Good morning, and welcome to the Cue Biopharma Virtual R&D Day. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentations. If you'd like to submit a question, please use the Q&A text box at the bottom of the webcast player. Today's call will focus on a review of Cue Biopharma's lead asset, CUE-401, in development for the treatment of autoimmune and inflammatory diseases. Joining me on today's call is Cue Biopharma's Interim President and Chief Executive Officer, Lucinda Warren, Chief Development Officer, Dr. Daniel Baker, two recognized researchers in T regulatory cells and cytokines, Dr. Richard DiPaolo and Dr. Jonathan Kay, and other members of Cue's management team. Please note that this presentation and discussion is being recorded and will be available under the Events in the News and Publications section of the company's website at cuebiopharma.com. The webcast will be archived for the next 30 days. Additionally, some of the statements we make on this call will include forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results could differ materially from those stated or implied by these forward-looking statements due to important risks and uncertainties associated with the company's business, including those set forth in the Risk Factors and in Management's Discussion and Analysis of Financial Condition and Results of Operations section of Cue Biopharma's annual report on Form 10-K for the year ended on December 31st, 2025, filed on March 16th, 2026, and any other filings that we may make with the SEC. In addition, any forward-looking statements represent our views as of today, April 7th, 2026. Cue undertakes no obligation to revise or update any forward-looking statements, whether written or oral, that may be made from time to time, whether as a result of new information, future developments, or otherwise, after the date of this conference call. Now, I would like to hand the call over to Cue Biopharma's Interim President and Chief Executive Officer, Lucinda Warren. Please go ahead, Lucinda. Thank you, Tara, and good morning, everybody. Welcome to Cue Biopharma's Virtual R&D Day event. The agenda for today's call, as shown here on slide three, will focus on highlighting the significant potential of our lead asset, CUE-401, a potential first-in-class bifunctional molecule leveraging both TGF-β and IL-2 pathways for treating autoimmune and inflammatory diseases. I'll start by providing an update on our current pipeline, as well as milestones achieved and upcoming. I'll then turn the call over to Chief Development Officer, Dr. Dan Baker, who will discuss the unmet need that CUE-401 aims to solve in autoimmune diseases, as well as its differentiated design and demonstrated mechanism of action. He'll also share promising data in multiple animal and in vitro studies. In addition, we have two immunology key opinion leaders joining us on today's call. Following Dan Baker, Dr. Rich DiPaolo, a leader in regulatory T cells, will share his perspective on CUE-401's mechanism of action for generating Tregs through the co-delivery of TGF-β and IL-2, including in vivo data generated from his lab from an autoimmune gastritis disease model. Following Dr. DiPaolo, Dr. Jonathan Kay will share his perspective on the relevance of cytokine reduction in autoimmune disease and CUE-401's ability to dampen inflammatory responses beyond enhancing immune regulatory mechanisms. Dr. Kay has three decades of clinical experience treating the broad spectrum of rheumatic diseases. As a practicing rheumatologist and immunologist, he will discuss the potential of CUE-401 to change the treatment paradigm for patients suffering with autoimmune diseases. We'll conclude with a question and answer session, which will include members of the Cue management team. Finally, I'll conclude the call with a few closing remarks. Before moving into CUE-401, which is the focus of today's call, I want to provide a quick overview of our current pipeline and upcoming milestones. Our lead candidate and primary business focus is CUE-401, a first-in-class bifunctional molecule leveraging both TGF-β and the IL-2 pathways. We have completed manufacturing and IND activities and plan to file an IND in this second quarter and then move to initiate a phase I trial. We believe that CUE-401's mechanism of action presents tangible benefits and a novel potential which we're excited to dive into today. CUE-501, which was licensed to Boehringer Ingelheim last April, represents a monetized asset with significant value. The agreement included up to $345 million in potential milestone payments, along with meaningful commercial upside. I'm excited to share with you today that this morning, we announced that the first preclinical milestone of this collaboration has been met, and Cue will receive $7.5 million. Importantly, this partnership also helps de-risk and validate the broader CUE-500 series, for which we retain full rights outside of B-cell depletion. Our CUE-100 series was licensed to ImmunoScape at the end of 2025, allowing Cue to focus on our autoimmune disease programs while continuing to advance the Immuno-STAT platform for oncology with ImmunoScape. The CUE-100 series represents another monetized asset for the company. This agreement included a total upfront payment of $15 million, along with high single-digit royalties on future sales, and in addition, Cue received a 40% equity stake in ImmunoScape, further aligning long-term value creation. ImmunoScape continues to make progress through potential IND submissions for additional trials in 2027. As a reminder, previous phase I clinical data sets generated by Cue demonstrated clinical activity of several CUE-100 series candidates in multiple metastatic cancers without the significant toxicities that are often caused by traditional immune-activating IL-2 delivery. Importantly, the CUE-100 series has been foundational to the evolution of our platform, including the CUE-500 series and CUE-401. Various key functional components of the CUE-100 series have been deliberately incorporated into these subsequent programs to enable specific mechanistic properties in these molecules. I'm excited to be driving this next stage of growth for Cue alongside other seasoned members of our leadership team. Now, I'd like to hand the call over to my colleague, Dr. Dan Baker. Dan? Thanks, Cindy. To set the stage for a review of the potential of Cue's platform in autoimmune diseases, let me highlight a few aspects of the pathophysiology of these conditions. In healthy individuals, the immune system maintains tolerance using the regulatory function of T cells, in effect, T regulatory cells or Tregs. Autoimmunity occurs when the immune system begins to recognize self-antigens as foreign, and an inflammatory reaction against those antigens occurs. Loss of tolerance usually occurs when Tregs either function poorly or are reduced in number, or both. The resulting inflammatory process can further suppress Treg function and exacerbate the autoimmune condition in a cyclic fashion as the inflammation spreads and intensifies. CUE-401 was designed to restore tolerance in autoimmune diseases by suppressing autoreactivity in several ways, both by directly inhibiting inflammatory pathways and enhancing T cell regulation. Next slide. Our molecule 401 was designed to address the challenge of restoring tolerance and controlling autoreactivity by directly modulating autoreactivity at its core. CUE-401 is a highly differentiated, bifunctional cytokine therapeutic leveraging a unique TGF-β component in combination with a modified interleukin-2. The supporting evidence behind CUE-401 is the findings of researchers such as Sakaguchi, DiPaolo, and others that demonstrated that concurrent signaling through IL-2 and TGF-β receptors in recently activated T effector cells induces and stabilizes FOXP3, and therefore converts autoreactive effector cells into autoprotective T regulatory cells, in effect, reducing pathologic inflammatory cells while markedly increasing tolerogenic antigen-specific Tregs. However, we were also determined to understand the direct effects of CUE-401 on other inflammatory immune cell types that express both receptors, which would allow CUE-401 to provide additional support for the Treg response by directly reducing inflammation. Parts of this data will be presented today. While TGF biology is pretty well understood, its therapeutic potential has remained largely untapped for several reasons, poor pharmacokinetics, off-target toxicity, and poor manufacturability. Thanks to the innovative design of our protein, developed by our engineering team, we've overcome these limitations. To improve the PK, CUE-401 is built on a sophisticated knob-in-hole Fc backbone structure that combines a TGF-β component with an IL-2 element, both of which have been attenuated. As you will see, alone, these cytokines bind poorly to off-target cells such as fibroblasts. However, not only does the design improve PK, but also promotes concomitant binding to both receptors. In addition, the avidity that results when both receptors are engaged allows a biased binding to immune cells that express both TGF and IL-2 receptors. This delivers minimal but sufficient concurrent signaling to achieve the desired biologic effect without overstimulation. It should be noted that recombinant TGF-β is very hard to produce at clinical scale since it is toxic to the cells that produce it. This toxicity results in very poor yields. In order to improve the manufacturing capability, CUE-401 also incorporates a masked version of the TGF-β receptor that prevents toxicity to producer cells, allowing efficient and productive cell lines. We will discuss the mask in more detail in the following slides. The IL-2 component is well-validated by the extensive clinical experience in over 150 patients as part of our clinical trials with the CUE-100 series. IL-2 plays a critical role in promoting the generation of regulatory T cells. When combined with TGF-β signaling, this approach not only expands natural Tregs, but also drives the formation of induced antigen-specific memory Tregs from cells that would otherwise become inflammatory autoreactive cells. Mechanistically, this creates a powerful trifecta of effects that builds on IL-2 based approaches. As we have discussed, by incorporating TGF-β in combination with IL-2, CUE-401 unlocks additional mechanisms to regenerate tolerance by generating induced Tregs with specificity. In addition, CUE-401 directly suppresses T effector function and cytokine production, NK cell activity, and suppresses pathologic B cell functions. Together, these mechanisms position CUE-401 to comprehensively rebalance the immune system in a targeted and highly effective way. This slide describes the attenuation of cytokine affinities for both TGF-β and IL-2. The red line represents CUE-401, while the black lines show the unmodified molecules. The attenuation for both is up to 10,000-fold, and so enhances safety by reducing the potential of off-target effects on non-immune cells while preserving some targeted biologic function. The safety and efficacy of CUE-401 have been demonstrated in multiple animal models and toxicologic studies. Additionally, the function of the mask has been confirmed since CUE has successfully completed production of 2,000 L batches using a master cell bank with a production titer of approximately 8 g per liter. The half-life of CUE-401 in non-human primates is about three days, but the PD effect, i.e., the number of Tregs, lasts much longer, allowing for intermittent therapy. On the left, this slide emphasizes the benefit of coupling TGF-β with IL-2 and how the mask works. The mask is a shortened and attenuated TGF-β II receptor that covers the TGF-β on CUE-401 when it is in its soluble form. Importantly, the interaction between the receptor mask and the TGF-β on CUE-401 is attenuated so that it has a lower affinity interaction compared with the binding of TGF-β to the wild type receptor on the cell surface. As a result, when CUE-401 encounters the wild type TGF-β receptor on the cell surface, the mask can open and allow the TGF-β and CUE-401 to bind and signal through that higher affinity interaction with the normal TGF-β receptor. It is important to note that despite the attenuation of the individual components, the ability of CUE-401 to bind to both IL-2 and TGF-β receptors concurrently results in avidity, so there is increased functional affinity at the cell surface. Thus, the innovative design allows preferential binding to immune cells containing both IL-2 and TGF-β receptors, while avoids off-target binding. On the right, we emphasize the difference between CUE-401 and simple IL-2-driven Treg expansion. As noted previously, immune tolerance to self-antigens is primarily maintained by the body's regulatory T cell system. Bluestone and others have suggested that a strong inflammatory environment can destabilize Tregs and convert them into pro-inflammatory effector cells. Efficient restoration of immune balance, therefore, requires both induction of Tregs and suppression of effector T cell-driven inflammation. The uniqueness of CUE-401 lies in its multiple mechanisms of action. As you will hear from Dr. Kay, CUE-401 suppresses T effector function and has direct anti-inflammatory effects, targeting multiple components of the inflammatory cascade. This combination of mechanisms makes CUE-401 a powerful tolerizing agent. How do these findings translate into in vivo models? The next part of the discussion will emphasize the effect of CUE-401 in in vivo biology. We evaluated CUE-401 both in vitro and in vivo across multiple preclinical models of autoimmunity. In all studies, the molecule consistently modulated immune responses as expected, suggesting potential applicability across multiple autoimmune indications. This slide demonstrates the effect of three early doses of CUE-401 on survival in a model of graft versus host disease. On the left, you can see that with just three doses of CUE-401 given early in the experiment. As shown in the blue line, 50% of animals survived out to the last evaluation at day 95. While, as seen in the purple line, all the control animals died by day 62. The CUE-401-treated animals showed the expected increase in Tregs in the spleen and other targeted tissues, as shown in the middle graph. Of interest, as shown on the far right, donor human T cells survived out to day 95, indicating the generation of tolerance of those cells to the host. Here on the left, we see how CUE-401 extends disease-free survival in a commonly used model of multiple sclerosis. The blue line reflects the survival of animals treated with CUE-401 and is compared with animals treated with vehicle in purple. In this model, generation of Tregs and suppression of relevant cytokines were demonstrated, as well as the increased survival. On the right, we show suppression of T cell-driven inflammation in a model of delayed-type hypersensitivity. In this model, only a single dose of CUE-401 was administered on day one, as shown in blue, and was compared to daily treatment with the immunosuppressant cyclosporine, shown in yellow. A single dose of CUE-401 was as effective as cyclosporine in suppressing immune activity in this model. Let me now introduce Dr. Richard DiPaolo, Professor and Chair of the Department of Molecular Microbiology & Immunology at Saint Louis University. Dr. DiPaolo will share some of his data demonstrating the biologic activity of CUE-401. For those of you who are interested in more detailed experimental methods and data, these can be found in his manuscript, which was recently uploaded to bioRxiv. Rich? Thank you, Dan. Good morning, everyone. Today, I'm excited to share our work on a fundamental question in immunology: how can we selectively activate and stabilize regulatory T cells, or Tregs, in vivo without broadly stimulating conventional T cells? This question sits at the heart of treating autoimmune disease, transplant rejection, and chronic inflammation. While we've known for years that IL-2 and TGF-β are essential for Treg biology, coordinating these signals pharmacologically in vivo has remained a major challenge. This work represents a collaboration between members of my lab at Saint Louis University and the folks at Cue Biopharma. Autoimmune diseases arise when peripheral tolerance breaks down. Regulatory T cells play a critical role in maintaining this tolerance, but selectively activating them in vivo has remained a major challenge. Although IL-2 and TGF-β are both essential for Treg biology, delivering these cytokines in a way that specifically activates Tregs has proven difficult. The rationale for combining IL-2 and TGF-β is well-established. IL-2 promotes STAT5 activation and supports Treg activation and survival, while TGF-β induces SMAD signaling, drives FOXP3 expression, and stabilizes the Treg lineage. In vitro, the combination of these two cytokines efficiently generates potent induced Tregs. However, translating this approach in vivo is challenging due to their short half-lives, potential toxicity, and the difficulty of ensuring coordinated delivery to the same cell. To address this, a strategy was needed to deliver both signals simultaneously to individual cells. CUE-401 was designed to overcome these limitations. Now I'd like to introduce CUE-401. CUE-401 is an Fc-based fusion protein that links an attenuated IL-2 to a receptor-masked TGF-β III variant. Both cytokine components are human-derived and cross-react with mouse receptors. The IL-2 mutein is engineered to reduce off-target activation, while the masked TGF-β III prevents constitutive signaling. This Fc scaffold enables coordinated cell-associated delivery of both signals, extends the molecule's half-life, and enhances manufacturability. In terms of mechanism of action, the combination of attenuated IL-2 and the masked TGF-β III creates a coordinated signaling environment that's hypothesized to induce a distinct regulatory program, one that preferentially supports Treg expansion and function while limiting effector T cell activation. In the next few minutes, I will highlight key results demonstrating the biological activity of CUE-401, and for those that are interested in a more detailed experimental methods and data, these can be found in a recently updated manuscript to bioRxiv. In vitro, extensive testing of CUE-401 produced three major outcomes. First, it induced FOXP3 positive iTregs from naive FOXP3 negative CD4 T cells at very high efficiency. Second, it expanded endogenous Tregs that maintain FOXP3 expression. Third, it reprogrammed effector memory T cells towards a less inflammatory state, reducing cytokine production. Next, we tested the activities of CUE-401 in vivo. A single dose of CUE-401 expanded Tregs dramatically six days post-administration, from about 20% to over 60% of the CD4 T cell compartment. Importantly, this expansion was selective. Conventional CD4 T cells showed minimal activation. We next tested whether these Tregs were stable. Sorted CD4 positive FOXP3 positive Tregs from CUE-401-treated mice showed full demethylation of the FOXP3 TSDR, identical to natural Tregs. Furthermore, they maintained FOXP3 expression even after reactivation for seven days in vitro. This indicates that CUE-401 expands lineage-committed stable Tregs. These Tregs weren't just stable, they were activated. Multi-parameter flow cytometry showed CUE-401 expanded Tregs expressed higher levels of CD25, CTLA-4, GITR, CD103, and Ki-67 compared to Tregs from vehicle-treated mice. RNA sequencing confirmed upregulation of several genes associated with Treg suppressive functions, including CD103, LAG3, GITR, genes associated with tissue residency, and genes associated with IL-2 responsiveness. This is a robust Treg activation program. To determine the role of TGF-β III, we compared CUE-401 to an IL-2 only variant of CUE-401 without TGF-β III. After a single injection, the IL-2 alone variant expanded Tregs, but failed to produce a subset of genes in Tregs compared to the TGF-β III containing CUE-401. Those are highlighted here in red. Importantly, the IL-2 only variant also activated conventional FOXP3 negative CD4 T cells and induced proliferation in effector-associated genes like KLRG1, Ki-67, granzyme B, highlighted here in blue, whereas CUE-401 did not induce these genes. Therefore, coordinated signaling of IL-2 and TGF-β with the CUE-401 induced TGF-β dependent regulatory genes in Tregs and prevented effector activation, demonstrating that TGF-β III is essential for Treg cell activity. Next, we assess CUE-401 in a stringent Treg deficiency model of autoimmune gastritis, including Treg depletion and cell transfer models that were also used in studies by recent Nobel Prize winner, Dr. Shimon Sakaguchi, to identify the role of Tregs in suppressing autoimmunity. Mice received CUE-401 only twice, on days one and 14 after cell transfer. 60 days later, autoreactive T cells in the stomach were reduced from 44% to 10%. Furthermore, disease scores, which assess the severity of inflammatory tissue damage, were cut in half in mice administered CUE- 401. In fact, some of the CUE-401-treated mice showed complete protection. This demonstrates that early administration of CUE-401 induced a durable immune tolerance long after treatment. To address the mechanism by which CUE-401 treatment was inducing immune tolerance in this autoimmune model, we performed single-cell RNA sequencing on immune cells from vehicle- and CUE-401-treated mice. This analysis revealed that Tregs in CUE-401 treated mice were present at twice the frequency, expressed higher levels of CD25, the high affinity IL-2 receptor, and expressed enhanced IL-2/STAT5 signature genes. They also expressed enhanced activation receptors like 4-1BB and survival genes like Bcl-xL. These features suggest that early establishment of regulatory dominance in the autoimmune setting. To summarize, coordinated IL-2 and TGF-β III signaling with CUE-401 induces, expands, and stabilizes Tregs, avoids effector activation, and produces durable immune tolerance. This represents a pharmacologic strategy for in vivo Treg programming. We believe this approach has broad potential applications in autoimmunity, transplantation, and chronic inflammation. Lastly, I'd like to thank our collaborators and those of you listening today, and I'll now turn the call back to you, Dr. Baker. Thanks, Rich. In addition, we're pleased to have Dr. Jonathan Kay with us today to discuss our findings in multiple relevant immune cell types. Dr. Kay is the Timothy S. and Elaine L. Peterson Chair in Rheumatology at University of Massachusetts Chan Medical School. He's Professor of Medicine and Population and Quantitative Health Sciences. Take it away, Jon. Thank you for the introduction, Dan. As you've just heard, we've demonstrated the powerful effect of CUE-401 on both the expansion of naturally occurring Tregs and the induction of stable antigen-specific Tregs, thereby restoring immune balance and enabling tolerance. However, it has long been known that TGF-β can have tolerizing effects on multiple immune cell types independent of Treg generation. We studied the direct effects of CUE-401 on a variety of other immune cell types, including conventional effector T cells, NK cells, and B cells. In the following slides, I will present data demonstrating that CUE-401 can inhibit the production of TH1, TH2, and TH17 cytokines and suppress both NK and B cell function. These immunomodulatory capabilities further differentiate CUE-401 from other IL-2 muteins and expand the potential of CUE-401 as a treatment for multiple autoimmune diseases. Cytokine release by activated T effector cells is a major component of the autoimmune response, not only inducing inflammation that causes tissue damage, but also suppressing the effectiveness of immunomodulatory cells such as Tregs. We hypothesized that the TGF-β component of CUE-401 will directly suppress the production of pro-inflammatory cytokines by CD4 positive T effector memory cells in a dose-dependent manner. To demonstrate this, human CD4 positive memory T cells were isolated from peripheral blood mononuclear cells and were stimulated with anti-CD3/CD28. The stimulated T cells were then re-stimulated either with one of several concentrations of CUE-401 or with an IL-2 mutein Fc fusion protein. After three days, before the generation of Tregs, supernatants were collected and analyzed for multiple relevant cytokines that are listed on the right side of this slide. These include TH1, TH2, and TH17 derived cytokines. Here we show data demonstrating that CUE-401 inhibits the production of a variety of TH1, TH2, and TH17 cytokines. The blue bars indicate levels of cytokines produced after re-stimulation with CUE-401, whereas the gray bars indicated cytokine levels after re-stimulation with an IL-2 mutein Fc fusion protein. CUE-401 clearly suppresses secretion of the TH1 cytokine Interferon gamma, the TH2 cytokines IL-4 and IL-13, the TH17 cytokines IL-17, Mutein-1, and IL-22, and GM-CSF and IL-6. Since these assays were performed on supernatants collected three days after re-stimulation, which is before the generation of Tregs, these results support a direct suppressive effect of CUE-401 on cytokine production by T effector cells, whereas IL-2 muteins lacking TGF-β are incapable of such suppressions. Natural killer or NK cells play an important role in autoimmunity. NK cells are responsible for antibody-dependent cell cytotoxicity, which results in cell death and tissue damage. IL-2 alone induces NK cell proliferation and activation. Thus, without a counterbalance, treatment with IL-2 alone can result in unwanted effects of NK cells on the immune response. Since TGF-β is known to inhibit NK cell function, we designed two experiments to study the effect of CUE-401 on NK cells in vitro. In the first experiment, peripheral blood mononuclear cells were obtained from healthy volunteers and exposed to a range of concentrations of either CUE-401 or an IL-2 mutein Fc fusion protein. TGF-β alone was not studied because IL-2 is necessary for NK cell survival. After five days, NK cell proliferation, NKp30 and NKG2D receptor activation, and granzyme B expression were measured. Granzyme B is relevant because it contributes to barrier dysfunction and inflammation, and its levels are elevated in a variety of diseases, including atopic dermatitis and psoriasis. The results of this experiment are shown in the graphs on the left in the middle of this slide. At doses as low as 10 nanomolar, CUE-401 markedly inhibited both IL-2-induced NK cell proliferation and granzyme B production. In the second experiment, purified NK cells from healthy volunteers were incubated with either CUE-401 or an IL-2 mutein Fc fusion protein, as in the first experiment. After 18 hours, the proportion of NK cells producing the cytokines Interferon gamma and TNF was assessed. As shown in the graph on the right of this slide, CUE-401 resulted in a significant dose-dependent reduction in the proportion of cytokine-producing NK cells. These findings support the conclusion that in contrast to simple IL-2-based therapies, CUE-401 promotes selective Treg expansion and should protect against the unwanted effects of NK cell expansion. The important role of B cells in autoimmunity has been well described. We studied the effect of CUE-401 on B cell differentiation and subsequent antibody production. B cells were isolated from healthy volunteers and activated in vitro, followed by treatment with either CUE-401 or an IL-2 mutein Fc fusion protein. After five days in culture, the number of differentiated B cells were counted by FACS analysis. As shown in the graph on the left of this slide, CUE-401 had little effect on mature B cells. However, as shown in the middle graph, the number of B cells that were differentiated into plasmablasts was markedly reduced. In addition, CUE-401 markedly suppressed antibody production in these cultures, as is shown in the graph on the right of this slide. These data support the conclusion that although CUE-401 has minimal effects on mature B cells, it suppresses the differentiation of plasmablasts into plasma cells, thereby reducing antibody production. These findings further support the potential for CUE-401 to both suppress ongoing inflammation and regulate overall immune balance. To summarize, I now return to the slide that I showed first. The ability of CUE-401 to suppress inflammation by inhibiting T effector, NK, and B cell function has unique implications for the treatment of autoimmune diseases. Although IL-2 by itself can stimulate proliferation of existing T regulatory cells and Tregs, it can also induce the proliferation and activation of T effector, NK, and B cells. The additional TGF-β signaling provided by CUE-401 not only stimulates proliferation of nTregs but also promotes the transformation of autoreactive T effector cells into antigen-specific iTregs. By doing so, CUE-401 suppresses the activation by IL-2 of other cell types involved in autoimmunity. This broader suppression of the inflammatory response by CUE-401 both protects against tissue damage and enhances maintenance of cell tolerance by the T regulatory cellular compartment. I view CUE-401 as a unique therapeutic agent that combines TGF-β and IL-2 signaling to both suppress inflammation and maintain self-tolerance by regulating immune balance. Thus, CUE-401 has great potential to treat the wide spectrum of autoimmune diseases and positively impact the lives of the many patients who suffer with these disorders. Thanks. I will now turn the call back to Dr. Baker. Dan? Thanks, Jon. Well, CUE-401 is rapidly approaching its first human trial. All IND-enabling studies are completed, including the four-week GLP toxicology study. The IND is in preparation for submission in June, and the first-in-human phase I program in healthy volunteers is scheduled to begin shortly after, with results of the single ascending dose study expected the end of 2026, and the results of the multiple ascending dose study expected in the first half of 2027. This slide shows the design of the phase I trials. The SAD study is a blinded, randomized, placebo-controlled trial which will enroll 40 subjects over five dose levels as five cohorts. We will then move to the MAD study, also a blinded, randomized, placebo-controlled trial, which will enroll 32 subjects over two dose levels as part of four cohorts. This trial will be pharmacodynamically marker heavy and will inform us about the best clinical doses that can be used in patient trials. Those trials will start rapidly following our understanding of the likely dosing regimens. In closing, we believe 401 provides an opportunity to make a difference for patients with multiple autoimmune conditions. The choice of a lead indication will be made to provide early proof of concept while providing pharmacodynamic data that will inform dosing and the best fit for adjacent indications. CUE-401 may provide a unique paradigm of treatment options, both alone and in combination with other drugs. Let me say that the Q team is very excited for the potential to bring life-changing therapies to patients. Let me pass it back to Cindy. Or Tara. Thank you, Dan. We'll now conduct a question and answer session with the management team who's currently on the line. We had a question come in, and I'd like to introduce Dr. Natasha Girgis, who's joined us as the Director of Translational Pharmacology. The question that's come in is about the TGF-β mask. It seems to be a reduced avidity binder, not a true conditional mask that turns on in the presence of IL-2. What have you done to de-risk the TGF-β toxicity concerns at high enough doses? Tasha? Thank you, Cindy. That's a great question. There are a couple of points I think that are important to point out. First, that's correct. Our TGF-β is a very reduced affinity binder to the TGF-β receptor, and the mask is not conditionally activated by proteases or in specific tissues. That said, there are a couple of things that do de-risk CUE-401 in terms of the risk of continuous TGF-β signaling. First, the mask does significantly reduce affinity up to 10,000-fold, resulting in very attenuated TGF-β signaling. Given the roughly three-day half-life of CUE-401, this also means that direct TGF-β signaling also occurs for a short period of time after dosing. This is part of the reason the addition of IL-2 is important, and there are a number of reasons for that. IL-2 increases the avidity of CUE-401, which has the potential to bias binding of the TGF-β component towards IL-2 receptor positive cells, because that TGF-β interaction on its own is so reduced in affinity. Second, because the combination of IL-2 with TGF-β induces and expands Tregs, that allows for CUE-401 to be dosed intermittently, as we've seen with other IL-2 based Treg expander approaches, most prominently Neoleukin. What that means is that TGF-β signaling is not activated by CUE-401 for long periods of time. It means that when you induce and expand those Tregs, they take over immune control, allowing for intermittent dosing. In terms of de-risking, we've performed multiple repeat dose studies in non-human primates with more intensive dosing than we're anticipating using in the clinic. In these repeat dose toxicity studies in NHPs, repeated dosing with CUE-401 did not result in any evidence of organ fibrosis. Great. Thanks, Tasha. We have a question here for Dr. Jonathan Kay. From a rheumatologist standpoint, what would make this mechanism clinically differentiated versus existing immunology drugs? Better durability, cleaner safety, steroid-sparing potential, or activity in hard to treat patients? Where do you think CUE-401 can make the most impact? Dr. Kay? The mechanism whereby CUE-401 increases Tregs as well as converts the T effector cells into Tregs, increases the efficacy. Certainly, this molecule is going to have tremendous effects in all autoimmune diseases by increasing immune tolerance. It certainly has potential to be steroid sparing as well as a direct therapy for diseases such as atopic dermatitis, systemic lupus erythematosus, inflammatory bowel disease. Inflammatory arthritis. This unique mechanism certainly has potential to reduce toxicity and increase efficacy. Great. Thank you, Dr. Kay. I have a question for Dr. Baker. The preclinical data shows that CUE-401 induces both natural Tregs and induced Tregs, which is the core differentiation from pure IL-2 muteins. How durable is this effect in your view after you stop dosing? Well, what we know is that the peak generation of iTregs, of Tregs basically, is about seven days. Those Tregs stay around for at least 28 days, and in peripheral blood, and may stay around longer in peripheral tissues. It's well known that it doesn't take a lot of specific Tregs to maintain a tolerogenic response. We think that that response will last up to months, and will lead to some intermittent dosing. Yes. Great, thank you. We had a question as well about the upcoming IND filing, how it's coming together. I think that I can answer that one. As Dan had mentioned earlier, the IND enabling studies have been completed, including the four-week GLP toxicology, and we're preparing the submission right now for June. Our first-in-human phase I program in healthy volunteers is scheduled to begin just shortly after, with the single ascending dose study expected to end in the end of 2026, and the multiple ascending dose study expected in the first half of 2027. Let's see. We have one other question here. Perhaps, Natasha, again. The TGF-β component is the most novel part of the molecule. How are you thinking about its safety profile in humans? Thanks, Cindy. I think that also relates to the first question that I answered about de-risking. I think that it has the potential for an excellent safety profile for a number of reasons. It is highly attenuated, so keep in mind that wild type TGF-β is produced anytime you have tissue injury or immune activation, and it's much more potent than our TGF-β. The major benefit is that by combining with IL-2, we induce regulatory T cells for long-term immune control. In terms of if we had to continuously agonize TGF-β, I don't think that would be a very safe approach. Because we combine with IL-2 and both of the cytokines are extremely attenuated, we allow for immune control and suppression of inflammation over the short term, and then induction of regulatory T cells for long-term immune control. Does that answer the question? Great. Thank you, Tasha. It looks like that concludes our questions. I want to just thank all the participants of today's call, Dr. Jonathan Kay, Dr. Rich DiPaolo, Dr. Daniel Baker, and Dr. Natasha Girgis. I also want to thank all of those of you who are listening in today's call and express my sincere appreciation and gratitude for your continued interest and support of our important work at Cue. Cue is committed to progress forward to help patients suffering from debilitating autoimmune diseases. Once again, I want to thank you all very much, and have a pleasant day.