Good afternoon. Thanks for joining our 46th annual healthcare conference. I'mJ. Stacy Ku, part of the biotech team with my colleague, Ms. Shaw. It's my pleasure to introduce Bradley Burnam, CEO of Turn Therapeutics. Please take it away.
Thank you. I'm just gonna do a quick double-check. Can everybody hear me okay? I've got sort of a microphone here. Are we good back there? Okay. I just wanna check the pointer. Okay, we're good. Hi. Thank you to TD Cowen. Thank you everybody for being here. Thank you to Stacy Ku for the questions that I know and the discussion that we're gonna have. My name is Bradley Burnam, as she mentioned. I'm founder and CEO of Turn Therapeutics. I'm just gonna jump directly into the slides. The origin of Turn Therapeutics is probably different, a lot of pharma companies out there. I was actually a medical device rep for 10 years. I was the pacemaker guy. I worked for St. Jude Medical, did the defibrillators, the pacemakers. I was in the operating rooms.
I managed a large team actually for a lengthy period of time. I understand the commercial portion of medical sales very well because I actually was in it. I dealt with the VAC committees, I dealt with, you know, corporate accounts and reimbursements and whatnot. The other thing is, because you're in the hospital all the time, you're interacting with patients. One of those patients was very sick, and I ended up getting septic with an organism called CRE. Those of you who know organisms, you know that's not a good one to get. It's got a pretty high fatality rate.
One of the symptoms of it is you get soft tissue infections about 25% of the time. I had a series of abscesses over the course of 5 years, over 20 surgeries. I became what could best be referred to as a chronic wound patient for a long time. Learned that our wound care products were not quite up to par at the time, that's where the company started. They were putting things like honey on my wound and calling it advanced. I set about trying to formulate my own product initially for myself. I found an API that is still the workhorse in TT-03, which is the formula that we're gonna spend a lot of time talking about today in Europe. It is a novel polymer.
It's a new chemical entity. It's never been utilized as an API in the U.S., we get the NCE status. Problem was it was in a liquid state, I wanted it in an ointment state. I developed a process of actually fusing this liquid inside of an oil carrier without an emulsifier, it was obviously a great deal of trial and error. It was my mom's favorite thing to say that her son patented mixing oil and water, here we are, we call that process PermaFusion. Visually, if you could just imagine berries in a bowl. I'm just gonna keep going even though the microphone's jumping in and out.
The APIs are suspended in these blueberries inside of a three-dimensional matrix of petrolatum, and because of that suspension rather than dilution, we can use a very low ingredient weight overall and still achieve a very high bioavailability. This is what we're gonna talk the most about today. This is the lead asset that I developed actually originally as a wound care product for me. I have an extensive amount of experience with this product. Actually had an FDA clearance in wound care, and I did some initial sampling and so we have a lot of actual human data and human uses to fall back on as far as the safety profile. What we discovered over time is that it was good at a number of things.
In particular, it's very good at things like dermatitis, we will talk about the fact that it is an IL-36, IL-31 inhibitor. It is the first IL-36 inhibitor of its kind. It is a novel mechanism of action. It's also an IL-31 inhibitor, which is very important. We do have an active phase 2 as we speak, 114 to 120 patients. It's happening inside the United States. We're expecting both the interim assessment and the final data to read out in the first half of 2026. It's going to be a fun first half of the year for Turn Therapeutics. This is our pipeline as I mentioned. Moderate to severe eczema is active.
Q2 interim assessment, then they'll probably be, because it's an eight-week treatment period, kind of a short trigger before we see the final top line. That's gonna be a fun quarter. We also have a phase III ready onychomycosis drug. With the recent updates with the FDA, that of course could be amended to a phase 2b/3 single registrational trial. Everybody's still sort of catching up a little bit on the new regulations. It has a great deal of human data, and I can go into that in a bit. I mentioned eczema. I did not initially think to use the product in eczema. I take no credit for that. The doctors are very clever people with, you know, coming up with off-label uses for things.
It made sense when they were putting it on severe eczema to me because these were patients that the biology of eczema had just progressed to the point that the skin was very injured. I mean, the real difference between moderate and severe eczema is just more injury to the skin. You know, more breaking, more infection likelihood. They were using it initially in these wound clinics and skin clinics to try and heal these wounds. What they were noting to me is the patients were getting significantly less itchy and reporting, "Hey, I want some more. It's helping my eczema." I had a theory that we were inhibiting what I like to call the epithelial distress cytokine. It is quite literally the first signal that the skin sends off in the case of barrier distress.
If you have too much staph colonization, if you have cold weather and it breaks, if you have a disruption, you know, in the force, if you want to use a cliché, the skin sends off this IL-36 signal, and it starts that whole eczema cascade. You might notice Th2 differentiation. Everybody's probably heard of IL-4 and IL-13 because of the biologics that act on them. That happens after IL-36 release. Later on in the chain, we also get the IL-31 release, which is the patient discomfort, the itching signal. That's obviously a very important target to hit and sort of a hot one because it actually leads to a quality of life change. I wanted to determine, validate whether or not this IL-36 theory was true. We set about doing some in vivo studies.
In the first one, we used a Johns Hopkins model by a gentleman by the name of Lloyd Miller, who was at Johns Hopkins at the time. He's now at Johnson & Johnson. He created sort of the seminal work on connecting IL-36 to eczema. We replicated his model. We created an IL-36 environment, we applied the product, and we wanted to see if there was a clinical effect. In that particular case, we had a 57% reduction in Investigator Global Assessment over 7 days. We now knew that at least there was a clinical effect in the in vivo model. Now, mechanistically, what was happening in terms of the actual cytokines? We ran a very large Western blot cytokine analysis using tissue analysis, protein expression, and basically said, "What's happening in there? Which signals are being expressed?
How much are we inhibiting them?" We ran a pre-treatment model that was actually an NIH model that they used in Candida auris studies, where we put ointment on the animals for four straight days, and then we induced, and we wanted to see, in terms of a comparator, which one was being reduced. Now if you see, we actually hit IL-36-alpha and IL-36-gamma. If you're familiar with these cytokines, you know that IL-36-gamma is strongly associated with psoriasis. Generalized Pustular Psoriasis drug, in fact, acts on that. eczema is alpha dominant. We also hit IL-31 downstream, a very significant portion of IL-31, and also IL-4. We have an extensive safety history on the product, as I mentioned, but of course you need to validate things with controlled clinical trials.
We sponsored a phase I study, a traditional RIPT study, ran, you know, repeat insult patch test. Over 53 patients, 580+ applications under occlusion. The Tegaderm, the Saran Wrap style dressings. We didn't have a single adverse event reported. This was not surprising to us 'cause the formula's already been blessed as non-cytotoxic, non-irritating, non-sensitizing. It's a non-systemic, but it's nice to see it validated. This is our phase II that is ongoing. We are now doing a moderate to severe eczema trial. This is happening in the U.S. It's got three PIs. It is enrolling on time and very well, especially with the winter enrollment surge.
We did it as an adaptive trial, whereby the interim committee, if you can imagine sort of a group of people where they swallow the key and hide behind a door, they look at the data and they say, "Okay, you can add some more in if you need to. We recognize that dermatitis can actually have a high placebo effect with vehicles." We don't anticipate a futility. We anticipate either keep going or keep going and potentially add a bit more patients, either of which, of course, are a win. We still are planning to read out probably in June. I will say by the end of Q2. Primary endpoint is the usual EASI index, Eczema Area and Severity Index, change versus vehicle. Secondary endpoints of IGA and itch score.
I anticipate we will actually be equivalent to systemics, so that could be a fun quarter. As far as the model, it was actually a really smart analyst who told me to think about this. When a patient goes to the doctor for eczema, there's a traditional treatment model, especially. They start with something topical, usually a steroid. It's a pretty big commitment to jump to these injectable systemics. Usually you wanna try something as a first line, and right now the first lines are not great options in terms of safety and efficacy. Nobody wants to just slather steroids all over themselves. Doctors don't love prescribing JAK inhibitors with side effects warnings on the side. We actually think because we're non-systemic, non-sensitizing, non-irritating, and non-steroid, that this could become first-line treatment for eczema. I just mentioned the topical milieu.
I don't need to go over each one of these in detail. As far as the eczema market, I'm sure most people know it's a very large market. A fascinating random statistic though is I started looking at other countries and they tier the countries in terms of like bigger markets, 1st tier, 2nd tier. The U.S. is actually a second-tier market for eczema. It turns out countries like Sweden, you know, Norway, Denmark, they can have as high as a 34% eczema incidence because it's cold and because the barrier is under distress a lot, and you get that IL-36 signal. We're obviously exploring international markets as well.
Quickly on the onychomycosis, another fun off-label, I'll call it program that was brought to me, this time by the head of the American Podiatric Medical Association, who reached out and wanted to run a clinical trial on our product for toenail fungus. He had a theory that because we're a fat-based product with a broad-spectrum API, that he could treat toenail fungus. He ran a 100-patient trial. This was an APMA study. It was in the journal. I can send the poster. He had 70%-85% efficacy, which is incredibly high for toenail fungus. He did the nail clippings. He sent them out to a lab. I wanted to know why, because that's just me. I don't like saying just because. I like to know why.
We ran an in vivo nail penetration study where they inoculated the nails with actually Trichophyton rubrum, the traditional organism that causes nail fungus, and we were one of the first topicals to actually penetrate the nail and kill the fungus. The current options for topicals are not fantastic. 6.5, 8.9, and 17.8. The last branded topical comes off of patent in 2026, and sort of this cliff that everybody is seeing. It is an interesting time to have a potential branded product in the toenail fungus market, which lacks almost any and all competition at this point. Just mention the topicals. You can see they are not cheap either, and people still like...
I sometimes call onychomycosis the last bastion of reimbursable vanity. This is a very deceptive TAM because only 15% of people actually go to the doctor to treat their toenail fungus 'cause they sort of already know they're gonna have to take a pill, Lamisil, or the topicals out there aren't great. If you could actually open up that market, a lot of people have toenail fungus. I feel like you can throw a rock in any group I talk to, you're gonna find a few people that have it. This is a massive untapped reservoir of patients. I mentioned our science. IL-36 has a number of diseases associated with it. It's sort of the golden goose to me of the cytokines. It's the initiating punch of the inflammatory cycle.
IL-31, given the quality of life and the other indications associated with itching. We have a very fun 2026 coming up. I mentioned this timeline. This deck will be online for people who wanna review it again. This is probably something you're not used to seeing at conferences like this, which is our unbelievably low burn rate. That is not a typo. Because I built this company on a shoestring, literally built my own lab in the beginning, I got used to outsourcing and vendors and choreographing, and we still extensively use vendors to this day. Built this company entirely on family office money. We've raised a total of $21 million to this day and produced everything you're seeing right now.
When it came time to, I'll say, go toward our phase III trials, our phase II is fully capitalized, it was either go public via microcap or direct list, which we did in October, and then utilize this fully capitalized phase II trial as an opportunity to actually approach institutional investors. So far right now, it's actually, it's working out. We're doing pretty well. Extensive patent and protections, 7 families, 17 issued patents, current coverage through 37. We should be expecting further coverage in the late 2040s. I think this is my favorite slide. I call this the Oracle slide. I was acutely aware in the beginning that I knew nothing about the pharma industry. I knew how to sell pacemakers and program them, but I started just cold calling these brilliant people. One of the first ones was Arthur Golden.
He's the senior-most M&A lawyer at Davis Polk & Wardwell. He's been a mentor of mine for at least half a decade, maybe more at this point. He's on our board. Andrew Gengos, CFO of Terns Pharmaceuticals, which is very confusing 'cause we're Tern sometimes. They raised a couple of dollars a few weeks ago or a month or so ago, and Callum was on that deal. Kent Kester is the head of CEPI. Martin Dewhurst was global head of McKinsey Life Sciences for seven years. He was at McKinsey for 30 years. If you look at this board, we just hired Dr. Redfield, the former director of CDC, to help us with regulatory and policy. We've got an incredible group of minds and brains that I get to reach out to. That's the conclusion of the presentation.
If I could just end with, you know, not a lot of people knew about us because of that, quote-unquote, non-traditional way that I said we went public, and we hired an incredible PR person named Sasha Damouni. She was with Bayer, and she was a Bloomberg health reporter, and she sort of helped us frame the story much more for the institutional crowd. Now given that we have a novel mechanism of action, we've got potentially phase III trials in the next 12 months to start an active phase II, we really think we're well-positioned for investment. Thank you.
obviously open up to Q&A.
Does this work or is it just that?
Opportunity to ask some questions. Otherwise, I have a couple. All right, jump in anytime. What a great comprehensive presentation.
Thank you.
Maybe let's go to the MOA slide.
Sure.
Talk through that in a little bit more detail. I know you talked about the oil and water aspect of things.
You mean the loop slide?
Yes, exactly.
This one. Sure.
Just talk about maybe clearly you've done a lot of work to look at the IL-36, potential role of your drug. Can we also talk about maybe the pathogenic skin bioburden?
Absolutely
...barrier dysfunction piece of all that, just maybe.
Absolutely. I mentioned a gentleman named Lloyd Miller before, who was at Johns Hopkins. He had a theory that eczema was closely associated with excess bioburden in the skin, dysbiosis. You know, it feels like everything keeps coming back to the microbiome lately. There is a strong connection with excess staph colonization in the skin, which tends to in the literature's theory, tends to lead to that distress signal. There's also the chicken or the egg back and forth because you may get more staph because of the fact that you have a weakened skin barrier, which can be a genetic deficiency.
The fact that we are a non-sensitizing that also eliminates the dysbiosis because we can eliminate the staph burden as well as heal the skin barrier, it's a working theory that we may work from both sides, especially and including the staph bioburden portion.
You also talked about at the very end the IP protection that gets you out to 2040s.
Oh, very much.
...the, maybe the hurdle, that you yourself faced to try to bring forward.
The hurdle that I'm trying to inside of oil? Yeah, it was, it wasn't easy. Because of the fact that we have literally the world's worst emulsifier re-emulsion, it's the best. A lot of it was what's not just, we're able to get method, though, and patent family on the indications such as onychomycosis pending for inflammatory skin disease, including the compositions as well. We've spent more money on IP than any other aspect of this company. I've become a little bit of a nerd. Never will have a single family filing continuation feel like somebody could throw a dart at the family, and the whole tree could fall. We continue to sense of additional families. We do have patent families, including the as well as the.
Okay, understood. Of course, work for the mid-twenties-
Yes.
-in atopic dermatitis talk about, de-risk have taken to the moderate to severe patient.
Absolutely.
Maybe speak that off-label you're seeing.
Sure. I mentioned that it was in wound care in the beginning. The fun story behind that is that I literally got that, a 510(k) clearance at a Kinko's in Woodland Hills, California by myself. I submitted all the data via phone. This formula passed our use on skin disease, including breached tissue because chronic wounds, diabetic ulcers, whatnot, good for that, but I was able to actually in this space. Thousands of units have been used on patients. It's a register. There's never adverse event reported to the public database. We have a huge amount of experience on the sale of this product. In terms of a lot of eczema to me is safety, especially what the options are out there.
In terms of the safety, as you said, we're very on an efficacy, you know, math, some of the systemic. I really don't think anybody's gonna hold a candle to us.
Okay. if you could go to the phase II design.
Sure.
-maybe walk through that adopted design where we are right now, just to level set the outcomes that we're expecting.
Sure. It is a one-to-one trial, simple in that sense. Vehicle on one side, active on the other, moderate to severe is the inclusion. A double blind randomized vehicle controlled all of the fancy acronyms that we want to is called various people the index before is going to be, are we better than the V? As an eight-week from enrollment out, which actually the treatment protocol, we recommend two to three times since we will use more than that, but for the trial, recommending two to three times a day. Secondary endpoint, the change in get a global assessment of the traditional drop in two point, which means you have to at least drop two, and I think it should be two, one or clear is what I believe the endpoint say.
The itch assessment is literally how bad are you with, very bio indicator of the eczema itself. Having breach issue, you know, with no itching, there could be the question of is this eczema or not? If you have the breached tissue and the itching to me, that's the indication of biological activity if that goes down.
Okay. Number of patients that you're gonna disclose, and we should expect all these updates to be also expected, all these different metrics to be disclosed as well.
The interim assessment will be conducted between 50 and 60 patients. We anticipate it'll be probably about 51 patients. That will be the add a few patients for statistical precision or futility, that we anticipate to be in Q2, and then we also anticipate the top line in Q2.
Okay. Understood.
The top line will have all of these specific data points in there. The interim will just have thumbs up, you guys designed it well.
Understood. When it comes to dermatology, and obviously you're gonna talk about toenail fungus and the opportunity there, but are you thinking about anything else within dermatology when it comes to this?
Very much.
I'm guessing you're waiting for the results here, but can we talk about some of the other places?
Yeah.
where it could be leveraged?
I have a very strong interest in hidradenitis suppurativa, and I've actually learned to say that correctly very fast, by the way. Hidradenitis suppurativa is a bioburden-driven inflammatory disease of the skin that results in huge painful lesions all over the body for these patients. Very similar mechanism of action, IL-36 driven bioburden connected. According to the physicians that I've spoken to, the only things that really work right now are things like topical clindamycin and oral antibiotics. There's a very large lack in that space, and it's a huge quality of life and issue for the patients. Given that we hit IL-36 gamma, psoriasis is obviously on our radar. I like the fact that HA is a relatively large but very high need market.
I was a patient for a long time, so it has that appeal to me, and there's also really nothing else out there that targets the very similar MOA.
As we think about maybe then beyond dermatology and your level of interest in toenail fungus, what kind of clinician target kind of sales force when you're thinking about maybe all the different indications?
I think that this force, I recognize that maybe force. Partner with another company or with a strategic sales force of some kind that already has that channel sale. We're actively working toward developing relationships with dermatology KOLs, bringing on staff that are in the dermatology space. It was fun because we found out we were a great derm asset because people told us. Now we're almost backing into it, but it's really nice when you sort of have information on your own asset before you begin the trial.
Yeah. To that point, what work are you doing nowadays to increase awareness in the dermatology community?
We have trials and peer review as we speak that I got a chance to co-write. We're going to be at the academic conferences, the American Academy of Dermatology. We submitted an abstract for that. I'm also actively trying to hire people in the medical affairs space and build out the advisory panel, with derms, and thankfully Sasha Damouni and her partner, David Patti, have a ton of experience. David Patti, who's another person who works in our PR, he ran the atopic derm, marketing at Leo. He's got a number of contacts in the space. We're very much leveraging our team that has a lot more experience in that space.
Okay, wonderful. Any last questions?
Yes, sir.
You mentioned that on the protocol you're recommending patients administer the drug two to three times a day. What if they're administering it only once a day? What if it's less? Would that blunt the efficacy that you think that you'll see?
In my opinion.
Can you repeat the question before you answer?
The question was, "If they don't use it two to three times a day, would that blunt the efficacy?" I will say that there are controls in the trial, such as tubes, to make sure that the appropriate . I do that using less and having more to the element, potentially skincare items or whatnot might blunt, but I also don't know applying it once and on the whole it might have a ton of effect. We're doing our best to control. We've had really good compliance thus far. We work extensively on a weekly basis. The weighing has been in keeping with the Eczema Area and Severity Index, the size of the lesions, and the using of the amount thus far.
That does bring up 1 last question. Your trial, how are you working on keeping the control arm within historical ?
Sorry, can you elaborate a bit more?
In your control arm, you're just trying to make sure. How do you make sure to stay within a control arm type outcome? Kind of working with the CROs to make sure you're maximizing the effect.
Maximizing the effect of the asset?
Yep.
We just designed the trial with a very heavy understanding of the fact that a vehicle such as ours would have a strong reduction in eczema. I mean, it's eczema. You put an emulsion on somebody's skin, it's gonna make them feel better. We have enough information on the product with the way we built the trial that we just believe strongly the delta will be high enough.
Wonderful. Any last questions? Thank you so much.
Thank you, Stacy, and thank you everybody for being here.