Great. Good morning, everyone, and, and thank you for joining us today. We have with us Omega Therapeutics. I'd like to welcome Mahesh Karande, the CEO, and Thomas McCauley, the CSO. And to kick us off, Mahesh, for those less familiar, do you want to start off by describing the Omega platform and the snapshot of the company today? Sure. Elizabeth, thanks a lot for having us. Thanks to you and Goldman for hosting us here. Look, Omega Therapeutics is a company. We are a clinical stage company right now, and we are engineering a completely new class of medicines called epigenomic controllers, which, you know, as the name suggests, control genes at the epigenetic level. And these are programmable mRNA medicines. We are the first systematic use of mRNA therapeutics as programmable epigenomic medicines. And the way we do this, if you think about, you know, if you think about disease, disease occurs because genes are either overexpressed or underexpressed, right? And if you could correct gene expression, and you could do that pre-transcriptionally, then the central dogma should work well. And that's the premise that we set up the company with. The way we do this is we have taken a biology-first approach. We essentially go to genes, single or multiple genes that are housed in these, you know, conserved genomic loops of DNA and have all the regulatory elements that control only those genes. What we are able to do is exactly like mother nature does. We are able to lay epigenetic marks at these different regulators that then in turn tune the gene to the right level of expression. We engineer in properties like the regulation, up or down, the level of regulation, as well as the durability of response, and that is disease-dependent. That's how we have actually built the platform, and we took a biology-first approach and created epigenomic controllers with the technology that made complete sense to control genomic expression. Got it. That's super helpful. And, before we jump into your clinical stage programs, maybe we can start with the Novo Nordisk partnership for obesity that you announced at the beginning of this year. Yep. If you could describe the financial terms, but also the scientific rationale here. You mentioned delivery is kind of a big priority for you and Novo to figure out, and just how you're going about figuring that out? Yeah. No, absolutely. Would love to talk about that program because it's truly emblematic of what Omega Therapeutics can do. So a couple of things. You know, I talked about gene regulation for direct disease control, right? So if you think about genes, there are two things, you know, at the highest level that you could do if you can control genes at the right level of expression, right? First and foremost, you could tune genes down to the right level of expression and directly control disease, like, direct correlation. The second thing that you can do, and that Omega's platform absolutely has demonstrated that we can do, is cellular control and cellular reprogramming. So that's. You know, for example, in our MYC program, we are doing two things. One is direct tumor killing by directly downregulating MYC, but we are also changing the tumor microenvironment by which intrinsic factors then, you know, come into play, and the immune system basically starts working. So the Novo program is in that realm. So I'll—I'm gonna ask Tom to explain the science as the CSO of Omega, but let me tell you this before I hand it over to Tom. So essentially, Novo wanted to work on the science of thermogenesis, and they were really looking at different approaches to it for many, many years, from small molecules, large molecules, to even siRNA, to engender thermogenesis, which is essentially transdifferentiation of white fat to brown fat. And they laid their faith in us because we are the company who can actually do that. But Tom can talk a little bit about that. I can talk about the terms of it in a bit. Go ahead, Tom. Sure. Yeah, no, just, just to step back in terms of the sort of historical approach to obesity, you know, with culminating most recently with GLP-1s, right? They're working on things like slowing gastric emptying time or satiety, sort of, you know, neural centers in terms of, you know, moderating appetite. But if you think about it, that's only one of the two key pillars in terms of managing obesity. The other one really is energy expenditure. And so people have, you know, Novo, chief among them, has known for a very long time that driving thermogenesis, which is sort of the, you know, physical generation of metabolic energy and heat by the, you know, by cells, is another key mechanism to drive weight loss. But people have tried over the years to drug various targets associated with thermogenesis without a lot of success. And so I think it was the confluence of a couple things. One is narrowing in on a couple of key targets in the thermogenesis pathways, and I think the other is what Mahesh alluded to, which is, you know, the development of a technology like ours that allows, you know, uniquely allows us to target and reprogram cell types, in this case, adipocytes, where, you know, we're all born with brown fat, which is highly metabolically active, but as we age and our diet changes and things, you know, we end up with quite a bit of white adipose tissue, which is not metabolically active. And so the whole approach here is in the simplest approach, you know, direct administration of an epigenomic controller that can reprogram the state of those adipocytes and take them from a white, non-metabolically active phenotype to a beige or even brown phenotype type, again, sort of turning back the clock on them, where they become metabolically active, and then ultimately, you know, those fat deposits will essentially sort of burn themselves off. So this, in the best case, this is something unlike a chronic therapy, you know, as GLP-1s currently are sort of daily or weekly. You could think about this being an acute treatment, where at some point you might not need further therapy, or you might need a very infrequent maintenance therapy. Yeah. I mean, I think, you know, you talked about delivery. We'll get into that in a second. But remember, epigenomic controllers, we can engineer in durability of response, right? So we have shown now in many, many disease areas, durability of downregulation upwards of six months in many disease areas already with our preclinical work. We have shown durable upregulation for over two months, which nobody else can do, by the way, right? So if you think about the obesity program with Novo, we'll be developing an epigenomic controller that has to be dosed once every X number of months and directly into the adipose tissue, and that's where you were getting at with delivery, right? Imagine if you create a therapeutic that every few months, you actually inject the adipose tissue, your white fat changes to brown fat, burns itself off. At some point, you don't need that drug, right? You do that three, four, five, six times, depending on your obesity level, and then potentially stop, and after that, maybe get into maintenance therapy. This is next generation. And the beauty of this is. Look, you know, for all genomic medicine companies, whether they are, you know, gene therapy, gene editing, what we are doing in epigenomic control, you know, over time, delivery will expand to all sorts of tissues. Like, we are at the forefront of this, right? We have our own delivery in terms of. We should, we should definitely talk about it in terms of lung, et cetera, and many, many other tissues that our A team is working on. But with. In this program, Novo didn't balk at the idea of not having a ready-made delivery, that a lot of people actually worry about all the time. And they said: Look, let's develop it together, because I think this is such a path-breaking approach and such a path-breaking therapeutic, that let's develop delivery to the adipose tissue. Because at the end of the day, right, whether you consider LNP or other nanoparticle delivery, the chemical space and the physical space that you have to deal with in terms of getting these LNPs into the right, or any nanoparticles in the right cell, you know, has exploded over the last so many years. So, you know, let's not think about the first-generation LNPs, which only went to the liver. Now, you can actually deliver a lot more. That's what we are doing with Novo, and that's what we expect to do, hopefully with many other pharmaceutical partners across the spectrum of disease, that we can pretty much treat any human disease. Mm-hmm. Mm-hmm. Then a few follow-ups here. Can you share with us some of the targets that you may be exploring for this program at this point? Actually, those are not yet revealed. Okay. You know, it's obviously a contractual obligation with Novo. So at some point, we will reveal the targets in the near future. Great. And then how should we think about the regulatory outlook? I know it's still pretty early for these next-generation obesity assets. We've learned a lot from kind of the muscle preservation initiatives going on right now with some other companies. But in terms of pure fat loss, how do we think about the approval pathway there? You want to talk a little bit about it? I mean, I can talk from a platform standpoint Right? Look, so Omega approach is a platform approach. I think when you're talking about regulatory pathways, you know, what the FDA typically is worried about when you're talking about completely new therapies is obviously, eventually efficacy, but the most important consideration is for safety, right? And if you think of gene therapy, gene editing, things like that, which can create collateral sort of issues with, you know, due to changing of nucleic acid sequences, there's long-term follow-ups, right? We got our first program cleared, you know, our IND cleared in one month with no long-term follow-up. The FDA understands exactly what we are doing. There is no safety concern on the Omega platform or with epigenomic control. So that's a starting point. So we don't believe there would be any major regulatory issue from the, from the technology and the platform standpoint. And then it's, you know, I mean, Tom can talk about it, but then I think it would be more about sort of the disease area that you talk about. Yeah, no, that's right. I think, you know, in analogy to the sort of endpoints that were used for the GLP-1, right? You know, control of glycemic index and weight, you know, weight loss is a very concrete clinical endpoint. And I do think, so as a, you know, for again, it's, it's far enough out that this is, this is speculative at this point. But I would say there's a very clear path towards an initial approval for this type of mechanism. I think it will be considered novel and modifying, which is their perspective, I think. But I think ultimately, as with the GLP-1, by being able to modulate this pathway, I do think that there we will also see a number of kind of corollary benefits in other areas that will eventually lead to certain expansion into a franchise opportunity for this as well. Yeah. And the beauty is that the way our collaboration works is, you know, we will develop the controller and at a particular stage, at the DC stage, hand it over to Novo, which is one of the world's expert in obesity and metabolic, right? I mean, I think, you know, they have all the disease models. They have all the relationships with regulatory agencies across the world. They understand this much more than what Omega can even try to do at this stage of the company, right? That's how we want to do partnerships. We want to essentially control the science, what we can do really well, and then hand it over to the partner that obviously Big Pharma has much more expertise. Having come from Big Pharma, I can vouch for that. Mm-hmm. Mm-hmm. That makes sense. And just to close the loop on obesity, what type of cadence of updates and the catalyst path can we expect from this program? And then if you could just remind us of the economics here. Yeah. So the economics were... You know, it's a single product, single target, and they will be taking a license to a single epigenomic controller. So it's a one target deal with total economic value of $530 million+ royalties, right? And $530 millions are milestones divided into upfront and, you know, other milestones that are short and long term. So as we hit these milestones, that's when we'll be talking about updates. Really, because I think this is a program—I mean, this is a contractual obligation that we have with Novo, that we will be sort of treading according to that obligation, and then at the right times, come out and talk about it. Okay and then cadence of updates, catalysts? Yeah, exactly. Oh, okay. So as we go through this and as we get to a DC stage, as we get to an IND stage, I think again, in conjunction with Novo. We will have to give the updates. Because even for them, this is a completely path breaking. I mean, they are literally trying to figure out the next generational therapeutic that eventually will either be used in conjunction with GLP because GLP-1s, because we are orthogonal in pretty much any therapy area. Because we are so orthogonal, we can be combined. But just given the biology behind this, this could eventually replace GLP-1s, right? Mm-hmm. Got it. So moving to oncology now, and your clinical stage programs, both targeting MYC with OTX-2002 and OTX-2101 in HCC and non-small cell cancer, respectively. Could you just kind of provide an overview of those programs, why the MYC target, and then what we can expect this year in terms of data? Yeah, absolutely. So I think let me start, and then I'm gonna hand over to Tom. Look, I think, you know, the program is going really well, OTX-2002, right? I mean, I think the idea of a phase I, and it's a 3 + 3 design that we were dose escalating, and if you see what we actually even talked about recently, right? We did dose level 3, which was at 0.06, and then we went to dose level 4 at 0.12, which was, you know, doubling. And then dose level 5, we went to 0.3 mg per kg, right? And the reason we escalated that much is because we were very confident in the safety of this drug, right? And the safety of this drug is driven based on all the data we have seen. It is driven exactly as we thought by the lipid nanoparticle, which is a liver-targeting LNP, and it's actually in, you know, next generational LNP that we have, right? And these are heavily liver-impaired patients. So we were fully expecting that at around 0.3, we might actually see some dose-limiting toxicities, which we did. So now the beauty of this is, in phase I, what you really need is bookends, right? So now we have hit a bookend. So what we have done now in dose level 6 is we have come down to 0.2. So anywhere upwards of 0.08, based on all our preclinical data. And the drug, by the way, has worked exactly as we expected, based on preclinical data on the mechanistic side as well. So we believe it will work the same on the biological side, right? So anywhere above 0.08 mg per kg, you are in the, you know, efficacious zone, right? So we are fully in the efficacious zone right now. Now, what we are really focused on in this, this part of the study is to make sure that we are able to get to a recommended dose for expansion. That is the idea of this, right? And once we do that, then we do the expansion later on this year, which will be basically phase II. And that will be, you know, at the right dose, in the right patient type, because that will be second line and second-line patients and more. This stage of the trial, we are getting patients who come in mostly with life expectancies over 12 weeks, and we have expanded their life expectancy. So the disease control rate is fantastic, right? People expect CRs and PRs in phase I. It would be great if we get a CR or PR, but the phase I, is not geared towards that. That's in phase II. So we'll have the right power and the right patient type once we embark on the expansion, which will be phase II, to actually deliver on that, right? So that's the update on the clinical trial. I think the most important thing for us is that the platform has delivered the proof of concept, right? And we are a platform company, so everything that we have learned in this program applies to the Novo program, applies to our entire pipeline. And now Tom can talk about why MYC going after these two. And NSCLC, by the way, before I give it to Tom, is a huge prize. It's tremendous, right? But Tom, you want to talk a little bit about MYC and why HCC and NSCLC, MYC? Yeah, no, absolutely. So MYC is implicated in more than half of human cancers, including both HCC, non-small cell lung cancer, as well as, you know, colorectal cancer and breast cancer. In HCC in particular, MYC overexpression's implicated in about 70% of the patient population. In the case of non-small cell lung cancer, it's somewhere between 25 and 40+. In HCC, as Mahesh said, from a-- in terms of un- a huge, a huge space for us as well. But the drivers, the thing that, you know, differentiates the two approaches in this case is that the drivers of MYC overexpression in the two cases, the two cancer types, are slightly different, right? They're overlapping but distinct. So what it allows us to do is generate, as we've done for HCC now and are doing for non-small cell, cancer-specific, you know, optimized molecules for the treatment of HCC and for the treatment of lung cancer. Completely aside from the delivery, which is, you know, liver and lung specific in particular. But it's allowed us to really use our—you know, the full benefit of our platform technology to have. You know, find a genomic, you know, sequence motif, particularly in the case of lung cancer, that allows us to optimize that, that molecule, you know, for that particular. I don't know if this is a good time to talk about the, the—in terms of combination, just to sort of close the loop on the- Yeah, absolutely. Absolutely. You know, the update that Mahesh gave in terms of the HCC trial. I mean, as we're, you know, very rapidly narrowing in, I think, on the recommended dose for expansion, you know, thinking about, getting into both monotherapy expansion, but also combinations. I mean, I think it's important to talk about why we're excited about those and what we think, where we think we should be able to go with those. One of the. So on the monotherapy side, you know, we've generated a significant amount of data preclinically, and now, you know, which has been borne out clinically, showing that we can, you know, site-specifically target MYC. You know, at the genomic level, we're able to modulate the epigenome. In the, you know, specific place we intend, and that that drives downregulation of the target gene in this case, you know, which-- And so that, that finding reads through from both the HCC program directly, you know, into the, the non-small cell program. The other, you know, from a, a data perspective, we have, as a monotherapy, Mahesh mentioned this, you know, MYC acts in two different ways. It will act at the cell-intrinsic level, you know, to stave off apoptosis and other things that the body would normally be trying to do to cancer cells, but it also acts at the level of the tumor microenvironment. So, you know, it acts to upregulate PD-L1 and other checkpoints that effectively mask the tumor microenvironment and the tumor cells from the host immune system. We, you know, one of the reasons we specifically went after MYC from a biology perspective is that because cancer is driving along those two different axes, we can attack the disease along both of those axes as well. In the monotherapy sense, we know, you know, we showed some data at ASCO this past year, where in an immune-competent mouse model, which is the best recapitulation you can get of a human, you know, clinical setting, we showed in a very robust study with 20 animals in it, that we had a 70% complete response rate. 70% of the animals treated every five days for a month had complete resolution of their tumors. So we took those animals then that were tumor-free, and then followed them for another 70 days with no intervention, and then at that point, re-implanted them with, both with the original cancer line, that the HCC line they'd gotten on one flank. On the other flank, they got an unrelated lung cancer cell line they'd not been exposed to. We then followed them for another 30 days. We again, no intervention at all. And what you see is that, for 100 days after their last treatment of EC, there was no growth of those re-implanted tumors, whereas in the control group, the lung tumor cell line that was re-implanted grew unchecked. So what it means is that we, as a monotherapy, again, we've been able to confer tumor-specific long-term immune memory in these animals. So it gives us, you know, huge prospect, I think, for activity in the monotherapy setting. And then on the combination side, we've shown preclinically just additivity and even synergy with both standard of care agents, including kinase inhibitors, as well as checkpoint inhibitors, either both PD-L1 and anti-PD-1 as well. And, you know, if you think about in the, you know, looking forward to those expansion and ultimately sort of further development, the real, you know, significant unmet need in, but in certainly in first line even, but certainly second and third line, is post-CPI patients, patients that are either refractory or have become resistant to checkpoint inhibitors. And that is something based on all of our preclinical data, where we think we can make a real difference there. Yeah. By the way, that's one of the reasons that, you know, we have a supply agreement with Atezo of Roche, right? A tezo/B eva is obviously, you know, first line. So as we, as we come out and talk about... We have always talked about our strategy at a higher level, but later on this year, when we come out and talk about data, we'll talk about, you know, which direction we are actually taking this program. You know, one of the possible directions is, like Tom said, looking at Atezo/ Beva, you know, could we potentially replace Beva? Could we potentially add on as a, you know, as a triplet? There's lots to explore here. And, and this comes back to, again, which, you know, the epigenomic controllers, they are orthogonal to any treatment. There is no overlapping toxicity, because there is other than the lipid nanoparticle-induced sort of side effects and toxicity, which are very well characterized, and even in this trial, we have seen them, you know, appear very transiently, even in where we had DLTs, for example, right? Where we had liver enzyme elevations. They were resolved without any intervention within four days, right? So a nd there is really no toxicity with the controller itself. So you can use this in combination with anything across any therapeutic area. So that's what is the super exciting part of this, as this program develops and as we are able to do other programs. Mm-hmm. How do you think about kind of capital allocation along all of those different clinical development paths, and kind of investing in, you know, bringing either the combinations or the monotherapies forward in addition to kind of your pipeline program as well? Yeah. See, look, that's a great question, right? I mean, I think we are, you know, given where the markets and given where everything is, right? We are really thinking that through really well. First and foremost, let me take you back. You know, Tom and I joined the company in 2019 when there was, like, very little early proof of principle, in terms of this completely esoteric science, right? We defined the biology, put boundaries around it. We defined the therapeutic modality. We defined a pipeline. We decided to go into HCC because of all of the reasons Tom talked about with MYC. But also a big reason was that four years ago, the only LNPs that were available were liver targeting LNPs, right? So that's why we went into HCC. We still absolutely believe in HCC based on everything that we just discussed, right? But we are at a point right now where we are really considering capital allocation. I mean, clinical trials are expensive, right? We have to raise money in these markets. So we will take this very, very judiciously. We have used our capital exceedingly well for the last five years, right? But as we go forward, we really are gonna be judiciously having these discussions within the company at the board level, with investors, because eventually, the big, big prize of Omega is really to expand the pipeline, do BD deals. That's why we just hired a chief business officer, right? Because business development partnering is so important to us. That's how we are thinking of capital, all these different avenues of capital, and then we'll figure out how to allocate it best. Mm-hmm. That makes a lot of sense. And is LNP delivery science something that's within Omega? Oh, absolutely. So look, I think, you know, what we did was, as we have developed the company, there's LNP sciences and other deliveries. By the way, there's a great team under Tom, and he should talk about that in a second. We just presented data at the TIDES conference. Like, we have- You know, I'm gonna let Tom brag about it a little bit, but we have our own internal LNPs that we have developed, for example, for lung, you know, intravenous as well as inhaled. But Tom, why don't you talk about that a little bit and overall development of not only LNP but, you know, other delivery techno. Because we're delivery agnostic, by the way. We can be delivered by any means, and we have looked at all delivery mechanisms, and epigenomic controllers can be housed in any delivery. Well, go ahead, Tom. Yeah. No, absolutely. You know, as Mahesh said, you know, 3.5 years ago, when we were, you know, launching our first portfolio program, the internal team was still being built in terms of delivery, but it was something from the very outset that we recognized was gonna be critical to our ultimate success. And so, you know, while we partnered for our- the LNP, for our HCC program, you know, to speed our path to clinical development, you know, we started really from day one building an internal expertise in delivery, focused initially on LNPs and mRNA. And, you know, certainly, I think, you know, there are a lot of very good reasons to continue to pursue that, and we are. But we- You know, as Mahesh alluded to, we are delivery agnostic. These can be, you know, in a particular tissue or cell type, particularly in a privileged compartment. Think about the, you know, the eye or the brain, for example. You know, these can be deployed using viral vectors, for example, right? The transcripts for the mRNAs that we use are very, very compact, and so, you know, cassette size is not an issue. We can get many, many copies of these into, you know, either viral cassettes or into lipid nanoparticles and things. But just to segue back, and so we continue to develop both, think about both viral delivery as well as other emerging technologies as they come forward. But on the LNP side, in particular, we have driven, you know, from the very beginning in our own compositions in liver and lung targeting, including both systemic as well as inhaled delivery for lung, and really have, I believe, have unlocked that. So the data that Mahesh referred to at TIDES, we have a collaboration with the Cystic Fibrosis Foundation, for example, where obviously on a, you know, a mission to develop a new therapy for cystic fibrosis. You know, one of the keys to unlocking that is delivery to the lung. And so the data that we showed actually shows one of our proprietary in-house lipids with very, very robust distribution to the lung with inhaled delivery, but also functional correction in that case. You know, in the case of, you know CF. CFTR and you know, ion transport. So we, you know, we remain very, very excited, you know, given the breadth of application that that allows for, you know, certainly in the, you know, the example here of rare disease, but also if you think more broadly about, you know, lung indications for some of the other, you know, products that we have thought about and some of which are currently in our pipeline, like the CXCL8 program you know, where any inflammatory lung disease could be targeted, either depending on which cell type you hit, either inhaled or through systemic delivery. So we really think this puts us in a unique position. Mm-hmm. And then are there any kind of specific points of differentiation for your inhaled EC for CF? I know it's definitely very early, but we just saw some data in that space last Friday from another company, and then I know Moderna and Vertex have a partnership there. So anything you can kind of say on the differentiation, program? Yeah, you can just speak at a high level. Yeah. On the high level is fine. We hate to sort of, you know, compare ourselves. Yeah To our big brother, Moderna, but, you know, Yeah, no, and certainly for patients, I mean, where there's unmet medical need, you know, it's all to the good for patients where multiple companies succeed in something. I mean, in our case, we are not directly pursuing, you know, a therapeutic approach from the payload perspective to CF. But I think it demonstrates what we're able to do, and I think one of the things that sets our efforts apart from many of those other folks is the fact that we are pursuing both inhaled and systemic delivery in parallel, which allows us, for example, in the lung cancer context. You know, we think systemic delivery, in many cases, is gonna make more sense because you wanna use the same sort of highways, if you will, you know, that the tumors are using to draw nutrients to deliver our therapeutic payload. Whereas for something like, you know, some pulmonary inflammation condition, for example, you probably want an inhaled approach, and we can do both. Yeah, but by the way, I mean, without getting into the specifics of it, when you compare our inhaled LNP, you know, to some of these others, actually, we are equal or in some cases, actually much better in terms of transfecting. Mm-hmm. Got it. At some point, we'll come out with those comparative data. Yeah. We haven't put those out yet. Okay, got it. Looking forward to seeing more from that program. I guess in the last few minutes here, if you could kind of run down your catalyst path for the next year or so, and as we look to believe it's that phase II, second line plus data in the future, just how to think about the bar for success there. Yeah. So look, I mean, I think, you know, you asked the question about how we will use capital, right? I mean, I think this goes, this all goes hand in hand. So if you think about the next 2-3 years of Omega, right? I mean, I think we are squarely positioned really, really well to actually bring, you know, 2-3 INDs, you know, successfully, right? In, in sort of, you know, programs in our pipeline, but honestly, even with some of the programs that are not in our pipeline, right? If we go to a program which is either, which has delivery, so liver, for example or even lung, for that matter, right? We have demonstrated with our first liver program that we got from scratch to clearing IND was 27 months. Right? So if you think of, even if we started a program de novo today, and we had delivery to that tissue, within 27-36 months, we can get an IND clear. That we know. Mm-hmm. This was 3 years ago. Now we have progressed the platform to that level, right? When you think of now catalysts, right? Outside of the HCC program, there are all these potential catalysts. Development candidates, you know, INDs, depending on sort of how we finance the company. Obviously, whether it's through partnerships or whether we raise money to do specific programs, right? Then obviously, you know, as a clinical company, you know, we have catalysts in the first program, which is OTX-2002. And like we said, later on this year, we'll be talking about dose levels 4, 5, 6. We'll be talking about a strategy in terms of expansion, combination, everything that we talked about, sort of put a stake in the ground as to where we get. A lot of it is finance dependent, right? I mean, you know, there's no two ways about it. But our expectation fully is based on all of the preclinical data that we have generated, right? Our expectation is that with the right patient types, you know, which you should see an expansion in later, as well as the right powering, you know, 15-25 patients, right, depending, we are pretty confident that we'll see ORRs. And then we obviously also think about combination. And the interesting thing about our drug is that we believe that it will work in monotherapy and combination. We have definitely shown synergies with TKIs or with checkpoint in the blood. So it's almost like an embarrassment of riches sometimes, but we need to be focused. Right? And that's, that's really what we'll do. So assuming, you know, continuing financing of the company, which I don't have any doubts about, right, what we will be able to do is deliver on all of these catalysts, not only in the clinical program, but also on the preclinical program. All that remains to be seen and thought through per your previous question. Mm-hmm. Got it. And, if you could just remind us of your current cash runway? Yeah. So in March, when we put out our Q, we talked about having $60 million on the balance sheet, right? And that takes us squarely in, you know, through into first quarter of 2025. So a nd then, look, a big part of our strategy has been partnerships, and we just did the Novo deal. We're talking to a lot of pharma partners. So there's various ways that, as with every biotech company in this market, that we are considering various avenues of financing. You know, as we do that, we will be unveiling and revealing what our exact plans are. Great. And then in the last minute here, anything you think is understood about or misunderstood about the Omega story that you'd like to emphasize? Yeah. No, look, Elizabeth, thanks for that opportunity. You know, I think what happens with a company like Omega, right? Which you're working on very esoteric science, you're the first in class, you are literally bearing the torch, you're paving the way, right? A lot of times people don't fully understand it, or even if they understand it, they're like, they're waiting for proof of platform or proof of principle. We have amply delivered it. We are the first company that is actually in the clinic, that has clinical data. We have demonstrated that this modality works, like Tom was saying. We've shown that epigenomic controller works, right? If your central dogma works, eventually you're going to get the results, right? So we have demonstrated site-specific targeting. We've shown site-specific epigenetic changes. We have shown that translating into mRNA changes. At some point, you know, we'll be doing tumor biopsies in these patients, right? Mm-hmm. We'll be able to correlate that. The platform works. What this means is, as a platform company, everything that we do in the MYC program, in the clinic, applies to every other program that's potentially possible with our platform. Except for the biology that changes, everything else remains the same, and we have honed this into a really good art and science that, you know, we can continue to expand the pipeline. I mean, to me, where we are is take a page out of Novo's handbook, right? Where they looked at something that they wanted to do that we could deliver on and said: Look, we are not worried about things like delivery, et cetera, because we are really focused on the next generation medicine. That's what this is all about, right? When you are pioneering, when you are creating a path, you want partners who believe in that and who want to do that. That's what I would say, you know, to the larger world, that this is a platform worth placing faith in, like Novo did. Mm-hmm. Right on time. Yeah. Well, thank you so much to Mahesh and Tom for joining us today, and we look forward to hearing more of the Omega story this year. Elizabeth, thank you very much. Thank you.