’m curious to see how that bears out as well.
I think we have other agents that are in play. I think there are other ones that we don’t even see here that are perhaps earlier in development, anti–IL-33 blockade, etc. I’m looking at alarmins. We haven’t seen benefit with anti-TSLP [thymic stromal lymphopoietin] therapy, but perhaps other alarmins might also have an effect.
Matt Feldman, MD: I would agree, and thinking back to the JAK inhibitors and how, yes, the ones that are approved now are JAK1 specific, but JAK1 transmits the cytokine cascade for many of these targets that we’ve talked about, particularly IL-31. I think of the Goldilocks effect here. In somebody who’s not a responder, maybe the anti–IL-4/IL-13 blockade, would combo therapy to hit another pathway or two, like adding nemolizumab, would that get you over the hump for that 80% responder for dupilumab? And would that be what you need? It may not be as immunosuppressing or with many of the other potential adverse effects as something like a JAK1 inhibitor, which has even more cytokine pathways. So, it’s like finding that Goldilocks effect for your partial or nonresponder.
It’ll be interesting to see, do we get combo therapy trials? Do we have head-to-head trials, now that we’re getting more and more of these tools that are coming to market? I think time will tell, but certainly, very exciting times for us.
Peter A. Lio, MD: I didn’t even really talk about yet some of these ones that are in such early stages, but I’m excited about the microbiome too. Can we influence the microbiome? Will there be treatments, both topical and oral? So, it is an exciting time, and I love the idea. I feel like that’s my signature, trying to use a couple of agents to get that perfect response, maybe, instead of hitting it over the head with something very strong. Will there be complements that we can figure out? I hope we’re going to have some more data on these, and people will start to study this, especially as we get closer to personalized or precision medicine.
Transcript edited for clarity.
