It's my pleasure to host Prime Medicine for a fireside chat. I'm joined by Allan Reine, CEO of Prime Medicine, and Greg Dearborn, Head of Investor Relations. Allan, Greg, thank you for being here. Thank you. Why don't we start off with a little bit of background? Allan, you've been in the CEO role at Prime for a couple of months. Tell us a little about that transition and your vision for the company. We announced on May 19th. As you said, I took over as the CEO. In addition to that, we finished what I would call the final stage of our pipeline prioritization, something that we started last year. I'd say we ultimately completed by that date. Obviously, it's an ongoing thing. We're always going to be looking at how to prioritize the pipeline and the right capital allocation strategy. I think importantly, we went from, I think when I joined the company, we had 18 programs in the pipeline, and now I think we're really down to three very high-value programs in both Wilson's disease, Alpha-1 antitrypsin deficiency, and cystic fibrosis. In addition to our collaboration with BMS, where we're working on ex vivo CAR-T therapies for immunology, hematology, and oncology. As I think about the vision going forward from here, it's really kind of twofold. I think about it both as what's my vision for the short term, the medium term, and the long term. As I think of that short-term vision, it's really generating clinical data for our two key programs in Wilson's disease and Alpha-1 antitrypsin deficiency. We expect an IND for Wilson's disease in the first half of next year, Alpha-1 just a little bit after that in the middle of next year, and data for both programs expected in 2027. 2027 becomes a really impactful year as you think about value creation for the company. If I think about the medium term, we've got cystic fibrosis that we're working on. That's being predominantly funded by the Cystic Fibrosis Foundation. We're going after many of the mutations that are not amenable to the current standard of care. Ultimately, we think we can treat, with a handful of editors, 93+% of the CF population. As I think about the medium term, it's another very high value program that we can ultimately drive towards the clinic into clinical data. Obviously, making some advancement with our BMS collaboration in terms of those programs, we got $110 million upfront, but we also got $185 million in potential, which we call preclinical milestones. Even early success there can be pretty fruitful to us in terms of our balance sheet. As I think about the long-term vision for Prime Editing versus other editing approaches, I think twofold. One, it's the most versatile way to edit the genome, right? We can do everything that CRISPR-Cas9 editing can do. We can do anything that base editing can do, and then we can do so much more, right? We're not limited to just knocking something out. We're not limited to just correcting one single base pair, but we can actually fix many different types of mutations. Through our technology, we can insert multiple base pairs into the genome. We could fix frameshift mutations. We can do what we call hotspot editing. We can fix transversion mutations. It's pretty endless in terms of what we can target. As I think long term, where we most differentiate, I think there is a lot of areas that I could see the company ultimately going into. Some of those are areas that we deprioritized in the last couple of years because, given our current cost of capital, I think those investments made sense at that time. As I think about neurological disease and other types of cell therapy, there's just a tremendous amount of opportunity for Prime Editing. I think if I'm going to do right by this company, it's how do we maximize that potential? Thank you for that. That was a very great intro. I want to touch on maybe something first that you haven't mentioned. You recently achieved the proof of concept for Prime Editing in humans in CGD. Let's start with that and how much read-through you see that program, that proof of concept data, flowing into your in vivo liver assets for both Wilson's and for AATD. Yeah, so one of the announcements that came on that May 19th date as well was that we had our first clinical data in a disease called chronic granulomatous disease. We've since announced a second patient, so we now have two patients' worth of data, but also announced we're discontinuing that program. We've deviated from that slightly, and I'll get into that. I'd say twofold. One, this is an ex vivo cell therapy. We're taking patients' hematopoietic stem cells, we're correcting the mutation, and then infusing this back into patients. What we saw was extremely rapid engraftment. Similar to making that single-stranded break, it's very gentle on the cells. We seem to get much more rapid engraftment than you see with CRISPR-based therapies. I think even at 15 days, which is pretty incredible. It's a disease where you have essentially defective neutrophils, so these patients get a lot of infections that really are very hard to treat. They also get inflammatory-like illnesses, like inflammatory bowel-like illnesses. There's a pretty reliable biomarker that you can measure that's pretty indicative if you could essentially functionally cure these patients. We know this from a lot of the experience that they've had with allogeneic transplant in the past. Just to cut to the chase here, we got extremely high levels, well above whatever threshold you'd expect, to really think about a functional cure in these patients. One of the two patients that we treated had a very high biomarker that was indicative of inflammatory bowel disease, 15 times normal. That essentially normalized within a month. It's pretty powerful data. That being said, there aren't a lot of patients to treat. In the U.S., we think the majority of patients have received an allogeneic transplant. There are probably, call it a few dozen patients, we think 30- 50 that are still out there. Either were unable to find a match or they, for whatever reason, aged out, because as you get older, an allogeneic transplant is more risk and is less effective. We think just based on the strength of this data, what I talked about before, deviating a little bit from the plan in May is we are going to go and have conversations with the agency, or what we said, I think we've called it FDA interactions. We think the strength of the data, even though it's only two patients, is that I see this as a much more effective way to treat these patients and a safer way to treat these patients in an they allogeneic transplant. You know, the FDA, they've talked about testing things in the commercial setting and other things. We'll see how the conversation goes, but we just think based on the strength of the data, it makes sense to have interactions, to use that word again. Just to be clear, because I think it's an important point, we are not allocating additional capital to this program. We're not going to be enrolling any more patients in CGD. This really is to assess if there's a way to get this drug to patients, but again, it's not going to be from further investment from Prime Medicine at this time. If you were to go positive with FDA and you were to gain approval for CGD, would you consider commercializing the asset yourself, or is this something that would be partnered? If it were financially in our favor to go for approval and market it ourselves, then we would do that. Okay, understood. Maybe shifting to the in vivo assets, I would just love to hear your thoughts on what makes both Wilson's disease and AATD good indications specifically for Prime Editing. Wilson's, I think you're unique in the gene editing space, but you have a competitor for AATD. I would just love your thoughts there. Yeah, so for Wilson's disease, the predominant mutations that we're going after, there will be probably a number of different mutations we ultimately go after, but the two prominent ones that we're going after, one in the Caucasian population, so the most prevalent mutation you see in both the U.S. and Europe, and also there's another mutation that's more prevalent in the Asian population. Those are the first two that we're going after. One's called 1069Q, the other one's called R778L, but those are both transversion missense mutations. There really is no other gene editing technology that can correct for that. We're very differentiated when we think about Prime Editing. When it comes to A1AT, investors obviously know a lot more about A1AT because there's about, I don't know, a dozen companies that are doing something within the space. Wilson's is becoming a bit more of an education, but for a lot of different reasons, we're actually really excited about Wilson's as well. First off, there isn't a lot of competition, but second of all, it's a very large market opportunity, which we can get into later. For Alpha 1, when we think about going into a disease, and this is some of the work that we did last year as we kind of analyzed all 18+ programs that we had in the pipeline, obviously you're looking at competition, you're looking at differentiation. We're thinking about the commercial opportunity, technical feasibility, clinical tractability, and everything else. For something like A1AT, we know there's a lot of competition. The question is, do we think we can really be a best-in-class therapy when it comes to A1AT? I think given the preclinical data that we've generated to date, we truly believe this can be a best-in-class therapy. As we think about Prime Editing versus other editing approaches or RNA editing, etc., there's really no other technology that I've seen to date that is taking a patient back to wild-type protein. We think ultimately, if you're thinking about curing these diseases, or fixing the mutation, the desired effect should be take a patient back to wild-type under endogenous control. There's no other technology that is doing that. With the RNA editors, obviously we're seeing some initial data that looks promising. There's still a question of, do you get the acute phase response and over what period of time? When you think about Alpha-1, that's a disease where Alpha-1 levels are going to go up two to fourfold in response to stimulus. Not sure that's going to be the desired approach. It's probably the reason the replacement therapies may or may not work. With base editing, we've seen some very promising data as well, but they do have the bystander edit, so it's not all wild-type protein. We really believe this is a secure technology when it comes to Alpha-1. Setting the bystander edit aside for a moment, when you're thinking about what the bar is that has been set thus far by the base editing approach, they're getting over 11 µM of MAT. I'm wondering, do you think that you need to go higher than that? Is there an advantage? Is it advantageous to go higher than that from a clinical perspective? I'm curious about your thoughts on what the actual bar is here when you are looking at wild-type AAT. Yeah, I mean, I don't, obviously, the FDA has had a bar in the past for replacement therapy, which I think is a very different approach where they've looked at that 11 micromolar level. You know, and there's some talk, has that gone up to 20 for new replacement therapies that are coming out. You know, it's a complicated question in my mind because again, I come back to when you're under endogenous control, what does that mean? That means in response to infection and response to inflammation, which is kind of what's propagating this lung disease, am I getting my Alpha-1 levels to the level they need to be to effectively inhibit what's called neutrophil elastase in the lung, which is what's protecting these patients and what these patients are missing. Do I get to those levels with a level of 11? Maybe you do, right? Because you have that acute phase response. If I have a replacement therapy at 20, maybe I'm not protective because I'm not getting to 30 or 40 or whatever I need to get to, or even higher. You know, we can have the same question when we think about the RNA therapy, RNA editing therapies. I think there's a lot of questions we have to answer. I just think we all compare across and just look at absolute levels. I think when you're thinking about endogenous control and gene control, you have to ask a bit of a different question: am I having the right response at the right time? I think you can get there with gene editing. Will the FDA look at 11 and say that's the right number? I don't know, right? I think the higher, the better. That's what we've seen. We want to see very low levels of Z protein in the periphery. We, at least, have seen historically that we think heterozygotes seem to be fairly protected and they seem to be in the 11 - 20 range. Normals are 20 and above. Again, I think the higher the better, but you want that acute phase response active and it's the gene editing approaches that are going to get you there. What do you think the market opportunity is for your AATD asset? I'm not going to put a dollar number on ours necessarily, but what I'll do is just give you what the market size is. There are a hundred thousand plus patients that have the mutation. It's what we call incomplete penetrance. Not all patients, not all people that have the mutation get the disease. It's estimated that there's about 10,000- 15,000 patients diagnosed in the U.S. It may be something that's underdiagnosed. There's a strong belief that could be the case as well. That's essentially what you're looking at. Now, when you think about a genetic disease, Alpha-1s, there aren't many like this, but it's really one mutation that makes up 99% of the disease. For example, in Wilson's disease, in the U.S., we can get into this later, but we can get to maybe 60% of the patients with a handful of different editors. In Japan, Asian countries, that might be a little bit higher, closer to 70% with a handful of editors. With Alpha-1, it's one drug product and you can get to 99% of patients. It always obviously comes down to pricing and people can do the math on how you think these things will be priced. I think ultimately these gene editing therapies are going to get fairly high market share within this disease. I think they should get high market share given the benefit they'll have in this disease. Within the U.S., within Europe, if you've got 20,000 plus patients to treat, I think you've got, I'll say $20 billion on the very low end, but this could be a $30 billion- $40 billion plus market opportunity. It's a little different with A1AT because it actually doesn't really exist in the Asian population. You've got the U.S., you've got Europe and maybe some other countries, but you're sort of limited to those markets just based off the patients affected. You're working towards an IND or CTA for mid 2026 for AATD. Yeah, how quickly, once you get clearance for that, do you think you could initiate a phase one study? Yeah, I mean, look, I think I'll probably make my CMO upset when I say this, but look, I think you can get these done pretty quickly. I think at sometimes, like, look, it's a gene editing therapy, and so it's not as trivial getting through IRBs, et cetera. There's a lot of pre-work that can be done though, so that you can get these done pretty quickly. We've seen competitors get from at least, you know, I won't comment maybe on INDs because some of these have been through CTA, not IND, and I don't have the exact dates always, but at least first patient dose to a pretty healthy data set even in nine months, right? You can go from a pretty rapid clip from patients getting dosed to first patient getting dosed to getting data. You can be sure we'll be driving as hard as we can to make sure we're getting sites up and rolling as quickly as we can. All right, looking forward to that. I know you can't comment on this directly, but I do want to ask, you are in arbitration with BEAM for your AATD program. When could we hear an update on how that's progressing? Not necessarily what we could hear, but when? Yeah, I mean, I don't think we're going to provide updates in terms of an ongoing arbitration. I don't think there's a lot I can say there. I think what we have said is we'd expect a resolution sometime in the first half of next year. That's really, I think, all we're willing to comment on. Understood. Okay. Maybe we turn it back to Wilson's then. Can you share a little bit about that opportunity? As you mentioned, some people are less familiar with this disease than AATD. What is the market opportunity? What% of the patients have the mutation that you're targeting? Yeah, so the 1069Q mutation that I talked about in the Caucasian population, you know, that's somewhere between, call it, 30% to 50% of patients, you know, so call it 40%. There's maybe a handful of additional mutations that are, you know, 8%, 7%, 5%. If you start to add those up, you know, we can get to, call it, 60% plus of patients. After that, it really falls off to like 1% or even just, you know, single mutations that will be a little bit, you know, likely won't have the, you know, make financial sense to develop, but, you know, we'll try and go down probably to even 1% at some point, might make sense. That's because we really think we can leverage, you know, sort of, all of the sort of preclinical work we do for one can be leveraged for the other. You're essentially using the same LNP, the same mRNA, you know, and you just have a slight change to your guide sequence. We think the ability to leverage that both to get into the same IND, but obviously ultimately if we have success with more than one, you know, potentially even just getting to approval at a pretty, pretty fast pace. We think each successive program within the same indication will be, you know, significantly less expensive to bring to market. If we think about 60%, you know, I think Wilson's, the estimates are somewhere between 10,000 to, I think, 11,000 patients in the U.S., I think a similar number in Europe. In Japan and some of the Asian countries, the prevalence of Wilson's disease is actually higher. There are more patients per capita, but there's also, if you look at the mutational breakdown, we can actually get at more of those patients, right? When we add up those, you know, R778L, there is, I think, 40% to 50% even, or 50% plus in Japan. Then we look at a few other mutations, you actually get to 70%. Japan could end up being almost as big of a market as the U.S. and Europe. When you kind of add that all up, you know, it's sort of on a gross patient basis to us, you know, it's almost a similar market size. When you think about Wilson's to Alpha-1, it might even be a larger market size, with a lot less competition when you start to include some of these other geographies. We think, globally this could be a $20 to $40 billion ultimate opportunity, with a reasonable kind of incidence rate as we think about that going forward. As I think about, we talk about vision before, if we ultimately get at a number of different diseases that have an incidence rate of, call it, 100 to 200 patients a year or more, and you start to increase that, now you actually don't have a, I just have to treat the curve, right? If you can kind of build those up on each other, now you've got a real long-term business with real long-term revenues that you can bank on beyond sort of treating those prevalence rates. Got it. Interesting. As you move towards IND, CTA, first half of 2026, I guess what is left to do for that filing? You have the development candidate you've disclosed, I believe. What are we looking for for those filings? Yeah, you know, we don't kind of give a step by step, but I can talk through some of the things that have to be completed prior to an IND filing. Obviously, you have to get through all of your IND enabling studies. Those include your GLP tox studies. There's a lot of other non-GLP tox studies, biodistribution studies, et cetera. You do your GLP manufacturing that you use for your GLP studies. Then there's your GMP manufacturing that you're going to use for your clinical studies. Obviously, writing your INDs, et cetera. There are a couple rate limiting steps in there, or we would do things even faster if we could. I can assure you we are doing things as fast as we possibly can to get this in as early as we possibly can. We know how important this indication is for the company, and the earlier we get into the clinic, ultimately the earlier we can get data. We're making good progress towards our IND and checking off the boxes that I just mentioned. What are you thinking about for a phase one design, and what would actually constitute proof of concept in that initial readout? Yeah, I mean, if you think about phase one, many of the patients, at least initially, will be on standard of care, right? These aren't patients that are naive. You can't really look at copper levels initially and really see an impact. That's something you'll do over time by removing standard of care. We'll do that ultimately, but I think there are different biomarkers that you can look at, that we're evaluating. You can look at ceruloplasmin levels, and if you're having a pretty consistent effect across patients, that's something that could be a good measure of if you're having that impact on enzyme levels. We're evaluating the potential to use copper PET in our studies. That's something where we actually do a radio-labeled copper PET study. The patients will actually come off standard of care for a few days while you do that study, and then you could really see if you're mobilizing copper in the right way. Wilson's disease is a, you have a defective enzyme in the liver that leads to copper buildup. Typically this enzyme would help shuttle that copper into the gallbladder, into the bile, ultimately excreted through the fecal route. When this enzyme is defective, the copper just builds up in the liver and then ultimately spills out into the bloodstream, where it's ultimately excreted into the urine. You get both liver disease from the toxic effects of the copper amounts in the liver. You have a lot of other tissues that are affected, but the most predominant is probably the brain where you get pretty significant neurologic and psychiatric disease as well. It's really the ability here to show with a copper PET that you are now getting sort of the proper shuttling of that copper now into the gallbladder, into the feces, and not really into the blood and ultimately to the urine. That's one biomarker we're looking at, but there are a few others that we think we can sort of, as you put this all together, can really paint a picture pretty early on in development if you're really seeing the effects of getting high efficiency editing in the liver. Will you build in, like, a tapering off of the chelators into the phase one design? Maybe chelate the label? Ultimately, you're going to want to get these patients off standard of care and show that, you know, they're essentially maintained. I think there's a number of other measures you can take. I mean, something we won't mandate, but even liver biopsy, if you can get to editing levels, can really tell you if you're going to have the desired effect. Remember, it's not really a biology question here. If you're getting high efficiency editing in the liver and you're getting the right amount of protein expressed, you know, this should be shuttling copper in, you know, in a normal way. Got it. Okay. You're using the same LNP, which is a proprietary LNP that you designed in-house for both of these programs for the liver. I'm wondering if you could just share a little bit about how that LNP itself and what you've seen preclinically on safety and biodistribution. Yeah, so I think on safety, we've seen, we have benchmarked against other LNPs, some that we believe to be in the clinic, or at least designed the ones that we believe have been in the clinic, and we've benchmarked pretty favorably. Any LNP with an ionizable lipid is going to have some mild to moderate LFT changes. These tend to happen pretty early, and they tend to resolve pretty early. We do see that, but again, benchmarked against some other lipids, it seems to be potentially favorable. We also have not seen at the relevant dose levels changes in any coagulation markers, which we've also seen with other LNPs that have been in the clinic, and effects on platelets, et cetera, and some inflammatory markers. Overall, I think we believe we've got a really strong preclinical profile in terms of our LNP, but ultimately, the true test of that is once you get to the clinic. Before I jump to CF, is there anything else you wanted to say on Wilson's or AATD? No, look, I think on Wilson's, it's important to kind of look through the preclinical data. I think we show very high levels of editing at very kind of relevant dose levels. We've shown really strong phenotypic data. You can see a reduction in liver copper that happens fairly quickly. You can see a reduction in urinary copper, and what you want to see is a corresponding increase in fecal copper. We've been able to devise these mouse models where you can really test that, which gives us a lot of confidence going into the clinic. I think for Alpha-1, we've got a really strong preclinical profile as well, in terms of the editing level, in terms of the Z versus M protein levels, and ultimately the total AAT levels that we're seeing at least preclinically. It all comes back to seeing that translate. I think from a positive sense, we've seen multiple companies now that have effectively shown they could deliver safely to the liver. We need to demonstrate that we can now do that with Prime Editing as well. Moving on to your CF program, I'm wondering if you could just talk through some of the challenges for that program as you're working to develop it, it being in the lung, delivery to the lung. Would it be LNP? Would it be AAV? How do you think about the types of mutations that you're going after? Just broadly, you know, level set where you are in that program and what you need to do to move it forward. Yeah, it's a really good question. I can give you the five-minute answer or the 30-minute answer, but I'll try for the five-minute answer. First off, you asked that question before about sort of the de-risking of CGD, right? The answer is, look, we're getting extremely high levels of editing in the tissue type that we're targeting, right? For ex vivo CAR-T, or sorry, for ex vivo HSC therapies, we use electroporation. That's a method of getting the cargo into the cell. Where I'm getting to with this is we've really de-risked the ability to edit, right? To prime edit, which is not trivial, right? If you think about where Prime Editing was when we first got a hold of it, you're looking at very low levels of editing. The thought was, this is an incredible technology, but can you get to high efficiency editing in different tissue types? We've demonstrated that in a dozen different tissue types at this point and many, many different diseases. The hurdle isn't, can we get to high levels of editing efficiency? The hurdle becomes, can you get the right delivery? I think for any gene editing company, it's, what's your editing technology? How are you getting that cargo into those cells? What's your delivery technology? Obviously, companies have been pretty successful in the liver, and we hope to follow in that. Companies have been successful ex vivo, which for obvious reasons is a little bit simpler. As you go in vivo into other organs, I still think there's a lot of de-risking to do when it comes to gene editing and even to gene therapy for that matter. When it comes to the lung, there are different ways to approach this, and different companies have done different things. There is an IV approach here that can work. You can reach the right cells through the IV approach. We found that the inhaled approach is probably better for the cell types that we're trying to get to. We haven't disclosed a ton of the state, although I think some of it at conferences, but we're developing two approaches, as you said. We have both AAV and LNP. Ultimately, I think if we're successful with one, we'd be pleased. If we're successful with both, we'd probably pick LNP over AAV, all else being equal, just because of the likelihood of being able to re-dose. That being said, right now we've made some great progress with our AAV approach. The complication or the hurdle, I would say, is it's not just trying to edit the secretory epithelial cells, but those are the cells that are ultimately producing the CFTR, so those are important cells to produce that. What you also want to edit or to have a long-term effect is you actually want to edit these basal progenitor, brachioepithelial cells. You really need a delivery mechanism that's going to deliver a vehicle that's going to get you to that cell type. We've seen, gotten there with AAV and shown some good editing. With our LNP approaches, fingers crossed, we're starting to make some progress as well. Nothing to share today, and there's still a lot of de-risking to do. I'd say this program has come a long way in the last year and a half to get to both very high levels of editing in the right tissue type in ALI culture. We've shown we can do it in the right cell type and the right culture, and now it's translating that to sort of the in vivo setting. Can we do this in the in vivo setting, get it to the right level of editing with AAV, LNP, or both? Yeah, looking forward to hearing updates on that program for sure. I guess bigger picture then, kind of building upon that. How do you think about target, both target and indication selection for Prime Editing? I know you have your focuses right now, but in the future you might be less constrained. You've mentioned Prime Editing is the most versatile gene editing therapy, and I agree with that. Just, you know, how do you think about being differentiated and really leveraging the capabilities of your technology? I always think it comes down to where are we truly differentiated, right? I kind of start off by saying we can do everything that CRISPR can do, but we can do it safer. That being said, if we went and did a bunch of knockdowns, yes, we're differentiated. We maybe don't have the same off-target issues. We don't have chromosomal rearrangements, translocations. We don't have really off-target editing. That's, we're not that differentiated when maybe it comes to efficacy. Is that really somewhere we want to go with it? Probably not. Where are we really differentiated? We're obviously differentiated going after the types of mutations that can't be targeted with either base editing the way they're doing it, or anything that obviously CRISPR can do if there's a true missense mutation or a frameshift mutation or a longer mutation or even a repeat expansion that we can excise. There are all these different things that we can do where we think we're very differentiated. Then it's sort of mirroring that to where is there true unmet need. Where do we think we can have a big impact on that patient population? The unfortunate reality is we have to look at where there's a real commercial impact, right? Because at the end of the day, we do have to create value for our shareholders. If we do that, we can create more Prime Medicines for more patients over time. Those are some of the things we look at as we sort of evaluate the next places to go. Take liver disease as an example, right? We've got higher probability of success in liver disease. We're not going to go for just some typical knockdown. Never say never, but I don't know that we're going to do the next LDL therapy, given the number of companies doing that. There might be other indications that are sort of interesting that we're the only approach that can really do that type of edit. We're evaluating some of those. We'll see if that goes anywhere. We're talking about the future, not in the next six months of what we want to do. As we think about some of the neurologic diseases, again, it comes back to delivery, right? Getting to show proving that you can do this preclinically. We're starting to generate some really positive data there. Both David Lu's lab has published some really promising data in the last few weeks, in a pretty rare disease showing with a Prime Editing approach, in three different mutations, very high levels of editing. That's pretty incredible data. We have some internal data that we've developed as well when we're working in neuro. These are areas where I think there's a lot of potential as we think about the future. When we kind of pick something to come into the pipeline, we want to make sure it's been de-risked enough or we feel the probability is high enough that we can really achieve success, that it's a good use of investor capital. We're not going to invest just because we have the capital to do it, right? The investment has to make sense at the end of the day. Got it. Okay. What is the outlook for potential future BD deals or partnerships? You mentioned a little bit about that neuro data. I think you said before perhaps those programs could be slated for partnerships. Even beyond that, what is the outlook? Yeah, I think as we sit here, you know, next year, my hope is that we've done, you know, one or more BD deals. I think there are areas of differentiation, like you said, that I mentioned before, where I think are sort of ripe for, I was about to say prime, are ripe for collaborations. I think the BMS is sort of, you saw the first one that we did within cell therapy. I think there's more to do within the cell therapy space. I think there are deals to do in the, you know, ultimately in the neuro space. I think, you know, there should be deals to do, you know, even in the, as we think about other cell therapy ideas, cardiometabolic and other. Those are just a few of the areas where I think we can be very differentiated, versus some of the other technologies that are out there where they're using like the virus or mRNA or anything else. Yeah, look, I think it's a promising technology. I think we're in conversations with a number of different pharma companies all the time about these things. Again, hopeful that some of these things come to fruition. Got it. We're running out of time, but Allan, maybe you can remind us of your cash runway and also share any closing remarks. Yeah, we just did a recent financing in August. As a result of that financing, if you look at our sort of pro forma from June, I think we had $260 something million, which takes us now into 2027. Decent runway extension. There are a number of other non-equity type things that can even extend that further if we're successful, that could potentially get us through our data sets, which we think is definitely possible. In closing, I just say, look, I came to the company because I thought this was just a very special technology in the sense that I've always sort of been enamored with the gene editing space. Just given the possibilities of what this technology can do, that's what really excited me. I think now that we've got the right strategy to push this company forward and this technology forward, that's what I'd say just excites me every day in coming in. I think we've got an incredible team of people to really turn this into a reality. Remember, the company's like five years old. People kind of forget that at times, but this is a company that five years ago was just out of a lab. Now we've got human clinical data, and we're about to get two more programs into the clinic next year. It's a great outlook in terms of strategy and vision from where we sit today. Nothing but excited for the future. Got it. Thank you so much, Allan. This has been a wonderful conversation and appreciate you being here. Thanks. Thank you.