Good morning, and thank you for joining Selecta Biosciences and Cartesian Therapeutics merger announcement conference call. At this time, all participants are in listen-only mode. Following management's remarks, we will hold a question-and-answer session. At that time, lines will be open for you. If anyone should require operator assistance, please press star then zero on your touchtone phone. Please also note today's event is being recorded. I would now like to turn the call over to Blaine Davis, Chief Financial Officer at Selecta. Please go ahead. Thank you, Rocco. Good morning, everyone, and thank you for joining today's call to discuss Selecta's merger with Cartesian Therapeutics. The press release reporting on the details of the transaction can be found on the Investor Relations section of our website. Joining me on today's call for prepared remarks are Dr. Carsten Brunn, Selecta's President and Chief Executive Officer, who will remain in the role for the combined company, and Cartesian's co-founder, Dr. Murat Kalayoglu. During today's call, we will be making certain forward-looking statements based upon the current expectations of Selecta and Cartesian, which include, but are not limited to, statements regarding the expected timing, effects, and potential benefits of the transaction, the expected timing and results of a stockholder vote to approve the conversion of the Series A preferred stock issued in the merger and concurrent private financing into common stock, and our future expectations and plans for prospects for the combined company. These statements are subject to various risks that are described in the filings made with the SEC, including our most recent annual report on Form 10-K and our quarterly report on Form 10-Q, which we expect to file later today with the Securities and Exchange Commission. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of today, November 13, 2023, and Selecta disclaims any obligation to update such statements, except as required by law, even if management's views change. With that, let me turn the call over to Carsten. Thank you, Blaine, and thank you all for joining us on today's call. Turn to slide 4. At Selecta, we're committed to advancing novel therapies for the treatment of autoimmune diseases with high unmet need. Today, we are thrilled to announce our merger with Cartesian Therapeutics, a private clinical-stage biotech company, pioneering RNA cell therapies for the treatment of autoimmune diseases, that shares the same mission. The transaction was a combination of thoughtful and thorough review of strategic opportunities to drive significant long-term value for stockholders. RNA cell therapy represents a profoundly exciting novel approach with the potential to overcome the limitations that have historically prevented the application of conventional cell therapies for treating autoimmune diseases. The merger establishes a publicly traded company focused on advancing the Cartesian pioneering pipeline with a clinically validated lead program, integrated capabilities, and a strong cash position to carry the company through multiple key catalysts. Cartesian's pipeline is backed by a strong IP portfolio and consists of several exciting programs with the potential to address some of the most pressing areas of unmet need for autoimmune disease. This includes the company's lead asset, Descartes-08. Earlier this year, Cartesian reported positive phase II data in which deep and durable clinical responses in patients with myasthenia gravis or MG were observed, underscoring the potential of this approach in autoimmune indications. Cartesian's previous Chief Executive Officer, Murat Kalayoglu, who has joined the company's board of directors, will walk us through the pipeline in greater detail shortly. Selecta and Cartesian each bring distinctive and complementary capabilities to the table. Our combined strengths result in a fully integrated company with in-house cGMP manufacturing, R&D and regulatory expertise, and clinical operations. Together with Selecta's existing public company infrastructure, we believe the combined company has a solid foundation and is well-positioned for success. With several potential near-term catalysts on the horizon, including data for the phase II-B trial in patients with MG, 2024 is poised to be an exciting year for Cartesian. Importantly, with our cash resources expect to support the continued development of Cartesian's pipeline through the phase III development of Descartes-08 in MG, as well as the advancement of several additional RNA cell therapy clinical programs. We firmly believe we are in a position to deliver on our mission to improve the lives of patients suffering from autoimmune diseases. Turning to the details of the agreement on slide 5. The merger was structured as a stock-for-stock transaction, under which pro forma ownership will be split across Cartesian stockholders, Selecta stockholders, and PIPE participants at approximately 58%, 21.4%, and 20.6%, respectively. Our pro forma cash balance of over $110 million includes $60.3 million in proceeds from Selecta's concurrent PIPE financing, announced in conjunction with the merger. The PIPE financing was led by Selecta board member, Tim Springer, and we're very pleased to have his support. We believe our strong balance sheet can support the continued development of Cartesian's pipeline through the phase III development of Descartes-08 in MG, as well as the advancement of several additional RNA cell therapy clinical programs. The combined company will be known as Cartesian Therapeutics, effective today, and our NASDAQ ticker symbol will change to RNAC, effective prior to the opening of trading tomorrow, November 14, 2023. It was important to us that any transaction we entered into not only offered an opportunity for significant value creation from the investment of our existing cash resources, but that the terms maximize the value of SEL-212 for existing Selecta stockholders without dilution. We feel that the structure of this merger agreement reflects those two key priorities. Notably, as part of the transaction, transferable contingent value rights or CVRs will be distributed to Selecta stockholders and holders of Selecta's 2022 warrants as of the close of business on December 4, 2023, the record date. Holders of the CVR will be entitled to potential semi-annual distributions, representing certain cash payments received by the company related to our legacy assets. This includes potential future royalty and milestone payments for SEL-212 made by Sobi, our commercialization partner. We remain excited about the potential of SEL-212 to serve as a once-monthly urate-based treatment for patients with chronic refractory gout, and we are pleased that through the CVRs, our stockholders will be in a position to continue to realize the significant value associated with this potential stream of payments. Moving on to an overview of the combined organizations, shown on slide 6. As we embark on this exciting new chapter, I'm thrilled to announce that I will continue to lead the combined company as President and Chief Executive Officer. The balance of our leadership team will be comprised of existing team members from both companies, all of whom are deeply committed to the mission of bringing meaningful therapeutic options to patients with autoimmune diseases. I'm confident that each of these exceptionally talented individuals will play a pivotal role in steering Cartesian towards continued success. Blaine Davis, Chief Financial Officer at Selecta, as well as Matthew Bartholomae, General Counsel at Selecta, will continue to serve in these roles for Cartesian. They will be joined by several members of the legacy Cartesian team, including Dr. Metin Kurtoglu as Chief Operating Officer, Dr. Milos Miljkovic as Chief Medical Officer, Dr. Chris Jewell as Chief Scientific Officer, and Dr. Emily English as Vice President of Quality. The combined company's board of directors will be led by current Selecta Chairman, Carrie Cox. Carrie will be joined by the remainder of the existing experienced Selecta board, as well as Cartesian's co-founders, Dr. Murat Kalayoglu and Dr. Michael Singer. Cartesian's success thus far is a true testament to the relentless dedication and hard work of Murat, Michael, and the rest of the Cartesian team. I look forward to Murat and Michael's continued contributions as members of the board. With that, I'd now like to turn the call over to Murat to tell you more about Cartesian and why we believe the combined company is poised for success, as we work toward our mission of advancing novel therapies for the treatment of autoimmune diseases with great unmet need. Murat? Thank you, Carsten. Thank you to everybody joining us on today's call. I'm excited to share more about Cartesian and the potential of RNA cell therapy. Let's begin on slide 7. As Carsten mentioned, Cartesian and Selecta hold a shared vision of bringing meaningful therapeutic options to patients with autoimmune diseases. We are confident that the merger marks a pivotal step towards achieving this goal. While conventional DNA-engineered cell therapies have demonstrated high efficacy in treating several blood cancers, the associated toxicities, need for lymphodepletion chemotherapy, and high costs have limited their use beyond oncology. RNA cell therapy, in contrast, has the potential to overcome these challenges, enabling patients to be dosed more reliably and repeatedly at safe therapeutic doses in an outpatient setting, and without the need for preconditioning chemotherapy. Ultimately, we believe this translates into the ability to expand the application of cell therapies into autoimmune diseases. Our confidence in this novel approach is underscored by clinical data from our lead asset, Descartes-08, a potential first-in-class RNA CAR T-cell therapy for autoimmune diseases. We previously reported positive data from a phase II-A trial in patients with MG, in which Descartes-08 was administered in the outpatient setting without preconditioning. Descartes-08 was observed to be safe and well tolerated and to induce deep and durable responses. To support our pipeline, we have built out wholly owned internal manufacturing and R&D capabilities, which allow us to optimize processes rapidly and in an iterative manner, offering unique strategic advantages that further position us for success. Beyond Descartes-08, we have a growing pipeline of RNA cell therapies, all of which are derived from our proprietary technology and manufacturing platform, the RNA Armory. The RNA Armory is designed to enable precision control and optimization for engineered cells for diverse cell therapies. This platform enables us to design therapies to fit patients' needs and target multiple modalities, including autologous, allogeneic, and in vivo transfection approaches. In addition to our novel approach, another key differentiator that we believe sets Cartesian apart is our in-house GMP manufacturing facility, located in Gaithersburg, Maryland. Slide 8. We believe having this in-house manufacturing enhances our control of product quality, production schedules, and costs, allowing us to move assets from preclinical to clinical development quickly and cost-effectively. Of note, in the last five years, all six of our IND application submissions were accepted, which we believe speaks to the strength of the team and quality of our GMP manufacturing management systems that are focused specifically on RNA cell therapy. Now, turning to slide 9, I would now like to spend some time talking you through Cartesian's approach, pipeline, and ultimately, why we believe that our RNA cell therapies have the potential to serve as meaningful interventions for the treatment of autoimmune diseases. Perhaps the best way to understand RNA cell therapy is to contrast it with conventional DNA-engineered cell therapies. When using DNA-engineered cell therapies, what we observe is gene transfer that irreversibly and permanently modifies the cell at the level of the cell's genome. Upon administering to the body, the cells find their target, become activated, and begin to proliferate. As this process occurs, the engineered DNA translates into protein that is also amplified exponentially. Now, these cells are administered at a subtherapeutic level and proliferate into a therapeutic window. Unfortunately, though not unexpectedly, the cell does not know to stay at the therapeutic window. As the cell continues to proliferate and cross the toxicity threshold, we begin to see the toxicities that have become synonymous with DNA cell therapies, particularly DNA CAR Ts, such as cytokine release syndrome, neurotoxicity, and increased risk of infections. What's more, in order to create the immunological space for these cells to be able to proliferate in the first place, these DNA-engineered cell therapies require administration of pretreatment chemotherapy. As we know, by design, chemotherapy results in cell ablation and induces cytopenias, which, of course, in and of themselves, are hematologic toxicities. This necessitates the need to administer these therapies in an inpatient setting in order to facilitate close patient monitoring. So as you can see, the risk-benefit profile associated with these DNA-engineered cell therapies generally limits application beyond patients with very advanced disease. Now, in contrast, as you'll see on the next slide, in slide 10, by leveraging our RNA-based approach, we believe we can develop potent, yet safer, cell therapies capable of being administered in an outpatient setting. Ultimately, this could expand the reach and potential of cell therapy for the treatment of autoimmune diseases. When we think about RNA-engineered cell therapies, an important component is the fact that RNA has a predictable half-life. As a result, we are able to control the pharmacokinetics and pharmacodynamics of our product candidates. When our RNA-engineered cell therapies are administered, similar to DNA-engineered cell therapies, they locate their target and become activated and proliferate. However, in contrast with DNA-engineered cell therapies, the CAR signal we've engineered is designed to enable the cell to dilute out naturally. What this translates to is the potential to administer our therapies at therapeutic doses without uncontrollable proliferation. Perhaps most importantly, since we're not administering these therapies at subtherapeutic levels and then expecting that they will proliferate into a therapeutic window, we expect that there will be no need to administer pretreatment chemotherapy. To date, we've administered our lead RNA cell therapy product candidate, Descartes-08, to over 60 open label patients that have not observed cytokine release syndrome, neurotoxicity, or infections. In addition, patients receive their treatments on an outpatient basis, and in fact, many of them at community clinics. So in summary, our RNA cell therapies are essentially designed to shift the risk-benefit profile in ways that favor treating more patients with various types of autoimmune diseases. Moving on to our pipeline on slide 11, it's important to call attention to the fact that through leveraging our proprietary RNA Armory platform, we can deploy three different modalities across our pipeline. In addition to the autologous RNA CAR T approach used in Descartes-08 and Descartes-15, which I'll discuss shortly, we also have an allogeneic approach, where we make a mesenchymal stem cell, or MSC, and engineer it with a combination of RNA therapeutics for use as both a factory and vehicle for creating and delivering the combination to the treatment site. Descartes-33 is an example of that approach, where we engineer the MSC with a hyperactive DNase to target neutrophil extracellular traps or NETs, key drivers of the pathogenesis of autoimmune diseases such as lupus. Finally, our third modality is in vivo lymph node transfection, which aims to turn a lymph node into a factory for making CAR T- cells and other types of RNA-engineered cells. The goal being that naive T- cells enter the lymph node and then exit it armed as engineered CAR T- cells. Now, turning to our lead program, the next slide, Descartes-08, and our lead indication, generalized myasthenia gravis or MG. MG is a rare autoimmune disease that causes debilitating muscle weakness and fatigue. It is believed to affect over 120,000 patients in the U.S. and Europe.... There are no known cures for MG, and the current standard of care consists of chronic use of steroids and other immunosuppressants, which of course, are not without their own toxicities. While there are some newer agents available, including complement inhibitors and anti-FcRN antibodies, they tend to only offer modest responses with chronic administration necessary in order to maintain those responses. We believe that applying CAR T-cell therapy to MG has the potential to induce deep and durable responses and would be a welcome addition to the toolkit for both physicians and patients with MG. Additionally, MG represents an excellent starting point for deepening our understanding of the potential that RNA cell therapy could hold in other autoimmune diseases, as the pathogenesis for MG is similar to that with which we see across many autoimmune diseases. That is, it involves an attack with both T- cells as well as on plasma cells. Turning to Descartes-08, which is our approach to treating patients with MG, which we describe on slide 13. I'd like to start by highlighting that Descartes-08 was granted U.S. FDA Orphan designation for MG in 2022, which we believe provides further support for its potential. To our knowledge, Descartes-08 is the first RNA-engineered CAR-T in clinical development for an autoimmune disease. From a manufacturing perspective, typical lot processing times for infusion are within about three weeks. Descartes-08 is designed to target B-cell maturation antigen, or BCMA. BCMA is expressed in the very cells that are pumping out or secreting the autoantibody, which are long-lived plasma cells that survive for decades and express this antigen ubiquitously. We believe this antigen represents a good target, not only for in MG, but in many other autoimmune diseases as well. The other cell type that expresses BCMA is the plasmacytoid dendritic cell, which secretes a type of interferon that has been shown to contribute to disease in lupus and other autoimmune diseases. So we believe BCMA is an encouraging target, given our capabilities of going after long-lived plasma cells as well as plasmacytoid dendritic cells. Turning to slide 14, our ongoing phase II study with Descartes-08 is broken into three parts. Part One, the dose escalation portion, aimed to assess the safety and manufacturability of Descartes-08, administered in three ascending doses to each of three eligible patients. Descartes-08 was well tolerated, with no cytokine release syndrome or other serious product-related adverse events. From there, we moved to Part Two, the dose expansion portion of the trial. This portion was intended to assess the safety and preliminary efficacy of Descartes-08 when administered repeatedly across three different treatment schedules at the highest dose identified in Part One. What we observed in Part Two is that six weekly infusions of Descartes-08, notably in the outpatient setting and without pretreatment chemotherapy, led to deep, durable responses in patients with MG. I will discuss these results in greater detail shortly. Finally, Part Three of the study is the phase II-B portion, which is a randomized, placebo-controlled study. Enrollment in phase II-B study is ongoing, and we expect to share top-line data in mid-2024. Now, moving to slide 15, let's talk about the phase II-A study, the results of which were published in The Lancet Neurology this past summer. Before I get into the data, I'd like to call attention to the study population, which was comprised of patients with particularly advanced diseases, assessed by both patient and clinical clinician-reported outcomes. More specifically, 79% of patients were classified at screening to have MGFA Class 3 or 4 disease, which means that they have moderate to severe weakness affecting their muscles. As I walk you through the data, it is important to keep this context in mind. Beginning on slide 16, DESCARTES-08 was observed to be safe overall and well tolerated. Notably, there were no reports of any dose-limiting toxicities, episodes of cytokine release syndrome, or neurotoxicity. As I discussed earlier, a key differentiator between RNA-engineered cell therapy compared with conventional DNA-based approaches, is that RNA cell therapy does not require pretreatment chemotherapy. Accordingly, there were no induced hematological toxicities observed. As a reminder, it is this impressive safety profile that enabled outpatient treatment with Descartes-08 for all patients. Beyond the safe, favorable safety profile, we were also highly encouraged by the clinical response data we have observed. Slide 17 highlights data from the 10 patients who completed all 6 doses of Descartes-08. The four graphs shown on this slide are scales commonly used to assess the severity of myasthenia. The MGADL and QOL graphs in the top left and bottom right, respectively, are from the patient's perspective, while the remaining two, the MGC and QMG graphs, are physician assessments. The ones with the red dotted line are quantitative, standardized, validated instruments that are used in registration studies, and a reduction underneath that red line is a clinically meaningful decrease in that score, indicating a clinically meaningful improvement. There are a few key findings I would like to draw attention to. First, the magnitude of clinical benefit appears to be relatively large, as you can see, based on the delta we see between the clinically meaningful red line and what patients are achieving. We're also encouraged by the fact that both the patient scores as well as the physician scores correlate with one another. Finally, we observe impressive durability. I'll note that we show on this slide data out to nine months, whereas our publication in The Lancet Neurology only went out to six months. This durability bolsters our belief that our unique approach has the potential to drive clinically meaningful disease improvement. Now, as I mentioned earlier, we're currently enrolling patients in phase II-B randomized, placebo-controlled, double-masked portion of the trial, which is summarized on slide 18. An important element of this study is its crossover design, which will provide any patient originally assigned to placebo the opportunity to receive Descartes-08 after completing study treatment. The study is designed to assess the primary endpoint of the proportion of patients achieving a six-point or greater reduction in their ADL score at day 85. Secondary endpoints are designed to assess a variety of additional clinical outcomes. We look forward to sharing our top-line results with you, which we expect in mid-2024. As we collect additional data in MG, we are also keenly interested in the potential to leverage our learnings to expand Descartes-08 into other autoimmune indications. I'll briefly call attention to data shown on the right side of slide 19 from a patient we treated under expanded access with autoimmune retinitis, a rare ocular disease where the autoantibodies attack the retina, resulting in a reduction in visual acuity. This patient was treated with the same course of therapy that we are assessing in our MG trial, and what we observed was a two-line, clinically significant improvement in their vision that correlated with the disappearance of three of the five autoantibodies associated with the disease. We are encouraged by these data, which we believe offer early support for Descartes-08's potential outside of MG. Looking ahead, we are in the process of initiating a phase II study in lupus, for which we have already received IND clearance in the first half of next year. In addition, we plan to initiate two separate phase II basket studies, one in ocular autoimmune disease and the other in vasculitic autoimmune disease, in mid-2024 and the second half of 2024, respectively. Beyond Descartes-08, we are also focused on advancing our next-generation anti-BCMA rCAR-T product candidate, Descartes-15, which, as with all of our assets, was derived from our proprietary RNA Armory platform. We designed Descartes-15 to be more resistant to recycling of the CAR upon multiple antigen exposures. This is a particularly important feature to increase the durability of CAR expression on the surface of these cells. As you can see on the graph shown on slide 20, there is a significant increase in potency between Descartes-15 and 8. We are excited to introduce Descartes-15 into the clinic, which we expect in 2024. Leveraging our proprietary RNA Armory platform, we believe we are uniquely positioned to advance and evolve our pipeline of novel RNA cell therapy product candidates across three different modalities, which we'll review on slide 21. In addition to our autologous approach, which is represented by Descartes-08 and Descartes-15, we are also working to advance allogeneic or off-the-shelf therapies that leverage mesenchymal stem cells rather than T -cells. As I discussed earlier, Descartes-33 leverages this approach, and we are currently assessing its potential for the treatment of certain autoantibody-associated autoimmune diseases. In preclinical studies, Descartes-33 was observed to induce potent degradation of disease-enabling neutrophil extracellular traps, or NETs. And finally, we look forward to sharing more about our earlier work, which employs our third modality, in vivo lymph node transfection, in due course. Before we open the call up to questions, I'd like to turn it back over to Carsten for closing remarks. Carsten? Thank you, Murat. Looking ahead, we can see on slide 22 that 2024 is poised to be a potentially transformative time for Cartesian, marked by what we anticipate will be multiple exciting, value-driving milestones. With the combined company's cash following the close of this merger, expected to be over $110 million, which includes proceeds from the concurrent PIPE financing, we believe Cartesian is well positioned to support the continued development of Descartes-08 through phase III, as well as the advancement of additional programs. In closing, Selecta and Cartesian each bring distinctive and complementary capabilities to the table to create a fully integrated, publicly traded company with in-house GMP manufacturing, R&D and regulatory expertise, and clinical operations. Through this merger, we believe Cartesian is best positioned for future success and value creation, and to ultimately unlock the full potential of RNA cell therapies for autoimmune diseases. I'd like to take the time and thank all those involved in this merger for their teamwork and collaboration. Most importantly, I'd like to thank the Selecta and Cartesian teams for their unwavering commitment to improving the lives of patients suffering from autoimmune diseases. Without your hard work, we would not be where we are today. We're excited for the journey ahead, and with that, we can open the call for Q&A. Operator? Thank you. If you would like to ask a question, please press star then one on your telephone keypad. If you are using a speakerphone, we ask that you please pick up your handset before pressing the keys. To withdraw your question, please press star then two. Ladies and gentlemen, that's star then one if you have a question. Today's first question comes from Kristen Kluska with Cantor Fitzgerald. Please go ahead. Hi, this is Jason Bouvier on for Kristen Kluska. One question from us. Can you talk a little bit about the size? Actually, two questions, sorry. The size of the other opportunities for Descartes-08 outside of MG? And then, it looks like for Descartes-15 is conferring a bit more potent properties. I'm wondering what the mechanism is there, and then what further indications that technology could extend into? Thank you. Yeah, Jason, that's a great question. I think first of all, we're really excited about the potential actually in MG. Given the results that Murat just showed you in the published in Lancet Neurology, we see a deep and durable response we believe actually is truly differentiated potentially versus other competitors in this marketplace and could be really transformational for patients. So that alone, we see tremendous commercial opportunity to begin with. As Murat mentioned, we are clear to start the IND and start a study in SLE the first half of next year. That obviously is a large unmet need. And we're also looking at other therapeutic areas in terms of where this therapy might be applicable. We're doing two or we're kicking off two basket trials, one in autoimmune, orphan diseases and the other one, vasculitic autoimmune diseases as well. So I think there's really multiple applications, but we're really excited about actually, you know, having really strong phase II-A data in MG, which we think is a, is a very strong commercial play. On Descartes-15, I, I'll hand over to Murat, just talk again a little bit about the differentiation actually, and why is it more potent, based on the recycling of the CAR T receptor? Sure. Thanks, Carsten. Yeah, so the Descartes-15 was engineered with an approach that has been years in the making that reduces the recycling of the CAR upon binding to its antigen. So, you know, typically, what happens is when a CAR binds its target there, that's, that the CAR gets internalized, and we've engineered the CAR to dramatically slow down that internalization and recycling. And as a result, even after multiple exposures, we see that Descartes-15 is capable of persisting in its killing activity relative to Descartes-08. We've actually now applied that technology across our platform of RNA CAR Ts for our next generation autologous CAR T programs. Thanks a lot. Thank you. Our next question today comes from Joseph Schwartz with Leerink. Please go ahead. Great. Thanks very much. I was wondering if you could talk a little bit more about the work you've done to establish the optimal dose, level, and schedule for DESCARTES-08. And do you think the dosing will need to be any different in different settings? And then I noticed that the retinitis data in your deck was from 2000. So I was wondering, you know, why wasn't that pursued initially? Does DESCARTES-08 readily cross the blood-brain barrier or get to the retinal compartment sufficiently? And, yeah, those are my first two questions. Thank you. Sure. Yeah. With respect to your first question around the dose optimization, on slide 14, you'll see that, in Part One of the study, we interrogated a, a low and then a medium and then a high dose in an intrapatient dose escalation arm, and then advanced the highest dose into Part Two, where we administered it at various different schedules, twice a week, once a week, or once a month. And what we saw is that the weekly administration of the highest dose that we administered from Part One, gave the deep, durable responses that you saw. In addition, of course, the once weekly schedule tends to be more convenient for patients as well as for clinic scheduling infusions. So, that was how we interrogated that dose. We're comfortable with that dose moving forward with Descartes-08, and of course, with our next-gen products, whether it's 15 or others that target other antigens, you know, that interrogation will need to be done again because of the differences in pharmacokinetics. So it could be that, you know, Descartes-15 has a less frequent administration schedule, for example. We'll have to determine that empirically. With respect to your question around the autoimmune retinitis data, so those slides, Sorry, those graphics, those photos were taken from an article from Heckenlively from 2000. They are not related to the patients that we recently completed treatment for. They're representative photos of what autoimmune retinitis looks like. Okay. Yeah, those are just photographs. Right. So, what about the ability of Descartes-08 to, you know, penetrate the retina and cross the blood-brain barrier, given, you know, it's a different disease compartment than MG? I'm just curious about that. Yeah, I think that it's unlikely that that is what is the mechanism is. I think the mechanism is first and foremost the elimination of the long-lived plasma cell niches that are actively secreting autoantibody that is attacking the retina, right? So the LLPCs are sequestered in various niches, including the bone marrow, et cetera, and pathogenic autoantibody producing plasma cells are, as well as the BCMA positive plasmacytoid dendritic cells, are what are being targeted with respect to an anti-BCMA RNA CAR T. That's very helpful. Thank you. Thank you, Joe. Our next question today comes from John Newman with Canaccord. Please go ahead. Hi there. Thanks for taking my questions. Just had a question on Descartes-08 in terms of the mechanism. Just curious as to what you currently understand regarding the long-term levels of B-cells, if the treatment eliminates the B-cells or if it just modulates the levels of B-cells long-term? Sure. Yeah. So the mechanism of, I think CAR T in general, in autoimmunity, is a work in progress, right? So it's important to differentiate B-cells in this regard from long-lived plasma cells. B-cells mature into plasmablasts and then into plasma cells, long-lived plasma cells, which persist for potentially decades. And along the path of maturation, they change expression of antigens. So B-cells, which really, for the most part, hang on to the antibody they make on their cell membrane, are expressing CD19 and not BCMA, whereas as they mature and become long-lived plasma cells, they are no longer hanging on to the antibody on the surface, but rather secreting that autoantibody and not expressing CD19, but expressing BCMA. So there are multiple targets within autoimmunity. We certainly think that B-cells that express CD19 are a viable target, as are the plasma cells that express BCMA, that are actually secreting the vast majority of the autoantibody. We think that it's important to go after and interrogate multiple targets in autoimmunity. There's likely, and I think the emerging consensus of CAR T therapy, not just our approaches, but others within autoimmunity, is likely more complex than even going after the target. These are complex cell therapies, and we and others are seeing other activities beyond killing BCMA positive or CD19 positive cells, such as reductions in inflammatory cytokines, such as dramatic shifts in T and B-cell repertoires, with some clones that, you know, come to dominate the repertoire and other clones that contract and disappear after infusion. It'll be quite interesting and important to define the different mechanisms at play, because I think ultimately, the capacity of CAR Ts to target multiple nodes of the disease process simultaneously, will help explain the deep and durable responses that are seen with CAR Ts in autoimmunity, in contrast to some of the more typical, you know, antibody therapies that might have more single mechanisms, that might have more modest and transient responses. Okay, great. And then I just had one additional question on the CVRs. Just curious, if you're able to talk a little bit about how much of the CVRs are tied to the royalty on 212 versus other assets or value? Thanks. Yeah. So, that's a good question, John. And, you know, if you kind of look at our disclosure the last couple of months, we really looked to get an unencumbered royalty stream, actually around SEL-212. The most recent announcement that we transferred the manufacture of ImmTOR for SEL-212 to Sobi, with, over 10 of our employees as well in manufacturing clinical operations. So, so we really have a truly unencumbered royalty stream, so that goes 100% of the CVR, plus all our legacy assets, ImmTOR, the IgA protease, Xork. So all those actually are part of the CVR and flow back to legacy Selecta investors, John. Great. Thank you. Thank you. Our next question today comes from Gil Blum with Needham & Company. Please go ahead. Good morning, and thanks for taking our questions. So maybe a quick one on the preclinical work that was done here. Do you have any ideas about what the durability is for a CAR T like this? I mean, I'm sure you tried and booked out on, you know, animal models to see how far it goes. And I have a follow-up. Sure. Yeah. So I would just draw your attention to slide 10 in thinking through the kind of area under the curve and exposure that we think about when we look at RNA cell therapy. We've designed these cells specifically to not have extended durability. This is a key area of contrast between RNA cell therapy and DNA cell therapy. So we are not actually interested in having a single administration with a cell that is potentially around for a very long period of time, because we don't want to risk the proliferation of the cells across the toxicity threshold. Instead, we've engineered these cells to be administered over a course of six weeks, once a week for six weeks, to achieve the relevant clinical benefit long term by dosing within the therapeutic window and achieving the appropriate exposure over the course of that six-week period. So, you know, in our preclinical work, we see that the expression of CAR wanes to undetectable levels after about a week. And we've chosen the once weekly schedule, in part, based on some of that work, as well as empirically showing that that dosing schedule appears to work the best relative to some of the others we tried. And finally, of course, because it's so convenient for patients and clinics alike to schedule weekly visits as opposed to, say, twice weekly or something like that. Yeah. That, that's very helpful. And, kind of as a follow-on, so these cells still expand on antigen interaction, right? I mean, they expand a little less, I guess, and then kind of lose their expansion over time because of dilution, but they still expand on antigen engagement. Is that correct? Yeah, you're spot on. So it's not that these cells don't expand upon, you know, binding antigen and activation, and then they start proliferating like any other T- cell. But unlike DNA CAR Ts, where every division leads to a daughter cell that looks genetically identical to the parent cell, with each division of an RNA CAR T, you have a dilution of the amount of CAR, right? As one cell becomes two, becomes four, becomes eight, if you're a DNA CAR T, you have exponential amplification of the CAR signal. But with an RNA CAR T, as one cell becomes two, becomes four, et cetera, you actually have a dilution of the CAR signal because it's RNA that has a half-life, and you're, you're in essence, have a natural break in the proliferation of the number of functional CAR-positive cells, which is why you don't cross that toxicity threshold, and which is why we, we believe we don't see the cytokine release syndrome, neurotoxicity, infections, et cetera. Okay. That makes sense. Maybe this is a little bit backwards, considering you have functional data, but is there a biomarker that you guys follow? So we're interrogating a number of different biomarkers. So, you know, these cells that we're targeting are not circulating in blood, right? So these cells tend to be sequestered in niches and in tissues and bone marrow, et cetera, so there's no direct way to sample them. But we've published on this. We've looked at a number of different markers. There's the plasma cell ligands, BAFF and APRIL, which tend to correlate directly with the total load of plasma cells, are decreased significantly after the treatment, and those decreases appear to correlate with an improvement in disease severity. We see an improvement, a reduction, a significant reduction in autoantibody levels, for example. So there are a number of indirect ways for us to be able to follow. Of course, as we gather more data, and in particular, gather data on this controlled clinical study, in phase II-B clinical study, we'll have an opportunity to, you know, fully interrogate the set of biomarkers, to see something that correlates directly. All right. One last one on your in vivo program. I'm assuming this is thinking about injecting naked RNA. Is that correct? No. So the RNA that we would be introducing into the lymph node would be packaged and introduced with a nanoparticle. That makes sense. It'll be interesting if you can find a, you know, nanoparticle that goes directly to the lymph nodes without directly injecting it into the lymph nodes, but something for next time. Yeah. Thank you. Thank you. Our next question comes from Boobalan Pachaiyappan with H.C. Wainwright. Please go ahead. Hi, good morning. Thanks for taking my questions, and congrats on the transaction. So do you potentially see opportunities to bring back any of Selecta's programs back into Cartesian's pipeline? Maybe, I mean, you you have not discussed anything about MMA program, except the clinical trial was old. So maybe just to tie this with the previous question, do you plan to share any updates on the MMA program? Yeah, that's a great question. So we actually, as we said in the remarks, we actually put all the Selecta legacy assets into the CVR. And, you know, we continue to do actively looking for partners. I think especially in ImmTOR is quite attractive since we went all the way through phase III with 212 and have, you know, hundreds of patient data. So I think... And it's truly proven to induce immune tolerance. So there's definitely potential for additional partnerships, and the proceeds from those partnerships would flow back to legacy Selecta shareholders. But we've been very mindful, actually, to keep it separate from the Cartesian pipeline. So all the proceeds basically go towards the Cartesian pipeline. On the MMA program, we actually, you know, have not moved that program forward, as we said, and we will not take the MMA program into the clinic. All right. Thank you so much. Thank you. Thank you. Our next question comes from Uy Ear with Mizuho. Please go ahead. Guys, yeah, congrats on the merger. So, big picture question, my first question is, could you sort of talk a bit about the idea behind this merger, and when did the process start? I just wanted to get a better sense of how long ago this was in the thinking. Thanks. Yeah, that's a good question. Obviously, as I said earlier, we've been really working towards unlocking value for our stockholders around the SEL-212 royalty stream and made, you know, excellent progress there. We actually have known Cartesian and Murat for over a year now, actually. There's been, you know, mutual interest in the approach, you know. Selecta was more of a T- reg approach. We, you know, we initiated those discussions and felt the time was right this time to work together. This came together all very quickly. I think it's a great fit, I think for our, you know, stockholders to really retain the value of the royalty stream and the CVR and the legacy pipeline. But then also, for Cartesian to go public, and kind of get the best of both worlds. You know, getting a functioning public company infrastructure, a very experienced board, and a very high-profile investor, we thought was a very good fit strategically. My second question is, have you spoken with the FDA? I guess just wanted a better clarification in terms of phase II-B studies, with respect to the endpoint, whether... I think Carsten mentioned going into phase III. Just curious, you know, maybe is it the data perhaps not sufficient to move forward into maybe accelerated approval or something? Just wanted a better sense of the regulatory pathway for this study. Thanks. Sure. Yeah. So there really isn't any predicate that we're aware of for a placebo-controlled, randomized, controlled study for cell therapy in engineered adoptive cell therapy, and then certainly not in autoimmunity. So, you know, we're gonna learn a lot from this study, and we're going to allow the data to inform the size and design of a registration study. So, when the data read out in mid-2024, we'll take a look at it and have the appropriate conversation with the agency at that time around the size and design of a pivotal phase III study. Do you, do you envision a similar primary endpoint, or? The agency encourages sponsors to interrogate a number of different endpoints in phase II development, which is what we're doing. We've picked the MG-ADL as our primary, but certainly are examining the array of different other endpoints along the way. So we'll take a look at all of it and make the appropriate decisions in collaboration with FDA for a pivotal study design. Okay. And could you also speak a bit about, you know, maybe the type of patient who would benefit from this, or the type of patient who would initially, I guess, benefit from this therapy? We envision that patients with generalized myasthenia gravis, who are Class 2, 3, and 4, would benefit from this treatment. phase II-B study includes that 93%+ of those patients that have non-MuSK disease, so acetylcholine receptor autoantibody, other autoantibodies, including as well as seronegative patients. So, you know, we'll again take a look at the data and design the phase III study in a way that we believe is the most commercially relevant, in helping the most patients with myasthenia. Okay. Thank you. Thank you. Ladies and gentlemen, this concludes your question and answer session. I'd like to turn the conference back over to Dr. Carsten Brunn for closing remarks. Thank you, Operator, and thank you again to everyone for joining today's call. As you heard, we look really forward to embarking on the next chapter of Cartesian Therapeutics and to providing future updates on the progress. And of course, if you have any questions or wish to connect in the near term, please don't hesitate to reach out to the team. Have a great day. Thank you. Thank you. This concludes today's conference call. We thank you all for attending today's presentation. You may now disconnect your lines and have a wonderful day.