Cartesian Therapeutics, Inc. ($RNAC)

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 Carsten Brunn, the CEO of Cartesian. [Operator Instructions] And with that, Carsten, maybe a good place to start as an introduction, just briefly walk us through Cartesian's core technology.

Yes. Thanks, Gil, for having me. So Carsten is an mRNA cell therapy company focused exclusively on autoimmune disease. Our lead asset, Descartes-08 is currently in a Phase III in myasthenia gravis. We also have published very promising Phase IIb results where we saw a deep and [indiscernible] 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 and go home the same day. It's a 2-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 a Phase II currently in myositis, both adult myositis and juvenile dermatomyositis. And last but not least, 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?

Yes. 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, upfront, 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, [indiscernible] cells, which play a role in early inflammatory responses, kind of dual mechanism of action. I think that's unique. So you have a much lower cell target to kill. But I think the reason we don't see CRS or ICANS is the fact that we use transient CAR T cells that they proliferate, but they lose the CAR signal. So there's never a risk of escalating CRS. You 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 indicating vectors. 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.

So targeting BCMA does and is associated with certain side effects that'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 Descartes-08. Maybe you can help us understand how you're kind of not seeing a complete wipe out of BCMA expressing cells.

Yes. Yes, you're right. I mean if you hear BCMA, and we started out 2 or 3 years ago, people heard BCMA say you guys are crazy. And it's really triggered by the DNA CAR Ts using BCMA, where you do see a wipe out of vaccine titers, reduction of IgG, but that's driven -- and they use lymphodepletion upfront 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 lymphodepletion. So naturally, the CAR Ts 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 primarily act to go after activated BCMA positive cells. So that means if you have a vaccine titer dose lung 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 BCM high cells, and that we primarily target actually when we -- so it's -- number one, it's targeting the lymphoid organs. So you don't have a migration to lung and gut where most of the memory B cells actually sit. And the other is kind of the 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 revaccinate patients, which is obviously, much safer and more practical. And we don't see a real reduction of IgG as well, which kind of makes sense.

So just to clarify and make sure I understand, is this because the activated cells express more BCMA on their surface?

Correct. Yes, you have basically more BCMA expressed what I call BCM high cells because they're secreting auto antibodies. So they're activated, sort of an activated state, and they're easier to target for CAR T cells versus more plasing cells like a memory B cell for a vaccine titer, they're not really activated at this point.

I do want to switch gears and talk about Descartes-08 product profile. So maybe starting with the comp here. VYVGART 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. With new formulations, using at home injectors, how do you think other modalities compete as it relates to the Descartes-08?

Yes. So let me start by saying we're actually grateful of all the work that the FcR antagonists have done around creating awareness about the disease. But having said this, I think fundamentally, the FcR antagonists are symptomatic therapy. So yes, you need 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, they were appreciative of FcR antagonist as 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 symptom relief and you don't get that with an FcRn antagonist. And I don't think that's mutually exclusive, to be honest as well. I mean physicians always try different modalities. I think where we're 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 with an FcRn antagonist, you're constantly rotating into your neurologist's office. Even if you sell those at home, you still have to come back to get a script refilled. And so it's a very involved regimen versus with the Descartes-08 It's one course of therapy over 6 weeks and then you're good for a year. I think that's really the differentiator and the durability of response.

So looking at some of the other modalities, I mean, any concerns around the new regimen for Uplizna that they can give every 6 months? Is there a reason -- any reason for competitive concern? And similarly, we recently saw an acquisition by Gilead of another BCMA CD3. Any thoughts on T cell engagers?

Yes. So I think Uplizna, I think it's definitely improvement every 6 months, but you know that you have to give every 6 months. So it's still a chronic therapy, whereas I think we believe that we don't have to give Descartes-08 chronically. We do have patients from the Phase IIb who've been 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 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, target CD3. So you do see CRS, ICANS in a number of patients. It still has to be given at least initially in patients. So I think that's quite a journey. But it's definitely validating BCMA as a target as kind of we kind of look at this as a positive that -- because when we started out, you remember 2 or 3 years ago, people said like why target BCMA. We're the only ones doing that. So I think that's helping us actually.

Okay. So circling back to Descartes-08 product profile itself, how much of a burden is the apheresis process? And have you guys done any market research on receptibility to Descartes-08 just given the dosing regimen, 6 weekly infusions and there is a potential redose.

I mean apheresis is not really a hurdle for patients or physicians. And yes, we've 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 of the Phase IIb data, about 1/3 of neurologists actually would use Descartes-08 ahead of a biologic, which surprised us because we haven't done any market conditioning at this point. And patients are still definitely looking for something that is more durable in terms of response. So I think there's definitely a path to be a commercially viable product. There is -- there are, of course, challenges in terms of just getting the neurologist comfortable using a CAR T, [indiscernible] CAR T, they're thinking DNA CAR T. Our experience has been from the Phase IIb, once the neurologists use 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 chair for 2 hours basically very similar to biologics. 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 -- on a DNA CAR T, you have to take 2 or 3 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.

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

Yes. I mean payer 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 this is a very targeted physician prescriber population. There's about 2,000 neurologists. Out of that, probably 100 to 200 are already initial prescribers. So I think that the key is to focus on your centers that you have in your Phase IIb and we have in the Phase III that have used Descartes-08 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 -- 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 biologic 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 FcR 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 have really unique modality that's differentiated and that's truly disease-modifying.

So this is a related question. Do you foresee a payer requiring a patient fail a biologic first? Or is just an open-end question at this point?

Yes. I mean we'll have to have that discussion. We don't think this is kind of a prior authorization kind of play. I think this is potentially more driven by physicians being more conservative. I think you always have early adopters in the launch. These are the guys that, hey, let's try this. This is exciting or I have done this. I've been part of the Phase III and keen to use this in the patient kind of as ahead of a biologic. And there's others, they're like, I haven't been involved in this. I read the paper, it looks interesting, let me try this first and there's a patient who failed an FcR antagonist. If they see good results in Descartes-08 they might next time use it ahead of an FcR antagonist. So I think the reality is it's going to take time to establish a treatment paradigm. But I don't think per se that payers will require. I think this is going to be a requirement if the DNA CAR Ts are successful, you probably have to fail in 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.

And how do you think payers are going to treat the potential for 2 dosing courses as it relates to reimbursement? I mean, would you reimburse for the entire treatment course, do you reimburse for both? Like how do you think this is evolving?

Yes. I mean I think it's too early to say. I think right now, we're kind of worrying about one course of therapy and getting a decent price for that. But I think the more data we have, I think we'll have to think through, I mean, is this truly a finite course of therapy? So meaning maybe patients need 2 courses of therapy. I think -- but then once we have data, we can engage with payers and look at that. The nice thing is that from a manufacturing perspective, we do get up to 2 full infusion cycles out of apheresis, not in every patient. But that means that the second course is kind of 0 cost for us. So I think it gives us some flexibility as well on the pricing perspective. But I would say we crossed that bridge once we're in the marketplace. I don't think there's going to be consideration at the time of launch.

And maybe kind of to go back to the pricing dynamics, as you mentioned prior. So it sounds like you're looking at treatment course for FcRns over a year as a comp. Is that fair?

Yes. I think I mean most payers think about 1-year cycles because patients do change plans every year. So I think that's kind of a natural. We have pretty compelling 12 months data. So I think we're going to walk into the conversation with 12 months data and assuming annualized costs of the FcR 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 lentiviral vector. We basically use electroporation, which is a lot cheaper, you just step the cells, simply speaking.

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

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

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

Yes. So I mean, we had a pretty comprehensive paper in Nature Medicine in January this year. So I think that was helpful, and we have a lot of inbound interest. I think the other piece that is interesting now, so I mean, so far, nobody had to redose the first 12 months. But we do have some -- we're going to have some redosing data. 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. But we've seen so far is very consistent. So I think I would look for some additional data that's kind of confirming the overall [indiscernible] of the data and specifically around redosing.

So maybe a question of comparability. So you have a few patients in the OLE who have maintained minimal symptom score for really long time unlike just a couple of treatment courses. Are there any examples of patients who received standard of care from a biologics that have shown such durable responses without chronic dosing? Is that the same?

Not that we have seen -- I mean, we have heard that patients have been on FcR antagonist 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 SPA. Can you elaborate on the benefits of having an agreed-upon plan with the FDA?

Yes. So we have -- we were one of the first -- I think the first company get RMAT 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 a 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 an MG has been always 2 studies. So we 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 they come back, hey, we don't like what you have and would have delayed the start of the Phase III. So we've taken somewhat calculated risk, but it was calculated because we knew from the 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 derisks that the study is positive that you can file a BLA with a single study. So that was -- that's the rationale we went through an SPA.

And maybe just to remind our viewers the choice of the 4-month endpoint in the pivotal study. What kind of was the reasoning around this? And how does that relate to potential for placebo responses?

Yes. So we wanted to derisk the study further based on the Phase IIb data, and we've done 2 things. So one, we narrowed the patient population to AChR-patients. It has to do with the higher placebo response, the seronegative patients, which creates noise. So we have done that. And most MG players have done that. I mean, AChR-positive patients 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 3, 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 we think it's going to be definitely back at baseline. If you -- and people ask us why didn't we do like 5 or 6 months? The risk is that they're getting 6, 7 infusions and they're on no therapy for basically 4 months. I think you push it out further there's a risk you lose patients when they have no benefit basically. So we felt 4 months was the sweet spot and to really basically further derisk the study from a statistical perspective.

So the Phase III also includes an open-label extension of 16 weeks for both arms. So assuming redosing will be provided in nonresponding patients only, will there be another point in time in the OLE where patients losing response could be redosed?

Yes. I mean after 4 months, whoever loses response defined as an ADL over 6 can be redosed actually. So that's very similar to the Phase IIb as well, where we kind of had that option. And the nice thing on the Phase IIb is that none of the patients in the active arm had to be redosed the first 12 months. It's actually a slight improvement over the Phase IIa data where we had 2 patients at month 12 that had to be redosed. So it's kind of a little bit unusual. It's a very small answer. 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 you're producing a lot for every patient lots of placebo patient, you have a chance to get this after the primary endpoint has been reached.

Excellent. I do want to switch gears to myositis. Maybe starting with the rationale for moving into this indication.

Yes. So we had -- and maybe kind of going back a little bit, we had a study ongoing in SLE. And it was kind of -- we inherited somewhat. It was an ongoing study, and we looked closer at the market and the disease and felt like it's a good indicator. It's a tough indication. So it's like a very heterogeneous disease. And what we liked about it is that in myasthenia gravis, it's mainly driven by pathogenic autoantibodies. SLE is driven by numerous pathogenic autoantibodies and by pDC. So where you have an [ interferent1 ] response, an inflammatory response. So mechanistically, we're interested in looking at SLE. And we saw very good responses actually. But then decided we kind of had a tough look at like what's going on in SLE in Phase II and III. 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 SME. So in dermatomyositis, you also have pathogenic autoantibodies drive it, but also pDCs play a role as well. So we saw that kind of nicely translates. It's a more manageable patient population, similar size to MG, less competitive. You have IVIg approved now, you might have [ Prebo ] approved later this year, like a daily oral JAK inhibitor, but it's a lot less crowded actually. So we felt -- and we had a lot of inbound interest in the last 2 years by the myositis community as well that we're 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 actually go about after dermatomyositis or myositis larger indication.

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

Yes. So we are -- so both studies -- both studies are basically getting up and running as we speak with sites getting ready. So in -- maybe let's start with JDM. 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 because if we have positive results and we get this approved, you are eligible for priority review voucher. The program has been renewed by Congress. So I think there's value in that. I mean there's obviously a huge unmet need, but there's also a value in that. And also, we're going to dose 3 patients initially. So it's basically a dose escalation study. It's open label. So we might have data this year. So I think that makes it 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, kind of a seamless adaptive design where we're starting a placebo-controlled study with 10 patients and where we're going to look at 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 to have that within our cash runway.

And as it relates to your competitors in the space, the DNA CAR Ts, why do we even see DNA CAR Ts in this sector? My understanding was that some myositis could be pretty severe, which is one of the reasons why they went into the space in the first place.

Yes. I mean it is -- I mean there are some more patients that have some lung involvement, maybe they're higher likelihood to be hospitalized. But we still think that the DNA CAR T is going to be last resort here as well. And I think we would go after less severe patients in an outpatient setting. So we're not really concerned here similar to MG, I think maybe SLE is the better indication for DNA CAR Ts because you do have more patients in crisis, especially you have lupus nephritis, you might be in a hospital setting already. So there's a higher chance. So I think the fundamental value proposition of Descartes-08 hasn't changed to actually go after earlier patients in an outpatient setting versus the DNA CAR Ts by definition, going to be more the train racks that are already in a hospital setting.

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

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 CAR Ts, 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 lentiviral vector because it's very expensive and you try to grow them. And they don't grow them well because you just give them 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 you don't -- we don't transceiral 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 [indiscernible], freeze it and ship it out. And we get up to 2 infusion cycles. It 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. We have capacity for probably the first 2 years of launch. That's what you have to show FDA to get the site basically approved. And -- but we see a potential to have a second site, maybe do a West Coast site or a European site through a CDMO 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 we have an [ MSA ] function and continuous -- thus 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 changing to potentially implement post approval. So that was the key driver. And it was also a bit of luck as well. When people hear, 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 1.5 years ago now. And we found actually in our backyard with a Chinese CDMO in AAV gene therapy just invested in this building, they got caught up in the uncertainty around the BIOSECURE Act and kind of decided to step out and we -- with minimum investment, we're able to take on and lease that building. So it's not a huge CapEx cost, but it helps tremendously to have full control of the process, not compete with anyone else at CDMO.

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...

I mean it's pretty standard to other CAR T therapies actually. So there's nothing specific. I mean we're not using a lentiviral vector in the process that helps you actually just from a monitoring perspective. 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 RMAT designation. We had -- and we have still significant and frequent interactions 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 QA/QC.

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?

Yes. 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 our data obviously in Phase III, and we have 3 patients with DC15. So -- 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 III, which is a near-term value driver. But we are actively in a couple of NTAs with delivery companies to actually test our payloads with targeted LNP. 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 with 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.

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?

Yes. I think I just want people to pay attention that we do have a late-stage asset that is pretty much derisked 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 CAR Ts, and 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.

Great, Carsten. At this moment, I will provide a full minutes for people to put down additional questions if they have them. Not seeing anything particularly pertinent at this point. So with that, Carsten, I do want to thank you for joining us today.

Thanks for having me. Gil. Appreciate it.