Conducting Additional Research to Improve PN Management

Sarina B. Elmariah, MD, PhD: I couldn’t agree more. Here’s my question to both of you then. When we started training, the idea of even a POSI [postprandial oxidative stress index] 100 was not that common. We were hoping for POSI 50 or POSI 75, and it’s taken nearly 20 years to really get there. How long do you think it’s going to take before we can get there for PN [prurigo nodularis]?

Shawn Kwatra, MD: I think it’s happening very quickly, to be honest. The pipeline is expanding. I think the main hurdle here is that we need to have more investigative research. What we learn in psoriasis is, it’s the subunit that you target that can make such a big difference. You look at some of these IL-23 inhibitors like risankizumab vs Stelara and you see these giant differences in terms of efficacy. I believe we need to have more research into the pathogenesis to narrow it down and target it a little bit more. If you look at some of the agents that are coming down, like say, for nemolizumab, which is coming out very soon, some of the H data are very strong. Some of the JAK [Janus kinase] inhibitors are going to have great data. I think we’ll always have to balance how much is it going to improve the H with how much it affects the safety profile. I think that’s the most important thing. To have more target agents where we can learn a little bit more about different immune subsets that are affected in these patients.

Raj Chovatiya, MD, PhD: I agree to an extent. I will say, with psoriasis, we ended up getting lucky a bit in that real time we learned about pathogenesis as we were developing therapies. What we ended up finding out was that psoriasis was probably far more homogenous than we thought as a disease in terms of the importance of IL-23 mediated skewing of Th17 [T helper 17] cells and then the pathogenic expression of IL-17A into a certain extent, IL-17F as well. It turned out that you could get to where certain drugs broadly get to a target of 100% in populations.

I’m liking this for atopic dermatitis. We’ve learned a bit since we’ve had some of our first systemic therapies and others that are far more heterogeneous as a disease. As it turns out that even with a very broadish blockade, you’re still not getting to that point that you’re getting to in psoriasis. A lot of this just comes when the drugs get there. We see what they work like in the real world. I think with PN it could go one of a couple of ways.

To Shawn’s point, I think we’re moving fast on that front. I think we’re going to learn a lot more when clinicians get these in their hands and we see what’s going on in the real world. We have more options. I’d say there’s probably a little more heterogeneity contained in this disease state. A little more on the AD [atopic dermatitis] end that’s psoriasis. We are maybe a little way off. I think we’re also going to learn that given that itch is such an important part of this disease, and that perhaps some of our agents targeting itch are really that good, will that mean that the other things we measure about the disease will catch up with PN, even more so with atopic dermatitis?

Transcript edited for clarity