Good afternoon, everyone, and welcome to Morgan Stanley's Global Healthcare Conference. I'm Sean Lummen, Head of U.S. Smith Cap Fire Tech Equity Research here at Morgan Stanley. Before we commence, for important disclosures, please see Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you do have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have the Centessa Pharmaceuticals CEO, Dr. Shahram Sahar. Welcome and thank you for your time today.
Thank you, Shahram.
We will come back to these macro questions, Katherine and Michael, but maybe just to commence proceedings, if I invite you to make some opening remarks, Shahram.
Yeah, no, thank you, Sean. Thanks for the invitation to speak. Incredibly exciting time at Centessa Pharmaceuticals, given the progress we've made with our orexin agonist program. I think more importantly, you know it's an exciting time for the orexin agonist space itself. Key members of our team have been on the ground at World Sleep Congress in Singapore over the weekend, and just the sheer excitement of what this class of drugs can do as completely transformative for patients who desperately need a drug to keep them awake and bring them back to being potentially functionally normal is just fantastic for the entire space.
Awesome, thank you. Maybe just for those that might be a little less familiar with the narcolepsy space, can you give us an overview of narcolepsy and other disorders with excess daytime sleepiness, and how do NT1, NT2, and IH differ in terms of pathology and diagnosis and treatment options?
Yeah, sure, I'm happy to. I mean, this is an area that's 25 years in the making with Emmanuel Walter at Stanford, a physician scientist who made that original discovery so many years ago that showed that narcolepsy in dogs at the time was caused by a genetic mutation in the orexin receptor 2, which led to deficient orexin signaling. Subsequent to that, it was found that this so-called medical mystery of why patients have cataplexy, loss of muscle tone, or excessive daytime sleepiness could give rise to this interesting human neuro condition. It was identified that deficiency in orexin signaling was the underlying cause. With narcolepsy type 1, there's a deficiency in just the orexin peptide itself below a certain threshold level that circulates in the brain.
Because of that, I think that it's an exquisitely sensitive population, a great population to study from a proof of concept standpoint, and whether a small molecule pharmacologic equivalent of what the orexin peptide naturally does could do to re-stimulate signaling of this receptor and bring these patients essentially back to normal again. Those patients suffer from narcolepsy type 1, from cataplexy, from excessive daytime sleepiness, and a number of other comorbidities. Narcolepsy type 2, defined as not having cataplexy generally, and then idiopathic hypersomnia, which is a large indication, has other diagnostic criteria that don't necessarily fall in narcolepsy type 1 and narcolepsy type 2.
Wonderful. What are your thoughts on the prevalence of the number of patients that are currently treated?
Yeah, so it's really remarkable that there are a large number of patients. It's 80,000 with narcolepsy type 1, more with NT2, and nearly double that with idiopathic hypersomnia. I think the important point here is, while only a subset are diagnosed, a very small number actually are treated because of standard-of-care drugs today that aren't really treating the underlying cause of the disorder itself, which is, in the case of narcolepsy type 1, a deficiency in orexin signaling. For the first time, with orexin agonists, you have actually a drug class that can treat the underlying cause, making it really one of the most exciting classes of drugs to emerge in decades in neuroscience.
We talk about these drugs as just affecting excessive daytime sleepiness and minimizing that, both cataplexy, but with the data we've seen from companies that have presented data on orexin agonists, that cognition, attention, these other features that, frankly, keeping everyone here sitting upright and hopefully paying attention is largely due to the orexin in your system. There is something to be said about this class and the potential beyond just the rare hypersomnias. That's what we're excited to explore with actually our second orexin drug that's already in the clinic right now, ORX-142.
Wonderful, Shahram. Maybe could you give us a bit more insight into the mechanism, particularly into NT1 with the orexin receptor 2 pathway?
Yeah, as I mentioned before, when you have a loss of orexin signaling, there isn't the orexin peptide, at least in narcolepsy type 1, that's present in orexin A peptide. Small 33 amino acid peptide stimulates orexin receptor 2 signaling, which then triggers a cascade of neurotransmitter release: serotonin, histamine, norepinephrine, acetylcholine. It's a beautiful kind of cascade that allows us to function, again, as I mentioned, in the morning and throughout the day. As the evening comes around, the levels of orexin decrease, at least in most of us who have the natural peptide circulating, and then we fall asleep. Stimulating this pathway through exogenous means through a small molecule is effectively modulating a system that's been hardwired since evolution, since the beginning of our species, which is remarkable science.
The precision in which you can do that with a small molecule now, and at least our company's understanding of how you can generate the pharmacokinetic curves necessary to mimic the pharmacology of the endogenous peptide, is quite remarkable.
Sure, thank you. Moving over to NT2 and idiopathic hypersomnia, what gives you confidence that orexin receptor 2 agonists will be beneficial in these two indications, given normal levels of orexin?
Yeah, so these patients suffer from sleepiness as an issue. What's, I think, very interesting, and we've shown this in our phase one setting, is that if you have normal orexin levels, you know, folks like hopefully most of us in this room, you can actually give an orexin agonist, like we did with ORX-750, to people at 11:00 P.M. at night, sleep deprive them all night, and then take measurements on kind of inducing, you know, forcing them to try to go to sleep under so perfect conditions at four time points during the night, all the way till 7:00 A.M. What's remarkable is you can keep people awake all through the night, as we've shown in our data at the 5 mg dose, single dose, and keep people essentially normal at 7:00 A.M. when they're neither alert nor sleepy.
That gives us confidence that beyond narcolepsy type 1, where there's actual lesion present in the orexin kind of pathway and they don't have the peptide, even in normal orexin tone settings like NT2 and IH and even beyond, these orexin agonists may be effective. There's also some clinical precedent to show that as well.
Yeah, wonderful, thank you. Is a kind of safety profile needed for Centessa in NT2 and idiopathic hypersomnia, you know, given that you might have to dose higher?
Yeah, so what we've noted, I think this is largely data that's been generated by others, is you need higher doses in the NT2 and idiopathic hypersomnia populations, as well as probably others where there's an intact orexin system because you're working on a system that's already in place where there's endogenous orexin levels present. It's different in NT1, where you probably need two to three times less of a dose because the system is essentially deficient in signaling.
Wonderful. Onto ORX-750 in the competitive landscape. For your lead program, ORX-750, can you help describe some of the PK/PD properties and structure-activity relationships that help to differentiate the molecule from other orexin receptor 2 (OX2R) agonists?
Yeah, we're obviously very super, super excited about ORX-750, especially after seeing the data from others this weekend, in that the molecule just has an exquisite PK profile. The properties of the molecule allow it to be dosed once daily. It is a once-daily drug. The properties of the molecule also allow it to be dosed in split dose settings. It's remarkable. You can do many things with this drug in terms of being flexible and whatever a patient would ultimately need. The way we designed this molecule is based on a proprietary crystal structure where the team was clever enough to introduce a couple mutations in the orexin receptor 2, which allowed a conformational change that allowed screening of the orthosteric binding pocket of the natural ligand.
That allowed for the med chem to be able to solve for the current structures that we have that are in the clinic today.
Wonderful. Looking back to the phase one healthy volunteer data, can you remind us what you showed on the maintenance of wakefulness test and the Karolinska Sleepiness Scale?
Yeah, at the 5 milligram dose, we've showed across the four time points during the night that we were able to keep people awake for greater than 30 minutes. I think we had an MWT of around 38 minutes on average for all four time points. Our TSS score was right in the middle, which is neither alert nor sleepy. It's exactly where you'd want to be at even 7:00 A.M. in the morning, which is remarkable. If you try to stay awake all night at 7:00 A.M., I think it's very hard for a normal person to do that. With an orexin agonist on board, you kind of are normal even at that point in time.
Wonderful, thank you. Can you give us an overview of the ORX-750 Phase 2a CRYSTAL-1 study for NT1, NT2, and idiopathic hypersomnia, and any feedback you've received following the presentation of the study design at World Sleep Congress?
Yeah, so at Centessa, we first entered the clinic with ORX-750, I think it was May of last year. It's remarkable, and now we're already thinking about pivotal studies. We were able to be very creative in our phase one design and go through that in just a matter of months. The phase two design, we did something somewhat non-traditional in drug development, which is real-time drug development. What does that mean? It's more than just adapting a study. It's doing it real-time in the setting of both NT1, NT2, and IH. Essentially, we have three studies ongoing, and we had a starting dose that we declared: 1 milligram for NT1, 2 milligrams for NT2, and 2 for IH. We run those cohorts with a small number of patients, with a minimum number that we dose. Then we unblind the data and we look at it.
We decide, okay, do we need to go up or do we need to go down? What do we need to do to get to a desired profile that maximizes on MWTs and efficacy in general, as well as is tolerable? That's very different from a priori picking doses and then randomizing and then waiting a period of time and seeing what the data looks like. This type of design allows us to be very flexible. It's important with the orexin pathway because it's an agonist. The PK matters. The dosing matters. Until you actually go into patients, you don't know really what to expect. We really wanted to give ourselves maximum flexibility to be able to optimize the doses we had into phase three.
Yeah, wonderful. Thank you, Shahram. When can we expect to see first data in all three indications? Would you plan to release them in tandem or separate top-line releases?
We've said, and we are reaffirming that in 2025, we intend to share data in NT1, NT2, and IH. We'll also have data from ORX-142 this year as well in healthy volunteers and our phase one data. We're sticking to that.
Okay, great. Thank you. Just to touch on it, your OX2R field has seen past liver toxicity and visual disturbances, urinary frequency or insomnia. Which of these do you think are on target versus off target effect? To what extent can the insomnia be managed?
Yeah, so I'd be guessing to be able to say which are on target, which are off target. I think the totality of data from others here will probably give directionality as to which ones are on target, which ones are off target. I think what's really important to understand is that each one of these orexin agonists is largely determined on a molecule-by-molecule basis on what their kind of pharmaceutic properties look like. What does the PK look like? As an example, in our screening funnel, we wanted to make sure we minimize the Cmax to Ctrop ratio. That was in anticipation of two things. One is that there may be inadvertent kind of triggering of the orexin signaling cascade if you have too high of a Cmax when you dose in the drug and you want to minimize that.
The second is that any AUC, any area in the curve under that is kind of not useful, if you will, because what you're attempting to do is to make sure the tail of that exposure curve stays above the wakefulness threshold through the duration of the intended time points you want, from 8:00 A.M. to early evening or beyond. I think that's something that's not discussed as openly as I would like folks to understand, is that an MWT is an average of four time points. Generally, when we test these drugs in patients, drugs given at 8:00 A.M., and then you do these MWT tests, you go in this room and you measure up to 40 minutes how long you're staying awake at 10:00 A.M., 12:00 P.M., 2:00 P.M., and 4:00 P.M. A person's day, a patient's day doesn't end at 4:00 P.M.
You want to maximize that MWT as long as possible. I'll just throw out hypothetical numbers to make a point here. If you have an MWT in your first session of 40 minutes, second session 30 minutes, third and fourth sessions 25 minutes, 25 minutes, that's an average of 30. That's pretty good. If you have 40 minutes, 30 minutes, 25, and 15 minutes, it's 27.5. If you looked at 27.5 versus 30, you'll say that's a two and a half minute difference. Not a big deal. You're looking at two completely different drugs. Because one drug, for the most part, will keep most people awake at 4:00 P.M. if they're at 25 minutes, let's say, versus the other drug, which you're at 15 minutes, and most of the people will be asleep.
When you look at patient-reported outcomes, it's fantastic to see that patients are feeling normal and they're benefiting, which is great. Those are done retrospectively. The bar is relatively low there. It's not as quantitative as an MWT is, especially at the later time points. You really want to be able to maximize your MWT as much as you can. I think to your earlier question, the pharmacology of the drug is to keep people awake. That's where you ultimately want to push as hard as you can to get, you know, I kind of jokingly say push them to insomnia, but that is the pharmacology of the drug. If you can get there and then you can back down, that means you're keeping them awake as maximally as you can.
What you don't want happening is you don't want something inadvertently preventing you from getting to the pharmacology of the drug, some untoward AEs, for example. That really would define a best-in-class drug. After seeing the data this weekend, we potentially have a best-in-class drug.
Wonderful, thank you. I do get a lot of inbound on this question. Just to try and be clear, can you help walk us through what was for ORX-750 in its phase one SAD and MAD safety data?
Yeah, you're testing my memory now. I believe we did, I'd have to go back and check, 1 milligram, 2, 2.5, 3.5, 4, and 5. I forgot what the MAD data ended at. We've since dosed much higher and feel very good about the safety profile. We've kept the phase one open for that reason. Largely, this is the way we like to think about developing drugs, not to presume anything. We want to give ourselves as much optionality and flexibility as possible should we need it. I think the data, if I recall correctly, that we showed in our phase one setting was very good data when it came from the tolerability aspect as we increased dose. There wasn't too much of a difference between placebo and our drug.
We saw some of these effects that were coming up in terms of polycarrier and others, but for the large part, the safety profile mirrored what you'd expect in orexin receptor 2 (OX2R) agonists to be.
Yeah, wonderful, thank you. I guess, you know, we just have gone past World Sleep Congress and there were some competitive data readouts. Does that inform the way that you'll release data? Maybe, you know, does it further emphasize to you, you know, the differentiation that ORX-750 might have?
Yeah, we weren't, you know, in some ways, the data that we saw was in line with what others had shown, I think, in their previous trial settings. There was some difference, obviously, in the MWTs on the lower end. Really, the way we like to think about it, especially after this weekend and seeing the competitor data sets, is we're largely, that's great, but now we're thinking commercial. I mean, we're thinking, how do we maximize the potential of this drug to make sure as many patients benefit as possible and to be the dominant Rx and franchise out there, starting with 750 in the rare hypersomnias? That's where our head is, and our head is really in just maximally developing this drug for optionality and as fast as possible to get into phase three and obviously the market.
It's less about, you know, it's more like just drive, forget the noise. You've seen that one movie. That's kind of what we've always been like. Let's just develop this as best we can. I think that that's hopefully what's going to serve us well.
Sure. Would it be best to push NT1 out the door first? Is it more trying to get them all together so it's kind of one option for a treating physician? What's the thinking around that? Given it looks like you'll be the first molecule potentially in all three indications, but others might be there first in NT1.
Yeah, I mean, look, it's a great place to be because having one molecule across all three indications, I'm a physician, you know, I think the MDs in the room can appreciate time is very valuable and you don't want to think very much. The patient walks in the door and you don't really know if they have cataplexy or not. You don't know if they're NT1 or NT2 or even IH. There's a lot of ambiguity there between what diagnosis the patient really has. You want to have one molecule that serves the entire population, so you don't have to think very much. You start them at a certain dose. If you think they're NT1, but maybe they're not doing well and you go up and maybe they're NT2, so they need a little bit more.
Maybe you go to a higher dose with NT2 and then they're really NT1, you go back down to a lower dose. That's the kind of optionality that one has with one molecule across all three indications. We aim to be best in class in NT1. We aim to be best in class and first in class with NT2 and IH. This is more reaffirmed by potentially the data that we saw this weekend to have that ability to say that. Our goal really is one molecule, three indications, and try to get that done all at once.
How do you expect this class will change the mindset of treating physicians? You think about Oxybate's out there, but you've got something now that potentially treats the underlying cause. Do you think there will ultimately be a polypharmacy approach? Do you think the orexin receptor 2 (OX2R) agonists, particularly ORX-750, might supplant Oxybate use? What's your best guess of how that plays out?
Yeah, the safe answer is probably to say, you know, all these drugs will have a place. My gut feeling says that the orexin agonists will dominate, likely be monotherapy for a large portion of the population. Why do I say that? It's because to date with the orexin agonists that have read out data in patients, I don't think the question's been answered completely on disturbed nighttime sleep. I think drugs with the pharmacokinetic properties that may be too short of a half-life, for example, or their MWT doesn't allow, based on what we've seen at least, that there's enough exposure of the drug on board into the evening where you need some orexin exposure tone potentially to deal with disturbed nighttime sleep. I think that's pretty well established.
I don't think the question has been answered by orexin agonists on whether or not disturbed nighttime sleep can be addressed. Hopefully, we'll be the first to do that. The question around oxybate then becomes, if disturbed nighttime sleep is addressed by orexin agonists, cataplexy is addressed by orexin agonists, and EDS obviously, then what role does an oxybate really have? I think that question is still unanswered, at least with publicly available data. I think that's something that's really exciting for us to redefine the space. The big question is, I think I've mentioned, is that ask patients, how do they feel between 4:00 P.M. and 10:00 P.M.? If the drugs that have at least shown their data from our competitors are not working in that time frame, then they're probably going to need polypharmacy, right?
They're going to have to take a stimulant of some kind or piggyback on an oxybate or another drug. Not ideal. While the data's been really good for the field and certainly a game changer for patients, and I think everyone can breathe a sigh of relief that the orexin agonist class is now de-risked, there's a lot of room for improvement, especially on your question of what happens in the context of polypharmacy.
Thank you. What sort of groundswell of feedback do you have from potential treating physicians on the class? Do you think this will, I mean, it's ultimately going to depend on the efficacy and the safety, but what's your feeling on the uptake and the ease of any ramp post-launch?
Yeah, I mean, look, you see all the data. You've done some of the work yourself, right? Others have, and we read it, and we've done our own work on talking to KOLs and a large number of physicians about what to expect, what might they, you know, want to see, and how are they viewing the Rx and class right now. Just tremendous excitement. I mean, this is, look, you're going from single-digit MWTs to the 20s, right? Hopefully better than that in the future. These patients are, you know, feeling more normal than they ever did. I mean, the bar is pretty low here. They suffer quite a bit. There's generally almost euphoric enthusiasm across the entire sleep community on the physicians who are treating these patients, which rightfully so. They finally have something. I think the definition of normal will change over time.
I think once you start getting the next gen, I think the first gen drugs that are out, you know, right, they're showing data now are good proof of principle, that kind of, you know, that situation. When the next gen drugs like ours come on, it should redefine what potentially a new normal could look like for these patients because they don't know yet. They don't know what we're possible yet. I think providing a drug that can act in the duration that they want it to act is probably the most important and with a good tolerability profile.
Thank you. You mentioned earlier you've done some pretty cool work on the crystal structure and the medicinal chemistry that you won't show us the crystal structure, but I'd love to see it. You know, how much confidence, knowing that you have that, that you've probably got the best fitting molecule to the binding site, and you know, you're going to be able to continuously dose lower than potentially competitors. Just to get your thoughts around that competitive dynamic and that neat medicinal chemistry.
No, it's great. Yeah, yeah. I mean, look, I'm taking all the, you know, I'm speaking about this, but the real credibility for Mario and his team, you know, Big Pharma have tried for a decade finding an agonist. They've successfully been antagonists, but not agonists, precisely for the reason that finding an agonist to a GPCR, identifying that orthosteric binding pocket, like I mentioned, being able to twist the conformation so it opens up so you can do med chem, you know, do DNA encoded library screening and then med chem, it's very difficult. I will say that the ability for us to have now generated so much interesting chemical matter that you're seeing now with ORX-750 and then with ORX-142, and I have to be careful because my GC will probably get mad at me, but I have a lot of excitement for ORX-142.
No one seems to pay attention to that. That's in the clinic. That's moving very fast.
That's a good question.
You are going to need it.
Yeah, go ahead.
A lot of excitement for that molecule. You'll see data this year. You know, every single one of these orexin agonists, which is, it's kind of, it's really interesting. They're all different. Until you go into humans, you don't really understand how different they could be in a very good way in terms of revealing properties of the molecule that may be advantageous for certain populations more than others.
Sure, wonderful. Thank you. Moving on to 142, can you give us an overview of the compound and how it improves upon 750's profile? I thought 750 was the best you could get, but.
We're super excited about the 750. I wanted to do some excitement there, obviously, but it's like, you know, the newest kid here. The 142, more potent than 750, almost approaching the potency of the natural orexin A-like peptide itself, you know, implying potentially lower doses, much lower doses. The PK profile is very interesting. I'll leave it at that, you know. Lower doses allow you to explore potential combination opportunities with standard-of-care and indications beyond the rare hypersomnias. That's where I think you've got to be very careful, just the general mass effect, the amount of drug that you're giving a patient on top of, you know, some pretty, pretty important drugs that people need to stay on, the neurodegenerative or neuropsych indications. A lot of polypharmacy there.
You want to be able to dose the drug as low as you can and have the right PK profile, you know, as best you can. I'll contain my enthusiasm for now, but you'll see the data soon.
Right. Maybe to ask you thematically about it. We've started writing about AI for a while, but we've started writing a regular publication last week. We've written regularly once. The title of that publication is Looking for My Mum, which is very good. Looking for My Mum, Maximally Optimized Molecule. Looking at, you know, directionally how pharma has developed drugs, it's this long, drawn-out iterative process. The point is that you get to the end game where a molecule can't be improved upon. Therefore, you can't get more patents, and then it goes generic in time. Just looking at what your model is, it seems to have mimicked what we might observe through an AI iterative process very, very quickly. I'm wondering on that thematic, when you've got 142, it's almost, it's mum. It's got to the maximally optimized molecule. Just to get your thoughts around that.
Yeah, I mean, we like to think we're continually optimizing more and more as we plan on, you know, the rare hypersomnias. ORX-750 is well positioned there. Outside of the rare hypersomnias and neurodegenerative neuropsych indications, ORX-142 seems, you know, potentially well positioned there as well. We have another molecule, 489, I think we've disclosed, it'll be disclosed. That's in IND enabling studies now that seem to go in the clinic. Our research team, small but mighty, is, you know, very clever. They continuously generate chemical matter and continuously optimize as much as possible. It's advantageous for us to build, as a pure-play Rx and company, to build a franchise of these molecules for different sets of indications for commercial purposes. I'll leave it at that. Continually innovating there is important.
Okay, maybe that was kind of leading into the next question I had, but I'll ask it anyway. Where do you see ORX-142 fitting into the therapeutic landscape? More specifically, how do you think about developing assets for more broad disorders like EDS and also chronic fatigue shift work?
I think some of the most important data that was released this weekend, which I'm sure many people hopefully paid attention to, is the cognition data, the fatigue data. I think that's remarkable. I've mentioned this. It's not just EDS, it's not just cataplexy. There's so much more that this pathway can stimulate and activate. A lot of these neurodegenerative neuropsych communications have these issues as comorbidities. To be able to kind of add on to their current therapies and address some of those issues, whether it's cognitive, whether it's fatigue, is going to be super important. For ORX-142, I think that's well positioned to do that.
Wonderful, thank you. I want to get these questions in, but with China's rising biotech innovation, how are you thinking about your competitive position here? Will it influence your research and development or BD activities?
Yeah, one of the advantages I think we have in this space, and a few of our competitors as well, is that the orthosteric binding pocket is relatively small. There's only so much chemical matter that one can generate that can fit in this pocket. Between, I think, the three of us, we probably commandeered as much of the IP space as possible. It's not impossible, but certainly, as I mentioned before, there were big pharmas with significant resources who have tried to find the orexin agonists unsuccessfully. That gives us some confidence that what we've been able to do, and all deference to our competitors, is that we've happened to land on scaffolds that really modulate the short sector really well. It's not safe and possible for others to do that, but it gives us a good moat, if you will, at this point.
Fantastic. How are you currently leveraging AI, and how do you think about AI as a potential disruptive force?
We use it when we need to. I think on clinical operations is certainly a place where it's, you know, it's certainly been super helpful. At the end of the day, you can't discount the fact of shaking hands, meeting with PIs, being in the room, motivating them. They don't really need much motivation. It's building that relationship that is important. We use it where necessary, and the human element just is important when we need it.
Sure. On the regulatory side, what's given you most thought more recently? FDA, MFN, tariffs?
Our team is very good at kind of predicting what might happen with those, with the tariffs and MFN and others. We have contingencies in place, but the reality is it really doesn't affect us. It doesn't keep me awake at night at this point. That's a good place for us to be.
Sure. Second to last, just remind us of the cash runway and your funding position.
Yep, $400 million as of June 30th, and cash into mid-2027.
Wonderful. Last question, what didn't I ask that I should have?
I think that probably what we did leave out is the potential of the market here in terms of just dollars. If you look at kind of backending the data that, I mean, just the numbers that our competitors, as well as analysts and others have backended, $6 to $7 billion just for NT1. Remarkable, absolutely remarkable. NT2 is an even bigger population. IH is an even bigger population. The rare hypersomnias alone, you're looking at north of $15 billion. All of this when it's a big pie, which is great. We're not even including the entire population outside the rare hypersomnias that we talked about with neurodegenerative psych issues for the orexin receptor 2 (OX2R) agonists. I don't know how many, I think John, our CFO, was saying there's only a dozen companies with a $3 billion product that are public today.
You're looking at just a rare indication that's $6 billion for one of the three rare indications. I think people should do their homework. They should do the math. A lot of conservative estimates come out at those numbers. There's a huge tan here. It's very exciting.
What's your market cap?
As of today, I don't know about it.
All right. That's all the questions I have. Thank you for your time today.
Thanks, Sean. Appreciate it.
Thank you.