Okay, excellent. Thank you, guys, for joining us. Super excited to have Merck Management with us. Just before I dig into my specific questions, I'll let you frame the broader discussion. We'll jump right in.
Great. It's great to be here. My name is Eliav Barr. I'm a Chief Medical Officer at Merck. This is a tremendous period of time for us. We have probably some of the most exciting pipeline products that I've had in my 30 years in the company and across oncology, vaccines and ID, and general and specialty medicines. I really look forward to talking to all of you.
Excellent. So I realize this is going to be a very R&D-focused discussion, and that's the direction I want to go. But just ahead of that, Peter, could you just refresh us on where we stand on the broader financials, especially as it relates to the Gardasil situation? And are we in all clear now after the third quarter, two to three quarters?
You tell me.
Okay.
So no.
No.
So we've had a
Oh, yes.
No, no, no. We are definitely, we've had a great year at Merck. Our current guidance is above where we initiated guidance at the beginning of the year. We expect 9%-10% XFX revenue growth on a full company basis. Gardasil we expect to be roughly flat year- over- year because there's been a slowdown in China, but the rest of the business has been extremely strong, and Gardasil has been extremely strong in markets outside of China
So in the third quarter, it grew strong double digits in just about every major region around the world, and we feel like we're in a very good position of understanding what's going on in China, and we are addressing that with our partners, Zhifei, and as we look out to 2025, we believe we will have a year of solid growth for Merck overall. So I feel like we're in a very good position commercially, including with Gardasil.
Okay, excellent. And maybe just one quick additional one just before we dig into some of the R&D programs. I know there was this, I think I would call it aspiration number, put out that oncology would go to $20 billion, pipeline, non-key pipeline. Oncology is $20 billion, cardiometabolic $15 billion, and immunology is multi-billion. Does that factor in on a risk-adjusted basis on some sort of long-term forecast? Is that something you guys would ever consider doing?
Yeah, so we've outlined what we believe our commercial opportunity is in several parts of our pipeline, not our entire pipeline. But as Umar mentioned, we've laid out an expectation for greater than $20 billion of commercial opportunity as we approach the mid-2030s from assets in our oncology pipeline, excluding anything that we're doing around Keytruda, including our subcutaneous program, which we just read out a successful phase three on. Those are all on a non-risk-adjusted basis. And we'll determine how we outline our future opportunities in future settings at some other time. But for now, we've outlined oncology, cardiology, and immunology as three major sources of opportunity. We also have opportunities in other areas of the pipeline, HIV.
Sure.
In vaccines, and also in our animal health business.
Excellent. So maybe let's start with oncology. That was the first line. That was $20 billion. And you just clarified that does not include any of Keytruda's new indications and/or Keytruda Sub- Q. However, does that include your new Chinese PD-1 VEGF, for example?
So not specifically.
Okay, not at the time it was given.
Yeah, not at the time it was given. We had not entered into the transaction with LaNova. So that is a future additional opportunity that would be incremental if it works out clinically.
Okay, so maybe let's start with that topic, Eliav. I remember I hosted you at our offices back in June. This was shortly after ASCO. Obviously, very interesting data from some of the therapeutic side with the hazard ratio they've put up on PFS. But we'll see how the profile plays out on an OS basis. Eliav, I'd be curious what your thoughts are on OS evolution and just your broad take on that data set, and I have some more specific ones on the program you guys brought in.
Sure. I think that the data are very interesting. They demonstrated a pretty substantial hazard ratio for progression-free survival. The issue for us and for everyone in the field is that the regulatory endpoint and the endpoint that payers and patients value most is overall survival. We just need to follow that to its conclusion. We've seen data sets with anti-VEGF drugs where the PFS didn't translate to OS, and we've seen some that have. The proof will be in the pudding. We'll see when the data read out and become more mature.
Okay, excellent. So I guess, and I have several follow-ups on this.
Sure, sure.
First one, as you think about the program you guys brought in, is that more insurance against anything that happens on the PD-1 VEGF space, or is that just your conviction in the target?
Yeah, I think it's the latter, not the former, because by the time the products get into the US setting, it'll be close to the US LOE for Keytruda. That wasn't really a factor to this. My interest was really more about seeing the data, reflecting back on the large number of studies that have been done, that we've done with various kinds of VEGF inhibition, whether it's through TKI mechanism or through direct anti-VEGF, and asking ourselves, if we were to look at the Keytruda database, where would we position this opportunity and how would we prosecute it? And so we thought about it. We looked at the data that were generated by Akeso Summit. And then based on that, looked at the profiles of what we wanted to see in a molecule. We looked at a variety of different drugs or candidates, I should say.
We ended up with the LaNova LM-299 as the one.
Got it. As I think about the signal seen to date, hazard ratio profound. It's on a PFS basis. Presumably, as we go into a Keytruda combination trial, would you expect a similar PFS hazard ratio to replicate? And because there's a lot of reasons to expect or not expect that.
Well, so we wouldn't, I mean, we'd be giving a trial against Keytruda.
A trial against Keytruda chemo?
Yeah, yeah, sorry. Yeah, so I think that where this will play out will depend again on the efficacy and safety profile, and if you look at the data that were presented, there was the data on greater than 1% frontline NSCLC, and there was the 1-49% data and the greater than 50% data, and you saw that the effect size in the greater than 50% data population was much greater.
You had that kind of hockey stick kind of thing for 1-49% that always worries one about with VEGF inhibitor combinations where you had a really big effect size at the beginning, and then it came back close, and one worries about that. How we'll develop the drug will depend on what we see in the phase one program. We've got a lot of insights from the Keytruda program that we think will help in managing efficacy, toxicity factors, and I think that that's going to be a very important thing with these drugs, is to ensure that you have the maximum on the efficacy and keep a vigilant eye on safety.
Got it. What do you think about Chinese patients and their responsiveness to VEGF, and how would that dynamic be relevant for the?
So a lot of the BEV studies had shown a higher response rate in Chinese patients. But the data, I think, were so spectacular. There was so much of a PFS benefit in the Akeso data that the Akeso Summit data. I think it's hard to imagine that it's just a.
And maybe just the last one on this because we have a lot of topics to get into. But in their EGFR mutant study, PFS is also still very robust. I think it's 0.49. But OS evolves into a hazard ratio that's above 0.8. Do you see a phenomenon like that happen on the trial that was just reported this past week?
We'll see. I mean, again, I think that that's why you do OS evaluations. You have to make sure that you get the right patients. I mean, part of it's also we have to remember that there's second-line therapy and third-line therapy adds more and more noise to the system. So you have to be careful about understanding what happened afterwards. But if you look at some of the trials that were done with pembrolizumab and anti-angiogenesis agents, you see this kind of profound initial and then slowdown afterwards. And so that's why we've been still, whenever I talk about it internally, externally, when we design our clinical program, we have to keep an eye out on the tail end, not the front end.
Got it. Any questions on this topic just before we move on? Okay, so maybe a couple of additional follow-ups on oncology then. HER3, the lung study, I guess. What are your, I think you guys met the primary endpoint on PFS, but your confidence in OS on that?
It was immature. I can't say. Happily, we've got a bunch of other further analyses ongoing.
Why did Astra pass on this one? That just never made sense.
Why did they pass on, oh, this asset?
Yeah.
I don't know.
Because they could have put this as part of the collaboration with Daiichi.
Ask Susan. I don't know. Okay, all right.
Excellent.
I'm glad we didn't.
On the PFS, is it reasonable to think there's at least a two-plus-month median PFS benefit?
I think that there, we haven't shown the data because even those data were relatively immature. So we have to wait and see how it goes. I think that what was interesting to me, and if you look at the study results, the study, it was HER3 against chemo induction followed by maintenance, and there were differential effects in the front and the back end.
Got it.
Differential effects in the front and the back end. During the induction and the maintenance, so you have to. That's why we keep on saying we just want to see how the data mature.
Okay, got it. Got it. I think there were two grade five ILDs as well.
Yeah, these drugs and a lot of the DS- DXd drugs, which is true across the Daiichi series, they do have some ILD. But one of the things we've learned, and this is true, I think, probably also with the Astra agents, is that they have a very strong program to detect and reduce and prevent it from happening. There were two cases, but compared with what we would have expected, it was about right.
Got it. CDH6, I think this ADC has, I think every time I see it in a conference update, the dose has stepped down. I guess, are we now hitting a point where you can get to a therapeutic index, which kind of works on both sides, efficacy and safety?
Yeah, I have to say that. So you worry about the dose. I think about this as one of the coolest of the drugs that we got.
Oh, is that right?
Yeah. Because between 4.8 and 6.4, 4.8 and 6.4, the efficacy is so extraordinary. And the things that I really love is the duration of response and the PFS. It's really, really good. And so I see this as being a real sleeper in the series. But for me, it's going to be we're excited to bring it into now later stage studies. And I'm very confident that it's going to be a big home run.
Okay, excellent. Anything else on oncology just before we transition further?
We had a lot of preclinical data. The clinical studies had just started, and we had maybe two or three patients. So I think that the configuration and the preclinical data and our profiling of that molecule versus others, we thought that was the best kind of stoichiometry between PD-1 inhibition and VEGF inhibition, the right kind of potential half-lives, projected half-lives, and so on. It's early. It's an early.
It's 1 to 1 on PD-1 and VEGF?
It's something.
It's something. Okay.
Yes.
That's good to know. Okay, excellent. And when's the first data update? I guess, what will be the cadence of data updates? How fast can you be in a randomized trial is the real question.
It's in dose escalation right now. So it'll take some time.
Got it, and could we envision a scenario where you run a trial like, assuming this target's active, but could you envision a scenario where a KEYNOTE-021G-like size trial could enable a path to registration?
I don't know. It's going to be it really depends on setting. We're going to look at.
Like a phase two 120 patients.
Yeah, I know. I mean, I think that that era may not necessarily be there anymore. One of the things that I think is important with these drugs is the safety database. And I think that regulatory agencies will want to see not just efficacy and not just a small safety database. They'll want to see longer-term follow-up. They'll want to see the effect size with OS. They'll want to see perhaps the proper dose and having an optimized-like dose. So when you think about all of that, 120 patients won't get you there.
So it depends. One of the things we have to remember is that this drug needs to pass the U.S. regulatory gauntlet, which means optimized, which means making sure that they're confident in durability and the long-term efficacy and safety profiles. So I'm not sure that it's reasonable to expect some small study to get to registration, besides the fact we have a variety of different drug combinations that we want to try.
Okay, got it.
Not just mono.
Okay, got it. Maybe, I guess my last one on this would be, if you put on a really skeptical hat, you could say, you know what, the entire curve separation happens at the first time point, that's week six, and you could make a case that the summit drug is basically a high-dose Keytruda. It's at a higher dose. How do you guys balance those things as you think about the development of?
It's a great question, and it's something that we have to address through dose selection and through looking at the effect size for not just that molecule, but also, for example, the one that is the Biotheus and BioNTech combo, because those guys are PD-L1 VEGF, so I don't know. They had good effect size in triple-negative breast cancer, and so you think about, is this just high-dose Keytruda?
Can you consider running a high-dose Keytruda trial versus standard dose Keytruda in lung?
I don't think we would. I think we optimize the dose of Keytruda. There was a lot of work that was done upfront. I don't think we would do that.
Okay. Okay. But are you leaving the door open that that could be a possibility, just a high-dose PD-1?
I don't think so. I think it's a combination of PD-1 and VEGF inhibition.
Okay. Excellent. Another trial that's important next year, at least to me, is the Group 2 PH trial. That's the left heart disease trial. But one of the things that worries me is the risk of background anticoagulant use driving a bleeding imbalance. Do you have visibility on how the bleeding profile is looking in that trial?
It's a blinded study, so I don't have any treatment group data. But I have to say that overall, there haven't been too many bleeding events. It's not been an issue.
Okay. And I know it took a while to recruit. And some of the feedback I've picked up is that the trial is designed for pulmonologists, but it's really intended for cardiologists. And there's some disconnect somewhere along the way, which is why it's slower to recruit. Any thought process in only taking CpcPH and not the IpcPH patients?
Yeah. So first of all, you're right. You're right in the sense that this is not a disease entity that people are warehoused, that they have a standard treatment approach, that they have the right drugs, and they're just looking for another drug in that category. These are patients who don't have very many options and where the diagnosis needs to be made in a more sophisticated way. CpcPH kind of patients tend to have a more severe disease.
They tend to go down faster. They tend to have more fibrosis. They tend to have more wall hypertrophy, the kind of biology that we've seen with PAH, with group one PH. And so we thought that that group would be more similar in terms of biology to PAH. And that's why we chose it. I think that the way I look at it is if the study is positive, people will have a rationale for going there, and there'll be a lot more diagnosis. I think it's a highly underdiagnosed disease.
Peter, does this have to be repriced? Is it out of step if this indication works?
Yeah. We've not spoken to what the pricing strategy would be for Winrevair if this works, so.
Okay. Okay. Okay. Makes sense. Oral PCSK9, that's another one that's important for next year. I think the food and diet restriction topic is coming up more and more and more. Could you just walk us through how significant is that issue or not? And knowing that, presumably, it will be as part of a cocktail, so there's some DDIs as well, so could you speak to that?
Yeah. The DDI issue is not, I don't think, going to be a problem. We have 30 minutes between administration and food. You can take it with water and sort of non-fatty liquids, and then you can have breakfast 30 minutes. This was similar to the bisphosphonates back in the day, and so I think that it hasn't been a compliance issue in the clinical studies so far, and obviously, it's something that we're going to have to make sure people are well educated about, but I don't see it as much of a problem compared with, let's say, having to get the injections and so on.
Got it. I guess the other one is on LDL reduction. There's a CETP inhibitor in the marketplace as well, which is reporting LDL reduction, which approaches what you guys are about to show. However, I recall Anacetrapib also had LDL reduction akin to the other CETP inhibitor from New Amsterdam. But the nuance was they were using this LDL measurement method, BQ, which may not be what's the standard. So could you just remind us all the LDL reduction data you guys have shown on an apples-to-apples basis, how different or similar is it versus the New Amsterdam molecule?
So we use the standard approach to measuring cholesterol. And the reductions that we see with PCSK9 are more profound. And I think that the issues with CETP inhibitors is that they have a pleiotropic effect. And the efficacy, the cholesterol reductions have been a little bit variable. And I think there's been some disappointment in some of the numbers. But overall, for us, it's the same measurement system that we use with statins. And throughout our program, we had reductions around 60% above and beyond maximum statins, high-intensity statins. So I'm very confident about that.
There was one death, I think, at the 18-mg dose, which was possibly drug-related. Would you happen to recall?
Yeah, it was a motor vehicle accident. There's someone who crashed their car, but the doctor.
But how would it be drug-related? Okay.
We never challenge our investigators.
Okay. Got it. There was very limited dose response above 12 mg, but you guys went to the 20-mg dose anyways.
Because you want to have the. It's not just the average. It's the percent of people with reduction. Remember, there's always variability in a drug and how much you reduce it, and so we want to make sure that everyone gets benefit.
And then my last one on this is really, I remember some of the initial studies on PCSK9s. One of the feedbacks was that if you enroll a population, which is very well controlled, and their LDL levels are already at 70 or 80, you're not going to get a massive hazard ratio on a CVOT. And I think that's kind of the framework you guys are using for the most part in your CVOT as well in the outcomes trial. I guess, how did you guys think through that? Having patients above 100 LDL could have resulted in a very different hazard ratio, presumably.
No. So the hazard ratio is a combination of, so first of all, there's no such thing as too low of a cholesterol level. So you will get benefit across the range. Hazard ratios for CVOTs are also dependent on time. And I think if you looked at some of the other PCSK9 inhibitors, they were truncated a little early. And that's why you had hazard ratios that maybe were not at the numbers that you'd want to see. We've done a lot of CVOTs. So we've modeled this so that the hazard ratio is good.
When should we get a readout on this?
When did we say? I think it's '8-ish.
'28?
'28-ish.
The outcomes trial? Yeah, 2028, 2029.
'28, yeah.
Got it.
It's still enrolling, so.
Peter, I don't know if you guys have said much on this. Do you guys expect this to be a meaningful launch before the CVOT?
We do, yeah. We will plan to launch based on the biomarker data.
To the extent you guys are putting in so much investment on this, would it make sense to have whatever you want to do in obesity also be in the marketplace around the same time? Is that how you guys are thinking about the preferences of whatever molecule you guys are looking into for obesity?
Well, I mean, I think we've got a bunch of different each molecule sings for its supper. So we're looking at, for this particular molecule, we're going to the data for MK-0616. We'll have the cardiovascular outcome data we said in 2028, but we'll have the cholesterol lowering by the end of next year, beginning of 2026. And so that's when we'll start that. MK-6024, which is our MASH compound, that's an injectable, you'll have phase 2b results, I think, late next year. And then phase 3 will start after that, should the data warrant it. Great enthusiasm with that drug. Our enrollment rates have been through the roof. And so I think that that's where our current metabolic play is. We'll see what happens with either business development or through our own labs in terms of other mechanisms of action.
Sounds like you guys may just go with an in-house approach. Because previously, it sounded like you guys were certainly looking at an external asset for obesity.
You know, I think so. Just to step back, the question in obesity is what can be added to what's already out there in the armamentarium. If you think about all the different assets that are there in obesity, there are injectables. There are all kinds of different orals. A lot of companies have gotten into it. And so the question is, what we've been looking at as we saw the field and we saw the wonderful work that's being done with injectables and now some of the orals.
You have to it's not good enough just to have something. You have to have something that's differentiated and that's relevant and that you can put into a suite of assets that make a difference for patients. And so we've been pretty disciplined about what we want to see, whether it's from our own internal folks or from the outside. It has to be something that's not just differentiated.
So differentiated at this point. So maybe let me just set the parameters. Weight loss, we're hitting 25% with injectables right now. Or the other way of doing it is orals, which is mid-teens. Or a third parameter is you go into the muscle. Amylin perhaps could fall into that. We need to see confirmation of that. Are there other parameters you see for the front page?
I think those are important parameters. There's tolerability, which is an important parameter. There's orthogonal. There's the question about whether or not if you had orthogonal mechanisms that are here or not yet been part of the all the names, the drug targets you've talked about, whether or not there's something that with lower doses of each, you can get something that's a little bit more effective.
But if you want to go orthogonal, don't you need a background GLP regardless to put the orthogonal onto?
Maybe. We'll have to see. I mean, I think that the point is, though, is that just having another equivalent of an oral agent when there, you can count a whole bunch of stuff that's, of course, some of them are in phase 1 or 1b/2. You don't know for a fact that they're going to get to the end. But these are serious companies with serious drugs. Just having another one of those and starting is not necessarily the case. So you have to have a combination, some sort of combination approach maybe, or some sort of unique feature that will help out with things like tolerability, as you mentioned.
How much weight loss? Any effects on drug-drug interactions? Can you eliminate the problem with muscle wasting? And you can go on and on about different things as the drugs evolve. The way I look at the obesity field is that there's this initial gold rush. Then the question is, what really will stay the course in the long term? That remains to be seen. That's going to be a more complicated question. We didn't get into the initial gold rush. It wasn't our thing. We have so many other things in the pipeline. Now as we look at this.
In obesity?
No, I'm talking about in general.
In general.
And so the question about obesity is a question about what is a Merck product? What is something that we can do that we can show differentiation? And it's not so simple and has to be a very thoughtful approach. And so we haven't run around and just bought things willy-nilly.
And just to be clear, Umar, that messaging has been consistent. So there's no intentional change. We have internal programs, preclinical, and we continue to look at BD as a potential opportunity.
Elliott, could you have anything in the clinic in obesity by next year?
I don't know. We'll have to see. I mean, we just have to it all depends. Again, we have very rigorous gates for everything that we do. Because I've got like 40 or 60, 40-60, depending on how you count it, molecules. I'm very confident in the amount of molecules that I have in the clinic so far. I think Merck has got a tremendous pipeline as it is, not including obesity. And so I'm really excited about the potential opportunities there, but I'm not wholly dependent on it. I'm going to use the same kind of strong stage gating that I do for anything else. And we're not going to run into the field like as if, oh my God, we have to be there.
Maybe a quick second on vaccines. You guys talked about a program called V118. So this is not 117. This is 118. Is this a potential 30-plus valent that could do infants and adults for pneumococcal vaccines?
What are the issues with pneumococcal vaccines that you want to address? You want to address maximize either pediatric or adult. And you also want to make sure that, ironically enough, as you add types and if your immunogenicity goes down, it's actually what's the residual of the types that have been in the vaccine already where the efficacy isn't 100%. That's actually where most of the disease is.
If you look at pediatrics and adults, Serotype 3 is a much bigger disease burden, although in the vaccines compared with all of these number 29, 30, 31, 32. So, what we're looking at with V118 is we want to make sure that we have robust vaccine that could address with high immunogenicity, not just new types and sort of say, oh, look, 30 is better than 25 is better than 20, but actually speaks to what we anticipate the burden of disease will be reduced, and that could be in adults or in children. We'll see where it goes.
So we shouldn't hold our breath on this being a 30-plus valent, for example.
I didn't say that.
The next-gen Gardasil that's moving forward, is that a 14-valent?
It's going to be to increase the number of types, particularly those patients who have from more diverse settings where we haven't been able to hit with Gardasil 9. The idea with this vaccine is to fundamentally change cervical cancer screening. So it's going to try to maximize the number of types. We haven't announced the number of types, but my goal with that is to have sufficient coverage that women won't have to undergo routine cervical cancer screening if they're fully vaccinated.
Got it. One last, sorry. On pneumococcal vaccine, I totally forgot. There's some evidence in the patent domain which suggests Pfizer for their really broad spectrum, so the 25-valent and the 30-plus valent, they're using a second carrier protein to fix for serotype 3. I know you talked about serotype 3 as well. So in the back of my head, I was wondering, is Merck now also considering two carrier proteins?
This has been so serotype 3 has been a real Achilles heel for people, and by the way, and also 19F and others, so it's not like the only one. I think that it's important to look at other approaches, at a variety of approaches. It could be adjuvant. It could be carrier protein. You see the literature. You see some of the other vaccines that are out there coming with different approaches to either conjugation or to sort of the system in which the vaccine is manufactured. We have a variety of approaches. There are many subtypes of V118. We'll figure out the right one based on data.
This one is entering clinic when? V118?
I don't know.
10 phase one.
phase one, yeah.
It is in phase one.
Yeah.
Oh, so in phase one, there's multiple formulations.
We're going to have a series of different V118s.
There will be a series of formulations.
Yes.
I see. I see. Okay. Makes a ton of sense. So last one for me in the last minute. I should know more about this, and I don't actually. MK-8527 in HIV.
Yes.
This is a readout coming up pretty soon. This is for PrEP with a single pill once a month.
Absolutely.
But the dose is really high.
No.
What is the dose?
The dose is really low. It's like I forget how much it is. It's much lower than that.
Wasn't it like 100 milligrams or something from what I recall?
Yes. It's going to be a once-monthly pill, small tablet regimen.
Okay. I guess how should we think about leukopenia risks or any CD4 issues that could happen by pushing it? So that's fine.
We'll find out soon enough. But 8527 is not like it's in the same family as a islatravir, but it's a different molecule, different threshold. So I'll tell you.
Is it same scaffold?
Yes. But it's same scaffold, different molecule. But I think this is going to be a big deal.
Should we not worry about CD4 drop then?
You should always worry about safety until you see the data.
Right.
So in my mind, the way I look at it is if you can have a single pill once a month that's not a horse pill that people can take, that is the sine qua non of what PrEP should be. Just ask the Gates Foundation. And those guys, they always are asking about this sort of stuff. We're very excited about this molecule.
I feel like no one ever talks to you guys about this program, and this is a readout coming up.
I was formerly head of ID vaccines at Merck, and I never know why people never talk about it. They always talk about that Gardasil issue in China. We talk about 8527.
So this is being developed only for PrEP, not for treatment?
Yeah, just for PrEP.
Wow. And why not for treatment too?
Because we've got 8591 for that. We've got the islatravir for that. No need.
But isn't the Islatravir like, in my mind, it's like a clouded path now with the CD4, and FDA might require monitoring or just be in a black box.
Just wait till you see the data are coming.
Just wait is my note on the slatravir .
Just, you know, we worked on the dose. The Q-day regimen data are reading out post-haste. And so you'll see it's soon enough. And I'm very confident that Merck is back in HIV. And I mean it. Yeah.
Okay. Got it. But not with the 8527 on both sides. Is that still?
MK-8527 is for PrEP.
Okay. Got it.
It's just like the right profile for PrEP. It'll be its own regimen. Islatravir is incredibly well characterized. Yes, including its high-end toxicity if you give too much of it. But we already have it in Q-week and Q-day. There's no reason to go with MK-8527 for that particular setting.
Got it.
We'll just have it for PrEP.
So last one to finish off on virology. Molnupiravir, any additional indications that you guys are putting in more investments? Because that looked like a promising molecule.
We are doing another efficacy study in COVID. I think it's really important. This is one of those drugs that I cannot believe that we had such weird press about. Because if you go to Asia and Japan and Australia and so on, that's been the drug that they've used for COVID. And it's been a smashing success. And so I don't know why. There's been all kinds of weird social media sort of stuff and whatever in the U.S. We've looked at a variety of different indications, other viruses with challenge studies. Data are mixed. But we are investing in another COVID study because we really believe in this drug for COVID.
There's viral challenge studies and other indications. Is that published somewhere?
No.
Not yet.
It's coming, and so we're.
Because mechanistically, I thought it lends itself to a lot of indications.
But you have to, that's why you always do the study. Just because.
The viral challenge was done with the right dose of the.
Right. So we have a variety of different viruses. And those data will come in due course. But I think the biggest place where we're sure that it's efficacious is in COVID. And but the regulatory authorities in the United States, FDA, has asked for another study. And that study will commence.
Got it.
And I'm confident that it's going to be positive.
Excellent. Anything in the audience just before we wrap up? All right. Thank you, guys.