Astria Therapeutics Inc (ATXS) 2021 Q3 法說會逐字稿

Good day, and thank you for standing by. Welcome to the Q3 2021 Astria Therapeutics Earnings Conference Call. (Operator Instructions)

I would now like to hand the conference over to your speaker today, Andrea Matthews, Senior Vice President, Corporate Affairs. Please go ahead.

Thank you, Elissa. Welcome to today's Astria Therapeutics conference call where we will provide a corporate update and review our third quarter 2021 financial results. With me today are Jill Milne, Chief Executive Officer; Andy Nichols, Chief Scientific Officer; Andrew Komjathy, Chief Commercial Officer; and Noah Clauser, Chief Financial Officer.

We issued a press release this morning summarizing our corporate update and our Q3 2021 financial results, which we will reference on today's call and is available on our website. We are also using slides during today's call that are available within the Events and Presentations section in the Investors part of our website.

I would like to note that during today's call, as mentioned on Slide 2, we will make statements related to our business based on current and future expectations that may be considered forward-looking statements under applicable securities laws and regulations. Actual results may differ materially from those indicated by these statements as a result of a variety of risks and uncertainties, including those discussed in our most recent annual report on Form 10-K, as well as discussions of potential risks, uncertainties and other important factors in the subsequent SEC filings, which are available on our website. Such statements represent our judgment as of today, and Astria undertakes no obligation to publicly update any forward-looking statements except as required by law.

With that, let me pass the call over to Jill who will provide our corporate update. Andy will share recent preclinical data on STAR-0215. Andrew will provide an overview of the need for new HAE treatments, and Noah will follow with the financial update. Jill will then wrap things up. Jill?

Thank you, Andrea. Good morning, everyone, and thank you for joining us on today's call.

Turning to Slide 3, I'm excited to introduce Astria Therapeutics. Our company name embodies our commitment to put patients first in all that we do. Astria comes from the Greek word for star, reflecting that patients are the stars that guide us and give us our purpose. Our mission is to bring hope with life-changing therapies to patients and families that are affected by rare and niche allergic and immunological diseases.

On Slide 4, you will see an overview of the Astria investment opportunity. Our lead program, STAR-0215, is a monoclonal antibody inhibitor of plasma kallikrein that we are developing to treat patients living with hereditary angioedema or HAE. We see STAR-0215 as an exciting opportunity to develop a product with the potential to be the most patient-friendly preventative therapy for HAE.

For important upcoming milestones, we are on track for an IND filing in mid-2022 and expect initial clinical trial results by year-end 2022. This first clinical trial has the potential to demonstrate clinical proof of concept for the differentiated profile of STAR-0215. We are also evaluating opportunities to expand our pipeline with the broader goal of addressing the unmet needs of patients with rare and niche allergic and immunological diseases.

We have an experienced team and Board of Directors backed by leading life sciences investors. At the close of Q3, we were in a strong position with cash and cash equivalents of $131.8 million, which is expected to fund the current operating plan through 2023. We have 18.3 million common shares outstanding on an as-[converted] (added by company after the call) basis, and we trade under the symbol ATXS on NASDAQ.

Slide 5 provides an overview of today's Astria corporate updates and STAR-0215 program highlights. We are making very good progress with the program and are on track for initial Phase I clinical results expected by year-end 2022. Our Chief Scientific Officer, Andy Nichols, presented new preclinical data last week at the American College of Allergy, Asthma and Immunology Annual Scientific Meeting regarding STAR-0215's binding affinity, potency, binding site and use of YTE modifications to enable a long duration of action, and he will review these results shortly.

Next, Andrew Komjathy, our Chief Commercial Officer, will highlight the potential market opportunity for STAR-0215 and our findings on the burdens of disease and treatment in HAE, which we presented at the National Organization for Rare Disorders Summit last month, supporting the substantial need to decrease patient disease and treatment burden. Subsequently, Noah Clauser, our Chief Financial Officer, will give an update on our financials.

For those that may be less familiar with HAE, Slide 6 provides an introduction. HAE is a rare, debilitating and life-changing disease. It is characterized by severe, unpredictable, painful and sometimes life-threatening edema. The edema can occur in the skin, the abdomen and airway. In most patients, it's caused by a deficiency in a protein called C1 inhibitor, which is an important component of the body's contact pathway. There are approximately 8,000 people affected in the United States.

Patients have a significant burden of disease and live with the fear of an attack. HAE is treated with preventative therapies to reduce the frequency of attacks and on-demand therapies when an attack occurs. Unmet need exists for effective preventative treatments with lower treatment burden. The global market for HAE treatments is large and estimated to grow from $2 billion in 2020 to more than $4.5 billion by 2026.

Slide 7 illustrates the differences between a healthy blood vessel and a blood vessel impacted by HAE and shows how STAR-0215 aims to prevent attacks in HAE by inhibiting plasma kallikrein. In a healthy individual, external triggers such as pressure from holding a tool, tissue stress or damage results in the production of plasma kallikrein. This system in healthy individuals is kept in check by a protein called C1 inhibitor, which blocks the function of plasma kallikrein.

In most patients with HAE, C1 inhibitor is either absent or defective. In an HAE patient without active C1 inhibitor, there is no break for plasma kallikrein, and what you get is a runaway contact pathway whereby plasma kallikrein continues to produce bradykinin, which leads to pathological swelling. With STAR-0215, our goal in HAE patients is for plasma kallikrein to be inhibited, even in the absence of C1 inhibitor, thereby reducing bradykinin production and preventing edema and pain.

Over the years, the therapeutic landscape for HAE has evolved immensely. On Slide 8, you will see that the recent -- that recently, the landscape changed in a positive direction with the entrance of plasma kallikrein inhibitors. However, there remains unmet need as more than 50% of HAE patients on approved plasma kallikrein inhibitors still experience attacks. We've heard from both patients and physicians that there is high interest in an effective preventative treatment option with infrequent dosing. We are aiming to deliver that profile with STAR-0215.

On Slide 9, you will see an overview of our lead program. STAR-0215 is a monoclonal antibody inhibitor of plasma kallikrein that we are developing to treat patients living with HAE. We see STAR-0215 as an exciting opportunity to develop what could be the most patient-friendly preventative treatment option for HAE based on our data generated to date and the existing HAE treatment landscape. We think of efficacy and dosing frequency as the key aspects that determine an HAE patient's experience with the treatment, and STAR-0215 was designed with a clear vision aimed at addressing the needs of HAE patients. What's exciting is its potential to provide long-acting, effective protection from the painful, recurrent and sometimes life-threatening attacks that are caused by HAE.

I'll now hand it over to Andy to give a more in-depth look at STAR-0215 and present our recent findings. Andy?

Thanks, Jill. Last week at the American College of Allergy, Asthma and Immunology Annual Scientific Meeting in New Orleans, I presented some of the preclinical data that describe the pharmacology and pharmacokinetics of STAR-0215, and the poster describing this is available on our website.

Turning to Slide 10. Plasma kallikrein binding affinity and plasma half-life have been shown to be key drivers of efficacy for the prevention of HAE attacks. We showed that STAR-0215 binds to plasma kallikrein in vitro with high affinity, about tenfold more potently than lanadelumab. In competition binding experiments, STAR-0215 was shown to bind to a different site on plasma kallikrein than lanadelumab.

To characterize the potency of STAR-0215, we use a physiologically relevant in vitro functional assay that follows bradykinin release from high molecular weight kininogen as catalyzed by plasma kallikrein, in other words, the exact same biochemistry that drives an HAE attack. Note that the concentration of the high molecular weight kininogen used in the assay is similar to the circulating level in humans. And the concentration of plasma kallikrein that we use is in the range of what has been estimated to be present in plasma during an HAE attack.

Importantly, the high binding affinity of STAR-0215 for plasma kallikrein translates into high functional potency in this physiologically relevant assay. We looked at the concentration of antibody that results in 90% inhibition of kallikrein activity because that is believed to be the therapeutically relevant level of inhibition to prevent HAE attacks.

In this assay, STAR-0215 has been shown to have about a tenfold improvement in potency over lanadelumab to inhibit plasma kallikrein by 90%. The potency of lanadelumab that we see in this assay is actually consistent with the plasma levels that have been reported to be required for clinical efficacy.

Moving to Slide 11. I also presented information about the half-life extension technology used with STAR-0215. The introduction of YTE modifications in STAR-0215 were designed to extend plasma half-life and enable a long duration of action. YTE modifications have been shown to extend the half-life of other monoclonal antibodies with the half-life in nonhuman primates being 20 to 40 days. In addition, there have been several antibodies with YTE modifications that have been in the clinic, and they have been reported to have half-lives in humans of 70 to 120 days.

As shown last week, enhanced pH-dependent FcRn binding enabled by the YTE modifications translated to a more than threefold increase in plasma half-life with STAR-0215 compared to its parental antibody without the YTE modifications. In nonhuman primates, STAR-0215 given at the same doses as lanadelumab has a more than threefold longer half-life of about 34 days and the potential for a longer half-life in humans as suggested by other antibodies with the YTE modifications. Together, these results support the potential for infrequent dosing with STAR-0215 possibly every 3 months or longer.

On Slide 12, we look at the data from both the in vitro functional assay and the pharmacokinetics in nonhuman primates, and we can begin to understand the potential relative duration of efficacy for each of the antibodies when given at the same dose.

In the middle panel for lanadelumab, you can see that the plasma levels fall below the IC90 by approximately day 10. This means that 10 days after the antibody is dosed, the levels fall below the therapeutic threshold that we are targeting of 90% inhibition of plasma kallikrein.

In contrast, you can see in the left panel that the plasma level of STAR-0215 remained above the predicted minimum therapeutic concentration for more than 84 days, which is the full duration of the experiment.

Lastly, in the right-hand panel, you can see a PK/PD model that synthesizes the same data together but in a different way. What is plotted here is the percent of plasma kallikrein inhibition expected that the concentration of antibody at each of the time points in the pharmacokinetic experiment. You can see that out through 84 days following STAR-0215 dosing, plasma kallikrein is expected to be, for all intents and purposes, fully inhibited.

In contrast, for lanadelumab, the inhibition of plasma kallikrein falls below that 90% inhibition level by day 10 and, by day 20, is about 50%. These preclinical data show that for the same dose of antibody, STAR-0215 is predicted to have a significantly longer duration of action than lanadelumab and that STAR-0215 has the potential to be a plasma kallikrein antibody with an increased potency and extended duration of action.

The CMC and nonclinical development of STAR-0215 are underway. Working with a CDMO that has significant experience in development and commercialization of biotherapeutics, we have identified a proprietary, high-producing cell line and an appropriate formulation, and these will be -- enable to supply our planned Phase I studies.

Our GLP toxicology program is in progress, and all relevant pharmacodynamic clinical assays are under development. Based on this, we expect to file an IND for STAR-0215 mid next year and to initiate our clinical program shortly thereafter.

Slide 13 outlines our plans for the first Phase I study design. We see an opportunity to establish clinical proof of concept for the differentiated profile we anticipate for STAR-0215 in the first clinical trial in healthy volunteers. We anticipate that this trial will be informative in terms of pharmacological activity and half-life of STAR-0215. We will monitor safety, determine pharmacokinetics and utilize a pharmacodynamic biomarker assay to assess plasma kallikrein inhibition.

Our goals for this trial with STAR-0215 are to demonstrate safety, establish the extended half-life, show prolonged plasma kallikrein inhibitory activity and to refine the dose and dosing regimen for our next trial. Initial pharmacokinetic and pharmacodynamic data from the first cohorts from this trial are expected by year-end 2022.

Due to the expected long half-life of STAR-0215, we will follow the treated subjects for an extended period of time before the full data will be available. If positive, we believe that this trial will set the stage for the differentiated profile of STAR-0215.

In summary, on Slide 14, STAR-0215 has the opportunity to be the most patient-friendly preventative treatment option for HAE patients. Our first objective was to identify a high-potency antibody that could inhibit plasma kallikrein to the same levels as lanadelumab but with less antibody, and this has been achieved preclinically.

The second objective was to engineer an antibody with a long plasma half-life, potentially allowing for less frequent dosing and preventing attacks for a long period of time. This has also been achieved preclinically.

The important next step is to demonstrate the differentiated profile of STAR-0215 in the clinic. With this, we are aiming to provide patients with a differentiated new therapy using a trusted treatment modality to prevent attacks in HAE over an extended period of time.

I'll now hand it over to Andrew to speak to the needs of the HAE community. Andrew?

Thanks, Andy, and good morning, everyone.

On Slide 15, we highlight that the need for improved HAE treatment options has been emphasized in recent publications from both HAE patients as well as physicians. Patients continue to have frequent attacks and experienced corresponding anxiety and depression. Physicians note that their patients are somewhat satisfied with existing treatment options and are interested in participating in future clinical trials.

On Slide 16, I'd like to highlight recent findings that we presented at the NORD conference last month, showing that there is a need to decrease both the burden of disease and also the treatment burden. These findings came from interviews from HAE patients using a structured interview guide. Patients were screened for inclusion based on self-identified disease type, HAE types 1 and 2; disease severity, moderate or severe when not on treatment; and eligibility for preventative treatment.

The findings suggest that HAE patients are seeking to reduce their treatment burden as well as disease burden, and many are open to trying new therapies that could address these needs. On average, patients tried 2 to 3 preventative treatments, most often switching for more convenient administration. Additionally, despite being on preventative treatment, half of the patients interviewed think about future attacks often or always. All patients shared that they would be compelled to switch from their current therapy if a new therapy offered similar efficacy with less frequent dosing.

I'll now turn it over to Noah to provide a financial update.

Thanks, Andrew, and good morning, everyone.

Turning to our financials on Slide 17, I will provide a brief summary. As of September 30, 2021, we had $131.8 million of cash and cash equivalents. We expect that we have sufficient capital to fund the current operating plan through 2023.

Our R&D expense was $3.8 million in Q3 2021 compared to $7.8 million in Q3 2020. Our G&A expense was $4.1 million in the third quarter of 2021 compared to $3.1 million in the third quarter of 2020. Our operating loss was $7.9 million in Q3 2021 compared to $10.9 million in Q3 [2020] (corrected by company after the call). Our net loss was $7.9 million or $0.61 per share in Q3.

As of September 30, 2021, we had common shares outstanding of approximately 13 million and 18.3 million common shares outstanding on an as-converted basis. Additional financial information will be available in our 10-Q, which will be filed with the SEC after market today.

I will now pass the call back over to Jill.

Thank you, Noah.

Slide 18 outlines the expected upcoming milestones as we envision the future for Astria. We, at Astria, listen to the voices of the HAE patient community to better understand their unmet needs, and this guides what we do. We are charting a new path for HAE patients, one that envisions an opportunity for a better quality of life with a long-acting preventative therapy that has meaningful efficacy with infrequent dosing.

We are not stopping there. We are also evaluating opportunities to expand our pipeline with a broader goal of addressing the unmet needs of patients. Our goal is to develop therapeutics that bring meaningful changes to patients' lives by pushing the boundaries of what is currently perceived as the standard of care for rare and niche diseases in allergy and immunology.

With that, I'll ask the operator to open the call for your questions. Operator, can you please repeat the instructions and poll for questions? Thank you.

(Operator Instructions) Your first question comes from the line of Hartaj Singh of Oppenheimer.

Thank you for the very nice presentation here, Jill and team. Just a couple of quick questions. One is, you indicated for your Phase I study, you'll be looking for biomarkers sort of antibody half-life inhibition of plasma kallikrein. Could those sort of serve as a Phase II/III kind of markers for sort of an accelerated approval type study? So that's number one. Or what would you need aside from doing a full Phase II and Phase III plan?

And then number two, in terms of your market research, you're showing that if you go up to about 3 months, you could have quite a few patients switch over. Could you give a little bit more color on what's the balance between decreasing attacks versus increasing the time between dosing? So I'm sure there's some kind of a relationship there also in patients' and physicians' mind. Could you give some color in your findings around that, meaning that you'd like to decrease attacks as much as possible versus increasing the time between doses?

Great. Thanks, Hartaj. Let me start and see if I can address both the areas of your questions and certainly have Andy contribute if I've left anything out and Andrew contribute on the market research side as well if I've left anything out.

So first, you asked about the biomarkers and the Phase I design in general. So you're absolutely right, we are incorporating pharmacodynamic markers in our Phase I study to understand the level of inhibition of plasma kallikrein. And we do see that as important as helping us chart our path into our Phase Ib/II and beyond to understand the level of inhibition that we're achieving.

I think this is -- HAE is a good space to be in as rare diseases go in terms of a relatively understood and known regulatory and clinical path to getting to registration. And we certainly will be looking at what has been done previously and optimizing it based on our program and the data that we're generating in that Phase I. And so we'll certainly be providing additional updates on our regulatory and clinical strategy in the coming months.

In terms of your question about the market research and what we've learned from patients and physicians, I think there's -- what we did learn and I think what's important here is that patients do want to decrease disease burden as well as treatment burden. And so we think it's important to both reduce the frequency of attacks and to do that for long durations of time, supported by infrequent dosing. We think that could be really a game changer for patients with HAE. We really, with 0215, hope to have a product that could allow patients to live differently with HAE. And really, with this infrequent dosing but robust efficacy, we hope to be able to achieve that. And certainly, we have a lot of work to do to get ourselves in the clinic and to establish that profile clinically.

And I'll pause for a moment and see if Andy or Andrew want to add anything to those comments.

Only to say that we will certainly be working with regulators to explore the most expeditious path to approval. Whether that could include an accelerated approval pathway is certainly not clear at the moment.

The only thing I'll add on the market research is it was very clear that patients really want to make sure, first and foremost, that they're controlling their disease. So maintaining a high level of efficacy is very important. And then from there, if you can reduce that burden of treatment up to 3 months, obviously, the further along you could go, the more convincing that is. So I would just say that you need to make sure that you're providing both of those elements to treatment going forward, and that's really what excited the physicians that we talked to about the possibility of 0215 providing both of those benefits.

Yes, great. Your preclinical profile suggests you've got some good ability to balance there.

Your next question comes from the line of Suji Jeong of Jefferies.

Congratulations on all the progress that you guys made. So I have a couple of questions about the clinical development time line for STAR-0215. So you said that in the presentation, since the drug has longer half-life, you are looking to follow the patients for a long period of time. So I was just wondering when you expect to have the full data from Phase I. And when you present the data, the interim data from Phase I by end of next year, what type of data do you plan to present and from how many patients? And I have follow-up questions.

Great. Thank you, Suji. Let me start with that and let Andy finish. So just to reiterate, our clinical development time line, we are on track to file an IND in mid-2022 and initiate the Phase Ia study soon thereafter. We'll have initial results from that Phase Ia in normal healthy volunteers by year-end of next year, so year-end 2022.

You asked what data, that initial data we hope will support the differentiated profile that we believe we have in STAR-0215 in terms of the extended half-life and also demonstrate inhibition of plasma kallikrein with STAR-0215. And you're absolutely right that this is a very long half-life antibody that we expect to see a very long half-life in human. And we will be following those patients from that initial normal healthy volunteer for a long period of time to collect the appropriate safety and pharmacokinetic data. So we'll be following those patients well into 2023.

And with that, I'll hand it to Andy maybe to comment on that. But that initial data will be at year-end 2022 to establish, we hope, that differentiated profile.

Yes. So our expectation is that we will have pharmacokinetic data from at least the first couple of cohorts and pharmacodynamic data from the first couple of cohorts by the end of the year to allow us to not necessarily definitively calculate the half-life, but to be able to say that it is extended and that it has pharmacologically -- has pharmacologic activity to be able to estimate what sort of doses could be pharmacologically effective.

Because of the extended half-life, it is, in fact, in that 70- to 120-day range. We will have to follow the patients for up to a year in order to be able to adequately assess the safety profile during exposure of the product. So it will take an extended period of time before the full data set is available from this initial study. But that does not stop us from actually looking at and making decisions based on the earlier data that we will be collecting.

And you asked about patient numbers. We hope to give an update in the coming months about the details around the Phase I design and, hopefully, more details about the full clinical development program for STAR-0215.

So that update would be sometime early next year?

Yes, we believe in the coming months. We're, as you might imagine, actively working on refining that plan and want to make it available publicly to let folks know what to expect at year-end next year and what to expect going forward with the program.

I see. So how long do you say the half-life was?

Well, the estimate is from other monoclonal antibodies that have the same half-life extension technology, the YTE modifications, they have demonstrated half-lives of the 70- to 120-day range in humans, so an average of about 90 days, 3 months. And you actually have to follow people for multiple half-life after the dosing. So you could imagine if the half-life is 3 months, we would actually have to follow patient -- the volunteers in the Phase I -- initial Phase I study for probably at least 9 months, possibly up to 12 months.

I see. So is your plan to start Phase Ib in 2023 still intact?

So our plan is still intact. We're obviously right now refining our clinical development plan, and that will be a discussion with regulators and also will be informed by the data going into that Phase I and the initial data from that Phase Ia.

Okay. And last question I have is, when should we expect to hear updates on the business development activity?

Yes. So we are actively evaluating opportunities to expand our pipeline in the area of rare and niche allergic and immunological diseases. We hope in the coming months to be able to talk about other opportunities that we intend to explore.

Your next question comes from Laura Chico of Wedbush Securities.

I actually wanted to circle back on the patient burden surveys that you mentioned. You indicated or the data shows that when patients are on preventive therapy, they're still having concerns about effectiveness. And I'm wondering if you could just elaborate a little bit more on why the concern is there. I just -- I'm trying to understand, is this just general disease concern? Or is there something specific about prophylactic therapy's efficacy? And if it is more of the latter, then I'm just kind of curious how 0215 -- or what attributes 0215 might have to demonstrate in clinical studies to kind of avoid those same kind of issues. So any attributes stand out as most important for clinical differentiation.

Yes, let me start and then hand it to Andrew. So that's a great point. And I think these patients generally live with a high level of anxiety and fear about the potential of an attack. I think one thing that we hope for STAR-0215 in the profile that we hope to be able to support clinically for these patients is that by having a potent inhibitor of plasma kallikrein that retains potency through a longer duration of action, so for up to 3 months between doses, we hope to maintain a level of inhibition of plasma kallikrein that prevents attacks from occurring for longer periods of time. So our hope would be that this could be a real benefit for patients and help alleviate some of the anxiety and stress that they live with in their everyday lives in thinking about this disease.

But I'll hand it over to Andrew to add any additional comments.

Sure. And thank you for the question. We're obviously learning a lot in speaking with both physicians as well as with patients. But I think with the advent of preventative treatments, the good news is that many of these treatments do reduce the frequency of attacks, and I think that's encouraging for patients. The challenge here is that they do still experience attacks. And some of those attacks, especially laryngeal attacks, can be life-threatening.

So I think the goal here is to make sure that we can prevent or reduce the frequency of attacks as effectively as we can with STAR-0215, but then in combination with that, reduce that treatment burden by extending the frequency of administration by up to 3 months. So again, I think it's just the anxiety that these patients deal with still being on preventative treatments, knowing that they could still be facing attacks.

Okay. That's super helpful. And maybe just one quick follow-up, and I apologize if this has been asked, but there was some recent competitor Phase II data at a meeting related to antisense therapies. And I think there's certainly been an evolution in the prophylactic space where we now have antibodies and oral agents. But I'm wondering if you can speak a little bit to what you view as probably what modalities are best suited for prophylaxis? And how do you envision the competitive landscape changing with kind of these different modalities advancing?

Do you want me to take that? Oh, go ahead, Jill.

Yes. So I think in -- you're absolutely right, there are multiple different modalities right now in use and more coming. So we have the monoclonal antibodies like STAR-0215. You mentioned, I think, the antisense data that was presented at ACAAI last week, which is yet another different modality coming in, and that showed effective reduction in percent attacks with every 4-week dosing.

What we hope with STAR-0215 is, here, we're using a very trusted modality in the form of a monoclonal antibody. And that profile that we've been able to demonstrate preclinically at this point suggests a profile that's very differentiated from what's currently on the market in terms of the different types of modalities for preventative treatment in HAE as well as what we see in the pipeline of candidates that are in development. And so we think STAR-0215, being a trusted modality in the form of monoclonal antibody with a highly differentiated profile that we believe could support once every 3 months or longer dosing, could really make a significant difference in the preventative therapy landscape.

Your next question comes from Joe Pantginis of H.C. Wainwright.

Jill, I wanted to start on the back end of your prepared comments about the potential pipeline expansion opportunities. If you were to take 0215 forward on your own, would you be looking at assets that could be marketed in the same sales bag? Are you more flexible with regard to the types of opportunities you're looking at with regard to orphan and niche indications?

Yes, thanks for that question. Yes, we certainly will be -- as we consider opportunities for the pipeline, we're going to be opportunistic. We want to stay in a somewhat related space for the reasons that you just suggest. We'd like to optimize the organization that we're building. And so that certainly makes a lot of sense for us. But I will say, if there is a great opportunity in the allergy and immunology space where we think we could make a significant difference for patients, we'll probably work on that.

Yes, that makes sense. And I guess switching to 0215, obviously, you provided a long list of, obviously, all your IND-enabling activities. And I guess I would ask it this way, what do you consider your rate-limiting step at this point? It seems like your CDMO is on board in having a drug ready to go. But I guess, are you experiencing any issues or things you've had to prepare for with regard to the global supply chain constraints?

Yes, that's a great question. So as with everyone, we are making sure that we are well ahead of any potential issues. Right now, we are working as efficiently as we can to get to that IND in mid-2022. We remain on track for that, and that's in large part because of trying to think well ahead and well in advance of any potential issues that could arise. And so just like many other companies in our position in IND-enabling studies and preparing for the clinic is we are doing things very far in advance to try to prevent any issues from cropping up between now and the time that we want to get into the clinic and get to that initial proof-of-concept data.

Got it. Got it. And my last question, if you don't mind, I guess it's truly speculative at this point because you don't have human data and the experiment hasn't been done. So if you were to assume that you were to go forward with once every 3-month dosing, one would assume, at least in the field with the current therapies, there are certain rates that you might be projecting for breakthrough attacks. And do you anticipate that those breakthrough attacks rates would increase as you get closer to the next dose?

That's a good question and something that is certainly on our mind as we develop the target product profile and refine it for STAR-0215 because what we want to be able to do is to support every 3 months dosing or longer, but to base that dosing frequency on the ability to reduce the occurrence of attacks to the greatest level possible. So you're absolutely right, this will be informed by the data in patients.

And so our hope is that we can optimize the dose and the dosing frequency to minimize the occurrence of breakthrough attacks. And so that's something that's going to be right out front as we design those clinical studies in patients and as we look at the data to design what we think the go-forward dosing frequency is. But that's spot on what we're going to be thinking about.

There are no further questions at this time. I would like to hand the conference back to Jill for any closing remarks.

Great. Thank you. Thank you all for joining our call this morning and for your continued support of Astria. We'll keep you updated as we execute on our STAR-0215 program and share other areas of progress at the company. We look forward to speaking with you again soon. Andrea?

That concludes today's call. A webcast replay will be available for 90 days via the Investor Relations page on our website at www.astriatx.com. Thank you.