Good morning, everyone. My name is Eun Yang, a biotech analyst with Jefferies, based in New York. Our next presenting company is Astria. Astria is a clinical stage company, and this is gonna be a hybrid format. Astria is going to give us a presentation, then we are going to go into Q&A. Presenting from Astria is Jill Milne, CEO of the company. Jill? Thanks, Eun. I'll start with an overview of the company, but before I get started, I'll note that we will be making forward-looking statements during today's presentation and discussion. Astria is a company that is developing first-choice therapeutics for patients affected by allergic and immunological diseases. Our lead program is STAR-0215. STAR-0215 is a monoclonal antibody inhibitor of an enzyme called plasma kallikrein, which is a clinically and commercially validated target for the treatment of hereditary angioedema or HAE. STAR-0215 has shown early proof of concept in our phase Ia clinical trial for its target profile, which is as a long-acting preventive therapy in HAE, with a best-in-class PK profile and the potential for dosing once every three or six months in patients. We are currently running our phase Ib/II trial in patients with hereditary angioedema. This trial is well underway, and we expect initial proof-of-concept results in patients from this trial in Q1 of 2024. Our second program, which we recently added to the pipeline, is STAR-0310, and we believe STAR-0310 has the potential to be a best-in-class OX40 program for the treatment of atopic dermatitis. We expect to file an IND for STAR-0310 in Q4 of 2024, and to be in phase Ia in early 2025, with results expected in the third quarter of 2025. Our expected cash runway is into 2026, and that's based on our current operating plan. This next slide is an overview of our strategy at Astria for how we think about building our company and specifically building our pipeline. Our focus is to develop what we call first choice products that improve the health and outcomes of patients affected by allergic and immunological diseases. We are taking the approach of advancing a pipeline based on established mechanisms. That is, mechanisms that have been validated clinically, but where we believe we can advance a best-in-class program. In terms of first choice, what we mean by that is that patients and physicians will choose our products based on their competitive efficacy profile, their low treatment burden, and their clean safety and tolerability profiles as well. STAR-0215 fits very well with this strategy. Again, STAR-0215, our vision for this program is to be as a first-choice preventative treatment to help normalize the lives of people living with hereditary angioedema. STAR-0310 also fits this strategy very well. We believe STAR-0310 has the potential to be a best-in-class OX40 program for the treatment of atopic dermatitis, and we also see great potential for STAR-0310 in additional indications as well. Shown here is our anticipated milestones over the next several years, including the proof-of-concept data in HAE patients with STAR-0215. Again, this shows the integrated pipeline with both STAR-0215 and STAR-0310. For STAR-0215, we just last week presented results from our phase Ia clinical trial with STAR-0215 in healthy volunteers, which again support the potential of STAR-0215 to be dosed every three or every six months in patients. We expect to release initial proof-of-concept results in patients from our phase Ib/II ALPHA-STAR trial in Q1 of 2024, and with positive results from that trial, anticipate initiating a single pivotal phase III trial in the beginning of 2025. For the STAR-0310 program, again, our expectation is to file an IND by the end of next year. We also intend to present the preclinical profile of STAR-0310 at a scientific conference in 2024. The phase Ia healthy volunteer trial for STAR-0310 will initiate at the beginning of 2025 and read out in the third quarter of 2025. I'll give a brief overview of the STAR-0215 program and talk about the upcoming milestones in more detail for this program. So again, STAR-0215 is being developed as a preventative therapy for the treatment of hereditary angioedema or HAE. HAE is a rare disease. It is a genetic disorder that is characterized by severe, unpredictable, painful, and sometimes life-threatening swelling. It affects about 8,000 people in the United States and about 15,000 in the EU. It's a disease that is truly life-changing and can be life-threatening. We hope to address both the disease burden and the treatment burden with what we are trying to accomplish with STAR-0215. So again, for STAR-0215, we believe it has the potential to be the first-choice preventative treatment in HAE, and that's based on the design of this program, as well as the clinical data that we've generated to date. HAE, in most patients, is caused by a deficiency of a protein called C1- inhibitor. C1- inhibitor is an important component of the complement pathway, and importantly, is a natural inhibitor of the enzyme plasma kallikrein. Without C1- inhibitor, patients with HAE have unregulated or uncontrolled plasma kallikrein activity. That leads to the release of bradykinin from the substrate of plasma kallikrein, high molecular weight kininogen, and it's the bradykinin that's the pathological mediator of the swelling that occurs during an HAE attack. By inhibiting plasma kallikrein with STAR-0215, we can shut down the production of that bradykinin and shut off the swelling that occurs during an attack for people who live with this disease. This mechanism is validated. It's validated both clinically and commercially by the market leader, Takhzyro or lanadelumab, which is also a monoclonal antibody inhibitor of plasma kallikrein. And so we share that validated mechanism with Takhzyro. However, there are some important differences between STAR-0215 and Takhzyro. Importantly, we have engineered STAR-0215 to have a very long plasma half-life. We've utilized the YTE half-life extension technology to engineer STAR-0215 to be able to support infrequent dosing with STAR-0215. So while Takhzyro is dosed in most patients every two weeks or 26 x per year, we have engineered STAR-0215 to be dosed 2x or 4x a year, so dosing every three or six months. Our initial phase Ia clinical trial results with STAR-0215 establishes the potential for this infrequent dosing. Here is an outline of the design of our phase Ia healthy volunteer trial with STAR-0215 that we've recently released results from. This trial is a randomized, double-blind, placebo-controlled trial in healthy adult subjects. We looked at five single ascending dose cohorts in this trial. The endpoints were safety, tolerability, PK/PD, and ADA. We just presented last week results from this trial through 224 days of follow-up for the first three cohorts, the 100 mg, 300 mg, and 600 mg subcutaneous cohorts. We released data through 112 days of Cohort 4, which is a 1,200 mg subcutaneous cohort, and 84 days for Cohort 5, which is a 600 mg IV cohort. The results and modeling of the data that we presented last week support, again, the potential to dose STAR-0215 as infrequently as every three or six months in patients, and we're currently testing that in our phase II trial, our ALPHA-STAR trial. What's shown here are the phase Ia healthy volunteer PK results, and what these results show is that we have, with STAR-0215, a best-in-class pharmacokinetic profile for an inhibitor of plasma kallikrein. What we see is rapid and sustained increases of STAR-0215 following single doses. The dashed green line on the chart to the right is the target threshold of drug levels that we are seeking to achieve, because this level of drug is associated with clinical benefit at suppressing attacks in HAE. What we can see is that we achieve those levels, about 12 micrograms per mL level of drug, out through 84 days, with all doses above a 100 mg. The 300 mg dose keeps drug levels above that 12 micrograms per mL threshold out through 84 days. The 600 mg level keeps... 600 mg dose keeps the drug levels above that 12 μg/mL out through 168 days. Again, this is following a single dose of STAR-0215. Importantly, there is a rapid onset of effect with STAR-0215 in terms of getting above that 12 μg/mL threshold. For example, the 600 mg dose achieves levels of drug above that 12 μg/mL threshold within 11 hours. That's critically important for patients with HAE because they want to have a rapid onset of effect with a drug that they're taking to prevent attacks. So we believe that's a key differentiator for STAR-0215 among the other preventative therapies either on the market or in development. The estimated half-life is up to 127 days for STAR-0215, so again, validating, the YTE half-life extension technology for this program. We've seen a very favorable safety and tolerability profile, no, SAEs, no discontinuations due to an adverse event. The most common treatment-emergent adverse events have been injection site reactions. We've taken the data from the healthy volunteer trial, the PK data, and developed models to simulate different dosing regimens that we plan to take into patients, and those models are shown here. The graph on the left is a simulated every three-month dosing model for STAR-0215, again, based on the clinical healthy volunteer PK data. And what you can see, again, the 12 μg/mL threshold is shown there, and that's what we're trying to achieve to keep drug levels above that threshold. What you can see is a loading dose of 600 mg, followed by maintenance doses of 300 mg every three months, keeps STAR-0215 levels well above that 12 μg/mL threshold. In fact, the Ctrough of this line you can see is about 25 μg/mL. So we believe this dosing regimen could be a regimen that could keep patients attack-free or have a significant benefit on attack rate reduction. The simulated model on the right simulates an every six-month dosing regimen, and you can see this has a 600 mg dose on day one, followed by maintenance doses of 600 mg starting at day 28 and then every six months thereafter. And again, you can see that the Ctrough levels with this dosing regimen are well above that 12 μg/mL threshold, in fact, are about 27 μg/mL. So we believe the data to date from our phase Ia healthy volunteer study supports the potential for dosing STAR-0215 in patients every three or every six months to suppress HAE attacks. This slide shows the pharmacodynamic biomarker results from our phase Ia healthy volunteer trial. We're showing the results here of the reporter substrate assay following single doses of STAR-0215. What we've overlaid on this graph is the data from lanadelumab, which again, is the market leader for preventative therapy in HAE. This data shown in the black dashed line is from the lanadelumab phase Ia healthy volunteer trial. And what you can see is that we see a statistically significant inhibition of plasma kallikrein activity through day 184 after single doses of both 300 and 600 mg subcutaneous, as well as the 1200 mg, which we see significant inhibition out through 224 days. And again, the STAR-0215 percent inhibition of plasma kallikrein is maintained through at least three months post single doses at levels that are greater than or similar to those achieved at peak for lanadelumab. The results from our Western blot assay of high molecular weight kininogen cleavage are consistent with that, and we have data pending for the 1200 mg cohort through day 224. We've just recently completed some market research with both patients and treating physicians. We talked with 92 HAE patients and 60 HAE treating physicians to explore the interest and potential of an every three-month and an every six-month dosing regimen. Importantly, what we heard back from both patients and physicians is great interest in both of these dosing regimens. Our intention is to move as quickly as possible to market, and we believe we can do that most quickly with the every three-month dosing regimen, followed soon thereafter with the every six-month. We're currently working on our phase III design, and we'll intend to share more details about that in the coming months. Shown here is the ongoing ALPHA-STAR phase Ib/II clinical trial with STAR-0215 in patients with HAE. What we're exploring in this trial is dosing regimens that can provide proof-of-concept data for attack rate reduction in patients following dosing every three or six months. There are three dose-ranging cohorts. There's a single dose, a 450 mg dose in Cohort 1, which we'll follow for three and six months post that dose. Cohort 2 is the 600 mg loading dose on day one, followed by a 300 mg maintenance dose on day 84, and again, we'll follow post that 300 mg dose for three and six months. Cohort 3 is a 600 mg loading dose, followed 28 days later with a 600 mg dose, which we'll follow patients three and six months post that last dose. What we'll be looking at, of course, is safety, tolerability, attack rate reduction, PK and PD from this trial. We intend to release initial proof-of-concept results in the first quarter of next year. We also have our ALPHA-SOLAR long-term open label extension trial that is now ongoing. This trial will enroll patients who complete the ALPHA-STAR trial, and we will continue to follow these patients in either every three-month or every six-month dosing regimens. So we believe that STAR-0215 has the potential to be a first-choice preventative therapy for the treatment of hereditary angioedema for several reasons. First, the strong data from our phase Ia healthy volunteer trial supports potential best-in-class PK profile that can potentially support every three and every six-month dosing regimens in patients. The proven mechanism of action and the trusted modality in the form of a monoclonal antibody, these are the same as the current market leader, and so I believe could provide confidence for both patients and physicians, who may want to switch to STAR-0215. We believe that STAR-0215 has the potential to provide rapid and durable protection against HAE attacks, and that, again, is based on the results that we've observed clinically to date with STAR-0215. We have developed STAR-0215 with a patient-friendly citrate- free formulation for low pain and for the ability for SC self-administration. And finally, we plan to develop two options for patients, both a Q3 and a Q6-month option, to allow patients to choose what's best for them. I will just spend a moment on the STAR-0310 program, which is a program we've recently added to our pipeline. STAR-0310 is a monoclonal antibody antagonist of the OX40 receptor that we're developing for atopic dermatitis. Atopic dermatitis is an immune disorder that's characterized by skin barrier dysfunction and itching. It's caused by a diverse set of mechanisms involving a variety of T cell pathways. There are approximately 5% of the adult population in the United States is affected by atopic dermatitis. Half of those patients have moderate to severe atopic dermatitis. And there is a huge unmet need in atopic dermatitis. The current market leader is Dupixent. There are two biologics that are currently approved, with Dupixent being the market leader here. But there are currently as many as 40% of patients that are not well served with current therapies that are available. And again, atopic dermatitis is caused by immune dysregulation. The current biologics that are on the market for atopic dermatitis target only one aspect of the T cell pathology that's involved in atopic dermatitis, and that's the Th2 pathway. And so these biologics do not address the full spectrum of the immune dysregulation that occurs in this disease. We became very excited with the OX40 pathway because of the potential of OX40 and inhibition of this pathway to modulate all of the aspects of T cell pathology that are occurring in atopic dermatitis. So not only the Th2 pathway, but importantly Th1, as well as Th17 and 22. The OX40 pathway itself is composed of two elements: the OX40 ligand, which is expressed on antigen-presenting cells in a wide variety of cells, and then the OX40 receptor, which is expressed only on activated T cells. We've chosen to go after an antagonist of the OX40 receptor because of the potential selectivity of targeting only activated T cells in this disease state. There have been three programs that have been taken into proof-of-concept studies in atopic dermatitis that are focused on the OX40 pathway, and those three programs are shown here. Amlitelimab is a monoclonal antibody that targets the OX40 ligand. Rocatinlimab is a monoclonal antibody that targets the OX40 receptor, and telazorlimab, which is the parent antibody to STAR-0310, targets the OX40 receptor as well. All three of these programs have established proof of concept in both phase IIa and phase IIb studies in atopic dermatitis. But they all have different aspects to them. Amlitelimab targets the ligand, which is expressed broadly on antigen-presenting cells and potentially on cell types that one doesn't want to target in atopic dermatitis. Rocatinlimab was engineered to be afucosylated, which increases ADCC and leads to T cell depletion and cytokine release, which causes pyrexia and chills, and also has the potential for an increased risk of infection. Telazorlimab was designed to be a full antagonist of the OX40 receptor to have low ADCC activity to preserve T cells. STAR-0310 is a next-generation version of telazorlimab that was affinity matured to have a tenfold greater affinity for the OX40 receptor and a 10x increase in potency against T cells, however, to be T cell preserving. And has been engineered with YTE half-life extension technology to allow for less frequent dosing than potentially amlitelimab or rocatinlimab. So STAR-0310, we believe, has the potential to be a first choice for moderate to severe AD and a best-in-class among the OX40 programs. Again, that's because of the high affinity of STAR-0310 for the OX40 receptor, the selective potency for activated T cells, and the design to be low ADCC to be T cell preserving. Again, we've extended the potential for long duration of effect with the YTE half-life extension technology. So we believe STAR-0310 has the potential to be a best-in-class and first choice treatment here as compared to rocatinlimab and amlitelimab, based on comparable effectiveness across a variety of T cell pathologies that are at play in atopic dermatitis. We believe that administering STAR-0310 every 4x to 6x a year is a possibility based on the YTE half-life extension, and that's in comparison to the 12x a year that are anticipated for amlitelimab and rocatinlimab. We believe that STAR-0310 has a potential to have a favorable safety and tolerability profile because of its T-cell preserving ability, low ADCC, and only targeting activated T cells in this disease. So, we do intend to expand the STAR-0310 program beyond atopic dermatitis into other immune indications as well. I will just end there. Thank you. One question here. Obviously, the two panelists see the data in the first quarter next year. What should we expect? You are measuring attack reduction, okay, reduction every three months and six months. Would it be from all three cohorts, or is that gonna be just the- Yeah, I'll have Chris Morabito, our Chief Medical Officer, answer. Good morning. Yeah, thanks. Great, great question. So the question is about what to expect with the Q1 data release. And this is an accelerated release. We have been talking about releasing these data in Q1, sorry, in mid-2024, now we're releasing in Q1. The reason for that is that we have always anticipated a pre-specified interim analysis. We just now know, just based on accelerated enrollment, that we can do this in Q1. And what we anticipate showing with this release is effectiveness, so that's efficacy of STAR zero of STAR-0215, to prevent HAE attacks, given once to look for prevention of attacks for three months and for six months. Along with that, we'll anticipate having PK/PD and safety information to support the overall product profile. We get it from all three cohorts? We will have data from all three cohorts to kinda contribute to this. Okay. So the last question is, you know, Ionis showed you open-label extension study. They have, and obviously, they have a different, they're targeting prekallikrein, since more upstream to the same kallikrein they are targeting. And every two months of dosing, they showed you over about 60%, 60, 60% of patients have attack free. So I want to ask you, what do you think about that data and then if you think we're better? So the question is about the profile of effectiveness, essentially, whether it's attack-free rate or something else. So you're referencing donidalorsen, which is targeting prekallikrein, and there is a small proportion of people that could probably benefit from that, given every 2 months. But most likely it's a once monthly medicine. 0215 is once every three months or once every six months. And just based on our modeling that we've done, as Jill introduced, we assess that we can have a proportion of people who are attack-free that's in the 80%-90% range. Thank you. You're welcome.