Good day, everyone, and welcome to the Mural Oncology Investor Call. Today's call is being recorded. At this time, I'd like to turn the call over to Dave Borah. Please go ahead. Hello, and welcome to Mural Oncology's investor presentation. I'm Dave Borah, SVP of IR and Corporate Affairs for Mural, and I'm pleased to be joined by CEO Caroline Loew, VP Clinical Research Oncology, Jessica Rege, Director of R&D, Josh Heiber, and Principal Scientist, Mark Whitmore. We look forward to telling you more about Mural, its protein engineering capabilities, how our lead asset, nemvaleukin, differs from other IL-2 approaches, and other exciting candidates in our pipeline. We'll leave time at the end for Q&A as well. Today, we're making forward-looking statements about our business, including our pipeline assets. Just to note, of course, that this is an inherently risky business, and we do our best to articulate the risks that we face. But for more information, we always point you to our SEC disclosures. Here's a look at what we plan to cover today. Caroline will start with a broad overview of Mural, our pipeline, upcoming catalysts, and the team we're assembling. She will also cover our proprietary protein engineering capabilities in general terms. Josh will describe the specific scientific rationale for nemvaleukin. Jess will cover the clinical results we've shown to date. Then Mark and Josh will discuss our IL-18 and IL-12 candidates. Finally, Caroline will finish with a brief overview of our financials before opening up the call for Q&A. Now I'd like to introduce our CEO, Caroline Loew. Caroline? Thank you, Dave. In the past 10 years, cancer treatment has made some amazing advances. I was very fortunate to have been part of that in my leadership role in BMS, as we built the [audio distortion] portfolio of indications. Now, while those steps were incredible, they still left many patients underserved, and the promise of additional mechanisms and modalities, even mono combinations, still haven't been realized. And this is the reason that I came to Mural. Cytokines, starting with IL-2, represent an extremely well-known area of biology and a known set of problems, which is the key here. We know that IL-2 is potent, and we know the specific drawbacks of native IL-2. And when you have a problem like this, you can work to solve it. It's a known known. So what excites me about Mural are a few simple, specific, and unique elements. Mural has taken a deep understanding of biology, a unique protein engineering approach, and has designed a cytokine, a fusion protein, that seeks to address the problems with native IL-2. That protein today is in late-stage clinical development in not one, but two registrational studies designed and powered for approvability based on earlier stage data. And finally, Mural has a pipeline built using its protein engineering capabilities, with two additional programs, an IL-18 and an IL-12. Mural is the leading late-stage cytokine company, and that positioning will allow us to build, starting with nemvaleukin, a portfolio of products and indications that will give us the flexibility to create the next wave of much-needed regimens for cancer patients. So to review our pipeline, we have two global registrational studies. The first, in platinum-resistant ovarian cancer, is reading out in the first quarter of 2025. The second is in mucosal melanoma, a rare disease with no current treatment, and it's also reading out in the first quarter of 2025. We also have a trial looking at less frequent IV dosing regimens, where we'll recommend phase II dose selection in Q1 of next year. And so far, we're very encouraged by what we see in that study. Preclinically, we have two programs, both approaching candidate nomination, an IL-18 and an IL-12. These both take the same protein engineering approach we have used with IL-2. We're very excited about both of these programs, and Mark and Josh will go into more detail on them later. I'm very excited by the people that are listed on this slide. We're assembling a board with many years of relevant experience in oncology drug development. Susan Altschuller is currently the CFO of Cerevel, was previously the CFO of ImmunoGen. Dr. Francis Cuss was the EVP and CFO at Bristol- Myers Squibb. Ben Hickey is currently the Chief Commercial Officer at Mirati and was previously the Chief Commercial Officer at Halozyme. Our chairman, Scott Jackson, was the CEO of Celator from 2008 to 2016 until it sold to Jazz. Our management team is coming together extremely well, and I'm just delighted about the team that we've assembled. Vicki Goodman, who's actually here with us today and will be available during Q&A, will be joining the company in November. She was most recently the CMO at Exelixis, and before that, held senior positions in oncology clinical development at Merck and BMS. Maiken Keson- Brookes joined our team earlier this summer and previously was the General Counsel and Chief Legal Officer at several biotechs, including Rubius, Synlogic, and uniQure. We've also hired a CFO, and we'll be announcing him before the spin, and also we are getting very close to hiring a CSO, and I look forward to announcing that shortly as well. Finally, a little bit about me. I'm an organic chemist by training. My experience ranges from most recently being the CEO of a platform biotech to periods in large pharma, including Bristol-Myers Squibb and Merck. I was very fortunate during that time to be at the center of the IO revolution. So since their advent, IO therapies have been incredibly effective and widely adopted in cancer. But even with this impact, their limitations are significant and real. Some patients don't respond, and others who do respond end up progressing. Cytokines play a critical signaling role in your immune system, both for innate and adaptive immunity. In the context of oncology, they really have a lot to offer. So at Mural, what we're doing is harnessing that cytokine biology to improve in the treatment of oncology patients. The result of our approach is that we're developing proteins that have activity where prior therapies, such as checkpoint inhibitors, have failed, and thus opening up the cancer market beyond today's available treatment population. Let's get off into how we do this a little more deeply. First, we build a deep understanding of the biology of interest, in this case, cytokines. Cytokines represent a natural, powerful, known biology, but they also have identifiable problems that we know can be addressed with our technology. We focus on targets with strong biological rationale as a start point. IL-2 is a great example of this. It's clinically de-risked. We know it's potent. It just has a specific problem to solve, the therapeutic window. We then use our unique protein engineering capabilities to try to address the issue with the target. This is a unique approach, approach across the industry. We're seeing screening and hit-to-lead. We're seeing mimicking. We're seeing therapeutic window being addressed with PEGylation. Those types of approaches are all valid, but they don't have the specificity of our approach or the technical robustness of our approach. The result of our approach is a molecule that works without activation, that works with extreme specificity to deliver the efficacy benefit of the target it uniquely binds to. And so, in summary, the approach we're taking is a platform to engineer novel cytokines, and it represents our key long-term value driver. So how does this approach translate into our programs? Let's first look at IL-2. The issue with native IL-2 is binding to the high-affinity IL-2R receptor that leads to Treg expansion. Our fusion protein is sterically blocked from that binding and binds only to the intermediate-affinity IL-2R receptor, upregulating CD8+ and NK cells. For IL-18, historically, this molecule has shown limited clinical efficacy due to the IL-18BP strongly binding to the IL-18 receptor. We've addressed that in our program with an engineered IL-18 design that has a half-life extension and is resistant to the strong binding of the receptor. Mark Whitmore will describe our IL-18 program later in the presentation. Finally, IL-12 use has been limited due to systemic toxicities, an issue that we seek to address in our program with a very elegant in situ assembly of the IL-12 subunits. Josh Heiber will provide more detail on that approach later in the presentation. Taken together, we have a portfolio of three modulators. They can be used alone or in combination, and there's a rational reason to combine them with, for instance, checkpoint inhibitors, as we have with nemvaleukin. We view this as a robust, purpose-built portfolio. Now we'll discuss our lead program, nemvaleukin, in more depth. Nemvaleukin is the poster child for the approach that Mural has taken to cytokine development. We've engineered a stable, active fusion protein that activates the IL-2 receptor site that drives CD8+ and NK cell activation, while directly blocking the high affinity receptor site that causes Treg activation and the adverse events seen with the native IL-2. To date, we've hit some critical milestones in this program. We've shown pharmacological proof of concept. We have clinical validation in mono and combination therapy, and importantly, we've recapitulated the responses seen in native IL-2-- native high-dose IL-2. Now we're in registrational studies with two indications with a potential for broad expansion. To talk more about the mechanism of nemvaleukin and what makes it so unique versus other IL-2 approaches, I'm pleased to introduce Josh Heiber. Josh is our lead scientist on both IL-2 and IL-12 and can speak in depth about the science of both. He joined Alkermes from Oncorus in 2017 and has been instrumental in the development of both assets. I'm delighted to turn it over to Josh. Thank you. Thank you, Caroline. This slide compares our IL-2 approach on the left to other high-dose IL-2 approaches depicted on the right. Nemvaleukin is an IL-2, IL-2 receptor alpha fusion protein that is sterically prevented from interacting with the high-affinity IL-2 receptor alpha on regulatory T cells or Tregs. This allows for the preferential and specific binding to effector cells of interest, CD8+ T and NK cells, at much lower doses than native IL-2. All of this, we believe, results in an enhanced therapeutic index. Importantly, unlike alternative strategies, nemvaleukin is a stable fusion protein, intrinsically active, and does not degrade to naked IL-2. On the right, we are highlighting the challenge of IL-2, which is the preferential binding to the trimeric high-affinity receptor complex expressed mostly on Tregs. This could actually benefit the tumor by creating a more immunosuppressive environment. As a result, high doses of native IL-2 are needed to achieve antitumor activity by dosing through the Treg window to stimulate CD8+ T and NK cells. This can be a stretch, as tolerability becomes a problem at higher doses not needed with nemvaleukin alfa. This slide nicely illustrates how nemvaleukin's design hypothesis, described in the previous slide, is confirmed by clinical pharmacodynamic data. Clearly, the CD8+ T and NK cells expand dramatically while the Tregs remain essentially flat. This is clearly encouraging as we think about how differentiation might appear in our clinical results. Now to talk more about the clinical trial progress we've made, I'm pleased to introduce Jess Rege. Jess joined Alkermes in 2020 after serving one year as clinical trials consultant for the company. Jess? Thanks, Josh. This is the overall ARTISTRY program for the development of nemvaleukin. ARTISTRY-1 was our foundational phase I/II study that established our monotherapy and combination activity with pembrolizumab and set us up for our current registrational studies. In addition, we have two alternative dosing studies, ARTISTRY-2 and 3, exploring subcutaneous and less frequent IV dosing regimens. We're focused on the less frequent IV dosing and are expected to have a recommended phase II dosage declared by Q1 2024. ARTISTRY-6 is our registration-enabling study as a monotherapy treatment in mucosal melanoma patients PD-1 pretreated with or without the CTLA-4. ARTISTRY-7 is our combination registration-enabling global phase III study with nemvaleukin plus pembrolizumab, compared with investigator's choice chemotherapy in platinum-resistant ovarian cancer. ARTISTRY-1 is our foundational study. It had three parts. The first part was the dose escalation, which enabled us to establish our recommended phase II dose, as well as our proof of mechanism. The second part, Part B, was to establish monotherapy activity in established tumor types in which high-dose IL-2 is proven clinically active. Then the third part, Part C, was to test nemvaleukin in combination with pembrolizumab in two major cohorts, the PD-1 approved and unapproved tumor types. Now, let me walk you through some of the established clinical data. This is our ARTISTRY-1 overall safety slide, depicting the monotherapy on the left and the combination on the right. Our safety profile is consistent with what is to be expected of a cytokine, with the most common adverse events being fever, chills, neutropenia, and hypertension, and the most common Grade 3 events were neutropenia and anemia. It's important to note that these events were transient in nature, not requiring growth factor support, nor were associated with any neutropenic fever. This is consistent when we look at the overall discontinuation rates associated with the adverse events, which were in the low single-digit percentile. Looking at the table on the right, when combined with pembrolizumab, there were no additional toxicities noted. As we talk about the efficacy data, this is important, as you'll see, the safety profile has enabled our patients to be treated over extended periods of time. Depicted here is the ARTISTRY-1 overall summary slide of our efficacy data. We saw a variety of responses in multiple tumor types, most notably in established diseases where cytokines are known to work, with responses in renal cell carcinoma and melanoma. Recall, our monotherapy responses are in patients previously treated, treated with a checkpoint inhibitor. Quite a different study population when high-dose IL-2 was approved. In addition, this was heavily pretreated study population that most had exhausted all other treatment options before joining this trial. Therefore, this is really promising clinical activity in a wide variety of tumors. It's worth highlighting that we had 24 patients with objective responses and two complete responses in platinum-resistant ovarian cancer, which is quite unexpected when you think about checkpoint inhibitors alone. Lastly, we had a combination of responses with pembrolizumab in tumors where checkpoint inhibitors are approved or not approved. As the data from ARTISTRY-1 has allowed us to move directly into our registrational studies, but it has also laid the foundation of our next stages of clinical development beyond ovarian cancer and mucosal melanoma. Now, let me walk you through some of the combination of monotherapy data within the ARTISTRY-1 trial. As you can see here, this is the overall combination data in the checkpoint inhibitor unapproved cohort with a focus on the ovarian cancer patient data. Let me highlight a few key elements on the slide. We had multiple responses in platinum-resistant patients, most notable, two complete responses and two partial responses. These responses were very durable in nature, with a median duration of 65 weeks. Our objective response rate was 28.6% and a disease control rate of over 70%. This in contrast to standard of care chemotherapy, which is lower responses and a median progression-free survival of only three months. Speaking of this, I want to highlight a few patients on the swimmer plot here. Focus your attention on the third swim lane. This woman had five prior lines of treatment for her ovarian cancer before joining our study. When she was on our study, she had very durable, stable disease and was on treatment for almost two years. This emphasizes the importance of disease control in this population. Now let's highlight patient OC-1, the topmost line of the swimmer plot. She came on our study as a sixth-line ovarian cancer patient. She achieved a complete response at cycle eight and remained on therapy in response for a total of 220 weeks. Finally, allow me to highlight one of the complete responses in the ovarian cancer, OC-2, in the next slide. This patient was an 83-year-old woman when she came on our study as a third-line treatment. She had a large 100 mm hemipelvic mass. After about 2 months of treatment, the lesion had shrunk by over 50%, indicating a partial response, and she continued to have a deepening of that response over time. Almost a year later, the tumor had 100% reduction in mass. As you can see, no longer visible, indicating a complete response. She tolerated the treatment well for two years with this response, but unfortunately, she did pass away due to an unrelated event. Now, this data laid the foundation for ARTISTRY-7 study, which I'll speak about in a minute. But first, let me walk you through some of the monotherapy activity. Shown here is the ARTISTRY-1 monotherapy efficacy in melanoma patients. Recall, our intentions of our monotherapy tumor choices of renal cell carcinoma and melanoma were to recapitulate the monotherapy activity consistent with high-dose IL-2. Although our patients were heavily pretreated and all were checkpoint inhibitor experienced, so in essence, we set a higher hurdle than prior high-dose IL-2 trials. Let me highlight a few key features of the data. In the table on the right, the overall response rate for mucosal melanoma was 33%, with a disease control rate of 67%. Again, a clinically meaningful result in this rare disease with no other treatment options beyond checkpoint inhibitors. On the swimmer plot, one patient, noted as M1 on the slide, who has been on treatment for almost 3.5 years and continues to remain on treatment today. This data presented here supported our FDA Orphan and Fast Track designations in mucosal melanoma and has laid the foundation for the ARTISTRY-6 study design. This is the ARTISTRY-6 study design, in which the registrational component of the study is highlighted here in pink. This study is aligned with the FDA as a single-arm study in mucosal melanoma patients with prior PD-1, with or without CTLA-4 treatment. The key endpoint of this study is objective response by central review. The additional two cohorts allow us to expand on the future development plan with nemvaleukin, particularly with alternative dosing flexibility for our patients. Like all biologics, we wanted to explore alternative dosing options of subcutaneous and less frequent IV dosing. We're particularly focused on cohort 3, which could allow us to expand this study to inform future registrational studies in cutaneous melanoma. Now, let's walk through our combination study in platinum-resistant ovarian cancer. Again, the ovarian data from ARTISTRY-1 has led us to design of the ARTISTRY-7 trial. This is a global registrational trial designed in consultation with the FDA to compare Arm 1, the combination Arm, to Arm 4, the investigator's choice chemotherapy, with a primary endpoint of investigator-assessed progression-free survival. This is a well-powered and novel combination study. Other key elements of the trial are two single Arms to be able to demonstrate a contribution of effect with built-in futility boundaries if lack of activity seen in those Arms. This study is well underway and is anticipated to have top-line results in Q1 of 2025. Now that I've had a chance to walk you through the foundational study data, the designs of our registrational trial, let me end with speaking a bit about our future plans of our strategy behind our dose optimization. Our development path has been deliberate and focused on delivering our two near-term registrational indications, mucosal melanoma and platinum-resistant ovarian cancer, both for patient populations where there's no current treatment, for mucosal melanoma, a rare disease of around 2,000 patients annually, and for platinum-resistant ovarian cancer, around 13,000 patients annually. Importantly, these initial indications are foundation for our market evolution in two key directions. The first, we plan to demonstrate efficacy potential of our IL-2 and then expand into earlier treatment lines or into other indications, such as RCC. Second, as a cancer treatment combination of choice, we'll add nemvaleukin to the armamentarium of cancer treatment options with a strong biological rationale for how to augment existing regimens. This leads us to believe there's a very broad potential for nemvaleukin as either a monotherapy or combination therapy across a wide range of patient populations. Now, let me finish by talking about our alternative dosing strategy we are building into our development plan. When nemvaleukin first entered the clinic, we wanted to control a number of variables, and we saw the frequency of dosing as something we wanted to emulate from the previous approved high-dose IL-2. So the once-a-day dosing for five days is modeled after high-dose IL-2. We understood alternative schedules, like less frequent IV, would be preferable, but also acknowledged we needed to walk before we could run. We're optimistic about the potential for our less frequent IV dosing and the progress the teams are making on ARTISTRY-3. As we shared earlier, we're expecting to have our recommended phase II doses no later than Q1 of 2024. This less frequent dose schedule will build upon the foundational efficacy that we've seen with our ARTISTRY-1 program and be implemented on our next phases of development. Now, it's my pleasure to hand the mic over to Mark Whitmore. Mark joined us from Genzyme over five years ago and has been particularly instrumental in the development of our IL-18 molecule, which we're all very excited about. Mark? Thanks, Jess. I'm really excited to talk about this program. It's worth mentioning that this program is relatively new. It was started in-house only a couple of years ago, and it was built with our in-house protein engineering capabilities. IL-18 has a very distinct biology from both IL-2 and IL-12, and was initially discovered as an interferon gamma-inducing factor. It has many powerful antitumor traits, but one big problem historically. The big problem is IL-18 binding protein, or IL-18BP. It's a strong binder to IL-18, which blocks its full therapeutic potential. This is a real barrier to meaningful efficacy in cancer. Fortunately, we believe we have a way to engineer around that. Using our in-house engineering capabilities, we are engineering an IL-18 variant that is designed to have an extended half-life and to be resistant to IL-18 binding protein. In preclinical studies to date, our resulting IL-18 variant has shown the desired effect with a relatively low toxicity profile. This slide is a good indication of what we're seeing preclinically. We have designed two versions of our molecule that differ only in potency compared to wild-type IL-18. As shown on the chart on the left, wild-type IL-18 bound prolifically to the binding protein, while no binding was detected between our two variants of IL-18 and the binding protein. On the right, you can see potency of our variants relative to the wild-type version in the presence and absence of a high concentration of IL-18 BP. Most importantly, we did not detect any suppression of our variants by IL-18 BP. In contrast, the wild-type version has to be dosed quite highly to break the chains of the binding protein. We are enthusiastic about this program and expect to publish meaningful preclinical data in the next year. We also intend to nominate a lead candidate in the next year as well. Now I'd like to hand the mic back to Josh for a brief description of our IL-12 program. Josh? Thanks, Mark. So IL-12 has been a challenging target in oncology drug development, mostly due to a narrow therapeutic window. IL-12 is a heterodimeric cytokine composed of p35 and p40 subunits. It is a potent stimulator of both the innate and adaptive immune systems and is extremely well validated preclinically. Additionally, clinical activity has been observed in humans. However, naked IL-12 has a narrow therapeutic index where safe doses are generally sub-efficacious. There is significant interest in IL-12, and many strategies are looking to improve upon the therapeutic index. Many focus on tumor-localized approaches, either via targeting or intratumoral injection, but these have also thus far had limited success. We have engineered a potential solution designed to be delivered systemically, but with limited systemic exposure and enhanced localized exposure of IL-12 in the tumor and tumor microenvironment. First, we split IL-12 into its p35 and p40 subunits, thereby inactivating the molecule. We then fuse these subunits to two non-competitive antibody fragments targeting the same tumor-associated antigen. Now, let me explain our dosing strategy that has been used in preclinical models. First, we dose p35. We then wait for p35 to clear systemically. p35 is, however, retained in the tumor and tumor microenvironment via targeting. Only after allowing most of the p35 to clear systemically is the second subunit, p40, administered. This limits the systemic formation of functional IL-12. However, levels of functional IL-12 complexes are maintained in the tumor and tumor microenvironment via targeting to our selected tumor-associated antigen. In summary, these subunits are designed to preferentially assemble and activate in the tumor and tumor microenvironment. The figure on the right is our first demonstration that our strategy of injecting p35 and p40 subunits separately in sequence works in vivo. We conducted this study in humanized mice. As you can see, the vehicle group, the first bar, has a low level of interferon gamma, indicating that T cells have a baseline level of activation in this experimental system. Single-chain IL-12, second bar, is a control to verify that the system is responsive to IL-12 and additional interferon gamma is produced in response to IL-12 stimulation. The two rightmost bars demonstrate a dose response to the sequential administration of our targeted IL-12 subunits. This data is very exciting, as only functional IL-12 can stimulate an interferon gamma response. This means that in the serum of these mice, sequentially administered p35 and p40 bound together and maintained function. As mentioned previously, we intend to nominate an IL-12 candidate next year. We are very excited about this program. At this point, I'll give the mic back to Caroline, who will run through our financials before wrapping up and opening up the line for Q&A. Caroline? Thanks, Josh. So here's a quick look at our financials. We're very fortunate to begin our life as a public company with such a healthy balance sheet, and this should give us enough cash beyond the key readouts, which are in less than 18 months from now. At this point, we can only give you a range of starting cash levels, as Alkermes has previously stated, and the exact cash levels will be made public before our spin later this quarter. So for over 20 years now, we've known that native IL-2 has driven strong responses across a range of tumors, but has just had an intolerable side effect profile. And since then, we've seen the advent of checkpoint inhibitors, which have also driven significant therapeutic effects, but those too have shackles. [audio distortion] sits at the intersection of these problems, and is positioned to address them and establish a leadership position in the process. We believe what nemvaleukin offers is the pathway to IL-2's deep and durable responses while mitigating certain of its hallmark toxicities, and it's doing so starting in indications where there are no other treatment options. There are just three things I'd like you to walk away from today remembering. We have a late-stage asset in two indications reading out within 18 months. We have a fast path to approval for mono and combination therapy. And those initial indications squarely position us in the oncology regimen armamentarium as a leading late-stage pipeline company. Thank you all for your time and attention today, and we're looking forward to answering your questions during the Q&A session. Well, thank you. If you would like to signal with questions, please press star one on your touchtone telephone. If you're joining us today using a speakerphone, please make sure your mute function is turned off to allow your signal to reach our equipment. Again, that will be star one if you would like to signal questions, please. Star one for questions. And our first question will come from Uy Ear with Mizuho. Hi, guys. Thanks for hosting the call. So I guess I just have a quick question. Could you sort of just help us understand your thinking with respect to. I know that this program has been ongoing for a little while, but, you know, with respect to IRA, how are you kind of, sort of factor in the, I guess, the decision to go to market first or perhaps wait for, you know, a study in a larger market for, for some of these, oncology, indications? Thanks. This is Caroline. Thanks, thanks for the question. So, you know, as you rightly point out, this development program was initiated sort of preceding the IRA, which has sort of, you know, I think, changed the calculus for how you know biopharma companies you know approach development. So traditionally, you know, particularly in oncology, it you know it's very common to approach development of drugs such as nemvaleukin you know with what we term kind of like a land and expand strategy, where you would try and pursue a foster market with a small indication to really establish sort of mechanistic proof of concept, but also try and you know meet the unmet need of patient populations that were underserved. There was a duality of approach that was occurring there, and that was absolutely the strategy that we were and are pursuing. So we have, you know, we're with the same monotherapy indication for a patient population that is, you know, extremely underserved and an orphan indication for mucosal melanoma and then the third-line indication for platinum-resistant ovarian cancer. And when we started that development program, there was no treatment available for that patient population. So. And today, still the broad population is still there is still no approved therapy only for a subset of the population. So the calculus in terms of coming to market now is different for us. As we look at, you know, potentially those the top-line readouts being around the same time for those indications, we will certainly be considering sort of the order of entry to the market for sure. And I think, you know, big picture, you know, it just highlights the very real choices that companies, you know, such as ours and across the industry are having to make. You know, when you look at an indication such as mucosal melanoma, where patients really don't have choice, and it's a very serious disease where patients have very poor prognosis and we're potentially faced with, you know, having to bring that to market after our platinum-resistant ovarian cancer indication, you know, I think that highlights the very real consequences of the IRA on biopharma companies. Right. Thank you. Thanks. Thanks for the question. Thank you. Once again, if you would like to signal with questions, it is star one on your touch-tone telephone. Again, star one if you would like to signal. We'll pause for just a moment. There are no further questions at this time. I'll turn the conference back over to you. Thanks, everybody, for your time and attention today. Please don't be shy about getting in touch if you have further questions, and we look forward to seeing you at conferences throughout 2024. Thanks. Well, thank you. That does conclude today's conference. We do thank you for your participation. Have an excellent day.