Seaport Therapeutics, Inc. (SPTX) September 9, 2026 Conference Transcript

The post-keynote session, the first one of the afternoon, day one of Citi's biotech back-to-school summit, I'm Miguel Nachamavitz, cover the next company we're going to speak with, Seaport Therapeutics. We have with us Lauren White, who's the CFO, and Michael Chen, the CSO of the company. So welcome, both of you. Great to be covering you since the IPO earlier this year. So I guess it's a new company, newly public company in neuroscience, obviously. But it would be great if Michael maybe just introduced the sort of premise of the company in terms of what the core technology is, why it's different. you know, where it came from. And then we'll talk about all of the various ways you're flexing it to do different things in neuroscience. Sure. Thanks.

Yeah, maybe I'll kick us off. Thanks so much for having us and a warm welcome to those in the room.

And I just also mentioned my colleague, Jeff Meacham is here as well. He co-covers the seaport with me.

Great. So again, warm welcome to everybody in the room. And thanks again for having us at the conference. We are going to be making some forward-looking statements based on our expectations and would encourage if anyone has questions can follow up with our sec filings so seaport is a neuropsych company we've got a clinically validated platform and a robust pipeline of three programs our lead program glyph allo is currently in phase 2b with the potential to be registration enabling and this morning we actually shared some interesting driving study data that michael will touch on in a few minutes our second program glyph ego is we currently we recently shared key phase one proof of concept data. And our third program is in preclinical development. All of our programs are based off of clinically validated mechanisms that were held back by some sort of an issue that we're able to address with our Glyph platform. Glyph is a lymphatic targeting pro-drug platform that's able to overcome limitations such as poor oral bioavailability, liver-related AEs, and other side effects. And the great thing is, is every time we Glyph a molecule, we create new IP. We've got a seasoned leadership team with a track record of success, both in delivering new medicines to patients and in delivering successful business outcomes. And as Yigal mentioned, we recently completed our IPO. So we brought in ample capital to help us deliver on our key upcoming clinical milestones. If we just take a step back and we look at the overall landscape, there's over 1 billion people living with mental illness. We at Seaport are focused on those struggling with depression and anxiety. Each of those impact over 300 million people. It can be very disabling. They're comorbid at times. And so it's clear that we definitely need better medicines in this space. And when you look at the landscape of existing medicines out there, you know, they're deemed commercial successes, billions of dollars of peak sales, millions of people helped by them, but they all have some similar limitations. They have modest efficacy. They don't work for one out of three patients. They can take weeks to stop working. And they have side effects that are unfavorable, such as sexual dysfunction, weight gain, and other items like that. And so we believe we're uniquely positioned across those parameters with the programs that we're bringing forward. You're probably aware that our CEO, Daphne Zohar, and our board chair, Steve Paul, founded and led Karuna. And we're taking a similar approach at Seaport as was taken at Karuna. So at Karuna, they knew that anomaline worked, but it was sitting on a shelf due to GI tolerability issues. And so the team was able to overcome them and create CAR-XT, now called Cobemphi. And so as mentioned, we're taking a similar approach to that in that we're targeting drugs that have clinical efficacy, but we're held back by some sort of an issue that we're able to address with our Glyph platform, and then we're also really focused on executing trials with a seasoned leadership team. So looking ahead, I know you all asked about kind of the next 12 to 18 months. We've got a really exciting horizon in front of us. We'll be sharing top-line data of our Bowie 1 trial and Glyph Allo in the first half of 27, and then looking ahead to our second program, Glyph Ago, we've got our Phase 2a data that will read out in early 28 and our phase 2b data that would read out in the end of 28. So a really exciting path ahead.

Okay, very, very comprehensive overview. Maybe we could just spend a few minutes just in a little bit of detail on exactly what Glyph does, because you're leveraging a novel pathway that really hasn't been leveraged before in the pharmaceutical space, as far as I know.

That's right, Yigal. So everything Seaport is doing is based on the Glyph technology, the glyph platform, which is really based on how the body absorbs dietary fat. So I know you all came from lunch, maybe had some fat during lunch. That is actually absorbed differently than many small molecules are absorbed. Typically, small molecules will transit through the portal vein into the liver, and the liver can exert what's called first-pass metabolism. And that can mean that the amount of drug actually circulating into the body or the brain can be extremely diminished relative to what was actually taken as a dose. So things like low oral bioavailability or even variable pharmacokinetics can result from that first pass metabolism, and that can limit drugs, including otherwise potent CNS drugs. Now, it can also stress out the liver to the extent that you can see liver enzyme elevations or hepatotoxicity. In contrast, dietary fats are absorbed through the lymphatic system of the gut. And what's important about that is it doesn't see the liver on its way into circulation. And so when we glyph a molecule, we cloak it so that it looks to the body like a dietary fat and then is absorbed like a dietary fat in that it doesn't see the liver on its way into circulation. But then what we release at the end of the day is a moiety, an API that is based on clinical validation, but we've been able to overcome limitations like low oral bioavailability and variable PK. We're able to address issues with safety and tolerability, including liver-related issues. And we create a new molecule with new composition of matter IP.

Okay. So that brings us to glyph aloe. You mentioned some of the data. We'll get into that in a second, the driving data. But before we get to that, just sort of explain. So allopregnanolone, it's, as you pointed out, a validated molecule. But just remind us, it's got some liabilities. The glyphing erases those, essentially. So talk to us about that. And then, you know, you're starting with MDD. So kind of go through the rationale of why glyph-allo for MDD is the right, you know, pairing.

Yeah, absolutely. So with glyph aloe, we're taking a mechanism, allopregnanolone, that, as you mentioned, has been validated. In fact, allopregnanolone, although it's a neurosteroid that we make in our brain, is also the basis of an approved drug. Now, that was a 60-hour intravenous infusion of allopregnanolone, but it worked. It worked in a form of depression called postpartum depression. It was rapidly acting as an antidepressant and also had anxiolytic and sleep-promoting activity. So all signs that this mechanism, allopregnanolone, which has a GABA positive allosteric modulation mechanism, is efficacious in depression. Now, the limitation, of course, is that it was a 60-hour intravenous infusion. And that was driven by the fact that allopregnanolone has high first-pass metabolism, low oral bioavailability, and just could not be taken as an oral therapy. Now, with glyph aloe, we apply the glyph technology, and we've shown in phase one studies that we're able to reach clinically relevant exposures, but now with once daily oral dosing, which really enables to take something that was, again, only an IV infusion and get it out of the clinic into outpatient therapy. We also showed in phase one that we not only had drugs circulating in the body, but actually pharmacodynamic activity, that is allopregnanolone that results in brain activity changes. And in a phase 2a study, we showed in a clinically validated model of anxiety that glyph aloe was able to blunt the salivary cortisol stress response in healthy volunteers, something that the only other neuropsych drug that's done that is alprazolam or Xanax. So on the basis of all that data, the PK, the pharmacodynamics, the safety profile, we took glyph aloe into a phase 2b study that is ongoing called buoy one in depression. And we started with depression really because of the weight of clinical evidence of allopregnanolone in depression, suggesting that it has activity in depression. And so now the question is with outpatient dosing of glyph aloe, can we see that activity?

Okay. So then the data this morning, let's get to that. It was important data, and I'll be in healthy volunteers, but it was still important data. So what were the key takeaways there? It's a driving study, which you don't typically see in biotech too often, but in this case, it was important to frame the risk relative to some precedents.

Yeah, absolutely. And some of the precedents in this space are oral synthetic analogs of allopregnanolone. One comes to mind, xoranolone. And xoranolone, which is approved in postpartum depression and has been shown to be efficacious in trials of depression, actually approved outside of the U.S. in depression. Xoranolone works, but has a black box warning for driving impairment and a 12-hour driving restriction, so 12 hours post-dose. and like allopregnial and seranolone is a GABA positive allosteric modulator now what we did was run a phase one driving impairment study using driving simulators and this is a validated method using validated study design in which you can detect next day driving impairment and the goal was to earlier than one would anticipate given the where we are in development, start to understand the potential differentiation of glyph aloe when it comes precisely to this driving impairment issue. So what we did was we ran a study in Healthy Volunteers that was a three-way crossover, which is very typical of the design. So essentially, this is a design where you have active drug glyph aloe at the doses that we're using in our phase positive control called zopoclone. And the primary endpoint, SDLP, really is a measure of lane swerving. So you don't want to separate from placebo in this study. You want to look like placebo when it comes to next day driving simulated lane swerving. And that's exactly what we found. So for our primary endpoint, on day five, after repeat dosing of glyph aloe, up to the doses 375 milligrams that we are using in Bowie 1, or our phase 2b study in MDD, we saw no statistically significant difference from placebo. That is, no driving impairment next day. Similarly, in our key secondary endpoint, after a single 250 milligram dose of glyph aloe, we did not observe any next day driving impairment. However, Zopaclone, the positive control, did statistically separate from placebo, showing that it's working as intended as a positive control. The overall experiment has assay sensitivity. And interestingly, zopiclone also statistically significantly separates from glyph aloe. So overall, our conclusions is that based on the study as designed, glyph aloe doesn't have any next day driving impairment in terms of that morning impairment. And when you compare it to the profile of something like xeranolum, we feel that these data, along with our Phase I data and our Phase IIa data with Glyph Allop, really add to the overall profile that's starting to build around Glyph Allop.

Michael, just maybe a broader question on the Glyph platform. I know as you go from Phase I, II to pivotal studies, your exposure is going to, you know, is going to increase dramatically the number of investments and number of patients. Talk about the regulatory kind of buy-in. Is there any extra hurdle that you have to do? Is there any body of work that you have to sort of finish before you, as you move to more pivotal studies?

And so what we've guided on is that the current study in MDD with glyph aloe, buoy one, is a potential registration enabling study. And we feel it's that way because of the size of the study, the adequate and well-controlled nature of the study. So it's a randomized, double-blind, placebo-controlled study in patients with MDD using glyph-allum. So it really looks like a pivotal style study. Now, there's always the open question of how many pivotal studies do you need given the regulatory statements that have been made from FDA around the interest in expediting single trial types of approvals. However, traditionally in neuropsych, you need two studies, two positive studies. So we're not necessarily banking that Bowie 1 is going to be the only study in MDD for glyph aloe. And we're anticipating that we may need additional studies to fill out the rest of that registrational package. But we do feel that Bowie 1 will be an important part of the registrational package.

Okay. And you mentioned the salivary cortisol related to the anxious distress component of MDD.

So maybe talk a bit about, you know uh sort of jeff's question in terms of looking to the future in the commercial setting mdd anxious distress the overlap there how are you going to position this molecule commercially assuming you can get efficacy in those groups yeah so as lauren highlighted mdd generalized anxiety disorder depression anxiety highly comorbid and in fact if you look at major depression, there's a major specifier in major depression called anxious distress that is present in more than half of patients with depression. You're talking 60% plus of patients who have anxious distress. Now, this is actually in the diagnostic workup for depression. It's in the DSM-5 as a major specifier, just like postpartum depression is a specifier of depression. And when you think about patients with anxious distress, these patients will often have elevated levels of anxiety, stress, and other symptoms. So allopregnanolone, as an IV infusion, had shown not only the antidepressant activity, but also anxiolytic activity, sleep-promoting activity. So our hypothesis is that with glyph aloe, given that we retain the pharmacology of allopregnanolone, that we can see a benefit in all comers major depression, but we may see even more benefit in the subgroup with anxious distress. And again, this is not based on a cutoff on a scale. This is based on simply how we diagnose depression in the first case. So really that provides a couple options in development. So we could see efficacy in all comers NDD, and I think that'd be terrific, and that would give us a really broad development path. We could also see extremely good efficacy see above and beyond with those patients with anxious distress. And again, major subset of depression, patients that don't respond well to SSRIs. And frankly, there are no drugs that are specifically targeted or labeled toward that anxious distress subgroup. So it provides a lot of flexibility as we think about next steps for development.

What kind of effect size or what kind of boost and effect size would you want to see in the anxious distress over the overall MDD to sort to claim meaningful differentiation there?

Yeah, I think it's a wonderful point because we have to emphasize that the overall study is really powered to observe differences between drug and placebo in all comers MDD. So we didn't necessarily power it to find a statistically significant difference between the subgroups. And what increasingly companies are doing is looking first at the all comers population and then doing a pre-specified but qualitative analysis to really look at the differential in effect if there is one. I'll also mention that beyond the pure effect size, we'll also be looking at the other potential benefits of glyph aloe. I mentioned that allopregnanolone as an IV infusion was rapidly acting. And so there are very few antidepressants that act quickly, SSRIs take weeks to start working. So glyph aloe beyond the overall effect on depression could also have rapidly acting activity. We'll also be looking at its potential anxiolytic effect, its sleep promoting effect. So really the totality of data and the totality of potential clinical benefit.

Okay. Before we move to Glyph Ego, I wanted to get your thoughts on some of the competitive data in the space, the Phenium's phase three data. How do you think about that in terms of resetting or changing the efficacy benchmarks to get your input there?

I think in general, what you've seen from that class, the overall space, is a real difference between things that have potential for unblinding, functional unblinding, for things that have intensive patient intervention. And at the end of the day, whether the effect size reflects the unblinding, the TRIP, something else, I think that what regulators are going to focus on is demonstrating in a robust study, statistical separation between drug and placebo. And so when looking at a treatment that has to be administered, you know, eight hours with supervision, et cetera, there's always going to be a different way of looking at that data compared to something that's a more conventional outpatient therapy. So I don't think it necessarily resets a bar in the space, but it provides additional options for patients, which given the unmet need and the scale of the diseases that we're talking about, I think more options are great.

Okay, that all makes sense. All right. So let's shift over to Glyph Ego. So tell us, this one, you're focused on GAD or generalized anxiety disorder. So we'd love to understand, you know, the drivers for this program being focused on GAD and also aglomelotin. Again, it's, you know, it is approved. I don't believe it's approved here, but it's approved in certain other territories. And so you're leveraging a known molecule, but it has some drawbacks. And you mentioned at a high level what those are, but we can drill down now and talk about that.

So agomelatine absolutely is validated. It is approved for not only major depression, but also generalized anxiety disorder. You asked sort of starting with GAD, and part of that is going back to our strategy on really starting where there's clinical evidence. And the clinical evidence for agomelatine in generalizing anxiety disorder, is quite robust. So there have been four placebo-controlled studies of agomelatin. And in all four studies, agomelatin statistically significantly separates from placebo. Pretty good battering average. So it's approved for GAD. From a childability perspective, the mechanism of action as a melatonin agonist and serotonin 2C antagonist means you don't have the SSRI baggage. So you don't have weight gain, sexual dysfunction, sleep difficulty. In fact, Agamalitine helps patients sleep. But that drawback that you're referring to is that it's a little bit rough on the liver. So due to its high first pass metabolism, some small proportion of patients can have elevations in liver enzymes. And what this does is necessitate liver function testing, blood tests. So for example, in the label in Europe, blood tests at baseline, three weeks, six weeks, 12 weeks, every time you increase a dose, it's a lot of tests and has really held back agomelotene. And frankly, it's also been held back by the lack of composition of matter IP. Now, what does Glyph do? As we review, Glyph allows us to bypass the liver, bypass that first pass effect. And so in some ways, it's almost like a perfect application of Glyph agomelotene. And so we created Glyph-Ago to address these shortcomings, to reach the same exposures that we know work in GAD, but reduce the amount of drug the liver sees. And in order to do that, we need to increase the bioavailability of Glyph-Ago compared to Agomelatine. And we had a bar going into initial clinical studies where we wanted to see about a two-fold increase in bioavailability, which we projected would reduce or eliminate that risk of liver enzyme elevations, which has held back aglomelatin. And we announced earlier this year data from our phase one study where we saw a nearly seven-fold increase in bioavailability, about 6.8-fold. But perhaps even more striking was a tenfold reduction in PK variability. So aglomelatin, due to that first pass, has highly variable PK. From patient to patient, you might get different exposures. But we saw a tenfold reduction in that variability with glyph-ago, again, due to that bypass of the first pass effect. We also start skirting the impact of drug-drug interactions on PK. So really a lot of positive benefits to glyph-ing agomelatin. And so those phase one data confirmed not only the PK profile that we were looking for, but a great safety profile. That is, Glyph-Ago was generally well-tolerated, no serious or severe AEs, no liver AEs. So from there, we're launching two phase two studies with Glyph-Ago. The first is a phase two-way proof of pharmacology study that will be really focused on sleep. I mentioned agomelatine has this sleep benefit. Glyph-Ago, we believe, will retain the pharmacology, will have that same sleep benefit, and sleep is a really core symptom for GAD and beyond for MDD, et cetera. And so we're going to be testing that explicitly in this study, where we're going to be looking at patients with GAD who will have sleep dysfunction, think insomnia, things like that. In parallel, we'll be spinning up a phase 2b, potentially registration-enabling study, of glyph-ago in patients with GAD. And the idea there is we know agomelty works, it's approved for GAD. We have GlyphAgo, which has an improved PK profile, and we're going to be launching a potential registration enabling study for GAD as a first indication.

And so the reason it was never approved in the United States is you mentioned the lack of IP, you mentioned the intensive liver monitoring. It just wasn't a commercially interesting thing to do in the United States, I gather. But of course, with glyphing, you get around a lot of that.

And there was development done with agomalatine, both in Europe, Australia, and also the United States. Some of that focused on depression. And you can see from that development history also things like trying to develop a buccal formulation to, again, fix the PK problem. It's a difficult problem to solve, really, because you don't want to put in more drug because then the liver is seeing more drug. So with glyphing and this bioavailability increase that we saw, we think that we've sort of cracked the nut on reaching this compromise of getting good exposures, but reducing the amount of drug the liver sees.

And I think another really important point that sort of come up in my conversations, you know, with clients is, yes, eventually the agamelitine, once it's, you know, de-lift, if that's the right phrase, and cleaved, you know, eventually it will obviously go through the liver at the end of the day.

But the point is, is that the concentrations are orders of magnitude lower because you've shunted it through the lymphatic system first that's right you're not losing 90 plus of the drug to the liver in the first place before it can even get to the brain yeah and that's a really important point because we have something like over four million patient years of history with agomelitine which teaches us that the liver enzyme elevations are linked to the amount of drug that the liver sees. It's dose-dependent, essentially. So to change that equation, we can essentially lower the amount of agamalitine that the liver sees overall, first pass, second pass, whatever, but still keep sufficient exposures that you see that clear efficacy signal that you saw in GAD.

Now, at various points along the IPO process and post-IPO, you'd mentioned potentially actually doing glyph aloe, doing the reverse, right? Doing glyph aloe in GAD and potentially doing with EGO in MDD, there's obviously a lot of overlapping symptomology there. So, but you decided to go the way we talked about a moment ago, but what would be the rationale to do this, the opposite approach eventually?

Well, I think the overlap is an amazing starting point, right? You know that patients with MDD will often report anxiety. That's why we have anxious distress. And with egomelatin, you also know that it's an effective antidepressant. So it's approved for depression, for the treatment of depression. It has a sleep benefit in depression, whereas SSRIs make sleep worse. So we think of MDD for glyphalo as a starting point and GAD for glyphago as a starting point. But in reality, we think the mechanisms are broadly applicable beyond that starting point. And as we get additional data and continue on in development. We'll look forward to using that data to motivate additional development.

Okay. I want to make sure we touch on the third program, which you briefly mentioned, I believe, at the beginning. We're talking about definium, but yours is a non-hallucinogenic neuroplastinogen. So love to hear about Glyph 2BLSD, and you can please tell us what that is and why it's unique.

So our third program is called Glyph-2B LSD. It's the glyph prodrug of a molecule called 2B or 2-bromo LSD. Now, like everything else that we're developing, that parent drug, that 2B LSD, has actually been in the clinic. Humans have been exposed to 2B LSD. It has actually shown some intriguing clinical activity in a rare and devastating headache disorder called cluster headache. But to me, the most interesting part is that 2B LSD, even though it has shared pharmacology with LSD, it has that classic psychedelic serotonin 2A agonism. And preclinically, it looks like an antidepressant and causes neuroplasticity, but it doesn't cause a trip. So when dosed in humans, you can dose up 2B LSD, it doesn't cause a trip. Now, there may be variable PK, side effects, things that we address with glyph, but fundamentally, it's maintaining that pharmacology, that psychedelic-like pharmacology, but without the trip. And then you think, what is the next generation of therapies beyond psychedelics, the in-clinic administration? And you imagine a drug that has the same effect, the pharmacology, but now you don't need administrative oversight. You don't need someone watching. You don't need to dose in the clinic. You don't need eight hours post-tose monitoring, but you could still capture some of that upside from a psychedelic pharmacology. That's the vision with Glyph-2B LSD. So we'll be wrapping up first in human enabling studies by the end of next year for Glyph-2B LSD. And we're really excited as the overall field advances to think about how Glyph-2B LSD will be optimally positioned there.

Just a quick one. As you look to the GAD and MDD indications, not as much on the non-tripping medications, the subject of professional patients has really caused a bit of a, you know, wreaked some havoc, you know, across the neuropsych field. How are you guys considering that as you, you know, move to maybe more later stage studies and maybe just philosophically?

Yeah, and it's something we think about already today and have put a lot of thought in from the very creation of Seaport because we're taking playbooks from Karuna, which did, in my view, a really excellent job managing not just having an active drug, but designing and executing clinical trials the right way. So professional patients is a great example. We use certain tools that allow us to identify patients that, for example, are trying to screen into Bowie One, but also trying to screen into a bipolar study down the street and a schizophrenia study in a different town. And there are ways of detecting those patients and excluding them so they don't end up in your study. You can also make sure you get patients that don't spontaneously improve between screening and baseline. That's probably not the right patient for a study like this. And then on a site level, you can use blinded data analytics. You can evaluate the raters actually doing the interviews. use every little thing you can do to try to reduce the placebo response, which ultimately things like this contribute to.

Yeah, no, that all makes a lot of sense. Any other ways to reduce placebo response or those are the big ones?

There's a lot of big ones. So I wish I could tell you there's a single thing that we do and then we're all set. Sometimes the design is really critical too. So I'll give you two examples. In buoy one, our MDD trial with glyph aloe, we only have two arms, drug, placebo. Now, sometimes you see studies like this that have three arms or four arms and three to one randomization. And it turns out that there have been studies where the number of active drug arms correlates to the magnitude of the placebo response, which kind of intuitively makes sense. Similarly, we've conducted meta-analyses looking at the frequency of clinician-administered assessments. So essentially, patients coming in and a rater or clinician sits down, interviews them, etc. And what we found is that the more clinician-administered assessments you have correlates with a higher placebo response in your studies. So this teaches us from past history how to design these studies. You don't want three active arms. You want one-to-one randomization. You don't want 10 assessments a week. You want to reduce or optimize the number of assessments. And these are small tools, but they all add up to the placebo response, which can even swamp out active drug signal.

Okay. So you mentioned the third program the non-hallucinogenic going into the clinic at the end of the next year or we'll be completing first in human enabling studies okay by the end of 2027 okay got it um and of course the point there or a point there is the lack of uh this functional on blinding given you won't presumably with this molecule you won't have a any tripping yeah and it'll be very interesting how this space sort of unfolds with that functional and blinding. I guess in the last few minutes, I just wanted to ask, we're asking everyone this one, just on the question of the use of AI tools. And let's see, to what extent are you leveraging those either, you know, for basic efficiencies like filing with the FDA or summarizing data or even in drug design? Just if you could give us a little perspective there. You know, we just heard from the former FDA commissioner, he gave us his two cents on the use of AI at the FDA.

Yeah, sure. I can start and Michael can definitely chime in. So we see a tremendous benefit of AI, I think, as we, you know, we're a small company, obviously, in the biotech space. And, you know, we are really looking at where it makes most sense to leverage it from an efficiency perspective, both on the R&D side and the G&A side. Obviously, as the CFO, we're driving as much as we can from a financial perspective to be able to leverage it in a way that makes us do our clothes more efficiently and things like that. And maybe Michael wants to add a little color on the science side as well.

Yeah, and I think on the R&D side, it's as tools become available and importantly have the rigor and the validation to be used, for example, in regulatory settings, we've seen more and more AI being used as a magnifier. So it allows small lean teams like ourselves to get more work done per pound, so to speak, relative to what we would have without AI tools, while balancing taking care around safety, compliance, quality, and as well as rigor that can stand regulatory scrutiny.

And then sort of final, like, you know, big picture question. I mean, this whole glyphing idea is a new idea. The technology comes, I understand, comes from important scientists in Australia who developed this. But it also seems like it has a lot of potential, not, you know, not just in neuroscience. I mean, if you're saying that, you know, we can remove the liver first past metabolism, there could be opportunities in other therapeutic areas. So, you know, while it's early, to what extent is Seaport thinking about, you know, this is more of like a platform technology where you could go into areas beyond neuro?

Yeah, it's a great point, Yigal. We as a company are very much focused on depression and anxiety, and that's where we've really focused our programs moving forward. But Michael and his team have glyphed over two dozen molecules across various therapeutic areas. So we remain really excited about what the potential of the glyph platform can be. We continue to receive significant inbound interest from other pharma companies that want to think about using the glyph platform to help solve their problems. And so we remain excited about that. We also recently announced, I think Michael mentioned, we have been working closely with ARPA-H and received some grant funding to help us think about Glyph in the gut lymphatic area. And so those are all just some examples, and we continue to be really excited about the Glyph platform.

All right. Very good. Well, we look forward to seeing the buoy data shortly. Thank you. Great.

Thanks for having us.

Thanks, Miguel.