Good morning and welcome to the Forte Biosciences Investor Webcast. At this time, all attendees are in a listen only mode. A Q and A session will follow the formal presentations. As a reminder, this call is being recorded and a replay will be made available on the Forte Biosciences Biosciences website following the conclusion of the event. I'd now like to turn the call over to Doctor.
Paul Wagner, Chief Executive Officer of Forte Biosciences. Please go ahead, Paul.
Great. Thank you very much and welcome everybody to the FV102 celiac disease phase 1b results conference call. It's a very exciting day for us and and I think for patients as well. On the call with us here today also is professor Jason Taidin. Professor Taidin is the head of celiac research at the Walter and Eliza Hall Institute at the Royal Melbourne Hospital.
And in addition to being a key thought leader in celiac disease, professor Taitin was also a principal investigator principal investigator in the study. I think enrolled close to twenty percent of the subjects who has direct experience with the study as well. And so thank you again for joining us, professor Taitin. So this is just the forward looking statements. And and as a refresher into a level set for people that may not be as familiar with f p one zero two, F d one zero two is an antibody to c d one twenty two, which is a subunit of the intermediate affinity receptor for IL two and IL 15, and it's expressed on NK cells and, certain subsets of T cells.
The idea behind f v one zero two, and we'll talk more about the mechanism here in just a minute, is that we wanted to intermediate both the IL two and the IL 15 induced proliferation and activation of reactive NK cells and T cells, particularly autoreactive T cells and NK cells. The celiac disease phase one b trial is completed. We're gonna be talking about that today, and we've we're really pleased to announce that we demonstrated positive histological and symptom data in the treated subjects compared to placebo. We're moving ahead very aggressively given the positive results, the phase two disease study is initiating, and the data is expected in 2026. And we also have a vitiligo study ongoing right now, and the top line results there are going to come in the first half of twenty six.
But on to, f v one zero two, one of the things that we think is really exciting about this is the connection between the mechanism of f v one zero two and the biology of diseases with very high unmet need. And on this table, I've highlighted some of those. But there's maybe 10 or 15 different, diseases that have shown activity and indications that have shown activity by blockade of, c d one twenty two. And we went through and did a thorough analysis of the biology of those different diseases and compared that up with the mechanism, and these really came up towards the top, of course, celiac disease, vitiligo, alopecia, and type one diabetes. And while these all look to be very disparate diseases, the reality is they're closely connected, by the autoreactive T cells, which we believe that we're having a significant effect on the mechanism of f one zero two.
And to that point, I'll just talk to the cartoon that's over on the right. As I've indicated, f d one zero two blocks the interaction of the pro inflammatory, proliferation cytokines IL two and IL 15, and it blocks the interaction with the intermediate affinity receptor receptor, which as I mentioned before is expressed on NK cells and certain subsets of T cells. And by blocking that interaction, we're able to prevent the proliferation and activation of those potentially pathogenic autoreactive cells. But what we don't do or we're trying not to do is to inhibit the I l two binding to the high affinity receptor, which is in the upper right hand corner, which is expressed on Tregs. And so the idea here is that we're able to impact the proliferation and activation of these autoreactive t and NK cells while not having any significant in excuse me, impact on the regulatory t cells, are helping to modulate the immune system, particularly in autoimmune diseases.
And this is data that that that that we generated recently, which really highlights the activity of f one zero two. And in this experiment, what we've done is we put f v one zero two into the media together with c d four positive and c d eight positive t cells. And when that happens without f p one zero two, what you see here is a very significant activation of those T cells, whether it's the c d eight positive T cells or the c d four positive T cells. Activation, of course, meaning, these are the cytotoxic. They become cytotoxic and release pro inflammatory cytokines.
And so without f d one zero two, what we see here is a 60% with the c d eight positive T cells, a 60%, activation. And when we put f d one zero two into the mix, there's really completely halts the inhibition, inhibits the the T cell activation. You can see that because the cell only on the far right hand side, that's with no cytokine whatsoever. And what we did in this experiment is we put IL two into the mix for twenty four hours and then IL fifteen for three days and able to completely inhibit that T cell activation. In terms of, celiac disease, this is a very high unmet need here, and professor Tayden can elaborate on that as well.
The the the incident here is around, two point five million people, but probably underdiagnosed because there really is no treatment option for celiac disease. At this point, it really is just attempting to avoid gluten. And in terms of the the biology itself, when gluten is ingested, the first thing that happens is the antigen presenting cell breaks down that gluten to gliadin and it presents it to a c d four positive t cell that then releases the I l two, which is a signaling molecule that causes the, the proliferation and activation of T cells that's supported by IL 15. And so what we're able to do here is block both that IL two and that IL 15 signaling, and so really well suited for, for celiac disease. And a significant amount of activity going on here.
Again, professor Ty Dan has been involved with many of these studies, but, Takeda, Shugai, Teva, Sanofi, Amgen, and now, of course, Novartis with the acquisition of Calypso. So a lot of activity in pharma going on here, again, because of the significant unmet need in celiac disease. I'll turn it over now to professor Taiden to talk more about the morphology and histology measurements in celiac disease. Professor Taiden?
Thanks very much, Paul. So what we're seeing here is a villous structure. So when we measure, gut damage in celiac disease, which is really, the the primary kind of a readout that we want to assess, celiac disease with the immune response that develops to gluten causes damage to the small bowel, and it's really these villi that get inflamed. And you can see the arrows here at the tip of the villi pointing out these T cells called intraepithelial lymphocytes. So we shorten that to IELs.
So increased numbers of IELs and increased density represents inflammation of the small bowel. This is what we really want to reverse in celiac disease. So in active celiac disease we get a lot of these inflammatory cells in the lining of the gut and these release mediators that lead to changes in the lining so that you get flattening of the villi and so you get what we call villous atrophy. So these cells are expressed as a density, usually the number of IELs per 100 small intestinal lining cells called enterocytes. So next slide.
So what we can measure here is what we call the villus height to crypt depth ratio. And you can see here on the figure, a villus structure standing out to the right. So it's finger like projections that help absorb nutrients, from ingested into the small bowel. The longer line there represents the length of the villus, structure, and then the smaller green line represents the crypts. The crypts are what produce the cells that make the villi.
So what happens in celiac disease is the villi become shorter, and so the ratio between the villus height and the crypt depth starts to fall. So a normal ratio is around two point five to three, in celiac disease this falls down. Next slide. The best way we're learning to conceptualize, both the inflammation with the IELs and the damage, that results from these IELs is a metric called the VC IEL. And what this does is it combines both those things, the IEL count and the villous high crypt depth.
So it's considered a very useful marker because it is, encompassing both those two independent metrics of gut damage, and it has high statistical precision. And because of this high precision, it's probably better to detect changes that do exist, more sensitively. So this is, likely to be a scale that's going to be adopted for many clinical trials moving forward. Next slide. Okay.
So let's jump into the actual data from the phase 1b trial. I'll pass across to you, Paul.
Sure. And I'll start off with just the design, the baseline, and then I'll turn it back over to professor Taitin to talk about the data. So this is just a refresher on the design of the study. It was a 32 subject study we enrolled at nine sites in Australia and New Zealand. It was randomized three to one, FV 102 to placebo.
So 24 were on active FV one zero two and eight were on placebo. And the subjects received a total of four doses of FV one zero two weekly. After receiving three of those four doses, they started a sixteen day gluten challenge, and we uptitrated the gluten from two grams to four grams and then eight grams for fourteen days. So this is a total of a sixteen day gluten challenge. And in part, the reason we did that uptitration was based on feedback, in part from professor Tai Din suggesting that we don't wanna see a lot of dropouts in this proof of principle study.
So we we started at a lower dose of Luton at two grams and then uptrend traded it to four and then up to eight. But as we'll show you shortly, there actually were a significant number of symptoms, and we're able to see some differentiation there. Again, the end endoscopy biopsies were taken at baseline and at the end of the gluten challenge so we could look at the morphology and histology inflammation as professor Taitin was just outlining. And then we also had gluten challenge symptoms that were measured. This was was done through the collection of patient diaries and AE reporting, and all of these subjects completed the thirty day day 32 biopsy.
In terms of the baseline demographics, you know, quite well balanced here across all of these different parameters, including the the villasite to crypt depth ratio and the IEL counts. And with that, let me turn it back over to professor Tidend to talk through the the the efficacy readouts.
Thanks, Paul. So jumping straight into things, this is the marker of inflammation in the small bowel. So this is the intraepith oh, no. So sorry. We've got the the VCIAL.
So this is the composite score of the intraepithelial lymphocytes as well as the villus high crypt depth. And what you can see here is clear distinction between the placebo group that worsens small bowel histology as expected with a sixteen day gluten challenge patients get damage and inflammation and quite a striking difference in the treatment arm with FB-one hundred two there is none of that deterioration to mucosal health and that is statistically significant. Next slide. So when you break it down, this is the intraepithelial lymphocyte density now. So this is the marker of inflammation, the the inflammatory cells that come into the small bowel that lead to the damage.
And again, you can see an increase of around 13.3 of these IELs per 100 enterocytes in the placebo arm and a decrease in the active arm with FB 102 of 1.5. And again, this is statistically significant. So it tells us that FB 102 is able to prevent the gluten induced inflammatory damage. Next slide. Okay so with the villous height grip depth ratio you can see that again there is this trend for FB one zero two to have a reduction in the worsening of villous damage.
This time it is not statistically significant, but there is a considerable difference between the placebo arm and the FB102 arm, again supporting the notion that both the villus inflammation and the villus structure is improved by treatment. What's really striking is the symptom protection that's afforded by the treatment arm. So here on the graph, you can see the sixteen days of gluten challenge that participants undertook, And you can see here shown the cumulative symptoms that each particular individual experienced. And you can see over time, not surprisingly, as they went along with their sixteen day gluten challenge, the number of symptoms per subject started to increase, but there was about a forty two percent symptom benefit in the f b one zero two arm. In other words, it abrogated the gluten induced symptomatology, which is a very striking finding.
And and, really the symptoms captured here were the most important ones induced by gluten, such as nausea, diarrhea, vomiting, abdominal pain, and bloating. And these are the common and very often disabling symptoms. You know, certainly in our group of patients that we had through the trial, there were some people who would typically vomit with the exposure to gluten, and these people were absolutely comfortable sitting there eating their gluten, having no issues. So this was quite striking to us. It was immediately apparent, not necessarily clearly demonstrated in this slide, but this slide does demonstrate how g, how FB one zero two is, reducing gluten challenge induced symptoms.
Excellent. Thank you so much. And we'll touch on just the the safety profile as well, very consistent with what we saw in the healthy volunteer study. Again, only one grade three severe AE, and that was in the placebo group that was associated with the placebo excuse me, with the gluten challenge. That was a patient who had two events during the gluten challenge.
One was nausea and one was vomiting, both grade three. But, again, that was the only grade three event. Everything else was predominantly mild AEs. And, again, quite well balanced in terms of the organ class as well, in fact, at favoring f v one zero two across all of the different organ types, including infections and infestations, and across all of these different parameters. So with that, you know, we're we are moving aggressively ahead.
Very positive data, and thank you again, professor Taitin, for your leadership in the in the study. As I mentioned before, professor Taitin enrolled about twenty percent of the of the subjects in the study. And moving ahead now, we're gonna be initiating a phase two trial in celiac disease looking to enroll a 100 patients. They'll be enrolled two to two to one to three different arms. Two arms will be on FD one zero two.
There'll be an induction period where they will get, five doses of FD one zero two followed by a maintenance of every other week at either three milligrams per kilogram or five milligrams per kilogram. And in this study, they'll be getting more gluten as well, so there'll be an eight week gluten challenge. It'll start out at eight grams per day for two weeks, and then it'll move down to three grams, for the next per day for the next, for the next six weeks. We, we are initiating the study, imminently here in the, in the second quarter, and we do expect The US IND late in '25 or early twenty six. The top line data readout from this study, should happen in 2026.
Again, we need to see the enrollment rate, but, you know, assuming that the enrollment looks similar to the phase one b, we should have that readout in 2026. So in terms of the development timelines, just talked about celiac disease. I mentioned earlier we have a vitiligo study ongoing as well. The top line data readout there in the first half of twenty six and starting that phase two also in '26, likewise with alopecia and type one diabetes where we've got some really compelling, data there that we've generated in house and and it's part of our corporate tech now. We're evaluating the study design and and looking at, at at the potential for initiation there as well.
So, again, thank you everybody for joining, and I'd like to open the call up to, to questions.
Thank you, Paul. Now we will begin our q and a session. At this time, if everyone can please hold for a moment while we poll for questions. Okay, our first question comes from Yaron at Cowen.
Hey, Yaron.
Hey. Good morning. Congrats on the data. Really great to see, and thanks for for taking a few questions. Maybe just the first one, can you put a little bit in context so that the baseline I IEL data looks really compelling.
I mean, you're starting on both of them at around $25.06 and $23.05. What what's considered clinically meaningful and maybe give us a sense. That's, like, obviously, showing a nice differentiation and separation early. But what what level do you wanna see, and how does that translate into clinical benefit? And then on the baseline villus, he'd decrypt that you're starting at 2.8.
So maybe do do you think that data gets better with time? Maybe put put put in context with how meaningful this data is. Thank you.
Professor Jaiden, did you wanna comment on that? And then maybe I can add a few a few comments as well.
Yes. Of course. Yes. So, Yaron, that that's some great questions there. So, typically, we'd consider a change of around 30% in IEL count to be, significant.
And really what the way we conceptualize things biologically is that the IELs are the key inflammatory cells that ultimately drive the the villous damage. So, we know from many studies, decades ago that this is a stepwise process. Early disease is often just the inflammation, and then with time, you get the villus atrophy developing. So with a two week gluten challenge, you probably saw that the villus change, the, the error bar was fairly wide there, which highlights that there is heterogeneity. Some patients got quite a lot of villus damage, some patients less so.
And I think over time with longer gluten challenges, you get much more consistency in the villous damage. So I'd be, very confident that given the compelling, reduction in inflammation that we've seen with f b one zero two, that would translate into much more statistically significant protection against villus damage with time. And I think this is really the rationale for the phase two to go longer with gluten to really get that consistency in causing the damage in the placebo arm and then showing greater differentiation in terms of the villus the villas structures. So, I hope that answers your question.
Great. So maybe on on the phase two, is it gonna be powered? It it be and what would be the primary endpoint? Is the primary endpoint gonna be still IEL, or is it gonna be azurelcyte to cryptep, and is it powered for that?
Excellent question. And, Yaron, this is Paul. So in the phase two study, yes, we're we're that that is powered to look at. And and not only are we looking at the histological and morphological parameters that we've demonstrated here, we'll have you know, there'll be a composite analysis. We're looking, of course, at the IELs, which, you know, are are critically important, the VHCD.
But also, we'll have using a a validated scoring tool for the symptoms as well. And given that in this study, in the phase two study, we don't have that dose escalation of the gluten, that two grams to four grams to eight grams as we did in the phase one b to try to mitigate symptoms to keep patients in so that we really could see histological effects. Here in the phase two, we're gonna start off directly with that eight grams per day for the first two weeks. And there, think we're gonna see some significant further differentiation on the symptoms as professor Taiden was just alluding to earlier.
Okay. And and maybe just a a final question for me, I'll jump back in the queue. The on the GI disorders side, the this there seems to be a little bit more it's well, it's both of them are sort of eighty eight percent. You have actually less nervous system disorders. Can you just put that in context?
Less than active than than placebo. Just put that in context. What are you seeing there? Thank you.
Yeah. It's those are just individual patient numbers. The actual event rates, as you saw in that symptom slide, is significantly less for for f d one zero two, and that that really is the important part. I mean, if we go back and we look into the symptoms specifically, I think about thirty percent of the patients on FD one hundred two had no symptoms whatsoever to the gluten challenge, that compared to only about ten or twelve percent of the patients on placebo. So again, a significant differentiation there.
It really has to do with, you know, number of events in terms of those symptoms relative to, you know, a patient maybe having recorded one. And also, think it's important to point out that the there was only one individual that had that severe grade three AE, and that was associated with the gluten challenge. That was actually that one patient, as I mentioned before, had two grade three AEs. One was nausea, one was vomiting. So, you know, a significant differentiation, not only in the number of events in those patients that had that had no symptoms on the gluten exposure, but also a difference in terms of the severity of the of the symptoms.
Okay. Thank you for the questions, Yaron. The next question comes from Daniel Gajalin at Chardan.
Hi, Daniel.
Yeah. Hey, guys. Thanks thanks for taking the question. Quick one. Just to kinda understand the thinking that went into your phase two design.
So so may maybe can you talk about key learnings from phase one b that informed the design of the phase two b study and what went into the decision of going with the single or high high the dose that you selected and high within challenge right away?
Yeah. Absolutely. Thank you very much. In terms of that dosing, you know, we have the induction and the maintenance. And one thing that's still being explored is the possibility that there is an immunomodulation that's happening so that it's not just a PK.
You know, we're still trying to understand this point, but the possibility exists. And it's been, I think, a view that's shared by others, you know, other researchers and other in the industry about the possibility that you're able to affect the population of these antigen specific tissue resident memory T cells. And if that's the case, then upfront we want to have this induction so that we can deplete those cells and have a longer durability of effect. We're going to be investigating that in the phase two, but that's the idea behind having that induction. Again, that ten mg per kg dose has shown very good safety and tolerability to date, now from the healthy volunteer study all the way through this celiac study.
And so we're gonna be continuing that, providing the good protection upfront, and then starting that eight gram gluten challenge with for two weeks without doing that dose escalation so that we can see even further differentiation on the symptoms. And as professor Taiden was saying, the IELs really are what are driving the damage to the villi, and and, frankly, causing the the symptom effects as well. And so the fact that we've seen such great control in the phase one b leads us to believe that, you know, in that longer gluten challenge, we're gonna see even further differentiation and even more positive data than the data we've generated here. So that really was the thinking behind it.
Yeah. Got it. Thank you. And and a quick follow-up, for the endpoints for two b. How critical, would it be to show, stat sig, improvement in, VHCD ratio?
Well, I'll turn it over to professor Zaiden to to provide his comments. As, you know, as we've talked about, IELs are are really the the mediators of the damage, not only in celiac disease, but also in these other disease indications that we're pursuing. And to see that level of control that we have here in this study, I think, is really, really encouraging, you know, leading to the symptom benefit, leading to, you know, what we saw with the VH the VHCD. And these composite endpoints, particularly the VCIEL developed by professor Murray at at Mayo, really is able to more holistically look at the damage to the gut. But, professor Tayden, what what what are your thoughts?
Yeah. Look. I agree. I mean, I think that the FDA guidance for industry is fairly slim on what the right histologic endpoints are. They talk about co primary endpoints of symptoms and histologic protection.
We've looked at as gastroenterologists for for decades, we've looked at both the villus high crypt depth and the intraepithelial lymphocyte count. And the sort of scoring systems we've used like Marsh in the past and nowadays with VCIL tend to sort of look at a a composite of both the villus damage and IELs. I think it would be nice to see both IEL protection and villus damage protection. I I'm actually pretty confident with what the phase one b data is telling us that this is likely to be the case as long as we drive enough damage into, the placebo arm. So eight grams a day, which is about it's almost about three slices of bread's worth of gluten.
So this is a decent amount of gluten that participants will be consuming. And we would imagine that after, the the seven or eight week period of the challenge, there will be much more substantial, damage both with the IELs and the villas high crypt depth. So I think it would be very, nice to see both, and I think this is what will happen. And I think that if you can combine that with the symptom and symptom readout, then you're essentially meeting that composite, co primary endpoints.
Got it. Thank you very much for, for for taking my questions. Congrats on the data.
Thanks.
Thank you
for the questions. The next question comes from Elmer Pirros at Lucid.
Are you on mute?
Good morning. Sorry. I was on mute. What I'd like to ask from doctor Taibin is if he could, put this dataset, which is obviously from a small trial, to perspectives of other, agents that have been examined in celiac disease and particularly when comparing it to other I o fifteen inhibitors. And if there is a thought process here that the combination of I o fifteen and I o two modulation may be more important than just focusing on a single pathway?
Thank you, Adam. I think that's an excellent question. To start with your latter query, absolutely agree. I think that the honestly, the IL fifteen data alone has shown, protection against gluten induced damage, but I haven't been completely, blown away by, that data in isolation when it's just IL fifteen blockade. And, certainly, I've not seen any data showing that this blockade can protect against gluten induced symptoms.
It may seem to abrogate some gluten induced gut damage. What I think is really the strength here, and and my background in celiac research has been very strongly focused on, interleukin two as a key role in, expanding the gluten specific T cells that cause celiac disease, is is the the blockade of interleukin two is, I think, a major, benefit of f b one zero two. And I think that's probably what is really, contributing to the substantial beneficial effect on blocking gluten induced symptomatology. So I agree. I think it's the combination of potent IL fifteen blockade as well as IL two blockade that's contributing to, the the therapeutic effects.
Now I've forgotten what your first question was. Sorry. Oh, yes. That's right. So it was just comparison to other other sort of, agents currently under development.
You know, I've been impressed by this data in all honesty and also, being involved in the clinical trial, with my nurses, and we've done seven other celiac disease sponsored trials in other agents. This has been by far the the the the most, the trial that they've enjoyed the most because participants were very tolerant of the agent. Many who were expecting to vomit with the gluten challenge did not, so they were able to push through. And I think that, you know, our experience and sort of insights into the other therapeutic compounds, you you know that there are tolerogenic approaches. There's a number of groups now looking at ways to try to induce gluten tolerance.
I think that's a very high bar. I was involved in the very first gluten tolerogenic study of NEXFAX two. That was a US and Australian, New Zealand, phase two trial that unfortunately failed. But then there's, you know, as you may be aware, there's other groups now developing tolerogenic therapies. I think biologically, that's a very high bar to to cross over to induce tolerance, against, gluten, which is very well strongly established.
And you have these tissue resident memory specific gluten T cells that are very hard population to get rid of. You have glutinases, which are gluten degrading enzymes, but these are really needed to be taken on demand really or regularly because while whenever there's gluten, you need to have this agent around. So this is not something that will hang around in the system. You'll need to take it every time you have a meal. So I think that's a niche need.
I think that might be useful for people traveling, but it's certainly different, effects than, an immune based approach. And there are other other groups developing other immune approaches such as bispecific antibodies that block the T cell response to gluten. And I I look. I think that it's still fairly early days with with that approach as well. So, on the whole, I think that if you can demonstrate I think the key is to demonstrate protection from gluten induced gut damage and symptomatology, and that'll really set you up for, futures trials and and demonstration of protection in both treated disease, but also an active disease.
Thank you very much for your perspective, doctor Diben. Congratulations, Paul.
Thank you very much.
Thank you for the questions. The next question comes from Kumar Raja at Brookline.
Good morning. Thanks for taking my questions and congratulations on the data. With regard to the density of the CD three positive cells, what are your expectations with the longer duration of treatment? Do you think there will be ability to further reduce it? And with regard to the starting the trials in The US, can you please share what are the next steps there?
Thank you.
Sure. I I I can provide some perspective on that, and then I'd be interested in hearing professor Taiden's perspective. You know, above 25 is considered, you know, of the IELs is considered, you know, celiac disease subject or patient. You know, healthy individuals, to my understanding, have IEL densities that are maybe closer to ten, ten, or 15. So, certainly, even even in the treated celiac patient population, to my understanding, and as evidenced here with the baseline characteristics of these treated celiac patients, we did have a baseline up around twenty five.
And so I think there is room to to continue to move that down towards normalization of the IELs in the villi, and we did see that. We did see that, you know, over this relatively short study, we're already seeing a decline in the IELs. You know, we'll have, you know, additional data on the TCR gamma deltas and the subsets of the k I 60 sevens that I'm very optimistic about, let's just say. But, you know, those subsets are also responsible for some of the cytokine release as well as the inflammation. And I think in totality, the dataset was really encouraging in terms of the, control and and further normalization of the inflammatory component of the disease.
Professor Taitin, did you have, any perspective on that?
Oh, I I guess I'd just add that, even though we're targeting treated celiac disease, what we know from other studies is there's no such thing as perfectly treated celiac disease. And I think this really underscores the fact that, a lifelong strict absolute, zero gluten, gluten free diet is is aspirational but rarely attainable. And so, you often find quite a high proportion of patients entering these trials with, you know, so called strict adherence to their gluten free diet who have evidence of some degree of inflammatory activity, both with raised IELs over 25 and also villous high grip depth ratios less than 2.5. And in some studies I've been involved in, sixty percent of patients with treated disease had VHCDs less than two point zero. So I think this underscores the importance of targeting the treated group who still have evidence of disease activity.
And, I think that, again, demonstrating that protection from gluten induced inflammation is the key.
Okay. Thank you for the questions, Kumar. I'll now hand the call back to Paul for concluding remarks.
Fantastic. Thank you so much. I really appreciate everyone joining this call and and for your support. I I also want to, to to thank I know there's gonna be they're they're gonna be listening in on this call. The, the investigators in this study, the colleagues of professor Taiden who who really did a phenomenal job, on this study, and also the Forte team.
Just incredible, incredible hard work to get to these results. And so thank you to the team, and look forward to following up with you all, throughout today and and tomorrow, and, look forward to continuing to have your support. So thank you again.