Yes, good afternoon, at the Leerink Partners Global Healthcare Conference. I'm Marc Goodman, one of the biopharma analysts, and very excited to have Definium Therapeutics, which is the old MindMed, if you remember MindMed, so get used to Definium Therapeutics now. Thank you, Robert, for doing that to us. Robert Barrow, the CEO, Brandi Roberts, the CFO, thank you for joining us. Why'd you change the name?
Yeah, that's an easy one.
I always told Brandi she could say it so this one.
Yeah, that's an easy one. I mean, I think when you think of the names Mind and Medicine, they're kinda out there all over the place. There's wellness groups, there's therapy groups. We couldn't even have mindmed.com because a therapist has that web domain, and we couldn't get it.
Yeah.
We're getting closer to commercialization. We wanted to have a place where people could find us and make it easily recognizable, so we came up with Definium. It stands for precision and boundlessness, two things that are important to us.
Yeah. I mean, when you first told me, I was like, "Oh, really?" I kinda, you know? Now I'm used to it. Now I'm really used to it.
Good.
I really am, so it's all good.
There you go.
By next year we won't even remember the old name.
That's right.
Rob, kick us off with, you know, just broadly the quick, you know, overview of the company and then we'll dive into each program and talk about data and what's to come.
Yeah.
You know, just kinda high level, like how the company kinda, you know, has come together.
Absolutely. We've been at this for a little over five years in current embodiment. Over that time we've progressed, you know, coming up on data from three pivotal studies for our lead asset. DT120 is an ODT formulation of LSD that we're developing in generalized anxiety disorder, major depressive disorder. Three ongoing phase III studies there, 2 in GAD, 1 in MDD, and starting our second MDD study very soon. I think it's a lot most of the air time. We also have the second program, DT402, which is the R-enantiomer of MDMA which we're developing to target the core symptoms of autism spectrum disorder.
Very different approach, very different program, one that we're equally excited about, but of course, being in an early signs of efficacy phase II study right now doesn't get nearly as much attention as the.
Yeah.
LSD program for anxiety and depression.
Talk about just the company itself, like the number of people and just how it's grown. I'm just kinda curious, you know, what.
God, yeah, over the last five years we've grown from pretty much zero to about 120 people today and likely a bit more by the end of the year. It's been an incredible opportunity to bring in some really talented drug developers to put their minds around what we think is one of the most exciting programs in all of psychiatry, and to take a drug that's been known for almost 100 years, it's been sitting on the shelf for the last 30, 40 years, and so far has shown the best efficacy we've ever seen to treat anxiety and depression.
Yeah. Yeah. I'd like to go through each of the programs that we're working on and talk about the data that we have and the reason to believe that it's gonna continue to work. Where do you think we should start? Should we start with MDD or do we start with D? 'Cause normally I start with GAD.
Anywhere you think.
Now MDD's coming before. By the way, why is that? Why do they kind of reverse? Not that the timing was that much different. Yeah. Yeah.
Yeah. Absolutely. Two indications and 2 very parallel programs. They're mirror images of one another. We did a 5-arm phase II study looking at dose response, establishing dose response, selecting a dose. They're the only dose response study that's been done in our entire field to look at the appropriate dose in a patient population. We used that. We received Breakthrough Therapy Designation for the program in 2024. That led us to launch pivotal programs in, and again, both GAD and MDD. The first study in each indication is a head-to-head, 2-arm, roughly 200-patient study in GAD and 149 patients that's fully enrolled in MDD that'll be reading out in late Q2. As you mentioned, the first pivotal readout we have ahead of us.
The second study is the same except we add on a second control, a 50 microgram intermediate dose control, and there's a bunch of reasons for that. It has no bearing on the statistics or the interpretation of the data. It's basically there as a functional methodological control to try to confuse people who take the drug and feel something to not be able to reliably guess that they've gotten the active dose of drug. That's the concept at least. We started the two GAD studies first and we set up the MDD program at the same sites as those that were running the GAD program with the idea of being able to bring patients officially through to the MDD study. A lot of times in GAD, what we do is we exclude patients who have an ongoing depressive episode.
There are a lot of patients who have both, who have GAD and MDD and are in depressive episodes. The thought was when patient comes in, if they have elevated depression, if they have a depressive episode, then they're gonna be lost from the study, and instead of just having nothing for them, we'd be able to move them over to the MDD protocol and enroll them potentially in that study. That's exactly what we saw. That's really why.
And worked so well.
The MDD study exceeded.
Yeah.
Exactly.
Was faster than expected.
We started out with a backlog of patients who were sort of waiting in the wings, waiting for the trial to get activated, and we're able to bring in very quickly. You know, I think the reality it also reflects a reality of psychiatry over the last 30 years has been very much sort of trained and equipped to handle patients with depression. This is the drugs we've had. It's 20 years since the last approval of a GAD drug.
Okay. Let's go back and let's talk. We have an ODT version of LSD, basically. It's your own, you know, kind of version, patented formulation.
Correct.
Very different from the regular product, so to speak. Talk about the GAD study, the phase II study. Talk about the data. I think that's where we should start.
Yeah. Phase two, 5-arm study, we wanted to establish the dose response, we wanted to pick a dose, and we wanted to answer a bunch of questions that are always asked about this field. Let's sort of start with each of those. We did. The 5- arms were placebo, 25, 50, 100, and 200 microgram doses of drug. That spans. It's about a tenfold increase across that range, roughly. It spans a bunch of sort of discrete points in the pharmacology and the activity of the drug. 25 micrograms is the barely perceivable dose. People may or may not be able to tell that they've taken the drug. Turns out most can. We found about 90% of patients, even at 25 micrograms, could correctly guess they were on a drug.
Going up from there, 100 is about what prior studies have shown is sort of the peak perceptual alteration. When people take LSD, they feel differently. Now, quantifying that is difficult because a defining feature of that experience is its ineffability, its inability to put it into words. From a number of studies, we saw that I think a maximal activity in terms of the perceptual effects at 100 micrograms. What we wanted to do is see if you go beyond that, do you incrementally pick up efficacy? Do you have a worse AE profile? The analysis of the phase two study was a dose response analysis.
The primary statistical assessment was something called MCP-Mod that established first, that there is a dose response, and second, what that response is based on pre-specified response curves from the protocol. All that is to say, we ended up proving that there is a dose response for this drug, proving that the 100 microgram dose is the recommended dose. It's where we have maximal efficacy without, as you go higher than 100, you increase the AE burden and the duration of a treatment session. That allowed us to have the evidence to move forward and to pivotal program with that 100 microgram dose versus a placebo. The one other thing I'll mention is that there's always the conversation about functional unblinding and the reality that patients can feel the effects of the drug.
While we saw a clinical dose response across that range, at every dose, virtually everyone knew they were on the drug. For the first time, we were able to say, "That cannot be what is explaining the clinical response." Really important finding because it also teed us up to do a really clean phase III development program, which we're now conducting.
Yeah. Talk about the data itself. Like how good was the data?
Yeah.
What were you excited about?
Patients came in with a mean HAM-A score in that study of around 30, which is quite severe. Single dose of drug, follow them for 12 weeks. At the end of 12 weeks, on average, patients had a 21.9, almost a 22-point drop from baseline on an absolute basis, which is extraordinary. It's the largest response we've ever seen in anxiety. That was 7.7 units better than placebo, which is also on a placebo-adjusted basis, more than double the standard of care and the best data we've ever seen on anxiety. We saw a very similar response pattern on the MDD endpoints on the MADRS.
Pretty impressive. From there, obviously a lot of excitement, and we started those two other studies.
That's right.
On MDD, what have we done so far on MDD?
In that phase II study, when patients with GAD didn't necessarily have elevated, depression symptoms or as picked up by the MADRS. We saw patients with around mid-20s on the MADRS coming in-
Yeah, okay, that was baseline?
Around mid-20s. It wasn't as equally as balanced because we were not sitting in a depression population.
Yeah.
There too, we saw about an 18-point drop, 18.5-point drop, which was 6.5 points better than placebo, roughly.
Yeah.
One of the other things we saw is that we pretty much bottomed out the scale, you know. We took the vast majority of patients into what would, if we were treating depression, be called remission, which means we lose discriminatory power.
Yeah.
As we think about moving into an MDD population in a higher starting point, that gives us the ability to potentially even separate.
Yeah
Separate further. There's also some prior academic data looking at LSD and depression with some really exciting results.
I mean, that's really strong data. The question is, how do we set up expectations for the data that's about to come? Because I mean, are you, are you telling people, "Well, we're gonna replicate that data," or what, you know? Like, what are you saying?
Well, we'd love to, of course. You know, we think that this molecule has really truly best in class feel like data so far that have just sort of blown.
Yeah.
Blown our socks off, right. It's just been amazing. As close as we get to that, it'd be fantastic. When we look at the landscape for anxiety in particular, it's been 20 years since we had a new drug. Last drug approved was Cymbalta, right? Most drugs have not been able to show even a four-point separation from placebo. If we are able to exceed a four-point bar, that is the best drug that's ever been developed in this indication, right? The same would roughly be true in depression. The sort of best in class is between four and five points on the MADRS. We think of that bar, again, we exceeded it pretty handily in the phase II study. Of course, we would love to blow it out of the water again.
Can I just say, best in class is 4-5, so if you come back even with 5, like that's still.
Extraordinary. Yeah
Best in class.
Exactly.
It's not even disappointing because it's best in class.
It would be an incredible outcome for them.
Yeah.
That study.
Yeah. I look at GAD, it's just, there's just nothing there. Even, I mean, even if you're 60% or 70% of that type of benefit, it's still outstanding.
It'd be a great outcome. When we talk to providers, of course, there's a degree of enthusiasm for this entire field and for our program that, you know, I don't think is going to hinge singularly on a single, you know.
Yeah.
Single digit changes in the MADRS or the HAM-A. We again think we have a best in class molecule, and we want the data, of course, to support that, hopefully.
Right. Let's just come back on the subtherapeutic dose for just one second to make sure we all understand just that again.
Yeah
Repeat that in the study.
In one of the depression studies, one of the anxiety studies, we include this 50 microgram control. It's there, and we aligned on this program, this design with FDA. It's there so we can tell patients in the consent process, there's a dose of drug that feels like something, but previously we've shown doesn't work, isn't clinically active. That's what we saw in the phase II study. The hope is that we're. There's always a concern, right, with any psychiatry drug that is clearly perceivable, which turns out to be all of them. There's always a concern that if a patient just knows that they're on the drug, they're just going to say that they're better.
Yeah.
It becomes concerning if they're not telling the truth.
Right.
If they are better, well, great. The idea is with the drug with sort of these profound effects that are clearly observable and we've seen in the vast majority of patients, regardless of dose, to have a dose where you can tell patients, "You may feel something, but it is not clinically active," hopefully leaves them guessing. Saying, "Well, I did feel something, but, you know, I'm not just gonna say I feel better because maybe it wasn't a dose that actually worked." This is somewhat theoretical, right?
We haven't s een this in many studies. Importantly, that dose is there as a sort of operational control, but we don't actually analyze it. We're not interested in separating from it. We don't care if it separates or not from placebo or from the active dose of drug. It's there to be there, but at the end of the day, the data from it did not change anything about the outcomes of the study.
Talk about the actual just, I guess I'd call, logistics of a patient coming in and just what's happening during the course. How long are they there? How long is the experience occurring on average? You know, prep time before, prep time after. Just give us a sense of what's happening.
Yeah. What we do in our studies is what you would do in any trial. Just informed consent, dose patient, follow up. The unique thing here is that patient comes into the clinic, they're given the drug, normally in the morning. We keep everyone under observation, regardless of the dose or whether they get drug or placebo. We keep them under observation for eight hours thereafter. Largely looks like they're laying on a couch. Not a lot happening.
In a room by themselves, basically?
There's a monitor there to make sure that they have what they need.
The monitor's there the whole time?
Monitor's there the whole time. It's there for their comfort.
Right.
Right? If someone needs a snack, they need bathroom, or rarely, but occasionally, someone says. You know, has a hard time, and the monitor's there to reassure them that they're safe and they're being cared for, as you would in any setting such as that. They don't do much. There's historically been a conversation about doing concurrent psychotherapy, but that's not done in our trials and really would. People who take high doses of LSD, of 120, aren't in a state where they want to talk all that much and just don't. It's a pretty internal process that plays out. The patient largely lays on a couch and often has eye shades or music. Writing materials, reading materials.
How long is the process? It's a full day, I think.
They're for 8 hours. Part of that is because we want to have a well-defined data set to establish when patients are ready to leave a monitoring session. There's always this perception of some of these drugs, and LSD is one of them. People say, "Oh my gosh, it lasts for so long." They're referring to, you know, use outside of medicine, use out in the real world where with a drug that's dosed in micrograms, you know, small changes in volume can mean huge changes in exposure, and we know that there's a dose-dependent duration. Really what we're saying, we're starting to assess readiness to leave in our studies at hour five, and we do that on an hourly basis until a patient is ready to go.
Really, we have accrued enough open label doses at this point where we feel really comfortable with that window, where by eight hours, you know, the vast majority of patients are in a state where they're able to leave the clinic.
I guess next to talk about is the market. Like, you know, maybe Brandi could give us a sense of just.
Yeah, this is a.
How do you-
This is a giant market.
How do you view this opportunity?
Yeah, I mean, there's 50 million US adults in the US with GAD and MDD, and so this is something where there's a significant unmet need. As Rob said, there hasn't been an approved drug in GAD since 2007, and the incidence of GAD has increased from 3.5% to over 10% in the last 10- 15 years. This is something where patients are really looking for options that can be helpful. I think we're seeing a tremendous amount of excitement on the GAD side, specifically because we have the phase II data to talk to people about. Because there are so many overlapping symptoms of both GAD and MDD, a lot of excitement about both indications and pursuing both of them.
Yeah. How do you think about just the landscape and, you know, your. Let's just fast-forward and assume your product is approved. Now what?
Yeah, absolutely. We know that there are about 7,000 providers out there right now who support patients with GAD, and those are a great place to start. A lot of those providers are also familiar with Spravato and are REMS certified to be able to use Spravato. You know, we expect that we would have a REMS for our product as well. One of our aspects in thinking about commercialization is, how do we prepare those sites to be as ready as possible to implement something like DT120 if it were approved? This is not just having sales reps.
This is also having people who can help with understanding the REMS, the administration that needs to occur, how to work with payers, how to make sure that insurance covers this. Really thinking about it from that holistic view of how to make this as easy as possible for sites to administer DT120. You know, this is something where they're gonna get paid for monitoring the entire time. When you think about a session that is somewhere in the 5-8-hour timeframe, they would look to get paid for and compensated for that amount of time, and we think that that's absolutely acceptable for a product like this as well.
Let's talk through the economics.
Sure.
Make sure we got this. Patient goes to a site. They're there for eight hours. The site is getting paid for the eight hours.
Yes.
From insurance, right?
Yes.
So hundred-
150.
$50 an hour.
Yeah. Sure.
The site's getting paid for eight hours. We've really got a problem. It's like we're in the middle of a hotel.
Yeah. To the people online, there are small gnats, yes, in the room.
Yeah.
Yeah.
It's Miami, it's fine. They come in for eight hours, the site gets paid for the eight hours, right? The patient is in a room blindfolded. Is there gonna be somebody in the real world having to sit with them in the room, or can they sit in the other room? Like, how's that gonna work?
There's of course gonna be a dynamic and, you know, the finalization negotiation of label and REMS that you know, it'd be premature to say firmly exactly what that is going to be.
It's possibly the way.
I think the reality is that we've gone to great lengths to document what happens in the trial, why someone who's monitoring a patient intervenes if they have to intervene.
Yeah.
Really it's something that we very, very rarely see there being a need for any sort of intervention.
Yeah.
There's gonna be necessarily a variety of practice patterns. Our goal in the development program has been aimed at trying to maximize the flexibility and adoption. If it's a site that has multiple providers that wants to see many patients at a time, that could be possible, or if it's a small office, a solo practitioner, there's a pathway for them to do that with their patients as well. It requires a ton of data, and of course, we have to do this really responsibly and thoughtfully. We've been aggregating those data across phase II and phase III programming and feel like we'll have a great data set to stand on to support that flexibility.
Let's come back to that line of thought. We have the patient comes in, eight, we'll just use eight hours just as a number. They get paid $100-$150 an hour, right? How much are you thinking about the cost for the product?
Yeah. I mean, obviously, it depends on the data, so it's a little premature.
Yeah
To talk about pricing, but Spravato pricing is roughly $28,000 a year low dose, low frequency, to about $70,000 a year high dose, high frequency.
Right.
When we talk about those ranges and we've, you know, had our preliminary conversations with payers, you know, those ranges are something that is acceptable. You know, the administration of Spravato is difficult. You have to come in, you know, up to 56 times a year, and so often you see patients not be able to continue through an entire, you know, course of a year because that's just a burden. That's a burden on being able to come in that often. We think that having a drug where there is a lot less administration, you know, we showed durability out to 12 weeks in our phase II. You know, we're following patients the whole way out to a year, so we're gonna see how long that durability stays.
You know, for something where a patient would only need to come in 1-3 times a year, that's a big difference in terms of the Spravato frequency. We think something in that price range absolutely makes sense, especially if we are able to show, you know, greater efficacy as well.
Let's just use 40. Whatever. Just something.
50's round.
50. We'll use 50. Okay, $50,000. Let's just say that in the open label, we do see that the therapy lasts 12 weeks. Every 12 weeks you've gotta come back. Are we pricing it for $50 for the 4 times you'd come in per year, let's just say? Is that how it would work?
I mean, we're thinking when we're talking about these prices, we're talking about annual pricing.
Annual.
So-
We would just take 50 divided by 4.
Divided by what the-
If it ended up being three, if it ended up being five, or whatever the number of times to come in, that's how you're thinking about pricing.
There's one obvious model that's the easiest sort of to take to talk about on stage. Let's-
Right.
You know, there's a lot of work. We just brought in an incredible head of market access who's gonna, you know, be doing a ton of work to make sure that we're optimizing for that. 'Cause one of the things that, you know, we think we believe is that the real world activity of the drug may even be able to outpace what we're able to show in trial. It's hard to monitor people for many years, right, in a clinical trial, and if you're seeing a multi-month or a multi-year effect in a lot of patients, that's incredible value that you're offering not only to those patients and their lives, but to the healthcare system at large.
'Cause these are patients who require a lot of medical care, a lot of attention, a lot of visits to the psychiatrist's office, and a lot of very high-priced treatments that often don't work. Those treatments are just effectively wasted money if they're not getting any benefit from them. If we're able to drive a consistent and high magnitude and durable benefit, this is an incredible value. Making sure that we approach this so that patients get the best care, that we can maximize the access and actually make a dent in the problems we're trying to treat and do so in a thoughtful, economic way, that's really how we're gonna approach all of this.
I wanna circle back to the duration because you threw out the 12-week number. Talk about the data that showed the 12 weeks. What study was it? How many patients? What was the performance at 12 weeks?
Yeah. The phase II study that I described before, the five-arm study, when we looked at head-to-head comparisons between 100 micrograms and placebo, the numbers I was saying, 22-point drop, 7.7 units better than placebo on the Hamilton Anxiety Scale, that was 12 weeks after a single dose of drug. Patient comes in, they sit in a room for a day. In that study, half of the patients who received 100 micrograms were in remission for 12 weeks after the treatment. Of every two people that walked in the room, one of them had no detectable anxiety three months later.
We didn't see any sort of reversion back to baseline, so these patients were one would like to be able to extrapolate and say, "Oh, maybe they would." We just didn't see that. For those who responded, and on average, we see this many month durable effect, and we just stopped looking at 12 weeks. In the phase III program, we're gonna be assessing patients for a year.
Yeah.
After 12 weeks, they have the ability to take open-label drug if moderate or worse symptoms return. For those who get a single dose and are just better or in remission, or have mild symptoms for the entire year after that, we could show up to a year of durability.
How often were the measurements taken in the phase II?
We took measurements at weeks 1, 2, 4, 8, and 12. Basically once a week, and then.
The numbers that you were quoting before, the performance, that was at 12 weeks?
12 weeks after
Did it start to break early? Did it get worse? Did it get better? Like, just give us a sense of how the 12 weeks progressed.
The Hamilton Anxiety Scale is a one-week recall instrument, so we can only measure it one week after dosing. As early as we measured it, we saw this same magnitude of effect, plus or minus a point or so.
Right.
We can use.
That was just, you know, almost straight.
Down and a flat is what we observed. We can look at more momentary assessments like the Clinical Global Impressions - Severity, CGIS, which is used here in a bunch of different disease areas. Within a day, we can pick up a change there. We measured it the day after treatment, and we already see a multi-category improvement from-
Yeah.
On the CGIS. The degree of impairment is helped within 24 hours and seems to be durable for many months. That kind of profile is just something that is far, far and away different, and we would argue better than anything we have today.
Yeah, it's interesting also, I mean, your studies have already started, so obviously, you know, we know exactly what you're thinking. But some of the other studies by some of the other companies in this space, they've done a dose and then short period of time later, another dose. You know, I guess you'd call it double dose, whatever you wanna call it. Like, you're not taking that approach. You know, I'm just curious, like, what your thoughts are just broadly about that.
Broadly, we're really confident in the efficacy of a single dose of this drug.
Yeah.
You know, we don't think on average we would need to redose patients, and we're gonna.
Right.
We're gonna do the studies to prove that out. Beyond that 12 weeks, in the 9-month extension phase of the study, we'll be able to see this, right? We'll be able to look at what will be more like real-world utilization patterns. As a patient who gets placebo, makes it through to the extension, takes open label drug and say they needed a second dose a few months later, we'll see not only what that use pattern is, but what the response is thereafter. So we can characterize, we can observe, we can describe that in a way that would be incredibly helpful and I think useful for prescribers and labeling and everything.
We don't need to discount the efficacy of our drug or the durability of our drug by having different dosing regimen that we're not just replicating the single dose activity of the.
In our last few minutes of time, let's talk about 402.
Yeah.
What is it? Why are we excited about it? Autism, there's really nothing.
Yeah.
You know, what makes you think that this should work, you know?
Yeah. 402. I mean, 402 is the R-enantiomer of MDMA, which we completed a phase I study, single ascending dose study. Obviously MDMA has been studied in a sort of session-based delivery modality alongside therapy and things like PTSD in the past, some pilot studies actually in the autism population. Our approach is quite different. We like to draw analogy with psychostimulants in ADHD, which is that the core deficit and the thing that patients with autism, individuals with autism say they want out of drugs are enhancements in social communication skills.
It turns out to be the very thing that MDMA or R-MDMA in particular seems to do in everyone, is enhance people's ability to perceive of emotions in themselves and in others and communicate about those, which is why it seems to work so well in addressing.
Makes perfect sense. Why no one else has done it?
That's a great question, Marc. No, I think when we look at this opportunity and we say, "This isn't gonna be." We're very clear about this is not intended to be sort of disease modifying or a single treatment that's gonna have some long-lasting effect. Really what we're doing now is a 20-patient open label study where we're bringing patients in and treating them and asking, you know, "Is it enhancing these things in the way that.
Right.
You know, everyone else says it does, and is that seemingly beneficial?
A real proof of concept study.
Real proof of concept, signal detection, trying to see.
Yeah.
Is there something there that's worth following up on? If so, then we start looking at more like regular use patterns, whether that be, you know, daily, weekly, some regular interval. The concept is while the drug's on board, someone would have the ability to engage and communicate socially better than they otherwise would. The drug comes off and that they return back to normal.
Why the R-enantio mer version?
The R-enantiomer has more serotonergic activity and in preclinical studies is associated with more of the prosocial effects of MDMA. The two enantiomers have quite distinct activity. S-enantiomer seems to trigger a lot more dopamine signaling and have more of the stimulant-like properties, whereas the R-enantiomer primarily drives those social connections and empathogenic qualities that we talk about with MDMA. Looking at that preclinically and then taking it into the clinic, we saw a very similar sort of response pattern.
Yeah.
Between the PK/PD profile of those two enantiomers and gave us confidence to go into an early efficacy study.
Yeah. atai is kind of thinking about the same idea, aren't they a little bit?
Yeah. No, I think there's multiple approaches for this molecule being considered. I think that one's a little bit differently, more of that sort of session-based.
Right
You know, trajectory altering, disease modifying kind of a approach that they've been taking. You know, we think there's, with a lot of these drugs, there's potential for multiple use patterns.
Yeah. Anything that we didn't hit? Any.
Oh, so much, but we only got 8 more seconds, so.
Well, I-
Three catalysts coming.
I'll explain.
Coming soon.
10 seconds over if you want. Like, obviously three catalysts coming this year is pretty-
Yeah
Amazing.
Yeah. We expect, you know, Emerge MDD data in late Q2, Voyage first GAD data in early Q3, and then Panorama, the second GAD study in the second half of this year. So a lot to look forward to.
Yeah, good to hear. All right.
Thank you so much, Marc.
Thanks.
Appreciate it.
Thanks for coming.
Yeah.
Good luck going 3 for 3.