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spk11: Good morning and welcome to the Selecta Biosciences third quarter 2022 financial results and business update conference call. Currently, all participants are in a listen-only mode. This call is being webcast live on the investor and media section of Selecta's website at www.selectabio.com and is being recorded. After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star then one on your touchtone phone. And to withdraw your question, please press star then two. For opening remarks, I would like to introduce you, Mr. Kevin Tan, Chief Financial Officer of Selecta. Please go ahead, sir.
spk07: Thank you, and good morning. Welcome to our third quarter 2022 financial results and business update conference call. The press release reporting our financial results is available in the investors and media section of Selecta's website, worldwidewebselectabio.com, and our quarterly report on Form 10-Q for the quarter-ended September 30, 2022, which we intend to file in the coming days with the Securities and Exchange Commission, or SEC. Joining me today are Carson Bruhn, 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, our 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 most recent annual report on Form 10-K and subsequent quarterly reports on Form 10-Q. Your cautions not to place undue reliance on these forward-looking statements which speak only as of today, November 3rd, 2022, and selected disclaims any obligation to update such statements as required by law, even if management's views change. I would now like to turn the call over to Carson Brun. Carson?
spk10: Thank you, Kevin. Good morning. I appreciate everyone taking the time to join us today. In the third quarter of 2022, we continued to make steady progress across the pipeline, and with an expected financial runway into mid-2024, we believe we're well-positioned to execute on our key priorities and reach multiple near-term value-driving events. In collaboration with our partner, Sobe, we expect to both complete the SEL212 Phase 3 dissolved trial and announce joint top-line data in Q1 2023. We also remain on track to advance SEL302, our proprietary gene therapy candidates, in combination with mTOR to treat metabolic acidemia or MMA into a phase one clinical trial in this quarter. Our key priority continues to be accelerating the development of our next generation precision and tolerance platform, mTOR-IL. We've made substantial progress in identifying a proprietary IL-2 candidate and continue to believe we'll have a clinical lead candidate by year end. Additionally, Our team continues to advance our preclinical pipeline, most notably the IMD enabling studies and manufacturing scale-up for our proprietary ITG Protease Zork as a pretreatment for AV gene therapies and IgA Protease candidate selection with our partners for the treatment of IgA nephropathy. On the cusp of these key milestones, we'd like to share details on how these programs, together with recent activities, align with our mission to solve the toughest challenges associated with autoimmunity and unwanted immunogenicity. Let us begin with the applications of our precision immune tolerance platform for autoimmune disease. Currently, over 24 million Americans suffer from autoimmune diseases, and while the current standards of care utilize immunosuppressive drugs or symptom masking treatments, These treatments leave patients vulnerable to serious infection and malignancies and fail to adequately address the underlying cause of the disease, which is an imbalance of T-regulatory cells versus T-effector cells. By combining intral with autoantigens, we hope to restore natural immune system balance by inducing and expanding antigen-specific regular T-cells in vivo. As we have highlighted before, we're very encouraged by our growing body of preclinical data in which we've observed the potential to amplify the magnitude and durability of end-specific immune tolerance by combining mTOR with an engineered T-REX-selective IL-2, an evolution of a platform we call mTOR-IL. By focusing on the induction and expansion of T-REX, specific to the autoantigens responsible for the pathogenesis of autoimmune diseases, we believe mTOR-L has the potential to be a truly differentiated, first-in-class treatment for those suffering from autoimmune diseases. The first autoimmune indication in which we plan to evaluate mTOR-L is primary biliary cholangitis, or PBC, a T cell-mediated liver disease driven by a well-defined antigen Co-administering mTOR-L with PDC-E2, the autoantigen implicated in PDC may result in the expansion of Tregs specific to PDC-E2 and restore immune system balance. We continue work on identifying additional autoimmune indications to expand, and we expect to select an IL-2 candidate by year end. We also plan to provide an update on the broader strategic development path for Intor-L in the near future. Moving on to our gene therapy vertical. In Q4 2022, we expect to initiate the Phase 1-2 trial of SAL302. As a reminder, SAL302 is a combination of Intor with MLA101, an AV gene therapy being developed for the treatment of metabolic acidemia, a rare genetic metabolic disease. The Phase I-II trial will evaluate the safety and efficacy of SEL302 in treating MMA and in TOR's ability to mitigate utilizing antibodies against the MMA101 AV capsid. We believe this trial will build on the growing body of evidence pointing towards the potentially multifaceted benefits of mTOR in enhancing both the efficacy and safety of AV gene therapies. By advancing SEL302 into the clinic, we believe we can help all of our current and future gene therapy partners accelerate the use of mTOR in their gene therapy programs by providing a clear clinical and regulatory blueprint for them to follow. This past October, at the 29th Annual European Society of Gene and Cell Therapy, or ESGCT, conference, the lecture showcased three presentations, including one joint presentation with our partner, Aspire. These presentations highlighted the immunogenic nature of MTAEV capsids in healthy volunteers, and the potential of mTOR and mTOR-IL in addressing key efficacy and safety challenges in gene therapy. Our evolving precision immune tolerance platform is designed to enable AAV vector redosing by amplifying the magnitude and duration of effectively inhibiting the formation of anti-AAV antibodies, while simultaneously mitigating adverse responses associated with high AAV doses. In our human-proof concept study, we evaluated mTOR's ability to inhibit the formation of neutralizing antibodies in healthy human volunteers and observed that with a single dose of mTOR, all subjects treated with 0.3 mgs per kg of mTOR maintained NAP titers of below 1 to 25 at day 30, and two-thirds of the subjects at this level of mTOR maintained NAP titers below 1 to 5 at day 30. Our preclinical data in non-human primates and mice indicate that two additional monthly doses of mTOR has the potential to provide durable inhibition of anti-AV antibodies. We plan to use this dosing regimen in our upcoming Phase I-II trial in MMA. We're also excited by our preclinical data, which indicates that mTOR or mTOR-L may potentially transform the treatment paradigm for AV gene therapy from a one-and-done to a low-and-slow, whereby patients could receive multiple lower doses of gene therapy, tighter it up to a therapeutic benefit, and avoid the risk associated with higher-vector doses of AV gene therapy needed in a one-time-only treatment model. The area of precision genetic medicine is here, and AV-mediated gene therapies have the potential to be transformational for those who can access them. However, 30 to 70% of the patient population are not eligible for treatment or trial inclusion due to preexisting anti-AV antibodies from natural AV infections. This prevents them from gaining access to potential life-altering therapies for which there may be few or no treatment alternatives. We're developing Zork, our proprietary ITG protease candidate that is designed to specifically cleave human ITG with the goal of expanding access to gene therapies to those patients who are currently excluded due to preexisting anti-AV antibodies. Zork is derived from a non-human pathogen and has low cross-reactivity to pre-existing anti-I2G protease antibodies. In addition to potentially enabling dosing of patients with pre-existing AV antibodies, we believe that the combination of Zork within TOR could open a therapeutic treatment window and enable repeat dosing of this enzyme therapy. At the same time, by increasing the eligible prevalent patient population, we aim to bring hope to those who may not have any other effective treatment options, enable companies to maximize the commercial potential of their gene therapy candidates, and help to make otherwise uneconomic gene therapy candidates viable targets for commercial development. Finally, we continue to work with Ginkgo Bioworks to design novel AV capsids with a goal of improving transduction efficiency, liver tropism, and immunogenicity profile. The Lector will conduct all non-clinical and clinical studies with Ginkgo's uniquely designed engineered capsids. By combining mTOR, With more efficient capsids, we could potentially further reduce the doses of AAV gene therapy needed to see therapeutic benefit. As you can see, we're taking a multidimensional approach to tackling immunogenicity challenges facing AAV gene therapies. mTOR and mTOR-L to mitigate the de novo formation of re-losing antibodies and enable re-dosing. Zork to those patients who, due to natural AAV infections, are ineligible for treatment by gene therapies and next-generation AAV capsids to improve both organ tropism and transduction efficiency of gene therapies. We're actively pursuing business development and out-licensing opportunities for Zork, mTOR, and our next-generation AAV capsids in gene therapy applications. And our goal is to maximize the value of our gene therapy vertical by becoming the leading provider of solutions to manage immunogenicity to AV gene therapy developers. Now turning to our biologics pipeline. Many biologics can be highly immunogenic as well, resulting in suboptimal responses due to the development of anti-drug antibodies after treatment. Patients who develop an immune response may be forced to discontinue treatment or experience adverse reactions to continued therapy. We believe the use of mTOR as an adjunct to biologics offers a promising approach to reduce the unwanted immune response and improve patient outcomes. Our most advanced program, SEL212, has served as clinical proof of concept for a precision immune tolerance platform with over 400 patients dose to date. As a reminder, SEL212 is comprised of IMTOR, co-administered with a proprietary URO case, Pagetri case, for the treatment of chronic refractory gout, and was licensed to SOBI in 2020. Our Phase III disorganizer program kicked off in the third quarter of 2020 and consists of two double-blind placebo-controlled trials of SEL212. In both trials, SEL212 is being evaluated at two dose levels of mTOR, 0.1 mgs per kg and 0.15 mgs per kg, with a single dose level of bagadricase at 0.2 mgs per kg. We believe SEL212 represents a potentially clinically differentiated asset for people with chronic refractory gout. In our Phase II trial, we observed a numerically higher percentage of patients responding to therapy on SEL212 versus Crostexa. A higher percentage of responders in patients with visible uric acid crystal tissue deposits, or TOFI, as well as statistically significant lower serum uric acid levels in treatment periods three and six versus Crostexa. These responses were achieved with no need for oral immunosuppressive or weekly methotrexate, and less frequent dosing of an eye infusion with monthly dosing of SEL212 versus biweekly infusions with Cristexa. Accordingly, with this tolerability profile, simplified dosing, and the avoidance of immunosuppression or methotrexate, we believe SEL212 is well positioned against the current standard of care and other drugs in the class that target this patient segment. We continue to work closely with our partners, SOBE, our clinical trial providers, and regulatory authorities to advance towards the successful completion of the DISSOLVE program, and we are on track to both complete DISSOLVE 1 and 2 and announce joint top-line data in Q1 2023. With extensive clinical data in SEL212 currently in Phase 3, we believe Selecta is well-positioned to leverage these learnings into our second biologic indication in IgA nephropathy, which is a kidney disease that occurs when immune complexes of an antibody called immunoglobulin A1, or IgA1, accumulate in the kidneys. By combining mTOR with an IgA protease to remove injurious IgA from the kidneys and improve markers of renal dysfunction, we believe our novel approach has the potential to address the underlying pathophysiology of the disease. We're currently working with our external partners to identify an IGA Proteus candidate for this program and plan to finalize clinical candidate selection by year-end. We're extremely excited about the advancements across our pipeline and the growing body of evidence showcasing the promise of our pioneering mTOR precision immune tolerance platform in a number of applications. We look forward to continuing our momentum and executing towards upcoming value-driving events. With that, I'll turn the call over to Kevin to run through our financial results for the third quarter. Kevin?
spk07: Thank you, Karsten. During the third quarter, our balance sheet was strengthened with the $10 million milestone payment from SOBE for enrollment completion of Dissolve 2. Additionally, we received a $2 million payment for extending SREPTA's option periods under our Research License and Option Agreement for mTOR to Q1 2023. and an additional $4 million payment for achievement of certain preclinical milestones. We ended the third quarter with cash, cash equivalents, marketable securities, and restricted cash of $148 million as of September 30, 2022, compared to $129.4 million as of December 31, 2021. We believe these funds will enable us to fund our operating needs into mid-2024. Turning to our financial results in the quarter ended September 30th, 2022, net cash used in operating activities was 19.8 million for the nine months ended September 30th, 2022, as compared to 28.9 million of cash used in operating activities for the same period in 2021. Collaboration and license revenue recognized was 20.7 million for the third quarter of 2022, as compared to 24.4 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 program through the license agreement with SOBE. Research and development expenses for the third quarter of 2022 were $16.5 million, as compared to $21 million for the same period in 2021. The decrease in cost was primarily the result of expenses incurred for the SEL 212 clinical program, preclinical programs, and the ASK-BIO collaborations. General and administrative expenses for the third quarter of 2022 were $5.8 million as compared to $5.4 million for the same period in 2021. The increase in cost was primarily the result of expenses incurred for stock compensation and personnel expenses. For the third quarter of 2022, Selecta reported a net loss of $7.9 million or basic net loss per share of $0.05 as compared to a net loss of $17.9 million basic net loss per share of 16 cents for the same period in 2021. I will now turn it back to Carson for closing remarks. Carson?
spk10: Thank you, Kevin. In summary, we've had yet another quarter of great progress here at Selecta, and we're excited about our plans to enter the clinic with SEL 302 in Q4 2022, the anticipated completion of the dissolved program with our partner Sobe, the advancement of IND enabling studies across our whole year on pipeline and supporting our numerous collaboration partners and our plans to move into the clinic. We remain deeply committed to solving the hardest challenges in autoimmune disease and helping patients overcome autoimmunity and immunogenicity through evolving into a precision immune tolerance platform. We believe IMTOR-IL could represent a generational leap forward for the IMTOR platform and for patients in need of alternative treatment options, and we look forward to evaluating its full potential across a wide range of autoimmune diseases of the liver and beyond. In parallel, we'll continue to seek opportunities to strategically partner in our routine therapy vertical to maximize the value of our platform. Before we conclude today's call, I would once again 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.
spk11: We will now begin the question and answer session. To ask a question, you may press star then 1 on your touchtone phone. If you're using a speakerphone, please pick up your handset before pressing the keys. And to withdraw your question, please press star then two. And at this time, we'll pause momentarily to assemble our roster. And the first question will come from Jo Schwartz with SVB Securities. Please go ahead.
spk01: Hi, this is Beth on for Jo. Congrats on the progress and thanks for taking our question today. So heading into the SEL212 joint phase 3 readout, it would be helpful to understand what you guys are hoping to see in terms of the serum uric acid response rate as well as the anti-drug antibody mitigation rate.
spk10: Yeah, that's a great question. Obviously, we're quite confident about this trial. We're in a unique position that we've run two phase 2 trials prior, one even head-to-head versus Cristexa, And we had response rate in the mid-50% range. And just to remind everyone, the actual Phase III is placebo-controlled, and we know from Prosexa there's no placebo effect. So, you know, we think from a technical perspective, the study is actually very low-risk. We also believe that the profile, as we understand it right now, is quite competitive with the response that we've seen in the Phase II, and the fact that the treatment frequency is a key differentiator as well, that we only need monthly dosing versus every two weeks, and this is a pretty uncompliant patient population. So that's kind of what we're kind of looking for. We're not looking at ADAs as a primary endpoint, so we're basically looking at SUA levels at month six for the top-line readout in Q1 next year.
spk01: Great, thanks. And if I could squeeze in a quick follow-up, I was also wondering if you're able to provide any color on the phase three discontinuation rates so far and comment on any read-through this might have into real-world duration of use.
spk10: Yeah, so we haven't guided any discontentation rates. We're obviously blinded in this phase three, and we'll report the top line in Q1 next year.
spk01: Great. Thank you.
spk11: Thank you. The next question will come from Kristin Kaluska with Cantor Fitzgerald. Please go ahead.
spk04: Hi. Good morning. This is Rick on for Kristin. Thank you for taking our questions. To start out with one, at ESGCT Selecta presented some data out today, 131 showing IL-2 mutine plus mTOR-inhibited anti-AAV antibodies in a preclinical model. Could you talk about any promising signals you've seen in these preclinical models with increased length of follow-up post-dosing? Thanks.
spk10: Yeah, I'll let the KRC answer the question. I see percentage of data. Okay.
spk09: Yeah, thanks, Karsten. Yeah, so in that study, we were specifically looking for the ability to mitigate immune responses to high vector doses because that's been an issue for the field. So we went up to vector doses of 5E13BG per kg. And what we were looking for is that durability of response that you referred to. as we have seen breakthrough in some studies, both preclinically and in our empty capsid study. So to remind you, we've shown that three monthly doses of mTOR can provide durable inhibition both in mice and non-human primates, and that's the regimen we're taking forward in our methylmalonic acidemia clinical trial that's starting later this year. And then at ESGCT, we presented data on the combination of mTOR plus engineered IL-2 molecule, as well as mTOR plus Benlysta, or an anti-BAF antibody. And both showed the ability to mitigate immune responses out to around day 131, as you indicated.
spk04: Okay, thank you. Maybe just one more then. Also kind of staying in the same lane, as you're looking at other potential autoimmune indications, what criteria are you weighing? We understand that a well-characterized autoantigen is a must-have, but are there any other key factors for the IL-2 approach in your view?
spk10: Yeah, that's a great question. Yeah, we definitely initially focus on diseases like PDC, where we clearly know the autoimmune PDC2 in this case. And we obviously see very broad applicability with this approach, which is, I think, important. We're not limited there. But initially, we will focus on liver-directed autoimmune diseases, such as PDC, as you know, into our accumulated liver, so we think that's kind of low-hanging fruit as an initial approach, but, you know, there's no reason why this wouldn't work in other systemic diseases, such MS, for example. But I think as a company, we want to focus initially on liver-directed diseases and adjacency also kidney as well, potentially.
spk04: Okay, thank you very much for taking our questions.
spk11: Thank you. The next question will come from Young Zong with BTIG. Please go ahead.
spk02: Hi. Good morning. Thank you very much for taking the question. So a question on the IO2. So what would you like to achieve with your identification of the engineered IO2 as compared to currently available IO2s? By any chance, is that going to be one that maybe you have used in clinical study? Sorry, not clinical, but preclinical studies and have shown data?
spk10: That's a good question. Maybe I'll start and then I'll hand over to Kay. Obviously, we see the key differentiation in our approach combining an engineered IL-2 with mTOR. So if you just use an IL-2, you just expand all pre-existing T-regs or cells, and you basically hope for a bystander effect, nonspecific. Whereas you can combine it with mTOR, we're aiming for an antigen-specific approach where we induce and expand antigen-specific T-regs. But we obviously want to have a differentiated IL-2 to begin with, so ideally have a best-in-class IL-2 that is competitive with the IL-2s that are out there right now, but I think the ultimate differentiation that we're aiming to be a first-in-class around, you know, antisemitic approach where we really target T-Rex specific to an antigen. But, Kay, do you want to add something to that?
spk09: Yeah, I think that's absolutely right, Kirsten. With regard to the ones that we've used in the studies that we've – presented, that's actually been with a mouse-specific IL-2 mutine. So it's just a model for us for our preclinical studies. But obviously, we've been working very diligently on identifying a proprietary molecule, and we think we're very close to being able to announce that to you.
spk02: Okay. Maybe a similar question then on the IgA protease And once the final candidate is identified, do you expect the selector to have 100% rights to that molecule, and is selector going to be mainly driving the clinical studies going forward? And also, does it make sense to add IO2 as well to IgA nephropathy indication, or maybe not necessarily?
spk10: Good question, Jun. So, yeah, so once we've selected and selected a enzyme candidate, an IgA protease, we will own this asset and we'll drive it forward ourselves 100%. So we'll be responsible for all preclinical, for manufacturing, and also for clinical development as well. As the IL-2, theoretically possible, I would say, but I think we've seen And this program, what's important, this program is really building on the experience we have with SEL212, where we are basically combining another enzyme, highly immunogenic, a fungal origin, with mTOR, and we're able to redose with mTOR. So I think the initial approach will be with mTOR alone. Okay, great. Thank you very much.
spk11: The next question will come from John Newman with Canaccord. Please go ahead.
spk08: Hi, guys. Good morning. Thanks for taking my question. Just wondered if you could remind us of the dosing strategy for mTOR in the upcoming gene therapy study that you'll be starting in the fourth quarter. I believe you'll be giving a higher number of doses of mTOR in combination with the gene therapy. We just wanted to review that. Thanks.
spk10: Yeah, I'll hand that question to Peter. He can kind of walk you through the design and some of the data leading us to the protocol we're moving into the clinic. Peter?
spk05: Yeah, thank you, Carson. Hi, John. Based on our data in the empty capsid study, we are starting with a dose level of 0.5 mg per kg. And Also based on the non-human primate studies, we're giving three monthly doses at that dose. So it'll be three monthly doses following the AAV at 0.15 mgs per kg. In the protocol, depending on the activity of neutralizing antibodies in the first several subjects, we do have the option of increasing the dose of mTOR should that be necessary. Great. Thank you.
spk11: The next question will come from Rahul Prasad with William Blair. Please go ahead.
spk00: Hi. This is Tiffany. I'm for Raj. Thanks so much for taking our question. I was just wondering if you guys plan to share any data on the selection process for the IL-2 or the IgA protease development candidate, and I guess any color or, you know, details on what the next update we can expect to see from either of these programs might look like. Thanks.
spk10: Yeah, hey, Tiffany, good question. So the key is that we gave guidance that will select clinical candidates by the end of the year for both the IL-2 and the IgA protease. And I think there's a good chance that we'll, you know, throughout next year at conferences, you know, we'll highlight those molecules in more detail and also share some on how we got to the selection of those. And as you know, we have various different approaches for each of those. For the IL-2, we're working with Cyrus, a protein engineering company out of David Baker's lab in Seattle. And for the IgA protease, we've got a dual approach. We have an option for an IgA protease from a small company called IGAN, and we're also working with Ginkgo Bioworks as well. So we'll definitely, once we have selected the lead candidates, share also a bit about the selection process.
spk00: Okay, great, thanks. And just one more. I know you're still on track to initiate the imaging therapy study by year end. Can you just detail any additional sort of activities you guys are working through in order to get that off the ground?
spk10: Yeah, I can let Peter speak to this, but I think there's not a whole lot new to report. It's going to be a single center study at the NIH. Chuck Venditti will be the PI there, and we are on track to kick the study off this quarter. Unless there's any additional color, Peter, you can share.
spk05: Yeah, that's correct, Carson. And we have all the requisite approvals that we need to initiate the study. So that will be initiated soon with enrolling the first subject with consent and screening.
spk00: All right, great. Thanks. That's it for me.
spk11: The next question will come from Bubulon Patayapin with A.T. Wainwright. Please go ahead.
spk06: Hi. Can you hear me okay?
spk10: Yes.
spk06: Okay. So following up on the MMA Phase I study, so you indicated earlier that you plan to assess initial efficacy and safety at three months for each patient before progressing to the next patient. So maybe can you remind us how many patients you want to enroll and what would be the approximate time to data?
spk10: I'll have Peter address that question as well in terms of the high-level design and how many patients and what kind of data will be available next year. I should see that Peter has technical issues. So, yeah, I can take the question, of course. So the primary endpoint is at one year, but we'll have an initial readout at month three. where we're looking at a couple things. One, obviously, primarily safety, but we're also looking at biomarkers of the disease, such as serum and the A. We have a unique breast test that looks at probiotic acid. And, of course, we're looking at what we're very interested as well at the level of utilizing antibodies. And there is a safe data monitoring board that will assess after each patient whether we can move forward or not. So it's going to be a sequential approach. And we haven't guided exactly when we'll have data, but we'll release data throughout next year.
spk06: Thank you. That's it from me.
spk11: The next question will come from Uwe Ehr with Mizuho. Please go ahead.
spk03: Hey, guys. Thanks for taking my question. So on the dissolve one, dissolve two. You know, as you indicated, you expect to join top line to data next year. Just wondering, like, how should we sort of think about your study versus Horizon's mirror study? What are the differences in terms of patients and, you know, in terms of the efficacy that will read out, at least numerically, should it be similar or different? Thanks.
spk10: Yeah, that's a great question that we do get a lot. And obviously, these are very different patients we're looking at. So if you look at the mirror study patients, there's a lot of exclusion criteria, actually. So patients are excluded. that don't tolerate methotrexate. You'll have to exclude patients that have chronic kidney disease, which is defined as an EGFR below 40 patients that have more than three drinks per week. So it's kind of starting out kind of the 100 patients. About 20 patients actually are eligible for that combination. So it's a more limited range. patient population you're looking at. And then it's quite, you have to have a very motivated patient population as well, since you're starting out the first month with daily folic acid, weekly methotrexate, where you don't really treat underlying disease, you have to ensure compliance, and then after that, two weeks of methotrexate, versus 212 is, you know, six-monthly infusions. What the studies do have in common is the endpoint, which is defined as SUA levels below six at month six. So basically, in short, you're looking at a different subset of patients. I think what's great for patients is to have potentially another treatment option available. The current penetration is below 5%. There are over 100,000 patients available. So there's a huge unmet medical need and obviously also a large commercial opportunity as well.
spk03: Thanks. And for Kevin, as you indicated, the R&D is down. It's low at least sequentially this quarter and year-on-year as well. because some studies was winding down. Just wondering how should we think about, I guess, R&D in the fourth quarter and going forward, given all the push and pulls? Thanks.
spk07: Yeah, that's a good question. The, you know, period-to-period kind of comparison, it went down, obviously, because we were enrolling dissolves. last year, and, you know, as you know, we completed enrollment in Q2 of this year, so obviously it's down year on year for the quarter comparison. But going forward, I would expect it to start to creep up as we start to enroll patients in the MMA trial and then continue to increase into 24 as we start to ramp up other things. So not significantly, but, you know, it will directionally be going up. Okay. Thank you.
spk11: Again, if you have a question, please press star, then 1. This concludes our question and answer session. I would like to turn the call back over to Selecta CEO, Mr. Carson Brunn, for any closing remarks. Please go ahead, sir.
spk10: Thank you, operator, and thank you to everyone who joined us this morning. Stay safe and healthy. This concludes today's call. Thank you.
spk11: The conference is now concluded. Thank you for attending today's presentation. You may now disconnect.
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