Conference Transcript - RNAC 2026-04-13

Gil Blum, Analyst — Needham & Company

Good morning, everyone. My name is Gil Blum, and I am a senior biotech analyst here at Needham & Company, covering the immuno-oncology and gene therapy subsectors. It is my pleasure to have with me today, Carson Brun, the CEO of Cartesian. As a reminder, any viewers who are watching through our conference portal are able to submit questions via the Ask a Question box below the video feed window. And with that, Karsten, maybe a good place to start as an introduction. Just briefly walk us through Cartesian's core technology.

Carsten Brunn, CEO

Yeah, thanks, Gil, for having me. So Cartesian is an mRNA cell therapy company focused exclusively on autoimmune disease. Our lead asset, Deckard 8, is currently in a phase three in Myosinia Gravis. We also have published very promising phase-to-be results where we saw deep and durable responses out to a year. What makes us unique, we're truly designed to be used in an outpatient setting, so no lymphodepletion. This is given in an infusion clinic. You can go home the same day. It's a two-hour procedure. There's no risk of CRS or ICANs, and we don't use integrating vectors, so there's no risk of secondary malignancies. We're also running phase two currently in myositis, both adult myositis and duvital dermatomyositis. And last but not least,

Gil Blum, Analyst — Needham & Company

we do manufacture in-house in Maryland. Excellent. So maybe just somewhere to start with the mechanism of action of mRNA CAR-Ts. How do you guys think they mitigate the side effects that we've seen with other cellular therapies?

Carsten Brunn, CEO

Yeah, so I think there's a couple of things. So first is the modality using mRNA, which is transient in nature. So the difference, as I said up front, we don't need to use lymphodepletion. So we give multiple doses at a therapeutic level. And the other kind of key differentiator is we're using BCMA as a target, which we think is a much more precision approach. BCMA is expressed on the long-lived plasma cells, the cells that actually produce the pathogenic autoantibodies. And it's also actually expressed on so-called PDCs, plasma autodidic cells, which play a role in early inflammatory responses, kind of dual mechanism of action. I think that that's unique. So you have a much lower cell target to kill. But I think the reason we don't see CRS or ICANNs is the fact that we use transient CAR T-cells that they proliferate, but they lose the CAR signal. So there's never risk of escalating CRS. We see mild fever, which is transient, doesn't have to be treated. That's really the difference from a short-term safety perspective. And then longer term, we don't have to follow those patients for 15 years. As I said, we don't use an indicating vector. you don't have that risk of secondary malignancies as well. So it's a pretty safe modality when you hear kind of CAR-T.

Gil Blum, Analyst — Needham & Company

So targeting BCMA does and is associated with certain side effects. It's actually considered pretty potent. A recent publication from you guys provided some insights as to the kind of therapeutic windows that you're seeing with the SCAR-T-SATE. Right. Maybe you can help us understand how you're kind of not seeing a complete wipeout of BCMA expressing cells.

Carsten Brunn, CEO

Yeah. Yeah, you're right. I mean, if you hear BCMA, and we started out two or three years ago, people heard BCMA say, you guys are crazy. And it's really triggered by the DNA Cartes using BCMA, where you do see a wipeout of vaccine titers, a reduction of ITG. But that's driven, and they use lymphodepletion up front, and then the cells proliferate and wipe out pretty much a lot of the BCMA-positive cells. Now contrast this with our approach. So we don't do lymphoid depletion. So naturally, the CAR T's kind of migrate to lymphoid organs to the bone marrow, where you want to go in the first place. And because they're transient in nature, they're primarily to go after activated BCMA positive cells. So that means if you have a vaccine-tied or dose, the long-lived memory B cell, they're not activated. Whereas if you have active MG, you're constantly exposed to the antigen. So those are BCMA-positive activated, or the so-called BCMA-high cells. And that's what we primarily target, actually. So number one, it's targeting the lymphoid organs. So you don't have a lot of migration to lung and gut, where most of the memory B cells actually sit. And the other is kind of a preference for BCMA high cells, actually, because, as I said, they're activated. And then combined with the transient nature, you don't see the, say, side effect profile that you mentioned. We don't see a significant reduction in vaccine titers. You don't have to re-vaccinate patients, which is obviously much safer and more practical. And we don't see a real reduction of IgG as well,

Gil Blum, Analyst — Needham & Company

which kind of makes sense. Just to clarify, I'm sure I understand, is this because the activated cells express more BCMA on their surface? Correct. Yeah. You have basically

Carsten Brunn, CEO

more BCMA expressed, that's what I call BCMA high cells, because they're secreting all the antibodies. So they're activated, so in an activated state, and they're easier to target or CAR T cells versus more question cells, you know, like a memory B cell for a vaccine titer, they're not really activated at this point.

Gil Blum, Analyst — Needham & Company

I do want to switch gears and talk about the SCAR to say product profile. So maybe starting with a comp here, BivGuard sales continue to grow. Feedback that we've gotten from some physicians suggest that they see pretty good efficacy, especially if you can increase the number of doses beyond the label. you know with new formulations using at home injectors how do you think other modalities

Carsten Brunn, CEO

compete as it relates to the scar to say yeah so let me start by saying we're actually grateful of all the work that the f-cell antagonists have done around creating awareness about the disease um but having said this um i think fundamentally the f-cell antagonists are symptomatic therapy So, yes, if you have more doses, you have control longer. But the moment you stop, you go back to baseline. And the longer you dose, you do have chronic immune suppression. That's basically what it is. And we had last year a patient ad board. And patients, if they were appreciative of XR antagonists, it was a short-term symptom relief, but they're not disease-modifying. So there's still a large subset of patients that are looking for long-lasting central relief, and you don't get that with an FCR antagonist. And I don't think that's mutually exclusive, to be honest, as well. I mean, physicians will always try different modalities. I think where we kind of unique in terms of TPP is that with a single course of therapy, actually, you get deep and durable responses. So you kind of, from a patient perspective, it gives you kind of freedom. because you can have your antagonist constantly rotating into your neurologist's office. Even if you self-dose at home, you still have to come back to get the script refilled. And so it's a very involved regimen versus with the DECARD-8. It's one course of therapy over six weeks and then you're good for a year. I think that's really the differentiator and the durability of response.

Gil Blum, Analyst — Needham & Company

So looking at some of the other modalities, I mean, any concerns around the new regimen for Oblizna that you can give every six months? Is there any reason for competitive concern? And similarly, we recently saw an acquisition by Gilead of another VCMA CD3. Any thoughts on T-cell engagers?

Carsten Brunn, CEO

Yeah. So I think Oblizna, I think it's definitely improvement every six months, but you know that you have to give it every six months. It's still a chronic therapy. Whereas, you know, I think we believe that we don't have to give Descartes 8 chronically. We do have patients from the phase to be whooping out for years with symptom control on a single course of therapy, I think. So I think there's still a significant unmet need. I think around the TCEs targeting BCMA, I think I welcome that, you know, the community now sees that BCMA is a viable target. We actually think all along that's a good target. I would say it's early days. I think what's enticing primarily actually to investors is that it's off the shelf. But I think the data so far is fairly early. And they're often recycled oncology assets that come with side effects. They're target CD3. So you do see CRS, ICANs in a number of patients. It still has to be given at least initially inpatient. So I think that's quite a journey. But it's definitely validating BCMA as a target. We kind of look at this as a positive. Because when we started out, Gil, if you remember, two or three years ago, people said, like, why target BCMA? We're the only ones doing that. So I think that's helping us, actually.

Gil Blum, Analyst — Needham & Company

So circling back to this card as a product profile itself, how much of a burden is the aphoresis process? And have you guys done any market research on receptability to discard, I say, just given the dosing regimen that seeks weekly infusions and there's a potential redose?

Carsten Brunn, CEO

I mean, apheresis is not really a hurdle for patients or physicians. And yes, we have done proper market research with neurologists, even quantitative. And as I mentioned, we have done an ad board with patients. I think for the neurologists, we're actually positively surprised about, and that's based on a TPP in line with the face-to-be data, about a third of neurologists actually would use DECARD-8 ahead of a biologic, which surprised us because we haven't done any marking conditioning at this point. And patients are still desperately looking for something that is more doable in terms of response. So I think there's definitely a path to be a commercially viable product. There are, of course, challenges in terms of just getting the neurologist comfortable using a CAR-T. When you hear CAR-T, you're thinking DNA CAR-T. Our experience has been from the phase to be, once a neurologist has used this, they're like, wow, this is basically like biologic-like from a use perspective. If you have an infusion clinic, you have somebody sitting in a chair for two hours, basically, very similar to a biologic. So you send them home the same day. And for the patient, they can continue to be working. They don't have to take time off. If you're on a DNA CAR-T, you have to take two or three weeks off, at least reserve the time in case something happens. So this is very doable. It requires education around the fact it's an mRNA CAR-T. And maybe looking back, we shouldn't have called it a CAR T. Maybe it's more of a cell therapy, but it's definitely, it's very doable, both from a prescriber and from a patient perspective.

Gil Blum, Analyst — Needham & Company

So this is a related question. What do you think is going to be your biggest challenge, assuming you're launched in Mystina Gravis? Are we talking education pieces, as you just mentioned, the payer, something different?

Carsten Brunn, CEO

yeah i mean pair will definitely play a role but i think in order to have a successful launch and we're kind of working through that right now we definitely think we can pull this off ourselves and we think um this is a very targeted physician prescriber population there's about 2 000 neurologists um out of that probably 100 to 200 are the initial prescribers so i think the key is to focus on your centers that you had in your phase two B and we have in the phase three that have used Deckard Aid that are familiar with the setup. I think that's going to be the biggest kind of hurdle or education around the practicality of this. Like how do I actually, how do I use this as a physician, right? How do I get reimbursed? How do I set up my clinic to run this? I think the payer piece, If we've done some initial payer research, we're looking kind of annualized pricing of an FCR antagonist. So I think that's acceptable. We don't think we have any access issues around that. We have to do more work for sure. But so I think it's going to be all about having a targeted launch and a clear patient profile as well. The nice thing is that it's not that every patient out there has been dosed with a biologic. I mean, I think the latest numbers, it's about 70% have been biologically naive. Maybe the number is a bit lower now, given the penetration. But there's a huge pool of patients. You're not really directly competing head-to-head with the F's or antagonist. There is room for a new modality. And that's the other piece that we oftentimes hear. It's such a crowded market. Yes and no, it's competitive. But we're really unique modality that's differentiated and it's truly disease-modifying.

Gil Blum, Analyst — Needham & Company

so this is a related question do you foresee a pair requiring a patient fail a biologic first or

Carsten Brunn, CEO

it's just an open-ended question at this point yeah i mean um we'll have to have that discussion um we we don't think this is a kind of a prior authorization kind of play um i think this is potentially more driven by physicians being more conservative um i think you always have earlier doctors in the launch these are the guys that hey let's try this this is exciting or i've done this i've been part of the phase three i'm keen to use this in the patient kind of um as you know ahead of a biologic and there's others like i haven't been involved in this i read the papers looks interesting let me try this first and there's a patient who failed and that's your antagonist um if they see good results in bigger date they might next time use it ahead of an fcr antagonist so i think the reality is it's gonna it's gonna take time to establish a treatment paradigm but i don't think per se that you know pairs will require i think this is gonna be a requirement if the dna cartis are successful you probably have to fail on everything else and be a last resort and probably require kind of hospitalization already. I think that's going to be a bigger hurdle. I think for us, we don't think that's a requirement, at least at this point.

Gil Blum, Analyst — Needham & Company

And how do you think bears are going to treat the potential for two dosing courses as it relates to reimbursement? I mean, do you reimburse per the entire treatment course? Do you reimburse for both like how do you think this is evolving yeah i mean i think it's too early to say i think

Carsten Brunn, CEO

right now we're kind of worrying about put one course of therapy and getting a decent price for that but i think the more data we have uh i think we'll have to think through i mean is this truly a finite course of therapy so meaning maybe patients need two courses of therapy i think but then once we have data we can engage with pairs and and look at that the nice thing is that from a manufacturing perspective, we do get up to two full infusion cycles out of one apheresis, but not in every patient, but that means that the second course is kind of zero COX for us. So I think that gives us some flexibility as well on the pricing perspective, but I would say we cross that bridge once we're in the marketplace. I don't think there's going to be consideration at the time of launch.

Gil Blum, Analyst — Needham & Company

and maybe kind of to go back to the pricing dynamics as you mentioned prior so it sounds like you're looking at a you know treatment course for fcrns over a year as a comp is that fair

Carsten Brunn, CEO

yeah i think i mean most payers think about one-year cycles because patients do change plans every year so i think that's kind of a natural um we have pretty compelling 12 months data so i think we're going to walk into the conversation with um you know 12 months data and assuming annualized costs of the F0 antagonist. And luckily, that pricing is almost oncology-like, so it's a pretty high price point. So I think it works from a business model perspective for us as well, as we do have lower cost of goods because we don't use a lentil biorector. We basically use electroporation, which is a lot cheaper. It just sets the cells, you know, simply speaking.

Gil Blum, Analyst — Needham & Company

Great. I do want to shift gears and speak a little bit about your phase three, your Aurora study. So starting with kind of the basic stuff, any updates on enrollment, timing, anything that you can share?

Carsten Brunn, CEO

Yeah, so we are progressing nicely. We have all sides up and running. And to remind everyone, this is a truly global study, U.S. and Europe, both EU and non-EU. um we will give more detailed guidance uh probably by mid-year so probably next quarter just when we have full out of sight um but the study definitely is on track we're pleased with the progress um we had guided in the past and that's still standing that we have cash till mid 27 and that we would have the readout ahead of that and so some cash to spare so you can do the math when that needs to happen. And as I said, we'll give more guidance mid-year to give investors more line of sight and then also provide an update on our myositis timelines as well.

Gil Blum, Analyst — Needham & Company

Great. So what additional data disclosures do you think you're going to have from the phase two, the open label portion? If there's any timing you can provide or what kind of follow-up?

Carsten Brunn, CEO

Yeah, so I mean, we had a pretty comprehensive paper in nature medicine in january this year so i think that was that was helpful and we have a lot of inbound interest i think the other piece that is interesting now um so i mean so far nobody had to be redosed the first um 12 months but we do have some we're going to have some redosing data um so that's something we will hopefully be able to share the second half of this year and probably as part of a scientific conference. I mean, I don't think this is a major data drop. Whatever we've seen so far is very consistent. So I think, you know, I would look for, you know, some additional data that's kind of confirming the overall gestalt of the data and specifically around redosing.

Gil Blum, Analyst — Needham & Company

So maybe a question of comparability. So you have a few patients, and the OLA who have maintained minimal symptom score for really long times on like just a couple of treatment courses. Are there any examples of patients who receive standard of care from a biologist that have shown such durable responses without chronic dosing? Is that a thing?

Carsten Brunn, CEO

Not that we have seen. I mean, we have heard that patients have been on FCR antagonists for a long time. But the moment you take them off therapy, they're reverting back to baseline. So we haven't seen any publication. And it makes sense mechanistically. You're suppressing something. Once you take the foot off, it's going to go back to baseline. So we haven't seen any publication that any of those therapies are truly disease-modifying. And you guys have an SBA. Can you

Gil Blum, Analyst — Needham & Company

elaborate on the benefits of having an agreed upon plan with the fda yeah so um so we have

Carsten Brunn, CEO

we were at one of the first i think the first company get armored designation actually for an autoimmune trial of a cell therapy so we had and still have good access to fda and we took the decision to take the risk and do this under an spa it's always the risk because you can delay things so under an spa you basically tell fda look at the protocol and look at the statistical analysis plans tell us, if you agree that study is positive, it's an approvable study. And the reason we did it was that it's a single study, and in NG has been always two studies. So we just want to make sure that FDA is comfortable with that, and they are comfortable, and actually they didn't require any additional review time. That was the risk we took, that it came back, hey, we don't like what you have, and we would have delayed the start of the phase three. So we've taken a somewhat calculated risk, but it was calculated because we knew from interactions we have with the agency, they were quite positively inclined. And we have a very solid protocol, and we use placebo. And I think all the noise around cell therapy and FDA, I think the noise is really around using biomarker data versus we have a placebo-controlled study. I mean, that's rock solid. So I think we're not concerned there. And it kind of de-risks that if the study is positive, that you can file a BLA with a single study. So that's the rationale

Gil Blum, Analyst — Needham & Company

we went for an SPA. And maybe just to remind our viewers, the choice of the four-month endpoint in the pivotal study, what kind of was the reasoning around this, and how does that relate to potential

Carsten Brunn, CEO

for placebo responses? Yeah, so we wanted to de-risk the study further based on the phase 2B data, and we've done two things. So one, we narrowed the patient population to HDSR-positive patients. It has to do with the higher placebo response with seronegative patient, which creates noise. So we've done that. And most NG players have done that. I mean, the ACR positive patient are about 80% of the patient population. I think that's kind of a key driver. The second piece is that we pushed out the endpoint to differentiate even more versus placebo. And so we already saw that at month three, the placebo response is almost back at baseline. So we thought that by pushing out another month, you buy yourself a bit more of a buffer actually. So I think it's going to be definitely back at baseline. And people ask, why didn't you do like five or six months? The risk is that they're getting six sham infusions and there are no therapy for basically four months. I think you push it out further, there's a risk you lose patients because they have no benefit, basically. So we felt four months was the sweet spot and to really basically further de-risk the study from a statistical perspective.

Gil Blum, Analyst — Needham & Company

So the phase three also includes an open label extension of 16 weeks for both arms. So assuming redosing will be provided in non-responding patients only, will there be another point in time in the OLA where patients losing response could be redosed?

Carsten Brunn, CEO

Yeah, I mean, after four months, whoever loses response defined as an MGA-ADL over six can be redosed, actually. So that's very similar to the phase 2B as well, where we kind of had that option. And the nice thing on the phase 2B is that none of the patients in the active arm had to be redosed the first 12 months, which is actually a slight improvement over the phase 2A data where we had two patients at month 12 that had to be redosed. So it's kind of a little bit unusual. I mean, it's very small and so I wouldn't read too much into it. It was just luck. But I think so it's not a likely event to occur. And I think the crossover of the placebo patients makes this attractive because you know, once you sign up for this trial, you're going to be on therapy at one point, right? So versus some of the other placebo-controlled studies, you're on placebo, you're kind of out of luck. But here, because we're producing a lot for every patient, also placebo patient, you have a chance to get this after the primary endpoint's been

Gil Blum, Analyst — Needham & Company

reached. Excellent. I do want to switch gears to myositis, maybe starting with the rationale for

Carsten Brunn, CEO

moving into this indication yeah so um we had and maybe kind of going back a little bit um we had a study ongoing in sle um and i mean it was kind of we inherited it somewhat it wasn't it was an ongoing study and we looked closer at um at the market and and the disease and felt like it's a good indicator it's a tough indication um so it's like a very heterogeneous disease And what we liked about it is that in Mycena Grav, it's mainly driven by pathogenic auto-antibodies. SLE is driven by numerous pathogenic auto-antibodies and by PDC, so where you have an interferon-1 response, an inflammatory response. So mechanistically, we were interested in looking at SLE, and we saw very good responses, actually, but then decided we kind of had a tough look at what's going on in SLE in phase 2 and 3. And I think there's 30-plus trials or 40-plus trials. So it's going to be very difficult to recruit. It's unclear endpoints. It's very crowded. We said, what other indications actually do make sense? And we always had myositis kind of on the radar as an interesting mechanistic carryover from SLE. So in dermatomyositis, you also have pathogenic autoantibodies drive it, but also PDCs play a role as well. So we saw that to kind of nicely translate. It's a more manageable patient population, similar size to MG, less competitive. You have IVHG approved now. You might have PREVU approved later this year, like a daily oral check inhibitor, but it's a lot less crowded, actually. So we felt, and we had a lot of inbound interest the last two years by the myositis community They were pushing kind of for open access. And now we said, okay, let's do a trial. And then we also already had rare pediatric disease designation for juvenile dermatomyositis. So there's a lot of reasons I actually go after dermatomyositis or myositis, a larger indication.

Gil Blum, Analyst — Needham & Company

Can you provide a little bit of detail as it relates to the clinical study, timing, and what should investors expect?

Carsten Brunn, CEO

yeah so we are um so both studies or both studies are basically getting up and running as you speak with um sites um you know getting ready um so in maybe let's start with jdm um i think that's been of a sleeper indication i think people didn't really pay attention i think this has become a lot more interesting now um because if we have you know positive results and we get this approved um you are eligible for prior review voucher that program has been renewed by congress so i think there's a value in that i mean there's obviously a huge unmet need but there's also a value in that and also um we're going to dose uh three patients initially so so um basically at those escalation study, it's open label. So we might have data this year. So I think that makes this attractive. And these are patients 12 to 18. And the diseases, JDM and DM are very similar. So whatever you see, I think are good indicators for the adult as well. The adult, and so the JDM study is called the Helios study. The adult study is called the Triton study. It's kind of a seamless adaptive design where we're starting a placebo-controlled study with 10 patients. And where are we going to look at, you know, the initial data and decide on that, how to progress. And we said we have funding for the first 10 patients, and hopefully we'll be able

Gil Blum, Analyst — Needham & Company

to have that within our cash runway. And as it relates to your competitors in the space of the DNA CAR T's, why do we even see DNA CAR T's in this, in this sector? My understanding was that some myositis could be pretty severe which is one of the reasons why they went into this

Carsten Brunn, CEO

into this space in the first place yeah i mean it is i mean there's some some more patients um that have some lung involvement maybe they're higher likelihood to be hospitalized um but we still think that the dna cart is going to be a last resort here as well and i think we would go after less severe patients in an outpatient setting so uh so we're not really concerned here similar to mg um i think maybe sle is the better indication for um for dna cartis because you do have more patients in crisis especially you know lupus nephritis um you might be in the hospital setting already so there's a higher chance um so i think the the fundamental value proposition of decartate hasn't changed actually you go after earlier patients in an outpatient setting versus the DNA CARTs, by definition, going to be more the train racks that are already in a hospital setting.

Gil Blum, Analyst — Needham & Company

Great. I do want to spend a few minutes on manufacturing. You guys own your own manufacturing. You mentioned the differences in cost as it relates to DNA CARTs. Can you elaborate a little bit about capacity? I mean, the doses that are provided for patients here are pretty big.

Carsten Brunn, CEO

They're pretty big, but maybe I want to step back a little bit and talk about the process, actually, how we make. So if you kind of look at DNA CARTs, and there's been a lot of innovation around manufacturing there as well, but fundamentally, you collect the T cells, and then you transfect them with the lentil vial vector, because it's very expensive, and you try to grow them. And they don't grow well, because you just give them a viral infection, right? So that's kind of rate limiting. We take a fundamentally different approach. So we harvest the cells, and then we grow them into the billions. And because we don't transfect, we don't even have an infection, they actually grow much better. So you get billions of cells, and then at the very end, we transfect them with mRNA, and we use electroporation. We basically run an electrical current to introduce the mRNA into the cell. So it's pretty simple, and then we aliquot, freeze it, and ship it out. and we get up to two infusion cycles. Depends a bit on the age of the patient, the weight of the patient, not in every patient, but we're doing more process improvements. And I think the big advantage having this in-house is that we control the process. It's our own operators. We don't have to pay a premium to transfer this to a CDMO, at least initially. At the same time, the process is simple enough. We can transfer this to a CDMO. um you know we have capacity for probably the first two years of launch that's what you have to show fda to get the site basically approved um and but you know we see a potential to have a second site maybe do a west coast site or a european site through a cd mall potentially so it's really to kind of have full control the other advantage is you learn so much when you actually manufacture with your own operators and you know we have an m set function and continues does continuous process improvement and so if you have your operators you can share this directly you actually can work in real time to improve the process and these are all changes you can potentially implement post-approval so that was the key the key driver and it was also a bit of luck as well when people hear oh you have your own manufacturing i think this is a huge capex commitment. It's not actually. It's a leased building. We were somewhat lucky. We did a nationwide search about a year and a half ago now. And we found actually in our backyard was a Chinese CDMO in AVG and therapy just invested in this building. And they got caught up in the uncertainty around the Biosecure Act and kind of decided to step out. And we, with minimum investment, were able to take on and lease that building. So it's not a huge capex cost, but But it helps tremendously to have full control of the process, not compete with anyone else at a CD mall.

Gil Blum, Analyst — Needham & Company

So just given that this is a CAR-T, what sort of quality assurance and release criteria do you anticipate here? I mean, it's not as complex as a TIL therapy where your product numbers are really small, but any difference?

Carsten Brunn, CEO

I mean, it's pretty standard to other CAR-T therapies, actually. so there's nothing specific. I mean, we're not using a lentil viral vector in the process that helps you actually, just from that monitoring perspective. You know, you don't have that kind of risk. So I think it's pretty standard QA, QC. And we, as I said, we're doing this under ARMA designation. We had, and we have, you know, still significant and frequent interaction with the FDA. So I feel pretty confident that they're very comfortable. And also I think we're the only cell therapy player that doesn't have the 15 year kind of monitoring requirement, which shows the FDA has realized that this is a different process. But I would say it is pretty standard in terms of QAQC.

Gil Blum, Analyst — Needham & Company

Excellent. So we're reaching a little towards the end here. Maybe a couple of really general questions This has been a lot in the news. Any thoughts on potential risk for your product from the in vivo approaches?

Carsten Brunn, CEO

Yeah, so there's been a lot of noise in the marketplace. But I think I want investors to think rather that we actually are in a unique position that all those in vivo approaches use mRNA. And we do have proven payloads. So we have demonstrated our payloads are safe. We have Descartes 8, obviously, in phase three, and we have three patients with DC15. So, you know, and we think our payloads are probably agnostic to the delivery system. So we, and I think we've been pretty open about it. We don't want to distract from our autologous programs in the phase three, which is a near-term value driver. But we are actively in a couple of MTAs with delivery companies to actually test our payloads with targeted LMPs. So I think it's quite attractive. At the same time, it's still early days, I would say. We haven't seen a ton of data yet. We have some healthy volunteers. We have seen some treated patients from China. But I would say this is still early days and not an immediate competition for us. But it's something that we're working on more of a longer term life cycle management, because we all agree that you want to do this off the shelf if possible.

Gil Blum, Analyst — Needham & Company

Excellent. And before we take audience questions, any information that you feel like we should share with the street or anything we didn't cover here that you'd like to emphasize?

Carsten Brunn, CEO

Yeah, I think I just want people to pay attention that we do have a late stage asset that is pretty much de-risk and addresses a large patient population, something we can execute ourselves. So I think people overlook the commercial potential here and oftentimes group us with the DNA Cartesian. I encourage everyone to do a bit more work and reach out to us and we can walk through the story that we just did.

Gil Blum, Analyst — Needham & Company

great question um at this moment i will provide a full minutes for people to put down additional questions if they have them not seeing anything particularly uh pertinent at this point so uh with that person i do want to thank you for joining us today thanks for having me again gill appreciate