Good morning, everyone. Welcome to the Q32 Bio conference call. At this time, all participants are in 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 Investors section of the company's website following the call. I will now turn the call over to Lee Kalowski, President and Chief Financial Officer of Q32 Bio. Lee, you may begin. Thank you, operator, and thank you all for joining us on today's call. Before we begin, I would like to remind you of the disclaimer outlined on slide two. During today's presentation, including during the question and answer portion of the call, we will be making certain forward-looking statements. A summary of these forward-looking statements and the related risks and uncertainties are outlined on the slide. These can be referenced in our company filings made with the SEC, including our most recent 10-K filing for the fiscal year ended December 31, 2025, and our subsequent 10-Q filing for the first quarter 2026 and subsequent filings. With that, we are thrilled to be sharing positive 36-week top-line results from Part B of our SIGNAL-AA, phase II-a clinical trial evaluating bempikibart in patients with alopecia areata, or AA. On today's call, we will provide an overview of bempikibart, a detailed review of the Part B results, and our next steps for the program. We will also review the unmet need, landscape, and commercial opportunity in alopecia areata. Joining me for prepared remarks are Jodie Morrison, our CEO, and Dr. Shelia Violette, our founder and Chief Scientific Officer. Following prepared remarks, we will have a Q&A portion where we will be joined by Dr. Arash Mostaghimi, a leading dermatologist in the research and treatment of alopecia areata and a central reviewer in SIGNAL-AA Part B. Arash serves as an associate professor of dermatology at Harvard Medical School and Vice Chair of Clinical Trials and Innovation at Brigham and Women's Hospital. We thank Arash for being with us on this morning's call. With that, I will now turn the call over to Jodie. Thanks, Lee. Today marks a significant milestone for Q32 Bio, our bempikibart development program, and most importantly, for patients living with alopecia areata. Building on the strong clinical activity and proof of concept observed with bempikibart in Part A of SIGNAL-AA, we initiated the open-label Part B portion of the trial with an expanded dosing regimen in patients with severe and very severe alopecia areata. Today, we are thrilled to report positive 36-week top-line results from Part B, achieving our target efficacy and safety profile and providing compelling evidence supporting the therapeutic potential of bempikibart in this indication. We believe the efficacy, durability, and safety results from Part B have the potential to set the bar for biologics in the treatment of alopecia areata and address the shortcomings of JAK inhibitors. On the pre-specified mITT primary analysis, we saw a clinically meaningful 35.3% mean reduction in score on the Severity of Alopecia Tool, or SALT, over the 36-week treatment period, and bempikibart demonstrated promising results with 40% of patients showing robust hair regrowth on the pre-specified SALT-20 endpoint. In the most conservative population on a full ITT basis, this data remains compelling, with 30.3% of patients achieving SALT-20. As a reminder, SALT-20 is the currently accepted registration endpoint. We are encouraged by these results, which we believe support bempikibart's profile as a biologic with an efficacy profile comparable to available JAK inhibitors at week 36. These results are especially meaningful when considering that greater than 35% of patients in Part B had previous exposure to JAK inhibitor therapy. Beyond the efficacy data, bempikibart continued to be well-tolerated, with no Grade 3 or higher adverse events and no new safety signals. We continue to see a favorable biologic profile with the inclusion of the loading dose regimen and look forward to sharing detailed data on today's call. As we put this data into context, patients with severe or very severe alopecia areata often face significant life-altering impact, including high psychosocial burden. JAK inhibitors are the only currently available advanced therapeutic for these patients, but carry significant safety risks and require chronic treatment to maintain hair regrowth. Unlike other JAK markets across the I&I landscape where biologics are the preferred choice, there are no approved biologics in alopecia areata. The Part B results support the potential of bempikibart to address this significant unmet need by filling the biologic gap and setting up for bempikibart to become a standard of care first-line option in alopecia areata. We are continuing the Part B off-drug follow-up period through week 52, and based on physician and patient demand, are now enrolling eligible patients in an open-label extension portion of the study. In parallel, we are evaluating next steps, including plans to advance into a registration-directed program in severe and very severe patients in the first half of 2027. Before we move on, I'd like to personally thank the investigators, our central reviewers, and most importantly, the patients who participated in SIGNAL-AA Part B. I'd also like to thank the many Q32 Bio employees and clinical development partners who helped make today's announcement possible. With that, I'll turn the call over to Shelia to provide a brief overview of bempikibart. Shelia Thanks, Jodie. On slide five, I'll summarize bempikibart's mechanism of action and impressive biomarker results from our phase II trials. To begin, bempikibart is a fully human antibody that binds to the IL-7 receptor alpha subunit at a region that is shared for binding by two very important cytokines. This includes IL-7 and TSLP. As a result, bempikibart naturally has bifunctional activity, allowing us to broadly remodulate the immune system and have the potential to go across many different T cell-mediated autoimmune and inflammatory diseases. IL-7 has the ability to support the generation of autoreactive pathogenic T effector cells that become hyperresponsive in an otherwise low antigen microenvironment. IL-7 is also importantly involved in the maintenance and survival of antigen-specific T memory cells. Pathogenic T effector cells not only locally drive inflammation and disease but lead to the suppression of regulatory cells. By blocking IL-7 signaling, bempikibart has the ability to inhibit the production of pro-inflammatory cytokines, such as interferon gamma by pathogenic T effector cells, and the ability to allow T regulatory cells to impart their immunosuppressive properties, and thus restore balance to the immune system. TSLP is a very different cytokine, known for its ability to induce TH2 immune responses where you have an epithelial barrier, including the lungs and skin. In part B of our alopecia areata trial, we have replicated prior biomarker data sets in which we've seen bempikibart achieve meaningful reduction in biomarkers of IL-7 blockade, as evidenced by reductions in CD3 positive lymphocytes and TH2 biomarkers such as TARC, IgE, and eosinophils. Bempikibart has the potential to address the root cause of immune dysregulation in alopecia areata, where local inflammation and hair follicle destruction is driven by the infiltration of cytotoxic CD8 positive, NKG2D positive T cells in what would otherwise be in an immune-privileged environment. This inflammation is further sustained by CD4 positive T effector and T memory cells. These cells also produce pro-inflammatory cytokines such as interferon gamma and suppress the restorative function of T regulatory cells. By directly inhibiting both the generation of pathogenic T effector cells and the maintenance and survival of antigen-specific T memory cells, bempikibart has the potential to inhibit T cell-mediated hair follicle destruction and durably restore immune tolerance, providing a differentiated mechanism of action with clinically meaningful therapeutic effects in alopecia areata patients. Now I'll turn the call back over to Jodie to review our SIGNAL-AA program. Thanks, Shelia. Our SIGNAL-AA clinical program has been thoughtfully designed to support a registration-directed program as a next step. The program comprises two parts. On the left, the previously completed part A trial, and on the right, the ongoing part B trial. In part A, bempikibart demonstrated encouraging clinical activity with 24 weeks of dosing, establishing proof of concept, robust pharmacologic data, and a well-tolerated safety profile. While not originally planned, we initiated the part A open-label extension for eligible part A patients based on demand following continued emergence of data suggesting remittive effect and durable responses following completion of dosing. In total, eight patients spanning responders, non-responders, and placebo patients from part A enrolled. These patients were off drug in part A prior to redosing for various time periods ranging from 26-55 weeks. There were several key learnings upon redosing in the part A OLE. First, redosing with bempikibart was well-tolerated with no safety issues over extended time periods. Second, we observed durable or further hair growth in patients who maintained hair prior to OLE enrollment, including multiple patients who maintained response more than 100 weeks. Third, we believe the varying response patterns observed across the full part A OLE patient set support a plan for reduced dosing schedule over time versus these extended off-drug windows of up to a year. These findings support the part B design, where the open-label extension begins in these patients after only 16 weeks off drug. Following analysis of the part B 16-week off-drug period, we will establish the plan for the long-term chronic maintenance regimen for our registration-directed program, which could include a regimen such as monthly, bimonthly, or even quarterly dosing. Taking a closer look at the part B design, the four key changes from part A include the introduction of a loading dose regimen, longer duration of treatment, a maximum duration of current episode of four years at baseline, and the introduction of a central review for diagnostic confirmation. Part B is an open-label trial in severe and very severe patients, as defined by SALT scores of 50 - 100. Similar to part A, no cap was placed on JAK experienced patients, who were allowed in the trial with appropriate washout. The treatment period is 36 weeks. Patients in the trial receive a loading dose of 200 mg weekly over a period of four weeks, followed by 200 mg every other week over a period of 32 weeks. Bempikibart is administered subcutaneously. Following the treatment period, there is a 16-week off-drug period through week 52 driven towards expanded learning on the potential long-term maintenance regimen, such as monthly, bimonthly, or even quarterly maintenance dosing. The pre-specified primary endpoint analysis is mean percentage change from baseline SALT in the mITT population at week 36. Additional efficacy analyses include the percentage of patients achieving relative and absolute SALT improvements, including SALT≤20. Moving to slide nine, we provide the baseline demographics of Part B patients. In the mITT population, the mean age of participants is 42, with a 76% majority of female participants. Average baseline SALT score is 76.9, with a minimum of 51 and a maximum of 100. Approximately 76% of patients were severe and 24% were very severe. 40% of patients had prior oral JAK exposure. Notably, the mITT population excludes a total of eight patients based on a pre-specified criteria. Of these eight, five patients discontinued prior to week 18, having received less than 50% of dosing, including two patients who discontinued during the loading phase and never returned for SALT assessment post-baseline. Importantly, none of these treatment discontinuations were related to the safety of bempikibart. The remaining three patients had unstable disease. Of note, the baseline demographics of the mITT population are largely consistent with the ITT population. As we look at the PK results, we are pleased to see a robust pharmacokinetic profile in Part B, and importantly, data that confirms the loading regimen included in Part B had its intended effect. Mean C-trough levels were approximately three-fold higher in the first month of dosing compared to Part A, and steady-state concentrations were achieved approximately 10 weeks earlier versus Part A and sustained through week 36. With the introduction of the loading dose regimen, we did not see a change in the safety profile of bempikibart. Additionally, negligible ADA with no impact on PK was observed in Part B. The right side of this slide shows bempikibart concentrations throughout the treatment period as well as the off-drug period. While we are pleased to see the robust concentrations during the treatment period, we would also draw your attention to the decreases in drug concentration after the completion of the treatment period, which suggests that the durable responses being observed are attributable to bempikibart's mechanism of action rather than the drug staying in the system. Now, we will turn to the efficacy results. From a pre-specified primary analysis, we are thrilled to report a clinically meaningful mean SALT reduction from baseline at week 36 of 35.3% in the mITT population. These data demonstrate clear and sustained hair regrowth as patients progress on the study, with deepening responses over time and no evidence of plateau. We notably saw robust hair regrowth in both severe and very severe populations. Looking at the severe population only, we saw a mean SALT reduction of 37.8% at week 36. In the very severe population, we saw a mean SALT reduction of 27.4% at week 36, a strong outcome in this more difficult-to-treat group. Shown here is the waterfall plot of the change in SALT score from baseline, with the SALT-20 responders identified on the right. We see clinically meaningful achievement of SALT-20 at week 36 in both severe patients, shown in blue, and very severe patients, shown in green. In the mITT population, we observed a 40% SALT-20 rate and a 30.3% SALT-20 rate in the most conservative ITT population. We believe this is a profound result for a biologic, with only 36 weeks of treatment, and combined with its well-tolerated safety profile, positions bempikibart as a potential leading treatment option in alopecia areata. Beyond the robust SALT-20 responses we observed, bempikibart demonstrated clinically meaningful efficacy on additional analyses measuring proportional hair regrowth in patients. On this slide, we've presented both the mITT and the most conservative ITT population for both the 30% and 50% responders. In both populations, we see clinically meaningful results. Collectively, these results have the potential to set the bar for biologic efficacy in alopecia areata. Now we'd like to share a few case studies from SIGNAL-AA Part B that really illustrate the therapeutic potential of bempikibart, including its durability and the impact it can have on patients. First, we highlight a 48-year-old female with severe alopecia areata and a duration of current episode of more than a year at entry. As you can see, this patient achieved a robust response, which was maintained off drug, achieving SALT 10 at week 24 and week 36, deepening to 100% SALT reduction at week 44, our first SALT 0. This patient is currently enrolled in the open-label extension. This is a compelling example of the potential of bempikibart to regrow hair and impact the quality of life of patients with alopecia areata. Next, we'd like to highlight a unique example on the potential of bempikibart to meaningfully impact patients. Shown here is a 33-year-old female with severe alopecia areata and a duration of current episode of 1.4 years, who notably had previously received JAK inhibitor treatment. This patient experienced a robust response, achieving SALT-20 at week 24 and SALT 10 at week 32. Ultimately, this patient decided to hold on dosing at week 32 to focus on family planning, consistent with trial guidelines. While the patient is no longer taking study drugs, she is continuing to have off-drug follow-up visits. We are encouraged by the durability seen in this patient's off-drug follow-up, highlighting the unique nature of the lasting effects of bempikibart. While the safety of bempikibart in the context of pregnancy has not yet been clinically evaluated, based on its mechanisms of action and the experience of biologics in other indications, bempikibart may have the potential to be an option in the future for this critical unmet need in alopecia areata patients of childbearing age. On slide 16, we see a 41-year-old female with severe alopecia areata with a duration of current episode of 2.5 years. This patient experienced a robust response on treatment, achieving SALT-20 at week 36 and a continuing response off drug, achieving SALT 10 in the off-drug period. This patient is now enrolled in the open-label extension. Rounding out our example case studies, we see a 32-year-old male with very severe alopecia areata and a duration of current episode of 3.2 years. Despite having a baseline SALT score of 100 and a longer duration of episode, this patient experienced a robust SALT-20 at week 36. His hair growth was maintained through the off-drug follow-up period. This patient is now enrolled in the open-label extension. These case studies, and more from Part B, demonstrate clearly the potential of bempikibart to regrow hair with durable responsiveness, which can have a meaningful, long-lasting impact on the lives of patients with alopecia areata. In addition to the robust efficacy results, bempikibart was also observed to be well-tolerated, consistent with our prior clinical studies. There were no new safety signals observed, and all adverse events were mild to moderate, with no serious Grade 3 or higher adverse events reported. Overall, we observed a mean 35%-40% reduction in absolute lymphocyte count, consistent with an on-target mechanism that stabilizes around 24-28 weeks. No relationship was observed between lymphocyte reductions and infection. The most common treatment-emergent adverse event was injection site reaction, which occurred in approximately 36% of patients. It is important to note that the majority of these patients experienced singular events, resulting in an incidence of injection site reaction of only 4% across all Part B dose administrations. All ISRs were mild and resolved with no intervention, with the majority resolving within a day. There were no discontinuations related to safety findings. With results across our SIGNAL-AA phase II program in hand, we are encouraged by the differentiated target product profile emerging for bempikibart and believe it could redefine the long-term management of alopecia areata. First, today's outcome has the potential to set the bar for biologics across efficacy, safety, and durability in this indication, bringing us one step closer to delivering a meaningful biologic option in the sole I&I condition where the only advanced option is JAK inhibitors. With this data, we have greater confidence that our IL-7 and TSLP inhibitory mechanism can deliver both meaningful efficacy while not sacrificing safety, an important balance not fully achieved by JAK inhibitors. Further, bempikibart's profile provides flexibility ideal for the management of this lifelong condition, including the potential for a durable response, expectations for a step-down to less frequent chronic dosing, and future options for at-home dosing supported by our flat 200 mg dosing. Taken together, we believe bempikibart's profile is positioned for both first-line use and market leadership in alopecia areata. Now, I will turn the call back over to Lee to discuss the unmet need, landscape, and commercial opportunity in alopecia areata. Lee? Thanks, Jodie. alopecia areata currently affects approximately 700,000 people in the U.S. and can have significant life-altering comorbidities, including deterioration of quality of life and psychosocial impact. It can affect people of all ages and can be particularly devastating for children and adolescents and their families, as well as women of childbearing age. Despite the significant population size, there are no approved options for patients with moderate disease and very few options for patients with severe and very severe disease. As mentioned, alopecia areata is one of the few I&I indications where there is no available biologic option. Yet there are three available JAK inhibitors. We partnered with IQVIA to conduct a survey of 50 dermatologists, which included questions on the areas of current unmet need. The survey results identified the need for therapies with an improved safety profile, that is, products with no black box warning and minimal lab monitoring. Safety concerns and ongoing monitoring are hallmarks of treatment with oral JAK inhibitors. Dermatologists also rate better durability of effectiveness as a key unmet need. The quotes on the left are also from our market research work conducted by IQVIA. These underscore the findings we just mentioned. Patients are currently forced to choose between benign but often ineffective topical agents, painful injections, or oral systemic JAK inhibitors, which carry a class-wide black box warning. There are no approved options that provide meaningful and durable efficacy with the expected safety of a targeted biologic. Ultimately, some patients opt for JAK inhibitors despite the side effect risks, and yet they still lose their hair if they go off treatment, usually within weeks. Others stay on ineffective therapies such as topicals or seek off-label use of therapies, usually with minimal efficacy. Some patients avoid treatment altogether. Ultimately, it is clear from market research that a safe biologic delivering durable, long-term responsiveness would have the potential to transform the treatment paradigm for alopecia areata as a preferred first-line treatment. Turning to the commercial opportunity, despite the lack of safe and efficacious therapies as well as patient hesitancy to pursue treatment with JAK inhibitors, the alopecia areata market has continued to show strong growth as demand for systemic therapies grow. From 2022 through 2025, estimated U.S. net sales of JAK inhibitors in alopecia have steadily grown. In 2026, oral JAK inhibitors are expected to achieve approximately $500 million in U.S. net sales. The alopecia areata market is expected to grow substantially by 2037, with a prevalence growing to approximately 800,000 patients and 300,000 patients treated with advanced therapies in the U.S. Based on our work with IQVIA, we forecast a total U.S. market opportunity of at least $5 billion in 2037. I will turn the call back over to Jodie for closing remarks. Jodie? Thanks, Lee. To summarize, bempikibart's differentiated target product profile supports the potential to become standard of care as an efficacious, durable, and safe targeted biologic therapy for the treatment of alopecia areata. Across our SIGNAL-AA program, we established proof of concept with durable responses and safe redosing in Part A, observed meaningful efficacy data in Part B, and observed a favorable safety and tolerability profile with low ISR rates across the full program. We plan to share the full results from Part B at a future medical meeting. We believe this data supports advancement into a registration-directed program, which we intend to initiate in the first half of 2027, following planned regulatory discussions. With this success in severe and very severe alopecia areata, we believe there is expansion opportunity in moderate and pediatric alopecia areata patients. Based on the bempikibart mechanism, that there are opportunities in a broad range of additional T-cell-mediated I&I indications. We believe the SIGNAL-AA program represents a foundation for a compelling multi-billion-dollar bempikibart franchise in alopecia areata and beyond. We will begin our question-and-answer session shortly, but before we open the line, I'd like to once again thank Arash for being with us today and ask first if he can provide his perspective on the unmet need in alopecia areata and for his thoughts on the Part B data. Thank you, Jodie. Before I give you my thoughts on the bempikibart data, I think it would be helpful to give a lay of the land with regard to the current therapeutic landscape in alopecia areata. I'm excited that there is a therapeutic landscape. Before 2022, there were no FDA-approved medications for AA, and historically used medications were often toxic with very low success rates. Since 2022, we've had three FDA approvals, all JAK inhibitors, with a potential fourth JAK inhibitor likely to be approved next year. While the introduction of JAK inhibitors has been revolutionary, the same hesitance that restricts the use of JAK inhibitors throughout dermatology also exists in the treatment of alopecia. Prescribers are hesitant to prescribe these medications, and while patients want treatment, they balk at the black box warning, which specifically mention risk of cancer, cardiac events, venous thromboembolism, and even death. Their enthusiasm around wanting to treat their hair loss wanes when they learn that JAK inhibitors are a chronic long-term treatment where missing even a few doses can lead to recurrence of their hair loss, not to speak of the ongoing need for close monitoring and laboratory evaluation. Increased data on the medium-term safety of JAKs, while promising, has done little to change the general beliefs that these medications can be dangerous. Although I prescribe JAK inhibitors on a daily basis and encourage their use for patients with alopecia areata, it's clear that similar to atopic dermatitis, a targeted biologic option for treatment would be favored by both prescribers and patients. Based on the data we just reviewed, I think bempikibart has the potential to set the standard as a biologic agent with JAK-like efficacy that retains the safety profile familiar to dermatologists who have been prescribing biologic therapies for years. On top of that, we have early hints of durability with the potential for deepening responses over time. Let me walk through each of these categories in greater detail. Let's start with what's most important, efficacy. Whether you're using the pre-specified modified intention-to-treat or even a straight ITT analysis, we're seeing for the first time in a biologic therapy, JAK-like efficacy at 36 weeks. Based on this data, without stepping on the durability potential, I think we're seeing the tip of the iceberg for response. Looking at the pictures in the deck from patients who are still improving after completing their 36 weeks on therapy, it's clear that even deeper response is possible. Whenever you look at efficacy, it's important to consider who is in the study, which for me is one of the most exciting aspects of this data. Patients with both severe, meaning SALT 50-95 or 50%-95% overall hair loss, and patients with very severe or SALT greater than 95% hair loss, both regrew hair. JAK-naive patients did well, as did patients who previously responded to JAK therapy, suggesting that in addition to being a first-line agent, this drug may have potential as an off-ramp for patients who have had success with a JAK inhibitor but who would like to switch. From a safety standpoint, no new signals or other concerns were identified in this trial. High retention rates were seen. ISRs were low, only 4% of injections, and very mild, all resolved without intervention. This profile suggests a clean safety profile that, if validated in phase III, will not have a black box warning and should have minimal to no monitoring, correcting for two of the main challenges I mentioned before with the prescription of JAK inhibitors. With regard to durability, the results out to 52 weeks suggest not just maintenance, but deepening response off therapy. In the real world, I anticipate that patients will continue on their medication for longer than 36 weeks. This efficacy will likely be amplified. In the future, this profile suggests that extended dosing regimens should be explored for patients. I'm really excited to see how well these patients do with additional time to grow hair. To summarize, I have tremendous enthusiasm for this drug and its potential. It's important to think of this drug not as the fourth or fifth potential approved drug in alopecia areata, but as one with the potential to be the first targeted biologic for alopecia that provides a much-desired alternative to JAK inhibitors. The totality of the data set suggests strong efficacy with a well-tolerated safety profile and emerging signs of durability, which are really what differentiate bempikibart. If these results bear out the way we're hoping in a Phase III trial, this should be the first-line treatment for patients with alopecia areata. Thank you, Arash, for your thoughtful perspective. Now we'll open the call line for questions, either for us or for Arash. Operator? Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. Should you have a question, please press the star followed by the one on a touch-tone phone. Should you wish to cancel your request, please press the star followed by the two. If you are using a speakerphone, please lift the handset before pressing any keys. Once again, that is star one should you wish to ask a question. Your first question is from Jay Olson from Oppenheimer. Your line is now open. Hey, guys. Congrats on these landmark results, kudos to the Q32 team for the tenacity to make this happen. We had a couple questions. The loading regimen appears to have achieved the intended PK goal. Can you talk about how much the improved efficacy you would attribute to earlier target engagement with the loading dose versus simply treating the patients longer? Is this the current regimen, essentially, the one that you envision taking into pivotal development? I have follow-up if I could please. Thanks so much, Jay. Yes, this is the dosing regimen we would anticipate taking into the phase III program. I would indicate we're not yet fully able to evaluate what the contribution of the loading regimen versus the 36-week regimen are. Collectively, we believe this achieves our goals. Okay, great. Thank you. I guess, what are the key remaining questions to resolve before initiating your pivotal studies? Can you just comment on how you expect your interactions with regulators to evolve based on these impressive Part B results today? Thank you. Yeah, thanks, Jay. I think ultimately, we'll hold on any specifics on the future design of a phase III program, but our expectation would be we would have an end of phase II meeting by the end of this year, where we would discuss those details. Obviously, there's precedent within the space for a single phase III. We intend to leverage that given what we're seeing here in both safety and efficacy and look forward to providing more detail to the market as soon as we can. Okay, great. Thank you. We'll look forward to that. Congrats again on these impressive results, and thanks for the update and taking the questions. Absolutely. Thanks, Jay. Thank you. Your next question is from Imogen Mansfield from Cantor. Your line is now open. Hi. Good morning, everyone. Congratulations, Q32 team. Great to see these data out. Two questions from me. The first one is about the three patients with unstable disease in the mITT. Could you tell us a little bit more about those patients? Did we know that they had alopecia areata? I know that you had quite an extensive central review. The second question is, did you see any biomarker trends for response to therapy? For example, patients with high IgE at baseline. Let's take the latter first from Shelia, and then I can address the unstable disease. Go ahead. Hi, Imogen. Thanks for the question. We've been monitoring various biomarkers in the trial. We have data now on TARC, IgE, and eosinophils. We're seeing really tremendous reductions in those eosinophils as a good biomarker of inhibiting TH2 responses. We are seeing responses sort of across the board in patients that are showing reductions in TH2 biomarkers, but also in patients that are not high for these biomarkers at baseline. We're going to be doing some further analysis on biomarkers to see if there's anything else that can give us an indication. I think what it has allowed us to do is show replications that we're fully engaging the receptor, as we can see by PK levels, but also by these various biomarker changes. Thanks. Thanks for the questions, Imogen. Appreciate it. I think on the unstable disease, we had pre-specified criteria within the statistical analysis plan for the program regarding patients who showed an increase in hair loss over the initial period in the trial. If they lost more than 25%, they were predefined as unstable and removed from the analysis. We had three such patients in this data set, two of which were patients who came in with patient-reported stability but had no medical records. They were local ad campaign patients, they did not have medical records, certainly a lesson for us in making sure there's confirmation of stability coming into these trials in the future. The third patient had a long history of NASH and had an exacerbation of their NASH during that time, which we believe triggered a flare, which caused hair loss at that time. Those were the three that were removed. You did. Very helpful. Thank you so much, and congratulations. Thanks so much. Appreciate it. Thank you. Your next question is from Joe Catanzaro from Mizuho. Your line is now open. Hey, everybody. Thanks for taking my questions. Congrats on the great data as well here. Maybe first question from me, I know maybe patient numbers get a little bit small, but wondering if you could speak to the efficacy you're observing in the subgroup of patients with prior JAK inhibitor therapy versus those who are JAK naive. Would expectations moving forward be to continue to allow patients with prior JAK onto future studies? The second question, I guess on the opportunities outside of alopecia, wondering if there's specific indications that you think alopecia maybe provides the best read-through to, and maybe somewhat related to the last question, whether there are biomarker changes you're seeing that give you the most conviction in these additional opportunities, any specific ones. Thanks. I'll take the JAK experience one first and then hand off to Shelia. What I would say is we saw strong, clinically meaningful responses across some of the patients who were JAK experienced. We still are doing an analysis of the full data set there, and we certainly want to see the 52-week data for these patients as well. We'll provide more of that at a future medical meeting. What I would say is we had a series of patients who were post-JAK that responded quite well. We're encouraged by that finding. We think that bodes well long term for the program and look forward to providing a little bit more analysis on that in the future. Want to add anything to that, Arash? I think this is a key differentiator in this study. Other alopecia areata studies usually exclude patients that have JAK exposure, and particularly thinking about the avenue in real life for patients who may have had success with JAK inhibitors, but who may want an off-ramp to something else, whether it's for family planning, as was highlighted in one of our patients, they're tired of taking JAK inhibitors or just want something a little bit different that has a different safety profile. I think this is a really unique aspect of this that we should highlight and would be a wonderful opportunity for clinicians and patients looking for an alternative to a medication they're currently on. As for future indications, certainly there's a wealth of opportunity for bempikibart outside of alopecia areata, both within dermatology and beyond. I'll let Shelia speak to the sort of mechanism and the biomarkers in some of the areas we're thinking of expanding in, but we're not advising on the next indication at this time, although we're doing some preliminary work to refine our thinking on that over time. Thanks for the question because I think it's an important one. I think what our data are now highlighting is that inhibiting the IL-7 receptor alpha subunit is now providing clinical validation in this disease that we know is driven by pathogenic T effector cells, particularly CD8 positive and NKG2D positive T cells. I think this data set would suggest that there are other indications where we are generating data to look at IL-7 receptor expression on T cells in the dermatology space that we also know are driven largely by T effector cells. This could include things like lichen planus. It can include things like vitiligo. There are a number of other diseases, as you are probably well aware, that are driven by active T cells, such as celiac disease, MS, type 1 diabetes, a lot of big indications. I think what's also really important about this data set is the replication of our ability to inhibit TH2 biomarkers. I think we've put to rest that the IL-7 receptor antibody is not only impacting T cells, but it has the ability to inhibit TH2 responses. We're seeing beautiful reductions in TARC, IgE, and eosinophils. It really opens up the door for respiratory indications and the potential for other indications, maybe in the skin as well, that are believed to be driven by TH2 responses. Great. Thanks so much for taking my questions, congrats again. Thanks so much. Thank you. Your next question is from Joe Pantginis from H.C. Wainwright. Your line is open. Hi, this is Josh on for Joe. Congrats on the really exciting data. I had two questions for you guys. For the first, I was wondering how you view this data relative to historical Olumiant and LITFULO data. The second question is, how do you feel that this current data set, do you feel it supports first-line positioning, or do you feel like you would need to wait for a larger randomized study to be able to make that call? Thanks so much for the questions. I'm going to let Arash go on this one and certainly can add some color at the back end. Sure. In regards to comparing this data against existing data for Olumiant and for LITFULO, the data here is in the range of the Olumiant 2 mg- 4 mg data at 36 weeks. All of these medications show initial improvement in one group of patients, then deepening over time, which I think is the pattern that we're seeing here. There's no head-to-head, and it's hard to draw an exact conclusion, but I think as a clinician, it's easy to say that these are in the same vicinity and that there's not a major sacrifice being made with regards to efficacy if one was to select this medication over a JAK inhibitor. Of course, every patient might be a little bit different. For the second indication about where this drug would lie in regards to first or second line, I think this is where shared decision-making with the patient is critical. If we look across dermatology at other indications, maybe the easiest one to look at is atopic dermatitis. When patients and clinicians are given a choice of a targeted biologic therapy versus a JAK inhibitor, even if there are numerical advantages with regards to efficacy or speed of impact with the JAK inhibitor, consistently the decision is made to go with the medication that is seen as being more safe, with less laboratory monitoring, and with less black box warning. My anticipation here is that, while patients will make their, and clinicians will make the best choice for each patient individually, it would be very reasonable to anticipate that most patients, and most clinicians will select a targeted biologic over a JAK inhibitor as a first-line agent, and depending on how the patient outcome is, go from there. Yeah. Great. Thanks on the color. Again, congrats on the great data. Thanks so much. Really appreciate it. Thank you. Your next question is from Derek Archila from Wells Fargo. Your line is now open. Good morning. Let me add my congrats on the data. Looking very good. Just a couple questions from us. Two for management, one for Arash, if we may. First, can you just discuss the time to SALT-20 response? I'm just curious how that might compare to JAKs. On the strength of the data that you're seeing so far using the loading dose, some of those curves look pretty good on the patient anecdotes. I just wonder, is a shorter 24-week phase III trial possible, or would you anticipate replicating a 36-week trial? For Arash, just curious again, based on the data today, could you quantify how many more patients may look to seek treatment now with a therapy like this, that are not currently being treated by JAKs? Thank you. Yes. It's good to talk to you, Derek, by the way. Thanks for the questions. Time to SALT-20, when we look at this, we do anticipate, given the pharmacokinetics here, that it may take a little longer to get to SALT-20, but we do have examples of patients getting there fairly rapidly. Obviously in larger studies, we may get a better look at whether there are different profiles that emerge for time to response here. Either way, we're quite encouraged to see this level of results at week 36. We're encouraged by that. We do believe endpoints for the phase III would need to be in the range of 36 weeks. Certainly based on other data sets, may seek to dose patients longer, even if our endpoint is at week 36. We think there could be deepening effects if we continue dosing longer. That's something we can consider, but certainly encouraged here that a 36-week endpoint is on the table for our phase III. Second question, curves on the 24 weeks. I guess I spoke to that. We would not seek to do a 24-week trial for the phase III. We would anticipate this being a 36-week. I'll kick it over to Arash. Perfect. I think this is a really important thing to highlight that the number of patients taking these medications for alopecia areata will expand as new drugs enter the market. At present, it's estimated that approximately 25%-35% of patients who are candidates for JAK inhibitors based on their alopecia areata are taking a JAK inhibitor. About two-thirds of patients right now are not being treated or being undertreated with other medications. A great proportion of that will likely be because of either they don't qualify for JAK inhibitors due to safety concerns, or they or their prescribers have specific concerns themselves. Introducing a new drug that has the profile of bempikibart should give another opportunity to a large proportion of those patients and may convert many of them to active use. I would imagine up to maximum three times more than what we have right now. In reality, let's say half of those patients begin a therapeutic, it yields a lot of the market left to be realized. Excellent. Very helpful. Thanks again. Do you want to add anything on the time to response as well? Yeah, Arash might want to add to that time to response answer. Let me speak a little bit to time to response. I think the one really important thing to understand with this data is that time to response is important. The time to response that we're talking about, though, is a categorical outcome where you kind of pass this SALT-20 barrier. In reality, when you're taking care of these patients, they're getting better week by week by week, and they're seeing the hair regrowth. They're happy about it. They're seeing those changes, and that's really the exciting part. For purpose of a clinical trial, we have a sharp cutoff, right? Where if you have 21% hair loss, you're a failure. If you have 18% hair loss, you're a success, right? Real life doesn't work exactly that way. While patients want to see consistent improvement and success, when you look at the data for how they make choices based on what drugs that they pick, the number one decision factor for patients choosing a treatment for alopecia areata is safety profile. The second most important thing for them is depth of efficacy and durability of efficacy. The third is form factor, and the final thing they put on is velocity. While we may be focused on the shape of the curve and how fast they get there, if you do this properly, velocity only occurs once, right? You regrow your hair, and you keep it, and then your focus really ends up being on how much hair am I going to have, how much is that going to remain over time, and how safe is it for me to continue on this medication? For me, as a clinician, the exciting part about bempikibart is those last three parts in particular, where you're going to have that depth of response. If these data hold in future studies, you're not going to have the same concerns around safety. Arash. Thank you. Thanks for the question. Thank you. There are no further questions at this time. I will now hand the call back over to Jodie Morrison for the closing remarks. Thank you all for joining us this morning and for the questions, and we look forward to keeping you updated on future programs and future calls. Thank you. Thank you. Ladies and gentlemen, the conference has now ended. Thank you all for joining. You may now disconnect your lines.