Improving Quality of Life in Atopic Dermatitis With Targeted Therapies - Episode 8
Alexandra Golant, MD, highlights the positive clinical data of ruxolitinib, a topical JAK inhibitor used for the treatment of atopic dermatitis.
Linda Stein Gold, MD: We have the biologic agents that we just discussed, where they work outside the cell, very specifically targeting specific cytokines. Yet we have the JAK inhibitors that work. You almost take out a microscope and look inside the cell, and we see that they block more broadly because they can hit multiple of those pro-inflammatory cytokines. We have the topicals. We have the orals. Alexandra, why don’t you start us off? We have a first-in-class topical JAK inhibitor, FDA-approved for mild to moderate atopic dermatitis. What’s the data?
Alexandra Golant, MD: Peter said it best. The JAK inhibitors, topical and systemic alike, combine this unique rapid onset with steroid-like efficacy in a nonsteroidal molecule. Ruxolitinib is a topical JAK1 and JAK2 inhibitor. If you look at its phase 3 pivotal trials at its end point, it’s often a gold standard that [the Investigator’s Global Assessment score is] 0-1, clear/almost clear. You saw just over 50% of the ruxolitinib 1.5% patients achieving this, compared with 10% to 15% of the vehicle group at week 8. In their earlier phase 2 trials, they actually used an active comparator arm with the topical steroids. So, we can say to patients, or…at least in our minds, this is going to behave at least as good as a medium-potency topical steroid. That’s not something we really had the ability to do with topicals before this agent. So that’s been really powerful and gives you this predictable efficacy in knowing what type of patient this can clear. What’s been interesting, looking at the other data points for ruxolitinib, which remain equally as impressive, is its early itch improvement, as early as sometimes 12 hours after the first application, significant by 36 hours, which is new for us. It is exciting for us with a topical agent. This also extends to some of the post hoc analyses, looking at quality of life. So many of our drugs for atopic dermatitis are pulling in these quality-of-life outcome measures. Work productivity, improvements in daily activity. It really speaks to how better disease control impacts that whole patient picture. Whether it be sleep, sleep quality, sleep amount, or work productivity the next day, it really impacts the entire patient experience and also helps guide you in selecting something [so] that when you know the patient in front of you, you think it will aid you in getting that patient to your shared goal, whatever that shared goal is [that] you have with one another.
Linda Stein Gold, MD: When you talk about the efficacy data and you summarize the fact that we had 2 phase 3 clinical trials, they both had an end point at 8 weeks using this drug that was above 50%. And you might say that’s fine. This is a nonsteroidal option, and we’re getting more than half the patients to clear/almost clear. Is that unique?
Alexandra Golant, MD: Very unique and not something that we’ve had before. We’ve seen these types of paradigm shifts in atopic dermatitis. I’m sure all of you would agree when dupilumab first came out, and now with our novel topicals and our additional biologics and our JAK inhibitors, they’re really elevating what we can come to expect from our treatments, which 10 years ago would have felt like a fairy tale. It would have felt like fiction, really. We’re now here, and so it changes the way you look at a patient. It changes the patient who is in front of you, [to whom you’re] saying, “Where can I get you with an effective topical regimen?” It’s different than it was before ruxolitinib, just like it’s different for our moderate to severe patients before our targeted systemic agents. That’s been really exciting to have these new tools to play with to see how far you can push these patients and how clear you can get them with these new, advanced tools that we have.
Linda Stein Gold, MD: We do know topical ruxolitinib is for patients who have more localized disease. So, we talk about it for patients with up to 20% of affected body surface area. We want to keep it localized. We don’t dip a patient in the topical. This is for patients who have more localized disease, which I think is appropriate because if somebody has more than 20% body surface area, my goodness, they should probably be on a systemic agent just to try to get them under control. But…we want to not treat this continuously over the course of a year, but on and off as needed.
Transcript edited for clarity