All right, super afternoon, everybody. Thanks for joining us here for the next Fireside. I'm Matthew Harrison with Investment Banking here at Morgan Stanley. Very pleased to have Ambrx with us. Quickly, before we get started, I just need to read a short disclaimer statement. Please note that all important disclosures can be found on the Morgan Stanley public website at morganstanley.com/researchdisclosures. So with that, Dan, really pleased to have you here. I thought maybe a good place to start is, you're obviously an ADC company, but, you know, you have a unique technology, and I think people are familiar broadly with ADCs as a concept, but, you know, maybe aren't sure about the differentiation between each of the companies. Maybe you could talk a little bit about your conjugation technology and how you think you're differentiated from some of the other ADC companies. You got it. And first, thanks, Matthew, for having us, and thanks to the bank for having us. And thanks to Walker Sippl, who is a colleague, and appreciate him inviting me and the company here to present. So we are highly differentiated than every other ADC on the street. And it. You know, I'd like, I'd like to start, you know, describing the company as an overnight success that took 20 years to happen. And I think people have looked at our company and looked at our chart and said, "you know, what's you know, where are these guys coming from?" Like, "It's" You know, "Haven't heard of them," or, you know, "What's going on with this company?" Because we've had a pretty significant increase in our price per share over the last several months. You know, to me, it's important to understand that the technology that we have and have been developing for the last two decades is the reason why we're having success in clinical trials today. The differentiation really goes to the heart of what makes an ADC. When you're building an ADC, and I spent a good portion of my career at ImClone Systems designing monoclonal antibodies or helping engineers design monoclonal antibodies and being involved in that process. When you're building an ADC, you're taking a protein or an antibody and attaching it to or putting together two things that don't go together in nature, and you're putting that into the bloodstream. When it gets in the bloodstream, an antibody and a payload, or a protein and a payload, the body wants to destroy and break it down. And that's what happens to ADCs when it enters the bloodstream. The systems that are being used in all of the approved ADCs are either cysteine or lysine-based conjugation. The way to think about that is, it's the nature-provided portions on the protein where you could conjugate a payload. In cysteine, and lysine conjugation have, you know, between 30 and, I think, 80 different sites for conjugation. What that means is when you're building an ADC using either cysteine or lysine conjugation, you're going to have a very random, attachment, to the protein, which actually can also, be potentially be unstable, ergo, getting into the blood, falling apart. At Ambrx, it started with identifying, a nd, you know, there's an article in Nature that published a couple of weeks ago. I'm happy to provide it for anybody here that would like to see it, that describes, you know, "Hacking the genetic code." And what it was talking about was the ability to design a non-natural, a non-canonical, a synthetic amino acid. And the reason for designing those synthetic amino acids is to allow for a specific type of chemistry conjugation that is enabled by using a non-natural or a synthetic amino acid. And it was reasoned that if you could design a non-natural amino acid, and you could expand the genetic code to do so, you could deploy that in therapeutics to solve for bringing two things together that otherwise don't go together and holding them together for a point in time, over a point in time. So that's the main differentiation between us and the entire field, which is everyone else is using cysteine-lysine conjugation or some derivative thereof, or some other proven system that's engineered to create stability as much as possible. When they speak of their drug antibody ratios or DAR, they always speak in an average, DAR 4 average, which means DAR 0, you know, or DAR 5, you know, or DAR 8, or whatever. When we speak of our drug antibody ratio, it's always DAR 2. It's not an average; it's a precise number. Why? Because we know that when we use that synthetic amino acid and that chemistry, we can ensure stable conjugation. And, you know, that idea has taken literally 20 years to really progress to the point where we are today. So when it was invented at Scripps, it was, let's expand the genetic code. It's a big idea. It was a huge undertaking, and it was done. But it was basically stopped there. The idea was then spun into Ambrx through the researchers at Dr. Peter Schultz's lab, and they then started to embody the concept of forcing a cell to make a protein with an embedded synthetic amino acid or non-natural amino acid, which is not easy to do. And in that timeframe, we were starting with a bacterial cell line and evolved into a mammalian cell line. And so today, you know, we're the only ADC targeting PSMA. And if one were to say why, you know, PSMA is an obvious target. It's been known for a very long time. Pluvicto has shown it's a great target to, you know, to treat cancer patients with a radioligand. How come there's no ADCs targeting PSMA? And, you know, the answer is, it's not because it hasn't been tried. It's been tried multiple times, and each time it's tried, it's failed. And the reason it's failed is because cysteine or lysine conjugation was used, which created the situation I described before, which was protein, payload, and antibody deconjugating shortly after administration, resulting in the payload going to where it shouldn't go and causing toxicity, resulting in an inability to establish a therapeutic window. So, you know, when we look at our company, and to answer your question in a really long way, how are we different? That's how we're different. We're the only company that own, that can use and owns synthetic amino acid conjugation and oxime chemistry. And that combination enables us to have a PK profile that doesn't look anything like anybody else's ADC. When you look at the comparative PK profiles for the PSMA-targeting ADCs, and when you see ours at ESMO, you'll be able to make that comparison. And you've, we've already published a PK profile on ARX788. And HER2, when you look at, and a conjugated antibody versus antibody, and you look at those curves, they're overlapping with ARX788. With Enhertu, they separate early. And, you know, all of which is evidence that the conjugation, the stability of conjugation exists in our technology, and is what's differentiating us from others. And it's why we're, I think, enjoying a level of success right now in targeting PSMA. Okay, super. So obviously, PSMA is probably the thing most investors are focused on right now. So why don't we tick through a handful of things that are important there? I think the first question just is, remind people you've... I believe you've had six cohorts of data so far. Remind people what we know so far, and then obviously, you know, we're looking forward to some data. I think you've highlighted it at ESMO. What's the data we're gonna get there? Sure. So, the program started over two years ago, and this is the first in-human assessment of what we call ARX517, which is, you know, PSMA targeting ADC. It's engineered the exact same way our other asset in targeting HER2 is engineered. That program just had a positive phase III study readout in China in a large program. So the same, you know, non-canonical amino acid, same chemistry, same payload, different target, has been explored in probably over 1,000 patients now with HER2. So this is our first chance to do so in PSMA. The context for doing so was we appreciated that the companies who tried to target PSMA and failed, failed because they were unfavorably conjugated, and we felt like we could solve for that and potentially create a therapeutic window and an opportunity to treat those patients. That's what started probably about four years ago. When the study program started two years ago, it started as a traditional dose escalation program. This is 3+3, starting at a very low dose of 0.32 mg/kg, and escalating up to 2 mg/kg, which is significantly higher than we use in our breast program. 2 mg/kg was selected because we felt that we were already evaluating a lower dose with efficacy in HER2, so that would probably be a sufficient top dose for this program. Two years later, I joined the company in last November. I had the opportunity to start to take a look at the data, and we are now at the Cohort 6 point. And so it was a natural point in time to look, because again, that was the time that the protocol described Top's cohort. We've since gone beyond that. I'll describe that in a second. So when we looked at the data at that point in time, there were really three striking observations. The first was that we were not seeing the safety signal that was the Achilles heel of the other predicate ADC targeting PSMAs. So we were not seeing, at that point in time, up Cohort 7, which was 2.4 mg/kg, any Grade 3 SAEs or treatment DLTs. So I think that was important observation number one. Again, the failure in the other programs was because of safety. We were not seeing that here. We think that's because of the stability of our conjugation to your first question. The second observation, from my point of view, was at the second lowest cohort, 0.64 mg/kg, we started to see efficacy. It's important to take a step back and think about the context of this study. So like any phase I study, phase I dose escalation study, we're looking at an all-comers patient population that is not biomarker selected. So, that's again, I think, an important thing to keep in mind when we, when we look at our data. Other, you know, Pluvicto and their VISION study was in a biomarker-selected and enriched patient population with a best supportive care combination. So in our assessment, we're, we're taking patients who may or may not have the biomarker. Most do, but about one out of 10 won't. We're taking patients that have various levels of biomarker expression, so a traditional all-comers patient population. We were also not combining with anything, so this was a monotherapy assessment, so we could really articulate the effect of our drug as a monotherapy. So you know, that's the context in which we were bringing this study forward. In terms of eligibility criteria, patients had to have at least two prior FDA-approved treatment options, and then one of the following: or two consecutive rising PSAs, relapse or progression or new bone metastases. All of our patients in the study have had bone metastases. Almost all of the patients have had rising PSAs. And when we provided a data update in February, the median prior lines of treatment were five. So we were in a very, you know, heavily treated patient population in a non-biomarker selected monotherapy assessment. So, as I said before, when we looked at the second to lowest therapeutic dose, 0.64 mg/kg, we saw at least one patient seeing a reduction of at least 30%. To me, that was important because 0.64 mg/kg is a small dose, and you've got patients with bone metastases, rising PSAs, that are heavily pretreated and seeing some level of efficacy at a very low dose was encouraging. The next observation that we communicated in February is Cohort 6, which again, was the articulated top cohort under the protocol, 2 mg/kg. All three patients saw a PSA reduction of 50%, and two went on to get a PSA reduction of 90%, and one of those patients had a soft tissue RECIST response. So that was, you know, from our standpoint, encouraging data, and that's, you know, exactly what we communicated to people. We like this data. What we then decided to do was obviously continue the study, right? We were then encouraged really to continue to bring the dose higher, which we did do. We went Cohort 7, 2.4 mg/ kg, and then to Cohort 8, almost 3 mg/ kg. So that work went underway. At the same time, or around the same time, we made a decision to start to expand into pediatric RP2D cohorts. The primary endpoint or the primary purpose of the study is to establish a phase II dose. So we were looking at the efficacy that we were seeing in these cohorts, and we said we would like to expand and start to expand now. And that's the work that's been ongoing, the dose escalation work in parallel to dose expansion work. We also, at that time, said, we're going to... We would like to be at ESMO with an update. We identified ESMO as the next best moment for us to provide a full data update, as full as we could do in a medical meeting context, where patients and where people could really have an opportunity to fully evaluate our data. We then submitted the abstracts, and, fortunately, they've gotten accepted. So we have two abstracts that are being published, at least two abstracts, I should say, that are being published. We also, in that in-between time, applied for Fast Track status with the FDA. We gave the FDA not only the data we had back in February, but all the data we had at that point in time and asked them for Fast Track status, which we subsequently got. So, you know, today we're, you know, about a month away, I guess, from when the abstracts will publish. I think it's today the 15th. Is that right? Something like that. 13th. 13th? Okay, a couple of days ahead. Month and three days. Month and three days. Thank you, Matt. So you're better at calculating that than me. But, yeah, so, that's when the abstracts will publish. So anyway, that's... Hopefully, that answers your question. Yeah. So walk us through a couple of things. So I guess the first question is, obviously, at a meeting, we get the abstract before we get the full data. Help us think about what potentially comes in the abstract versus what you get at the meeting. And then secondarily, in that, you know, have you told people how big that expansion cohort is or what we should expect in terms of the denominator? Yeah, great. Thanks. I'll try to answer all those questions, Matt. So, let's talk about what's in the abstracts. So, the abstracts will publish on Monday, October 16th, and we, because we've not only been looking at the safety and efficacy data, we've also been evaluating the PK data. So we had a lot of data that we wanted to put into our abstracts, and so we made a decision to bisect the data, PK, separate abstract, safety and efficacy, in a separate abstract. So, we submitted both those abstracts, and they were accepted, so we'll be presenting those or providing those on October 16th. Those will publish. In terms of what's in the abstract, that relates to the safety and efficacy of the dose escalation portion of the study. You'll see the dose escalation portion of the study. So that's Cohort 1 through Cohort 8, safety and efficacy. So that means, you know, the safety events that we're seeing, as you would see in a standard report, the most common AE is being observed. If we've seen any SAEs, the prevalence of those SAEs, have we reached a DLT? All of that will be in the abstract. Also in the abstract, we're putting a grid, because when we did the space count, we determined that we could get more information by putting a grid than putting text. So in the grid will be PSA 30%, 50%, 90% by cohort. So you'll see, you know, for example, Cohort 4, PSA 30%, 50%, 90%, Cohort 6, Cohort 7, Cohort 8. This is a note, most people are interested to see Cohort 7 and Cohort 8 because of what we've seen in Cohort 6, they're interested to see if there was follow-through in Cohort 7 and 8 or if Cohort 6 was unique in some way. That question will be answered. You know, the other elements that will be in there is ctDNA, which is another surrogate for efficacy, which we've been monitoring. So we'll have some information in the abstract about that. We will also, I believe we're also going to have median duration of treatment in that, and ORR. So looking at overall response rate, not all of these patients, actually, a minority of the patients, have soft tissue measurable disease. But as I said, in Cohort 6, we already saw one response. So that's hopefully a good description of what's going to be in the abstract. The PK abstract will have similar information as much as we could, you know, describe in the required space about the PK that we're, you know, having to see. What we're hoping to see is a long half-life, a Cmax that occurs, you know, in long into administration. Those curves I described earlier for PK, antibody versus conjugated antibody overlapping, right? So no separation of those curves. Because I think that will again, you know, provide further justification as to why, if we're seeing good efficacy, why and good safety, why we're seeing that, whereas others were not able to do that. We'll look to, you know, juxtapose that because we have the PK data from those other programs, so we can situate our PK data vis-a-vis those other programs. The poster, which will be a week later, will have the dose expansion patients, right? So I know you know Project Optimus, which for those who don't know, it's an FDA guidance, which talks about how to define our P2D. And the part of the guidance is to just to look to evaluate what could be the lowest efficacious dose. So as I said earlier, we saw activity at the second lowest dose, and then we saw the activity I described in Cohort 6. So if you're us, and you're looking at saying, "Okay, I'm going to evaluate potentially the lowest effective dose," you probably would pick something in between Cohort 2- Cohort 6. And so, you know, we haven't described which cohorts we've expanded into, but I think one could reasonably think about it that way. In terms of, you know, the higher cohort, we'll also see patients in that expansion. Folks have been asking how many patients we are going to see. Traditionally, a dose expansion cohort would be anywhere from 10-20 patients, perhaps more. So I think, you know, it's reasonable to think we would have at least 10 in those expansion cohorts, plus the three that were in the dose escalation, so around 13, but perhaps more. We're looking to evaluate confirmed PSA responses. So in order to have a confirmed PSA response, you have to have at least two assessments. And so, you know, when we report that, in the expansion cohorts, we'll look at confirmed PSA responses for patients who have had at least two assessments, and then also have an opportunity to see further confirmation of responses to patients that have had still had one assessment, but we don't have, you know, two yet to make, you know, a PSA assessment. So, in those expansion cohorts, I think you'll see a lower cohort and a higher cohort. I think, hopefully, aspirationally, we would see a dose effect from the lower cohort to the higher cohort, right? So you can see efficacy in the lower cohort, but better efficacy in the higher cohort. But I think, you know, from overarching standpoint, I think it's going to be an opportunity for people to really get a sense of where this program is heading. So, you know, hopefully, that answered your question, Matt. It does. And so then I guess the follow-up, which is probably important, is what's the appropriate comparison? You know, is Pluvicto, is Pluvicto's early expansion cohorts, are they the right way to look at it? So, you know, how are you trying to set expectations? Yeah. So, I think, you know, I think Pluvicto would be a natural comparator for people to make because it's a PSMA-targeting agent, with a radioligand, and, you know, we are not. We're obviously a chemotherapy. But, you know, I think, you know, the commonality of both of us is, you know, targeting PSMA. It's really where the comparison stops because the MOAs are very different, right? One's a radioligand, one's a, a, you know, a micro tubule inhibitor, you know, MMAF, microtubule inhibitor. So, they are definitely different technologies. Nonetheless, you know, it's, I guess, natural for people to make a comparison because we're both addressing the same target. So Pluvicto, in their VISION study, PSA 50 rate was 47%, but that was in a patient population that was a biomarker-enriched, selected, and enriched patient population. So you not only had to have PSMA expression, one out of 10 don't, you have actually more than that, but around that, and you also had to have, meet the criteria for PSMA expression under the study. But they were looking to really find a homogeneous patient population vis-a-vis PSMA expression level, and that's what they achieved in the study. There were a significant number of patients who didn't, you know, didn't qualify for PSMA expression that were excluded from the efficacy assessment in their study. I'll come back to that in a second. So the Pluvicto VISION study, PSA 50% or 46%, was in a biomarker established and enriched patient population, and it was also in a combination setting. So Pluvicto plus best supportive care versus best supportive care was the study design for the VISION study. The best supportive care arm of the study had a PSA 50% rate of 7%. So, you know, one could logically assume that the, the contribution of the best supportive care to the Pluvicto, PSA 50% of 46% should be reduced by at least 7%, so around 39%. And then again, one would have to account for the, you know, the biomarker selection enrichment in order to try to make an apples-to-apples comparison to our, study, which again, is a monotherapy assessment in a non-biomarker selected patient population. So, you know, so when, when we think about what Pluvicto would do if it were in the, in our study, it's, you know, it's probably, you know, significantly less than the PSMA 46% that, was published in the VISION study. So from our point, I think anything that's in the, you know, around 40% or greater is, would be a very nice finding for us in those expansion cohorts. And so that's kind of, you know, how we think about it. If we can get to, you know, 40% or more, I think that would be, you know, indication that it's a very active agent and that it has an opportunity for further drug development. I think the other element of comparison is safety. And, you know, Pluvicto's SAE rate was 36%, with 3% Grade 5 or 2.7 Grade 5. You know, as I said earlier, our February data at 2.4 mgs per kg, and for a study that had been running for quite a while, we had not seen an SAE. So I think that's, you know, obviously a very big differentiator between the two programs, potentially, if we maintain, you know, that, the trajectory that we've seen on the safety. And then lastly, you know, as between the two technologies, Pluvicto, obviously, as a radioligand, requires special handling. It requires special instructions for patient post-treatment, including having to isolate from pregnant women and children for a period of time. So there's a lot of, you know, you know, qualifications that go around that. And then second to lastly, you can only stay on Pluvicto for four or six months. So, you know, aspirationally, we'd like to see a convincing PSA level. You know, we would like to see, you know, not only PSA 50%, but PSA 90%. You know, in that, in that Cohort 6, we saw two out of three get to PSA 90%, which I think was great. We would like to see, you know, continuation of the safety profile that we were seeing, supported by the PK data. That really gives the rationale as to why we're, you know, potentially being successful so far in the study. Okay, great. We only have a few minutes left, so why don't we just take a brief moment and talk about your HER2 agent? And maybe the simplest question is just, you know, you're obviously gonna look at the post-Enhertu HER2 markets. So So maybe just talk to people about, you know, why you think that's a relevant market, and what sort of data you need to generate to decide to move ahead there. Yeah, it's a great question. So I mean, post-Enhertu HER2, 25% of the patients come off of treatment within 12 months. So it's a great drug. It's, you know, helping patients, but a quarter of the patients come off within 12 months. So there's an absolute need for an option in that patient population, and there's not a lot of data that would suggest what would be an efficacious agent post-Enhertu HER2. So, you know, we think that's an opportunity for ARX788. ARX788, you know, as I described with PSMA, is built the exact same way. Synthetic amino acid, oxime chemistry, microtubule and MMAF payload, all designed to stably deliver an ADC, cause the internalization, lysosomal degradation, accumulation of payload, and cell lysis or cell death occurs. That's how our technology works. We engineer... We don't engineer for bystander effect. So that's, you know, again, to, to keep in mind as we talk about our tech. So the opportunity we think exists with a quarter of the patients progressing within the first 12 months and then 50% within the first two years. And, you know, then we think about our agent vis-à-vis Enhertu. So the payloads are different, right? Our payload is a microtubule inhibitor, MMAF. Theirs is a topoisomerase inhibitor, DNA-damaging agent. It's a much less potent payload, and that's for a reason, because the, the, you know, the, the dislocation of the payload, well, for Enhertu, happens, you know, within hours of administration. You know, whereas as we've already published in our PK data, our Cmax of free payload in serum over time occurs around day 7, and our half-life is around day 7. So it's much different MOA, the point I'm getting to. Theirs operates more like a slow-release chemotherapy, albeit under the rubric of an ADC. Ours operates more like a stable ADC designed to deliver fully conjugated payload to the target. And for those reasons as well, we think, you know, we have a kind of a fundamentally different MOA, you know, albeit within the, you know, within, again, the structure of an ADC. So those are kind of the two main drivers. And the third is, we've seen post-Kadcyla, we've seen some antitumor activity, small number of patients, post-Enhertu. In the United States, we've seen some antitumor activity. Again, small number of patients. HER2-low, same thing, small number of patients. That gave us, you know, some confidence to think perhaps we can address that post-Enhertu patient population. Lastly, although not directly relevant to that patient population, our partners in China, a company called NovoCodex, which has been running multiple clinical studies in China with ARX788, recently published ARX788 prevailed in its phase III study against the chemotherapy control. So obviously an active agent in a well-controlled study in a very large, you know, population. So all of those things combined really, you know, were the catalyst for us to think we should be looking at post-Enhertu in a small signal finding study, and that's what we're doing right now. Okay, great. Maybe just to cap us off, remind us where you are in terms of balance sheet and, and runway. Sure. So our last reported cash position is in our slide deck, so I believe it's around $220-ish, so go back and check on that. But. And we're burning about, if you look at our historical burn, it's about $5.5 million-$6 million a month. So if you extrapolate that forward, we think we have cash, you know, on a flat line basis into 2026. So, we're very appreciative of our shareholders. We've had a lot of great interest and support from shareholders. So, you know, we absolutely appreciate that, we're getting that support. We also appreciate the support we're getting from our doctors on our study and our patients. Great. Dan, thanks for being here. Okay, thanks, Matt. Appreciate it. Appreciate it. You bet. Thank you. Bye. Bye-bye.