Artiva Biotherapeutics, Inc. (ARTV) September 14, 2026 Conference Transcript

Good afternoon, everyone, and thank you for coming to the H.C. Wainwright 28th Annual Global Investment Conference. My name is Emily Bodner, and I'm an equity research analyst at H.C. Wainwright. I'll be doing a fireside chat with Fred Aslan, Chief Executive Officer of Arteva Biotherapeutics. Maybe to start, for those who are less familiar with the Arteva story, can you give us a bit of an intro to your alginate and case cell therapy, L-O-N-K, and your pipeline development currently?

Yeah, so thanks, Emily, for having us. So Arteva is a phase three company pursuing refractory RA. As you mentioned, we are one of the companies that's pursuing the very exciting mechanism of deep B-cell depletion. We have differentiated ourselves by actually pursuing refractory rheumatoid arthritis as our lead indication. And if we are successful based on the current competitive landscape, we should be the first of any deep B-cell depleting products to actually get to market if we're successful, and probably the very first approval in RA since 2019 when RINVOC was approved. So we'll come back to the RA market in a little bit and explain why it's so compelling. So Arteva uses NK cells to actually kill the B cells. So unlike AutoCart T, Allocart T, T-cell engagers in vivo, we don't use T cells to actually do the killing. we use NK cells. We don't engineer RNK cells, and there's a number of advantages of not engineering them, but because we don't engineer them with a car, we actually use a monoclonal antibody as part of our regimen. So monoclonal antibody binds to the B cell, and then the FC portion of the monoclonal activates RNK cells, which then does the killing. So we have been running a phase 2 trial, a basket study that includes RA as well as Sjogren's, scleroderma and myositis. And after a recent meeting with the FDA, we aligned on a registrational single phase 3 trial. We raised $300 million of capital, which takes us through the end of the phase 3 trial into 2029. And yeah, and we're located in San Diego.

Awesome. Given that you combine L and K with rituximab, what's giving you confidence that L and K is contributing to the deep B cell depletion that you're observing compared to rituximab when it's used as a monotherapy?

Yeah, that's a natural question because rituximab is part of our regimen, right? So people always want to know, well, what are you doing above and beyond what rituximab does. Now that we have phase two results with really encouraging results, high degrees of responses, significant decreases in disease activity across the board, it's pretty clear that the level of activity that we're having is above and beyond rituximab. But there's more ways in which we can describe that. The first way is the mechanism that we're going after is deep B cell depletion. And we utilize an assay. It's currently available, but very few companies have reported using that assay. But it's an assay that actually detects B cells in the periphery with a limit of detection of 0.1 to 0.2 cells per microliter. Most of the B cell depletion charts that everybody shows has a 5 to 10. If you look at rituximab specifically with assays that are that sensitive, one realizes that the average patient on rituximab still has B cells after they are treated with rituximab whereas in our patients we showed a series of all of our ra patients not a single one had detectable b cells using that assay so that combined with the efficacy that we have already seen so far i think is pretty strong evidence that it works significantly better than rituximab and then the final piece of evidence that we're going to be generating is our phase three trial is actually a randomized control trial against rituximab and one of the reasons we did choose to do a randomized control trial as opposed to an open label study is because if we were to come out with a very strong degree of efficacy, specifically ACR50, which is our regulatory endpoint, people would always ask that question. I wonder what rituximab would do in that population. And by running a randomized control trial against rituximab, then we will have very clear evidence of what we do above and beyond rituximab, assuming we're successful.

Given your lead program is in RA, what benefits do you believe that LNK brings relative to other autologous and allogeneic CAR-T or other cell therapies, given that it's mainly a community-based autoimmune disease?

Yeah, one of the biggest advantages of NK cells, I would say it's the biggest advantage of NK cells and why they matter, is because whether you're talking about autocar T, allocart T, TCEs, or in vivo car T, these all use T cells, and these all rely on T cells expanding in order to actually kill the B cells. When T cells expand, they cause cytokine release syndrome, CRS, they cause ICANs. We've recently seen with autocar T that there's other syndromes that they can also cause. Allo-NK, our NK cells, do not cause CRS. They do not cause ICANs. And so because of that, it has a safety profile that's very differentiated compared to the T-cell approaches. We have actually treated the vast majority of our patients in a community setting. So community setting is not the outpatient infusion clinic at Harvard. It's a community rheumatology practice where there's only one or two practitioners, and he or she is utilizing his or her infusion chair to treat the patients and then the patients are going home. This tolerability profile really differentiates NK cells from T cells. Now the one drawback of NK cells is that because they don't expand you have to give very high doses. So we for example give 8 billion NK cells as part of our regimen compared to something like 60 million T cells, which is the regular regimen that's given. Thankfully, we have a highly scalable manufacturing process. And because we don't engineer RNK cells, we're actually able to manufacture our cells in a way that the cogs look a lot more like a biologic than they do to traditional cell therapy. So this is the one thing that I feel like investors a lot of times don't appreciate with regards to our cells is the way you would use our cells in a community practice is you pretty much get a kit as part of the clinical trial. You get our cells in a doer, which you thaw by the bedside, and then you connect it straight to the IV. There's no specialized pharmacy. You receive the cyclophosphamide and fludarabine in an IV bag that, again, goes straight into the IV that you're administering, and then you use rituximab the way these clinics use rituximab. So there is no specialized pharmacy, no liquid nitrogen, no need for complex monitoring. It really is as simple as cell therapy gets when you compare it to a biologic.

Makes sense. You recently had a significant data readout at ULAR. Can you walk us through the data that you presented in RA efficacy-wise and how that kind of compares to what would be expected for available therapies in refractory RA?

Yeah, so we shared data on 21 patients that had 12 or more weeks of follow-up, and we honed in on the ones that had six months because ACR50 at six months is our regulatory endpoint. What we were able to show is that across the board, you know, for the vast majority of the patients, we were causing clinically significant disease activity reduction, and specifically the ACR50, out of the seven patients that were ACR50 evaluable, five out of the seven achieved an ACR50, which mathematically 71%, but those are small numbers, our bogey, the target that we are going after, is actually achieving a 50% or higher ACR50 compared to approximately 20% for rituximab. So we would like to show as part of the RCT that we can, in a way, double what the response is that rituximab offers and rituximab as some people may know you are retreated every six months with rituximab which means you keep the b cells low for this entire period and when that happens the patient is relatively immunocompromised compared to somebody whose b cells recover so in our case the b cells are able to recover they recover with a naive phenotype and then the patient is off any other biologic or targeted synthetic potentially giving the patient an opportunity to be less at risk of infection than if they were on any other chronic therapy.

Why specifically ACR50 as the endpoint and what's the significance for the the six-month time frame?

ACR50 is a pretty stringent measure of disease response, particularly as you get into refractory patients. ACR20 has been used in the past for regulatory purposes, But we find that the bar for ACR20, it's not so high for you to achieve an ACR20. So it doesn't provide as a robust dynamic range for what we're looking for. ACR50, on the other hand, has a pretty wide dynamic range. So pretty much every approved therapy only has an opportunity to drive a 10% to 20% ACR50 by the time you become a refractory patient. So coming in with a 50% or higher ACR50 is a very clinically meaningful way to demonstrate superiority over rituximab and as a proxy for everything else. Because rituximab pretty much works as well as anything else does in a refractory population.

Looking longer term, what are your expectations for longer term data and durability that you believe would be sufficient for kind of commercial use?

So, you know, the notion of durability in autoimmune disease really comes from the autocar T world where you treat the patient and then you want to monitor how long they receive a benefit because you're unlikely to retreat the patient, again, in the near term with autocar T given it's expensive, you have to do it in a hospital setting, there are side effects. In our case, because the COGS is pretty low, the tolerability profile is a lot better than when you use T-cells. And because you can redose our therapy, our expectation is that one would get the treatment with our therapy. They would benefit from that therapy for 12 months or more. And then when they lose their response, and if they lose their response, then they have an opportunity for another treatment. So this way, we can think of durability, not just in terms of how long do you benefit from one single treatment, but how many years can you derive benefit from our treatment with these very infrequent infusions. And in between those infusions, you have these periods where you're off any biologic or JAKS.

How are you implementing the redosing potential in the randomized controlled trial?

Right. So we are giving our patients that have a response. We're monitoring how long that response lasts. And then when the physicians deem that they are losing their response, that's when they would become eligible to receive a second treatment. So this gives us an opportunity to, number one, measure how long does it take from when they get treated to when a physician thinks that they're losing response, and now they have to consider something else, to treating a subset of those patients and then figuring out whether we're seeing the same pharmacokinetic results, the same pharmacodynamic results as the first time, but then more importantly, that they're actually benefiting the second time around the way they did the first time around. We have good evidence from our oncology data where we did retreat patients that we can see similar levels of PK between the second treatment and the first treatment, and we have no evidence that our cells are being rejected. So that makes us very confident that we can retreat patients multiple times.

Awesome. And you've discussed how you're planning to have an updated data presentation this year at ACR. Maybe just talk to us what that would look like from a patient follow-up perspective.

Yeah. What we guided is that we're going to be sharing updated data on at least 20 RA patients where 10 of them specifically meet all of the phase three criteria. We're going to have data on at least 10 Sjogren's patients and at least five scleroderma patients. All of those patients would have more than six months. Now, we have treated a lot more patients than that. They're just on earlier stages of follow-up. As of our last update in April, we had treated over 70 patients with autoimmune disease, which is in addition to the over 60 patients that we treated in oncology. So we have a very robust data set now across indications, demonstrating a good level of efficacy, which we did in oncology, and now across multiple autoimmune diseases.

Maybe walk us through where you are with getting ready for the randomized controlled trial and timelines that you've kind of provided in terms of enrollment and data completion.

Yeah. So we're using words like we are initiating the phase three trial so very specifically where we are is we had the meeting with the fda during the second quarter of this year where we aligned on what that phase three is and now we're going through the process of getting that phase three started and what we guided is that before year end we would provide an update just more concretely stating where we are with regards to site initiation and timing for enrollment. But the goal is to actually read out on this phase three trial by the end of 28. So as I mentioned before, with the 300 million that we raised, we have enough cash to get into 2029. So we are well-financed to run this trial and to report out on the phase three.

How many sites are you planning to have on the phase three trial? And kind of what is your confidence with achieving the enrollment timelines within that about 18-month time frame?

We're planning to have 80 sites or more. And again, we're planning to enroll 150 patients. So that feels like considering how strong enrollment has been for us as part of the phase two, we feel really confident that we can enroll within the time that we have set out. And again, I think this comes from the fact that we are doing most of our treatments in a community setting. So there's a lot less bureaucracy. You see, if you go into an academic center to actually test TCEs or to test cell therapy today, you need rheumatology to work with oncology under the guidance of the cell therapy department. When you go work in a community rheumatology practice, you don't have any of that bureaucracy, right? The rheumatologist can actually do all of the treatments. So because of the safety profile that our treatment has, we have the ability to go into these practices. So that opens up the possibility of going into many sites and to have enrollment happen pretty rapidly.

Maybe you've talked to us a bit about what the market opportunity could look like in refractory RA. And as you kind of speak to physicians in the trial or et cetera, what is kind of the, like, do they want new therapies? And how is the kind of cell therapy process kind of looked up?

Great. So the RA, I think, as everybody knows, is maybe the largest indication there is for pharmaceuticals or maybe the second largest. Now we have JLP1s. But it's a 20-plus billion-dollar market just in the U.S., and now we have many drugs that have been approved for RA. Historically, taking a product through phase three in RA cost a billion dollars because you have to do thousands of patients in order to get the approval. And today, we have so many drugs that are now competing to be that first drug that you take after you fail methotrexate or even to be that first drug you take following a failure with TNF. Typically, a TNF inhibitor is the first product that you would be on, and then you would go on to a second product. Most commonly, it's either Orencia or it would be one of the JAKs. And as I mentioned, RINVOC was the last JAK to be approved in 2019. Now, all the labels of all the existing approved drugs in RA are for that first or second line that I mentioned. There is no drug that was ever tested specifically for an approval in patients that have failed two distinct classes. Now, when you look at papers in the literature about the efficacy of existing drugs in this, what we're calling the refractory population following two failures, the ACR50s are in the 10% to 20%. So on the one hand, if you ask physicians, do you have drugs that you can use with your patients, they will say yes, because there's been many drugs that have been approved. And I think, as everybody appreciates, part of your role as a physician is to not let the patient leave the office without a script if they're desperate for something. So if that is your priority, there is another script that you can write. But if you ask them, how likely are you to actually really address the unmet need in patients that have failed two or more classes, that's when they recognize that the existing drugs don't really work there. And 25% of RA patients that ever start a biologic have actually failed two or more distinct classes. So we are talking about a quarter of maybe the largest autoimmune indication. No product has ever been approved for that segment. And it's been almost 10 years since the last drug was approved there, which means that this pool of patients that are refractory to the approved drugs continue to grow. So it's really one of those things. As you know, Emily, we started in oncology. And so as we were going into RA, I was expecting there to be a very crowded space, just given how big it is and how there is this unmet need with refractory patients. But it turns out that a lot of companies had this notion of how big the development had to be in order to get there, because one was using incremental benefits, which has been the reality of the prior drugs that have been approved in the space. If you can actually come in with an ACR50 of 50% or higher compared with an active control of an approved drug at 20%, you don't need that many patients in order to show a delta. And because it's a refractory population, the safety database can also be more modest than what has been required in the past.

Makes sense. Maybe with our last few minutes, If you can kind of talk about indications outside of RA, you touched on Sjogren's and scleroderma. So what could development in those areas look like? And are you kind of waiting to see the RA data or is there opportunity to kind of move forward with one of those earlier?

Well, we want to make sure that we actually do the best job we can in RA. And as I mentioned, it isn't just about the randomized control trial. It's about proving that retreatment works. And it's about being very thoughtful about how we measure that time to next treatment and the ability to actually retreat patients. Once we feel that RA is in a good spot, we can start thinking about what is that the lowest amount of cyclophosphamide and fludarabine that's actually needed in order to drive good results. Now, we believe that the doses that we're currently using are quite tolerable as they are. but everybody would prefer if you could find a way to actually give less cyclophosphamide and fludarabine. So there's an opportunity to optimize that. And then we can start looking at additional indications. Today, we use the additional indications in order to convey that the drug is very active, right? So in case people are wondering, oh, well, maybe you got lucky in RA, when we show high response rates in non-Hodgkin's lymphoma, high response rates in Hodgkin's lymphoma, good clinical activity in Sjogren's, and good clinical activity in scleroderma, that puts the RA efficacy into perspective. But we do see a lot of value in making this franchise be actually a lot broader, not just with one indication, but multiple indications.

And maybe to end just on a quick summary of upcoming catalysts and milestones for the next 12, 18 months.

Well, so we have been very specific with the milestones over the next six months, which is this updated clinical data with more patients, more follow-up, not only in RA, but in additional indications. Then as we look at 2027, again, the follow-up will be even longer. We will probably have at that point retreated patients, so we can start commenting on what that pharmacodynamic effect of retreatment is. Eventually, we can show what that clinical effect is in the patients that we have been retreating. We will continue to provide updates on where the RCT is, as well as updates as to how we're thinking about a second indication. So a number of catalysts happening in parallel to the phase three trial running.

Perfect. Thank you very much, Fred. Thanks to everyone who's been listening in. Hope everyone has a great rest of their day.

Thank you.