Protagonist Therapeutics, Inc. (PTGX) Earnings Call Transcript & Summary

Okay. Hello, and welcome back to the 39th Annual JPMorgan Healthcare Conference. My name is Matthew Bannon. I'm one of the biotech analysts here at JPMorgan. I'm happy to announce our next company presenting, Protagonist Therapeutics. And on behalf of Protagonist is CEO Dinesh Patel. Dinesh, the floor is yours.

Thanks, Matt, for the kind intro. It's a real pleasure to participate in the first virtual JPMorgan Healthcare Conference. As a reminder, on Slide 2, we are a publicly traded company, and today's presentation will include forward-looking statements. Let's go to Slide #3. Protagonist is focused exclusively on peptide therapeutics. We have a highly innovative platform. And admittedly, the schematic below does look complex, but that is how technologies are. So just look at it like a toolbox with very unique and diverse set of discovery goals, and this toolbox has enabled us to conduct de novo discovery against a wide range of diverse biological targets. The true validation, of course, comes from about half a dozen clinical development candidates discovered to date utilizing the platform. Slide #4 is our clinical development pipeline and time line slide. And what you will quickly appreciate is that we have multiple shots on growth. Numerous candidates in different stages of clinical development in multiple indications. Also, we have very good cash runway through the first half of 2024, which is more than enough to drive all of these studies to satisfactory conclusions. Today, we are also providing specific guidance on 8 different objectives for the year 2021. So our clinical programs, they fall in 2 broad categories of diseases. The first is hematology and blood disorders. And here, our principal asset is hepcidin mimetic 300, currently being evaluated in 2 different indications. The first indication is polycythemia vera where we have an ongoing Phase II study. So this is our crown jewel, and this is where we reported transformative data last year. We remain on schedule to complete the enrollment by midyear and intend to provide data updates at major medical conferences throughout the year. Based on the very strong and convincing data on hand, we plan to meet with regulatory authorities in the first half of the year and finalize a registrational clinical plan. The second indication is hereditary hemochromatosis. An open-label study is in progress, and we should be able to share our preliminary findings from this study sometime this year. 300 is a subcutaneously administered drug. So we are also working on next-generation [ oral ] hepcidin mimetics. Preclinical proof-of-concept data was presented at the December ASH Conference, and we plan to nominate a development candidate sometime this year. The second category of programs is targeted at inflammatory and immunomodulatory diseases. Here, we are developing orally stable peptides that work through intervening those biological pathways that have already been validated by injectable antibody drugs on the market, thereby derisking the biology but yet offering a strong differentiation. One such validated mechanism is the interleukin-23 pathway. And an exemplary drug here is the IL-12/23 antibody drug Stelara from Janssen Pharmaceuticals. So not surprisingly, we have a strong partnership with Janssen for over 3.5 years now, and our objective is to extend and strengthen the $6.5 billion Stelara franchise. It has been a highly productive collaboration with several candidates that could provide multiple clinical as well as strategic options for numerous indications down the road. Our final and fully owned asset is an oral, gut-restricted alpha-4-beta-7 integrin antagonist PN-943. This is the most safe, specific and validated biological target for inflammatory bowel diseases. PN-943 is currently in a 150-patient Phase II ulcerative colitis study, and we expect to complete this global study in 2022. So now let us begin by focusing on the most advanced asset and the most promising indication in our pipeline, that is PTG-300 for polycythemia vera. We will talk about the disease, we will highlight the unmet need, offer a mechanistic rationale for a hepcidin mimetic and outline the next steps, including the preparation for a registrational study. So now we are on Slide 5. Polycythemia vera is a disease of excessive erythrocytosis, which means excessive production of red blood cells, and that is why it is commonly also referred to as the thick blood disease. While classified as a rare disease, there are about 100,000 diagnosed patients in the U.S. alone. The disease occurs most commonly in elderly population, and it is a long-lasting chronic condition with a survival lifespan of around 20 years. There are significant thrombotic and cardiovascular risks for these patients. Hematocrit is the percentage of volume of red blood cells in the total blood volume, and the standard treatment goal in PV is to control and maintain hematocrit levels below 45%. First and foremost, as shown on Slide 6, it was very critical for us to understand the current treatment regimen, evaluate its true effectiveness and identify specific areas of unmet need. So we undertook a retrospective analysis of real-world patient data using the Symphony database, which is one of the most comprehensive sources of healthcare data in our industry. We focused on patients with confirmed PV diagnosis who received treatment over a 2-year time period. This inclusion criteria gave us a patient count of over 28,000 patients. Further, we obtained hematocrit measurements from blood test results for a subgroup of over 4,000 patients. And here are our 3 key findings: in terms of treatment patterns, the disease is predominantly managed by phlebotomy or hydroxyurea or a combination of both, similar to the literature data. None of this is ideal. As you can imagine, patients undergoing phlebotomy or bloodletting are burdened with numerous quality-of-life issues and hematocrit control will be erratic at best. Also by removing blood, you're not just removing RBCs, but also removing the iron, which can often lead to iron deficiency symptom burden in these patients. Hydroxyurea is a generic anticancer agent, which is not even formally approved by the FDA for PV. Finally, while not reflected in this analysis, we know that kinase inhibitor Jakafi is approved for hydroxyurea-resistant and intolerant patients and finds utility in very late-stage disease patients, which is a small fraction of the total population. So the current treatment regimen offers very few choices and now let us see its effectiveness in controlling hematocrit. This is where the results are actually very alarming and disturbing. While hematocrit below 45% is the main treatment objective, such control was not achieved in a majority of patients. In fact, only 22% of the patients had consistent hematocrit control below 45% in this data set. Even worse, half the patients had at least one measurement over 50%. Finally, while minimizing thrombotic events is the ultimate purpose of therapy, 8% to 40% of PV patients in this data set had at least one thrombotic event during their treatment. Overall, these numbers may be hinting at the ineffectiveness of current treatments and serious consequences of uncontrolled hematocrit. And the best example in that regard is from the literature shown on the next slide, #7. In this CYTO-PV study, patients were divided in 2 groups, a low hematocrit group with levels below 45% and a high hematocrit group between 45% to 50% range. Primary endpoint was time until death from cardiovascular or major thrombotic events. After 31 months, about 10% of the high hematocrit group unfortunately met this endpoint in comparison to 2.7% in the low group. In other words, high hemato group -- high hematocrit group was 4x more likely to die from cardiovascular or major thrombotic events. So the retrospective analysis and the literature data then basically leads us to 4 conclusions: current treatment options are very limited; hematocrit is not controlled adequately in a majority of patients; not controlling hematocrit poses significant thrombotic and mortality risk, and therefore, a new therapeutic agent is needed to address such unmet need. On slide 8, we offer a rationale for our hepcidin mimetic as a potential new therapeutic agent for PV. Hepcidin is a natural hormone and a master regulator of iron homeostasis and erythrocytosis in our body and it exerts its function primarily by blocking ferroportin, the major exporter of iron from intracellular stores in the body to the blood compartment. Shown on left, PV is characterized by excessive red blood cell production caused by the JAK2 mutation but requiring abnormal amounts of iron to fulfill this excessive demand for hemoglobin synthesis. Low hepcidin levels could be one venue facilitating this excessive iron transport from macrophages to bone marrow. Using our platform, we discovered PTG-300 as a mimetic with superior drug-like properties in comparison to hepcidin. Shown in the right graphic, 300 can downregulate ferroportin and normalize RBC production by controlling the supply of iron from the macrophages and other stores to the bone marrow. So such an intervention with a hepcidin mimetic can lead to a well-controlled and normalized RBC production in PV patients. So now let's go to the clinical study. Slide 9 is the schematic of the Phase II study designed with 300. This is a 3-part study. Part 1 is dose-finding phase, where patients are dosed on a weekly basis, starting at 20 mg and going up to 80 mg as needed to keep the hematocrit below 45%. Once the effective dose is identified, patients remain around that dose level for a total of 28 weeks, after which they enter the blinded withdrawal phase. And after completing that, they are offered an open-label extension. All patients with frequent phlebotomies, that is 3 or more phlebotomies in the past 6 months and with or without concurrent cytoreductive therapies were eligible for the study. As of November 18 of last year, 18 patients were dosed with a treatment duration ranging from 5 weeks to over a year, and the data is shown on the next slides. So Slide 10 is our money slide. As they say, a picture is worth more than a thousand words, and this slide is a good example of that. Our strong bottom line statement over here is that 300 essentially eliminates the need for phlebotomy in these patients. To grasp that, all you have to do is look at the red dots. Each red dot represents a phlebotomy event. Prior to treatment with 300, these 18 patients had very frequent and irregular phlebotomies. In contrast to that, in 6 months during treatment, phlebotomy is, by and large, eliminated in these patients. So this is a night and day difference in phlebotomy requirements before and after treatment. The 18 patients are a good representation of the broader PV population and represent the breadth of diversity, high versus low risk category and offer a good sampling of real-life concurrent treatment regimens with cytoreductive agents like hydroxyurea and interferon. On Slide 11, as you can see, hematocrit is decreased and maintained constantly under 45% for these patients, thereby achieving the key treatment guideline and objective. Now there are variations during the initial dose titration phase, but once the right dose range is established for each patient, the numbers become tighter. The same pattern is observed with red blood cell counts, that is the drug treatment controls the otherwise excessive production of RBCs in these patients. On Slide 10, we show that in addition to controlling hematocrit and RBC production, 300 rapidly normalizes iron stores, as indicated by a fact of ferritin levels. These patients are in an iron deficiency ferritin range at baseline and rapidly go towards normal levels upon treatment. Note that phlebotomy treatment can often lead to iron deficiency. So this reversal of iron deficiency could be a specific advantage of 300. Now let us look at the effect on markers of red blood size and hemoglobin content, that is MCV and MCH. As expected, with 300 treatment, as iron stores increase, the red blood cells are enlarging and are getting closer to normal size. Similarly, hemoglobin content is also increasing. So in essence, the drug treatment seems to be causing the desired shift from smaller microcytic RBCs to normal healthy red blood cells. We also analyzed MPN-related symptoms, such as concentration, fatigue and itching, and that is shown on Slide #13. The results of the preliminary are encouraging and seem to suggest that 300 treatment could be decreasing this iron deficiency-related symptoms in these patients. Now on Slide 14, we summarize the adverse events, and the drug appears to be very well tolerated. More than 90% patients just had grade 1 events. Injection site reaction was observed in 3 patients, but it was transient and the patients continued treatment. No SAEs were observed, and no subject stopped treatment due to an adverse event. So in summary, on Slide 15, 300 offers great promise in managing hematocrit, drastically reducing phlebotomy requirements and reversing iron deficiency. The drug appears well tolerated and offers great potential as the first non-cytoreductive natural hormone mimetic-based therapy for PV. We should complete enrollment in the ongoing Phase II study by midyear, and we plan to provide updates throughout the year at medical conferences. The drug has received orphan and fast track designations, and we will discuss the registrational path forward with the regulatory agencies in the next few months. So that concludes our overview of 300 and PV, and now let us go to Slide 16 and talk about the second indication, hereditary hemochromatosis. So HH is an iron overload disease, and it affects over 1 million people between U.S. and Canada. Phlebotomy is the only therapeutic option for these patients, and there are no drugs that are approved for HH. Excessive iron accumulation in key organs like liver and heart is a major concern. And if left untreated, this can eventually lead to more serious conditions. The genesis of the disease is mutations leading to absence or deficiency of hepcidin in the body, and that provides a good rationale for a mimetic like 300. We have a small, open-label proof-of-concept study ongoing. The key measurements are effects on phlebotomy rates, iron parameters like TSAT and ferritin and liver iron content. We should be able to share some of our findings from this study this year. So this finishes our overview of PTG-300. As you can tell, it is a one-product portfolio play. PV and HH are the first 2 indications, and we have every intention of identifying additional new indications based on the rationale of erythrocytosis, iron imbalance and the need for phlebotomies. Now let us briefly talk about our oral peptides in the inflammatory and immunomodulatory disease space. Slide 18 summarizes our first program, the IL-23 receptor antagonist program, which is being pursued in partnership with Janssen Pharmaceuticals. The core objective is to strengthen and extend the $6.5 billion Stelara franchise and to provide the much-needed and timely transition from injectable antibody to oral targeted therapy in various chronic indications. The partnership was initiated 3.5 years ago with a $50 million upfront and an additional $30 million have been earned so far from achievement of various milestones. It's a very lucrative billion-dollar deal with up to double-digit royalties and U.S. co-detailing rights. It is also a very productive collaboration with a portfolio of 3 candidates in different stages of clinical development and an ongoing research collaboration. The multiple products should provide numerous strategic and clinical development options, both for IBD and also for non-IBD indications. Slide 19 summarizes our other program in the immunomodulatory space. PN-943 is an oral, gut-restricted alpha-4-beta-7 integrin specific antagonist, and it is an unpartnered asset, fully owned by us. This integrin is the most safe and specific target for IBD and the exemplary drug here is the injectable antibody ENTYVIO from Takeda. We generated $3 billion in sales in 2019. In a head-to-head comparison study, ENTYVIO was shown not only to be safe but also superior in efficacy to Humira, the largest selling drug in recent years. 943 offers the potential for a first-in-class gut-restricted integrin blocker. This is our second-generation drug, and it is threefold more potent than the previous drug 100, through which we have validated the gut-restricted approach through a Phase II study in ulcerative colitis patients. 943 is currently in a global 150-patient Phase II study with completion anticipated in 2022. So this completes the R&D overview of our pipeline. Now let me -- allow me to highlight on Slide 20 that we have an outstanding team with very great breadth of experience and track record, and as they rightfully say, you are only as good as your team is. Slide 21 summarizes the financials. Long story short, we have a very good balance sheet with cash runway for the next 3.5 years. So now I would like to conclude the presentation with Slide 22 and with the following 3 specific remarks. First, we believe that our hepcidin mimetic 300 shows great promise for addressing a very large unmet need in polycythemia vera and to be able to seize a great commercial opportunity. Based on the outstanding clinical data that has been generated so far, we remain very optimistic about the potential clinical and regulatory success in the future. Finally, this is an orphan drug for a rare disease, which encourages us to envision independent commercial development with a small focused effort. Second, we have a diversified portfolio of products, which should come to fruition at different times in 2021 and 2022. We also have strong IP and a robust technology platform, which will continue to deliver new innovative products in the future. Third and final, we have great financial and human resources and bandwidth that should enable us to execute on all important value drivers, including completion of not just the studies listed here, but also initiating and completing a Phase III registrational study with PTG-300 in polycythemia vera. With cash runway to mid-2024, we are blessed to be able to take multiple shots on the ultimate goal of addressing unmet medical needs and returning great value to shareholders. Thank you for your attention.

Great. Thank you so much for that, Dinesh. We'll move into the Q&A session now. So maybe just to kick things off, you can introduce who from the team is on with you today, and then we can get into it.

Excellent. So we have our senior team, Samuel Saks is our Chief Medical Officer and much more than that, a very experienced drug developer and strategist; Tracy Woody heads up our commercial efforts, she has a ton of experience in that category; David Liu is our CSO and Head of R&D; Suneel Gupta, our Chief Development Officer; and last but not least, Don Kalkofen, our Chief Financial Officer.

Awesome. Welcome, everybody. And just a quick reminder for those on the webcast that you are encouraged to submit questions through the Q&A portal, and I will ask those on your behalf anonymously. We've got a few in the queue now, which we'll walk through, and then we can move down our list. So first off, the question is, do you expect to be able to file, this is for PTG-300 in PV, on hematocrit control alone or will you need to show benefit on other clinically relevant endpoints as well?

Sam, you want to take that?

Sure. I would just say that the backbone of any endpoint for approval will be the control of hematocrit below 45. That's what's in all the guidelines and all the textbooks, and that's what's been used with other products. But exactly what else could be in the endpoints, both primary and secondary, will be detailed after we have the regulatory dialogue that we're about to have in the first half of this year under the expedited treatment with the fast track and the orphan drug status.

Got it. Okay. And then the second question relates to cash runway and the PV trial and one of the questions that we had actually, the runway guidance into mid-2024, what exactly does that include? And does that specifically include the Phase III PV study?

Yes, the short answer is that while we don't have clarity on the Phase III study design, it will become clear once the regulatory dialogue is completed. But at the end of the day, this is orphan drug development. PV is a rare disease. So within the confines of that, we feel very confident that we should be able to not just initiate the registrational study but also complete it and march towards and even beyond the NDA filing, including even some -- initiating some efforts early on in the prelaunch kind of commercialization kind of activities.

Yes. I remember you guys had the presentation in September about the PV opportunity. And maybe we can talk about that a little bit actually. I guess from the work that you've done so far, maybe you can ballpark the size of an initial sales force needed for a launch in the U.S.?

Yes. And we have Tracy Woody with us. So I would ask Tracy to highlight our conclusions about the market opportunity and what are some of the efforts we should be undertaking.

Yes. So the great thing about this market, obviously, it's a very concentrated market with a concentrated group of physicians that are prescribing these products. About 11,000 is our estimate. While we haven't done a sales force sizing project, just with that estimate, you would think somewhere between 75 to 150 would be appropriate sizing. Well, we haven't done the formal sizing, but again, very focused, concentrated group of prescribers.

Okay. Got it. And then for the target population, obviously, there's going to be some low-risk and high-risk patients who fit the description. So maybe you can talk about the different opportunities as they're stratified kind of by risk status?

Go ahead, Tracy.

Yes. So just touching on the data that Dinesh presented, if you think about the 100,000 patients, in our study, about 70% of those were characterized as high-risk patients. So that's about what we'd probably most likely see in the market. Again, what the data -- the clinical development data shows is that we are going to be used in frequent phlebotomy and for those who can't get their hematocrit under control. What we saw in the Symphony data from a high level is about 70% of those patients did not have hematocrit under control. And I think what you'll see in 2021 is us begin to segment that market in more detail, to determine exactly which ones are appropriate for 300. And again, as the clinical work comes in, we'll look at that 70,000 pool and give you more input on that.

I mean our general look over here is that, look, there are already 100,000-or-so diagnosed patients in the U.S. alone, almost an equal number in Europe, and Tracy pulled out some data, which suggests that you are adding, unfortunately, 10,000 to 15,000 patients each year in the U.S., right? So these are big numbers and population sizes for a rare disease. And that is where I think we are focused right now. Now the question becomes what will be most appealing for PTG-300? So knowing the data that we have in hand, I think one statement, which is very simple and very accurate is like, "Hey, if your current treatment regimen is not working adequately and the best signal for that is if you are requiring too many phlebotomies, then that is where PTG-300 will come into play." So we'll be the first one to admit that if you look at the disease spectrum, in the very initial phase, if the business is controlled by a few phlebotomies, then hats off to you. That's how you should continue. Similarly, at the very, very late-stage when the disease is kind of moving towards myelofibrosis and other complications, that is where I think -- that is the space for Jakafi. And you know that Jakafi basically reported they have treated 5,300 patients, for example, last year. That sort of thing. But anything in between basically belongs to 300 theoretically. The other thing to -- that is very important, and Sam often points this out, is like this is a very nontypical hematological indication, right? The disease lasts for 20 years or so. So that is going to be a long treatment period for which 300 could be used effectively.

Any sort of initial work on the potential duration of therapy?

Suneel, do you want to comment on that?

The duration of therapy could be several years, at least, because we think it's going to be 5 to 10 years. Jakafi is, what we call, more of a late-stage disease. And most people with the PV, it would be as high as 10, 15 years before they get to Jakafi. So there's going to be several years. But it depends upon how much they're progressing, what their allele burdens are, where their phlebotomy burden is and other symptoms.

And we already have patients in the current study who have been treated for more than a year. And Suneel, remind me what is the open-label extension duration? I believe it's one full year, right?

Yes. Minimum one full year of medicine.

Okay. I've got some questions on PN-943, but first one more on 300. Do you guys plan to file for breakthrough designation for PV? Is that something that's been disclosed or you're willing to disclose?

We're operating under the fast track currently, and we've guided that we're having the kind of iterative expedited discussions that it allows in the first half of this year. So you can assume that, again, it's imminent.

Got it. Okay. Switching gears a bit then to PN-943. A couple of questions here. So what is the methodology by which you measured the receptor occupancy? Second question is for PN-943. How tightly is the correlation between receptor occupancy and efficacy?

Yes, certainly. So these are 2 very important questions. And I will have David Liu, our CSO, attend to this question. Go ahead, David.

Yes. The methodology for measuring receptor occupancy in the blood has been published by Takeda when they used it eventually for vedolizumab development. So it's a facts-based analysis, fluorescence sorting-based analysis.

And the second component about the -- what is the correlation? So I mean it's a great question. And in a way, I want to elaborate a bit on that. Ours is an oral gut-restricted drug. So meaning very little presence in the blood compartment at any given time. So in theory, when you talk of receptor occupancy, we are talking about blood receptor occupancy. So we didn't know what blood receptor occupancy percentage to expect. But making the long story short, with our previous drug where we did extensive preclinical studies, Phase I studies, including receptor occupancy and then ultimately, Phase II positive data where we got clinical remission rates similar to ENTYVIO and 44% histological remission data. So that convinces us that the drug works. But now if we backtrack to, like, "Hey, what was the receptor occupancy in the blood at -- in healthy volunteers," the magic number is 74%. So for us, our rule book is as long as we see 74% receptor occupancy in healthy volunteers, we feel confident about the eventual effectiveness of the drug to perform in Phase II. Now PN-943, the second generation drug. The reason we are so excited about it is like it is at least threefold more potent than the previous drug. Meaning whatever the previous drug did at 900 mg dose to get to that 74% receptor occupancy, 943 does that at 1/3 the dose, at 300-milligram dose. And in fact, if we go to 900 mg, we got near saturation, 95-plus percent receptor occupancy. So that is what we would say. Now at the same time, though, if your drug is systemically biovailable or it's an injectable or things like that, the rules are open-ended. Because, as you know, more recently, the Genentech antibody drug, alpha-4-alpha-E-beta-7 integrin blocker, there was no scarcity of achieving 100% RO. But still, at the end of the day, the drug is not moving forward.

As a reminder, there's 5 minutes left for anyone else who wants to send me the question. Another one on 943, is this an asset that you would be willing to partner or is this one that you are hoping to take the full line yourself?

Another fantastic question. Let me answer by saying that if Protagonist have an opportunity to do a partnership before we started the Phase II study, the answer is yes. And of course, what we opted for is like, no, we want to do this study on our own. And the reason for that is the high level of confidence that we have in 943, its superior potency versus the previous drug where we demonstrated efficacy. And if you look at the historical transactions, there is so much value-add after this Phase II study is done and assuming that the data is positive. So basically, it is that -- right now, we are focused on this robust 150-patient study. Suneel and his team are very busy managing different sites globally in multiple countries. And we believe we'll be able to complete the study sometime next year and then the data will speak for itself and make it loud and clear what are the right kind of strategies at that stage.

Great. I don't see any more questions coming in, but actually, I have one more. Tracy, you mentioned presenting some Symphony [ Health ] data potentially in 2021. And you presented a handful of that at ASH. And so we were just wondering what kind of feedback you got from the conference. If they provided any sort of metrics on how many people attended and whatnot, we think that would be helpful.

I wouldn't be specific on metric in terms of the attendance, but we've received quite a bit of feedback on the ASH abstract from KOLs. And I think people are -- have been quite surprised with the unmet need in the space, just how many patients were at thrombotic risk because of not being controlled at hematocrit. And then the further work, we'll explore that further as we look into 2021, what are some other health economics type of work we'll do this year using that database and looking deeper into the implications, both from a clinical perspective, but also from an economic perspective.

And I can add on -- I mean, this is a very indirect statement. But last year, in May, we had 7 patients. By November 18, we had 18 patients. And then by early December, we had 24 patients enroll. And now we are stating that, "Hey, by midyear, we will finish enrollment of 50 patients." So clearly, the KOL buzz is there and people are speaking very positively about this. The awareness is clearly expanding and building, and that basically is another way you can look at that.

Got it. And there actually was one more question submitted. And it is how do you think PN-943 matches up to other alpha-4-beta-7 inhibitors, like the oral ones, like the second-gen AJM molecule or MORF-057?

Yes. So I think, in a way 943 is not just alpha-4-beta-7 integrin specific. It is not just oral. It is gut-restricted, which is very different from the other overall approaches where there is actual systemic bioavailability. What we have in hand is that with the previous drug, which was also gut-restricted, we already have positive Phase II data, meaning clinical remission, histologic remission, that sort of thing. So the statement we would make is like we feel very validated and very confident about the gut-restricted alpha-4-beta-7 integrin. We are the most advanced. Our path is validated, and we are going full speed ahead with 943.

We're doing a very robust clinical study that shows our confidence. A lot of people in the IBD space do these small proof-of-concept studies, they're not very valuable. You really need to treat a significant number of patients to know what you have.

And last but not least, we are doing it on our own time. And we decided not to opt for a potential partnership before the study.

Awesome. Well, thanks so much, guys. This is really super helpful and informative. Thank you, everyone, for dialing in or linking in. We hope you all have a great rest of your virtual JPMorgan Healthcare Conference.

Excellent. It has been a real pleasure. Thank you.

Thank you.

Stay safe, everyone. Bye-bye.