All right, good morning, everyone. Thanks for joining us, the Morgan Stanley Global Healthcare Conference. I'm Mike Ault, one of the biotech analysts here, and it's my pleasure to introduce Natalie Holles, CEO of Third Harmonic Bio. Just as a reminder, the format for today is a fireside chat, but if anyone in the audience has a question, please feel free to raise your hand, and we'll get your question addressed. But before we get started, I just need to read a quick disclaimer. "For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative." With that, Natalie, thanks again for joining us today. I thought maybe, to get started, we could talk a little bit about KIT inhibition and why it's such an attractive target for mast cell-mediated diseases. Certainly, and thanks very much for having us. We're happy to be here as always. So what we know about KIT. One of the great things about KIT, first of all, is that the biology is very clear and very well understood. We know that KIT activation, KIT signaling is required for really all elements of mast cell function and survival, proliferation, differentiation, migration, activation. And when we look at diseases like chronic urticaria, the mast cell is clearly the effector cell that's driving, predominantly driving, the disease pathology. And so if we inhibit KIT, we're really inactivating, and if we sort of inhibit KIT signaling over time, ultimately deplete mast cells, and it gives us broad utility in treating mast cell-mediated diseases because that all happens sort of downstream of whatever is activating the mast cells. We know that there are multiple ways that mast cells can be activated. Certainly in different forms of urticaria and other types of mast cell-mediated diseases, you have lots of different signaling inputs that can activate the mast cell and trigger the symptoms associated with these diseases. Inhibiting KIT blocks them all. You get broad utility regardless of the source of activation, and you get a really deep effect that is playing out in what we view as really best-in-disease efficacy with these KIT inhibitors that are in the field for some really important diseases that for where there's a very high degree of residual unmet need. Yep. You mentioned sort of the broad potential of this approach. Yeah. Can you maybe talk about some of the diseases, you know, and how you think about those, and which ones make sense to target? Yeah, certainly. So we know that mast cells are resident in all of our barrier tissues, so skin, GI, airway. And we know that wherever mast cells are present, aberrant activation of mast cells can trigger disease. And so we see skin diseases, allergic inflammatory diseases, where mast cells are a key effector cell. Urticaria is one. KIT inhibitors are also being studied in atopic derm. Other, chronic rhinosinusitis is, although that's technically, I guess, more of an airway disease, is another one. Likewise, in the airways, there are clinical data out there actually supporting the utility of KIT inhibition in the treatment of asthma. And we also look at the gut as an interesting tissue where some of the symptoms associated with IBS-type diseases are likely driven by mast cells. We really look at KIT, KIT inhibition as a pipeline and a target opportunity. As we think about sort of the long-term trajectory for Third Harmonic Bio and how we want to continue to provide benefit to patients and value to shareholders, it's really looking at expanding out from urticaria. In terms of where we specifically go next, we've always talked about asthma. Yeah ... severe asthma, as being, an indication of interest for us. Again, good clinical validation for KIT inhibition in that space, but also from a commercial perspective, in severe asthma, we've seen a number of biologics that have been introduced over the last decade or so, but no new oral therapies since the anti-leukotrienes in the nineteen nineties. So there's a clear commercial white space in a big market where, if we're successful, we could have a tremendous opportunity. Yeah. But beyond asthma, we think about other diseases where that I mentioned, where KIT inhibition, you know, has sort of good validation around its approach. But I have the benefit of a number of colleagues in this space running studies and other indications that I'm gonna have the benefit of seeing- Mm-hmm ... before I have to make a decision about where I want to go next. Yeah. We are heads down, focused on the execution of our phase I study right now. We've guided to data in the first quarter, and I think next year, with the benefit of those data in hand, we will think and start talking more specifically about our indication- Yeah ... expansion strategy. Makes sense. Just given your initial focus on chronic urticaria, maybe just talk about, you know, that disease, you know, how patients are currently treated- Yeah ... and where the opportunity is. Yeah, certainly. So what we know about urticaria is that highly prevalent disease, point prevalence at any given point in time is estimated at or above 1% of the adult population. Only about half of patients with urticaria are adequately controlled with standard antihistamines. And post-antihistamine, there's really one approved therapy, which is Xolair, an anti-IgE antibody. And we know that the penetration of Xolair, the use of Xolair in the urticaria population, by the sponsor's own estimates, is pretty low, on the order of about 15% of the population. And so... And beyond Xolair, there is some use of more heavy-duty immunosuppressant therapy, but really, the residual unmet need is massive- Yeah ... in this space. And so when we think about the future of urticaria, we really see it as a story of market development, increasing the diagnosis, increasing the catchment of physicians that are diagnosing and treating urticaria, so that fewer patients are sort of lost in that diagnostic waterfall of trying to find physicians who can diagnose, have something to offer them, something that works. So, we actually think that all of the development that's ongoing in the space is a net positive. Certainly a net positive for patients, but I think a net positive for the development space as well. Yeah. You mentioned just Xolair, 15% penetrated. Like, why so low? Or what's the hurdle there? You know, at the end of the day, it's not our drug, so we can't- Yeah ... we can only sort of speak in speculative terms. But, there are limitations from a safety perspective. Xolair carries a black box warning for anaphylaxis. It requires in-office monitoring for the first couple of doses, which can be an impediment from- Yeah ... certain physician populations using it more broadly. I think the efficacy is good, but there's still a large segment of the population that doesn't even adequately respond to Xolair. So I think that there is opportunity for broader use of new therapeutics frontline, and then there's also the opportunity for new drugs to be used in patients who don't adequately respond to Xolair. So big opportunity, but it's also been noticed by a lot of other competitors in the space. So maybe just talk about, you know, your positioning relative to some of those competitors and what your key, you know, differentiating features are. Yeah, certainly, so first of all, I would say at this point in the game, we consider them colleagues, not competitors. Yeah. I don't have the privilege of worrying about market share yet. I'm still in the clinic, but I think, you know, KIT as a target, as a mechanism, as we talked about at the top, to argue, really has best in disease efficacy at this point. Certainly, the data that are coming out of the antibody program in front of us look really promising from an efficacy perspective, and I think that the safety, as, as the data are maturing over time, continue to look sort of better and better. I think the early concerns about the long-term safety profile associated with chronic KIT inhibition, I think those have not borne out. I think that it actually looks better than maybe people expected, and certainly in our own program with our first-generation compound, we took it all the way out through chronic tox and didn't see anything that was, I would say, anything that we believed that would translate into a clinically meaningful safety profile. So a little bit of neutrophil decline, but nothing to levels that would be associated with increased risk of opportunistic infection. And, you know, certainly the data from the antibody continue to look that way. Yeah. So we're excited about KIT as a target. Yeah. I think the one important differentiator between a biologic approach, an antibody approach, and a small molecule... Actually, not one, I think there are a number, but one that we're certainly focused on is the risk of anaphylaxis. Mm-hmm ... associated with an antibody-mediated approach to KIT inhibition. It is a low-frequency, high-consequence safety profile- Mm ... risk that is really specific to the antibody approach to KIT inhibition. With a small molecule, tyrosine kinase inhibitor approach to KIT inhibition, just mechanistically, that isn't one of the things that we worry about, and I think that has the potential to be a very important commercial differentiator. Yeah. And then, when you look at the other mechanisms that are in development for urticaria, BTK inhibition, Syk inhibition, Siglec programs, I think the clinical and non-clinical data that have been put out to date. I don't see anything that suggests the potential for the degree of efficacy that you're seeing with KIT inhibition. And so I think that an oral KIT inhibitor, in particular, is really optimally positioned- Yeah ... to be a really important therapeutic option for patients in this space. And then, you know, my KIT inhibitor versus other companies' KIT inhibitors, it's too early to say. Yeah. I think it looks like we and other people in this space have potent and selective oral KIT inhibitors. Yeah. It'll really be a matter of seeing how those profiles play out in the clinic. Yeah. And just relative to the monoclonals, you know, what other advantages does an oral give you? Is it just more flexibility in dosing and fine-tuning? Is that? For sure. Yeah, you said it. I think, the opportunity to more finely dose titrate, to finally answer this question of how much tryptase reduction- Right ... is required. I was gonna ask you if you know. Yeah, I don't know yet. I'm gonna run that study as soon as I can, so I think the opportunity for dose titration is certainly important. The lack of anaphylaxis risk is certainly important. Fast on, fast off is an important element of it from a safety perspective, but also just there's patient convenience, physician preference, all of those, and we know that there's a well-established preference for oral therapy in a lot of these inflammatory dermatologic conditions. Yeah. So I think that the profile of an oral KIT inhibitor, again, I'll say it again, I think we're pretty optimally positioned- Yeah, yeah ... as our program evolves. Yeah, makes sense. You mentioned earlier, you're in sort of phase one for your next generation program, but maybe you can just touch on your first generation program and the learnings you've had there. Yeah ... and how that's translated. ... Well, I'll start with the positive, which is that with our first-generation program, we initiated a program, a clinical study in induced urticaria, cold-induced urticaria. And prior to the discontinuation, which I'll get to, we saw really profound clinical benefit in even five subjects worth of data. We saw two partial responses, two complete responses, and this was at our lowest planned dose of a three-tiered dose escalation study. So from our perspective, the clinical proof of concept was convincing, even with a really small data set. The bad side is that we saw drug-induced liver injury that made us terminate the program. But at the time, the sentiment among the team was, "This is clearly a drug if we can figure out what went wrong and how to fix it." And so we spent the first half of last year doing a lot of mechanistic work to understand the etiology of the drug-induced liver injury. We were able to identify that one of the major metabolic pathways of THB001 was generating a reactive intermediate, which was causing oxidative stress and liver tox. And by doing careful metabolic analysis of the compound, we could figure out sort of where the structural liability was. We were able to make a new molecule that functionally blocks that metabolic pathway that's generating the reactive intermediate, and then did a tremendous amount of work preclinically to really convince ourselves that that was the problem and that we had fixed it. Coming to the starting line of filing an IND and starting our clinical work with 335, we're much better informed with respect to the metabolic profile and the risk of hepatotoxicity, and really needing to convince ourselves that this was a worthy endeavor to take it forward. In moving to our next gen molecule, we were able to maintain all of what was good about 001. The potency, the selectivity, the overall pharmacologic profile of the molecule is intact, with an improvement in the metabolic profile. Yeah. Maybe you could talk about some of the additional sort of preclinical work you've done on the second gen program- Yeah ... relative to the first, that sort of gives you confidence that, you know, you've eliminated this potential. I would say not even sort of. I would say it does. I mean, we needed to convince ourselves, and even more importantly, we needed to convince- Yeah ... the regulators. Yeah. So I mentioned the more in-depth metabolic analysis that we did on THB335- Yeah ... versus 001. One of the good things about the profile of both compounds is that they are very metabolically stable. Good thing when you're delivering a drug orally for systemic administration. But what that means is, you know, your standard short incubation ADME studies that are required for an IND, like a four-hour incubation in human liver microsomes, for example, isn't gonna tell you a lot because there's not a lot of metabolisms actually happening in that time course. So we developed some test systems where we were able to study these molecules in vitro on the order of weeks rather than on the order of hours. Mm. We used a human liver microsome test system that was ended up being sort of our workhorse study, system, in which to understand the metabolism and the hepatotoxicity or lack thereof, of these molecules. All of those studies were sort of above and beyond the baseline ICH guidance, you know, IND-enabling studies that you need in order to get a drug into the clinic, because we knew we had a specific liability that we needed to make sure that we fixed. And so in those studies, we were able to discern very different metabolic profiles, and very different phenotypic profiles in terms of hepatotoxic effect on these human liver microsomes and culture. So after three weeks of daily incubation with either THB001 or a next generation compound, after three weeks, you see very clear upregulation of transcriptomic signals that are, or, signatures, excuse me, that are associated with oxidative stress. THB001 lights it up like a Christmas tree, and you see nothing- Mm-hmm ... with the next gen. So again, as we're coming to the starting line, because we knew that there was a problem that we had to fix, we did much more de-risking. Mm ... preclinically, heading into the clinic the second time around. Yeah. Makes sense. So pretty confident you've identified the issue, eliminated it, and, you started talking about this before, but you also were able to enhance the molecule in other ways with some... You know, or engineer out other sort of negative things with- Yeah ... the first gen. Maybe talk a little bit more about that. Yeah. So I mean, the next-gen work was always going on in the background. Yeah. So even as THB001 was moving forward, unfettered in the clinic, there were. were. It's just good housekeeping to always continue to iterate and do medicinal chemistry when you're in the small molecule world. So there were things that we were looking to improve. One was we wanted to improve solubility, because a more soluble molecule is just easier to work with from a CMC perspective. With THB001, we started with twice daily dosing. We were formulating our way into once daily dosing. With THB335, we actually believe, based on our preclinical data, that it's going to be a once daily dosing drug right out of the gate. But if we're wrong, and preclinical DMPK models are often wrong, I've learned, we're in a much better position to formulate our way into once daily dosing with a more soluble compound. It has improved lipophilicity versus the first generation. It is peripherally restricted. Mm. THB001 was broadly restricted, broadly distributed and, you know, sort of broadly speaking, if you don't need a drug in the brain, it's better to not have it there. Better half or better PK profile, I would say. As I mentioned- Yep. We believe this is a once daily drug right out of the gate. And then, you know, also importantly, this molecule represents a selection invention within the prior art, so it actually resets the composition- Mm. composition of matter patent clock. So we now base IP protection out into the early 2040. Yep. What about the impact on fertility? Because I know that was sort of a point of discussion for the first generation program. Yeah. So it was in the early days, but we actually went all the way through the repro tox with THB001, and saw no functional effect on fertility. So you definitely see a histologic effect, but when we ran the functional fertility studies in rodents, there was no effect, meaning that they were able to reproduce even while on drug. So that element of the safety profile had already been de-risked- Yep ... along the way with THB001, and we are doing our repro tox studies for THB335 now. Got it. And you mentioned you're sort of in this, the phase 1 healthy volunteer study. Maybe just talk a little bit about the design of that in terms of patient numbers, et cetera. Yeah. And then anything notably different compared to your prior phase 1 with the first-gen? Certainly. So it is, a very standard phase one, healthy volunteer, SAD, MAD food effect study. So single ascending dose, and then fourteen-day multiple ascending dose cohorts. Healthy volunteer study, as I mentioned. You do your single dose studies and, you know, your starting doses set off your tox margins, your non-clinical tox margins. You dose escalate from there, you get into what you believe to be, sort of a clinically relevant dose range in your SAD, and then you can start your MAD cohorts. The important elements of the data that will be coming out of this study, first, of course, safety- Yep ... is an important component or the most important component at this point. But we'll also... We will be able to test those non-clinical DMPK models and confirm that this is indeed once daily dosing. We have a very good sense of the PK/PD relationship with small molecule KIT inhibitors. Mm-hmm. So I'm gonna see what sort of exposure levels I get, and then I will also get a look at PD from serum tryptase, which is a fantastic biomarker for efficacy in this space with this mechanism. So it's an important study, and that I will actually get a really good read-through on what I can expect from an efficacy perspective- Yep as I move into the disease population from the phase one. And then, you know, also what my dose ranges and my dose frequency will look like. We can take a peek at MetID to start answering that question or confirming what we saw non-clinically in the clinic with respect to the liver tox risk. But with the first generation program, we didn't actually see the asymptomatic transaminitis until week eight. Mm-hmm. And so if you are a bear, we need to wait for the 12-week study to really sort of completely discharge that risk. But again, I sort of felt like I was 90% of the way there with a cleared IND this time around. Mm-hmm ... based on all of the additional work I did pre-clinically- Yep on the second generation. Yep. Can you talk about the doses you're testing? I don't know if you've mentioned that yet. We haven't talked about them yet. Right. You know, the dose, you start with a starting dose. Yep Which is set by your tox margins. We do our tox in rats and dogs. Rats is the more sensitive species when you're talking about KIT inhibition. So you start there, and then you dose up. In the first quarter of next year is when we've guided to data, and it will be sort of a full showing of safety, PK, and PD across all dose ranges. So all will be known- Yep in a couple of quarters. Yep. Maybe just on safety, other than liver tox, which is a big one, but anything else beyond that, you know, you're paying attention to or? We have the benefit of a very well-characterized safety profile with KIT inhibitors, so I know what I'm looking for. Yep. You know, I think as we talked about earlier, the long-term safety profile of chronic KIT inhibition, I think, is quite encouraging. And we see a lot of consistency in our preclinical data from the first generation and what's been disclosed publicly from the biologic programs. So, we can get a peek at that, certainly in the first two weeks. In two weeks of dosing, we should get a look at, you know, presence/absence of KIT-related safety signals, and then we also follow these patients for, you know, some weeks after dosing, so we'll also show recovery. Yep. Maybe on the PD, you know, we joked about it before, about the amount of tryptase you need to sort of translate into a clinical benefit. Yeah. Maybe just remind us again what you showed in the prior phase one? Yeah. And is there any sort of minimal threshold that you know was sort of accepted out there, or is it just not... Nobody knows? If I had a dime for every time I got that question. So I'll answer your questions in turn. So in the first study, this was our lowest planned dose, 200 mg BID. We kind of overshot, actually. Right. We found 83% reduction in serum tryptase, which was a greater effect than we were actually hoping to get at our lowest- Mm planned dose because we wanted to get something up more in the 50%-60% range to start answering that question. Yep. So in that, with an 83% reduction in serum tryptase, we saw two complete responses, two partial responses that very much looked like they were on their way to complete responses with longer term dosing, which exceeded our expectations. That wasn't what we thought we were. It's not what we were shooting for with the lowest planned dose. Yep. Yep. ... So, it was good news in that we were able to drive down tryptase and see these really profound clinical benefits. But it didn't get at the question of, is there a threshold? So we're going to ask the same question again with 335. And the way that what we're planning to run our phase 2 CSU study is to have a range of doses that give us a range of target coverages and, you know, different levels of tryptase reduction to start getting at that question. Yeah. Is there a 200-milligram dose in the mix? That was 001 - Right. versus three three five. And if there's one thing that I've learned in this space, is you cannot sort of project your doses from one molecule to the next. So if the question is, is there going to be a dose that drives on the order of 83% tryptase reduction? Yes. I hope there's gonna be one lower, too. Like, I—we really do. Like, the low end of the dose range, my hand is going up because I'm thinking about the tryptase curves on the plot, but the lower end of the dose range is, for us, what's really interesting. Yeah. I want the reassurance that if I need to bottom out tryptase- Yeah ...... I have a dose that can do that. We certainly showed that with THB001. All the preclinical data with THB335 suggests we're going to be able to achieve the same. But the question of, do I need that much? That's still to be answered. Yeah. Is there a risk of getting too much tryptase reduction? I think if there were, we would have seen it- Yeah ... in the biologics programs, because you're administering really high doses of a really potent KIT inhibitor. And if there were, it would be on the safety side of the ledger. And again, I think everything that we're seeing, anaphylaxis notwithstanding, I put that in its own category- Mm-hmm ... everything that we're seeing with respect to the safety effects associated with long-term KIT inhibition, it all looks good from our perspective. I think the neutropenia that we were all wringing our hands about two years ago, I just don't think it's actually- Mm ... come to pass, that you're seeing clinically relevant neutropenia in patients. Assuming if you get some positive phase 1 data, as we expect, you know, how fast can you sort of move into, you know, phase 2, and what could that design- Turn and burn. Yeah. Yeah. What are you doing now to sort of help accelerate that? Yeah, great question. I ask my team that every day. So one of the things that we did was we're running our phase 1 study in the U.S., so we have a U.S. IND open. With 001, we started in Europe. An open U.S. IND, we really did that for two reasons. Number one, we just sort of wanted the U.S. regulators' imprimatur on the program, just starting- Mm ... that, like, they were convinced that we had a drug that was safe to put into humans. But number two, with an open IND, I can turn from phase 1 to phase 2 more quickly, because now it's just an amendment to an open IND versus a whole new IND for the regulators to review. But in terms of what's on critical path, there's the clinical data from the ongoing phase 1 study. We've guided to Q1 data there. There is the data from the subchronic tox studies, which we're running in rats and dogs currently. And then there's the CMC development to get us to get enough drug product to dose the study. So, but we haven't guided formally to when we'll start that study, but I think I can say as fast as possible is the plan. And one thing that we're doing differently with THB335, or I should say another thing that we're doing differently, is we are moving directly into a single robust phase 2 study. So rather than a smaller 1b, 2a prior to moving into the bigger phase 2 study, from our perspective, clinical proof of concept is established. Yeah. And we're really most interested in moving as aggressively as possible through development, recognizing that we have time to make up. So the plan for the phase 2 and CSU is a single, robust, multi-dose study powered for efficacy, certainly powered for safety, twelve-week study that will put us in a position from there to hopefully move directly into registration studies. Gotcha, and we touched on this earlier, but also just thinking sort of next indications and how rapidly you move that forward. Yeah. Yeah. How is that decision impacted by, like, you know, others sort of going after mast cell diseases? Yeah, it- Is it somewhere different or? It's actually very heavily influenced- Yeah ... by where my colleagues are running the experiments. So we've talked about asthma as being a place that we're excited about. From our perspective, the data that are out there suggest that you really need to dose for six months to get at kind of a clear signal in asthma. That's gonna require chronic tox in order to do that. You run your chronic tox in parallel with your phase 2 study, so asthma will have to start later. One of the things that the team is doing right now is looking at where are there indications where we can generate convincing proof of concept data in a 12-week study above and beyond urticaria, where, to your point, someone else isn't already doing it? And I can, you know, sort of get that up and running and we're enrolled in kind of a relevant timeframe. So, all of that is ongoing, and my expectation is that once we get a look at the phase 1 data and have a really clear sense of what the drug looks like, we can start thinking and talking more specifically about indication and expansion beyond urticaria. ... Yeah, and how large do you go? You know, in other words, like, is two more good, three more? Yeah. Like, where does it end? That's a great question. It's a great question. I think particularly it's a great question in the age of the Inflation Reduction Act, where you sort of have this, you know, negative incentive to continue stacking additional indications- Mm-hmm on asthma, on the same molecule because you lose your pricing protection on the back end. And we continue to do medicinal chemistry, iterating on THB335, you know, with the notion that if there's a best-in-class molecule out there, we want it to be ours. But also, different mast cell populations, like skin mast cells, are not necessarily like gut mast cells and airway mast cells. And so it could be that I can kind of fine-tune molecules for different tissues and different diseases. So I don't have a clear answer on that. Part of that is because I need the data, and part of it is because I wanna see how the field evolves. Yeah ... and make sure that I'm plotting both the most efficient path, but the one that is going to create the most durable value over time. Yeah. And maybe we've got just, you know, two minutes left, but maybe just last question, just maybe touch on your cash position and runway and kind of- Yeah - where that goes. So, $255 million at the end of the second quarter. Guidance is that will, that gives us cash runway at least through 2026. The way that we're running the business is that, we really view. We've got a couple of really important clinical inflection points coming up. We have the phase 1 data, which is gonna be really a pretty meaty readout for us because we have this beautiful biomarker in serum tryptase. But then the phase 2 CSU is also gonna be an important, data readout for us. And so we're running the business that we can get through both of those, catalysts with, you know, ample cash on the balance sheet, and so it's a careful daily exercise in investing. Mm-hmm in the success of the program and, you know, maintaining the financial discipline to keep ourselves in good stead with respect- Yeah - to the balance sheet. Okay, great. Oh, someone's got a question. Oh, yeah, please. Yeah, a couple of questions, actually. First... Oh, thank you. I guess the first is, have you released the chemical entity itself that was- No Going to DILI? You have not. No, no. This is a competitive space, and we learned the hard way, frankly. And so, I don't want to enable others. Sure ... based on the chemistry, the structure-activity relationship that we were able to discern in our own hands. Okay. And was it subject to polymorphisms in P450s, or? 'Cause it wasn't-- it didn't seem, at least on reflection, to be broadly across human populations. It must have been a polymorphism related. We didn't get that far. We- This was two of the first three subjects that reached week eight of dosing, so I don't think we have enough experience in the human population to be able to extrapolate. And when you were going IPO, we spoke about select like PK partitions between the bone marrow compartment and the skin. Are you seeing similar kind of pharmacokinetics with the second compound you saw with the first? I don't remember the details, but we did speak about that, I remember. I don't actually remember the details either. So are you meaning like differences in tissue PK? Yeah, that it was possibly a little bit less in the bone marrow than it was in the skin, if I remember correctly. I think maybe what you're recalling is that we saw we were looking sort of on an apples to oranges basis across studies, an antibody study in healthy volunteers versus the small molecule study, and it looked like there were differences in heme effects at any given level of- Yeah - tryptase reduction. Does that- That- Does that ring a bell? Oh, yeah. Yeah. Yeah. You have a better memory than I do, but... Yeah, I haven't thought about that for a while. So the answer is, I don't know. That was human clinical data, and we're not there yet with THB335. Mm. All right. Well, great. Looks like we're out of time. Thanks so much, Natalie. Yeah, thanks, Mike. Appreciate your time, and- Yeah We're looking forward to your update next year. Thanks.