Good morning, and thank you for joining us. I am Luis Peña, the President and CEO of Evommune. Yesterday, we announced our agreement with Hinova for global development rights, excluding Greater China, to EVO570, an oral VAV1 molecular glue degrader. Over the next few minutes, we will explain why we did this deal, what the science shows, and how EVO570 fits into the rest of our portfolio. I am joined today by Greg Moss, our Chief Business and Legal Officer, who will cover the deal terms and the competitive landscape, Jeegar Patel, our Chief Scientific Officer, who will take you through the VAV1 biology and the 570 data, and Mark Jackson, our SVP of Clinical Development, who will walk through the development plan. Before we begin, a reminder that today's presentation contains forward-looking statements, including statements about the potential benefits of our product candidates, the timing of our clinical trials and data, and our cash runway. These statements are subject to risks and uncertainties, and actual results may differ materially. Please refer to the disclaimer on this slide and to the risk factors in our SEC filing. This webcast is pre-recorded, so we will not be taking live questions. Please send any questions to our investor relations team, and we will be glad to follow up. Let me start with why we are excited about EVO570 and why now. EVO570 is an oral molecular glue degrader of VAV1, a protein found almost exclusively in immune cells that drives signaling through both the T-cell and B-cell receptor. Our goal is simple: JAK-like efficacy without the JAK liabilities. The case rests on three points. First, the biology. Human genetics support VAV1's role in inflammation. It has broad potential across autoimmune disease, and because it is restricted to immune cells, we expect a more selective profile than the JAKs. It is also an emerging target, which makes the timing right for us. Second, the clinical path. We will start in rheumatoid arthritis, or RA. Many RA patients remain underserved by current therapies. RA reads through to many other T and B-cell diseases, and it gives us a fast, well-precedented proof of concept for an oral drug with a novel mechanism. Key opinion leaders support these assumptions and are excited about the program. Third, the molecule. We ran parallel diligence on 11 programs and chose EVO570. It is about 20 times more potent than MRT-6160, the Novartis VAV1 degrader, with a sub-nanomolar DC50. It has a distinct scaffold with its own composition of matter IP and freedom to operate, and it is close to the clinic, with phase I data expected mid-2027. One housekeeping note: EVO570 was previously known as HC118, so you may see that name in earlier publications on some of our slides. Greg will now take you through the deal terms. Greg? Thanks, Luis. We've secured global development rights to EVO570 from Hinova Pharmaceuticals on capital-efficient terms. The program comes with expected composition of matter IP protection through 2045, plus potential patent term extension. Upfront, we paid $20 million in cash plus $10 million in warrants, exercisable for Evommune stock, issued at signing. Hinova is eligible for tiered royalties on net sales from the mid-single digits to the low double digits. It's also eligible for modest development, regulatory, and sales milestones in line with market terms. The first is a $10 million milestone payment when a phase II study is initiated. Alongside the license, we raised $30 million in a private placement with specialist institutional investors. We see their support as a strong vote of confidence in EVO570, our team, and in our broader pipeline. The proceeds will help fund EVO570 through phase I and into phase II in rheumatoid arthritis. We'll keep executing on EVO301, EVO756, and EVO646 in parallel, and are committed to advancing all of these programs forward in our pursuit of new treatment options for patients suffering from chronic inflammatory diseases. With the transaction and this financing, we expect our cash runway to extend into the second half of 2029. Back to you, Luis. Thanks, Greg. Why does this matter? Because VAV1 could become the next major oral class in immunology and inflammation. About 160 million people worldwide live with an immune inflammatory disease, and only about 3% of them are on advanced therapy. There is a lot of room for an oral drug that patients and physicians are comfortable using earlier. The JAK inhibitors show what an oral class can become. They generated about $12.5 billion in sales in 2025 and are approved in more than 12 I&I indications, all from one mechanism. But their safety profile, including a boxed warning, has kept most use in later lines of therapy for more severe patients. That is the opening for VAV1, and our plan has three steps. We start in RA, a $23 billion global market with a clear development path, clinical precedent, and a disease biology driven by both B and T cells. We then aim to displace the JAKs in diseases where they're already approved, such as ulcerative colitis, Crohn's disease, psoriatic arthritis, axial spondyloarthritis, and atopic dermatitis. And we go beyond the JAKs in B and T-cell diseases they do not treat, such as MS, Sjögren's, dermatomyositis, myasthenia gravis, and lupus. Before we go deeper on EVO570, let me show you where it fits in our portfolio. Two of our programs are already in phase II. EVO301 met its primary endpoint in our phase IIa trial in 70 patients with moderate to severe atopic dermatitis. We saw a 34% placebo-adjusted improvement in EASI at week eight. At week 12, 23% of patients reached clear or almost clear skin versus none on placebo. There were no treatment-related serious adverse events and no conjunctivitis. That was a single dose level given twice, and the PK supports dosing every four weeks or less often. We plan to start phase II-B in mid-2027 with the data in the second half of 2028. We also plan to start a trial in ulcerative colitis in phase II-A in the first half of 2027, with data expecting in 2028. EVO756, our oral MRGPRX2 antagonist, is in a phase II-B dose-ranging trial in migraine prevention. About 330 adults with refractory migraine received 25 or 50 milligrams twice daily or placebo for 12 weeks. The primary endpoint is a change in monthly migraine days, the standard endpoint in the field. Top-line data in this trial are expected in the second half of 2027. Both programs read out within the next two years. Alongside them, EVO646 and EVO570 give us a potentially leading oral autoimmune franchise built on complementary biology. EVO646 is an oral TLR7/8 antagonist. It acts on innate immunity and autoantibodies. It blocks type 1 interferon production by plasmacytoid dendritic cells, a pathway validated by anifrolumab in lupus, and it reduces B-cell activation and autoantibody production, a pathway validated by belimumab, also in lupus. That makes systemic and cutaneous lupus and myasthenia gravis among our main diseases of interest for EVO646. EVO646 enters phase I in the first half of 2027, with data expected in late 2027. EVO570 acts on adaptive immunity through the receptors that switch on T and B cells. By degrading VAV1, it damps signaling downstream both the T-cell receptor and B-cell receptor. We start in RA, with IBD, MS, and Sjögren's among the expansion options. Phase I data are expected in mid-2027. Two oral mechanisms covering different drivers of autoimmune disease alongside EVO301 in atopic dermatitis and IBD, and EVO756 in migraine. Here's how the four programs fit together. Evommune has always been a portfolio company focused on chronic inflammation. We manage our programs with discipline and are always looking to optimize the mix through our own research and through business development. When we see exceptional science, we act on it, and EVO570 is an example of that. Each of our four programs targets an upstream driver of inflammation, and together, they could reach large patient populations of about 6 million U.S. adults with moderate to severe atopic dermatitis for EVO301, about 30 million migraine patients eligible for preventative therapy for EVO756, about 6 million patients in EVO646's initial indications, and about 18 million RA patients for EVO570. With four programs, no single readout decides our future, and we have many distinct opportunities to potentially help patients. Here's a timeline for each program. I covered the phase II programs a moment ago, so I'll pick out what's added here. Beyond atopic dermatitis, EVO301 has a phase II-A ulcerative colitis planned to start in the first half of 2027, with data expected in 2028. We see other indications where their IL-18 pathway drives disease. EVO570 phase I data with key biomarkers are expected around mid-2027, and EVO646 phase I data with key biomarkers in late 2027. That is a steady flow of data from four programs over the next 18 months. I'll hand it over to Jigar Patel, our CSO, to take you through the VAV1 biology. Thanks, Luis. What makes VAV1 attractive is where it sits. In T cells, it is activated downstream of the T-cell receptor and the CD28 co-stimulatory receptor. In B cells, it sits downstream of the B-cell receptor and CD19. One target controls signaling through both of the receptors that drive adaptive and autoimmunity. Once VAV1 switches, the cell goes on to activate, produce cytokines, and migrate to sites of inflammation. We also remove VAV1 with a molecular degrader approach, which is a precision approach to tag and use the cell's own protein disposal machinery. VAV1 is also immune cell restricted. It potentially gives it benefits over other mechanisms. This slide shows how broad VAV1 biology is. Across the top are nine key indications, split between diseases driven mainly by T cells and those driven by both T and B cells. Down the slide are seven drug classes used in I&I today. Each of those classes work only on some of the disease attributes, and most are injectables. The bottom row is VAV1, and there is direct biological evidence in all nine indications. Human genetics link VAV1 to psoriasis, RA, MS, and myasthenia gravis. Disease models support it in colitis, arthritis, MS, and lupus. Additionally, patient cell data supports it in lupus and Sjögren's. Competitor phase II trials have now begun in psoriatic arthritis and Sjögren's, though no efficacy data has been reported yet. The breadth is one reason we are starting in RA. RA is driven by both T and B cells, so what we learned here reads across through many of the other diseases on this chart. Here we compare VAV1 with the JAK family, TYK2, and T and B cell depletion approaches across C7 attributes. On these attributes that drive efficacy, VAV1 looks like JAK. It modulates T cell function and B cell function, it modulates cytokine production, and it affects immune cell chemotaxis. That is why we describe it as potential JAK-like. Where VAV1 differs is where it acts. The expression is limited to immune cells, whereas JAK signaling crosses most tissues of the body. We believe that selectivity is what gives VAV1 the potential for a better safety profile than JAKs. The short version, JAK-like efficacy with more selective profile. Now let me show you why we think EVO570 is the best molecule to test that. Why EVO570 specifically? We tested it head-to-head against MRT-6160, the Novartis VAV1 degrader that is now in phase II. EVO570 degrades VAV1 with a DC50 of 0.3 nanomolar versus seven nanomolar for MRT-6160. That is about 20 times more potent in vitro, and it reaches deeper knockdown, 99% versus 97%. In addition, EVO570 binds cereblon about 10 times more tightly and forms ternary complex about four times more strongly. That potency carries through to function. It is at least 10 times more potent at blocking IL-2 from T cells and blocking IL-6 from B cells. The degradation is also durable, with more than 85% of VAV1 still degraded at seven days post-dose, which gives us potential for durable activity and less frequent dosing. The selectivity is clean, like MRT-6160, and the safety window is large, with no dose-limiting toxicity identified in toxicology studies. Taken together, this suggests that EVO570 could work at low doses, which could help for depth of activity, safety, and dosing convenience. In vitro potency only matters if it translates in vivo, so we tested EVO570 in three standard and relevant disease models against both MRT-6160 and standard of care comparators. In rheumatoid arthritis models, like the CIA model, inflammatory bowel disease models, like the T-cell transfer model, and for multiple sclerosis models, like the EAE model, EVO570 met or exceeded both MRT-6160 and standard of care at low doses in all the models evaluated. Greg will now put EVO570 into the context of the VAV1 field. Thanks, Jeegar. Let me put EVO570 in the context of the VAV1 field. The most advanced program is MRT-6160, which Novartis licensed from Monte Rosa. In a phase I study in 70 healthy volunteers, it achieved more than 90% VAV1 degradation and was well tolerated. Novartis is now running two phase IIa/b studies in Sjögren's disease with about 344 patients and in psoriatic arthritis with about 220 patients, and we expect more phase II study starts. That matters for us. We estimate Novartis could report part A top-line data as early as the fourth quarter of 2027 or the first quarter of 2028. That could validate the class about a year before our own RA data, which we expect in the fourth quarter of 2028. We are in a distinct lane. Novartis is in Sjögren's and PsA. We lead with RA, where we plan to be the first to advance to later-stage studies and eventually to approval. In addition to MRT-6160, the other clinical-stage VAV1 programs that we are aware of are earlier and China-only. InnoCare's ICP-538 in phase I healthy volunteers and Haisco's HSK56630, about which there is little public disclosure. To date, neither has disclosed U.S. development plans. Of importance, EVO570 is based on completely novel chemistry and has the potential to be both first in class based on our development execution and, as Jigar mentioned, also best in class based on its unique and fully IP ring-fenced chemistry. Mark will now walk through how we plan to develop EVO570. Thanks, Greg. We are starting in rheumatoid arthritis because there is a large underserved patient population that still needs new therapies. Treatment usually starts with conventional DMARDs, such as methotrexate. Patients who do not respond to methotrexate add a biologic or JAK inhibitor, typically a TNF inhibitor first, and those who still do not respond switch to another biologic or to a JAK. Even so, more than half of RA patients are not in remission. The efficacy of anti-TNFs wanes over time, and there has been no new mechanism in more than 10 years. There is a large population of patients who have failed TNF therapy or who cannot tolerate current options, and there is still no convenient, well-tolerated oral option. There are four main reasons we chose RA first. Mechanistic fit. RA is driven by T and B cells, and VAV1 signals downstream of both receptors. Second, fast proof of concept. A 12-week placebo-controlled study in methotrexate inadequate responders pairs clinical endpoints with target engagement. Third, an established pathway. Standard endpoints and regulatory precedent speed up dose selection. Finally, a first and best-in-class potential. The other VAV1 programs are in other indications, and our RA dose, PD, and safety data will help guide where we go next. On the right is the wider opportunity, 12 prioritized indications in total. RA is our lead proof of concept. Expansion candidates include IBD, lupus, MS, myasthenia gravis, and systemic sclerosis, as well as PsA and Sjögren's, where phase II trials are already underway. Lifecycle options include dermatomyositis, psoriasis, hidradenitis suppurativa, and ankylosing spondylitis. The sequence is simple. Phase I for safety, PK, PD, and food effect. We are also exploring a phase I-B cohort in RA patients in order to be the first to deliver patient data on the target. Then the RA phase II program to set the dose and show clinical activity. Then the potential expansion, prioritized by our own human data and by readouts from the class. Here is the phase I design. It is a first-in-human, randomized, double-blind, placebo-controlled study in 146 participants, run in China, and designed to support a global phase II program. Part A is a single ascending dose, eight cohorts of 10 patients, randomized eight to two, active to placebo, starting at 0.1 milligrams. Part B is multiple ascending dose, four cohorts of 12 patients, randomized 10 to two. Part C is a two-way crossover food effect study in 18 participants. The primary endpoints are safety and tolerability. Secondary endpoints are PK and PD, which includes VAV1 degradation in T and B cells, and the ex vivo response to T and B cell receptor stimulation measured through CD69, IL-2, IL-17A, interferon gamma, and IL-6. The design is adaptive, so a safety review committee can adjust doses based on earlier cohorts. On timing, the China and U.S. INDs were submitted in September and October respectively, and the U.S. IND is now open. We expect phase I to start in January 2027, with data around mid-2027. We are also exploring an RA patient cohort with Hinova for early proof of concept as an additional phase I-B cohort on the MAD portion of the study. A phase II in RA follows. With that, back to Luis. Thanks, Mark. Let me put it all together. We started with the JAKs as the model for what an oral class can become, and with the boxed warning that holds them back. VAV1 keeps the oral convenience, but differs in two ways that matter. It is substantially restricted to immune cells, and it acts on a targeted pathway downstream of the T and B cells. We have a series of milestones ahead across the portfolio. EVO570 phase I data are expected around mid-2027, with a phase II program in RA planned to start in the second half of 2027. EVO756 phase II-B top-line data in migraine are expected in the second half of 2027. EVO646 phase I data follow in late 2027. For EVO301, we plan to start a phase II-A in ulcerative colitis in the first half of 2027, with data in 2028, and a phase II-B trial in atopic dermatitis, where we expect data in the second half of 2028. We are funded to deliver them all. Cash runway post-transactions expected into second half of 2029. To sum up, EVO570 is a potentially best-in-class oral VAV1 molecular degrader that could deliver JAK-like efficacy with a better safety profile. Together with EVO646, it gives us a potential leading oral autoimmune pipeline alongside EVO301 in atopic dermatitis and IBD, and EVO756 in migraine. We are well-funded to deliver the data. Thank you for joining us. A replay of this webcast and the slides are available on the investor section of our website. If you have questions, please contact our investor relations team.