Amgen Inc. (AMGN) Earnings Call Transcript & Summary

Excellent. Thank you, guys. Thanks for joining us. Pleasure to have Amgen management join us. But before we start, I always love turning it over to Arvind, who I feel like framed it so well. So Arvind, over to you.

Umer, thanks so much for inviting us to your conference. And I was just talking to Dave earlier that there's great news that you're planning on having this conference in Miami this year or next year.

That's right.

Let me just kind of tee up some of the kind of the broader picture or some of the key topics. I've been obviously delighted that we have David Reese, our kind of research and development with us. And with all of what we have going on with the pipeline, I think it will be -- it's just a great opportunity to kind of dig into some of the opportunities that we have there. So I will start by saying that despite the fact that we have confronted some macro headwinds, we have had a year of solid execution so far as we near the end of the year. And our focus, our strategy of focusing on volume-driven growth, I think, is a very effective strategy. If you look at many of our priority products through the first 9 months of this year, we have generated some very good unit volume growth for these products. Notably, products like Repatha, products like Otezla, Prolia and EVENITY. And of course, with some of the recently launched products, TEZFIRE for severe asthma is off to a very good start, LUMAKRAS continues to do well. Obviously, a lot more development work that has to be done there as we think about moving LUMAKRAS to earlier lines of therapy or in other tumor types. I will also note over that our recently closed acquisition of ChemoCentryx that brings a newly launched, innovative product to our implant portfolio, a product called TAVNEOS. So I get more to come on them. And then also, we continue to make very good progress with our innovative pipeline. And you might recall that recently at the American Heart Association, we presented some data, some detailed Phase II data on Olpasiran, our Lp(a) inhibitor. And what we demonstrated in this data is that Olpasiran dose 75 milligrams or higher every 12 weeks reduce the Lp(a) concentration by more than 95% in patients with established cardiovascular disease. Now we conducted an investor call in conjunction with the American Heart meeting, and you might recall that we also presented data from single and multiple dose cohorts of a Phase I study on AMG 133. This is our Phase I obesity molecule, very novel mechanism targeting GLP-1 and the GIP receptor. And we are going to be presenting a more detailed data set from this Phase I study at the upcoming congress on insulin resistance, diabetes and cardiovascular disease, which is going to be held here in December. And of course, planning is underway to initiate the Phase II trial, but happy to delve in to that in greater detail, depending on the questions that we might get from you and others.

Got it.

LUMAKRAS, as I've mentioned before, the development continues. We have a very broad, comprehensive program as we look to move this into earlier lines of therapy and other tumor types. And then just a couple of other comments that I would make. Biosimilars, will continue to add new biosimilars to our portfolio over the next several years. We have had positive Phase III data from 3 programs this year. Our biosimilars against STELARA, SOLIRIS and EYLEA. And of course, we are very much looking forward to launching our biosimilar version of HUMIRA. Our product will be called AMGEVITA towards the end of January of next year. The last comment that I would note is we have a strong balance sheet, continue to generate significant cash flow. We generated almost $3 billion in free cash flow in Q3, and we retain significant financial flexibility to continue to look at strategic business development. So with that, let me turn it over to you and happy to jump into any questions that you might have for Dave and myself.

Sure. And Arvind, maybe -- and I feel like there's a ton of R&D specific questions I want to get into, but just ahead of that, can you remind us what specifically are you guys seeing on BD? Is ChemoCentryx like the focus right now?

We have been fairly consistent in our posture that we are size agnostic. We have a fair amount of financial flexibility. Our quest for BD really emanates with the strategy of the company. Does it allow us to strategically -- after the portfolio of the company, does it allow us to expand our geographic footprint? Perhaps most importantly, is this something that's going to allow us to create value for our shareholders? Can we be the best buyer of that asset? So those are some of the criteria that we look at, and size, of course, is secondary to that. If you look at some of the deals that we have done of late, if you think of the Otezla acquisition as an example, this is a product that has been launched and had been approved in a number of markets, but have been commercialized in a limited number of markets. And with our global infrastructure, we are able to take this product in these markets where the product had yet to be launched. And really, the same applies for TAVNEOS. We have a significant amount of experience in in-plan, in the rheumatology space, and we can leverage that as we commercialize this asset.

Got it. And Arvind, also, sorry, just one other quick high level one, was on the 2030 numbers, can you remind us if that guidance is all organic? And how much denosumab do you guys assume in there? Because there's always this question of do you guys have additional patents beyond the 2027 or not?

Yes. Again, what we have mentioned, Umer, is that in terms of our own modeling, we have estimated that we retain exclusivity on denosumab through 2025. And the projections or the growth outlook that we have communicated through the end of the decade is indeed organic. Of course, it takes into consideration certain assumptions that we have made on our growth products, notably products like Repatha and Otezla, some assumptions that we have made on the biosimilars business. We have estimated that off of the revenue base that we have for biosimilars in 2021, which was just a little over $2 billion, we can more than double that by the end of the decade. It takes into consideration pipeline contributions, and some of those, of course, will continue to be derisked as we get additional data. So all of that translates into an organic outlook that we had communicated of mid-single-digit growth as far as revenues are concerned and low double digits -- or high single-digit, low double-digit EPS growth on average over this period between now and 2030. So any business development activity that we undertake between now and then should be additive.

Got it. And denosumab is not modeled in through 2030, correct?

Denosumab, like I said, we have assumed that there will be biosimilar competition post 2025 in terms of our own model.

Yes. Got it. Got it. Okay. Excellent. So there's a ton to talk about, David, so let me jump right in. And let me start with the -- not so much because I think this is the highest profile program in your pipeline, but more because that's the data that's coming up, on the obesity side. So let me start with this. One of the questions that often comes up is, should there be an expectation for an A1c benefit or not considering Amgen's only developing in an obesity setting.

So what I would point out is we'll be showing the data in a couple of days. Actually now here in Los Angeles, at the hybrid conference, a poster will go up on Thursday, then there will be an oral presentation on Saturday afternoon, where we'll share the full data set from the Phase I trial. In that trial, we enrolled only individuals with normal hemoglobin A1C levels. So these are not individuals with the history of diabetes or hyperglycemia. However, based on the mechanism of action, we would expect anti-hyperglycemic effects in the Phase II trial, which we'll talk more about in due course as that gets up and running. We plan on enrolling both patients with a history of type 2 diabetes as well as those who are normal glycemic where we'll directly address that question.

Got it. Got it. The other one -- so that's really helpful, David. I appreciate you clarifying that. So there's no reason not to expect A1C benefit. The other one is a lot of -- I feel like there's a lot of mismatched cross-trial comparisons going on. People are taking your data at a certain time point comparing it versus some of the other data sets at similar or slightly later time points. But one of the important differences is the relevance of a titration regimen. And can you speak to how that was done in this study?

Yes. In the Phase I study was a very standard design. So there were a single dose cohorts and then there were multiple ascending dose cohorts. And those individuals received 3 doses basically 4 weeks apart. So a total of 12 weeks of dosing. Monthly dosing is the easy way to think about it. What I would pay attention to when we released the data in a few days here are the kinetics of that weight loss. So the rapidity, sustainability, and then also, of course, the adverse event profile. So these are things that we all think are important, and we'll potentially differentiate if we're able to maintain a favorable profile through Phase II.

Got it. So I guess, Dave, you're saying since it's multiple ascending, there technically is a titration first versus second versus third shot?

No. No, I'm sorry. Those were different cohorts.

Okay. But there's no titration?

At different doses, but they were not dose titrated within cohorts. Go ahead, sorry.

No, it sounds like you're saying you may not need titration.

That's one of the questions that we will address in Phase II. So we will -- and this is planned to be a very robust Phase II trial. One thing that I really want to have coming out of that study is optionality in terms of further development. So we will look at both dose escalation, i.e., titration as it's commonly referred to in this field as well as fixed dose regimens and a variety of doses.

Got it. So Dave, I guess, let me just say back to the way I understand it. It almost sounds to me like you're fairly comfortable with where the profile is tracking right now on the AE side. You think there might be room to further improve by [ trying titration ] as well.

Yes, the question is -- of course, always in Phase I, you have relatively limited numbers of patients. And the question is, can we optimize the dose and schedule, and that's why we're planning a fairly robust Phase II to investigate a range of dosing and scheduling paradigms.

Got it. And where -- I mean, as you envision this program on a longer-duration studies, you're getting close to mid-teens in weight loss already. And we know sort of the big bogeys are Mounjaro getting to 20% at a much later time point, and Novo modeling, never showing, but modeling that they can get to maybe 25% with CagriSema. Do you think -- considering you're approaching mid-teens at such an early time point, do you think there's a plateau coming at a certain point? Are you tracking those patients beyond the early dosing as well as what's your expectation? Do you think you can get to that mid-20s or higher perhaps?

We are following those patients. This is, of course, a key question for Phase II. What I can tell you is that based on the kinetics and the curves that we've seen in Phase I, again, that will be shared in a few days, we don't appear to have reached the plateau, number one. And so the question is how much weight loss can we actually drive with continued dosing? Remember, this was a total of 3 doses maximum for these patients. I will say also that it was relatively well sustained, as you'll see from the curves. Patients maintained weight loss for a decent period of time after that third dose. That suggests mechanistically that there's still room to go in terms of additional weight loss. But obviously, that's a key question for Phase II. But I'm relatively optimistic based on the data we've seen so far.

Got it. And David, at a patient level, was it generally consistent, the percentage that hit, let's say, a certain threshold versus not? Because Lilly and Novo Nordisk have always shown certain thresholds of weight loss. And like patient distribution, are you comfortable with what you're seeing, or is there outliers, too?

Yes. I mean I would say we're relatively comfortable with that with the caveat that Phase I always has relatively small numbers of patients, typically 8 in a cohort, a couple of them are getting placebo. So you've got small numbers of patients. But for these sorts of studies, we're quite happy with the data.

Got it. And perhaps my last one on this topic is really just around the mechanism, because I know there's been questions raised on what Mounjaro is doing on the GIP side is kind of the opposite of what you're doing in this regimen. And nobody really understands because Lilly says one thing and [ Amgen ] says another thing. In my simple mind, I'm just wondering, maybe it's just all GIP that matters, and then the other part of me want to be doing something.

Well, yes, so I would say a couple of points here. Number one, there's very good genetic evidence, including a lot of our own data, both published and unpublished, that suggests that variance of the GIP receptor that are associated with decreased activity of that pathway associated with the lower BMI, lower weight. And so based on that in our own preclinical mechanistic studies, we were very, very confident in GIP receptor inhibition as the appropriate approach. I think that chronic agonism of the receptor probably ends up leading to receptor exhaustion in the same sort of thing over time, i.e. pathway down regulation. We chose to directly go after that. In addition to the second part of your question, is this all potentially GLP-1? I don't think so. And we certainly have preclinical data suggesting that this combination of GLP-1 agonism with GIP receptor antagonism has a synergistic or additive effect on weight loss.

And David, one last one, sorry, on this topic is -- is there any one-off side effect we should be aware of because it's an antibody approach? Is there something like that?

We'll share that with you. What we've said publicly to date is the -- it's the -- for these pathways, we're not seeing adverse events that are anything unexpected for these patents. Most of them are associated with the first dose and are transient. We'll give details on, of course, the safety profile, the tolerability profile in just a few days here.

Got it. Okay. Makes sense. Maybe transitioning next to -- and I don't want to spend too much time on this, but I do want to touch upon the KRAS program, obviously. I guess one of the confusions I've had is when I comped the Phase I safety profile for LUMAKRAS versus the Mirati molecule, I felt like at least on those early comps, LUMAKRAS looked cleaner. But then when I look at the PD-1 combination data generated to date, the Mirati data, at least what's been reported so far, looks like it's tracking better on the tolerability. And I guess, why is that? And is that something you guys have thought about internally?

Yes, of course, we thought about this. I'll let others speak to their data. The one thing I would point out here that's important is to follow these patients for a significant period of time. One of the things that we saw in terms of the elevation in liver enzymes, it's the dose-limiting toxicity for the LUMAKRAS PD-1 combination is the fact that, that actually appeared often 30, 60, 90 days into therapy, sometimes, later. And so you need adequate follow-up to really define that profile. So of course, we'll wait for data to emerge in the field. As we've mentioned before, we're now taking an approach where we're using a lower dose of LUMAKRAS, 240 milligrams as a lead-in, and then layering on top of that the PD-1 inhibitor to see if that improves the tolerability profile. We're actively enrolling that right now. And over the course of next year, we'll share those data, we hope.

Got it. But as of right now, no plans for a pivotal trial in PD-1 combo, but you're not shutting the door on it either.

Yes, absolutely not shutting the door. I think we need to do further investigation here. The other thing to point out is that we are moving forward with potentially pivotal trial with a chemotherapy-LUMAKRAS combination in patients who have PD-L1 negative tumors. That's roughly 1/4 to 1/3 of patients with [indiscernible].

What's the comparator in that? Is that KEYTRUDA chemo?

Yes, it will be chemo checkpoint inhibitor, what would be considered standard therapy.

Got it. So presumably, the active arm could get PD-1 on crossover, but even with that, I think what I recall is if it's within 90 days of KRAS exposure, then you could have more side effects. Are you guys gating on that?

Yes, potentially, depending on exactly the timing of exposure. But this is a trial where we'll look, especially a progression-free survival. So before any sort of crossover that will be one of the primary endpoints.

Got it. And then also, David, I'm curious sort of internally in your organization, what was the feedback on? Because ORRs tipped a bit, but that's okay, going from Phase II to the pivotal trial on to the Phase III trial in monotherapy setting. But then what got my attention was the PFS of 3.5 months? Like I wouldn't have thought it would be sort of in the 3s. I was thinking more like 5 to 6 months. So what was sort of the internal feedback on that? Because it sounded...

Are you talking about tarlatamab now, the DLL3 program, or...

Oh, I'm really sorry. I was switching, I was switching, yes. I should have clarified. On the DLL3, the 3.5 months.

Scary that I immediately knew which one on that PFS number. Well, first of all, these are patients with advanced small cell lung cancer, where there's very, very little therapy available. The disease is often quite aggressive. So a median PFS, I think, it may not be particularly helpful in that setting. What actually really encourages me on this program is, number one, the response rate. But beyond that, the duration of response in the 13 months area, which is really just remarkable for these sorts of patients. We have some of the -- many of them now still on therapy ongoing where the expected survival is often measured in a matter of a few months. And then the overall survival, median overall survival of over a year in that particular population. So I think if in the potentially pivotal Phase II trial, we can replicate those sorts of results. This is something that will really be welcomed by the field. When I talk to these investigators are really enthusiastic about what they're seeing in the clinic.

Isn't -- so I remember Lurbinectedin got approved in small cell on their Phase I/Phase II data set. Shouldn't your -- considering you're in mid- to high teens on the DLL3, shouldn't that technically potentially be registrational?

Well, so the Phase II trial is potentially registrational. Obviously, we've had ongoing discussions with the FDA and other regulatory authorities. It will all depend on the data package in the end.

And when do you expect that data, Phase II?

I don't think we've said publicly when we expect that. I can tell you, the trial is enrolling, number one, very briskly. And number two, we do have an agreed final dose with the FDA. You may recall that we took a couple of doses into that Phase II trial, consistent with the spirit of Project Optimus and dose exploration in oncology. We have -- we're very comfortable with this, the go-forward dose. And so all additional patients will be enrolled at that dose going forward.

Got it. Okay. Excellent. Okay. Eric, is there anything on oncology part that you want to touch upon before we move on?

Not so much oncology. But I do have a question from [indiscernible].

Sorry, on which one?

On the Lp(a).

Okay, go ahead.

Yes, I was curious about what your expectations on CD outcomes were given what you saw in the Phase II data.

Yes. I mean, I really like this program. Of course, we just presented the data a few weeks ago at the American Heart Association meeting. There was a concurrent paper in the New England Journal of Medicine. The molecule is really behaving beautifully in the clinic right now. As Arvind pointed out in his introductory remarks, we're seeing very profound suppression of Lp(a) levels at any dose, 75 milligrams every 12 weeks and above with quite a good tolerability profile in the Phase II study. So I think we absolutely have the tool in hand to address the Lp(a) hypothesis. The cardiovascular outcomes trial, we'll be launching, we hope before the end of the year, so within the next month or so. And our goal, of course, is to enroll that as expeditiously as possible. I had a chance to talk to a large number of physicians at the AHA meeting regarding this program. There is great interest. One of the reasons being that there's nothing available, of course, right now. And many cardiologists, they have these patients where there's a family history, there's an elevated Lp(a), and there's not much that they can do right now. Many of them drive the LDL level down to very, very low levels to control the one risk factor right now that you can control. But there is tremendous interest. We saw that, I think, even in enrollment in the Phase II trial, which went -- which moved along very, very briskly.

And what happens to the background -- like some of them might inevitably have high LDLs. How does that bake into this trial?

Yes. So that needs to be well controlled just as we did in Phase II. And if you look at the Phase II data, you'll see that, in fact, patients were coming in with very well-controlled LDL levels.

So that needs to be well controlled on statin or even a PCSK9?

Yes. Exactly. Whatever therapy is required for control of that LDL level.

But I recall, David, PCSK9s have a pretty meaningful Lp(a) reduction as well. What percentage of your trial do you expect?

I think it's going to be a relatively small percent. I don't remember the figure offhand in the Phase II, but it was a relatively small percentage. The PCSK9 effect on Lp(a), is there, but it's nowhere near the magnitude that we're seeing with Olpasiran, not even close. In fact, there's no therapeutic now that's really -- that can produce a pharmacologic effect and induce Lp(a) lowering.

Got it. And Dave, remind me this outcomes trial is a must for a commercial launch -- for approval as well?

Yes. I mean, I think our expectation is that we need cardiovascular outcomes in hand for approval.

Because there's no marker that like an LDL that would form the basis.

Yes. What we don't have here that we had in the LDL field was, of course, a half century of data showing that if you reduce LDL by a certain amount, you can predict very accurately what the reduction in event rates will be. We're actually going to be generating those data within the context of this trial.

Got it. So this is 4 years out or something like that?

Yes. I mean as enrollment moves along and as we get event rate projections, we'll provide updated guidance periodically as to when we can expect data.

Okay. Excellent. All right. Perhaps switching to a program, which I personally find fascinating, and then I think there's a lot of interesting things about it, but a lot of nuances about it, too. The OX40 program. David, like the first thing that stands out to me is, do you expect -- do you -- first of all, I guess, let me start with this. The durability of efficacy -- how have you thought about that? I know that was an observation seen in the Sanofi program too. There have been some questions that whether a related mechanism on the small molecule side CXCL might be showing something like -- are those related or not? And how do you think about that?

Yes. I mean one potential explanation, I think, in our program is the partial depletion of pathogenically activated T cells. The OX40 pathway is one of the primary drivers of that -- of pathogenic T cells in atopic dermatitis. That partial depletion may actually account for the duration of effect because, of course, with cessation of dosing, it would require time to repopulate that pathogenic T cell population, and that may be what gives you the duration of effect. This is something that we'll obviously be tracking quite carefully in the suite of Phase III trials that we're going to be conducting.

So you do think the depletion of pathogenically active T cells across your program, the Sanofi program, the small molecule. These are all related mechanisms?

That would be my leading hypothesis right now. But I would view that as a very good strong hypothesis, but something that we need to nail down with the large amount of Phase III data.

Got it. Got it. So you're -- okay. But I guess the reason I was asking was there has been questions around could this be a false positive of sorts on this durability we're seeing. But the fact that it's happening in 2 or 3 different trials makes me wonder what are the odds.

I think if you look across the field, it looks like a real phenomenon.

The other point that comes to me, David, is the pathogenically active T cells, are they always peripheral or could they also be central as well? Because I know you act on both sides, some of the approaches are doing peripheral.

They could be, and many of these are actually probably tissue resident, meaning present at the site of active lesions.

Got it. Okay. The other one is, when I think about your efficacy, given the mechanism here, there's reasons to expect that you could put up an efficacy signal in dupi resistant patients. Is that something that's being explored or thought about?

Yes, that's absolutely going to be part of the development program. In the Phase II study, about 14% of patients had prior Dupixent. And based on that data set, we didn't see any apparent differences in the efficacy or safety profile of rocatinlimab. So that is part of the development program. We're actually going to be exploring a wide swath of patients here, age, or adolescents and adults, different ethnic backgrounds as well as prior exposure. So whether patients have had no biologics prior to Dupixent or prior JAK inhibitors. So we're going to be taking a look at all of that in the suite of Phase III trials.

And David, was there ever a consideration to start, let's say, a 200-patient dupi experience or dupi refractory trial? Put up some easy 50 score in there and use that to form the basis of an accelerated approval, because theoretically, that should exist.

Yes. That's -- one thing you need to also recall here is the FDA requires relatively large safety databases for these sorts of indications and for patients to be followed for a good amount of time. So it's a little more challenging in terms of accelerated pathways than something like oncology might be?

I see. Okay. No, no, that makes a lot of sense. But I guess on the flip side, if the efficacy is so durable, like you can just do 1 shot or 2 shots in a dupi refractory and say, that's that. We're not aiming for more, at least not for the early.

Yes. So we're taking a look at some of these questions within the Phase III program. We are actually planning to restart Phase III study in the very near future. And in addition, you'll see additional studies starting at that time to start rounding out the suite of about a half dozen studies or so that will constitute...

Okay. So that was my next one because I only see one Phase III in clinal trials. So you have a bunch more coming, it sounds like.

Yes. Yes, I would say stay tuned in the relatively near future. Amgen will provide more guidance and information on what other studies will look like.

Is this one of your highest profile programs on your top 3 David, if I may?

Yes. I think this is certainly one of -- I would say, a handful of programs that I always don't like to pick my favorite child. But this is certainly a very important program. There's a huge unmet medical need in this disorder, which is quite prevalent around the globe. And we're just -- we're optimistic based on what we've seen so far.

Makes sense. Now the one thing, David, which I have been like on the efficacy side and everything, I feel like there's a lot of very strong momentum behind this program. The only part about it that has confused me every time I looked at the data is, when I looked at the tolerability profile, I felt like I was looking at the tolerability of the COVID vaccine with the pyrexia and everything. So how should we think about that? And how relevant is that from a development perspective, especially in a population like this?

Yes. It seems to -- so fevers and chills, we're seeing in a number of patients in the Phase II trial. It's very transient and it appears to be largely a first dose phenomenon. So in the large majority of patients, it happens with just the first dose. Certainly, in talking to the clinicians here, it was clinically managed. It wasn't something that they really -- the investigators I've talked to see as any sort of barrier at all.

I see. Okay. And what do you buy into that mechanistic explanation why Sanofi didn't necessarily see that?

Yes. I don't know. I think this is something that we need to sort out. And mechanistically, I'm not sure why you might see different reports that we've seen across the field.

Got it. Okay. That makes sense. And then perhaps just switching briefly to TEZSPIRE. There's a bunch of new indications coming up. Is there 1 or 2 in particular that you find most promising and your expectations on efficacy in those trials?

Yes. I mean, we've got...

Knowing that the derm trial was kind of hit or miss.

Yes. So chronic sinusitis with nasal polyps, our Phase III trial ongoing now. You may recall that we presented some data from the pivotal trials of TEZSPIRE where we looked at the subset of patients who had overlap between severe asthma and concomitant chronic rhinosinusitis with nasal polyps. Those 2 are actually not infrequently travel together. We saw an 86% reduction in the exacerbation rate in those patients. And then looking specifically at the chronic rhinosinusitis component, there was a 22% improvement in clinical symptoms which was considered by clinicians quite significant in this patient population. Quality of life impairments and challenges are quite common in these patients. They often undergo multiple surgical procedures for the nasal polyps, for example, and have ongoing symptoms. So that gives us a lot of confidence, I think, and optimism regarding that Phase III trial. We are planning a Phase III trial in eosinophilic esophagitis based on all of the mechanistic data that we've accumulated in the program to date. And then we've got ongoing studies in chronic spontaneous urticaria as well as chronic obstructive pulmonary disease.

Got it. And Dave, maybe just the last one for you, and I have a couple of quick ones for Arvind as well. But just very quickly, what would be the top 3 or so programs that you would have put? Like I remember you mentioned OX40. What would be the other ones, you would say, commercially most important from your perspective, the highest priority?

Yes, highest priority in the nonmarket, I think we've talked about them. In the cardiometabolic portfolio, it's obviously the Olpasiran trial. Our program in the lead, AMG 133 moving into Phase II. Rocatinlumab in the inflammation portfolio in Phase III. And then tarlatamab, ongoing LUMAKRAS development, and then AMG 509, which is a bispecific targeting STEAP1 in prostate cancer, also one to keep an eye in the oncology portfolio.

Excellent. Arvind, just 2 very quick ones for you. One, Otezla, any impact or any feedback from your commercial team to launch, or any impact there because that was always a big question in the past.

Yes. The fact that we have a broad spectrum of indications that we can now cover with Otezla, over the fact that we can cover from mild to moderate to severe disease, I think that has been quite meaningful in terms of the commercialization. There are no laboratory monitoring requirements. So I think the overall profile of Otezla is very well understood. So we'll continue to press on. We think we are very well positioned. We do get a lot of questions on [ dupra ] in terms of [ when and where ] does that get positioned. And our thinking is that for patients who perhaps aren't appropriately responding to Otezla and before they commence a biologic, that may be the niche that [ dupra ] was after. But like I said, based on the profile that we have now established with Otezla from a safety and efficacy standpoint, we feel that we are very well positioned in this market.

Got it. And Arvind, is there any feedback you're sharing on sort of where the numbers stand into next year, any pushes and pulls you flagged for people?

We haven't. I mean, obviously, we have provided the guidance for the year, and we stand by that as far as 2023. As we have done customarily, in conjunction with our full year results presentation at the end of January, we'll provide the guidance at that time.

Okay. Sounds great. Thank you guys so much for making time. Really appreciate you joining us.

Sure. Thank you, Umer. Thanks for having us.

Thank you, guys.