Great. Good afternoon, everyone. My name's Jessica Fye. I'm a large cap biotech analyst at JP Morgan, and we are delighted to be continuing the conference today with BioCryst. A little bit different format this year from years past. We're gonna stay in this room for Q&A. If you have a question at the end of the presentation, just raise your hand, somebody will bring you a mic, or you can submit them electronically as well. With that out of the way, let me turn it over to BioCryst CEO, Jon Stonehouse. Good afternoon. Thank you, Jess, for inviting us to this year's conference. I was telling her before I got up here, I honestly can admit that I'm happy to be live in San Francisco. I didn't think I'd get to that point during COVID, but good to be here. I'm gonna be making some forward-looking statements. Those statements have risks. The risk factors can be found in our most recent filings, found in our website, listed at the bottom of slide 2. How do we create value at BioCryst? We do it by bringing oral drugs to patients that suffer from rare disease. Why is that important? It's important because not only are patients looking for reduction in the burden of their disease to have control or have a drug that works, but if you're able to give them a reduction in the burden of therapy by not injecting themselves, not having an infusion, but giving them a capsule or a tablet, you have the potential to change their life. That's the value that we're creating at BioCryst. We're creating that value today in the marketplace with our first oral drug, ORLADEYO. It's a kallikrein inhibitor, and it's the first and only oral prophylactic for a rare disease called hereditary angioedema. If you're looking for reduction in the burden of therapy, I don't think you can get much better than once-a-day oral therapy. Does the drug work? Because nobody's gonna take the drug because it's convenient if the drug doesn't work. If you look at the data from our clinical trials, APEX-2 and the long-term extension up to 96 weeks, we see an 86% reduction in the baseline attack rate, so that's real control. 16 out of the last 17 months of treatment, the median attack rate was zero per month. Again, very good control in our clinical trials. Then in the real world, you know, we've been on the market now for two years and what are we seeing in the marketplace in terms of control? This is data we presented at the college meeting in November. These are switches. This is a switch market. It's a mature market. You see patients switching from prophylactic therapy. The therapies are listed in the graphic on the left. You see over the course of a little more than a year, the reduction in their attack rate. Again, there's control. The median attack rate over the little over a year is less than a half an attack per month. Again, control. ORLADEYO doesn't work in everybody, but it works in many. When it works, it works very, very well. No drug's perfect. The most frequent adverse events with ORLADEYO are GI related. You can see in the table on slide 7, the types of GI adverse events and the dose most frequently prescribed in the marketplace is 150 mg once a day. You can see the percentages that we saw in the clinical trial on the right-hand side of this table. The good news is that these GI adverse events tend to go away in a month or two. This is data from our pivotal studies, and you can see that after the first or second month, that it gets down to close to what you're seeing with placebo. Let me talk a little bit about the marketplace, and let me describe the U.S. marketplace for you first. There's 7,500 treated and diagnosed patients in the United States. About 70% of them are on prophylactic therapy, and the other 30% are on acute. As I said earlier, there's been eight drugs in the last 13 years that have been brought to this population, and a lot of them work really well, but most of them are injectable. You know, the opportunity for BioCryst to get patients onto ORLADEYO is they have to switch from what they're currently on. That's no small task, but we've been pretty successful to date. You can see, since the start of launch all the way through to October of last year, that a little more than half are coming from prophylactic therapy, and the other half are coming from, on-demand therapy. You can see the breakdown of what drugs they're coming off of, TAKHZYRO being the one that's most frequent. On the graphic on the right, we pulse the market on a quarterly basis and get a sense of what is the physician's perspective on prescribing today and what do they plan to prescribe in the future. We do a robust job of surveying physicians. This is a survey from September of last year, 60 allergist immunologists that have on average about seven to 10 patients in their practice. You can see in the current prescribing, what percentage of their patients are allocated to ORLADEYO. More importantly, we ask them, "What do you see as you're prescribing in the future?" You can see that it's increasing. This has been consistent with every quarter that we've pulsed this survey, and it's very encouraging for additional prescribing in the future. What kind of value are we creating with ORLADEYO? We're pretty proud of this. I think by any measure, this has been an exceptional launch. We believe it's on a path to $1 billion. The first year, we sold $122 million, first full year of launch. This year, we more than doubled that with $251.6 million, and we're a quarter of the way to our path to $1 billion. We've given guidance now that no less than $320 million this year, so almost a third of the way in the third year. We think we're well on our way and on our path to $1 billion. The math is pretty straightforward. You don't need crazy market share, like 50%, 60% of a market in order to get to the $1 billion. You can see 25%-30% in the U.S. gives us about $800 million at peak. The last thing that I think is really important is you can choose... You can draw a line through the three data points we have on this slide and decide where you believe we'll get to a $1 billion, at our peak. We have a composition of matter patent protection out to 2039. It's not like we're gonna have a couple years of peak sales, we're gonna have many years of peak sales, and that's real value creation. Just one last note before I leave ORLADEYO, and that's around guidance. Let me say this very succinctly and clearly. The only people with the data are BioCryst. We have a sole-source specialty pharmacy, so the normal channels of getting information about prescribing are not accurate. We have the data, what we've been trying to do is be accurate with guiding. You saw in 2021 and 2022, we start out with saying no less than, 'cause these are numbers that we're confident in. We put a greater than or equal to sign because if things go a certain way over the course of the year, it could be adjusted upward. You see the results of what we delivered at the end of each year. Again, we're very accurate. When we say no less than 320, what you should put in your model is $320 million for this year. What's next? What if we were able to replicate what we've done with ORLADEYO and HAE in another rare disease or multiple rare diseases? What if we had a platform, a discovery platform, that allowed us to make more oral drugs for patients suffering from rare disease? We believe we can, and we believe that can create significant value. Our platform is structure-based drug design. This has been around for decades. Many companies do it. What's unique about what we do at BioCryst is where we apply it. We go after validated targets, but targets that, in order to get an oral drug for a rare disease, come from large families like proteases. It's not just good enough to have a potent inhibitor, you've got to have a selective inhibitor. Then, of course, to make it oral, it has to be bioavailable. Doing all three of those is hard. Let's start with potency. In order to get a potent binder using structure-based drug design, you need to know the physical shape, so the pockets, the flat spots, the turns in the enzyme active site. You need to know the electrostatic charge. If it's a negative charge in one spot in the active site, you need to have a positive charge on the molecule to bind more tightly. Then you build it atom by atom, chemical segment by chemical segment, to fit tightly into the space to create a potent molecule. Wouldn't it be nice if the protein stayed the same shape when you put the inhibitor in it? It doesn't. It has a conformational change. One of the things that we've gotten really good at to deal with the conformational change in the protein shape is we do something called co-crystallization. What we're able to do is take the protein target and the molecule inside it and get the crystal structure and understand if any of the spots became less tight binding or other areas where we could make it an even tighter binding molecule. This is an important part of getting to a potent inhibitor. Selectivity is the next piece, and as I said, we go after targets that are more challenging 'cause they come from big families like proteases. There's more than 300 in the human genome, and many or most of them are serine proteases. They're similar in shape and function. What is the trick to do is to get it to bind to the target you're going after, but not bind to something closely related in the family. What we've gotten good at is understanding the shape and charge of the other closely related family members, and we can specifically get it to bind to the target, but not the family member. In the case of serine proteases in HAE, plasma kallikrein is the target. You want it to bind tightly to that, but you don't want it to bind to tissue kallikrein, for example. Over the 30 years that we've been working at BioCryst, we've built a really large database of other related serine proteases and understand the shapes to be able to be selective and specific to the target we're going after. Last but not least, probably the hardest part of this is oral bioavailability. The reason it's hard is because the things that make a molecule potent and selective are the things that make it difficult to cross the gut and get into the bloodstream. Things like electrostatic charge and size and shape, make a drug potent and specific, but could get it stuck and not get it across, the GI tract and get it into the bloodstream. Again, our scientists, you know, over 30 years, have done a fantastic job of understanding the balances of getting a potent molecule, a selective molecule, and having a molecule that can cross the gut as well. The balance of all three. The last piece is have a long half-life. Right? It's super important that not only is it oral, but that we can strive towards getting it to once a day like we've done with ORLADEYO. This is what we're good at. This is something we've perfected over the past 30 years. I think it's something that's unique to being able to bring oral drugs forward for rare disease. The tools have improved as well in structure-based drug design, robust screening systems, databases that have all of the protein crystal structures, and then virtual reality to give you a better view of the three-dimensional shape of an enzyme active site. We have access to all of these, so do others, but if you have the tools and you don't have the skills, you can only get so far. If you have the skills and you don't have the tools, you can only get so far. We have both, and we take advantage of both. Where are we applying this platform to get to the next oral drug for a rare disease or the next oral drugs for rare disease? That's the complement system. Why are we going after the complement system? 'Cause it's rich with protein targets, and if you block one target in a pathway, you have the potential to affect multiple rare diseases. That's what makes it really interesting. The function of the complement system is to fight off infection and be kind of a clearing house for damaged cells and tissues. There are three pathways, the classical pathway, lectin pathway, and alternative pathway. When it's working, it removes... It'll tag pathogens and damaged cells and tissues, and macrophage will come in and gobble it up. It activates or triggers inflammation by activating immune cells and then membrane attack complexes can get attached to pathogens and damaged cells and tissues and cause it to have poke holes in it. Ultimately, these pathogens and cells break apart and lyse. That's when it's working. When it's not working, and it's dysregulated, it can create a number of rare disease problems in a number of different systems in the body; rare neurologic diseases, blood and immune diseases, kidney diseases, skin, and others. We're going after the alternative pathway first, and you can see on the graphic on the right, the diseases that are associated with dysregulation of the alternative pathway. The target that we're going after is Factor D. I'll go over the data here in a minute, but we think we have potentially a best-in-class molecule. We're also interested in other pathways in the complement system, the lectin and classical pathway. We've come up, and you can see the diseases, distinctly different diseases that we can go after for treating rare disease patients. The target where we now have potent and selective molecules that are going into lead optimization in our discovery program are targeted to C2. The binding affinity that we have to C2 is when C2 binds with C4 at the convergence of the two pathways, the lectin and classical pathways. We think not only does this give us an opportunity to go after a bunch of other diseases other than the alternative pathway, but it could be used in a disease like IgAN or PMN or lupus nephritis, diseases where two pathways affect the disease. We could combine our Factor D inhibitor and a C2 inhibitor, put it in one molecule and possibly be able to treat more patients. We're really excited about advancing more targets in the complement system. Let's talk a little bit about the data that we announced yesterday with 10013. We're still in a SAD MAD healthy volunteer study, but you can see from the slide, this is slide 30, that when you give a 110 milligram dose, you drop suppression of the activation of the alternative pathway, and it stays at zero basically through 24 hours on a single 110 milligram dose. The graphic on the right shows that there's, on average, at 110 mg at 24 hours, suppression of almost 98% of the alternative pathway. We don't think that's the dose yet, but we think that this profile supports once daily dosing, which could make it a best-in-class molecule. Far, from a safety and tolerability profile, slide 31 shows the treatment adverse events and any of the other tolerability safety summary data. It's still blinded, but what you see is there's no serious adverse events. There's no grade 3, 4 adverse events. The most common adverse events in grade 1 and 2 are things like headache that you typically see in a phase I study. So far, we haven't seen any clinical abnormalities. So far so good. Early still, but looking good so far. Our goal is to wrap up the SAD MAD by the middle of the year and start a patient study in PNH to do dose ranging. From that, the data from those two programs, make a decision on what we believe is the best dose at the end of this year so that we can go into a pivotal study in IgAN in 2024. You know, as rare disease programs go, this is pretty fast, and we're really excited about where we're at with BCX10013. Lastly, in terms of cash, we're in a really solid position. We have, at the end of third quarter of last year, $463 million on our balance sheet. I told you we're expecting $320 million in net revenue this year. If you take out the interest on the debt that we have, the net cash use is going down because the revenue is going up and the cash is not going up as fast. That puts us in a really solid position, especially as we continue to move towards the $1 billion in peak sales with ORLADEYO. I started out by saying, the way we create value is by bringing oral drugs to patients who suffer from rare diseases. We're creating that value in the marketplace today with ORLADEYO, and we believe we're on a path to $1 billion, and we believe we can repeat it over and over and over again. That, we believe, creates meaningful value for patients and for shareholders. With that, I'll invite some of my colleagues up to join me, and we'll take your questions. Let me just introduce who's with me so that people who aren't in the room might know. Anthony Doyle, our CFO, Helen Thackray, our Chief R&D Officer, and Charlie Gayer, our Chief Commercial Officer. Great. As a reminder, if you wanna ask a question, just raise your hand or send it to me in the portal. Let's start with ORLADEYO. You're coming off a really strong year in 2022. What were the factors that you were considering when you put out your guidance for 2023? I think the biggest factor really is the consistent demand. Looking at, are we still driving new patients in the same way as Jon described patients switching over? That's a big piece of it. Patient retention, which we saw in 2022 really stabilizing. You know, what percentage of the patients are we getting to paid therapy? Those are the three big pieces. Looking at, as Jon mentioned, we have access to all the data that's what points us to no less than $320 million for the year. I think for 2022, you came in slightly below essentially like a point estimate you had given us with three key results for the full year number. Can you just walk through kind of what happened with the fourth quarter that led to that number not lining up? There were two factors. First of all, we ended the year, we ended the fourth quarter at the number of patients on therapy that we expected. What we didn't achieve quite to our expectations is getting the number of paid patients, so we have a higher percentage on our long-term free goods, so patient assistance program, than we'd anticipated. We think that's solvable 'cause most of these patients are actually insured, and it's really just about giving the insurance companies all the information that they need to approve ORLADEYO for these HAE patients. The other somewhat lesser part of it is just how many patients took shipments in, particularly in December. We're at the point where every ship day is about $1 million, right where we are with the current number of patients. Just two or three ship days made a difference at the end of December in terms of how many people took their shipments late in the year. None of this has anything to do really with the underlying trends, which we see as being really strong. Now that you've been in the market for a couple of years with this product, I know you kind of flagged, some 1Q dynamics. Maybe you can talk a little bit about what those are and also whether there's any other seasonality or other variables to consider as we think about the quarterly cadence in the year. The biggest thing in the first quarter and for those experienced in rare diseases is no surprise, but most of the patients have to go through a reauthorization in Q1 from their insurance companies to get it reapproved. What that means is for some patients, as we're helping them through that process, they're gonna step back to free product for a month or two before returning to paid therapy. That is the revenue we would expect to be similar to Q4, but the patient number will still grow. What that means is for the year, then Q2 will have a higher growth, will sort of have the highest percentage growth in the year, and then small, more regular growth in Q3 and Q4. Can you tell us what ORLADEYO's penetration is in the U.S. market right now and kind of what your guidance implies for how much higher that means you're gonna go this year? Yeah. One of the slides, I forget which number it was, that Jon showed in his presentation is from market research that we do regularly every quarter with physicians, ask them what percentage of their patients are on all the different products. That survey is, I think, a pretty, you know, pretty good approximation of market share, and our latest survey showed that ORLADEYO is at about 20%. With our sample, that may overstate our actual market share a little bit, but I think that's pretty representative. The other number that we put out at the college, the Allergy College meeting in November, is that at that point, 1,500 over 1,500 U.S. patients had been prescribed ORLADEYO. They're not all still on therapy, but that was our penetration number across the whole patient base of, as Jon was saying, about 7,500 diagnosed and treated patients. One of the questions I get sometimes when, you know, investors are trying to reconcile that market research number is, I think, you know, one of the slides talks about to get to your peak U.S. number, that sort of implies 20% or 30% share. If the current market research says you're already at 20% share, kinda how do we get there? Yeah, I think that's where, you know, we always try to do big, robust samples, but what's gonna end up happening is more of the respondents in those surveys tend to be larger prescribers. That's where I think the share is actually a bit overstated. I think we will regularly do those surveys, and I think it's more a direction of where we're headed. The other key part of those surveys is what do they intend to do over the next 12 months. What we see at this point is that consistently ORLADEYO is the product that they see growing the most. You're right. To get to peak, if we get 2,000 patients on ORLADEYO stable, that's what gets us to about $800 million out of our peak sales estimate of about $1 billion. The other $200 million would come from ex-U.S. markets. I think it was mentioned in the presentation that the persistence has kind of stabilized. What does it look like currently, and what percentage of the patients who start on ORLADEYO stay on it? What we see in our data is that the. If we can get patients to six months, and particularly a year, then the persistence is really strong. When we lose patients, we lose about half of those. Half of the discontinuations that we have happen within the first two or three months. The one-year retention is around 60%, a little bit higher than that. Once we get them to 12 months, that means that the patient's really having a good experience, and most of them stay on long term. Our goal is to get as many patients in the marketplace to try ORLADEYO and really trying to show both patients and physicians that that's a very low risk for potentially tremendous benefit of being able to take one pill once a day to control their disease. You know, if half are coming off in the, half of those who come off are coming off in the first couple months, is there anything you're putting in place to kind of support patients in their first couple of months to kind of help them stay on therapy in the beginning and kind of turn them into one of those long stayer-oners? Yes. The number one thing that we can and are doing is to make sure that the appropriate expectations are being set. You saw in some of Jon's slides that there are really two things, two main reasons for patient discontinuation. One is breakthrough attacks, perceived efficacy, and the other is GI side effects. You saw that from our clinical data, the side effects tend to go away within the first couple of months. If it happens, we want the patients to know that this is possible, but if it happens, it tends to go away. If you have a breakthrough attack, that's normal. If you're having persistent breakthrough attacks after three or six months, maybe this isn't the drug for you. It's not for everyone. We wanna make sure that no patient gives up too early, and that's where we think, we can have more of an impact in those first few months. What's the current split among new starts between treatment-naive patients and switch patients? It's been remarkably consistent since launch. Again, you saw on the slide that I think we have data there through October. Roughly 50% of the patients have been switched from other prophylaxis therapies. The other 50% is switching mostly from patients who are diagnosed, but they were just treating their attacks acutely and then are coming over to prophylaxis now that they can do it with one pill once a day. The smallest portion of that is patients who were treatment naive or newly diagnosed. In the U.S. market, it's pretty mature, so most of the patients, we believe, are already diagnosed and treated. Yeah. that percentage is- Very ... less than 10%. What about the patients who are staying on injectables? Do you guys understand what their main reasons are to not go to oral? Yeah. Here's what we know, which is that all else being equal, the great majority of patients would rather be on an oral. That said, you know, 10, 15 years ago, patients didn't have any good targeted options for HAE, so they have a history of many more attacks. Some really good therapies have been launched. These patients are under good control. There's, as much as they would like oral, there's some hesitancy around, you know, how is this drug gonna work for me? The doctors have the same feeling. If they've solved the problem for a patient, they wonder, you know, "Why should I rock the boat and switch a patient over?" This is a long-term process of convincing them that the risk of doing that is low, but the benefit in terms of being able to, you know, not have to deal with needles, not have to prepare medicines, not have medicines that you have to refrigerate when you travel, all of that, you know, it versus just taking one pill a day where they can basically forget that they're sick. It takes time to convince some physicians and patients of that, and that's why we see this is a very consistent long-term growth as we convince more and more of these patients and physicians. Yeah. The approach our field force is using is we either haven't convinced you there's enough benefit to being on an oral, or we haven't convinced you that there's a really low risk that if you switch onto our drug, you can't go back to your old one if it doesn't work, or we'll help you with the, you know, the reimbursement process and dot, dot. But that we chip away at that with every visit that we have with the doctor. You know, you can see with, you know, some guys that weren't prescribing a year ago, now they're prescribing four or five patients, and we'll keep chipping away. I think one of the things that has the biggest impact is when they see somebody really well controlled on a once-a-day oral and talk to that patient, and that can have a cascade onto further prescribing of Orladeyo for other patients. Mm-hmm. Are there any new promotional activities planned for ORLADEYO this year? How should we think about your SG&A spend on ORLADEYO in 2023 relative to last year? One thing, it's not so much new, but we're constantly looking to make any adjustments to our team add where we think we can have more of an impact. We did add a bit to our team to our field team. The main thing we did was expand the number of sales regions. It wasn't a massive territory increase, but it was shrinking the span of control for our regional sales leaders so that they can spend more time with their teams and also have develop more relationships with some of the key customers. The other thing, and this is not new, but we're really focused on, and we're able to do this more and more, is live patient meetings, because that's if there's one thing that we've missed launch to date or missed the opportunity to do as much as we'd like, is really getting patients aware and activated because that's a, that's a key part. If the patients are asking their doctors about ORLADEYO, we've got the most of the doctors really primed to prescribe. Those. The last couple of years, a lot of those live patient events were limited. We expect to do more of those this year. Anthony, you wanna hit the SG&A? I think in terms of the investment, right? It's not a visceral reaction to something not working. It's gonna be incremental investment in optimizing what we can do. It'll increase year-over-year from an SG&A perspective. It won't be as much like Jon said, as the revenue will grow. We've already announced when, you know, we announced the earlier date on BCX9930 and BCX10013 in December, that R&D was going to be year-over-year. We weren't gonna see growth in it. We will see some growth in that SG&A. Again, more than compensated by the amount of revenue growth that we foresee in this year. Got it. Maybe lastly on ORLADEYO, as the product gets approved and reimbursed in more countries outside the U.S., is ex-U.S. revenue gonna become more important this year? What we've seen most of our ex-U.S. launches at this point have been in Europe. What we said is, at the point we get to about 10% of sales, we'll probably start breaking that out. That could happen this year. Ex-U.S., just the pace of growth is or and the impact of the growth is less because the... It takes about three or four European patients, for example, to add up to one U.S. patient. It's gonna take a little longer as we get through all of the market access processes in the various markets. It's gonna take a longer time to get to the 20% of our peak sales ex-U.S. So far, the signs we see are very promising and gives us confidence that we will get to $200 million plus, ex-US sales at peak. We can switch and talk about the pipeline. I really wanna better understand the key differences between 10013 and its predecessor 9930 from, like, a chemical structure perspective. The chemical structure has a similarity in terms of backbone, but BCX10013 is a very different molecule. The R groups that you add to give the molecule its particular characteristics and its, different qualities are the ones that make that difference, and we see that now in the clinic. Specifically, we see the pharmacokinetic properties are different. We have exposure that goes far longer with BCX10013. We see that then bearing out also in the PD data with that also going longer, which gives us the potential for once-daily oral in BCX10013 as a result of that difference in structure. Way less drug, right? We're at a single dose of 110 mg when we're up to 1 g with BCX9930. Okay. Can you walk through what makes you believe that BCX10013 won't bump into the same issue that BCX9930 had, given that you only saw that sort of later in development with BCX9930 when for in-patients for a longer period of time? Yeah, sure. We've learned a lot with the BCX9930 program, and we've applied that with BCX10013. We've assessed a number of things in looking at it and reached our conclusion that we have fairly good confidence in that point we won't see that. Specifically, there are a couple points. One is, the with BCX9930, we saw in the preclinical models, in an animal model, we saw crystals developing in the kidneys at a dose level that was consistent with the dosing in the clinic. That was one of the findings that we had emerging around the same time as the serum creatinine in the clinic. With that, we've learned the animal model that is most relevant then for that, we've been able to test that specifically also at the therapeutic range and above with BCX10013, and we do not see that crystallization, that crystal forming in the kidneys. We also know the point that Jon Stonehouse made on BCX10013. We're seeing exposure with the molecule such that at a lower dose, we think we will get to therapeutic range we want to be in, at a lower dose and substantially lower dose potentially than BCX9930. That may be very relevant as well. Remember we were talking about saturation and super saturation in the kidney. That is a direct consequence of dose and the amount of drugs. As we see, you saw the 110 mg data here at BCX10013. We're at a far lower dose and achieving PD activity out through 24 hours. We do think we need to dose higher with BCX10013, that will be one of the things that's a big difference also. Higher than what? Sorry, higher. Let me clarify. We're at 110 mg with the single ascending dose data here. We do think we want to dose at that level and higher in patients, and we think the ultimate clinical dose is likely to be higher. Even so, we're at a substantially lower dose than the clinically relevant dose of BCX9930. Yeah. As Bill says, we're within shooting distance at 110, so it's not like we're going to have to quadruple it. Great. I think it sounded like the SAD MAD was kinda keep running through the first half. What's still going on in that study? Yeah. So like maybe clear around that as well. We have what we need to advance into patients. One of the things that we wanted to see is that we could get to the therapeutic dosing range, and we know we're there with that PD activity, so we're ready to go into patients. One of the things also that healthy volunteers studies allow you to do is get a rich PK data set that helps you build your PK/PD model to confirm dose and to... and also as part of your rationale for dose as your regulatory filings go. We will continue to work in the SAD MAD study to define that data set for the PK/PD model. It's not, we have what we need, and so it's not slowing us down and getting into patients. We'll do some further dose ranging in patients, but it's building on now what we know from healthy volunteers. Yeah, you can sample patients in a phase I study way more frequently than you can in a patient in the outpatient setting. Okay. It looks like we're out of time. Thank you. Thank you. Thank you.