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Turn Therapeutics' Atopic Dermatitis Candidate Achieves 57% Reduction in Disease Severity in 7 Days


Bradley Burnam discusses results from an in-vivo model of atopic dermatitis.

In an interview with Dermatology Times, Bradley Burnam, the founder and CEO of Turn Therapeutics, discussed Turn's latest candidate for atopic dermatitis, which recently demonstrated a remarkable reduction in disease severity in a widely cited in-vivo model.

Over a 7-day treatment period, the candidate reduced the ISGA score, a standard measure of atopic dermatitis severity, by 57% compared to just a 10% reduction observed with placebo.

Burnam delves into the details of this innovative therapy, its development process, and the impact it may have on the future of dermatologic care.


Bradley Burnam: I'm Bradley Burnam, founder of Turn Therapeutics. I began as a survivor of a hospital-acquired infection, turned into the development of a series of products, and I'm focused very intently right now in dermatology.

Dermatology Times: Can you provide a detailed overview of the in-vivo study design and methodology that was used to evaluate Turn Therapeutics' atopic dermatitis candidate?

Burnam: There have been a lot of studies and a lot of validation to the notion that Staph aureus precedes atopic dermatitis. There's sort of been a chicken and the egg concept for some time. In 2017, I would say, a series of studies focusing on the subject came out. One of them actually showed, via an infant study, that followed 149 infants from birth through when they actually show a symptom of atopic dermatitis. It showed that infants with atopic dermatitis had more than 100 times, or 100 times more Staph on average, than people who don't. It's as if the chicken or the egg concept has been determined at this point: Staph precedes eczema.

Then studies started coming out, especially from the group at Johns Hopkins, where they were trying to determine: What is it about Staph that leads to atopic dermatitis? We all have Staph on our skin, even if there's excess amounts in our in our skin mantle. Why is it driving this incredibly large inflammatory response? The Johns Hopkins group determined that it was related to an interleukin called IL-36 which is part of the IL-1 beta group. I would call it high up in the chain of the inflammatory cascade receptor, and the toxins that Staph releases signal the release of IL-36, and in the determination of these studies, that leads to eczema. We've sort of got the chicken or the egg thing solved now, and then, not just the what, but the how, and they used that to make a mouse model for inducing eczema. The mouse model, which has now become pretty widely accepted, is essentially, you apply Staph on a bandage at a particular concentration for 7 days, and you end up with eczema. It's incredibly true; that is the in-vivo induction method that we use.

What we did is we started with 30 mice, which, with all the studies, have shown to be the best model for inducing eczema. We induce eczema. All 30, we ended up with a 3.3 on the ISGA scale across the board, as you know, somewhere between moderate and severe. We have photos on the website. In the study, you can see some of them were pretty intense inflammation. At that point, I also wanted to see whether or not the IL-36 was truly elevated. I couldn't measure whether or not we were inhibiting it, because then we'd be going on the way down. But it was also a verification of the mechanism of action that the studies have discussed.

We took 10 of them, and we did a tissue analysis for the expression of IL-36, and it was extremely elevated. It was in the 7000 as the peak for some of them; I think the mean was about 5700. Then the remaining subjects: Half of them were treated with our product, to reduce the ISGA score in theory. Half of them were not. The mean reduction over 7 days for the treatment group was 1.89 in 7 days, which is a dramatic drop in ISGA, or 57% reduction. The immune reduction was only a 10% reduction in the placebo group, and the p value was 0.0003, so it was a very clear differentiation between the 2 groups. A relatively simple study; 7 days of induction, 7 days of treatment with a pre-treatment control to verify the IL-36 expression. Our next study will be a pre treatment model where we try and measure which cytokines, in addition to or including IL-36A, in theory, we inhibit.

Dermatology Times: Can you elaborate on the significance of the study findings within the context of atopic dermatitis treatment?

Burnam: Number 1, while you can't generalize mice to humans, you definitely see a dramatic drop in ISGA very quickly. 1.89 over 7 days is dramatic. I see the options in atopic dermatitis now as sort of on some polar spectrums. You have steroids for the most part, and then you have the injectable biologics on the other. They both do their thing respectively. Steroids will reduce the inflammation after you have it. The injectables, once they're loaded into your system, can theoretically stop it from happening. I'd like to give people that in-between option where they don't necessarily have to use steroids, and they don't necessarily have to use injectables. The significance, to me, is, number 1, an option for people who don't want to use either. Number 2, a very well understood mechanism of action for our API and our product in terms of how it's working. We know that we reduce Staph colonization via historical data on our product. We know that we have no sensitization via historical clearances on our product, and we now verified in-vivo that we can reduce eczema symptoms. The significance, to me, is that maybe there's a happy medium between steroids and biologics, and even if it's just a bridge, to me, some people will end up on the injectables, and they're very effective. We all know that. But there are some people who either don't want them, are still suffering before they've reached their levels in their system where they are working. Even if we can be a replacement for some and a bridge for others, I think it would be highly significant.

Dermatology Times: What are the next steps in the research and development process following these promising in-vivo results?

Burnam: I have become rather obsessed with the cytokine concept, and all the different ways that the different interleukins and cytokines actually affect even different portions of the chain of inflammation, even different symptoms of it. For example, IL-31 being sort of the itchiness one. We've run a number of simulation models that suggest that our mechanism of action inhibit a number of cytokines, IL-36 alpha, IL-36 gamma, IL-4, IL-13, IL-31. Again, these are simulations, so I haven't verified this yet. We have designed that protocol, and we plan on running that protocol in July using a model that was designed by the National Institute of Health for pre treating for Candida auris colonization and subsequent IL-17 activation. We're hoping to have the results of it by the end of July, and if at that point, we can prove that we actually inhibit these interleukins without being an injectable, to me, that's extremely significant, potentially, in my mind, I think that would be a groundbreaking discovery. I'm looking forward to seeing those results.

Following that, we hope to jump into a phase 2 study as quickly as possible, so that we can get the efficacy data in humans. We're at an interesting point as a product, because it's an expansion of indications. This is not first in-human. When we go and we work on eczema patients, or we go and study on eczema patients, it's 200,000 plus in human. We have a very good idea of what the safety database or what the safety results are going to look like, because we have seen it used so many times. But given the in-vivo data that we have, given the mechanism of action understanding that we have now, and given the safety database that we have and all of the anecdotal, if not, some are more than anecdotal reports from physicians, we're very excited to see them in a formal clinical trial, and we're hoping to have the result of that, conservatively, I'd say within 2 years. Clinical trials require a lengthy period of enrollment, but I'm hoping we can push it to a year and a half.

Dermatology Times: What are some of the key messages you want dermatologists to take away from the study or from future ongoing studies and development?

Burnam: What I'd like to say is there's a place for everything in the continuum of care, to me. There are people who are against one thing, for one thing, something causes more side effects than another, for some people. But right now, there are very limited choices, I believe, in terms of safe and effective options. You're either using steroids, you're using injectables, and there are people that don't want either. I would simply like doctors to know that I'm working very hard to give them an affordable option that is neither a steroid nor an injectable, in theory, patients might be more apt to use because the safety profile is higher.

I have a 3 and a half year old, and eczema has become much more on my radar since he developed pretty moderate to severe eczema, and it's been amazing actually helping him with it, because I have access, and I cannot wait to get people access to this product. I've seen it, and it's gone so that I am as excited about this as I have been about any program I've worked with before. If anybody knows my history, you know I will fight to get something to the market, no matter what I have to do. I am extremely excited about this asset.

[Transcript has been edited for clarity.]


Turn Therapeutics atopic dermatitis candidate reduces disease severity by 57% in-vivo. News release. BioSpace. June 20, 2024. Accessed June 26, 2024. https://www.biospace.com/article/releases/turn-therapeutics-atopic-dermatitis-candidate-reduces-disease-severity-by-57-percent-in-vivo/#:~:text=All%20(816%2C573)-,Turn%20Therapeutics%20Atopic%20Dermatitis%20Candidate,Severity%20by%2057%25%20In%2DVivo&text=LOS%20ANGELES%2D%2D(BUSINESS%20WIRE,in%20disease%20severity%20versus%20placebo

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