All right. Good morning, everyone, and thank you so much for taking the time to join Citi's 2022 Virtual Bus Tour. I am very pleased to be joined by the management team from atai Life Sciences for our next session. We have the company's CEO, Florian Brand, and the company's Chief Scientific Officer, Srinivas Rao. I just wanted to remind everybody, since this is a virtual bus tour, you are free to raise your hand and ask questions. We do want this to be interactive. If you do raise your hand, I'll call on you, and you can unmute yourself and ask your question. If you prefer, you can also just email me, and I can ask your questions for you, whatever is best for you. Before we jump into questions, I did want to turn it over to Florian and Srinivas if you guys want to make any opening remarks. Sure. I'm not sure if everyone knows us. I see some familiar names here. Srinivas, why don't you do a quick introduction on yourself, and then I do a very short one on myself. Sounds good. Thanks. Yeah, just very briefly, my name is Srinivas Rao. As Nina mentioned, Chief Scientific Officer and co-founder of atai. Background, I'm an MD/PhD, neuropharmacologist. I've been in drug development now for about 22 years, and primarily in the CNS space, but kind of in a diversity of indications broadly. Been pretty much exclusively at small companies and worn a bunch of different titles: CEO, CSO, or CMO. Last couple of gigs were actually Chief Medical Officer jobs. One was at Axial, which was focusing on brain-gut interactions for autism and Parkinson's disease. Before that, I was CMO of a company called DepoMed that was actually fully vertically integrated, essentially, with both six products in the market as well as phase III assets. Again, great to be here. I'm going to hand it off to Florian. Thanks, Srinivas. Yeah, Florian, co-founder, CEO of atai. We started atai around about three and a half years ago, really, because of very personal reasons, and primarily because we saw friends and family members suffer and not finding sufficient help in the available treatment options. Basically seeing a friend of ours, Lars, ultimately, after he was diagnosed to be treatment resistant, to find healing in psilocybin-assisted therapy. Basically, the therapy that one of our subsidiaries or one of our largest investments, or most advanced companies, Compass Pathways, is developing now in a, they just read out their phase II. Seeing him finding healing and seeing him going through the very positive transformational experiences was for us kind of the initial starting point to initially focus on psychedelics as a catalyst for innovation. We quickly broadened out the focus and are now really looking at everything from non-psychedelics, psychedelics, digital therapeutics, which we would love to talk about today because we believe there is a great potential in those in mental health disorders as well, standalone and primarily also combined. In this, to really make a truly forward for mental health patients with a strong focus on developing more efficacious, more durable, more rapid-acting pharmacological interventions for mental health patients. Great. Awesome. I will start out asking some questions. Like I said, if anybody does have questions that you want to ask, feel free to raise your hand. I guess maybe just starting off talking a little bit about the business model before we get into some of the individual assets because you are going to have a lot of data over the next 12 to 18 months. Maybe just starting more generally, you, of course, have a pretty broad portfolio right now. Maybe if you could talk a little bit about what some of the priorities are in terms of adding to the portfolio. You've got, obviously, discovery kind of discovery companies. You've got some companies that are in clinical stage. You have digital therapeutics and other supporting technologies. Is there any particular area within that or beyond that that we should be thinking about in terms of priorities for future BD? Yeah. I'm really happy to. At atai, we're really interested in achieving clinically meaningful and sustained behavioral change in mental health patients. Basically, see three major ways to get there. I think it's, in terms of what I just said, basically applied to depression, it's in a simplified way, how do we get people out of depression, and how can we keep people out of depression, and how can we do that in a more targeted way, given the kind of spray-and-pray approach that we often see today in psychotherapy? How can we move towards more precision mental health approaches in our sector? How we believe we can make a true difference and be a leader in this field is by being focused on basically three areas. One is, and that's what I said in the introduction, being very much focused on pharmacological interventions that are truly differentiated from what we have here. That is our core focus area. That is where we have the, you mentioned our pipeline, a very diverse pipeline. We intend also here to add on further compounds and basically ranging from discovery to clinical assets. The second pillar is basically digital ongoing patient support. These are our digital therapeutics that we're developing. Also here, we see a great benefit, again, standalone in the mental health field. That is what we are currently focused on by combining them with our compounds and with the first pillar. Ultimately, the third pillar is exploring biomarkers to enable us to make much more targeted decisions when it comes to treating those patients. In all of those areas, we intend to be, yeah, to remain very, very active. We have already programs and initiatives running in all of those. The clear focus will be on the very first pillar in our drug development programs. We will continue to be as active as we have, I would say, over the last year. That is a good indicator, a good proxy when it comes to, yeah, how active we will be. In terms of indications, I think, not surprisingly, we're very interested in Neuropsych. DSM-5 are kind of the indications that we remain focused on and are also cash-wise in the position to add more compounds to the pipeline. Okay. Great. That makes sense. I know you did obviously mention in the intro about digital therapeutics and kind of the potential for incorporating those within kind of your broader portfolio. I guess maybe you could talk to us a little bit about how you do that, how you kind of see digital therapeutics being incorporated with your other programs, and specifically some of the work that you're doing right now kind of with your pilot program. Yep. Srinivas, do you want to take that one? Yeah. So there's a couple of different ways. I think it's important when we go back to talking about our psychedelic compounds, what that entails, right? What does it take to actually deliver a psychedelic therapy? It takes some preparatory work, right? This can be done by a therapist. It can be done, we believe, digitally as well. It takes support during the psychedelic experience. What's commonly referred to as a setting or a guide, I mean, I really do believe in the concept of a digital guide. It takes support after the psychedelic effect. There's really, again, sort of two phases to that. There's an acute behavioral plasticity period, and then a longer-term phase. That longer-term phase is pretty important to think about when you may want to read those. What can we monitor there to make some decisions? That's broadly how we think about digital therapeutics. There's actually an app-based approach that is really covering the pre and post-psychedelic effects. We also have a device in the context of Psyber that's really more focused on the setting and kind of helping the patient along. Part of the reason, I mean, there's multiple reasons that we're doing this. Of course, one is to improve patient safety. Also, we think we can improve patient efficacy. I think the other really important piece here is that we can use this for scalability, right? Essentially allowing for a commonality of therapy across geographic areas, etc. Right now, I think one of the questions or concerns is there's lots of variability with these therapists. Using this app-based approach, it puts things on a more structured, and it puts things in a more structured manner so that everybody has the same thing. We think that that allows for more stability and better separation of the signal as well. Now, the other piece of this that's very important with many of our psychedelic compounds, but other compounds as well, we want to actually develop these agents and digital technologies as combination products. These are so-called drug-device combinations. That means that the actual device itself ends up in the label. That, of course, adds another level of ability to block for these assets. I mean, both because it's actually in the label, and it's going to be very specific to our app, which is not going to be accessible outside of a prescription for our product, but also that we will have a lot of opportunities for IP generation, both within the app and certainly within the context of combination. Okay. Great. That makes sense. I do want to, there's a lot more questions I think we can kind of ask about the general business model and those sorts of things. I do want to get into some of the specific clinical studies that you're running right now because I do get a lot of questions on those. I guess maybe the first one is just a general question. We are seeing, particularly, I mean, in the psychedelic space and then actually just more broadly as well, we are seeing the FDA, I think, issuing a lot more clinical holds than we've seen kind of historically. I know in the psychedelic space, it's largely been around kind of concerns that the FDA seems to have around the adequacy of patient monitoring and support during studies. I guess, can you maybe talk to us a little bit about the level of interaction you've had with the FDA kind of to date on some of your programs and your portfolio and how comfortable you kind of are that you may not face those same kind of clinical hold issues that others have? Yeah. Where we've interacted so far with the FDA is really perception. We just announced that we did get clearance to start a phase I trial here in the United States. I think we've mentioned also that we'll be broadening out our phase II study here in the United States. RL-007, the Recognify asset, also had an IND in place. In fact, that phase II A Proof- of-M echanism study was actually conducted here in the United States. Those are the places where we had primary interaction, neuronasal as well, primary interactions here with the FDA. Marketing is a little bit different, right? I mean, sure, it's derived from a psychedelic or dissociative compound. Of course, our investment thesis on this particular molecule is that it is non-dissociative at the efficacious doses, in other words, as a therapeutic index. That really didn't come up in that context with our FDA interactions there. It should be noted that no such issues came up with Compass either. Now, of course, they're going to be moving forward to their end of phase II meeting, and they publicly mentioned that. Maybe some of the stuff will come up. I don't think so. I mean, they've been very careful, very thoughtful on how they approach this. I think that's really important. There's a lot of training that's been involved with their guides, with their therapists. I think that's going to really help them. Again, it's been a very thoughtful, lots of thoughtful approach, lots of training. We won't deviate from that, essentially. As I mentioned, the digital therapeutics over time are going to play an increasingly important role. There is a lot of training for the digital therapeutics that we're going to be going through over the course of the next couple of trials. The idea is to shift a lot of the heavy lifting from the person to the digital therapeutic again over time. Certainly, by the time we get to end of phase II, I'd anticipate that there will be a lot more standardization because of the digital therapeutics. I think that's going to really appeal to the FDA. Okay. No, that makes a lot of sense. Okay. Great. I do want to talk about PCN-101 just in terms of the phase II study that you're running. I guess just thinking about what the objectives are kind of of this phase II study, what are the key questions that you're really looking to answer with this study, and how is the study designed, I guess, to answer those questions? Yeah, that's a good question. It is important to ascertain efficacy, right? That's the most important thing. Do we, in fact, get a rapid-acting antidepressant effect, right? Can we see something in 24 hours? Secondarily, it's what is our redosing frequency, right? We are looking at 4 days, I believe, and 14 days, and 7 days, I believe. The question is, when do we redose? Of course, esketamine is redosed twice a week. We would love to get that down a little bit to once a week. Again, it's probably not as critical if the drug is administered at home, which actually gets to the third point, perhaps the most important point, which is around therapeutic index. We have two doses that we're looking at. Based on the phase I results, we know the 30 mg dose is completely sub-dissociative. I mean, essentially, the CAD scores were well within the normal range there. At the 60 milligram, it was riding the line, essentially. There was a couple of scores that were at or just above the 4, but essentially non-dissociative as well, but again, riding the line. We want to understand how 30 mg and 60 mg look, 30 mg in particular. Do we have a very strong, do we have a strong argument to make with the FDA for at-home use? Again, there's a lot of other extenuating circumstances here. It's going to be a relatively short-term therapy in the sense of it's several months at most. That's how we anticipate this. The idea is to drive patients to remission and then kind of do this on an as-needed basis going forward from there. I think we have some latitude. Of course, treatment-resistant depression is an indication with high unmet medical need and significant mortality and morbidity associated with it. Again, we think that we do have some latitude here. Okay. No, that makes sense. In terms of getting the FDA comfortable with the idea that you can use a form of ketamine in an at-home setting, I mean, is it as simple as kind of showing kind of normal CAD scores, or do you think that there is some other baggage associated just with the fact that this is ketamine from a regulatory perspective? I've done some regulatory work on this, so I'm just kind of curious how you're thinking about that. Yeah. It's a little tough to speculate, to be honest with you. I mean, the premise is a reasonable one. Insofar as the agency tends to be very data-driven, I think we'll be in good shape there. Of course, it all comes down to these results, right? These results are going to be quite key to making these arguments coherently. Again, we'll see at the end of this year. We're obviously very enthusiastic. We do believe that this will be borne out. Again, the preclinical data is what it is. It's preclinical, but it's a large amount of preclinical data. It's not a single study in a single lab. It's multiple models all showing the same thing. Of course, we have that open-label trial out of Brazil that is also consistent with the general hypothesis. Again, it's a little tough to speculate. If you ask the question now, you'll get it's a review issue. Of course, that's the correct answer, right? Because we do need to generate that data and truly understand what that therapeutic index looks like. Okay. Got it. No, that makes sense. I guess just going back to the study design itself, I guess how should we think about the types of patients that are being enrolled, what the baseline characteristics could look like, previous suicidal ideation or behaviors, those sorts of things? I think, obviously, with the Compass Data, people are really interested in kind of understanding the patient population and getting a better sense of what's kind of separating the indication from kind of what we see from a therapeutic perspective. Yeah. Just so that everybody in the audience knows, actually, a lot of the details here are publicly available. It's on the UDRAC site. It's not on the clinicaltrials.gov site because the trial is primarily being conducted there at this moment. To get to your question, of course, it's treatment-resistant depression. I would say that we are generally more open compared to a lot of other TRD trials, which of course helps. In terms of suicidal ideation, nothing within the past year. Of course, nothing active, right? No suicidal ideation, no homicidal ideation, no thoughts of self-harm, etc. The usual kind of criteria that are important for these kind of studies. You can't really rule out suicidal ideation broadly. For treatment-resistant depression population, that would exclude a nice chunk of your population. It's just not tenable in a TRD study to do so. MDD is a possibility, but not TRD. In terms of other baseline characteristics, they're allowed to have other medications. It's a shorter list, but you can have con meds here. HAM-D of greater than 18 is the other important piece here. Of course, we're looking at the MADRS as the primary endpoint. Again, a pretty typical design. Okay. Great. I guess just in terms of the types of patients that we should expect to be enrolled, I mean, should we expect something similar to kind of what the Compass Study showed? Enrolled something similar to I think the esketamine study has had slightly more severe patients. I guess how should we think about that? I'd say it's very comparable in many ways to the Compass Trial. I mean, again, these are not particularly unusual inclusion criteria for a TRD study. It is important that you obviously get those patients that are kind of on the more severe end. That is important that our criteria should accommodate that. By the time you get to TRD, by the time you get to HAM-D's in the 18 and above range, really kind of obsessing over those sites and working very closely with the investigators, you'll end up with more severe patients. This is pretty consistent, again, with Compass. It's also very consistent with the initial IV study that was conducted with esketamine. Okay. No, that makes sense. I guess just in terms of enrollment and how that's progressing, I know you mentioned expanding into the U.S. I mean, how should we think about the timeline for completion of enrollment and then top-line data? Yeah. I mean, what I can say is that so far we're on track. The plan is, as we've guided, to have top-line results by the end of this year. I know we talked a little bit about this initially, but just what you would define as kind of success. I know you're obviously looking for the therapeutic window, but I guess what would be a highly successful outcome in your view? How would that guide essentially the next steps of development? Yeah. I mean, it's important to think about the TPP, right? What's the end goal here? That is we want at-home therapy with a rapid-acting agent. Not surprisingly, it's exactly what you just said. We need to see efficacy, and we need to see efficacy ideally, we'll ideally see it in the absence of any significant dissociation or no dissociation, right? Basically, CAD scores for the vast majority of patients that are under the 4 threshold. That's what we're really looking for. Of course, maintenance over the course of certainly several days, ideally a little bit longer, right? That would be fantastic. Even in the context of at home, if you can do it less frequently, that makes life easier for everybody involved. Those are kind of the main things. Certainly, if we have a compound that is dosed twice a week, right, but has a therapeutic index that we believe makes for a very compelling argument to the agency, that would be a win. Okay. Okay. Great. I guess just my last question on PCN-101 is just I know you're working on a subcutaneous formulation as well. I guess what specifically you're looking for from a PK perspective in the bridging study that you're working on? Yeah. That'd be great. That's a good question. I mean, right now, it's a 40-minute infusion. The subQ tends to, I mean, subQ is a little bit variable, depending on the molecule, not necessarily so much on the person. Ideally, we'd like to see, obviously, we're going to target exposures that are comparable, right? The total exposure should be similar. Of course, the overall PK profile, we'd like to see something similar as well. We don't want it to be too peaky, right? If you start seeing very high Cmaxes to obtain a certain amount of exposure, that's something we'd have to think through a little bit because one presumes that the peakiness is what's going to drive some of the dissociation. Rate of rise is the other one. I mean, we kind of have to balance some of these parameters a little bit once we see the results. Of course, as part of this relative bioavailability study, we'll be assessing these parameters, right? How much dissociation the patient, the subject in this case, is experiencing, relatively speaking, between different formulations. Got it. Okay. That makes sense. I wanted to move on to your ibogaine program, so DMX-1002. I guess maybe if we could start at a high level, just going through the design of the phase I, phase II. I know I've gotten some questions from people just around how to think about really the goal of the phase I portion of the study versus the phase II. Maybe if we could talk about that too, that'd be great. Yeah. The phase I is a relatively straightforward design. It's a single-ascend dose study. A couple of things that we'll be looking for, obviously, are safety and tolerability as well as psychedelic effect, right? Safety, tolerability, not a big surprise. If you look at the literature, we're, of course, looking at cardiovascular parameters here. The literature really supports the notion that you need to get around 7-9 mg/ kg to get a real psychedelic or an entheogenic in this context effect. That's what we're going to be looking for. Does that get borne out in our normal healthy volunteer study? What does that look like in terms of we need to look at the PK in a more structured manner than what's been done in the past? Of course, again, looking at safety and tolerability. The idea, of course, is to pick one of the doses here and then go to a double-blind, placebo-controlled trial. That is going to be a pretty rigorous study, right? This is really going to be giving a single administration, looking at acute withdrawal parameters, but more importantly, looking at urine-confirmed abstinence for an extended period of time, 90 days. We are really looking for harms reduction here, right? That is the most important parameter here. Can you markedly reduce the amount of opioids that these individuals are taking based on a single administration of a compound? Absolutely. From just the phase I portion, I know I've gotten some questions from people around. I think you are using people that have a history of kind of opioid use, and you are incorporating some efficacy or kind of clinical endpoints as well, I believe, in the phase I portion of the study. Maybe if you could talk about do you expect to really what do you expect to kind of see on those kinds of endpoints in that sort of a patient population? I do want to talk about dose selection, but we'll. Okay. Yeah. We've actually softened that up pretty significantly. It is healthy volunteers at this point as well as those that have taken opioids in the past. Part of this is pragmatic. You can obviously find many more people that are healthy volunteers. We are looking for individuals that have some sort of past psychedelic use. That's mainly because the experience with ibogaine has been characterized as being somewhat challenging, right? In terms of a psychedelic experience, the anecdote is it's making you walk through all the bad decisions you made in your life and sort of confront them, which sounds great. It's something that's going to be rife for abuse. That's why we're looking at those individuals that have had psychedelic experience. Other than that, we're not really looking for any kind of efficacy there because of the broadening of the entry criteria. Okay. Okay. Got it. Just in terms of the dose selection for the phase II randomized placebo-controlled portion of the study, how are you thinking about assessing the therapeutic window? I know, obviously, cardiovascular side effects, as you mentioned, that's a key consideration with ibogaine. How are you going to be weighing some of the psychedelic effects and those sorts of things with the cardiovascular risk? I mean, clearly, this indication, opioid use disorder, has significant morbidity and mortality associated with it, right? That's what we're really trying to address here. There is a higher risk tolerance in many ways from a cardiovascular perspective, particularly because this drug is going to be, A, administered intermittently, and B, administered in a supervised medical setting. Again, this gives us a lot more latitude. It's not that we find any level of QT prolongation unacceptable. It just needs to be within parameters. Those parameters are things that we're working through with some very important and prominent cardiovascular experts. I mean, I think a lot of us are used to, myself included, thinking about QT prolongation in the context of an acute drug, I mean, a chronically administered drug, right? You start getting really freaked out when you get beyond 5 or 10 milliseconds. In the context of an acutely administered drug, things are very different. The FDA guidance does not really focus on this element, on this acute administration. When you talk to the cardiovascular experts, they are, yeah, much more nonchalant about even longer duration ones. I'm not sure that I am, but certainly they are. Yeah, again, we are just kind of balancing these things and working very closely with the experts to figure out what's going to be acceptable in this patient population. Okay. Okay. No, that makes sense. Okay. I guess maybe my last question on this one is just around timing. Timing of when we could see kind of the phase I and then maybe when kind of the phase II portion could start. Yeah. I mean, again, we're looking at phase I this year. Phase II, I don't think we've guided on that. I will get back to you on that point. Okay. No, that's fair. I did want to move to RL-007. I know you did have some data, of course, in that end of last year and earlier this year. I guess in terms of next steps and thinking about what a kind of Proof- of-C oncept study could look like in CIAS, anything you can kind of share at this point on the types of patients, the inclusion criteria, all that kind of fun stuff, endpoints, dosing duration? Yeah. I would say that a lot of this is still being sorted out. I mean, essentially, we're working very closely with, again, a very prominent group of KOLs in this space with our SAB and a little bit broader than that. I mean, that's really where we're at at the moment. It's not going to be a big shocker what this trial looks like, right? It's going to be a double-blind placebo-controlled trial. We saw that simple coding was important. Simple coding is an important element within the MCCB. MCCB is going to be an important endpoint in this trial. Simple coding is something that we want to look more closely at as well. These are kind of the broad parameters of the study and very focused on getting Proof-o f-C oncept here. We want Proof- of-M echanism in that first trial. We want to really get Proof- of-C oncept in the second one, something that really supports all the subsequent development, right? Again, duration things are still being sorted out. It depends very much on how the trial design is. Again, we do have a couple of different things that we're putting in front of our SAB and hashing out. We'll give guidance on this very soon, not surprisingly. Okay. No, that's totally fair. I guess are you thinking about potentially moving into other indications? I know we've talked about this before, but given the impact on cognitive tests, there are, of course, other potential indications that you could go into. How are you kind of thinking about that? I guess was there anything in particular in the Proof- of-M echanism data that suggested that there may be certain types of cognitive impairment or certain patient populations that may benefit particularly well from a drug with this profile? Yeah. That's a good question. If you, what did we, one of the key things that we focused on in that phase II A trial was quantitative EEG, right? Quantitative EEG was to essentially, it was extending the results of the old phase I scopolamine study into a patient population. What we saw was essentially beta, sort of to some degree gamma, augmentation. One way to think about it is focusing on those indications where this has some prominence, right? Another obvious indication would be autism. Autism is also characterized, at least large subsets of the autistic population are characterized by beta-gamma kind of lack of coherence as well as sort of lower absolute power level. That's something that would make a lot of sense in time. You could take that and broaden it out further. I mean, there's lots of potential indications all the way out to things like Alzheimer's. Right now, we're focusing on things that are relatively more homogeneous within that sort of window. Schizophrenia is kind of at the top. Then autism, if you can use a biomarker, in this case, some kind of EEG biomarker for enrichment, that might make a lot of sense. Of course, Alzheimer's is much more heterogeneous. Okay. Got it. No, that makes sense. In terms of GRX-917, I did want to ask a couple of questions about that because I know that is in phase I. I guess thinking about kind of what you're looking for in the phase I study here with this program, just given that it is based off of an existing molecule, yeah, I guess if you could just talk to us a little bit about that. I know you completed the SAD portion of the study. If you can give us any sort of quick takes from that data and what you're looking for in the rest of the study. Yeah. Some of the challenges that we faced with etifoxine because of the fact that it was an old approval is we really had no access to data, right? We had no understanding and no documentation of why they chose the dose they did. An important element of that SAD component of the trial was to do a real dose ranging trial, right? We did everything; I think it was 10 all the way up to 500. We had a very broad range of doses. We found very good safety and tolerability. I mean, I think that's kind of the long and short of it. That's very consistent with the nature of this compound. We were looking for greater metabolic stability because of the duration, right? That's obviously something that is widely seen, seeing if we can get some changes in serum half-life. Can't really say too much about it, but those were really sort of the foci of this trial. We also looked at quantitative EEG, a little preliminary there. We're going to have to combine all the data together with the SAD and the MAD to really have anything definitive there. That's something that we'll be talking about, certainly as the totality of the data comes in and when we discuss the results of this trial, which is sort of in the middle of this year. Okay. Great. I guess just thinking about kind of the next steps, I know obviously you mentioned we'll look at the totality of the data and kind of go from there. Just thinking about indications of interest at a high level, I mean, how are you thinking through that and how will the complete data set from the phase I kind of help guide that as well? Certainly the phase I data is important for dose selection, right? We're starting from scratch in a sense, I mean, intentionally so. We want to understand the compound itself, understand the safety profile, and make decisions around dosing in a rational manner as opposed to just sort of taking it sort of ad hoc. That's an important element that's going to come out of this phase I SAD/MAD. In terms of indications, I mean, part of our philosophy is to do a trial that gives us an answer in a short timeframe in a cost-effective manner, right? Something that's time-efficient and cost-efficient. That may mean that we do—we're certainly interested in anxiety. We're looking across a broad spectrum of potential indications there for the trial, right? There is a lot of predictive validity seemingly across different types of anxiety, be it SAD or MAD or situational type of anxiety disorder. There is a little bit more latitude if we want to get Proof- of-C oncept with this compound. We are looking at a bunch of different indications. Again, that does not necessarily read on what we ultimately end up developing. That is a different question. It is a way of really understanding the compound and getting a quick read on efficacy there. Okay. Great. I did just want to remind everybody, if anybody does have a question, feel free to raise your hand. We've got a couple more minutes left. I did want to just ask both of you, what other assets in the portfolio are you particularly excited about, especially if it's something that we haven't really talked about or something that you think the street is underappreciating? I mean, I can jump in with certainly the DMT asset. Pretty excited about that. I mean, again, it's a little bit like, what's your favorite child? I mean, there's a lot of really interesting assets. They are very different from one another. They target different indications. In terms of compounds, based on what we saw with psilocybin, a very good analog to psilocybin is actually DMT from a pharmacological perspective. Having this shorter duration of action, I think, is really exciting. We're going to be kicking off that phase I trial and not do this in the future. Really excited about that, understanding what our different formulation could look like, our transmucosal formulation. Yeah, very excited about that. Again, it's sort of a short-term thing. Of course, we have an MDMA derivative as well. I guess I'm really focusing on things that are coming up soon. Yeah. Yeah. Totally agree. I think zooming out a little bit when we look at the psychedelic compounds and our approach is to drive forward first-generation naturally occurring compounds. What Srini referred to is kind of what we call second-generation compounds where we tweak, I guess, through formulation and optimize the duration of effect for that window that Spravato established, right? This paradigm that J&J established. Because again, coming back to scalability, we believe we can leverage that to address the accessibility, the scalability question of the assisted psychotherapy therapies that we are having in development. I am also excited about this program. Again, we talked about digital because that's one of the more advanced ones where we will be in trials together with our digital therapeutics. Very excited to see data on that in hopefully not the too distant future. I guess the third pillar in the drug development approaches is to be third-generation. That is what we have been quite active in on the drug discovery side to also add more capabilities, orthogonal complementary approaches to EntheogeniX that you are, I guess, very much aware we are with Nina. In addition to that, added TryptageniX and Invyxis that in itself have, yeah, in our perspective, quite complementary approaches to that to, yeah, optimize those molecules that as a compound class have a lot of potential, but we believe that there is room for optimization. I do not know, Srini, if you want to go a little bit into detail how you think about that and where we are in terms of also EntheogeniX. Yeah. Don't get me started. We can talk for a long time. No. TryptageniX, I mean, EntheogeniX is the oldest of these companies, right? It's been around since 2019. It's done a lot of work, and we've got a lot of compounds that have come out of that. Because of the approach around computational chemistry, we have compounds that are totally different. They don't look anything like any other compound that's out there. That gives us a lot of benefits because we can make things a little bit more selective or a lot more selective. We're getting some really, we've got some unique properties. We've got compounds that hit the 5-HT2A receptor really hard but don't seem to elicit head twitch in animals. That's a proxy for psychedelic effects. We may have some very interesting compounds here that are non-psychedelic but very potent agonists at 5-HT2A. This is really interesting. Now, with TryptageniX, this is focused on biosynthetic approaches. This is intriguing because there are things you can make biosynthetically, enzymatically, that you can't make really with small molecule chemistry. At least you can't make them at any kind of scale. It is another avenue for improving a compound in a very site-specific manner and a very efficient manner. I mean, there are compounds that we have that are also synthetic or semi-synthetic. This is a means of getting those molecules in a way that's, of course, environmentally and, in this case, politically as well. Insofar as some of these compounds or these plants only grow in certain countries. There are a lot of advantages to that approach. Finally, there is a lot to be done. is still surprisingly a lot of white space around existing tryptamine compounds and ergolines and everything else. The Dalry-Adda collaboration Invyxis is really focused on that. It is partially IP but partially around pro-drug strategies and other ways of affecting better molecules around the existing structures. We are really focused on a small molecule from a small molecule angle. Yeah. I think if I had to sum it up or kind of summarize it in a nutshell, what I'm really excited about is really that we have this diverse pipeline that allows us so many different approaches that also addresses a very heterogeneous patient population. I think that's quite unique to us also that we have those multiple shots on goal, this rich density of news flow coming up. If you just look at the more advanced one, we have this year, as Srini alluded to, coming up with the perception readout, phase II Proof- of-C oncept, followed by Recognify initiation of a phase II, GABA phase I readout, phase II initiation, DemeRX phase I readout, again, phase II initiation. We'll keep you posted on that one, as Srini said, or I'll give you that information after this one. There are a lot of phase I initiations as well. All the programs where we also anticipate the digital therapeutic to be a core element, Viridia with DMT, EmpathBio, our MDMA derivatives, and Revixia, Salvinorin A, all phase I initiations over the next month to come. I think that alludes to the fact how much is going on and how excited we are to drive those programs and also receive data on the progress of those programs too. Absolutely. Awesome. I think we are a couple of minutes over, but I really appreciate you guys taking the time to chat with us. Everybody who listened in as well, I appreciate you taking the time. Yeah, it's been great. I'll let everybody go. Thank you so much for joining us again. I really appreciate it. Hopefully next time, next year, it'll be in person. Yeah. Looking forward to that. Looking forward. Yeah. Great. All right. Thanks, Nina. Thanks, all. All right. Thanks so much, guys. Okay. Bye.