Merck & Co., Inc. (MRK) Earnings Call Transcript & Summary

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 will let you frame the broader discussion and we'll jump right in.

Well, great. It's great to be here. My name is Eliav Barr. I'm Chief Medical Officer at Merck. It 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. So 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, 2 to 3...

You tell me. So no, no. We thought I -- 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% to 10% ex FX 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 we -- 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 partner, 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-KEYTRUDA pipeline. Oncology is $20 billion. Cardiometabolic, $15 billion. And immunology is multibillion. 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?

Yes. So we've outlined what we believe our commercial opportunity is in several parts of our pipeline, not our entire pipeline. But as Umer 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 III 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, that's -- we've outlined oncology, cardiology and immunology as 3 major sources of opportunity. We also have opportunities in other areas of the pipeline, HIV and 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 subcu. However, does that include your new Chinese PD-1/VEGF, for example?

So not specifically.

Not at the time it was given.

Yes. 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 the Summit Therapeutics side with the hazard ratio they've put up on PFS. But we'll see how the profile plays out on an OS basis. A, I'd be curious what are your thoughts 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. Well, I think that the data are very interesting. They were -- they demonstrated a pretty substantial hazard ratio for progression-free survival. And 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. And we need to -- 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. So 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 want to -- I have several follow-ups on this. First one, as you think about the program you guys brought in, is that more an entrance against anything that happens on the PD-1/VEGF space? Or is that just your conviction in the target?

Yes. I think it's the latter, not the former, because by the time the products get into the U.S. setting, it will be close to the U.S. LOE for KEYTRUDA. It wasn't really -- 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. And we ended up with the LaNova LM-299 as the one.

Got it. As I think about the signals 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 would be -- even in a trial against KEYTRUDA...

A trial against KEYTRUDA in chemo.

Yes, sorry. Yes. So I think that the -- where this will play out will depend again on the efficacy and safety profile. And if you look at the data from -- that were presented, and there was the data on greater than 1% frontline NSCLC, and there was the 1% to 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. And you had that kind of hockey stick kind of thing for 1% to 49% that always worries -- one always worries about with VEGF inhibitor combinations, where you had a really big effect size at the beginning and then it come back close, and one worries about that. So how we'll develop the drug will depend on what we see in the Phase I 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' responsiveness to -- Chinese patients and their responsiveness to VEGF? And how would that dynamic be relevant for the...

So a lot of the bev studies have shown a higher response rate in Chinese patients, but the data, I think, are -- were so spectacular. So there was so much of a OS -- of a PFS benefit in the Akeso data that -- the Akeso-Summit data, that I think it's hard to imagine that it's just a [ little ].

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 happening on the trial that was just reported this past [ week ]?

Well, we'll see. I mean, again, I just -- I think that's why you do OS evaluations. You have to make sure that you get the right patients. I mean, part of it is also -- we have to remember that there is -- 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 -- we're 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. We think -- happily, we've got a bunch of other further analyses ongoing.

Why did Astra pass on this one? That just never -- I mean it's...

Why did they pass on this asset?

Yes. Because they could have put this as part of the collaboration with Daiichi.

Ask Susan. I don't know.

Okay. All right. Excellent.

[ On that ], we didn't.

And on the PFS, is it reasonable to think there's at least a 2-plus month median PFS benefit?

I think that there is. We haven't shown the data because it was that -- even those data were relatively immature, so we have to wait and see how it goes. I think that the -- what was interesting to me, and if you look at the study results at 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. So differential effects in the front and the back end?

In the -- 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 2 Grade 5 ILDs as well.

There was. Yes, these drugs and a lot of the -DXd drugs, which true for -- across the Daiichi series, they do have some ILD. But their -- 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, rid and reduce and prevent it from happening. There were 2 cases, but it was -- 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 any conference update, the dose has stepped down. I guess, are we now hitting a point where you can get to therapeutic index, which kind of works on both sides, efficacy and safety?

Yes, 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?

Yes. It's because between 4.8 and 6.4 mg per kg, 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?

Well, we had a lot of preclinical -- there's a lot of preclinical data. There's no -- the clinical studies had just started, and we had maybe 2 or 3 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 or projected half-lives and so on. It's an early [ scenario ].

It's what? The one on PD-1 and VEGF?

It's something.

It's something. Okay. That's good to know. Okay. Excellent. And when is the first data up? Like 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 will take some time.

Got it. And could we envision a scenario where you run a trial like -- assuming this target is active, which is -- but could you envision a scenario where a KEYNOTE-21G-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...

The Phase II, 120 patients.

Yes, I know. I mean I just -- I think that it's -- 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 the regulatory agencies will want to see not just efficacy and not just a small safety database. They will 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 Optimus-like dose. So when you think about all of that 120 patients, it's not that -- it won't get you there, so it depends. We're going to -- one of the things we have to remember is that this drug needs to pass the U.S. regulatory gauntlet, which means Optimus, which means making sure that they're confident in durability and the long-term efficacy and safety profile. 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. I just want to...

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 6. And you can 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/VEGFs, so I don't know. There, they had good effect size in triple-negative breast cancer. And so you think about, is this just high dose?

Can you consider running a high-dose KEYTRUDA trial versus standard-dose KEYTRUDA in lung?

I don't think we would. I think we optimized the dose of KEYTRUDA in there. 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, and that could be a possibility? It's 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 like by treatment group data. But I have to say that overall, there haven't been too many bleeding events. That has 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 as well?

Yes. So we -- so first of all, you're right. These are -- this is -- 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 1 PAH. And so we thought that, that group was -- 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 building -- for going there, and there'll be a lot more diagnosis. I think it's a highly undiagnosed disease.

Peter, would you -- does this have to be repriced, sotatercept, if this indication works?

Yes. We've not spoken to what the pricing strategy would be for WINREVAIR, if this works, so -- yes.

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?

Yes, 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's -- I don't -- it hasn't been a compliance issue in the clinical studies so far. And obviously, it's something that we're going to be -- have to make sure as well, people are well educated about. But I don't see it as much more -- 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 NewAmsterdam. 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 NewAmsterdam 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 what...

Yes, it was a motor vehicle accident. There was someone who crashed their car, but the doctor...

How would it be drug related? Okay.

We never challenge our investigators.

Okay. Got it. There was very limited dose response above 12 mgs, but you guys went to the 20-mg dose anyways.

Because we want to have -- you want to have the -- it's not just the average, it's the percent of people above the -- with reduction. Remember, there's always variability in the drug and how much you reduce it, and so we want to make sure that everyone gets the benefit.

And then my last one on this is really -- I remember some of the initial studies on PCSK9s. One of the feedback 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, I don't -- so the hazard ratio is a combination of -- 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 a 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.

And when should we get a readout on this?

When did we say? I think 8-ish?

'28?

The outcomes trial, yes, '28, '29.

'29, yes. 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, yes. We will plan to launch based on the biomarker data. [ Reach out late next year ].

And 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 0616 or enlicitide, we'll have the cardiovascular outcome data, we said, in '28. But we'll have the cholesterol lowering by the end of next year, beginning of '26, and so that's when we'll start that. MK-6024, which is our MASH compound, that's an injectable. It -- you'll have Phase IIb results, I think, late next year. And then Phase III will start after that, should the data warrant it. Great enthusiasm with that drug. Our enrollment rates have been through the roof. And so we're -- I think that that's where our current metabolic play is. We'll see what we -- what happens with either business development or through our own labs in terms of other mechanisms of action.

It sounds like you guys may just go with an in-house approach because all -- previously, it sounded like you guys were certainly looking at an external asset for obesity.

Well, 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. But it has to be something that's not just another oral.

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 differentiation?

So 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 on to?

Maybe, we'll have to see. I mean, I think that the point that I'm -- the point is though -- is that just having another equivalent of an oral agent when there is -- you can count a whole bunch of stuff that's -- of course, some of them are in Phase I or Ib/II. You don't know for a fact that they're going to fit -- 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 it goes -- you can go on and on about different things as the drugs evolve. So the way I look at the obesity field is that it's -- there's this initial gold rush. And then the question is what really will stay the course in the long term. And that remains to be -- 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. So now when you look at this...

In obesity?

No, I'm talking about in general. And so the question about obesity is a question about what will -- what is a Merck product? What is something that we can do that we can show differentiation? 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, Umer, 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.

Could you have anything in the clinic in obesity by next year?

I don't know. We'll have to see. I mean I just have to -- it all depends. Again, I -- the -- we have very rigorous gates for everything that we do because we've got like 40 or 60 -- 40 to 60, depending on how you count it, molecules. I've got -- 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 I'm -- 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 any other, anything else, and we're not going to run on to 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, it's 118. Is this a potential 30-plus valent that could do infants and adults for a pneumococcal vaccine?

So the issue -- so 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 don't want to -- one has to -- 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.

Okay. Okay. And 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 -- we haven't announced the number of types. But my goal with that is to have sufficient coverage that patients won't -- 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 on the back of my head, I was wondering, is Merck now also considering 2 carrier proteins?

This has been -- so serotype 3 has been a real Achilles heel for people. And by the way, also 19F and others, so it's not like the only one. And so 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. And you see the literature, and 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. So we have a variety of approaches. There are many subtypes of V118, and we'll figure out the right one from -- based on data.

This one is entering clinic when? 118.

It's in Phase I.

Phase I, yes.

It is in Phase I?

Yes.

Also, in Phase I, there's multiple formulations.

There'll be -- we're going to have a series of different 118s.

There will be a series of formulations?

Yes.

I see. I see. Okay. It makes a ton of sense. So last one for me in the last minute, it's -- I should know more about this, and I don't actually. MK-8527 in HIV, 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 at -- I forget how much it is. It's much lower.

Wasn't it like 100 milligrams or something? From what I recall.

It's not -- 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...

We'll find out soon enough. But 8527 is not like -- it's in the same family as islatravir, but it's a different molecule, different threshold. So I'll tell you, it's...

Is it same scaffold?

Yes. But it's same scaffold, different molecule. But I think it's -- 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. So in my mind, the way I look at it is if you could 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. It's really a...

I feel like no one ever talks to you, guys, about this program. And this is a readout coming up given the...

I was formerly head of ID and vaccines at Merck, and I'm -- I never know why people never talked. They always talk about the GARDASIL issue in China. You're talking about 8527.

8527. So this is being developed only for PrEP, not for treatment.

Yes. Just for PrEP.

And why not for treatment too?

Because we've got 8591 for that. We've got islatravir for that. Don't need...

But isn't islatravir -- like in my mind, it's like clouded path now with the CD4 and FDA might require monitoring or just do a black box.

Just wait until you -- the data are coming.

Just wait is my note on islatravir.

Just -- we're working on the dose. The Q day regimen data are reading out post haste. And so you'll see it soon enough, and I'm very confident that Merck is back in HIV, and I mean it. Yes.

Okay, got it. But not with the 8527 on both sides. Or is that still...

8527 is just for PrEP. It's for PrEP.

Okay. Got it.

It's just got the right profile for PrEP. It will 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 the Q day. There's no reason to go with 8527 for that particular setting. We'll just have it for PrEP.

So last one, to finish off on virology. Molnupiravir, any additional indications? Are you guys putting in more investments? Because that looked like a promising molecule.

Well, we are doing another efficacy study in COVID. I think it's really important to -- this is one of those drugs that I cannot believe that we had such a weird press about. Because if you go to Asia, in Japan and in 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 -- well, 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.

Is that a -- and there's some viral challenge studies in other indications. Is that published somewhere?

No, not yet.

Not on COVID?

No. It's coming. And so we're...

Because mechanistically, I thought it lends itself to a lot of indications.

It could. But you have to -- that's why you always do the study just because it's...

And the viral challenge was done with the right dose of the [ drug ]?

Right. So we have a variety of different viruses, and those data will come in due course. But I think the biggest -- the place where we are sure that it's efficacious is in COVID and where -- 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.