Great, good afternoon, everyone. Tyler Van Buren here, Senior Biotech Analyst at TD Cowen. Thank you very much for joining TD Cowen's 46th Annual Healthcare Conference. For our next session, excited to have a hybrid presentation and fireside chat with Artiva, and it's my pleasure to introduce Dr. Fred Aslan, the President and CEO of Artiva. Fred, privileged to have you here. Thank you for joining me. I'll go ahead and hand it over to you for the presentation. Thanks, Tyler, and thanks for inviting us to the conference. I'll be making some forward-looking statements as I go through this presentation. The deep B-cell depletion space, I think promises to be one of the most transformational mechanisms that we have seen in a while in the autoimmune disease space. There are many different companies and many different mechanisms going after autoimmune diseases, but I don't think we have seen efficacy in any other mechanism that mirrors the efficacy that we've seen with autologous CAR T, specifically in the variety of different diseases that it has shown. For us, it's a matter of how do you go from being one of many deep B-cell depleting companies that enter the space to actually maturing to that next level? We feel that it's about choosing an indication where place towards the strength of your product and where you can be first. In our basket study, which we initiated, in the middle of last year, we're exploring four indications: RA, Sjögren's, scleroderma, and myositis. We started, like most other people, in the lupus nephritis space because that's where Dr. Sheth demonstrated activity with AutoCAR T. What we decided to do, and we announced this last October, is to choose rheumatoid arthritis as our lead indication. We did that because we're trying to play to our product strengths, which we have learned about over the last five years. Just to review, from the efficacy side, we treated a number of patients with aggressive non-Hodgkin's lymphoma, and we saw really good complete responses and really nice durability, which is in line with what AutoCAR T has seen. We also ran a trial with Affimed in Hodgkin's lymphoma, which is a CD30-directed product, and we saw very nice complete responses with some nice durability. Again, proving that the drug is very potent in its ability to eliminate B cells. Very importantly, the one advantage of NK cells is that you have a much safer product profile than you do with agents that modulate T cells. NK cells have an ability to actually kill B cells without expanding and without inciting cytokine release syndrome or ICANS. In the history of clinical development with NK cells, there's been very little CRS that's been reported, oftentimes because it was a fever and because it was a cell therapy trial, therefore, that's how it was called. As we shared data, back in November, we treated 32 patients in the autoimmunity setting, and we saw no CRS. The tolerability profile and the fact that most of our patients have been treated in the community setting leads us towards indications that are actually big, that you need to be treating in a community setting, and where a product like ours that has really good scalability compared to traditional cell therapy can have an impact. RA is the indication that we chose as our lead indication, and our goal is to be the very first agent in the deep B-cell depleting space to start a registrational trial in RA and to potentially become the first to market in rheumatoid arthritis, which has the largest population of refractory patients. We are interested in other indications. We have decided against prioritizing lupus and lupus nephritis because it has become extremely competitive with lots of questions as to who has the opportunity to be first and what the target profile looks like. In rheumatoid arthritis, as far as we can tell from watching the competitive landscape closely, we appear to be on the lead. In this first half of 2026, we'll be having an interaction with FDA to discuss what a pivotal trial could look like in this area. We're interested in Sjögren's, scleroderma, and myositis, and we have a particular interest for Sjögren's for the same reasons that we have an interest in RA. It's a very large indication, community access is very important, and we have an opportunity to also be first. Let's first discuss why RA and what the opportunity is there. Rheumatoid arthritis is the largest autoimmune indication, and typically what happens to patients is if you need a targeted agent, a TNF or a JAK, and this is the first agent that you are having, you have a decent chance of a response. ACR50s at six months in patients that are seeing a JAK for the very first time, a targeted mechanism for the very first time, either a TNF or a JAK, they have ACR50s in the mid-30s to mid-40s. If you have an inadequate response to your first targeted agent and you move on to your second targeted agent, so for example, if you had a TNF first and then you move into a JAK, or you had a JAK first and then you move into a TNF, the ACR fifties decline. Now they're in the 20%-35% range. If now you have actually had an inadequate response to two distinct targeted mechanisms, the only option that physicians today have is to cycle you through a third, a fourth, and a fifth. The ACR fifty opportunity with these patients is in the 10%-20%. If you look at it the other way, if your physician is debating, "Now, do I put this patient on a third targeted mechanism?" If they choose to do that, 80%-90% of them are not going to have a response, and they're gonna have to cycle to a fourth and a fifth drug, and while that happens, the disease is worsening. We're coming in at that point. That is the unmet need that we are defining and where we hope to have an intervention. Our goal is to drive the ACR50 responses at six months in this population that has had an inadequate response to two targeted therapies up to 50%. Potentially a higher ACR50 than any of the other approved agents, and not in an earlier line, but at a line where patients have already had an inadequate response and have a low probability of having a good response. 25% of patients that receive targeted therapies become refractory to two distinct classes. Out of the approximate $20 billion in sales in RA today, approximately $5 billion of that is on patients that are receiving that third drug with only a 10%-20% chance of having a response. There's a big unmet need here, and our goal is the opportunity to become the very first B-cell depleting product to enter the market targeting this unmet need. Our mechanism of action, we're different than most other cell therapy in that we are not genetically engineered. Because we don't engineer in a CAR, we actually use a monoclonal antibody to do the targeting. Monoclonal antibody binds to the antigen on the B-cell. The FC portion of the antibody activates our NK cells, and once the NK cells are activated, it attacks the pathogenic B-cell. five years ago, people asked the question, "Well, can a non-genetically modified NK cell with a monoclonal find the cells and orchestrate all that killing?" Well, all of the cell therapies, NTCs, went into aggressive NHL, and the data speaks for itself. We had complete response rates in the 60% range, which is in line with AutoCAR T. Our durability, which had not been met, was at 19.4 months. We have patients now that are two years after they've been treated with our therapy that are walking around free of their non-Hodgkin's lymphoma, aggressive non-Hodgkin's lymphoma. Now, where we source our NK cells, this is probably the most scalable cell therapy that we are seeing today. We source our NK cells from umbilical cord units. We specifically select units that have a KIR-B haplotype and a high-affinity CD16. That way, our drug product is not genetically engineered, but the entire drug product has that high affinity to bind to the monoclonals and do the killing. From one umbilical cord unit through a two-step process, we can actually generate thousands of vials like the one you see here on the right, where each one of these vials can be cryopreserved for three, four years. The cells are vialed in an infusion-ready media. The vials can be thawed at the bedside, and it's a five, 10-minute IV infusion. From one umbilical cord unit, we can make thousands of these vials. We have a 9,000 sq ft facility in San Diego, which if used at capacity, could treat 1,000 patients. That's a 9,000 sq ft facility that could treat as many patients because the process is so scalable. The best part is because we're not engineering the cells, the COGS are actually very low. We expect that 1 of these vials with 1 billion cells would have a COGS of $1,000 or less. Our low dose as part of our one-and-done treatment is 3 billion cells, so $3,000 COGS. Our high dose is 12 billion cells, which would be $12,000. You could price this therapy pretty much anywhere one would want in this indication, given its potential efficacy, and you would have a 90%+ margins. This is as scalable and easy to form a supply chain perspective and COGS as we've seen with cell therapy. In November, we presented data on the 1st 32 autoimmunity patients that we treated, and here we make a comparison between the safety profile of AlloNK and Rituximab with the data that was coming out from Erlangen with autologous CAR T as well as with T-cell engagers. In our 32 patients, we saw no CRS at all compared to what is typically seen. Even low-grade CRS, if there's a percentage of patients that require TOCILIZUMAB, that means that careful monitoring is required of these patients. We have no CRS at all. We have no ICANS at all. There was no TOCILIZUMAB, usage required for escalating CRS. The infection rates were in line with what RITUXIMAB would do on its own. This is really important because with both AutoCAR T and the TCs that have worked really well, one does see an elevated rate of infections. It would be acute infections if it's a more potent TC or chronic infections if it's used more chronically. We saw infection rates at the same rate as RITUXMAB, which has been used by hundreds of thousands of patients in autoimmunity since its approval. We see no HYPOGAMMAGLOBULINEMIA. There's been no IVIG usage in order to address HYPOGAMMAGLOBULINEMIA.. Despite the fact that we use CYCLOPHOSPHAMIDE and FLUDARABINE in the community setting, we're seeing a tolerability profile that is actually quite attractive and compatible with a community setting. This is the slide on hospitalizations, and this tells the whole story. Before we started, people have a lot of misconceptions about CYCLOPHOSPHAMIDE and FLUDARABINE. There's an assumption that because at these doses, one causes cytopenias, that one would see a very high rate of hospitalization. That is just not the case, and this is what we're hoping to educate people as we continue to make progress. On this chart, each row represents one of the 32 patients with autoimmunity that we treated, and each one of the columns represents a day in the first 28 days of treatment. A green box is the patient going into the infusion chair at their community rheumatology practice, receiving the infusion, and going home. A blue box were the two sentinel patients in each one of the trials where the FDA asked for an overnight observation. There were no AEs there. Then an orange box is actually a hospitalization for any cause. As you can see, out of the first 32 patients, there was only 1 patient that required hospitalization for an ear infection. They received IV antibiotics, and they went home. Truly demonstrating that this is extremely compatible with the community setting. The vast majority of these patients, in other words, other than a handful of patients that were treated in academic medical centers, all the rest were treated in community setting. These are community rheumatologists who are giving the CYCLOPHOSPHAMIDE and FLUDARABINE in their infusion chair, sending their patients home, and managing them. We were really pleased with these results. From a mechanism of action perspective, we also shared data in November that demonstrates that our drug, not surprisingly, is doing what it's supposed to do, which is a very deep B-cell depletion. Unlike others, we developed our own high sensitivity B-cell assay because a lot of the assays that are typically used have a limit of detection of 5-10 cells, and that's still a lot of cells that are flying under the radar. We developed an assay similar to the Roche Genentech assay that was developed when Rituximab first came out, that has a 0.1 cells per microliter, which means that you can really detect the presence of low levels of B cells that when people have studied RITUXMAB. Let me orient you to the y-axis on this chart. This axis is% of patients that still have quantifiable B cells using a high sensitivity assay. As you can see, when RITUXMAB is used, this was a series of 99 autoimmunity patients, you still see B cells present in 40% of the patients. When we ran all of our samples at the time of the disclosure, every single one of these patients had no detectable B cells utilizing a high sensitivity assay. This is further validation that we can achieve a really deep B-cell depletion, which again, shouldn't be surprising considering that we cured a number of aggressive NHL patients that are now two years out and still cancer-free from the time of the treatment. Just to summarize before we go to questions, we believe that our A represents a significant area of unmet need. Yes, there are 12 products that have been approved, and the first one or two provide a lot of relief, but 25% of patients do not respond to the first two distinct mechanisms, and then they go on cycling between all the other approved drugs. There's an opportunity to come in after that failure of the second drug with something that has a high opportunity, perhaps an ACR50 or 50% or greater with a durable effect. We have the potential to be the very first drug in the B-cell depleting space across cell therapy, across biologics to get into the market. This would give this product a very compelling commercial opportunity considering the unmet need there. We will take a data-driven approach to select our additional indications. We're doing one at a time. Enrollment has been going very well for us, which speaks to the tolerability of the product and the ease of use in the community setting, and we feel we are in a strong position to actually deliver on our goals. We have a very experienced team that has enrolled as many patients as any other company in the deep B-cell depleting space so far. We have a cash balance of $123 million as of the end of Q3 of last year, which gives us runway into Q2 of 2027. Great. Thanks very much for the presentation, Fred. Maybe we'll start at a high level. It's been a few years now since we got the initial data by Dr. Sheth. Now that we're in 2026, what do you think the B-cell depletion space has learned, and how do you think Artiva is competitively and clinically positioned to stand out amongst the pack? I think we've learned that this is a very powerful mechanism and that it is very likely to wash over all autoimmune indications. It does seem like a lot of the products are actually working. What we've also learned is that a lot of the T-cell-based approaches do exhibit a level of therapeutic index. There are some therapeutic index limitations. The most potent ones, which have shown some of the best efficacy, do show a higher rate of CRS and infections. The ones that are used at a lower dose in order to avoid those tolerability issues are more tolerable, but they usually have to be used chronically because you're not seeing durable results, and the efficacy is a little lower. Where we're hoping to differentiate ourselves is to actually specifically bring that potent efficacy, which we've seen in oncology, we've seen in the deep B-cell depletion, but with a product that is compatible in the community setting. The other thing we've learned is it's a very crowded space. For a while, people have been asking the question, "Who's going to win?" That is a very naive question because there isn't such a notion of one winner. You have to look indication by indication, figure out the target product profile of the companies that are likely to be the first or the second, and then judge, you know, the merits of that product in that indication. That's how we have differentiated ourselves, is by choosing indications where we seem to be on the lead with a product that seems to have the right TPP to go after that. Great. From the first clinical data that was reported in the fall, can you elaborate on the feasibility of community administration and what you observed, or what you've observed so far that gives you confidence in that? Those first 32 patients were actually extremely telling, number one, whether we could do this in a community setting, because again, the vast majority, as I mentioned, were dosed and treated by community rheumatologists in their practice. That demonstrated that it is very feasible. Enrollment has been going really well. The second question that it answered is, what does administering Cy/Flu look like? A lot of people ask questions about the tolerability of Cy/Flu in a community setting. That also answered that question. It was nice to get validation in autoimmune disease that the depletion of B cells would also happen with the same level of potency as we saw in oncology. Just to follow up on the Flu/Cy comment, I think there's a lot of people out there that don't think Flu/Cy can be used in the community. What do you think are the biggest kind of misconceptions among the investor audience with respect to that, and why should they be thinking differently about Flu/Cy in the community? I think that it's important to put Flu/Cy in the context of the overall TPP for the regimen, right? I think that there's a lot of noise in the space. If you're developing a T-cell engager, you immediately point to the lack of chemotherapy as one of the advantages. We need to look at what is the clinical impact from a safety perspective, and a tolerability, and an ease of administration of actually utilizing Cy/Flu. First few things. There have been tens of thousands of patients that have actually used Cy/Flu in the context of auto CAR T. Most people don't appreciate this, but the Cy/Flu is actually done in an outpatient setting. They only get hospitalized once they're getting the auto CAR T or once the side effects of the auto CAR Ts come in. That is very feasible to administer. The next thing to look at is what is the impact of that Cy/Flu? At the doses that we're using it only once, what you get is a pancytopenia that lasts a period of two to three weeks, right? That pancytopenia, usually in the vast majority of patients, recovers within a two to three-week period. During that period, because you are concerned and monitoring patients for infections, it covers these patients. The way this happened initially, and this was kind of the story of our clinical trial, initially PIs were asking the questions, "Oh, what is it gonna be like for me to be managing the CYCLOPHOSPHAMIDE and FLUDARABINE?" The next thing that happened is they saw neutropenias in these patients, and they started calling us, "Oh, should I do something about this neutropenia?" We would ask the question, "Look, are you seeing any symptoms? Because you should just manage it on the basis of you seeing symptoms." In the end, as I showed you in that chart, a neutropenia is a lab value that you're following. You have to monitor these patients for infections, but we're not seeing this low level of cytopenias with the antibiotic coverage, you know, influencing, making this a high-risk infection. What are you left with? You're left with fertility concerns, which are hypothetical, but this is a hard battle to fight, which is one of the reasons why we prioritize RA and we like some indications where the patients are a little bit older. Because in indications like lupus, that's when it becomes a big problem because there's a larger proportion of patients that are of reproductive age. But once you start looking at RA, that population is a lot smaller, that's of reproductive age. CYCLOPHOSPHAMIDE and FLUDARABINE turn out to be something very tolerable. You don't have any acute issues the way you do potentially when CRS occurs. There's no ICANS that happens. I think that over time, as we continue to treat patients, as we continue to enroll and add additional sites, this is gonna be a misconception that hopefully will go away. Great. Since you mentioned RA as the ideal first indication, can you just elaborate on that a bit? Are you gonna focus on the more moderate to severe RA patients, the later line patients? Do you think you have the opportunity to go to earlier lines over time? Again, just more broadly, why RA? In RA, it's important to note that most clinical development activities in RA are focused on that first or second line, right? Most people that are in development today, and you look at other public companies that presented here at the conference, they're trying to develop a, you know, seventh mechanism that can compete with the existing mechanisms, so they can go after that market. The data that we have seen so far from most people that are in late-stage development look to be in line with what the JAKs do and the TNFs can do. We are specifically targeting a population, which is after you have had an inadequate response to two targeted agents. We have not seen any company seek an approval or even run a large trial in that population. Most people are focused on the earlier lines. We see a big unmet need for patients where the alternative would be to go to a third, a fourth, and a fifth with a very low rate of response with a treatment that you could do one time and could offer you durability of 18-24 or more months. That's a big unmet need area, and if you can be first providing this type of relief to patients, that could have a big impact. For the upcoming data in the first half, can you remind us how many RA patients you plan to report on, how much follow-up we will have, and what types of data or what endpoints will get reported on? We guided that we would be sharing data on at least 15 patients, where most of those patients would have 6 or more months of follow-up. The bar that we have been setting is that we believe that this would be a very compelling therapy if we can give 50% of patients or more an opportunity to hit an ACR50. What our objective during that, during that disclosure is to actually demonstrate that the drug does have that potential, that in a much larger trial, which would be the basis of a pivotal trial, that we stand to have a high chance of actually hitting that endpoint. We started off in an IIT, and then we transitioned to a company-sponsored study. We don't have all of the components that one usually collects for an ACR 50, but again, our desire is to show enough data with all the components present so that people can take comfort if the data holds that this would be a successful registrational trial. I know you showed some of this data in the presentation. What gives you the most confidence that AlloNK can reach that bar and hit the ACR50 in this ongoing trial? I think we are going off of the extrapolation that autologous CAR T worked really well in NHL, and that's why it's working really well in autoimmune disease. We've demonstrated really solid efficacy in NHL, so we have no reason, given that the mechanism is the same, to not deliver that, but we need to collect the full data set and follow these patients. I think in the near term, we'll have a good sense of what the response rate is, and then we'll need a little bit more time to follow these patients to have an understanding of how long the durability actually is. Our goal is to have a one-and-done therapy that you can treat, patients can have a relief, and this is a durable effect for some time. How long do you need to follow these patients in this initial trial? What level of follow-up and durability do you need in order to start a pivotal? I don't believe that one thing is tied to the other because generally, what the FDA looks for in rheumatoid arthritis trials is generally an endpoint like an ACR50 at six months. There is no durability requirement per se from a regulatory standpoint. The durability becomes really important from a market research and commercialization perspective, where the longer that durability is, the more compelling the product becomes. You're going in to do Cy/Flu once with a treatment that lasts a total of 20 days. If you can get relief for 18, 24, 36 months, that's really compelling because during that entire period, you're not on another immunomodulatory drugs, so your infection rate should be lower. You're not exposed to the side effects of these other medications. The more durability data we collect, the better off we are. We will be following these patients for as long as we can because for all we know, there's gonna be some patients that are gonna have a pretty long response and others that may not respond for so long. Time will tell what that durability will look like. Any preliminary thoughts on size and design of a pivotal trial? Do you think the FDA will require an active comparator? From a design perspective, because we wanna go after RA, because RA is a very big indication, because there's always questions about what is the contribution of Rituximab versus the whole therapy in your trial, we have a preference to run a randomized control trial. Why would we do that? We would do that because the signal that we hope to show, we set the bar that we wanna have an ACR50 at six months of greater than 50%. That is a lot higher than any other drug, particularly drugs that are being offered to patients after they've had an inadequate response to two therapies. We believe that with a relatively efficient trial, you can actually have a randomization of patients to RITUXIMAB as opposed to our therapy, and still do that with relatively small numbers of patients. You know, as you know, the total number of patients that need to be treated, we need feedback from the FDA in order to have a better sense of what their expectations are, but there's two major drivers in that. One is, how many patients do you need to establish a signal of efficacy, statistically significant and well-powered to do that, as well as you have to think about what is that safety database that FDA will wanna see before the product is approved? Our goal is to not only share the data from the first 15+ patients in this first half of the year, but also to provide some feedback from our FDA interactions. Assuming you start the pivotal in refractory RA, what other additional indications are you most excited about, and when could we get proof of concept data in those indications? Yeah. As I mentioned, you know, the indications in the basket study are our priority indications. The other indications outside of RA is Sjögren's disease, myositis, and scleroderma. We particularly like Sjögren's disease for all the reasons we like RA. It's a really big indication. You have to be out in the community setting. You need a product that's very scalable. There's been less validation of Sjögren's from a B-cell depletion perspective. We also think that in myositis and scleroderma, there could be value in a product that can be done in a community setting. We know that most physicians don't like referring, providing efficacy and, you know, I think one of our taglines is going to be a cell therapy that a rheumatologist can actually own without the need for an oncologist. We're gonna take a data-driven approach here, one indication at a time, as opposed to just sharing all of the data as it matures. We're up on time, so, to wrap up, I'll ask you, Fred, what do you believe is the most underappreciated aspect of the Artiva story by investors? I think that people are trying to figure out who's going to be the winner? What is that silver bullet amongst all the different modalities that are in the deep B-cell depletion space? I think they need to start looking at the picture of, let's work backwards. Who's gonna be first, in what indications? Are they a lot better than the standard of care? Could they do well commercially because of the impact they're going to have? Wonderful. Fred, thank you very much for your time.