Good morning, everyone. Thank you for joining us. It's three of the Goldman Sachs Healthcare Conference, and it's my pleasure to introduce Seaport Therapeutics. With us, we have Lauren White, CFO, and Michael Chen, CSO. To start here, and thank you so much for being here, given the recent IPO, could you provide a brief overview of the Seaport story and the 12 to 18 month catalyst outlook for the company?

Sure. First off, we'd love to thank you for having us here, Selvian. We're super excited to be here. So, Seaport is a neuropsychiatry company. We've got a clinically validated platform, and we've got a pipeline of three robust programs. Our lead program is currently in phase 2B and has the potential to be registration enabling. Our second program, we just shared phase 1 key 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 items like that. And the great thing is that every time we glyph a molecule, we create new IP along the way. We've got a seasoned leadership team with a track record of success in this space, both in developing medicines for new patients and in driving successful business outcomes. And as you mentioned, we recently completed our IPO where we raised over $260 million of gross proceeds, which provides ample capital to take us through our next set of milestones. If we take a step back, there's over 1 billion people living with mental illness globally. When you think about prevalence, it's similar only to hypertension and obesity, and so we here at Seaport are really focused on depression and anxiety. Those are areas that typically tend to be comorbid. They each impact over 300 million people globally, and it's clear we need better medicines in that space. If you look at the current landscape of medicines that are prescribed, you know, there's millions of patients that are on them. There's huge commercial successes, but they're held back by some limitations. They can take weeks to work. They have modest efficacy. They don't work for one out of three patients. And they have unfavorable side effects, such as sexual dysfunction, weight gain, and sleep disturbances. And so we at Seaport believe we're uniquely positioned across those three parameters. You're probably familiar with the fact that our CEO, Daphne Zohar, and our board chair, Steve Paul, founded and led Karuna. And so we have some similarities to Karuna. Specifically, one example is Karuna knew that Zomaline worked, but it was held back and sitting on a shelf due to GI tolerability issues. So the team was able to go in, fix it, and invent CAR-XT, now called Cobemphi. So we at Seaport, as I mentioned, have similarities to that. We go after drugs that have validated efficacy, but have some issue that's holding them back, and we're able to apply the Glyph platform to support that as well. And so looking ahead over the milestones for the next 12 to 18 months, we've got a really healthy set of cadence of milestones. First, we'll be sharing data from our phase one driving study for glyph aloe that'll be in the second half of 2026. Next we've got our buoy one readout of our glyph aloe program in the first half of 27 and then we've got some interesting milestones related to our second program glyph ago. We've got a phase 2a readout in the early 2028 and we've got our phase 2b readout in the end of 28 and so we're really excited about the path forward. We've got a great set of capital from our IPO to take us through these next set of milestones. Great.

At a high level, how does the Glyph platform enable a differentiated product profile, and how de-risk is it at this point?

Sure, I'm happy to describe it. So Glyph, as Lauren mentioned, is a lymphatic targeting prodrug technology. So the way it works is that it takes a small molecule that might otherwise be chewed up by the liver and cloaks it so that it looks like a dietary fat. And when we do that, we create a new molecule with new composition of matter IP, but importantly, that molecule now goes into the body via a side road, via the lymphatic system of the gut. And what this enables is to bypass the liver. So that can mean for small molecules for drugs with limitations like poor oral bioavailability, highly variable PK, pharmacokinetic profile, or even liver toxicity due to, again, the liver seeing a lot of drug. we're able to overcome these particular issues. And this is a technology that we have now validated through multiple programs. So first with our Glyph-Aloe program, in which we successfully demonstrated an increase in oral bioavailability. And most recently with our Glyph-Ago program, where, again, in the clinic, we're able to validate that the platform works. And with Glyphago in particular, demonstrate that we're able to bypass that first pass effect and get to an exposure that we need to get to while reducing the dose. And so this is really critical for not only generating the new medicines that are in our pipeline, but for also taking molecules with the limitations that we know about, addressing those limitations, and creating new potential medicines.

In terms of the data that you've generated with this platform, you know, have you been able to completely eliminate the side effect profile that you're trying to?

I'll give you one great example, again, from the data that we announced very recently with glyphagomelatin, including the multiple sending dose data that we announced recently. This is a program in particular where the parent molecule, so to speak, agomelatin, is actually an approved drug. It's not approved in the United States. It is approved in Europe. It's approved in Australia for the treatment of both depression and generalized anxiety disorder in Australia. But it's held back by a key limitation, which is really tolerability associated with the liver. So agomelatine has dose-dependent elevations in liver enzymes. And this occurs in a small percentage of patients, but it's notable and it must be monitored. So practically for clinicians, for patients. What this means is liver enzyme testing, blood tests, before initiating treatments at three weeks, six weeks, 12 weeks, 24 weeks, every time you increase the dose. And this is not something that clinicians or patients really love. With agomelty, we know that the liver enzyme increases are dose dependent. They're really dependent on how much drug the liver sees. And the issue is that the brain sees less than 10% of the drug that the liver sees. The liver chews up so much of the drug before it can actually reach the brain. So we've now demonstrated by glyphing agomelatine with our glyph-ago molecule that we're able to bypass the liver. So for example, in phase one data, what we showed was an increase of bioavailability that can be as great as 9.6 to 14.5 fold greater than agomelatine. And so practically what this means is we know the exposures of egomelatin that work in the clinic. Part of our strategy is looking at clinical data and going towards that. So we can reach the same exposures of egomelatin that we know are efficacious, for example, in generalized anxiety disorder, but dose less drug because we don't lose so much drug to the liver before it gets to the brain. So in our phase one, not only did we show that PK difference that enables that, but from a safety and tolerability perspective, glyph AGO was generally well-tolerated, there were no serious or severe AEs, and there were no liver-related AEs, all while hitting this PK profile. I'll mention one last fact, again, to the advantages of the glyph platform that can play out clinically. We know agomelatine actually has a drug-drug interaction. So again, not an AE, not a side effect, but something that patients must be cautious about using, in this case, estrogen-containing oral contraceptives because they can interact with agomelatine at the level of the liver, and you can see this in the PK profile. But when we dose glyph-ago, we don't see this difference in patients or in healthy volunteers, in this case, with or without oral contraceptives. And that's because that drug-drug interaction is happening in the liver, and the glyph platform allows us to bypass the liver. So to your point, we're able to hit the profile in this case PK-wise that we believe will translate into a reduction in liver enzyme elevations and a new molecule without the burdens that has really held back aglomelatine from having a significant impact.

Can we dig into that reduction in liver enzyme elevations? So when you look at the parent asset that's approved, XUS, what is that rate of liver elevation and in what proportion of patients, and then what are you seeing when you say reduction?

Right. So this is actually something that you're able to model because of how much clinical data there are out there with agomelatine. So with agomelatine, in thousands of patients who have used this and in reports, it's been found that these liver enzyme elevations can be as high as two to three percent of the patient population, which doesn't sound like a lot, and indeed it's not a huge number, but it is several times greater than the placebo background rate. So it is a notable increase, and it is dose-dependent. The more aglomelatin a patient receives in terms of drug, the higher likelihood that they're going to have these elevations. Now, I should caveat, these are elevations that tend to be three times greater than the upper limit of normal. It's not necessarily bilirubin increases or Heye's Law or things like that, but it is a notable increase. What we were able to do before we actually set out on phase one was to actually create a bar for ourselves, which is to use a program called DILI-SIM to help model the liver injury risk with aglomelatin and how that's associated with the PK profile, how much dose of drug. And through that modeling, we were able to set a bar for ourselves of how much we need to increase the bioavailability of glyphago relative to agomelatine in order to eventually show those reductions in liver enzyme elevations. And so that bar was two X, twofold. And so when we went into phase one, we ran single ascending dose, multiple ascending dose, but importantly also a crossover, where healthy volunteers received agomelty, the parent molecule, without glyph, and then glyph-ago. And what we saw was actually nearly seven times increase in bioavailability. So our bar was 2x. What we saw was nearly 7x. And taking away the complication of oral contraceptives, it goes as high as 14.5x. So we're clearly exceeding the threshold that we've modeled will result in a reduction of liver enzyme elevations. And that's where we're excited to now launch two Phase II studies with glyphagomelatine, a Phase IIa clinical pharmacology study and a Phase IIb potentially registration-enabling placebo-controlled study where we will look at efficacy and safety for glyphago.

Maybe starting here with glyphalo, which is a glyph version of alopregnalone in major depressive disorder. Can you walk us through your data to date and the clinical rationale here?

So I think the clinical rationale goes back to our strategy on looking at compounds that have clear clinical activity but are held back by a shortcoming. In this case, allopregnanolone is an endogenously incurring neurosteroid we're all making in our brains right now. It's a GABA-positive allosteric modulator, and it's actually an approved drug. So it's been approved for the treatment of a form of depression, postpartum depression, where it's effective. It's actually found to be rapidly acting with anxiolytic and sleep-promoting activity as well. But allopregnanolone has poor oral bioavailability. So that approved drug was in the form of a 60-hour intravenous infusion. Drug that works, 60-hour IV infusion. so with glyph aloe we were able to glyph alopregnanolone create a new molecule with by the way a new composition of matter ip and in phase one what we're able to show is that we're able to reach clinically relevant exposures of alopregnanolone but now with glyph aloe with once daily oral dosing so in that phase one we're able to show not only that drug gets into the body, but also gets it into the brain. So allopregnanolone, as it's released from the glyph prodrug system, actually gets into the brain and has pharmacodynamic activity. That is things like EEG markers, eye movement markers, all consistent with allopregnanolone in the brain. So drug in the body, drug in the brain, and at well-tolerated doses. In fact, we don't see AEs that might be associated with the glyph platform itself, but the most common AE is from allopregnanolone's pharmacology. As a gabapam, that means mild transient somnolence was the most common AE, and we're actually dosing glyph aloe once daily at night. So on the basis of these clinical data, what we did was actually launch a Phase 2A proof-of-pharmacology study with glyph aloe. And what we did there is use a clinically validated model of anxiety called the Trier Social Stress Test, or TSST. And in this model, we take healthy volunteers in a randomized placebo-controlled trial, and they receive drug and then are given a task, which is to prepare and then give a speech in front of a panel of judges on why they deserve a job, and then to do math live in front of this panel, subtraction, 2,000 minus 17, over and over again, and then they're told wrong, start over, wrong, start over. As you expect, this might be stressful, and so individuals who are dose placebo will show a big spike in the stress hormone cortisol, which is the primary endpoint of that trial, which we can just swab. And that big spike in salivary cortisol is potently and statistically significantly blunted in healthy volunteers randomized to glyph aloe at a single well-tolerated dose of glyph aloe, P-value of less than 0.000, sorry, P equals 0.0001 in that case. And the only other neuropsychiatric drug that has shown that effect is actually Xanax, Alprazolam. And this is consistent with the role of allopregnanolone as not only a known antidepressant, but also with that anxiolytic activity. But importantly, we know allopregnanolone as an endogenous molecule is very different than a benzodiazepine. And so what we have in glyph aloe is a molecule where the parent allopregnanolone has been shown to work, antidepressant activity, anxiolytic and sleep-promoting activity, but it's held back by a key limitation that in phase one, we demonstrated we were able to overcome by increasing the oral bioavailability. That 60-hour IV infusion is now once daily oral dosing of glyph aloe. So on the back of that, as Lauren mentioned, we're currently in a phase 2b potentially registration enabling study in major depression with or without anxious distress using glyph aloe. That's a randomized placebo-controlled study, global study, and it's one that we believe is adequately well-powered to be a potentially registration-enabling study, and that's something that we'll read out in the first half of next year, 2027.

And just to step back here, we're all familiar with this asset when it went through U.S. trials for major depression, the parent compound here through SAGE and Biogen. Helped us understand what the challenges were with regard to outside of tolerability, but what really played out here and how you aim to overcome them, including trial design.

Yeah, I think it's a great way to look at what we view as the third pillar of what we're doing here at CEPOR, only having the right molecule, but actually having the right clinical trial, both in terms of design and in execution. So to your point, Sage had developed an oral synthetic analog of allopregnanolone because, of course, allopregnanolone, as we talked about, has very poor oral bioavailability. So that means 60-hour IV infusion. So a synthetic oral analog called xoranolone was developed and was tested in MDD. And interestingly, it has antidepressant activity. So in five out of six trials, it met its primary endpoint. It's actually approved for major depression outside of the United States, for example, in Japan. However, it was studied as a two-week course and is given as a two-week course. And so while it met its primary endpoint, if you look at the FDA guidance for antidepressants, the agency is really looking for durable efficacy out to six weeks or greater. And so if you give patients drug for only two weeks and then you take them off of drug and then ask for efficacy at six weeks, that can be a different challenge. And so that durable efficacy was never really established in those trials, even though clearly xeranolone has antidepressant activity. And even though xeranolone is approved for MDD outside the U.S. and is approved for postpartum depression in the U.S., there is nothing in this GABA-positive allosteric modulator class that's actually approved for the broader major depression indication. And so we can learn from these past experiences, and for our glyph-alove program, the BUIE-1 Phase IIb, one of the important things we're doing is dosing for the full six weeks. We're also taking other learnings from past neuropsychiatric programs, including the successful examples of Karuna, and taking these design and execution patterns from these previous programs to inform our own development program. I'll give you one or two examples. We know the placebo response can really bite programs. And so we're trying to reduce that placebo response by carefully studying what contributes to that placebo response. We've put out meta-analyses, for example, showing that the frequency of clinician-administered assessments can actually predict the magnitude of the placebo response. The more you interact with patients in a site during a trial, the more likely they are to generate a placebo response. So we are tuning and calibrating the number of clinical assessments to not have an excessive number of clinical assessments. It can be very tempting to put in many, many assessments to look at how wonderful your drug activity looks, but the more you do that, the more you drive the placebo. Another one is the number of active arms in a study. It can be very tempting to range across a number of doses, have three active arms, one placebo arm, but every active arm you add to a neuropsychiatric study actually increases the placebo response. Participants know they have a 75% chance of getting a potentially active compound, and And that can contribute to the expectancy and the placebo response. So in our Bowie 1 study, we have one-to-one randomization. Drug, placebo, and that's it. So it's these little tricks of the trade that we're adding to try to control the placebo response and maximize the likelihood of success. And there's not one silver bullet, but it's a number of these small things that we have to do to make sure that the drug's activity can really show itself.

And the survey has a black box warning for driving impairment, and I believe you're going to initiate a driving study later this year with results in the first half of next year. What do you hope to confirm or establish with this study?

Yes, so we've initiated a driving study. The results, which will come out later this year, second half of this year, will really inform the overall profile of glyph aloe in this program. And so to back up, we know that xeranolone as a synthetic analog of allopregnanolone has different PK characteristics. Allopregnanolone, when it's infused, for example, clears relatively rapidly. And this is something we observed with glyph aloe, the oral lymphatic targeting prodrug of allopregnanolone, that by the time you get to 68 hours post-dose with glyph aloe, you have something like 15% of the CMAX of the drug remaining. So it pretty rapidly drops from its peak at three to four hours to six to eight hours. And we actually saw this in phase one, not only in the PK data, but in the pharmacodynamic data as well. So if you look at those brain markers, the EEG markers, they peak at three to four hours and they're back to baseline by six to eight hours. And we feel this is consistent with a drug that can be dosed at bedtime. And so that's what we're doing in Bowie 1. we're dosing glyph aloe once daily at bedtime. Now, in the United States, there's a driving restriction in Bowie 1 in that patients cannot drive while taking Bowie 1. In the EU, it's actually a six-hour driving restriction. So once daily at bedtime, and then six hours, no driving, and then the next morning, fine. And so the goal of the driving study is to add more information to the overall clinical knowledge around glyph aloe. And we feel that based on the PK properties of glyph aloe, that the outcome of this study, the driving study, which we'll get actually ahead of the Bowie-1 study, but that driving study plus Bowie-1 will be very informative towards the overall clinical picture of glyph aloe, and it's something that we believe has the potential to, over time, reduce that driving restriction as we continue to gather key data. The driving study itself is a driving simulator study. It's actually, I hate to use the word canned, but it's a little bit of a canned study. It's a very standard study with dosing of glyph aloe at night and then next day driving and looking at the simulator-based driving, not an actual in-car experience.

So when we see this phase 2b data in the first half of next year, I believe, what is the bar for success that you're looking for here?

I think in these antidepressant trials, and Bowie 1 is no exception, the table stakes are a statistically significant separation between drug and placebo. And the way we've designed and powered Bowie-1 is that a statistically significant result will be a clinically meaningful result. And this is on top of other benefits of allopregnanolone that we believe could have an impact with glyph aloe as well. So for example, we know allopregnanolone is rapidly acting, very rapid antidepressant effect. And we also know that allopregnanolone has anxiolytic activity and sleep-promoting activity, and those are facets that we'll be looking at in addition to that sort of top-line key efficacy. And so we'll look at the activity of glyph-aloe, but we'll also look at the side effect profile because I think one key potential differentiator, is that allopregnanolone, and we believe glyphalone, does not have sexual dysfunction or weight gain or insomnia or some of the other baggage that has really held back standard of care like SSRIs or SNRIs in major depression. But table stakes, statistically significant separation between placebo and drug.

So when you think about the HAM-D delta that one would want to see, typically whatever you see in phase two just gets more narrowed as you get to kind of that bigger phase three trial. So what do you think is an appropriate delta here as you look at the approved drugs that have played out to be meaningful?

Yeah, if you look historically at approved antidepressants, you can see effect sizes in the 0.3 and up range. And so for us, again, table six is just demonstration of that statistically significant difference between drug and placebo. And that change between phase two and phase three, some of those design factors that we talked about may contribute to that change. We think that even though it is a potentially registration-enabling trial, historically there have been multiple trials run to have a drug successfully approved, and so we believe that we'll need to do additional trials beyond Bowie 1 to confirm efficacy and safety, if that's a signal that we see in buoy one. And so really what we'd be looking at for here is data to inform those phase three programs and something that you can interact with the agency as part of an end of phase two meeting, for example.

For glyphago, can you outline the differences between the planned phase two A and phase two B studies and what you would consider a successful outcome for each of those?

Yeah, maybe I can just back up and give a little bit more background on agomelatin as well, because I know we sort of jumped straight into the very exciting top-line data that we recently put out. So Glyph-Ago, I think, is another great example of our strategy where it's based on agomelatin, which, as I described, is actually an approved drug. And it's approved for major depression and generalized anxiety disorder. And we're actually starting development of Glyph-Ago in G80, in generalized anxiety disorder, which, as Lauren mentioned is a huge unmet need. Over 300 million patients around the world affected. And it's startling that despite this unmet need, in the U.S., the last approved GAD drug was about 20 years ago. It's been a dearth of innovation in GAD, despite, again, the unmet need. Agomelatine, we know, works in GAD. So, for example, there have been four placebo-controlled trials of agomelatine in patients with GID, where agomelatine statistically significantly separates from placebo in all four trials. In addition, it does not have side effect profiles similar to SSRIs. It's actually in a different class altogether. It's a melatonin receptor agonist and serotonin 2C antagonist. And so a part of that, it doesn't have sexual dysfunction, doesn't have weight gain. It actually helps improve sleep. this has been something that's been shown in MDD, and we'll come back to that when we talk about our phase 2A. But the profile of agomelatine is something that in meta-analyses and reviews has been described as both more efficacious and better tolerated than standard of care like SSRIs, benzodiazepines, with that one exception, with the liver enzyme elevations as the exception that has caused that label restriction and onerous liver function testing and monitoring requirement. And so with glyphago, we're starting where the clinical data take us, which is in generalized anxiety disorder. And we put out that phase one data supporting that we hit the PK profile that we believe will lead to a reduction or elimination. What we're doing now with these positive first in human data in hand is to launch two separate studies, the phase 2A and phase 2B. Now, I talked briefly about sleep with aglomelatine. So with aglomelatine, the parent molecule, head-to-head against an SSRIs, which makes sleep worse. You can actually worsen insomnia. Aglomelatine in the past has been shown to actually improve sleep. And not only the subjective experience of sleep, but actually the objective sleep architecture. When you look at EEG, polysomnography of sleep, it actually improves with chronic daily treatment of agomelatine. And that was shown in major depression, and that's something that we're going to be exploring in a Phase 2a proof of pharmacology study with glyph-ago. And so we'll be looking at patients with generalized anxiety disorder, not MDD, but in this case GAD, with sleep disturbance, and we'll be looking at measures of sleep. And this proof of pharmacology study will be a randomized double-blind study of two different dose levels of glyphago to look at a potentially dose-dependent effect on sleep outcomes in that population. And we believe this is really important because of how central sleep symptomatology is in GAD. So many patients with GAD and MDD actually have complaints of sleep, difficulty falling asleep, staying asleep, waking up too early, et cetera. So that's the Phase 2A. That's, sometimes I joke, the appetizer study that will be starting soon and will read out in the sort of first part of 2028. Where it really differentiates, the Phase 2B is a potentially registration enabling, very much a placebo-controlled, randomized, double-blind, very sort of weighty study. And that will be in GAD without the bells and whistles. Again, we talked about trying to do too much with patients in these potentially registrations. So that phase 2B will be taking the same learnings. We'll be looking at sort of standard endpoints with anxiety rating scales, et cetera. And that's really designed to be a primary look at safety, efficacy, tolerability with Glyph-Ago. That, again, could be one of potentially several registration enabling studies.

Remind us what happened here with regard to the U.S. process, like why it was approved ex-U.S. but not in the United States.

Yeah, and I think this comes down to a contribution of the liver enzyme elevations and the lack of composition of matter IP, which is actually an important point. Agomelotene currently doesn't have composition of matter IP, so that and the PK challenges, the lack of oral bioavailability leading to that high first-pass metabolism and the resulting liver enzyme elevations led to some development in the U.S., but never any attempts at having it registered for either MDD or GAD. And then, frankly, patent life has really been a challenge. And so you see that in the EU, for example, it's only approved in MDD, where, by the way, agomelatine has also demonstrated efficacy. But in Australia, it's approved for MDD and GAD. So with glyph-ago, with our glyph-pro-drug of agomelatine, not only do we improve the profile by having a radically different PK due to this first-pass-avoiding lymphatic transport, but we actually create a new molecule with new composition of matter IP. But at the end of the day, what's circulating, what gets to the brain is agomelatine, which we know works, and we know the exposure that works. And that's, again, back to our strategy of taking compounds with known efficacy and addressing their shortcomings.

What is the overlap between GAD and MDD, and then how would you position these drugs in the context of that? And then secondly, just speak to where else you could go with the glyph platform outside of Neuropsych.

Yeah, I'm glad to answer this, and Lauren, if you want to chime in as well. So there is substantial overlap, and this is something that can be a comorbidity between MDD and GAD, for example. It can also be the presentation of anxiety within depression. So this is something we're actually exploring in Bowie 1. I noted earlier that's an all-comers trial, MDD, and that's the primary outcome we're looking at is drug versus placebo and MDD. But we will have a qualitative look at what's called anxious distress within major depression. It's a specifier. It's actually a major specifier. Over 60% or more of patients with MDD will have anxious distress. And due to that, the fit pharmacologically with glyphalo, the data that we've demonstrated with the TSST, we believe that glyphalo could have an even more beneficial effect in those patients with anxious distress. So there's a lot of overlap. between this. And you see this with agomelatine. It's approved for both GAD and for MDD. So with glyph aloe, we're starting with MDD, but we are looking at that anxiolytic profile of allopregnanolone. And with agomelatine, we're following the clinical data where it's very strong in GAD. So we're starting in GAD, but we know it's approved in depression. And I'll just briefly comment on the glyph platform itself. It's not specific to the brain. In fact, we believe we can have the impact on a wide variety of molecules that are limited by first-pass metabolism or liver toxicity to that first-pass, poor or bioavailability, et cetera. And so, actually, we are exploring outside of the CNS. For example, we recently received up to $15 million as an award from ARPA-H to explore metabolic disease, oncology, and INI applications of the glyph technology because we as a company, CEPOR, are going to be focused on neuropsych.

And maybe just to compliment that, we retain worldwide global rights to the Glyph platform and any programs that come out of it. So just to reiterate, the IP piece is a big play here where every time you Glyph a molecule, you create new IP. So we're really excited about where the platform can go as well.

And Lauren, our last question here. Where does the cash runway take you to in the context of these trials that you're running?

Sure. So with our recent IPO, we raised gross proceeds of over $260 million. So that combined with our Q1 cash on the balance sheet takes us into 2029. So then to reiterate, that covers the driving study that Michael touched on in the second half of 26. That covers our key Bowie 1 trial in the first half of 27, and it includes the Phase 2A and the Phase 2B trial of Glyph-Ago in early 28 and the end of 28.

Well, with that, thank you so much. Really appreciate the time today.

Thanks so much, Selvian.