Good morning, everyone. Welcome to the Zenas BioPharma Conference Call. At this time, all participants are on a listen-only mode. There will be a question-and-answer session after the prepared remarks. Be advised that this call is being recorded at the company's request, and a replay will be available in the investor section of the company's website following the call. I'll now turn the call over to Jennifer Fox, Chief Business Officer and Chief Financial Officer of Zenas. Jennifer, you may begin. Thank you, Operator, and thank you all for joining us to discuss our transformational global collaboration agreement with InnoCare Pharma. Before we begin, I would like to remind you of the safe harbor provisions outlined on slide number two. During today's presentation, including during the question-and-answer portion of the call, we will be making certain forward-looking statements. Any statements contained in this call that relate to expectations or predictions of future events, results, or performance are forward-looking statements. Forward-looking statements speak only as of the date of this call and involve risks and uncertainties that may cause actual results to differ materially from those expressed or implied by such forward-looking statements. These risks are described more fully under the heading risk factors, as well as elsewhere in our company filings made with the Securities and Exchange Commission, including our quarterly report on Form 10-Q for the second quarter and our subsequent SEC filings. You are cautioned not to place any undue reliance on these forward-looking statements. Except as required by applicable law, we undertake no obligation to update or revise any forward-looking statements. We will begin today's call with prepared remarks from Lonnie Moulder, our CEO, Lisa von Moltke, our Head of Research and Development and Chief Medical Officer, and Haley Laken, our Chief Scientific Officer. For the Q&A portion of today's call, we will be joined by Joe Farmer, our President and Chief Operating Officer. I'll now hand over the call to Lonnie. Thank you, Jen, and thank you, everyone, for joining us for today's announcement about our strategic global collaboration with InnoCare, a well-established and respected, fully integrated biopharmaceutical company that we've had a long relationship with. This collaboration is not only transformational for our organization, as you will see in subsequent slides, it also has the potential to be transformational for patients living with autoimmune diseases, especially progressive forms of multiple sclerosis, an area of extremely high unmet medical need. Zenas now has a deep differentiated development stage pipeline of potentially best-in-class molecules. This transaction advances Zenas' stated corporate strategy and leverages our global development capabilities and commercial experience. For a potentially best-in-class phase III product candidate, orelabrutinib, and two novel earlier stage autoimmune development candidates, InnoCare will receive upfront consideration that includes $35 million in cash plus five million Zenas common shares. The phase III registrational study for orelabrutinib in primary progressive multiple sclerosis, or PPMS, has already been initiated. Upon first patient treated in the upcoming phase III secondary progressive multiple sclerosis, or SPMS study, an additional $25 million and two million Zenas shares will be paid. Subsequent milestones for orelabrutinib are tied to regulatory submissions, approvals, and commercial sales milestone achievements. There are additional regulatory milestone payments, as well as commercial sales milestone payments, for the oral IL-17 AA/AF and brain-penetrant TYK2 programs. There are also tiered royalties on net sales for all three programs. This exciting transaction, closed our collaboration agreement with InnoCare, is a significant step toward our goal of becoming a global, fully integrated commercial-stage biopharmaceutical company making a meaningful difference for patients living with autoimmune diseases, including multiple sclerosis. As we head into 2026, we aspire to leverage our team's experience and strong track record of success and our global development and commercialization capabilities to potentially launch, over five years, three best-in-class franchise molecules across five indications in three therapeutic areas, including rheumatology, multiple sclerosis, and dermatology, each representing significant commercial opportunities. Our I&I pipeline portfolio now consists of obexelimab, with regulatory submission activities and launch preparations for an IgG4-RD indication as our highest priority in anticipation of phase III Indigo top-line results expected around year-end. We are also on target to report top-line results from the Moonstone relapsing multiple sclerosis, or RMS, phase II study this quarter, and results of the Sunstone phase II lupus, or SLE, study, mid-2026. Orelabrutinib, our newly acquired, highly selective, CNS-penetrant and potentially best-in-class BTK inhibitor, is currently in a phase III trial for PPMS, with the first clinical site having recently been initiated in the U.S. A phase III study of orelabrutinib in SPMS is planned to begin next quarter. We will further discuss our exciting oral IL-17 AA/AF inhibitor, ZB021, and our brain-penetrant TYK2 inhibitor, ZB022, both of which we plan to advance into the clinic next year. As you can see, we have multiple potentially value-creating milestones expected over the next several years, ranging from a phase III readout for obexelimab in IgG4-RD to phase II readouts in RMS and SLE. Our expanded pipeline further builds upon these milestones, with two phase III trial initiations for orelabrutinib in progressive MS and initial data plan from both our oral IL-17 and TYK2 programs. I'll now turn the call over to Haley, who will review progressive MS, the promise of BTK inhibitors to address disease progression, and the unique profile of orelabrutinib. Haley? Thanks, Lonnie. As Lonnie previously mentioned, preventing disability progression is the highest unmet medical need in multiple sclerosis, a need unfortunately for patients which has been overlooked historically. A considerable percentage of the overall MS population are living with progressive forms of the disease. SPMS, an advanced manifestation of RMS, where relapses become less frequent or stop, but gradual worsening of disability occurs, represents at least 20% of MS. PPMS, where progression of disability occurs from disease onset without distinct relapses or remission, represents approximately 10%-15% of MS. Currently, there are only approved therapies for relapsing SPMS and only one approved therapy for PPMS, ocrelizumab, already a blockbuster in RMS but less impactful at delaying progression in PPMS. Progressive forms of MS represent a significant, largely untapped commercial opportunity. Preventing disability progression is the highest unmet medical need in multiple sclerosis, an unmet need that we believe orelabrutinib has the potential to address. MS stems from a complicated inflammatory process, both in the periphery and compartmentalized in the CNS. BTK is a validated target in MS, and the enthusiasm for BTK inhibition stems from its ability to also address compartmentalized inflammation through a central mechanism of action. While BTK inhibition also impacts peripheral B cells, similar to today's leading RMS therapies, the unique advantage is the ability to cross the blood-brain barrier and inhibit macrophages and activated microglia, which are strongly implicated in compartmentalized neurodegeneration. This dual peripheral and central activity of BTK inhibition underpins the promise of the mechanism to prevent disability progression in progressive MS patients. Tolebrutinib has laid the foundation by validating the potential for BTK inhibition to prevent disease progression, as captured in two studies published earlier this year. Tolebrutinib has shown success in a phase III SPMS trial, the first program to succeed in non-relapsing SPMS. In addition, tolebrutinib demonstrated a positive impact on PIRA, or progression independent of relapse activity, in an RMS trial. These outcomes underscore the excitement around BTK inhibition. The mechanism, centrally targeting compartmentalized inflammation and neurodegeneration, is compelling, provided that the molecule has the right selectivity and potency. I'll show how orelabrutinib fits that profile. As previously mentioned, there are no drugs approved for non-relapsing SPMS and only one approved for PPMS. tolebrutinib is in development for both PPMS and SPMS. While it has a head start in these indications, we believe orelabrutinib has the potential to be best in class. Fenebrutinib is being developed only for PPMS. This represents the core BTK inhibitor competition in progressive MS. In addition, frexalimab is advancing with a promising mechanism for SPMS. We see a significant market opportunity here, grounded first in the pharmacology and second in the clinical data we'll share. In progressive MS, several BTK inhibitors are in development, but we believe orelabrutinib's selectivity is a clear differentiator. In a study of 15 BTK inhibitors, orelabrutinib had the highest selectivity of the BTK inhibitors in development for progressive MS, an important attribute to limit off-target binding and activity. Equally important is the combination of CNS penetration and potency. Orelabrutinib is a covalent inhibitor of BTK, which is dosed once a day. Orelabrutinib has demonstrated concentrations in the CNS that well exceed its potency, which presents an advantage over tolebrutinib when you consider a ratio of CNS concentration to IC90. Fenebrutinib, in development only for PPMS, is a non-covalent inhibitor employing higher doses given twice a day. These data support the potential of orelabrutinib to deliver meaningful impact on disability progression in progressive MS patients, and orelabrutinib's profile validates our view that it has best-in-class potential for addressing disability progression in both SPMS and PPMS. Now I'll turn the call over to Lisa, who will review the data from the successful orelabrutinib phase II RMS trial. Lisa. Thanks, Haley. The phase II trial for orelabrutinib was a classic RMS study evaluating multiple doses in a dose-finding design versus placebo. The primary endpoint was the standard assessment of new T1 Gd-enhancing lesions on MRI over a 12-week period. During week 12 through week 24, placebo recipients were switched to the lowest dose, 50 mg once daily, and by the end of 24 weeks, all participants were transitioned to the lowest dose. Secondary endpoints included new or enlarging T2 lesions at 12, 16, 20, and 24 weeks. Evaluating the safety profile was also a principal objective of the study. The entirety of the trial generated 96 weeks of data, providing a robust dataset for diligence and evaluation. The baseline characteristics in the phase II study were as expected for the RMS population studied at that time. As is typical, there was a female predominance with a mean age in the mid-30s and with a time since diagnosis of just under six years. The EDSS score median was 2.6. The mean number of T1 Gd-enhancing lesions at baseline was 1.8, and the number of participants with T1 Gd-enhancing lesions present at screening was 33.5%. All three treatment arms demonstrated statistically significant improvement over placebo. The 80 mg daily dose achieved a greater than 90% reduction in new lesions compared to placebo. Importantly, the 80 mg dose also had the highest Cmax, which is critical for blood-brain barrier penetration, and it is the dose selected for the phase III trials. The time course of the appearance of new T1-enhancing lesions over 12 weeks shows separation from the control arm as early as week 4, underscoring the rapid onset of effect. These impressive phase II RMS results were complemented by data that went out to 96 weeks. We would like to highlight several outcomes at the later time points. These data support that there was sustained clinical activity as well as an impact on measures tied to disability progression. There was a nearly 10% drop in the EDSS score from baseline to week 96. Serum NfL levels, a potential marker for neurodegeneration, dropped over 50% during that same time period, and slowly expanding lesion volumes dropped by 40% between week 48 and week 96. Taken together, these findings suggest orelabrutinib could play a meaningful role in slowing disability progression in progressive MS patients, supported by the impressive phase II lesion data. The overall safety profile of orelabrutinib is consistent with expectations and similar to a number of other BTK inhibitors in development for MS. Treatment-emergent adverse events were observed in 53% of the orelabrutinib population versus 30% in the placebo population. Serious treatment-emergent adverse events were present in 2% of the orelabrutinib population versus 0% in the placebo arm. Liver-related treatment-emergent adverse events were 10% in the orelabrutinib arm versus 7.5% in the placebo arm. Transaminase elevation-related adverse events occurred primarily in the first eight weeks of treatment, and most were present as lab abnormalities only, without any clinical manifestations or symptoms. Multiple BTK inhibitors, including orelabrutinib, were placed on a partial clinical hold by FDA, but not by EMA, for studies in relapsing MS because of the potential risk of hepatic toxicity. Two cases of drug-induced liver injury in orelabrutinib trials met Hy's Law criteria, which is elevated transaminases and bilirubin in the absence of another cause. These two cases, as well as all others involving transaminase elevations, resolved without clinical sequelae upon cessation of dosing. After further analysis and given the high unmet need for treatments for progressive MS, the FDA cleared protocols for development of orelabrutinib in progressive MS patients that included risk-mitigating weekly LFT monitoring and specific stopping rules. It should be noted that many of the routinely prescribed oral therapies for MS have also been associated with liver enzyme abnormalities. Phase III protocols for primary progressive MS and secondary progressive MS have been cleared by both FDA and EMA, and we are proceeding with development activities. In fact, the first site for the phase III PPMS study has already been initiated in the U.S. That trial design uses a 2-to-1 randomization to study orelabrutinib dosing of 80 mg a day versus placebo. The orelabrutinib arm is planned to be comprised of approximately 470 participants, while the placebo arm will contain 235. The primary endpoint will be the time to onset of composite-confirmed disability progression events confirmed over at least 12 weeks, known as the 12-week CCDP. The secondary progressive MS study design will also employ a 2-to-1 randomization scheme with approximately 660 participants receiving 80 mg of orelabrutinib daily versus 330 in the placebo arm. This primary endpoint will be time to onset of confirmed disability progression events confirmed over at least 24 weeks, known as the 24-week CDP. I'll now turn the call back to Lonnie. Thank you, Lisa. With significant unmet need, we believe progressive MS represents a very large market opportunity: approximately $12 billion in potential peak sales in the U.S. alone across both PPMS and SPMS, after accounting for access, compliance, and pricing consistent with high-efficacy MS therapies. We also believe we have a best-in-class product candidate. While tolebrutinib has a head start, history shows that many blockbuster therapies were not first to market but succeeded by being differentiated. To summarize, we believe orelabrutinib provides a tremendous opportunity with a clear path to registration in a significant, largely untapped progressive multiple sclerosis market. Orelabrutinib has a unique mechanism of action targeting not only pathogenic B cells in the periphery but also those in the central nervous system, as well as microglial cells addressing the key pathogenic drivers of progressive disease. Potential best-in-category pharmacology and convenient administration provide best-in-class potential. Importantly, a pure BTK inhibitor is currently under FDA review for secondary progressive multiple sclerosis, and a growing body of data supports the ability of this class to address neurodegeneration and so-called silent progression. We've seen highly positive results in the phase II relapsing multiple sclerosis trial with 96 weeks of data. Our phase III primary progressive multiple sclerosis trial is already underway in the U.S., and we plan to initiate our phase III secondary progressive multiple sclerosis trial in the first quarter of 2026. We have a clear regulatory path forward with alignment from both the FDA and EMA. From a market perspective, multiple sclerosis is expected to exceed $30 billion globally by 2030, with progressive forms representing over 40% of that market. In the U.S. alone, the more than 200,000 patients living with progressive multiple sclerosis represent a commercial opportunity of over $12 billion. Now I'll turn the call back to Haley, who will describe our exciting earlier development stage product candidates. Haley. Thank you, Lonnie. IL-17 targeting biologics have made a significant impact for patients with immune-mediated diseases. The IL-17 market is large, around $10 billion, and has grown over 50% year -over -year. Oral cytokine targeting programs based on small molecules and peptides have had some challenges, including bioavailability and activity. The InnoCare team dedicated an effort to targeting IL-17 based on structural modeling and profiling for attributes set up for success in the clinic. ZB021 is a potent small molecule with well-characterized ADME properties: high bioavailability, low clearance, and high metabolic stability. In preclinical testing, we highlight one experiment, the rat CIA model, where ZB021 shows compelling activity compared to an IL-17 targeting antibody. IND-enabling studies are ongoing, and clinical studies with ZB021 are anticipated to start in 2026 after IND clearance. We plan to include both healthy subjects and patients in our phase I program. We are also enthusiastic about the potential for our brain-penetrant TYK2 inhibitor, ZB022. In immune-mediated diseases, TYK2 is a well-established mechanism, and there is increasing evidence of a role for TYK2 in neuroinflammatory and neurodegenerative diseases. This concept is currently being explored clinically, and emerging data will help guide Zenas' investment. I'll now turn the call over to Lonnie to discuss our obexelimab program. Lonnie. Thank you, Haley. Moving on to obexelimab, our IgG4-related disease program remains our highest priority. The phase III Indigo trial is fully enrolled, and the last patient out will be in mid-November with top-line results reported around year-end. Our multiple sclerosis global phase II Moonstone program, which will provide new blinded clinical data on today, completed enrollment in June with 116 patients, and we plan to report the 12-week primary endpoint data this quarter. And finally, our systemic lupus program is enrolling patients. Enrollment should wrap up about year-end with 24-week BICLA endpoint top-line results expected mid-next year. So, three really important data readouts within the next year for obexelimab. Many of you may be familiar with this molecule and its unique mechanism of action. It combines binding to two markers on B cells, one being CD19, which is broadly expressed across B cell lineage. The other is Fc gamma R2b, also known as CD32b. This is really the natural inhibitory pathway to shut down B cell response or B cell activity, specifically after an infection with antigen-antibody complexes eventually binding to Fc gamma R2b and initiating this inhibitory pathway. This clever design of the antibody to be an inhibitor is unlike that of anti-CD20 and anti-CD19 B cell depleting antibodies, and we believe provides certain advantages which we will discuss. Leveraging this biology, obexelimab is highly potent in decreasing B cell function, which includes antibody production, cytokine production, proliferation and differentiation, and the processing of antigens for T cell presentation. I'll now hand the call back to Lisa, who will provide an update on our obexelimab phase II RMS study Moonstone, including the new blinded data. Lisa? Thanks, Lonnie. Slide 32 shows an overview of the phase II Moonstone trial, which enrolled 116 participants. This is a standard phase II design with MRI endpoints, and these studies have been highly predictive of phase III success using an endpoint of annualized relapse rate in an RMS study population. The Moonstone trial used a 2-to-1 randomization with treatment once a week for 12 weeks. The primary endpoint is the number of new T1 Gd-enhancing lesions at week 8 plus 12. Secondary and exploratory endpoints include using standardized assessments, imaging, and biomarkers to evaluate the impact on disease progression through week 24. On the next slides, we are going to walk through the baseline characteristics and blinded aggregate data from the Moonstone study. Slide 33 shows the Moonstone baseline characteristics. The average mean age was early 40s with a female predominance. The average time since diagnosis was about seven and a half years, and patients had a median EDSS score of three. The number of T1 Gd-enhancing lesions at screening was 0.71, which is consistent with the lower disease activity characteristics of relapsing MS patients currently entering many clinical trials. The percentage of participants with T1 Gd-enhancing lesions at baseline was 21.6%, again reflecting a broader trend of less active RMS patients entering into clinical trials. Slide 34 has some historic benchmarks for Gd-enhancing T1 lesions at the time of endpoint assessment in phase II RMS trials. The relative difference between drug and control has remained fairly consistent, but the absolute number of lesions per scan has dropped substantially. For example, in the most recent successful fenebrutinib readout, the drug drove lesion counts to near zero. However, the control arm also had very low baseline and 12-week activity, reflecting today's less active trial populations. Slide 35 shows blinded aggregate data from the obexelimab Moonstone trial. Recall that the study has a 2-to-1 randomization design. The first graph shows new T1 Gd-enhancing lesions per scan over 12 weeks, with a decline from 0.71 to 0.09. The second graph shows new and existing lesions per scan over 12 weeks, with a drop from 0.71 to 0.18. While the data remains blinded, they show the potential that obexelimab is active. We expect to report 12-week primary endpoint data this quarter and 24-week data early next year, but we are aware that development of new drugs in relapsing forms of MS is challenging due to the evolving treatment landscape and current pivotal trial endpoints. Available B-cell-directed therapies are highly effective in controlling relapse rates, and this is shifting the population available for clinical trials. RMS patients entering trials in the U.S. and some other areas generally now have less active disease. Regulatory endpoints that involve improving the annualized relapse rate versus an active comparator are challenging on that backdrop of substantial reductions in annualized relapse rates for patients. The need for alternate endpoints has been a topic of active discussion. And finally, development in relapsing MS continues to require substantial resources, given the need to conduct two large randomized trials. As discussed earlier, we are excited about the potential of orelabrutinib in progressive forms of MS, and consequently, Zenas expects to make a decision on obexelimab development for RMS in early 2026. With that, I'll hand the call back over to Lonnie. Thanks, Lisa. An important and emerging concept across many inflammatory and some neurologic conditions is that of smoldering disease. For IgG4-RD, this is ongoing disease activity below the quantitative ACR/EULAR flare score of 20. IgG4-RD patients with a score below 20 still have inflammation, and it is clinically important to control that smoldering disease and potentially diminish the possibility of long-term organ damage. This could be measured as complete remission, an endpoint included in our Indigo phase III trial. But first, let's look at the obexelimab phase II IgG4-RD trial previously conducted. This graphic shows the outcome of the trial. On the y-axis, you see the IgG4-RD responder index, a measure used to determine disease flare. A score above three indicates a flare, and the median at baseline was 12, meaning these patients had significant disease activity. The drug was used to both induce remission and then maintain remission, and you can see how rapid the onset of effect was. The primary endpoint of the study was a two-point decrease in the index, and all patients met this endpoint. One patient dropped out early because they were not actually eligible. They had a score below three. Only one patient in the study experienced a flare, which is less than a 10% flare rate while on treatment. These are impressive results and served as the basis for moving forward into the phase III trial. In addition, obexelimab was well tolerated, and we believe our subcutaneous dosing regimen has the potential to further improve tolerance while optimizing PK parameters, which could further improve efficacy. We'll touch on that in a moment. That brings us to the phase III trial design. This design was developed in agreement with regulatory authorities worldwide and closely mirrors the design of a now-approved drug in this area. Patients enter the study while in flare, and a central committee confirms the flare status. They are then treated with a steroid regimen to induce remission. Once remission is confirmed centrally, patients are randomized one-to-one to receive either obexelimab or placebo. Steroids are tapered per protocol over eight weeks in both arms, identical to the competitor study, and patients are then monitored for flare over 52 weeks. As mentioned earlier, the study completed enrollment last November, so the full cohort of patients is now in study with the last patient expected to finish in mid-November. Once data are cleaned, database locked, and unblinding and analysis is completed, we will release the top-line data anticipated around year-end. The potential differentiation for obexelimab versus the only approved therapy for IgG4-RD is clear. Our therapy offers at-home subcutaneous dosing, which aligns with typical practice in the rheumatology community. Self-administration will be via prefilled syringes or an autoinjector, unlike the marketed product, which requires IV infusion center access. In addition, we are actively evaluating vaccinations as part of a dosing pause and reinitiation approach within the obexelimab open-label extension study, something investigators are very enthusiastic about. From a patient standpoint, out-of-pocket costs under the Medicare Part D pharmacy benefit that covers at-home subcu administrations are lower than under the Part B medical benefit associated with IV infusions. In terms of clinical outcomes, the marketed product's six-month IV dosing regimen allows for B cell repletion in a significant percentage of patients. When that happens, patients can potentially lose benefit, which is captured in a clinical study complete remission endpoint. As pointed out earlier, that endpoint goes beyond flare control and looks at residual or smoldering disease activity. Because obexelimab is continuously dosed with consistent exposure, target engagement, and clinical benefit, we believe we have the opportunity to outperform the marketed product on complete remission rates and potentially demonstrate a stronger clinical profile. And IgG4-RD is a significant commercial opportunity. Experts estimate there are 30,000 to 40,000 patients in both the U.S. and also in Europe. Of these, about 20,000 are currently diagnosed and medically managed. Roughly one-half of that group experiences frequent flares and would be candidates for ongoing therapy. When you apply current market pricing in this field, that translates to a market opportunity of approximately $3 billion in the U.S. and $2 billion in Europe. We believe the obexelimab profile positions us well to capture a meaningful share of that opportunity. It is also recognized that IgG4-RD is currently underdiagnosed, and with the potential approval of obexelimab, we and others will be positioned to grow the market by increasing disease awareness. Our lupus program builds on prior work with this drug in a phase II-A study. In the prior study, the primary assessment for the intent-to-treat population showed a 17% effect size compared to control. That result is in line with two currently marketed drugs for lupus, but we believe we can do better. What we discovered is that patients who achieved the proper exposure, measured by the concentration trough level or C trough, had double that effect size. In fact, they demonstrated a 35% benefit over control. Achieving this level of efficacy would be very meaningful for patients. The subcutaneous dosing regimen we've selected for all our studies is designed to ensure a C trough in the range associated with this substantial 35% benefit. It's important to note that the prior phase II-A lupus study was relatively small, with only about 50 patients per arm. Our ongoing Sunstone study is nearly double that size, with close to 100 patients per arm, providing much stronger statistical power. Another critical element in lupus trials is ensuring we enroll the right patient population, specifically those with moderate to severe disease. To address this, we established an adjudication committee that reviews and confirms eligibility, thereby protecting the integrity of the study. This approach reduces the risk of placebo overperformance and strengthens our ability to detect a true treatment effect. We believe the study is well designed to succeed, and we enthusiastically anticipate the results. Revisiting the catalyst for the next two years, now in the context of what we discussed today, we hope you recognize why we're tremendously excited about our expanded pipeline portfolio, the numerous potentially value-creating milestones it creates over the next several years, and the incredible potential it has to benefit patients with autoimmune diseases, both in the short and long term. To summarize, we are approaching the end of what has been a truly transformational year for the company. We completed major financings, and with today's announcements, have significantly advanced and expanded our pipeline. That pipeline now includes two late-stage potential franchise molecules, obexelimab in rheumatology and orelabrutinib in progressive multiple sclerosis, as well as two exciting next-generation assets, our oral IL-17 inhibitor, ZB021, and our brain-penetrating TYK2 inhibitor, ZB022, both expected to enter the clinic next year with best-in-class potential. Together, these programs create a robust and balanced pipeline portfolio aimed at addressing critical unmet needs in autoimmune disease while also offering significant commercial opportunities. With this pipeline, combined with our team's deep experience, proven track record of success, global development and commercialization capabilities, and strong financial position, we are well positioned to execute on our vision of becoming a globally fully integrated commercial-stage biopharmaceutical company with the potential to launch three best-in-class franchise molecules across five indications in three therapeutic areas, including rheumatology, multiple sclerosis, and dermatology, each representing significant commercial opportunities by 2031. Before we open up the call to questions, I'd like to thank the InnoCare team for their collaboration and commitment to working alongside our team as we advance orelabrutinib, ZB021, and ZB022. Importantly, I'd also like to thank the Zenas people who helped make today's announcement possible, as well as the entire Zenas team for their steadfast commitment to enabling patients with autoimmune disease to reimagine life. With that, we're ready to take questions. Operator, please go ahead. Thank you. To ask a question, please press star one one on your telephone and wait for your name to be announced, and to withdraw your question, please press star one one again. We would ask that you please limit to one to two questions. You may re-enter the queue, and we will get remaining questions if time allows. Please stand by for the first question, and our first question will come from Roger Song with Jefferies. Your line is now open. Great. Good morning, team, and then congrats for this BD deal with the enrichment of your I&I franchise. I have two questions, one related to the new asset, orelabrutinib, and then the other one is the new data from the blinded MS Moonstone study, so with this high CNS penetration and potency ratio for the orelabrutinib, how do you believe it could differentiate clinically in PPMS and SPMS with other BTK, given a couple already ahead of you, and then in terms of the efficacy and the safety, and then maybe talk a little bit about the PIRA endpoint as well. I have a follow-up on the Moonstone. Thank you. Thank you, Roger, for the questions. So if we look at the molecule, I think the potential clinical differentiation really starts with the pharmacology, as Haley described, so if you think about progressive forms of MS, it's really about impacting the compartmentalized inflammation and neurodegeneration, and of course, as you know, to do that, the molecule needs to get to those targets within the central compartment, and that includes not only B cells, but the innate system, macrophages, and importantly, microglia, so the differentiation we would anticipate because of this much greater CNS to IC90 ratio, which I think is a really good way to summarize, getting into the brain, getting to the target, and then the covalency staying at the target would be obviously impacting disability progression in a more compelling way than the data sets already available out there. And those data sets include, of course, tolebrutinib in SPMS and Ocrevus in PPMS. So it's really the pharmacology of the molecule that we believe can lead to clinical differentiation from an efficacy standpoint on what's important to measure in this disease, disability progression. As far as tolerability, what we have, fortunately, is several years of experience with orelabrutinib. In China, it's indicated for five leukemia and lymphoma indications, actually at a much higher dose. The dose for multiple sclerosis is 80 mg per day. The hem/onc dose is 150 mg per day. It is now the number two prescribed BTK inhibitor in China. And a lot of that has to do with not only the efficacy, but it's considered the best tolerated of the BTK inhibitors. And your second question, I believe, was related to Moonstone, Roger? Yes, thank you for the first one and then for the Moonstone, appreciating this blinded study, the data so far, but with this low baseline Gd lesion, T1 lesion, and other baseline characteristics, how do you expect the placebo arm will perform over the 12 weeks with understanding less lesions than the old studies? Yeah. I think when looking at blinded data in a controlled study, that is always the question, how is the control arm going to perform? Of course, in this case, it's placebo. So if we just look across the various studies that have reported out in the past of similar design, we know what the placebo arm does. And I guess one could point to the fenebrutinib curves because that is one of the more recent studies and happens to have had a much lower baseline lesion rate, similar to, actually slightly lower than even our study. So I would point to that. But of course, it is blinded, and we will all know in a number of weeks. Got it. Thank you. Congrats again. Thanks, Roger. Our next question will come from Judah Frommer with Morgan Stanley. Your line is open. Hey, everyone. Good Hey, everyone. Good morning and congrats to the team. This is Nick on for Judah. Thanks for taking our question. Just have a couple. Really quick, can you just give us a little bit more background on how the deal came about? I know you said you've had a long relationship with InnoCare, but when did the conversation start? And were you actively looking for a BTK inhibitor, or did this opportunity come to you? And then just another question on development for orelabrutinib. I know that tolebrutinib didn't be an active comparator in its phase III relapsing MS study, but would you consider further development in relapsing MS if just depending on your discussions with FDA on alternative endpoints or maybe emerging data from the fenebrutinib phase III program? Thanks. Thanks for the questions, Nick. And good morning to you. So the history here obviously goes back to the founding of Zenas. As you know, we build our pipeline through business development and licensing, just as we built our prior companies. So we are always continuously talking to a variety of parties. And as you know, there's been a great deal of emphasis most recently in licensing assets from China. For us, because we actually have an Asia team based in China, along with our European team, our U.S. team, we have a lot of contacts and a substantial network. So I would say perhaps over 50% of what we've looked at over the last several years are actually molecules that were discovered or being developed in China. The actual relationship with InnoCare started about three years ago, having the opportunity to get to know Jasmine, the CEO, who is just such a high-quality individual leading a fantastic company, a former longtime Merck development executive, building this company in such a way that now, with being Hong Kong exchange traded, having several thousand people, large discovery operation, two drugs on the market, headed to profitability, this is a fantastic partner. And we've tracked their pipeline over the last several years and have had continual discussions. At the same time, we've been talking to other parties. And we have a lot of interest in BTK inhibition because of that mechanism's applicability to MS and other diseases, frankly. And in having the opportunity to do deep diligence on this one, obviously with marketed commercial data available, data from actually studies in other indications, and of course, the robust MS data that Lisa reviewed, this went to the top of the list. So as we were tracking this, we were quite interested in the outcome of the discussions with both FDA and EMA on trial design. And when it became apparent that there was excellent alignment on what would be studies to support the type of indications that could be transformational for us, we decided to act. And as we were doing that, of course, as a late-stage program, it became a competitive process. And we, because of our long relationship and how we're situated, we ultimately won out in that process. And here we are today announcing the transaction. Regarding your other question, of course, the tolebrutinib RRMS studies you referred to had the challenge that Lisa was discussing, and that was comparing to an active agent, teriflunomide, with a primary endpoint of annualized relapse rates. You may know that, for instance, Ocrevus, the market leader in RRMS in pivotal trials, had an annualized relapse rate around 0.15. Teriflunomide and its approvals had an annualized relapse rate of twice that, greater than 0.3. But more recently, controlled trials utilizing teriflunomide have demonstrated teriflunomide annual relapse rates down in the 0.1 range, which is what occurred in the tolebrutinib study, clearly indicating the patients had much less active disease. And that poses a challenge to an active drug such as tolebrutinib or any active drug in the clinic today actually winning in a phase III trial with annualized relapse rates as the primary. So it's a challenging field. And I think that will need to evolve for us to consider moving into RRMS. For now, our hands are full with two major progressive MS trials starting. I hope that's helpful. Yeah, thanks. Super helpful. Congrats again, guys. Thank you. And the next question will come from Yigal Nochomovitz with Citigroup. Your line is open. Yeah. Hi. Thank you very much. Hi. Thank you. Lonnie, I just was curious on the blinded data. It looks like you have basically all the patients at week 12, 115, and you started with 116 at baseline. So it seems like everyone's basically met the endpoint. I'm just curious what else needs to happen before you can show the data because it seems like you're basically almost done with the study. Yeah. So obviously, these are data we have in-house. But at the same time, having last patient out in September, we're still going through the final process of cleaning data, some queries, and that will lead shortly to the unblinding and, of course, the analysis followed by the quality assurance checks on the output from that analysis. So we're just a number of weeks away from having the unblinded results. And of course, we'll release that. And based on what we're seeing, we're really excited to do that. Okay. And just one other question regarding the thesis for the transaction with orelabrutinib. Was there a thought that perhaps combining with obexelimab would be something to do down the road or not? And in your diligence process, was there any preclinical work that you did to test these two molecules together in any MS models? To answer the second part, no, we haven't done preclinical work in combination. Those models take a little while to run, of course. I think you're making a point that's interesting, not only in multiple sclerosis, but in other inflammatory conditions. Combinations have not been explored to the extent perhaps they could be. As we all know, in the oncology world, really making a difference in certain diseases requires combinations. And there's always the consideration around pricing when you put two drugs together. But if you'd assemble a portfolio of programs where you're the sponsor for all of them, you can sometimes manage that pricing complexity when it comes time to commercialization. So over time, we'll be thinking about combinations. I don't know whether obexelimab combined with a BTK inhibitor would be the way to go. We don't have data. I think you could imagine the biology behind that, why perhaps maybe it would be interesting. But there are no plans at this time. All right. I appreciate it. Thank you. Thanks, Yigal. As a reminder to ask a question, please press star then one on your telephone. Our next question will come from Yatin Suneja with Guggenheim. Your line is open. Hi. This is Iris on for Yatin. Thank you for taking my questions and congratulations on the deal. My question is also around MS. So we know that obexelimab RMS study has some secondary exploratory endpoints related to PIRA progression. So even if the endpoints would be positive, would there still be interest in proceeding obexelimab with PMS? And also, I wonder for the execution of the progressive MS trials, is it going to be PPMS being managed or executed by InnoCare while SPMS by Zenas? And any details on how the studies are powered? Thank you. On the PPMS and SPMS trials with our global rights to orelabrutinib, we will manage both, and all potential future indications we would consider pursuing with orelabrutinib. As far as the powering, I'll come back to that and let Lisa address that, but if we're thinking about the obexelimab program, and I believe you were referring to the data that's going to be associated with the 24-week readout early next year, that's up to almost 20 secondary and exploratory endpoints, and some of those would apply to giving us an indication that the drug could be beneficial when looking at disability progression and ultimately the clinical endpoint. We will have that data in hand first quarter of next year, and as we think about going forward, an important consideration is the regulatory aspect of this. Is the primary endpoint in RRMS going to continue to be annualized relapse rate? I think we've talked about the challenges of that. So we'll keep an eye on any changes in regulatory thinking. We know there are parties talking to the FDA and EMA about primary endpoints for RRMS. And we'll look out for how that proceeds. For now, of course, we're dedicating our efforts to progressive MS with orelabrutinib in two indications. And if you think about this, we've really pulled forward our whole MS strategy because we are now already in phase III with a really important drug. Lisa, on the sizing of the trials, any comments? Sure. Both studies are 90% powered for a hazard ratio of 0.7 or a relative risk reduction of 30%. And we think this is a conservative sizing that we can easily manage. And our assumptions around progression rate in the secondary population are around 27% over a two-year period. And in the primary population, it's about 45% over two years. Thanks a lot. Thanks, Iris. I am showing there are no further questions in the queue. I would now like to turn the call back over to Lonnie for closing remarks. Thank you all for joining us today. And we really look forward to updating you in the future. Have a great day. This concludes today's conference call. Thank you for participating. You may now disconnect.