Good morning, and welcome to the Selecta Biosciences first quarter 2022 financial results and corporate update conference call. Currently, all participants are in a listen-only mode. This call is being webcast live on the Investors and Media section of Selecta's website at www.selectabio.com, and it is being recorded. For opening remarks, I would like to introduce Kevin Tan, Chief Financial Officer of Selecta. Please go ahead. Thank you and good morning. Welcome to our first quarter 2022 financial results and corporate update conference call. The press release reporting our financial results is available in the Investors and Media section of Selecta's website, www.selectabio.com. Our quarterly report on Form 10-Q for the quarter ended March 31st, 2022, which will be filed today with the Securities and Exchange Commission or SEC. Joining me today are Carsten Brunn, President and Chief Executive Officer, Peter Traber, Chief Medical Officer, and Kei Kishimoto, Chief Scientific Officer. During today's call, we will be making certain forward-looking statements, including, without limitation, statements about the potential safety, efficacy, and regulatory and clinical progress of our product candidates, financial projections and our future expectations, plans, partnerships, and prospects. These statements are subject to various risks that are described in the filings made with the SEC, including our quarterly report on Form 10-Q. You are cautioned not to place undue reliance on these forward-looking statements which speak only as of today, May 5th, 2022, and Selecta disclaims any obligation to update such statements even if management's views change. I would now like to turn the call over to Carsten. Carsten? Good morning. I appreciate everyone taking the time to join us today. Despite geopolitical turbulence, macroeconomic volatility, and sector-specific headwinds, we believe Selecta's proactive approach to managing risk, which included opening additional SEL-212 clinical trial sites in the U.S. in the face of heightened geopolitical instability, prioritizing our product portfolio to manage our resources, and raising additional capital ensures that Selecta can build on the exciting progress made in 2021, and realize the full potential of our leading precision immune tolerance platform. We continue to make steady progress across our proprietary pipeline, as well as deliver on several key strategic and financial milestones. Most notably, we recently announced that the clinical hold on SEL-302, our wholly owned gene therapy candidate for methylmalonic acidemia or MMA, was lifted on March ninth, and we successfully completed an underwritten offering in April, which raised approximately $38.7 million in gross proceeds. With our modality-focused wholly owned portfolio and financial runway into mid-2024, we believe Selecta is well-positioned to execute on our clinical-stage assets in biologics and gene therapies, advance our proprietary IgG protease Xork into the clinic, complete our IgA protease clinical candidate selection for our program and accelerated development of ImmTOR‑IL for our next-generation antigen-specific precision immune tolerance platform. We're incredibly excited to advance our ImmTOR platform and bring hope to the over 24 million Americans suffering from autoimmune diseases daily. Our sharpened strategic approach has allowed us to support and accelerate the development of our wholly-owned pipeline with a focus on autologous therapies for autoimmune diseases and therapeutic biologics, as well as provide transformative solutions for our gene therapy partners to unlock the true potential of adeno-associated virus or AAV gene therapies. I would now like to walk you through key updates and recent strategic partnerships pertaining to the three pillars of our pipeline. The current standard of care for autoimmune diseases utilizes immunosuppressive drugs which are associated with side effects that often leave patients vulnerable to serious infection and malignancies or treatments that provide only symptomatic relief. Our approach is to reimagine the treatment paradigm for autoimmune disease by using our precision immune tolerance platform to restore natural immune system balance by inducing and expanding antigen-specific regulatory T-cells, thus avoiding the need for systemic immune suppression or chronic symptom masking treatments. Recent preclinical data generated by our scientific team showed synergistic activity when ImmTOR was combined with engineered IL-2 molecules that are selective for Tregs. This combination, which we call ImmTOR‑IL, shows a substantial increase in antigen-specific Tregs when co-administered with a target antigen well beyond what we see with ImmTOR alone, in which we already have observed clinically meaningful benefits. We tested ImmTOR‑IL for the ability to induce durable immune tolerance to a co-administered AAV gene therapy vector in mice. We observed complete inhibition of anti-AAV antibody formation after multiple doses of gene therapy through 117 days. Most excitingly, this effect was observed and will be considered sub-therapeutic doses for ImmTOR alone. These results suggest that this combination of a Treg-selective IL-2 with ImmTOR has the potential to increase the potency, durability, and efficacy of the antigen-specific immune tolerance that ImmTOR elicits. Our programs of engineered Treg-selective IL-2 molecules focus on a generalized expansion of total existing Treg, but not Treg specific for the autoantigens responsible for the pathogenesis of autoimmune diseases. Thus, we believe ImmTOR‑IL has the potential to be a truly differentiated first-in-class antigen-specific immunotherapy for autoimmune disease that restores immune system balance in vivo. We believe that our ability to induce antigen-specific Treg in vivo is potentially the most elegant solution to the intractable problem of restoring balance to the immune system. Further, we believe ImmTOR-IL represents a transformative evolution of our precision immune tolerance platform, with implications across all three pillars of our pipeline, in particular, the potential to create breakthrough therapies for the treatment of autoimmune disease. A key priority for Selecta in 2022 will be to accelerate the development of a proprietary engineered IL-2 molecule. We have partnered with Cyrus Biotechnology, a world leading protein engineering company, spun out of David Baker's lab at the University of Washington, to speed the development of a next generation, highly differentiated IL-2 mutein to combine with ImmTOR. We believe our ImmTOR platform is ideally suited to address primary biliary cholangitis, or PBC, a T-cell liver disease driven by a well-defined antigen. In PBC, the immune system mistakenly attacks tissue in the liver and damages the small bile ducts. Treatments to help slow the progression and prevent complication in PBC are available. However, these medications ultimately fail to control PBC, and patients often require a liver transplant. As shown in animal models of liver injury and inflammation, the ability of ImmTOR to target the liver, coupled with the expansion of antigen-specific Tregs when co-administered with IL-2, suggests that ImmTOR‑IL may be beneficial in the treatment of patients with PBC. We are continuing IND-enabling studies for this program. In parallel, we are evaluating additional targets and indications that'd be well suited for our first in class antigen-specific immunotherapy, and we'll update the market as we add indications to our pipeline in autoimmune disease. Moving on to our work in gene therapy. We believe Selecta, with a combination of ImmTOR and our proprietary IgG protease Xork, has the potential to solve some of the most difficult challenges facing the AAV gene therapy field. Patients who have pre-existing antibodies against the capsids due to prior natural exposure to the AAV virus are often ineligible for treatment. Additionally, the anti-capsid immune response prevents the ability to re-administer AAV vectors. As a result, gene therapies are considered one time only treatments. Currently, 30%-70% of the patient population for gene therapy trials are ineligible for inclusion due to pre-existing neutralizing anti-AAV antibodies, which are a result of natural infections. Thus, many patients in need are unable to access potentially life-altering therapies for which there may be few or no treatment alternatives. IgG proteases have shown promise as a pre-treatment to transiently clear pre-existing neutralizing antibodies and create a window during which AAV gene therapies could be administered. However, IgG proteases are derived from bacteria and are themselves highly immunogenic. Additionally, some IgG proteases are derived from a common human pathogen, and consequently, the vast majority of individuals have pre-existing antibodies against these proteases. Xork, our proprietary IgG protease candidate that is designed to specifically cleave human IgG, is derived from a non-human pathogen and we observe low cross-reactivity to pre-existing anti-IgG protease antibodies. We believe that the combination of Xork with ImmTOR could enable repeat dosing of this enzyme therapy. This combination of Xork and ImmTOR has the potential to simultaneously address two of the biggest issues currently limiting AAV gene therapy. Xork, to bring the power of gene therapies to those patients who would be otherwise ineligible for treatment due to pre-existing antibodies, and ImmTOR to mitigate the novel immune responses to AAV gene therapy and enable redosing. We believe that the combination of Xork and ImmTOR has the potential to provide safer and more effective gene therapies to more patients and truly unlock the potential of the gene therapy modality by transforming a treatment into a durable long-term cure. Preclinical studies suggest multiple potential benefits of ImmTOR in AAV gene therapy, including increased transient expression in the first dose, mitigation of hepatic inflammation, more durable transient expression, and inhibition of capsid-specific B and T cell responses. We are proud to have multiple presentations, both independently and in partnership with AskBio, at the upcoming annual meeting of the American Society of Gene & Cell Therapy, or ASGCT, this month. Our presentations will highlight the ability of ImmTOR and ImmTOR-IL to mitigate anti-AAV antibodies and enable repeat vector dosing. In a single-dose clinical study in healthy human volunteers conducted in partnership with AskBio, we observed the ability of ImmTOR to mitigate the formation of anti-AAV nucleosome antibodies out to 30 days, and our preclinical data in mice and non-human primates suggests that control of antibodies can be maintained with 2 additional doses of ImmTOR. Another major challenge for the gene therapy field relates to the serious toxicities associated with vector doses of 1 × 10¹⁴ vg/kg or higher. Solving this problem will likely require a multipronged approach, including engineering more efficient capsids. The ability to re-dose AAV vectors could provide a complementary strategy by enabling the administration of multiple lower doses of capsids. We would like to see the dosing paradigm for AAV gene therapy change from one and done to low and slow. By giving multiple lower doses of a gene therapy, we could potentially titrate up to the intended therapeutic level while avoiding the unfortunate adverse events that have been seen at high doses of gene therapies. Initial studies in mice suggest that ImmTOR-IL has the potential to mitigate anti-AAV antibody responses at high vector doses up to 5 × 10¹³ vg/kg. We're also excited about our collaboration with Ginkgo Bioworks to design novel AAV capsids with the goal of improving transduction efficiency, liver tropism, and immunogenicity profile. Ginkgo will design and engineer the capsids, and Selecta will conduct all non-clinical and clinical studies thereafter. This partnership leverages Ginkgo's cell engineering and high-throughput screening capabilities, and Selecta's ImmTOR precision immune tolerance platform to advance gene therapy delivery. By combining ImmTOR with more efficient capsids, we could potentially reduce the dose of gene therapy needed to see therapeutic benefit and further mitigate the risk of serious adverse events associated with high vector doses. Moving on to our wholly owned gene therapy asset, SEL-302. On March 9, the FDA cleared the IND application for our phase I gene therapy clinical trial of SEL-302, a combination of ImmTOR with MMA-101, being developed for the treatment of MMA, a rare metabolic disease in which the body cannot break down certain proteins and fats. The trial is expected to initiate in the second half of 2022 and will evaluate the safety and efficacy of SEL-302 and the mitigation of neutralizing antibodies against the MMA-101 AAV capsid. We are hopeful that the phase I trial of SEL-302 will build on the growing body of evidence supporting the potentially multifaceted benefits of ImmTOR for enhancing the efficacy and safety of AAV gene therapies and the learnings from our anti-AAV8 capsid study in healthy volunteers. We believe development of a wholly owned asset in MMA will provide an important regulatory and clinical blueprint for our leading gene therapy partners, including Takeda, Sarepta, and AskBio. We are seeing excellent progress across our gene therapy platform, and we look forward to continuing to progress ImmTOR in our wholly owned gene therapy programs. To maximize the full potential of our platform, we plan to actively pursue business development and out-licensing opportunities for both ImmTOR and Xork for gene therapy applications. Lastly, I want to provide an update on our biologics pipeline, which houses our most mature program. SEL-212 has served as an important clinical validation for a precision immune tolerance platform with over 450 patients dosed to date. Many biologics can be highly immunogenic, resulting in suboptimal responses due to the development of anti-drug antibodies after multiple treatments. Patients that develop an immune response may be forced to discontinue treatment or experience adverse reactions. We believe that the use of ImmTOR as an adjunct to biologics offers a promising approach to minimize the healthcare and economic burden of anti-drug antibodies. SEL-212 is comprised of ImmTOR, co-administered with a proprietary uricase, pegadricase, for the treatment of chronic refractory gout, and was licensed to Swedish Orphan Biovitrum, or Sobi, in 2020. As a reminder, our phase III DISSOLVE clinical program kicked off in the third quarter of 2020 and consists of two double-blind, placebo-controlled trials of SEL-212. In both trials, SEL-212 will be evaluated at two doses of ImmTOR, 0.1 mg/kg and 0.15 mg/kg, and one dose of pegadricase, 0.2 mg/kg. The original enrollment target for both studies was 105 subjects. On December 1st 2021, we closed enrollment at 112 subjects for DISSOLVE I, which is being conducted in the United States. DISSOLVE II enrollment is continuing apace and is being conducted in four countries across Eastern Europe and the United States. We have proactively undertaken steps to prioritize the safety of our patients and investigators, as well as mitigate any potential disruptions due to the evolving geopolitical situation in Ukraine and Russia. Firstly, we have temporarily suspended screening and randomization for new patients in both Russia and Ukraine, and have reserved existing clinical trial supplies in these countries for those already enrolled in the study. Secondly, to mitigate the risk of any delays, we proactively added 11 additional sites in the United States to offset the potential loss of subjects in Ukraine and Russia and speed enrollment in DISSOLVE II. We now have 55 active sites and are on track to complete the study in Q4 2022. Finally, in agreement with our partner Sobi, we have increased enrollment in DISSOLVE II to approximately 140 subjects in an effort to replace subjects enrolled in Russia and Ukraine who may be lost to operational issues. We anticipate that these mitigation efforts will see us complete both DISSOLVE studies in Q4 2022, with joint top-line data available in Q1 2023. We will continue to work closely with our partner Sobi, our clinical trial providers, and regulatory authorities to ensure the successful completion of the DISSOLVE program. With extensive clinical data and SEL-212 currently in phase III, we believe our biologics pipeline is mechanistically de-risked, and Selecta is well-positioned to leverage these learnings into our second biologic indication in IgA nephropathy, a kidney disease that occurs when immune complexes of an antibody called immunoglobulin A1 or IgA1 accumulate in the kidneys. Current treatments fail to address IgA protein de-deposits, the underlying pathophysiology of the disease. We believe our novel approach, which combines ImmTOR with an IgA1 protease, has the potential to remove injurious IgA from the kidneys, improve markers of renal dysfunction, and have a transformative impact on patients' lives. We are currently working with Idun Pharmaceuticals on the first-generation IgA protease derived from the Haemophilus influenzae bacteria. Additionally, in October 2021, we entered a collaboration with Ginkgo Bioworks to generate a second-generation IgA protease designed to have lower immunogenicity, and when combined with ImmTOR, have a potentially transformative therapeutic profile. We plan to finalize clinical candidate selection by the end of the year. We're extremely excited about the advancements across all three pillars of our pipeline and the value-driving milestones ahead. With that, I will turn the call over to Kevin to run through our financial results for the first quarter ended March 31st, 2022. Kevin? Thank you, Carsten Brunn. During the first quarter, we proactively took several steps to further bolster our balance sheet. We prioritized our wholly owned portfolio to conserve resources, restructured our loan agreement to defer principal payments for an additional 12 months, and most notably, on April 6th, we priced an underwritten equity offering, raising approximately $38.7 million before fees and expenses. As a result of these initiatives, we announced approximately $154 million in cash equivalents, investments, and restricted cash on hand as of April 11th, 2022. We believe our current liquidity will be sufficient to meet our operating requirements into mid-2024. Selecta enters the second quarter of 2022 with a strengthened cash balance that we believe will allow us to execute on our priorities despite geopolitical uncertainty, macroeconomic volatility, and biotechnology-specific headwinds. We have multiple clinical readouts and IND filings anticipated within our cash runway, and we will continue to be careful stewards of stockholders' capital and execute our strategic plans expeditiously. Reviewing our financial results in the quarter ended March 31st, 2022. Net cash used in operating activities was $11.9 million for the first quarter of 2022, as compared to $12.1 million for the same period in 2021. Collaboration and license revenue recognized was $34 million for the first quarter of 2022, as compared to $11.1 million for the same period in 2021. Revenue was primarily driven by the shipment of clinical supply and the reimbursement of costs incurred for the phase III DISSOLVE clinical program under the license agreement with Sobi. Research and development expenses were $17.7 million for the first quarter of 2022, as compared to $13 million for the same period in 2021. The increase in cost was primarily the result of expenses incurred for the pre-clinical programs, salaries, contract license, and milestone payments. General and administrative expenses were $5.5 million for the first quarter of 2022, as compared to $5.2 million for the same period in 2021. The increase in cost was primarily the result of an increase in stock compensation expense. For the first quarter of 2022, Selecta reported net income of $28.8 million, or basic net income per share of $0.23, compared to net loss of $24.6 million or $0.22 per share for the same period in 2021. I will now turn it back to Carsten for closing remarks. Carsten? Thank you, Kevin. In summary, we're pleased with our progress in Q1 2022. With a financial runway into mid-2024, we believe Selecta is positioned to reach potentially transformational inflection points across all three pillars of our pipeline. Most notably, we are excited by our plans to enter the clinic with SEL-302, complete the DISSOLVE program with our partner, Sobi, advance IMD mapping studies across our whole pipeline, support our numerous collaboration partners, and rapidly progress our next generation precision immune tolerance technology, ImmTOR-IL, into the clinic. We believe ImmTOR-IL could represent a generation leap forward for the ImmTOR platform. The strong synergistic effects we've seen in our pre-clinical work support our belief that ImmTOR-IL has the potential to unlock first-in-class antigen-specific immunotherapies for autoimmune disease, as well as improve the efficacy and safety profile of therapies in biologics and gene therapy. We'll continue to deliver on our unrelenting commitment to solving the hardest challenges in autoimmune disease and help patients overcome autoimmunity and immunogenicity through our evolving ImmTOR precision tolerance platform. Before we conclude today's call, I would also like to thank the entire Selecta team, our investors, and the many people who have been supportive along the way, including our patients and their families. With that, we're happy to take questions. We will now begin the question-and-answer session. To ask a question, you may press star then one on your touch-tone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star then two. At this time, we will pause momentarily to assemble our roster. Our first question will come from John Newman with Canaccord. Please go ahead. Hi, gentlemen. Good morning, and thanks for taking my question. You know, I had a question about the work you're doing with IL-2. Really interesting here. What I'm wondering is, you've got a proprietary IL-2 program running here with Cyrus. I'm wondering, when you take ImmTOR into the clinic in combination with IL-2, do you think you'll be taking it into the clinic with your proprietary IL-2? Or might you investigate ImmTOR on its own first with an available formulation? Thanks. Hey, John. It's a good question. So as you rightly said, we are working with Cyrus to develop a proprietary IL-2 mutein and, you know, plan to take it into the clinic with that IL-2. You know, having said that, I mean, there are other IL-2s in clinical development and you know, there's always a chance to look at those as well. For now, the plan is to take the combination with the IL-2 from Cyrus into the clinic first. We believe that the data we have at least demonstrated so far, combining ImmTOR with IL-2 in the mouse studies, where we see really a profound increase both in induction and expansion of Tregs, will be really meaningful in autoimmune disease. The other piece which we're excited about is that this not only limits us to autoimmune disease, but we're also really encouraged by the data we have seen in gene therapy, where the combination actually was dose-sparing, which is very encouraging. We also see potential application combining it with biologics as well. Okay, great. I just had one additional question, if I may. You've also got some interesting work going on with your IgG protease, and I know that, this is a bit early, but just curious as to how you might like to study that in the clinic, once you get there. Just wondering if you'd look at antibodies against gene therapy vectors, or if there are some other things that you'd like to evaluate that you think would be more meaningful. Thanks. Yeah, that's a great question, and I'll let Peter answer this, but just to kind of frame it up for everyone. Our proprietary IgG protease is from a non-human pathogen, so that we haven't seen any cross-reactivity with human sera, which we believe is a major advantage. There are multiple applications, but the one we're most excited about is as a pre-treatment for patients that had a prior AAV infection are not eligible for gene therapy. Peter, maybe you can elaborate. Well, we haven't really guided the detail, but you know how we might look at this from a proof of concept. Yes. Thank you, Carsten. Hi, John. The ability to test the IgG protease in healthy volunteers, we think is a real advantage because there is an incidence of AAV antibodies in the population. We think that we would start with a healthy volunteer study to look at the abrogation of AAV antibodies in that population. That would set up the potential for looking at multiple different gene therapies with pre-treatment with Xork. We think that the initial c linical development is relatively straightforward in that way. Of course, then we are looking for either with our proprietary MMA program or OTCD potentially or other programs, looking for those programs where we could then test it clinically with a specific gene therapy. The first relatively straightforward approach is to look at antibodies. Okay, great. Thank you. Our next question will come from Rick Miller with Cantor Fitzgerald. Please go ahead. Hi. Good morning. This is actually Kristen. Sorry about that. Wanted to ask just based on the abstracts that were published for the ASGCT conference earlier this week, and I know the presentations are very near term here, but could you talk about from a high level, the questions you're looking to really answer with some of these studies that you haven't reported on yet? It looks like you had some promising effects on inhibiting AAVrh32.33 IgG antibodies versus methotrexate, and you're looking at different capsids and routes of administration. Essentially, how might some of these studies that you plan on presenting on help shape future directions of ImmTOR for gene therapy, either by you or a partner? Yeah. Hey, Kristen. That's a great question, and actually, I'll let the man who actually conducted the studies speak to it, since we have Kei on the call. Kei. Hi, Kristen. Yeah, we have a lot of really interesting presentations at ASGCT, both our own and also ones that we are presenting with our partner, AskBio. The study you referred to with the AAVrh32.33 capsid was actually being presented by our colleagues at AskBio. It's a very interesting study because although in humans it's often seen that you get this increase in capsid-specific CD8 T cells that hasn't been so much noted in animal models. With the exception of this one capsid which has been previously published by the Wilson Group to induce capsid-specific CD8. In this study the AskBio group used ImmTOR and also compared it to a multi-dose regimen of methotrexate. The results are really pretty impressive that ImmTOR inhibited capsid-specific CD8 T cells as well as the anti-AAV antibodies as expected. Whereas methotrexate really had pretty marginal effects. The other abstracts that we're presenting relate to kind of getting to being able to redose AAV. As you know, we had the healthy volunteer study that we also did with AskBio, and we had previously reported on that and the finding that we could inhibit neutralizing antibodies out through 30 days with IMTOR with a single dose of IMTOR in healthy volunteers. Our preclinical studies in both mice and non-human primates indicate that by giving additional monthly doses of ImmTOR, we can sustain that inhibition. In addition, as Carsten was alluding to earlier, I think one of the aspirations that we have, and I think really the whole field is mitigation of these high-dose vector toxicities. Of course, one aspect is to engineer more efficient capsids or transgene cassettes. Certainly we're working with our partner, Ginkgo, on better capsids. We also feel like by changing the paradigm from dosing one and done to being able to do multiple doses or slow and low would be a significant benefit, so instead of giving one large vector dose, if we could give multiple smaller doses. We present in two different posters, one combining IMTOR with IL-2, so IMTOR-IL, and the second combining ImmTOR with an anti-BAFF agent. We show that we can inhibit antibody formation to capsid doses as high as 5 × 10¹³ vg/kg. To our knowledge, no one has been able to mitigate antibody formation at such high vector doses. Okay. Thank you for that. Looking forward to the presentations in a couple of weeks here. Just on ImmTOR-IL, I know, you know, you're doing a lot of work here and you're extremely excited about the potential, but could you maybe share for us some of the work you're doing to at least narrow down some of the potential indications you might look to start with here? Thanks again for taking the questions. Yeah, that's a great question. We actually have started with an area we know really well. Which is in gene therapy, and that's what Kei just referenced. We're extremely excited with results we see there. We have guided to PBC as our lead indication, but we are working through a process right now to identify additional indications that are, you know, Treg-mediated. We're looking at this, you know, both from a scientific perspective, you know, where do you have a high chance of technical success? Looking at available data, I mean, there is some data available already from phase I and some phase II from other companies that pursue IL-2s in autoimmune disease. That definitely, you know, helps to guide as well. We'll likely guide to another indication this year or a range of indications that we might potentially pursue. It's really a combination of, you know, what's a good proof of concept where there's clear biomarkers. We think there's a high chance of technical success, balanced with commercial potential of course, as well. I think that's kind of where we are right now. We are conducting additional studies right now in animal models in autoimmune disease, which are always a bit lengthier and, you know, you can expect for us to share some of this data as they come in. Our next question will come from Yun Zhong with BTIG. Please go ahead. Hi. Thanks very much for taking the question. It's a full question about ImmTOR-IL. It's very interesting data, and you showed there seems to be a big difference between the combination and ImmTOR alone. Also you said you are going to explore potential use in gene therapy as well, not just the autoimmune disease. I guess you're now going to use ImmTOR-IL in the planned MMA study. At what point and in which way do you think you will be introducing ImmTOR-IL into gene therapy programs? Is that gonna be more likely your own gene therapy program or more for potential partnership discussions? Yeah, that's a great question. So, you know, as you know, ImmTOR alone induces antigen-specific Tregs, whereas IL-2 alone only expand pre-existing Tregs. Really the combination, you get the best of both worlds. You get an induction and expansion of antigen-specific Tregs, which really is differentiated. We see, really, the main application in autoimmune disease, where we wanna, you know, tip the balance between T- effector cells and Tregs and that's what we're really excited about. But you're right, we're also, you know, seeing this being used in gene therapy. But we will not, at least initially, include this in MMA. I mean, in the MMA program we're testing ImmTOR based on the, you know, pretty compelling data we've generated in the anti-capsid study. I mean, there's always a chance to amend this IND and add ImmTOR-IL down the line, but at least for now, we're really focused on, you know, getting the study started in the second half of this year. It's definitely something that we continue to explore further, to really fine-tune the treatment paradigm in gene therapy. A quick follow-up, if I may. Mm-hmm. You mentioned the next generation IL-2 in the press release. With that next generation, are you able to comment what exactly are you trying to achieve or what kind of improvement as compared to the current version? Yeah. We haven't exactly guided to our approach, but I think we've been pretty clear. We're working with a leading protein engineering company, Cyrus. They come out of David Baker's lab in Seattle. You know, obviously we're trying to optimize the Treg specific component, you know, and not have any effects on T- effector cells. There are multiple approaches. If you look at the IL-2 field, you know, from fusion proteins, muteins, there's various approaches, but we haven't guided the approach that we are taking for this program. Okay, great. Thank you very much. Our next question will come from Raju Prasad with William Blair. Please go ahead. Thanks for taking the question. Just curious to know, kind of in your conversation with KOLs on the gene therapy side, with ASGCT coming up, what the duration of effect to kind of is for gene therapy, and kind of the use of ImmTOR in the clinical setting. Thank you. Yeah, that's a great question. Obviously, if you look at the data we have generated so far, is that in the human proof of concept study with a single dose of ImmTOR, we're able to control NAb titers at day 30. We know from the animal studies that ImmTOR extends the half-life of AAV capsids. So we see a rebound of the titers out to day 90. Which is expected. We've seen this in non-human primates, but we've also shown that once you control titers at day 30, if you give two additional doses, actually, you are able to control the titers long term. We also believe that after day 90, there's no more capsid around, so no more antigen. Our hypothesis and speaking with KOLs but also the FDA, we believe that three monthly doses actually is, you know, a reasonable path to go, and that's how we approach it in our MMA program, where we plan to give three monthly doses of ImmTOR. Great. Can you give us some color or context on the PBC model preclinically and how well that mimics the immune features of the disease and when we can expect data? Thank you. Was it PBC? Yeah. Okay. I'll let Kei speak about the model. Kei, you're on mute. Sorry about that. Yeah, there's actually a couple of interesting models for PBC in that these are genetic models, so the disease is spontaneous, so you don't have to induce disease in these animals. So we think it's a more accurate reflection of natural disease and certainly they're pretty well established in this field. Our next question will come from Mr. Uy Ear with Mizuho. Please go ahead. Hi, guys. Thanks for taking my questions. I guess my first question is on SEL-212. Just wondering if you need to consult with the FDA to increase the number of patients, and if that's the case, whether you have done so. I guess my second question is sort of jumping ahead a little bit. Regarding the gene therapy phase I MMA study, just wondering about how you will disclose the data. Will you do it either by patients, by cohort, or wait until the study completes? Thanks. Thanks for your questions. I'll give the first question to Peter around how we handle the increase of number of patients. Yes. Hi. Could you please repeat your question? Sure. Just wanted to know whether you need to consult with the FDA to increase the number of patients in the phase III gout study. Whether you have done so. If I may, can I also add, you know, the top line data is now pushed out to first quarter of 2023, and just wondering if that's a result of the additional patients and additional clinical sites, or is it something else as well? Thanks. Yeah, sure. Yeah. We did consult with the FDA on the changes that we made to the protocol, as well as we will handle the data from Russia and Ukraine. We'll be continuing discussion with the FDA. The increase to 140 subjects is underway. The issue of the reporting in Q1 of both trials is related to the increase in the number of subjects in the trial. As we reported, we'll complete both trials this year, meaning last patient, last visit will be completed this year. Because it'll be near the end of the year, it'll take a couple of months to lock the data and. Thanks, Peter. Your second question is around MMA. We will likely report patient by patient, you know, as we get results. We get the first results basically 90 days after we dose the first patient. We'll likely report it patient by patient basis as the data comes. Okay. Thank you. Again, if you have a question, please press Star then one. Our next question will come from Swayampakula Ramakanth with H.C. Wainwright. Please go ahead. Hi. Can you hear me okay? Yes. Thank you. All right. Great. A couple of questions from our side. Firstly, with respect to MMA, phase I trial that's out. Do you plan to include patients with isolated MMA only or those with MMA plus high homocysteine levels? What would be your rationale for that? I'll give this question to Peter. Yes. All the subjects in the trial will have null mutations, and they have clinically severe disease. Secondly, with respect to your DISSOLVE data release, your previous guidance for the top line was fourth quarter 2022, and per today's release, it's actually pushed to first quarter 2023. Just curious, is there any advantage of combining the data from both the trials and then releasing it in one first quarter 2023 versus, you know, releasing the DISSOLVE I data in fourth quarter of 2022 given that DISSOLVE I enrollment was completed last year? Yeah, it's a good question. I mean, as we have decided. First of all, the good news is that we have clarity now on the timing. We've decided to increase the patient numbers to up to 140 in DISSOLVE II. Both studies will read out by the end of this year in Q4. Then we've decided to do a joint release, you know, because they're so close together. It is cleaner to report both pivotal studies at the same time. Obviously ImmTOR-IL is pretty interesting. I think you've been hearing this a lot today. Just curious, can you comment on or what kind of safety and tolerability characteristics you're looking for before initiation of your phase I? Yeah. I think obviously we have a pretty good understanding of the safety and tolerability of ImmTOR. I mentioned it in the main call over 450 patients dosed. We'll obviously do tox studies with our proprietary IL-2, but we see some indications from the phase I, phase II studies of the other IL-2 molecules, you know, which look pretty promising as well. Okay. That's it from me. Thanks for taking my questions. Our next question will come from Gil Blum with Needham. Please go ahead. Hey, this is Gil Blum. Thank you for taking our questions. Our first question is there any near-term update or potential milestone from Selecta's partners? Yeah, good question. We get a lot. We do have multiple partnerships. It's always difficult to guide, but obviously, we've publicly disclosed that we are eligible to receive milestones of up to $80 million around clinical investigatory milestones from our partner, Sobi. We haven't disclosed the exact timing, but obviously there's some important milestones coming up. We also have guided that Sarepta, their option period basically expires in June of this year. There's basically three scenarios. One is they opt-in. We have a fully negotiated commercial term sheet. The second is they, you know, they discontinue the work, but there's also an option for them to extend the option period versus a pre-negotiated payment. There's potential other milestones, and it's very difficult to guide as they come in. I think what's important to note as well is that our cash guidance into mid-2024 doesn't include any of the milestone payments from any of the partnerships. Thank you. Considering the higher activity of ImmTOR-IL, is there any logic to moving forward with ImmTOR in earlier programs such as autoimmune diseases like PBC or IgA nephropathy? Yeah, that's a great question. I think what's important is that we see very good clinical activity with alone. I think that's very important. But we're clearly, especially in autoimmune disease, are especially excited about ImmTOR-IL in the context where you have to, in autoimmune diseases, restore balance between T- effector and T reg, and we believe that ImmTOR-IL is ideally suited to that. But we stay, you know, focused on the programs we use ImmTOR alone, such as SEL-212 and MMA. But for autoimmune disease, specifically PBC, we will likely take ImmTOR-IL into the clinic in that indication. Great. Thank you. This concludes our question and answer session. I would like to turn the conference back over to Carsten Brunn for any closing remarks. Yeah. Thank you, operator, and thank you to everyone who joined us this morning. Stay safe and healthy. This concludes today's call. Thank you. The conference is now concluded. Thank you for attending today's presentation. You may now disconnect.