Welcome to the Alpine Immune Sciences investor call. Currently, all participants are in a listen-only mode. As a reminder, this event is being recorded. I would now like to introduce Michelle Greenblatt, Director of Investor Relations and Corporate Communications at Alpine. Ms. Greenblatt, please go ahead. Thank you, Operator. Good afternoon, and thank you to everyone for taking the time to join us today. With me on today's call from Alpine are Dr. Mitchell Gold, Executive Chairman and Chief Executive Officer; Dr. Stanford Peng, President and Head of Research and Development; Paul Rickey, Chief Financial Officer; and Dr. Remy Durand, Chief Business Officer. Before I turn the call over to Mitch, I'd like to remind you that we will be making forward-looking statements during today's call. These forward-looking statements represent our views as of today and are based on our current expectations and consequently involve risk and uncertainties. Actual results could differ materially from those anticipated in such forward-looking statements as a result of such risk and uncertainty. I encourage you to refer to the most recent SEC filings regarding the risk factors associated with these statements. Due to today's announcement regarding Alpine's anticipated acquisition by Vertex Pharmaceuticals, we are unable to take any questions at the end of today's call. Mitch, please go ahead. Thank you, Michelle. T hank you to all of those who are participating in the webcast today. I'd first like to make a few comments about the merger agreement we announced this afternoon with Vertex Pharmaceuticals. This is a historic moment for Alpine, for our employees, and most importantly for patients who may benefit from our pipeline of products, in particular povetacicept. Our team has done a tremendous job in demonstrating povetacicept's potential in a very short time since beginning clinical trials less than two and a half years ago. It became clear during our discussions with the Vertex team that we share many core values, including a commitment to patients, our employees, and an intense drive for innovation. Povetacicept has demonstrated potential best-in-class attributes in IgA nephropathy and has a broad development potential across a number of other autoimmune and inflammatory conditions with significant unmet needs. We look forward to the opportunity now, more than ever, to make a meaningful difference in the lives of patients worldwide as part of Vertex. We will focus the remainder of today's call on the updated data announced this afternoon for povetacicept and IgA nephropathy, and that will be shared again Monday during a late-breaking presentation at the World Congress of Nephrology. After I provide an introduction, Stanford Peng, our President and Head of R&D, will provide an overview of povetacicept, including the mechanistic rationale for targeting BAFF and APRIL and IgA nephropathy, as well as review key data. Stanford will then discuss next steps for povetacicept's development in IgA nephropathy, including the planned initiation of a phase III study later this year, and provide an overview of our upcoming milestones and development plans in additional indications such as SLE and other indications. I will then conclude with closing remarks. We believe today's update confirms the potential best-in-class profile in IgA nephropathy of povetacicept, a wholly owned, potent dual antagonist of both the BAFF and APRIL cytokines that is administered in a convenient once every four-week subcutaneous regimen. The depth of proteinuria reductions at 36 weeks, combined with stabilization of eGFR, strongly support our pivotal trial plans for povetacicept and IgA nephropathy. Importantly, we have completed our end-of-phase II meeting with the FDA, and they are supportive of our plans for a phase III registrational trial in IgAN, which we plan to initiate in the second half of this year. The design of this study will be similar in size and duration to other ongoing placebo-controlled phase III trials in the space, with an accelerated approval endpoint based on UPCR at 36 weeks and full approval based on using a two-year eGFR endpoint. While we plan to carry forward the 80 mg once every four-week dose schedule into the pivotal study, as we previously disclosed, we also find the 240 mg once every four-week data compelling, given the deep Gd-IgA1 reductions noted to date. We'll continue to track the 240 mg data and plan to report additional follow-up at the ERA meeting in May. IgA nephropathy is the most common primary glomerulonephritis worldwide, with a prevalence of approximately 130,000 in the United States and 265,000 in G8, according to our own market research. With limited effective treatment options, up to 50% of IgAN patients will progress to end-stage renal disease within 10 years, causing significant morbidity and cost to the overall healthcare system. Given the high rate of progression to end-stage renal disease and the typical onset of disease before 40 years of age, there is an urgent need for the development of disease-modifying therapies for IgA nephropathy. Based on our market research, there are three key trends emerging in IgAN that support a significant commercial opportunity. First, there may be significantly more patients than many initially anticipated. This is a result of increasing awareness among nephrologists to screen patients for IgAN earlier, and this is consistent with the strong investigator enthusiasm we've experienced in our ongoing RUBY-3 trial. Second, there is a shift towards earlier treatment, with the current understanding that patients with previously accepted or low levels of proteinuria are indeed at risk for progressing to end-stage renal disease. T hird, more aggressive intervention with disease-modifying therapies such as povetacicept may drive deeper reductions in proteinuria and stabilize or possibly even improve eGFR. Based on these emerging trends, povetacicept's profile in IgA nephropathy is extremely attractive, given its deep proteinuria reductions, convenient once-every-four-week dosing regimen, and dual inhibition of BAFF and APRIL. Looking ahead in IgAN, we anticipate several meaningful milestones in 2024 and beyond. In May, we plan to present additional data on povetacicept in IgA nephropathy, including longer-term follow-up data from both the 80 mg and 240 mg once-every-four-week dose cohorts at the European Renal Association meeting. Following these data in the second half of the year, we plan to initiate RAINIER, a registrational phase III study of povetacicept in IgA nephropathy, as well as a phase II study of povetacicept in SLE called DENALI. While our primary focus in 2024 remains on the initiation and execution of these critical studies, we are only in the early stages of exploring the full potential of povetacicept. Given its broad applicable mechanism of action and extended patent life, we continue to advance development of povetacicept as a potentially disease-modifying new therapeutic option in autoimmune and inflammatory diseases, including multiple nephrology indications within our ongoing RUBY-3 study and hematology indications within our ongoing RUBY-4 study. In addition to these updates on our clinical studies, we look forward to sharing translational data that further support the best-in-class potential of povetacicept in multiple disease areas, including neuroinflammation. A critical aspect of povetacicept not to be overlooked is its best-in-class dosing convenience of a single, low-volume, every-four-week injection. This profile is enabled by povetacicept's high potency and rational design as selected for using Alpine's directed evolution engineering platform. While other programs in the class may deliver up to 52 injections annually, povetacicept's once-every-four-week dosing regimen confers a significant advantage for patients, especially in our lead indication of IgAN and SLE, which are heavily comprised of younger adults with full and busy lives. W hile we anticipate commercializing with a once-every-four-week dosing, we continue to explore the potential to dose povetacicept even less frequently, potentially once every two or even once every three months, to help ease the burden on both patients and the broader healthcare system. Stanford, I'll now turn the call over to you to give an overview of povetacicept and walk us through our most recent data update. Thank you, Mitch, and good afternoon, everyone. Let me begin by reminding everyone about the target rationale and preclinical data. BAFF and APRIL are two cytokines thought to play a key role in the pathogenesis of many autoimmune diseases, including IgA nephropathy. Although they play a role in the function of several pathogenic immune cell subsets, they have primarily been described in the context of B cells, where they play key roles in the differentiation and activation of multiple B cell subpopulations, particularly antibody-secreting cells, which include plasmablasts and plasma cells. B cell populations are of particular clinical relevance due to their predominant responsibility for the production of pathogenic disease-related autoantibodies. In IgA nephropathy, the generation of pathogenic immune complexes consisting specifically of aberrantly glycosylated or galactose-deficient IgA1 are thought to lead to kidney inflammation and injury. Povetacicept is designed to interrupt this disease process, resulting in reversal and/or resolution of renal inflammation and damage. In many different autoimmune diseases, both BAFF and APRIL appear to contribute significantly to disease pathogenesis. In IgAN and other glomerulonephritis conditions, both cytokines have been found to be elevated, often correlating with disease activity and/or severity. In addition, genetic studies have identified significant disease-risk alleles associated with both cytokines, as well as their receptors, emphasizing the key importance of this cytokine pathway in the underlying pathogenesis of glomerulonephritis. Much recent attention has been focused on APRIL-specific inhibitors due to their promising clinical data in IgAN. However, BAFF has also progressed in clinical validation, with data in IgAN with the BAFF-specific inhibitor blisibimod and, more recently, the approval of the anti-BAFF antibody belimumab for the treatment of lupus nephritis. Wild-type TACI-based drugs, which are structurally related to povetacicept, have also shown promising findings in IgAN, as well as at least anecdotally in lupus nephritis and primary membranous nephropathy. Such observations altogether indicate that both BAFF and APRIL are clinically validated targets, and the combined inhibition of both may result in superior outcomes. Povetacicept is a dual inhibitor of both BAFF and APRIL, engineered using our proprietary directed evolution protein engineering platform from wild-type TACI for higher affinity against BAFF and particularly APRIL. Structurally, it is a decoy receptor consisting of a single active domain, as shown in green, fused to an Fc. It thus resembles but is smaller than other molecules in the clinic, which are based on the whole extracellular domain of wild-type TACI shown in lavender. We have previously published that povetacicept is quite potent compared to wild-type TACI and other clinically relevant comparators. This table shows IC50s of povetacicept in a cell-based assay used to assess BAFF or APRIL activity. Note that in this assay, the IC50s for APRIL appear particularly improved versus wild-type TACI, and in general, povetacicept is at least comparable, if not superior, to monoclonal antibodies against BAFF or APRIL. Povetacicept appears to possess multiple biophysical attributes that may confer significant advantages as a therapeutic. In addition to its smaller molecular weight and higher affinity compared to wild-type TACI, it possesses a significantly more acidic isoelectric point, as shown on the left of this slide. All of these characteristics may increase its ability to distribute to disease-relevant tissues, particularly in inflammatory disease states. Indeed, in a tissue distribution study in mice shown on the right, povetacicept was found at significantly higher amounts in multiple organs of particular relevance to IgAN, or the kidney, ileum, and lymph node, which includes the Peyer's patches that are considered to be one of the major sources of pathogenic antibodies and/or autoantibodies in the disease. This greater tissue distribution correlates with greater effects in lymphoid organs and other tissues. In a KLH immunization model, povetacicept reduces the production of anti-KLH antibodies more potently than wild-type TACI, as shown in the right in green, but also reduces B cell populations more potently in lymphoid organs, as shown on the left, including particularly the follicular B cell subset but also the germinal center B cells and plasma cells. These findings further correlate with results we've described in multiple preclinical disease models. On the left is the NZB/W model of lupus and lupus nephritis, where povetacicept in green was superior in reducing renal histopathology compared to wild-type TACI in blue and conventional B cell depletion with an anti-CD20 antibody in orange. In the middle, this same model also develops an autoimmune hemolytic anemia, and povetacicept was similarly superior in controlling the anemia with largely normal hemoglobin levels versus the other two comparators. O n the right, povetacicept in green was also effective in a model of myasthenia gravis, superior to FcRn inhibition in purple and CD20 depletion in orange. With such compelling preclinical data, we initiated clinical development of povetacicept with a single ascending dose study in healthy adults, exploring both intravenous and subcutaneous routes of administration. All doses were well tolerated overall, and we observed dose-dependent pharmacokinetics and pharmacodynamics. Results from the study supported consideration of two dose regimens for multidose patient studies: 80 mg and 240 mg subcutaneously every four weeks. The rationale was based on data shown here. In the middle column, pharmacodynamic reductions in circulating immunoglobulins were noted, similar between the dose levels, suggesting maximization of pharmacodynamic activity over the dosing interval. Similar observations were also seen in Gd-IgA1 in the upper right and in circulating antibody-secreting cells by flow cytometry on the lower right. However, target coverage of both BAFF and APRIL shown to the left differed, with the 240 mg in purple suppressing both cytokines effectively throughout the four-week observation period, while the 80 mg in teal or turquoise suppressed them for approximately only two-three weeks. These findings suggested that while it could be possible that 80 mg every four weeks could be sufficient for efficacy in a disease population, 240 mg may be warranted for more complete target coverage, especially if disease states mean higher levels of circulating or tissue BAFF. We therefore plan to explore both 80 mg and 240 mg subcutaneously every four weeks in our initial patient studies. To summarize this portion, here are four key takeaways regarding the preclinical and translational aspects of povetacicept. One, povetacicept is an engineered dual inhibitor of the BAFF and APRIL cytokines designed to achieve more potent inhibition of both cytokines than other comparators. Two, povetacicept demonstrates a highly compelling nonclinical profile with superiority in preclinical efficacy models versus wild-type TACI, FcRn inhibition, and conventional anti-CD20 B cell depletion. Three, povetacicept has been well tolerated and demonstrates on-target pharmacodynamic activity in healthy adults, where single doses have been well tolerated at up to 960 mg subcu or IV. And four, povetacicept's development profile supports a convenient dose regimen, initially with 80 mg-240 mg subcu every four weeks. We'll now move on to the update of povetacicept's experience in IgA nephropathy. As a reminder, RUBY-3 is an open-label parallel cohort multiple ascending dose escalation basket study of povetacicept in multiple glomerulonephritis conditions, including IgA nephropathy, primary membranous nephropathy, lupus nephritis, and ANCA-associated vasculitis. Participants are being enrolled in disease-specific cohorts initially at 80 mg subcutaneously every four weeks, escalating to 240 mg after adequate initial safety review. They receive initially six months of povetacicept, which is extendable to up to two years, and are assessed for various standard outcomes, including safety, UPCR, eGFR, and disease-specific biomarkers such as Gd-IgA1. The data today focus on the IgAN cohort, where the majority of patients have been enrolled and, in fact, over-enrolled. They are required to have biopsy-proven disease within 10 years, UPCR of at least 0.5 g per gram, eGFR of at least 30, and be on maximal ACE inhibitor or ARB therapy. Stable SGLT2 or endothelin antagonists are permitted if stabilized prior to study entry. Note, however, that new initiation or change in dose of such or other antiproteinuric agents is not allowed during the study. As of March 1st, 12 and 29 patients had enrolled at the 80 mg and 240 mg dose levels, respectively. Their baseline characteristics appear generally similar to other IgAN studies, including a baseline UPCR of approximately 1.2 g-1.3 g per gram and eGFR of 60-70. A minority of patients had previously been treated with corticosteroids, and some entered the study on a stable dose of an SGLT2 inhibitor. Both the 80 mg and 240 mg dose levels appear well tolerated in IgAN. As shown here, there have been no reports of severe or serious infections or severe hypogammaglobulinemia as defined as IgG less than 300 mg/dL among these patients. Let me comment on a few events of note, though. The grade three event at 80 mg was a patient who developed breast cancer on study. She had a history of breast cancer, and retrospective evaluation indicated that she likely had a preexisting breast nodule at the time of study entry. Therefore, the event was considered by the investigator and safety monitoring committee as unrelated to study drug. Also, one injection site reaction of rash has been reported in a single patient at 240 mg. However, this reaction has not recurred despite subsequent doses in the same patient without any specific intervention, such as premedication. Updated data indicate that povetacicept continues to be associated with significantly meaningful improvements in disease activity. At 36 weeks, the endpoint for accelerated approval, six patients on 80 mg had achieved a 64.1% reduction in UPCR, and a single patient on 80 mg had achieved a 78% reduction at 48 weeks. Among these, four out of six, or 67% at 36 weeks, as well as the patient at 48 weeks, had achieved remission as defined as a UPCR of less than 0.5, reduction in UPCR of at least 50% from baseline, and stable renal function as defined as no worsening of eGFR of more than 25%. Povetacicept treatment was also associated with resolution of hematuria as defined as negative or trace or small hematuria in patients with non-negative trace hematuria at baseline. All, that is, 100% of patients with data available at 36 or more weeks have achieved hematuria resolution by these criteria. Note, initial available data from the emerging 240 mg cohort in purple demonstrates similar reductions in UPCR and remission, with follow-up available in 13 and two patients at 12 and 24 weeks, respectively. Importantly, renal function as assessed by eGFR appears stable with both dose regimens. These improvements in proteinuria and stabilization of eGFR were associated with rapid reductions in the key disease-related biomarker Gd-IgA1. Both dose regimens were associated with a reduction of over 40% within the first four weeks. The 80 mg dose cohort was reduced by almost 68% after 36 weeks, while the 240 mg dose cohort was reduced by over 70% within the first 12-24 weeks. For some further insight into the potential disease impact of povetacicept, IgA to C3 and Gd-IgA1 to C3 ratios were examined. These have been proposed in several studies to be significant disease severity and/or prognostic biomarkers in IgAN, incorporating C3 as a biomarker of alternative and/or lectin complement pathway-mediated activation of IgA1-containing immune complexes. As shown, both ratios were reduced by over 40%-50% from baseline in the 80 mg cohort beyond six months, while the 240 mg cohort reduced by over 60%-70% after as early as three months. As previously noted, povetacicept treatment is associated with pharmacodynamic reductions in circulating immunoglobulins, including IgE. The differences, if any, between 80 mg and 240 mg are not as dramatic here. In summary, povetacicept administered subcutaneously every four weeks continues to demonstrate significant, clinically meaningful reductions in UPCR by over 60% at 36 weeks, associated with stable renal function, resolution of hematuria, and evidence of remission. Both 80 mg and 240 mg dose regimens demonstrate improvements. These doses do not yet appear to differentiate by UPCR based on the available data with 240 mg through 24 weeks, but other biomarkers such as Gd-IgA1 suggest a potential quantitative pharmacodynamic difference, which prompt interest in further follow-up to ascertain any possible later differentiation in primary clinical endpoints such as UPCR. Importantly, both dose regimens have been well tolerated in IgAN with no severe serious infections or instances of severe hypogammaglobulinemia. Altogether, these findings strongly continue to support further development of povetacicept in IgAN and other autoimmune diseases. Looking ahead, we are pleased to have recently completed a successful end-of-phase meeting with FDA, which enables advancements of povetacicept to a single randomized placebo-controlled registrational trial in IgAN. This study is called RAINIER, and we plan to initiate it in the second half of this year. We also plan to initiate a phase II study in systemic lupus erythematosus called DENALI later this year, while continuing to explore other glomerulonephritis and cytopenia conditions in the RUBY-3 and RUBY-4 studies, respectively. I'll now turn the call back over to Mitch. Thanks, Stanford. As Stanford highlighted, we are highly encouraged by the updated IgAN data for povetacicept and are just beginning to explore the full potential of this unique, best-in-class molecule. We look forward to the initiation of RAINIER, our pivotal phase III study in IgAN, and DENALI, our phase II study in SLE. In addition, we will continue to evaluate the potential for povetacicept in additional indications beyond IgAN. Povetacicept's favorable commercial profile, including a once-every-four-week dosing regimen, truly allows for a pipeline and a product development plan. In closing, let me thank our investigators and patients who participated in our clinical trials. Through your courage and support, we are blazing a new trail in developing therapies for autoimmune diseases. I would also like to thank our investors. Some of you invested in us very early and supported the company through multiple fundraising rounds, enabling us to achieve our goals of developing an innovative, best-in-class medicine from our directed evolution platform. We could not have accomplished this without your support. Thank you, everyone, for your time today, and have a great day. This concludes today's conference call. Thank you for your participation, and you may now disconnect.