Shattuck Labs at 24th Annual Needham Conference: Strategic IBD Focus

On Wednesday, 09 April 2025, Shattuck Labs (NASDAQ: STTK) presented at the 24th Annual Needham Virtual Healthcare Conference. CEO Taylor Schreiber outlined strategic developments in their DR3 blocking antibody program for inflammatory bowel disease (IBD). While the company expressed optimism about their innovative approach, challenges such as high placebo response rates and market impacts from tariffs were also discussed.

Key Takeaways

• Shattuck Labs is developing SL-325 and SL-425, targeting DR3 for potentially improved IBD treatment efficacy.
• The company has completed GLP toxicology studies for SL-325 with a favorable safety profile.
• A Phase 1 study is planned soon, with data expected by the end of the year.
• Shattuck aims for a subcutaneous dosing regimen, potentially reducing dosing frequency.
• Positive early interactions with the FDA were reported regarding IND submission.

Financial Results

• Shattuck Labs is financially equipped to fund its Phase 1 study and operations into 2027.

Operational Updates

• SL-325 (DR3 antibody):

- Completed GLP toxicology studies in non-human primates, showing no adverse events.

- Phase 1 study initiation is planned for the next few months, with initial data expected by year-end.

- Receptor occupancy data indicated full receptor occupancy at the lowest dose tested.

• SL-425 (half-life extended version):

- Developed alongside SL-325 to achieve less frequent dosing.

- Chronic toxicology studies are planned to compare safety and pharmacokinetic profiles.

Future Outlook

• Shattuck is targeting the initiation of Phase 2 studies in IBD patients in the second half of next year.
• Aiming for subcutaneous dosing formulations in Phase 3, with a preference for Q8 weekly dosing.
• The decision between advancing SL-325 or transitioning to SL-425 will depend on Phase 1 and chronic toxicology data.
• Development of DR3-directed bispecific antibodies is underway.

Q&A Highlights

• Dosing Regimen: Focus on subcutaneous dosing for maintenance in Phase 3, preferring less frequent Q8 weekly dosing.
• Placebo Response Rate: Acknowledged high placebo rates in IBD trials; importance of considering patient therapy history in studies.
• Tariffs and FDA Changes: Tariffs impact business elements; positive pre-IND interactions with the FDA were noted.

Readers are invited to refer to the full transcript for a detailed account of Shattuck Labs' presentation and strategic insights.

Full transcript - 24th Annual Needham Virtual Healthcare Conference:

Ethan Markowski, Member of the biotech research team, Needham and Company: Good good afternoon, everyone, and thank you for joining us at Needham and Company's twenty fourth Annual Healthcare Conference. My name is Ethan Markowski, and I'm a member of the biotech research team here at Needham. Joining me today from ShadowCloud is Taylor Schreiber, chief executive officer who will provide a presentation on the company followed by a Q and A session with the remaining time. And with that, I'll go ahead and turn it over to Taylor.

Taylor Schreiber, Chief Executive Officer, ShadowCloud: Great. Thanks, Ethan. And thank you to Needham for the opportunity to present at the healthcare conference this year. These are my forward looking statements. So I'll start with providing you all with an overview of t l one a and d r three biology and and outline the reasons why we think that targeting d r three may lead to higher rates of complete remission than what has currently be seen with been seen with t l one a.

Then we'll talk through the antibody candidates that we're developing themselves. So most people are probably aware, but this is a snapshot of the now published phase two data from Prometheus in developing tulisocobart that Merck is now in control of. And the data presented here and and showing complete placebo adjusted complete remission rates in the range of twenty five percent was was incredible to see, was the first data point that started to provide clinical validation that blocking t l one a in IBD patients could be clinically efficacious. And what's been even more exciting is to is been seeing that since that time, the results have really been replicated by both the Roche antibody that came from Royvant and now, of course, with the Teva antibody as well. And so, you know, it's it's relatively uncommon to have, you know, three independent placebo controlled trials with antibody different antibodies going against a similar mechanism like this with, you know, no clear leader in terms of getting toward approval.

And so that provides really great optimism for patients that are suffering from IBD for for what this might yield in terms of benefit in the future. And to go through the axis itself, the t l one a d r three axis is fairly straightforward. For many so t l one a d r three are both members of the TNF superfamily, and many TNF superfamily receptors are promiscuous, meaning that one ligand binds multiple receptors or one receptor binds multiple ligands. And when that's the case, there can be a very obvious reason to target either the ligand or the receptor to maintain specificity and and reduce off target effects. And that's not the case with this axis.

T l one a is the sole known signaling signaling ligand for d r three, and it does not cross bind any other signaling receptors. The only other protein that t l one a is known to bind is soluble molecule called d q decoy receptor three or d c r three, and this was a protein that evolved in humans. It doesn't exist in non primates. And whenever that happens, it tends to give you an indication that this is an evolutionarily important pathway. And the role of d c r three is is to neutralize serum t l one a.

And so because of the simplicity of the access, we believe that the clinical data to date showing the safety and specificity of t l one a blocking antibodies is highly likely to predict the safety profile of a d r three blocking antibody. The fundamental biology around this axis began to be published in in the early two thousands. So t t l one a was first described as the signaling ligand for d r three in 02/2003. And since that time, a limited number of labs in the world, including my academic mentor, Eckert Podak, the University of Miami, have been the folks that really have defined the rules of engagement for how this access works. This figure on the right here came from Richard Siegel, was another one of those early investigators that was important in defining how this access works.

And what he showed in this publication here was that if you have mice that express high amounts of t l one a, those mice become highly prone to developing spontaneous inflammatory bowel disease. And you could fully neutralize that phenotype if you cross those t l one a over expressing animals onto background of animals that do not express d r three. And this is one of many data points from those days that proved the monogamous nature of the axis and that and that t l one a was the sole signaling ligand for d r three. If you look across all of that early literature, you will not find examples of where where either genetic deletion of d r three is inferior than genetic deletion of t l one a or where pharmacologic inhibition of d r three is inferior to pharmacologic inhibition of t l one a. But you will find a few examples including this one where and this came from Fabio Caminelius, group at Case Western University, where he has a mouse strain here that is highly prone to developing spontaneous Crohn's disease like ileitis.

And what he then did is he crossed that those animals onto animals that either lacked d r three or animals that lacked t l one a. And what he found was that the animals that were crossed onto a d r three knockout background had a much higher degree of protection from inflammation than the animals that were crossed onto the t l one a knockout background. And so these are are some of the preclinical data that get us excited about the the prospects of neutralizing d r three. The other data comes from translational data, and then what these authors were doing in this figure here was taking biopsies from either healthy volunteers or patients with Crohn's disease. And they were biopsying the GI tract either in parts of the bowel that were not actively inflamed, or they were taking biopsies a few centimeters down the bowel in in places that were actively inflamed.

And what you can see here is that in a in a normal non Crohn's disease patient, about three and a half percent of the cells in the GI tract will stain positive for t l one a, whereas about eight percent will stain positive for d r three. If you then look in the uninvolved part of the bowel, you'll see that there is no upregulation of t l one a whatsoever, and you only see upregulation of t l one a in the actively inflamed part of a Crohn's disease patient bowel. Whereas when you look at d r three, you see that d r three is both more abundant and evenly upregulated both in the inflamed and adjacent uninflamed parts of a Crohn's disease patient's GI tract. And so this could be an important difference in expression in terms of targeting one side of the axis versus the other to fully neutralize inflammation. And the data from that publication is one of several that showed the same thing at the protein level, but obviously there are a limited number of patients that are included in those manuscripts.

And so what we then did is we pulled data from the Mount Sinai Crohn's and Colitis registries, and we asked, do those data confirm now in a cohort of about twenty five hundred ulcerative colitis and Crohn's disease patients that d r three is indeed more abundant in the GI tract than t l one a. And what you can see in red is that those those data from a large cohort of patients do confirm that conclusion to t l one a is is much less abundant. And the reason for that is that t l one a is a tissue restricted ligand primarily induced in antigen presenting cells. And as I'll show you in another slide, it's expressed in a pulsatile manner. In contrast, d r three is a stably expressed target, and the cells that express d r three are primarily lymphocytes.

And that's the reason why if you look in the blood of those very same patients, you find lots of d r three present and really no t l one a being expressed. And so these this again, these are two figures from a series of older publications where these authors were asking, what is it that turns on t l one a and and how is it regulated? And NT in this figure stands for no treatment. And so what you can see is that the note the non treated groups of antigen presenting cells here do not express t l one a. When you stimulate those antigen presenting cells with a variety of different innate immune signals though, you see that transcription of t l one a gets turned on and then gets turned off fairly quickly.

This is a figure from a different publication that was looking at the same thing. Here in human antigen presenting cells, you can see that there is no expression of t l one a baseline. And when you expose those antigen presenting cells to bacterial cell wall components like lipopolysaccharide, which is probably a predominant driver of t l one a expression in patients with IBD when you have barrier disruption. You have rapid induction of t l one a expression it reaches a maximum in six six hours or so. But then importantly, you'll notice that there is no ongoing expression of t l one a twenty four hours later.

And so it's a moving target on a transcriptional level and there's a secondary means of regulating t l one a on the protein level because once t l one a goes to the cell membrane, there's a a membrane proximal protease cleavage site that cleaves the extracellular domain and that leads to shedding of t l one a from cells. That's the reason why you have soluble t l one a that you can detect in patients, and that's also the reason why humans evolved a decoy receptor to neutralize shed t l one a. And so these basic biological parameters of of d r three and t l one a expression and localization are what drove generation of of this figure here. And so in the actively inflamed parts of an IBD patient bowel, you have t l one a being expressed in red and you also have d r three, and d r three is more abundant than t l one a in the actively inflamed parts of the gut. But you then go to the adjacent not yet inflamed tissue, you still have lots of d r three present, but you don't yet have t l one a.

And what that means is that there is no means of retaining an anti t l one a antibody at that margin of inflammation. And the and the reason that's a problem is that as inflammation spreads in these patients, it will then become a race whether that newly expressed t l one a has the opportunity to interact first with locally abundant d r three, or whether that newly expressed t l one a is immediately neutralized by an anti t l one a antibody that is passively diffusing through that tissue site. And so this is the reason why we believe that targeting d r three may lead to higher rates of complete remission than what has already been seen with anti t l one a antibodies. And this this this sort of biology is not unique to the d r three t l one a axis. If you look at the differing expression patterns of p d one and p d l one, you walk away with the same conclusions where in that case p d l one is the tissue in restricted inducible ligand, p d one is constitutively expressed by circulating lymphocytes, and this is one reason why the efficacy of anti p d one antibodies may be superior to the efficacy of anti p d l one antibodies.

So turning now to our lead antibody program, s l three two five. This is a humanized monoclonal antibody that is going into phase one in just a few months. This we also have a similar antibody. It's based on the it has the same d r three binding regions, but where we have now added a series of half life extending mutations. That's s l four two five, and at the end, I'll show you what the interaction between s l three two five and four two five looks like, and I'll also touch on what we think some of the advantages of developing d r three bispecifics might be relative to t l one a bispecifics.

So three two five was designed with a few parameters in mind. First of all, we wanted a super high affinity antibody, and we found one that binds d r human d r three with a 1.3 picomolar binding affinity. We designed the antibody to spare the decoy receptor so that the natural degradation mechanism of t l one a would remain intact. And then we found an antibody that binds an epitope that both interferes with trimerization of d r three and also interferes with trimer to trimer binding between t l one a and d r three. And then finally, we found an antibody that does not trigger d r three internalization on cells that express it, and that that comes through clearly in the receptor occupancy data from our monkey studies that I'll show you in a minute.

So there's a lot more information available on our website that I can cover in a short presentation, but this is one example of the sorts of assays that we have run-in developing s l three two five. Here, what we're looking at is whether s l three two five can interfere with t l one a binding to d r three and how the potency of that inhibition compares to the potency of the Merck antibody or the Roche antibody and we've subsequently tested the Teva antibody. And in all cases, there's about a tenfold improvement in blocking t l one a binding to d r three relative to those leading antibodies. Ultimately, the gold standard functional assay for whether you have a good inhibitor of the t l one a d r three axis is taking lymphocytes from patients with either ulcerative colitis or Crohn's disease, stimulating them with an artificial t cell receptor agonist, in this case, c d three, c d 28 beads, and then titering in t l one a in the presence of your antibody and asking whether your antibody can fully neutralize the costimulatory effect of t l one a on these IBD patient lymphocytes.

And so, first of all, the orange here, you can see that we can add in our antibody and it in and of itself does not cause any induction of interferon gamma from these T cell receptor stimulated IBD patient lymphocytes. When you bring in t l one a, you can see a dramatic induction of cytokine production from t l one a. And then as you tighter in your antibody, you can fully neutralize that t l one a mediated co stimulatory effect in patient samples. And so we took our lead antibody into GLP toxicology studies in synovalgus macaques. This study was completed last year, and what we did is we gave the antibody at one ten or one hundred milligram per kilogram doses.

We gave three doses over a month long period separated by two weeks each, and then had a four week recovery period. And as is typical in GLP tox studies, we're first and foremost looking for signs of any safety events. And fortunately, there were no infusion related reactions observed in any animal at any point in time. There were no changes in clinical chemistry parameters, gross path, or histopath. And so the NOA L was defined as a hundred milligram per kilogram, the top dose that we administered to these monkeys.

One of the benefits of targeting a receptor like this is that because it is expressed by lymphocytes in the peripheral blood, you can draw blood samples from these animals and measure receptor occupancy on those lymphocytes. And this is a particularly important question for a first in class antibody like this because, as I showed you before, their their d r three is more abundant than t l one a. And so one question was, were we gonna have to go to a a fundamentally higher dose of antibody to fully block d r three than what has been seen so far with t l one a. And what the receptor occupancy data shows that even at the lowest dose of one milligram per kilogram, we achieved full receptor occupancy immediately following the first dose. We could then look at each dose whether the antibody remained bound to the receptors following the two week inter dose intervals or the four week inter dose interval in the recovery group, and what those data showed is that full occupancy was maintained through at least those intervals and probably longer.

And so this speaks to the fact that this antibody does not get internalized by cells that it binds. Now three two five is a humanized antibody and so you do expect to see some evidence of immunogenicity in non human primates. And we did. We saw just a couple animals that developed anti drug antibodies, and this actually became a very helpful data point for us because we also noticed that in those two animals, there was a drop in receptor occupancy when the animals became ADA positive. And also at that same time, the concentration of free drug in the blood fell below one microgram per mil.

And in all other animals who remained ADA negative, they retained full receptor occupancy and the concentration of free drug in the blood remained over one microgram per mil. And so these data now become extremely helpful in forecasting what trough concentrations might need to look like in a phase one trial, and we use that in our POP PK modeling that I'll show you in a few minutes. I I think, you know, a common question that we get is is why hasn't anybody else gone after d r three? Why is everybody focused on t l one a? And one reason for that is that, you know, Steph Targan and the group of Prometheus started with t l one a, And once something works, there's there tends to be a herd mentality to stick with what works.

As I've outlined, I I don't think there that there's a good biological reason to do that. Another reason folks probably preferred t l one a versus d r three is that when you're going into any given antibody generation campaign, your chances of success are higher if you wanna have a ligand blocker versus a receptor blocker. And the reason for that is that all the t l one a blocking antibodies really need to do is interfere with primer t l one a binding to d r three. When you're building a receptor blocking antibody, you also have to make make sure that there is no evidence of untoward receptor agonism because your antibody can always potentially bring together at least two subunits of d r three. And I think that's the bigger reason that has caused folks to shy away from this or or perhaps not be successful.

And I showed you some of the preclinical data that convinced us that we did not have any evidence of agonism, but ultimately the best test of that is looking in non human primates to see whether there's any evidence of lymphocyte proliferation, activation, or cytokine production a week after administering your antibody. And so we looked carefully for that in nonhuman primates. There was no evidence of of lymphocyte proliferation or activation of any kind, and so these data give us great confidence that this antibody is a pure play antagonist. So these figures here are looking at the preliminary POP PK models from the nonhuman primate data. We've highlighted in black the one microgram per mil trough concentration that we believe is necessary to maintain full receptor occupancy.

And then we've looked at what absolute doses would exceed that trough concentration either at a q four week or a q eight week maintenance dose. And what these data suggest is that at a q four week maintenance, we'll we will exceed that trough concentration at either one or three milligram per kilogram dosing. And if we wanna go to an eight q eight weekly maintenance regimen, we will likely need either a three or six milligram per kilogram maintenance regimen. Now a caveat to these models as they currently stand is that we do not yet have a complete assessment of how long the receptor occupancy may actually last in humans. If you look, for example, at patients that were treated with the anti p d one antibody pembrolizumab, which also does not get internalized, Folks remain functionally blocked for PD one six months after their last dose.

And if that ends up being the case here, then these POP PK models could underestimate what the true absolute dose is to maintain full RO. But we we don't we certainly don't wanna be wrong about that. And and so this is the reason why we're developing s l four two five in parallel. As I said, it's the exact same antibody as s l three two five, except that it contains some half life extending mutations. And so as the healthy volunteer study, phase one study initiates for three two five, we will also be initiating chronic toxicology studies for both three two five and four two five.

Chronic tox is necessary no matter what before initiating phase two trials in IBD patients for three two five. And what this will set us up to know is, you know, in around the second quarter of next year, look at the actual PK data from our single and multi ascending dose study in in human patients or human volunteers I should say, and then look at both the safety and the POP PK modeling data from the chronic tox study comparing three two five and four two five and ask ourselves, do we have evidence that three two five can move forward and ultimately be administered no more often than a q eight week regimen subcutaneously? Or are we better off bridging to s l four two five to achieve that maintenance dosing goal? And that's the reason for aligning these two programs so that four two five could bridge in to the phase two studies at at the necessary time if that's the profile that we need. So we're in a unique position in in our clinically validated access like this where we are the first to be developing an agent to the receptor side.

And hopefully, I've convinced you that there are very good reasons to go after the receptor side. In addition to the fundamental biological reasons to target d r three as opposed to t l one a, One of the things that we also now know is that all of the t l one a antibodies have fairly high rates of immunogenicity. And the reason for this is that the t l one a antibodies bind, stabilize, and slow the degradation of serum t l one a. So what what many companies who have shared data focus on is what happens to the concentration of free t l one a after administration of an antibody. And that qualifier free t l one a is likely used because something different is happening in the to the concentration of total t l one a.

And Pfizer actually published this with the antibody that Roche is now developing. And what they published is that the concentration of total t l one a goes up two logs after treatment with that anti t l one a antibody. And what you're actually measuring there are immune complexes between the anti t l one a antibody and serum t l one a, and that is a prominent source of immunogenicity. The secondary benefit of going after d r three from an immunogenicity perspective relates to the opportunities to develop bispecific antibodies. And Amgen was was the first to develop a t l one a directed bispecific.

They made a drug called AMG nine six six, which was a t l one a by TNF alpha bispecific. They brought it through a phase one trial and published a really nice paper in Frontiers in Immunology. If you search for AMG nine six six, you'll find it. And what they showed in that phase one study is that every single patient developed rapid high titer neutralizing ADA, and they defined the reason which was that in that case, you had an antibody that with one arm was binding and stabilizing t l one a, with the other arm was binding and stabilizing TNF alpha, slowing the degradation of both. That led to even larger immune complex formation, and thus every patient developed those rapid high titer neutralizing ADA.

And that's a cautionary tale for for the future development of t l one a directed bispecifics that you don't have to tangle with if you are instead going after a membrane restricted receptor like d r three. So we're excited about that opportunity, and and we'll have more to say about the bispecifics that we're developing soon. So here we are. We're we're we'll be in phase one in just a few months time. We expect to look at initial data from the single ascending dose cohorts by the end of the year.

We've completed the single and multi ascending dose study by around q two of next year and be in a position to start those phase two studies in IBD patients in the second half of next year. We currently have cash through our phase one study and into 2027, and so we're certainly looking forward to generating some of that phase one data in humans soon. That's all I wanted to go through for for today, and I I welcome any questions people have. Thanks for the chance to speak.

Ethan Markowski, Member of the biotech research team, Needham and Company: Yeah. Thanks for the presentation, Taylor. And as a reminder to any viewers who are watching, you can ask a question through our conference portal, ask a question feature. And while that list is compiling, maybe I can go ahead and and start us off. So I think from our research into IBD, administration convenience has definitely become a priority of late as in the the less frequent dosing you can achieve, the better.

You talked about how you have a half life extended version in the pipeline. But curious what dosing regimen do you think you need to create in order to be competitive? And then are you guys also considering subcutaneous dosing formulation?

Taylor Schreiber, Chief Executive Officer, ShadowCloud: Yeah. So few thoughts. Yes. We are developing a subcutaneous formulation, and that is the plan for phase three study, would be to move to sub q dosing minimally for the maintenance portion of the study. The approved you know, patients with IBD are used to getting treatments every four or eight weeks.

And so you don't wanna have a drug that you have to give any more frequent than that. And I think as time goes on, even the q four weekly will be less appealing than the q eight weekly. So those are the goals, and and those are the reasons why we're developing both three two five and four two five in parallel. And the programs, as hopefully I outlined, are are aligned in a manner so that if the data tell us that four two five is is the direction to go, we're not looking at a delay there. That being said, there are biological reasons in the t l one a d r three access why that that cause you to question whether blocking the axis permanently may not be a no brainer goal.

And it may be a no brainer goal in IBD, but in lots of the other indications where t l one a d r three biology is implicated, you have less control over when the offending antigen that's driving disease is present. And in diseases where the offending antigen is not ever present, you may not want to always block t l one a d r three signaling. And happy to follow-up with anybody who wants to learn more about that, but that could be the reason why the same Teva antibody that looks wonderful in IBD failed in asthma. And so I think folks need to be thoughtful about more than just what's convenient for patients when making these decisions.

Ethan Markowski, Member of the biotech research team, Needham and Company: That that's a good point. And, you know, when we do, I guess, look at the space, I think another thing that jumps out is there's typically a very high placebo response rate in clinical trials. And if you actually adjust clinical remission rates, you usually get about twenty to thirty percent is is the rule that you usually see. This is kind of more of a curiosity question, but is there anything that can be done to either reduce the placebo rate, or are you really just relying on boosting the efficacy to kinda counteract that effect?

Taylor Schreiber, Chief Executive Officer, ShadowCloud: If you look at so first of all, you're correct. There's a there's a huge range in placebo rates. Just if you look at the Teva and Prometheus study, it can vary by 20%. So, you know, one thing that you you should do is make sure that you make conservative estimates for what the placebo rate should be and power your studies accordingly. Elementiv had a really nice poster at ECHO this year where they did a retrospective analysis across multiple studies over time, and they zeroed in on about nine percent placebo complete remission rate in UC as, you know, the centering point.

So you can think about that as an anchoring place for power calculations, but you need to think about the upper and lower bound of that as well, and and we're working with our statisticians to do that. The other variable that has a large impact on where your placebo rates end up is looking at how the split of patients that are advanced therapy experienced versus advanced therapy naive lands for the folks you enroll in your study. And all of the studies that have been done have, I think, put in reasonable criteria to try to, you know, put guardrails around not having too many of those folks, not having too few of those folks, and and not having too many of those folks is what drives lots of enrollment outside of The US. But, you know, you still have to just go into these eyes wide open that that you could plan for nine percent and end up with eighteen. Yeah.

Ethan Markowski, Member of the biotech research team, Needham and Company: And then, obviously, one topic or, I guess, maybe two topics. We've been asking a lot of the companies this week, sort of broader macro. Obviously, there's a lot of uncertainty in the market right now, particularly around two two key topics, which are tariffs and recent changes at the FDA. I won't quiz you too hard on tariffs because I know that's evolving at by the minute, I believe. But, you know, just in general, what sort of impact, if any, do you expect from tariffs as well as recent recent leadership changes at the FDA?

Taylor Schreiber, Chief Executive Officer, ShadowCloud: Yeah. Well, all you have to do is open your eyes today to know that even companies that may not be directly impacted by tariffs like us are still impacted by tariffs. So, you know, and that can relate to various facets of your business, you know, in our case, raw materials that you're purchasing from different places, you know, wherever you're conducting your clinical trials, how the, you know, pharma wallet gets pushed one way or the other to adjust tariffs and how that affects the m and a appetite around the industry. So, you know, everybody's affected by tariffs. In terms of changes at the FDA, we have we have some recent data points, and given that we're in the middle of submitting our first IND, I can tell you that we've we've been in the pre IND interaction process for the last couple of months.

And, you know, I'm happy to report that we weren't expecting a response on our pre IND questions until later in the month in in this month, and we actually got them today. So that's great. You know, does that stay around forever? I hope so. But so far, so good.

Ethan Markowski, Member of the biotech research team, Needham and Company: Yeah. And I think, you know, having those data points is reassuring to some investors out there because it's really the best you could hope for at this point. It's just things continue as normal and the more recent interactions you have to justify that, the better. I am looking at the chat. I don't see any further questions at this time.

So I will give you the floor. I think you already kinda summarized, where the company stands and what you're looking for, but, any final thoughts here?

Taylor Schreiber, Chief Executive Officer, ShadowCloud: Yeah. I mean, look, we we are we are heads down. Glad to be close to the clinic. Excited to get those first data with a first in class d r three antibody and look forward to engaging with folks who are who are watching and our our investors moving forward. I think we've got something really special here and that's gonna unfold over the course of the year.

Ethan Markowski, Member of the biotech research team, Needham and Company: Great. Thanks, Taylor. Thanks for attending the conference. It's always it's always good to have the conversation.

Taylor Schreiber, Chief Executive Officer, ShadowCloud: Thanks, Ethan.

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