All right. Great. Good afternoon, everyone. Tyler Van Buren here, Senior Biotech Analyst at TD Cowen. Thank you very much for joining us at TD Cowen's 45th Annual Healthcare Conference for our next session. Very excited to have a hybrid presentation and Q&A discussion with Artiva. It is my pleasure to introduce Neha, the CFO of Artiva. Neha, privilege to have you here. Thank you very much for joining me. I will go ahead and pass it over to you to start the presentation. Thank you, Tyler. Excited to be here today to talk about Artiva. Artiva is a clinical-stage company that's focused on allogeneic NK cell therapy for patients suffering from autoimmune diseases and cancer. We were founded in 2019 as a spinout of a Korean company called GC Cell, who pioneered the technology of manufacturing these NK cells at scale over a decade ago. We are exploring AlloNK in Phase I autoimmune trials across a number of different autoimmune indications. AlloNK, which is our lead program, is an allogeneic, off-the-shelf, non-genetically engineered NK cell that we utilize in combination with monoclonal antibodies to target these various autoimmune indications. There is a large market in autoimmune disease, with, in 2023, the top 10 IMiD drugs selling about $65 billion in sales. Yet there still remains an unmet need for patients to receive treatments that either have adequate response or that avoid the use of background medication in these patients. Emerging data that you've seen has shown that a deep B cell depletion in the periphery and in the tissue has shown to lead to prolonged periods of drug-free disease remission. We look forward to looking at that clinical signal in our trials in autoimmune. We've generated data in aggressive NHL patients with AlloNK in the combination with rituximab that we'll cover today that gives us confidence around the potency of B cell depletion as we move into autoimmunity. From a cash perspective, we have $199.6 million in cash as of the last reported financials. From a runway perspective, that gets us at least through the end of 2026. We have guided to initial data from at least one of our ongoing clinical trials in autoimmune disease in the first half of this year. This slide captures the three elements of our strategy. The first, as I mentioned, is that we are a spinout of a Korean company called GC Cell. The decade-long head start that they have had in optimizing the manufacturing process, we believe, gives us a head start in BLA readiness as well as commercial scalability of our platform. We source our NK cells from umbilical cord blood with two different attributes. First, high affinity CD16 and a KIR-B haplotype. To give you a sense of our process and the scalability of it, from one of these umbilical cord blood units, we can manufacture greater than 4,000 of the vial you see on the slide. Each of these vials is a billion cryopreserved NK cells. We now have drug product stability out past three years. This drug product is a lot more like a biologic than it is a traditional cell therapy. We can do that from a modest 9,000 sq ft facility in San Diego. At scale, our COGS are projected to be less than $1,000 for a billion cells. Much more like a biologic than a traditional cell therapy. The second element of our strategy is the mechanism of action for AlloNK. As I mentioned, AlloNK is a non-genetically engineered NK cell. That means we do not introduce a CAR. We believe that has multiple advantages. First, from a scalability standpoint, we do not introduce lentivirus. From a COGS perspective that has advantages, as well as the ability to manufacture yield that is much greater than an engineered product. Secondly, since we use a monoclonal for targeting, we do have the ability and the versatility to utilize different monoclonals, CD19 or 20, or CD38, for example, to target different B cell compartments. The mechanism of action is enhancing ADCC for these monoclonal antibodies. Monoclonal binds to the antigen on the B cell that you see in blue. Fc portion of the antigen binds to the CD16 on the NK cell. The NK cell does the killing. In our clinical trials, we explored rituximab in NHL patients, a CD20 monoclonal. That's where we've generated data in oncology to date. That's the monoclonal we're starting with in autoimmune disease. It's been shown in the literature that high affinity CD16 in patients that naturally have it in oncology studies have better survival and in autoimmune disease have better outcomes. Again, this is a key attribute of our NK cell that we believe differentiates us in terms of the outcome we are getting. In our aggressive NHL patients that we treated, we treated 29 patients with our full regimen. As we benchmark this data against what auto CAR T showed in CAR T naive patients, our data is looking to look a lot like auto CAR T from a durability standpoint and a response standpoint in these patient populations. We again believe this has read-through into autoimmunity as we move forward into that setting. The third element of our strategy, which is critical in autoimmune, is the ability to go outpatient. Right now, a lot of modalities talk about administering their therapies in an outpatient setting. Yet approved T cell engagers and auto CAR Ts, for example, have mandatory hospitalizations in their label and are enabled to sort of break out of that hospital setting. This is where a majority of rheumatologists exist and prescribe drugs to their patients. We believe that the safety profile of an NK cell as a modality does give them benefit to be able to go into the community. We have shown that in our oncology trial in terms of majority of patients, elderly cancer patients, not spending a single night in the hospital. Mechanistically, NK cells do not induce the same escalating CRS that T cell derived therapies do. That gives us an advantage in terms of adoption in the community setting. Why NHL? We believe that NHL data has read-through into autoimmune. Another way to describe it, the reason why auto CAR T works in NHL is the reason why it's working in autoimmune disease. They're both diseases of B cells in the same relevant tissues. A CR in NHL is a deep B cell depletion in the periphery and then, of course, the tissues. What's been described as an immune reset from a mechanistic perspective is a deep B cell depletion in the periphery and the tissue. In the next slide, we'll show you our oncology data that again gives us confidence in the deep B- cell depletion, as well as a safety profile that we hope to demonstrate in the autoimmune studies as well. From a B cell depletion perspective, as I mentioned, we treated 45 patients in our NHL trial, 29 of whom received the combination regimen. From a peripheral B- cell depletion, all patients who had B- cells at baseline saw that reduced to below the limit of quantitation for up to 60 days. In the middle panel, from a swimmer's plot perspective and efficacy standpoint, we saw durable complete responses. Importantly, these were aggressive NHL patients. There was one MCL patient that you see on this chart, a total of 14 patients that were CAR T naive, a 62% complete response rate. Importantly, as the time of the last cutoff, six of the eight CRs were ongoing, with the majority of those, five out of six, out past six months, which is where a lot of the allo data started to falter. We are starting to look a lot more like what auto CAR T showed with the limited follow-up that we have. Last but not least, patient access. This was the statistic that I was referencing. Majority of patients treated as outpatient. You can see that with the uncolored boxes in the top half of this chart. That tolerability profile, along with the patient journey of this being a drug that's a 5- 10 minute IV push, thawed at bedside, is a lot more conducive as we move to an autoimmunity setting. As we step away from NHL and move into autoimmunity, we think there are a number of different factors that play into what modality and what therapy would likely succeed. There are a lot of therapies that are being explored in this space. We think the greatest potential for AlloNK to differentiate, given we are an NK cell therapy, is in the community setting by being the important therapy that can be utilized by a community rheumatologist for their patient population. This captures the patient journey of a patient in our autoimmune clinical trials. This represents one treatment cycle for the patient. We plan to administer one treatment cycle and watch for follow-up for these patients. They receive three days of fludarabine, one day of cyclophosphamide. The conditioning regimen is similar to what Schett used in his data that he's generated. This is followed by three weekly doses of AlloNK. As a reminder, thawed at bedside, 5- 10 minute infusion of AlloNK. They will receive the monoclonal antibody, so either rituximab or obinutuzumab, depending on the trial, at least 14 days apart, which is per label or guidelines for the monoclonal. This patient journey is a lot different than what auto CAR T is typically done. This can be done in an outpatient setting, as I described earlier. Importantly, the doses of fludarabine and cyclophosphamide that we are using is a fraction of what has been used historically, whether it's cyclophosphamide in terms of guidelines in rheumatic diseases or fludarabine, which has historically been used in rheumatic diseases. To give you perspective of the tolerability profile of the treatment, we have two trials ongoing currently in autoimmune disease. The first is a company-sponsored trial in lupus, including patients with lupus nephritis. Here we're exploring rituximab and obinutuzumab, both CD20 agents in combination with AlloNK. We are exploring 1 billion cells per dose and 4 billion cells per dose in this trial. The second trial we have ongoing is an IIT, but importantly, it's being done in a community rheumatology practice. No oncology involved. As far as we know, we are the only cell therapy company that's being able to do this. We think that bodes well in terms of the safety profile of the therapy. This trial is important for a number of different reasons. First, it is to demonstrate the utilization of cell therapy in the community setting. Secondly, utilization of cell therapy in other indications beyond lupus. For example, we are exploring RA in this trial, pemphigus, and vasculitis. The way we look at the universe of indications that we could explore, AlloNK being an NK cell-based therapy and the patient journey it has, has a greater possibility to explore indications where the disease prognosis or the manifestation of the disease is different from what it might be in, say, a more severe lupus patient and gives us the potential to potentially address a larger market. We are exploring the typical clinical endpoints in this study for each of the indications. SLEDAI, for example, for lupus, DAS-ESR and SLEDAI for RA, translational biomarkers that have typically been shown in these studies, safety, of course. Importantly, the reduction in meds in the patients, which we believe, again, is an important piece that a lot of standard of care does not have today. In conclusion, we're excited about AlloNK and the ability to demonstrate the utility of our therapy in autoimmune disease. Thank you for the time. Wonderful. Neha, thank you very much for the presentation. We'll go ahead and get started with some Q&A. Maybe we'll start with both the trials you just outlined. What's the current status of enrollment for both the internal phase I and the basket IIT study? How should we think about how many patients will be treated in those trials? Yeah. From a guidance perspective, what we have said publicly is that we have treated our first patient in each of those trials. We announced that last year. For the company-sponsored trial, we announced that in April of last year. In the basket trial, we announced that as part of our Q2 earnings, which was in the middle of the year. We have not guided in terms of enrollment and how that's going to date. I think we're all learning from our peers to not box ourselves in and providing those updates. From a guidance perspective, what we have said is initial clinical data from at least one of these trials in the first half of this year. So, I just want to spend some time focusing on your development strategy with CD20 monoclonal antibody. As you start in these early trials, do you start with rituximab or can you move to obinutuzumab or Gazyva pretty quickly? I'm curious to get your thoughts on the Gazyva lupus data that we've seen relatively recently and how that might impact your development strategy. Yeah, absolutely. Just to take a step back in terms of our monoclonal strategy in general, right? Because we're not engineered, we need to combine with the monoclonal. In general, we've been ensuring that we're combining with the monoclonal that either has been utilized in the guidelines, is approved for the indication we're going after, or looking to be approved, right? Obinutuzumab would fall in the category of looking to be approved in that indication. Actually, this morning, Roche announced that the supplemental BLA has been accepted for lupus nephritis for Gazyva. That means it's going to be approved soon, presumably this year. We think about that as an advantage to combine with something that's more established versus novel because it does shorten the path from a dose finding and a regulatory perspective as well. Just to touch on, that's the reason why we included obinutuzumab in our company-sponsored trial in lupus, to give us the ability to generate a data set in a monoclonal that is looking to get approved in that indication. The protocol allows for rituximab and obinutuzumab to be dosed in parallel, right? To answer your question, we have the ability to dose them in parallel. Physicians are very excited about obinutuzumab. We heard that yesterday in the KOL panel as well. The good part, again, is they're used to administering these monoclonals, right? To add on an NK cell for them is not that high of a burden because they are very comfortable with monoclonal administration at this point. Just to touch on the REGENCY study in the Phase III trial. First and foremost, again, we are excited to see that it is looking to get approved, right? From a strategy perspective, the opposite would not have been a good thing, right? The fact that it met its primary endpoint and it is looking to get approved. A couple of things to highlight on that data set. First, they show the primary endpoint, 46% response, in the patients at 18 months. That was on top of background medication, so MMF and steroids. The control arm also had background medications and steroids. It was a specific steroid taper that was required in the patients in that trial. While the headline 46% is a great response, right, much better than what monoclonals have done historically, if you look at it adjusted for background meds, it's a 13% separation from control arm. That, to us, highlights the unmet need, right? The 13%, if you take away the background medication, which is really what you're trying to do, is get patients to respond, but also importantly, get off of the MMF with steroids in this case, there is a lot of room for improvement from what even Gazyva has shown, right? We look at that as a positive. There are a couple of other things I'd highlight about that data set as well. I mean, things we don't know yet, right? One is the chronicity of the disease. There are a huge range of patients they enrolled. We don't know how fast the proteinuria resolved, for example. These are all things that, again, it's helpful to have that data set out there now with a large number of patients for us to understand. I think overall, we viewed it as a positive, both from the fact that it's going to be utilized in these patients, but also from what it demonstrated from an efficacy standpoint. Do you think there's room to improve because Gazyva is not getting complete B- cell aplasia and it's not durable? Is it one of those or both? Yeah, I think it's a combination, right? I think we know that in order to get a response, it's not enough to just deplete B cells in the periphery. You have to get in the tissues. We have, I think, shared this before. Monoclonals do not do a great job of even depleting B cells in the periphery. Therefore, why would they do a good job depleting B cells in the tissue as well? Gazyva is looking better than rituximab. I think we can say that, right? I think, as we have said before, our strategy of we have a high affinity CD16 NK cell. The biggest difference between Gazyva and rituximab is this affinity for CD16. If you can enhance that ADCC even more, right, does that produce a more durable response, but also being able to get these patients off of their medication. For the initial clinical trial data update by the end of the first half, will it be from one of the two trials, or could it be from both? Love these questions, Tyler. I'm going to repeat our guidance, which is we'll have data from at least one of the trials. OK, at least one. How many patients will likely be included? I have to ask. Yeah, no, I know you do. OK. I mean, what I'd say is, listen, we are all looking at what everyone else is presenting, right, in terms of our peer set. So far, we've seen a lot of auto CAR T data from commercial companies. We've seen some allo CAR T data. We've seen TCE data more from an academic setting. We're seeing how people are presenting, what level of follow-up, all those questions that everyone's looking to get answers for. I think for us, given that we are a unique approach versus what everyone else is going after, being an NK cell, being a non-engineered NK cell in combination with monoclonals, we know there's a lot of questions people want to answer, right? There's a lot of questions we ourselves need to answer as we move forward into registration, whether it's what indication, what dose, right? Where are we going to take this? Where in the line are we going to be? What does the registrational study look like? We're not going to answer all of those questions, right? I think we do think there is utility in answering, starting to answer some of those questions, given our modality and our differentiation, and to start to thread the needle from where we were in NHL and what we demonstrated there and how that's translating into autoimmune. What questions might you start to answer with the update by the end of the first half? What might you guys provide us? I think I'll go back to saying we're not going to answer all of the questions that everyone has, but I guess we'll start to early B- cell aplasia data and safety, essentially, probably? I would point back to the trials we have today, right? The fact that we've said it's at least one and that we're looking at all of the above in those trials, right? We're looking at all the translational markers, the safety. We do think safety is important. I don't want to minimize safety. I think people take that for granted. We're not providing any guidance beyond that. Yep. Obviously, after this update, these phase ones, I imagine you'll continue to enroll and you want to collect enough data prior to thinking about the next stage of development. Do you guys have any perspective at a high level how many patients you might need in totality of confidence moving forward to the next stage of development? Yeah, I mean, it's a direct question to ask. I think what we've seen, also, we do believe that being best part of CBER versus CDER, TCEs, for example, versus us does give us an advantage in terms of speed in which one could move from early stage development to later stage development. I think one thing we are watching very closely is our auto CAR T peers and what kind of registrational trial design they have and what kind of data sets they needed to get there or need to get there. Kyverna, of course, is exploring a much more ultra-rare patient population with stiff person syndrome where they announced earlier this year that they have a single-arm registrational study. That is a fairly small study. Again, that is an indication that is specific to that. You could argue it is because of that. It will be really helpful to see what Cabaletta will show, will bring to the agency in terms of a data set for registration. We do think that will be important for us to watch to see where we are and very much could inform the strategy we take. We have always been pointing to this notion of if we have six patients with the follow-up that we need to start to have those conversations as a reasonable view to have. A lot of that comes from what we have seen other people say or do, but to be continued. OK, that is helpful. Regarding lymphodepletion and in particular with AlloNKs to continue to develop it, what do you think is the likelihood of being able to reduce or potentially even remove it? Yeah. Just to take a step back on cyclo or lymphodepletion and what its purpose is in the therapy, right? I think it is well understood that lymphodepletion does play a role in reducing the B- cell burden, helping with persistence, and generally contributing to activity, right, within a cell therapy. Oftentimes, if you ask a PI, would you rather have a therapy without lymphodepletion or with lymphodepletion? The answer is always, of course, without, right? We get that. I think the way to frame the question is for a therapy that looks more like ours, right, where the patient journey is in outpatient, it's off the shelf. A patient has three days of lymphodepletion. They get their monoclonal. They get the AlloNK. By getting this treatment, right, they are able to get, in a portion of patients, 18-24 months of drug plus a drug-free disease remission. For the first 30-60 days, they have to watch, and they can watch from home, right, for infection risk, so less than 10% infection risk. Would you put your patient through it? The answer is usually yes, right! It is more of the what are you getting for it that we believe matters. I think there are perceptions that the reason why patients are hospitalized is the conditioning regimen. It is really the CRS and the risk of CRS escalation that keeps patients in the hospital. The conditioning, and we have shown this in our oncology study with the patients we have treated, there is not that same risk of patients needing to come back in, for example, into a hospital setting. I will go back to the doses, the doses we are using. The cyclophosphamide dose, which rheumatologists are much more familiar with, is a fraction of the Euro-Lupus protocol and what is used in lupus indications. At the higher dose, there was minimal risk of fertility or infection. Fludarabine, there was a chapter in the 1990s in RA patients where they utilized fludarabine. It didn't work. We're using a fraction of that dose, but it was safe, right? We look at it in totality. Of course, over time, we'd want to optimize. For a first-in-human study, we want to make sure we are minimizing the variables we are changing and trying to control the experiment, if you will, to start to tease out what our drug can do in the various indications. Fair enough. With your oncology experience, you mentioned, or in general, you mentioned the ability to dose outpatient. In the oncology experience, you mentioned that the vast majority did not have to go into the hospital. For the minority that did, how long were they generally in the hospital for? It was a median of three nights, right! These are elderly cancer patients. There is a lot of social, we call them social hospitalizations, where just because of other comorbidities or their age, they had them stay in the hospital until their next dose. We do not anticipate that being the case in autoimmune where the patient population is different. I think the other thing I would highlight about that is they were treated empirically, right? Treatments that you can get in a rheumatology clinic, for example, or an outpatient clinic versus a specialized center where you need tocilizumab to be available and the protocols that are required. You touched upon the NK cell value or the AlloNK value proposition for autoimmune versus other modalities. I just want to follow up on a competitive landscape question. Is there other data sets or proof of concept data across other modalities over the last year that stand out in particular as you think about forming the AlloNK development program? Yeah, I think there's been a lot of data. I think I mainly kind of parse out what I would point to in particular that I think continues to reiterate our thesis of being the therapy of choice or the differentiation thesis in the community setting, right? I think the one comment I'd make is a lot of companies that moved into NHL, moved into autoimmune and in general modalities. There was a lot of perspective that burden of disease in autoimmune is lower, so the rates of CRS may be lower and hypotheses, if you will, that that might be the case. Even with T- cell engagers, there is a therapeutic window that could achieve a meaningful response but not have the same risk of CRS. I think what we're seeing from the data that's emerging is that for a mechanism that involves T- cells, there is a correlation between activity and tolerability. One data set we point to is the teclistamab data at ACR. It's a BCMA TCE. They showed 10 patients of data in autoimmune diseases. It was great data. It showed activity in those indications. From a tolerability profile, 8 out of 10 patients had CRS, majority of them required tocilizumab. There are other concerns, of course, also hitting the BCMA. That is one example of where they saw the efficacy, but there were challenges in tolerability. What does that mean for us, right? That means we do think, for example, therapies are going to fall in two camps. There's going to be therapies that a lot of things are going to work, right? We do believe in the scattering things are going to work. But the ones that require this more specialized treatment protocols, et cetera, are going to be utilized more in the hospital setting, large hospital centers where they have the ability to treat these patients. Whereas for NK cells, we have the ability to decouple activity from tolerability. And we could have the greatest potential to go in that community setting where they are less tolerant, right? The hospital is across the street. It's not in the same center. You could put a more benign TC in the same category, right, where it's more of a repeated dosing. Monoclonals, right, are much lower on the activity bar, but they're tolerable. They also require background meds. We kind of see the data that's emerging as starting to sort of plot in that matrix that we showed in terms of where people are stacking from a safety and tolerability and continues to leave room, we think, for us in that top right quadrant. That's helpful. Just remind me, in the oncology trials, was much Toci used with AlloNK? No. No. Great. We've got 30 seconds left. We'll go ahead and wrap up the conversation. I'd like to ask a final question. Neha, what do you believe is the most underappreciated aspect of the Artiva story by investors? Yeah, I think the room for differentiation of a non-engineered NK cell in combination with monoclonals and autoimmune, right, the ability for our NHL data to translate, I think, is one of the many things underappreciated about a therapy. The idea of decoupling this activity and efficacy to have the greatest value proposition in a number of indications in rheumatology even beyond lupus, I think, is one of the biggest things that's underappreciated. Wonderful. With that, Neha, thank you for your time. Thank you for having me.