Pleased to be joined today by the team from Altimmune. Maybe we'll just start with an overview. I think it's helpful to level set. So I don't know which one of you want to take that, but an overview of the pipeline, in particular key value drivers.
Well, thank you for having us. So, as you know, at Altimmune, we are developing a GLP-1 glucagon dual agonist for obesity and for MASH. We recently announced our phase ll obesity data. The drug is called pemvidutide. So again, it's a GLP-1 glucagon dual agonist. And the idea is that we're combining two different mechanisms: the pure GLP-1 incretin effect, which is appetite suppression, but we're combining it with glucagon, which brings in this additional component of energy expenditure. So really, by combining the two, we're able to show not only significant weight loss, but also a profound effect on serum lipids, on liver fat reduction. And we think that's all going to have benefit in terms of addressing some of the very important comorbidities of obesity.
When it comes to MASH, obviously having anything that's direct acting in the liver, having the fact in liver defatting, and on top of that, the overall weight loss, we think that'll benefit the MASH indication. We'll talk more about that. MASH, we have a phase ll- B study ongoing right now. It's enrolling as we speak, and we expect to have data in the first quarter of next year. So we're very excited about all of the upcoming events. We have an end of phase ll meeting coming up with the FDA at the end of the third quarter. So a lot of exciting things happening.
Great. I think we'll definitely spend some time on NASH, particularly given some recent updates. But maybe we'll start with obesity. You talked about this, but you reported phase ll data last December. Maybe you could walk through some of the key details from those results as you see them.
Sure. So we achieved, at the end of 48 weeks, 15.6% weight loss, but the shape of the weight loss curve or the trajectory was downward pointing. We think that at the end of 72 weeks, which is where tirzepatide read out their data, we could have substantially more weight loss rivaling the numbers they came up with. In patients who had high lipids at baseline, we saw very profound reductions in serum lipids, LDL cholesterol reduction of 21%. While not directly looked at in that trial, we also saw great reductions in liver fat. This was not an apple-to-apple population, but 80% of their people defatted their liver, which is very important for cardiovascular risk. One of the more important readouts from that study was body composition. We have best-in-class preservation of lean mass. We're still looking at that data.
We think there's the potential of getting even better effects as we mine the data more. We'll make a presentation of that in a meeting later this year. But this is extremely important for something that's not gotten enough attention right now in the minds of investors, which is maintenance and safe and effective maintenance of body weight. The focus has been on how much weight loss you have in a year, but some of these drugs are having profound loss of lean body mass. Semaglutide, for example, was associated with bone fractures in the elderly and in women. That's not really going to cut the mustard in terms of long-term treatment. So as a cosmetic drug, getting weight loss, that may really suit a lot of people, but for effective long-term management, will you safely reduce cardiovascular risk while also preserving lean body mass? That's very important.
Our lean body mass preservation is commensurate with, and probably even better as we see it now, than diet and exercise. So we're really gearing our program right now towards maintenance of safe maintenance of weight loss. We'd like to have that discussion with the FDA and build it into our studies when we talk to the FDA at our end of phase ll meeting, which will be late in the third quarter of this year.
Yeah. In the obesity arms race, there's obviously a lot of things that you can talk about, but efficacy and tolerability sort of come first. On the tolerability side, can you walk through what you guys showed?
Yeah. So you have to look at tolerability by phase of development. In phase ll, sponsors aggressively dose their drugs. That's what we did. And typically, you see adverse event discontinuations between 20%-30%. And we saw that recently with various readouts. Orforglipron was 20%. So was retatrutide. We were actually below that at 19.9%. It's important to realize we actually achieved that without allowing for dose reduction, which is actually employed by about 30% of patients in these other trials. In the structure trial, 40% of patients, in order to maintain their enrollment in the trial, had to reduce their dose. We didn't allow that. So the fact that we were able to hit that 19% with our drug is impressive considering the fact that we didn't allow for that. In addition, the great majority of these drugs are titrated over 16-20 weeks.
Our drug is not titrated at effective doses. At the highest dose, it's a four-week titration. We think best-in-class tolerability. We think we have potential and optionality to improve that like other companies do by making changes in our dosing regimen going into phase lll and have the best tolerability profile in the incretin class.
Okay. You mentioned the body composition data. Obviously, early signals and intriguing there. I guess, could you talk to us about the mechanistic basis you think that's providing that benefit with pemvidutide?
Glucagon, which is the key component in pemvidutide, shifts metabolism from carbohydrate to fat. We know that. We saw that in our data when we saw a rise in ketone bodies in our studies. So glucagon acts by inducing what you might say is a ketogenic diet. We know that's preserving for lean mass. So what it does is it takes away the reliance of muscle to provide the substrate for glucose in the liver and therefore robs the liver of its amino acids and protein in order to supply carbohydrate. It shifts it over to fat and it puts the burden on fat. We think that's the mechanism of preserving the lean mass.
Okay. One of the things that people talk about sometimes with glucagon is it obviously doesn't have the positive effect on HbA1c that you see with some of the GLPs. I guess, how would you characterize that aspect of this product profile relative to other agents? And how do you see that shaping sort of where it's used?
Well, only 20% of the obesity marketplace is diabetic, first of all. We are not out to bring hemoglobin A1c from 8.5 down to 6.8. Admittedly, there are better drugs to do it, but there is a huge part of the marketplace of people with stable diabetes who do not need the hemoglobin A1c reduction who would benefit from all of the things that we just talked about. So in that class of either non-diabetics or stable diabetics, we've shown excellent maintenance of glucose homeostasis.
Okay. As you look across all the data and think about next steps of the program, I guess, what are your priorities going to be? And you maybe alluded to this in your first comments, but what are your priorities going to be as you go speak to regulators through this year?
I think the most important thing we're going to bring out are the attributes and the benefits of glucagon. So we could take the approach that we're going to just target the entire obesity population. That's going to be a huge population. There's really no need for this. We saw hypertension divide into 10 drug classes, each having its own role. We think that we need to concentrate in this huge marketplace on what glucagon actually brings to the table, which is going to make it desirable for doctors to prescribe. So things like lipids, liver fat, body composition. So it's important for us to identify for the marketplace where this is going to fit in in the treatment paradigm and to actually design studies and get agreement with the FDA on those studies in order to drive home that value.
Based on that, we think that with the studies that we're going to propose to the agency and discuss with them at the end-of-phase ll meeting, which will concentrate on those glucagon-specific attributes, we think that meeting will be confirming of our statements about glucagon and actually drive our value up tremendously.
Okay. To what extent is this going to drive kind of the patient inclusion/exclusion criteria versus the endpoints that you evaluate?
Well, I can't talk specifically because we haven't had that meeting, so it's not public information. But just to paint a broad picture so that you can understand it, in terms of body composition, enrolling a population susceptible to body composition of lean mass loss. For example, elderly people, women with osteopenia, these are huge populations, or people with sarcopenia. It's known that about 15%-20% of people with obesity actually have lean muscle mass at baseline. And the reason is because they're so obese, they have insulin resistance. They can't maintain their muscle mass. So despite being 100 kg, the amount of lean mass they have is actually low for their height. And these people are very susceptible to injury. There's a direct correlation between lean mass or inverse correlation between lean mass and mortality. It's well established in the literature.
Consequently, we could design a program that looks at people, a pivotal study that looks at people with lean mass susceptibility. We could look at people who have hyperlipidemia because a lot of these patients in our studies had hyperlipidemia, were already taking statins and not getting the desirable benefit. Because of the fact that we have class-leading effects in liver fat reduction and liver fat is known to be a risk factor for cardiovascular disease, we could do a study aimed at that and also at a MASH-type population.
Yeah, just wanted to add, Corinne, that one of the advantages of obesity phase lll program is that you're looking at fairly large patient population just for the safety database. So that gives you the flexibility to look at various subclasses within that subgroups. So you can actually, within that phase lll program, include these patients and hope to get those on your label. And that's really what we will be talking to the FDA at the End of phase ll Meeting.
As you look forward then and think about what kind of outcome studies then you could run successfully with an asset of this profile, I guess, what are some of the most interesting outcomes you think you could be proving out here?
Well, I think a long-term study to show that we're preserving lean mass in susceptible populations better than other drugs, but also relating it to outcomes with enough patients. As Vipin mentioned, these pivotal studies are large enough to look at outcomes like bone fractures. For example, the reverse was seen in the semaglutide program where they had a 40% loss of lean mass. We're at about 25%. We're about diet and exercise at this point. They actually had in their label an increased risk of bone fractures. It is possible within a pivotal program to show an impact on bone fractures. Obviously, we would try to show the opposite and try to get that into our label.
So we think that that's really what we want to design into our program, really take a focus towards the long term in terms of the safe and effective maintenance of weight loss and also the safe and effective maintenance of reduction in serum lipids and liver fat.
Yeah, I just wanted to add that to date, there's been a lot of focus on acute weight loss, what happens in 12, 24, 48 weeks. That's not what it's going to be about. It's really going to be about weight management and weight maintenance. So we think, again, a glucagon-containing compound is really going to shine there. Lipid profile, long-term lipid profile, and actually manage.
Yeah, let me add to that, Corinne. Right now, I firmly believe, we firmly believe that in the near future, 3-5 years, approvals will also be based on safe and effective maintenance of weight loss. We saw this in other indications, for example, in Crohn's and ulcerative colitis. It could be in the 1990s you could get an approval for induction of remission of one of those diseases. By the mid first part of the mid part of the first decade, that shifted to you have to show maintenance of effect. So you couldn't just get an effect on inducing remission in Crohn's disease. You had to show maintenance of remission to get approval. So we think that right now the field is still young.
Drugs are getting approved in acute weight loss, but I think in the future there'll be a shift to showing maintenance of weight loss safely and effectively as well. We think that's happening in the near future.
You recently disclosed some plans to think about pemvidutide in adjacent indications for proof of concept studies. What was the impetus behind the thought to put that out strategically? Flavor, you can give us around what kind of adjacencies are most interesting?
Yeah, so some of those things we are already talking about. I mean, again, we can't really be very specific right now until we talk to the FDA. But again, our goal is to enhance as much of the benefits of glucagon as we can. And we believe that there are subpopulations out there within the obesity space that we can show that, as well as in the MASH space. So our goal is to really enhance those advantages of glucagon when we design these studies.
Yeah, I would add to that that obviously taking on the entire obesity marketplace is a huge effort. We've announced that we want to do it with a partner. There are related indications that would be more narrow, that would be a faster approval, that would also bring out all of those effects without having to go through the path of a full obesity approval and a pre-obesity spend. Consequently, these are indications that we could do on our own that are related to obesity that would enhance the value of the compound, lead to earlier approvals in a financial territory that we'd be very comfortable.
Okay. Maybe another question here. Obviously, on one level, obesity is quite crowded. There's tons of different products in development. On the other, there's slices of the market based on mechanism and delivery, etc. As you look within the slice of glucagon and GLP targets, what are the benefits for your program?
Well, there are going to be multiple classes of obesity drugs. This marketplace is not fully differentiated. I'd like to quote Louis Aronne from Weill Cornell, who says that obesity is the new hypertension. I think that's exactly correct. Back in the 1980s, we had poor drugs for hypertension. Now we have a multitude of drugs in 10 classes, very differentiated attributes known to primary care. Primary care docs use it. Obesity is going in that direction as well. I think the easiest differentiation right now is between the compounds that do glucagon and the compounds that don't have glucagon. Because when you take one and you combine it with GIP or amylin, you're really looking at the same effect, which is reducing appetite just by different mechanisms. So all of the effects in obesity are by stymieing caloric intake.
All of the effects you're seeing are related to weight loss. If you don't get weight loss, you don't get the effects. So it's really a pursuit of weight loss. Now you shift over to glucagon and you get other attributes, as Vipin mentioned, increased body metabolic rate, energy expenditure, which could have effects on the metabolic set point chronically, the lipids, the liver fat reduction, and now we know body composition. So we see that our part in the marketplace is in that glucagon space. And we think that based on a variety of readouts, we have the best glucagon-containing molecule.
Okay, great. Maybe we'll switch to NASH. Obviously, a lot of updates last week for the particular GLP-NASH kind of complex. Maybe walk through what you thought were the most intriguing takeaways as it relates back to your program.
Yeah, well, I think the two main readouts that we were interested in were tirzepatide and survodutide. And let me talk about it in that order. We thought the tirzepatide readout was very interesting. There's been a lot of controversy since that readout about the statistical treatment. I don't want to get into that because there's a lot of detail there. What we would say in summary is that we do think that they had benefits, both in NASH resolution and fibrosis improvement. It's hard to know from a regulatory sense and a statistical sense whether they really had fibrosis improvement because the statistical analysis was complicated and, in fact, perhaps too liberal. But there possibly is an effect there. And quite frankly, if you give any GLP-1 or GIP and you give it long enough, you will see an effect in fibrosis improvement.
It's a question of the potency and the speed. For example, we know that bariatric surgery has effects in fibrosis, but it takes 5 years. So the question is, if you have a mechanism that works by restricting caloric intake the same way bariatric surgery does, how long will it take? It's not the debate about whether you will eventually get there, but how fast it is and what you need to accomplish in the period of time in front of you with the patient. So their trial was 1 year. I think their readout in fibrosis was borderline. It was not as potent as related in the abstract because of the statistical concerns. And I think other people have focused on that. But that's fine. We agree. We think that can happen. The question is, how do you do better than that? Right?
So right now, the GLP-1s are kind of being used or looked at in the early stages for NASH, F1, F2 fibrosis. And the thought is that you really need to have potent reduction in fibrosis. You have to go to other mechanisms. And that's other drugs that you've seen in that space. Now, with the survodutide data, they initially presented very potent improvement of fibrosis. And we congratulate them for that. We think that's directly attributable to glucagon. However, the detail in the statistics, if you look at the New England Journal publication, the authors rejected the analysis they did, and they relegated it to the supplementary appendix. Apples to apples compared to other drugs, looking at it in that fashion, the treatment effect was a bit greater than tirzepatide, but probably in the range of about 17%. So that increase over tirzepatide is glucagon.
But there's not much glucagon in that molecule. Our ratio of glucagon to GLP-1 is eight times higher. We have better reduction of liver fat, which has been shown to be the strongest predictor of fibrosis improvement, as well as we have data showing that pemvidutide directly decreases fibrosis independent of liver fat. The bottom line is the more glucagon, the better, the more liver fat reduction you have in fibrosis improvement. So we think survodutide is a great step forward in terms of showing the benefits of glucagon in fibrosis. We're going to do better. They read out at 52 weeks. We believe that our drug is so potent that it will fibrosis improvement over 24 weeks, like the other drugs that are known to be potent reducers of fibrosis in NASH. But even more importantly, we have a great tolerability profile.
In survodutide and their phase ll trial, the adverse event discontinuation rates were over 20%. They presented another abstract at the meeting, which didn't get a lot of attention in cirrhosis, where they actually had changes in fibrosis biomarkers in the cirrhotic population. And again, we congratulate them on that. We show that we feel these glucagon-containing compounds are very potent to be used eventually in F4 cirrhosis. But if you look at that study, they had a control group of MASH patients without cirrhosis, and the adverse event discontinuation rate in that trial was 47%. 47%. So this drug is not well tolerated. It gets its efficacy by being pushed very hard at the sake of tolerability and dropouts. And we think that we're clearly superior to survodutide on the basis of tolerability.
Okay. Maybe with those 2 data points in mind, can you walk through the phase ll trial design and some of the key parameters you're evaluating with the update in the first half of next year?
Sure. So we have two endpoints in the trial: NASH resolution or fibrosis improvement. It's a dual endpoint trial, meaning to be successful, you hit either. And the statistics are developed that way to give success for either. We are looking at a typical MASH population with F2 and F3 fibrosis. We're not looking at F1. We don't really think the benefit is there in F1. Also, the ability to hit fibrosis improvement is better in the more severe stages of fibrosis. So we're requiring at least 50% F3s to be in the trial. We're taking the 1.2 mg and the 1.8 mg doses forward. They're not titrated at all. The reason we didn't take the 2.4 mg dose forward was that we saw the effects plateauing at 1.8 mg. We thought that was enough into this trial.
We could always take 2.4 into phase lll if we feel that that's going to add additional benefit. The trial has 190 subjects, as you mentioned, Corinne. It's supposed to read out in the first quarter of next year. Enrollment in this trial has been excellent. I think we're going to enroll this trial faster than any other MASH trial. I think the reason is that patients want to come in and get the weight loss matched to them as a silent disease. It's like cigarette smoking. I'll try to stop next month. But for weight loss, it's right in front of people that want to lose weight immediately. So we've had no problem getting people into the trial. And we think that reflects the market opportunity as well, is when this drug gets out, when the pen hits the pad.
I've been there before for many years as a prescribing physician. You talk to the patient, and ultimately, prescriptions and negotiation with the patient, if you've ever been on the other side of the discussion, people want to get the weight loss. They're going to see that first. We think that this drug is going to be a winner.
Okay. One of the questions that came up for me as you were talking, sorry, and I'm losing it. So I'm going to go to my next on the list. Oh, I know what I was going to say. So in the past, you've talked about the basis for why you think you could see fibrosis improvement at 24 weeks, and it has to do with the liver fat reductions that you've seen in prior trials. So could you talk to us about what you've seen with respect to liver fat reductions in prior studies in this patient population and how that maps to some of the other NASH assets that have come before and shown 24-week histology data?
Yeah, 24 weeks, our liver fat reduction is in the best of the class. It's 76%. But importantly, we also saw it in 12 weeks. In fact, we saw it at 6 weeks. So not only is this potent liver defatting, it's rapid. So when you think about the constructs of a trial with this restriction on time points, to hit that endpoint at 24 weeks, you have to have a rapid effect. And we have it. In addition, we have preclinical data in a model of fibrosis that does not involve liver fat, showing a 33% reduction in fibrosis in just 2 weeks. We'll announce on this data at a meeting later in the year. So not only do we have potent effects in liver fat, which is a big driver of fibrosis, we actually have a direct effect on top of that.
All of our data, all of our non-invasive markers, we presented some of this at EASL, our computational models, we presented that at EASL as well. Our non-invasive endpoints like corrected T1 imaging, our ALT, they all point to a very potent and rapid effect. And drugs that are potent in MASH don't need to wait till 52 weeks. Potent drugs have actually read out at 24 weeks on their NASH resolution and fibrosis endpoints. And we want to be in that category. And assuming we hit that, we'll be the most potent incretin in NASH in development.
In terms of the powering, I guess, what are you looking to see in terms of delta with respect to fibrosis and/or NASH resolution?
Yeah, you got to be a bit careful when you're taking week 52 endpoints and translating it to week 24. Because obviously, your absolute changes at week 24 will only be better at week 48. So if I give a number and you compare it to the 52-week data, you're going to get confused. The important point is that it's statistically significant. It means it didn't happen by chance. So we hope to have the best treatment effect possible. But the more important readout will be that it's statistically significant.
This study also includes a follow-up out to 48 weeks, as you just said. It's primarily focused on the non-invasive endpoints. I guess, what's the rationale for looking at non-invasive endpoints at that time period? And which of the non-invasives are you most focused on?
Yeah. So it's typical to tell patients they're going to get 2 biopsies in a year. In fact, assuming they had a biopsy come into the trial, to demand it at week 0, week 24, and week 48 would be a deterrent for patients to enter the trial. So we really felt that we had one shot at this. And consequently, we put that endpoint or that biopsy at week 24. But we're quite interested in having 48-week data. So it is possible to project out the effect to week 48 by following the non-invasive markers. And as well, we'll get additional information for safety, which is also part of the regulatory discussion. So our primary readouts in fibrosis will be the FibroScan, the ELF, the Pro-C3 in this study. And those are all recognized markers of fibrosis.
I guess, what's your view on the role that non-invasive tests can play in NASH space, both in the drug development and then as you get into patients' kind of monitoring basis?
Well, they're very helpful to help predict effects in the absence of a biopsy. Where they stand in terms of approval at the FDA, I think we're years away from that. I think the FDA made it very clear in their symposium several months ago that non-invasive tests are not ready for approval. We could talk about the rationale for that. But these non-invasive tests are very useful, like at week 48, to see the progression. To look at populations where a biopsy may or may not be readily available, it will give you guidance as to what's actually going on in the liver.
Okay. We talked about with obesity expecting a stratified market. I guess, how do you think the NASH market is going to shape up over time as more drugs come to market?
Well, that's interesting. Right now, the way investors see the NASH space and drugs in development with the GLP-1s and everything else, and maybe resmetirom might fit into that space. The reason is because you have the drugs that have weight loss and the drugs that don't have weight loss. The question is always how far out to F4 and cirrhosis with the GLP-1s go. Right now, they're kind of being held up in that F2, F3 phase. If you're starting to get the complications of cirrhosis, maybe you want something that's more potent. Now, we would contend with our drugs that if we have potent effects in fibrosis, that we're going to span the entirety of it. In other words, we can have weight loss. We can have the effects on lipids. We can have that in the F1, F2, F3 space.
If we have potent effects in fibrosis, we'll have it all. Eventually, we can even be used in some cirrhotics.
Okay. As you think about next steps, like post-phase ll data, I guess, what would come after that? Would you be able to initiate kind of between the 24- and 48-week endpoint, or do you need to get through 48 weeks?
We'll have that discussion with the agency and see what their feelings are. But that data can be coming in as we speak to the FDA and roll it in. But we clearly think, and I'll let Vipin talk to the finances on this, that this is in our wheelhouse that we can execute a phase lll study in MASH because the spend is not as acute and as focused in such a short period of time with no outcomes trials, right? So that's an indication that we can actually execute on our own. So we believe, and I'll let Vipin comment on this as well, that after that readout, we would progress to an end of phase ll meeting and start phase lll right after that.
Yeah. I mean, look, our strategy has always been to pursue MASH on our own. Obviously, as we've said, for obesity, we're looking for a partner. But MASH can continue on its own path forward. We think by combining these two mechanisms, both weight loss and a direct effect on the liver, we have a unique profile. And I think our tolerability is also going to shine. It's going to add to that profile as the data becomes available. So we have a unique drug for MASH, best-in-class liver fat reduction that's going to show up in long-term studies as well. So we think we will move forward very aggressively, as Scott said. We'll actually try to meet with the FDA soon after the 24-week data. And in parallel to collecting the 48-week data, we'll begin to plan for the phase lll program in MASH.
It's a good segue to my next question, which was going to be around kind of status update around potential partners for phase lll. Anything you can provide there in terms of color?
Well, our goal still remains to have a partner before we initiate phase lll. We think the end of phase ll meeting would also help with that, will provide more clarity, and really focus on some of the attributes of the molecule itself. If the FDA agrees with our hypothesis, that would be very helpful in those discussions. It's hard to really pinpoint the timeline. There's a lot of information coming in this space. So people are evaluating everything. Clearly, our belief is that there's going to be a role for glucagon-containing compounds. And if that's the case, we are the best glucagon-containing compound out there. And that's really the basis of our discussions in all our partnership discussions.
As you think about the adjacent indications, you've started talking about the NASH data next year. I guess, to what extent could those kind help inform partnership conversations from a more robust, full pipeline perspective?
Yeah, that's a good question because most partners are really looking at pemvidutide more like a cardiometabolic drug. Obesity, MASH, and some of the comorbidities, dyslipidemia, hyperlipidemia, they all fit that category. So some of those discussions are centered around what are the other indications? Because just going after the broad obesity market is a very significant undertaking for anybody. So as a result, there is interest in trying to explore some of the benefits in smaller indications. So those discussions are also part of our partnership discussion.
One of the questions that comes up in the obesity space, particularly in the incretins, is the supply chain, right, like manufacturing capacity. What do you guys currently have? And how much would you need to build out to support registrational trials in obesity and then commercialization?
Yeah. So we're working with the CDMOs at this point. These are very well-known CDMOs that are very familiar with this space. They actually manufacture some of the products that are on the market. So we have very good relationships with them. We're well set in terms of phase lll supplies for obesity as well as for MASH, including commercial launch of the drug. But obviously, we'll need more capacity as the market grows. There are many, many CDMOs that are coming online. Everybody sees the opportunity in this space. It's also part of our discussions with strategics because some of them already have these types of facilities. Some would like to make an investment. So all of that goes into that discussion.
But for now, we are in a very good place in terms of being able to supply material for our phase lll program as well as commercial launch of the drug.
Remind me how COGS compares to the other GLP-1 onlys in space?
Very similar. There's really not a significant difference. We're using similar devices in terms of the weekly injection of the drug as well as the peptide manufacturing is very similar.
Okay. And then finally, we've talked around some of this, but cash runway, remind me the current status and what that takes you through in terms of both endpoints and trial execution?
Yeah. So at the end of first quarter, we had approximately $180 million that we announced. We are well positioned to have all of the data that we've been talking about, the end of phase ll meeting as well as the MASH data. We have cash into 2026 at this point.
Okay. Great. That wraps up all of my questions. Thanks so much to both of you for joining us today here at the Goldman Sachs Global Healthcare Conference. Beautiful. Thank you.
Thank you.