Start Time: 11:20 January 1, 0000 11:58 AM ET
Amgen Inc. (NASDAQ:AMGN)
Evercore ISI HealthCONx Conference
November 29, 2022, 11:20 AM ET
Company Participants
David Reese – EVP, Research and Development
Arvind Sood – VP, IR
Conference Call Participants
Umer Raffat – Evercore
Umer Raffat
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 frames it so well. So Arvind, all you.
Arvind Sood
Umer, thanks so much for inviting us to your conference. And I was just talking to Dave earlier that it was great news that you’re planning on having this conference in Miami this year, or next year.
Umer Raffat
That’s right.
Arvind Sood
Let me just kind of tee up some of kind of the broader picture of some of the key topics, and then obviously delighted that we have David Reese, our Head of Research and Development with us. And with all of what we have going on with the pipeline, I think 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. It has been 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 trials through the first nine 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 TEZSPIRE 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 would also note, Umer, that our recently closed acquisition of ChemoCentryx, that brings a newly launched innovative product to our implant portfolio, a product called TAVNEOS, so more to come on that. 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 2 data of Olpasiran, our LP(a) inhibitor. And what we demonstrated in this data is that Olpasiran dosed 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 1 study on AMG 133. This is our Phase 1 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 1 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 a Phase 2 trial, but happy to delve into that in greater detail depending on the questions that we might get from you and others.
Umer Raffat
Got it.
Arvind Sood
LUMAKRAS, as I 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, we’ll continue to add new biosimilars to our portfolio over the next several years. We have had positive Phase 3 data from three programs this year, 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, continued to generate significant cash flow. We generated almost $3 billion in free cash flow in Q3. And we retained 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.
Umer Raffat
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 deals the focus right now?
Arvind Sood
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 add to 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 had been launched and had been approved in a number of markets, but had 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 and in plan [ph] in the rheumatology space and we can leverage that as we commercialize Otezla.
Umer Raffat
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 it’s always these questions on do you guys have additional plans [ph] beyond the 2027 or not?
Arvind Sood
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 have communicated of mid single digit growth as far as revenues are concerned and low double digit — 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.
Umer Raffat
Got it. And denosumab is not modeled in through 2030, correct?
Arvind Sood
Denosumab, like I said, we have assumed that there will be biosimilar competition post 2025 in terms of our own modeling.
Umer Raffat
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 is only developing an obesity setting?
David Reese
So what I would point out is we will be showing the data in a couple of days. Actually now here in Los Angeles at the Hybrid Conference, 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 1 trial. In that trial, we enrolled only individuals with normal hemoglobin A1c levels. So these are not individuals with a history of diabetes or hyperglycemia. However, based on the mechanism of action, we would expect antihyperglycaemic effects in the Phase 2 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 normoglycemic where we directly address that question.
Umer Raffat
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?
David Reese
Yes. The Phase 1 study was a very standard design. So there were single dose cohorts and then there were multiple ascending dose cohorts and those individuals received three doses basically four weeks apart. So a total of 12 weeks of dosing, monthly dosing is an easy way to think about it. What I would pay attention to when we release 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 will potentially differentiate if we’re able to maintain a favorable profile through Phase 2.
Umer Raffat
Got it. So I guess, David, you’re saying since it’s multiple ascending, there technically is a titration first versus second versus third shot?
David Reese
No, I’m sorry. Those were different cohorts.
Umer Raffat
Okay, but there’s no titration —
David Reese
They’re different doses, but they were not dose titrated within cohorts. Go ahead, sorry.
Umer Raffat
It sounds like you’re saying you may not need titration.
David Reese
That’s one of the questions that we will address in Phase 2. So we will — this is planned to be a very robust Phase 2 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.
Umer Raffat
Got it. So Dave, I guess — let me just say it 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 a titration as well?
David Reese
Yes. The question is, of course always in Phase 1, you have relatively limited numbers of patients.
Umer Raffat
Sure.
David Reese
And so the question is, can we optimize the dose and schedule? And that’s why we’re planning a fairly robust Phase 2 to investigate a range of dosing and scheduling paradigms.
Umer Raffat
Got it. And where — as you envision this program on longer duration studies, you’re getting close to mid teens in weight loss already. And we know sort of the big bogeys are Manjaro [ph] 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 their early dosing as well as what’s your expectation? Do you think you’d get to that mid 20s or higher perhaps?
David Reese
We are following those patients. This is, of course, a key question for Phase 2. What I can tell you is that based on the kinetics and the curves that we’ve seen in Phase 1, 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 three doses maximum for these patients. I will say also that it was relatively well sustained. As you’ll see from the curve, some 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 2. But I’m relatively optimistic based on the data we’ve seen so far.
Umer Raffat
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 Nova Nordisk have always shown certain thresholds of weight loss and patient distribution, are you comfortable with what you’re seeing or is there outliers too?
David Reese
Yes, I would say we’re relatively comfortable with that with the caveat that Phase 1 always has relatively small numbers of patients sick, typically eight 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.
Umer Raffat
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 Manjaro 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, Amgen says another thing. In my simple mind, I’m just wondering maybe it’s all GLP that matters, and then the other part may or may not be doing something?
David Reese
Well, yes, 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 variants of the GIP receptor that are associated with decreased activity of that pathway associate 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 and the same sort of thing over time, i.e., pathway downregulation. 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.
Umer Raffat
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?
David Reese
We’ll share that with you. What we said publicly to date is for these pathways, we’re not seeing adverse events that are anything unexpected for these pathways. Most of them are associated with the first dose and are transient, and we will give details on, of course, the safety profile, the tolerability profile in just a few days here.
Umer Raffat
Got it. Okay, make 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 1 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, it looks like it is tracking better on the tolerability. I guess why is that? And is that something you guys have thought about internally?
David Reese
Yes, of course, we’ve 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 is 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 is the 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.
Umer Raffat
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?
David Reese
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 a pivotal trial with a chemotherapy/LUMAKRAS combination in patients who have PDL-1 negative tumors, and that’s roughly a quarter to a third of patients with non-small cell lung cancer.
Umer Raffat
What’s the comparator in that? Is it KEYTRUDA/chemo?
David Reese
Yes, it will be chemo checkpoint inhibitor what would be considered standard therapy.
Umer Raffat
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 care as exposure, then you could have more side effects. Are you guys gating on that?
David Reese
Yes, potentially depending on exactly the timing of exposure. But this is a trial where we’ll look especially at progression free survival, so before any sort of crossover, that will be one of the primary endpoints.
Umer Raffat
Got it. And then also, David, I’m curious sort of internally in your organization, what was the feedback on, because ORRs dipped a bit, but that’s okay, going from Phase 2 to the pivotal trial onto the Phase 3 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 threes. I was thinking more like five, six months. So what was sort of the internal feedback on that because it sounded –?
David Reese
Are you talking about tarlatamab now, the DLL3 program or –?
Umer Raffat
I’m really sorry. I was switching, I was switching, I was switching, yes. I should have clarified on the DLL3, the 3.5 months.
David Reese
It’s scary that I immediately knew which one on that PFS number. 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 may not be particularly helpful in that setting. What actually really encourages me on this program is, number one, their 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 many of them now still on therapy ongoing where the expected survival is often measured in a matter of 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 2 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 who are really enthusiastic about what they’re seeing in the clinic.
Umer Raffat
So I remember [indiscernible] and got approved in small cell lung, their Phase 1, Phase 2 dataset. Shouldn’t your — considering you’re in mid to high teens on the DLL3 BiTE, shouldn’t that technically potentially be registrational?
David Reese
Well, so the Phase 2 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.
Umer Raffat
And when do you expect that data, Phase 2?
David Reese
Yes, 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 doses into that Phase 2 trial consistent with the spirit of Project Optimus and dose exploration in oncology. We’re very comfortable with is the go-forward dose, and so all additional patients will be enrolled at that dose going forward.
Question-and-Answer Session
Umer Raffat
Got it. Okay, excellent. Eric [ph], is there anything on the oncology part that you want to touch up on before we move on?
Unidentified Analyst
Not so much on oncology, but I do have a question for [indiscernible].
Umer Raffat
Sorry, on which one?
Unidentified Analyst
On the LP(a).
Umer Raffat
Okay, go ahead.
Unidentified Analyst
Yes, I was curious about what your expectations on CB outcomes were given what you saw on the Phase 2 data?
David Reese
Yes, I really liked 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 2 study. So I think we absolutely have the tool in hand to address the LP(a) hypothesis. The cardiovascular outcomes trial will 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 in 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’s tremendous interest. We saw that I think even in enrollment in the Phase 2 trial, which moved along very, very briskly.
Umer Raffat
And what happens to the background — like some of them might inevitably have high LDLs. How does that bake into this trial?
David Reese
Yes. So that needs to be well controlled just as we did in Phase 2. And if you look at the Phase 2 data, you’ll see that in fact patients were coming in with very well controlled LDL levels.
Umer Raffat
So that needs to be well controlled on statin or even a PCSK9?
David Reese
Exactly, whatever therapy is required for control of that LDL level.
Umer Raffat
But I recall, David, PCSK9s have a pretty meaningful LP(a) reduction as well. What percentage of your trial do you expect?
David Reese
I think it’s going to be a relatively small percent. I don’t remember the figure offhand in the Phase 2, but it was a relatively small percentage. The PCSK9 effect on LP(a), it 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) lower.
Umer Raffat
Got it. And, David, remind me this outcomes trial is a must for a commercial launch for approval as well?
David Reese
Yes. I think our expectation is that we need cardiovascular outcomes in hand for approval here.
Umer Raffat
Because there’s no marker like an LDL that would form the basis.
David Reese
Yes. When we don’t have here that we had in the LDL field was, of course, a half century of 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.
Umer Raffat
Got it. So this is four years out or something like that?
David Reese
Yes. As enrollment moves along and as we get event rate projections, we will provide updated guidance periodically as to when we can expect data.
Umer Raffat
Okay, excellent. All right. Perhaps switching to a program which I personally find fascinating and 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 — 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 and non small molecule site CXCL might be showing something. Like are those related or not? And how do you think about that?
David Reese
Yes. I mean one potential explanation I think in our program is the partial depletion of pathogenically activated T cells and the OX40 pathway is one of the primary drivers 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 to Phase 3 trials that we’re going to be conducting.
Umer Raffat
So you do think the depletion of pathogenically active T cells across your program, the Sanofi program, the small molecule, these are all like related mechanisms?
David Reese
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 3 data.
Umer Raffat
Got it, 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 two or three different trials makes me wonder what are the odds?
David Reese
I think if you look across the field, it looks like a real phenomenon.
Umer Raffat
Yes. The other point that comes up, 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.
David Reese
They could be, and many of these are actually probably tissue resident, meaning present at the site of active lesions.
Umer Raffat
Got it, okay. The other one is, when I think about your efficacy, given the modal, given the mechanism here, there’s reasons to expect that you could put up an efficacy signal in Dupi [ph] resistant patients. Is that something that’s being explored or thought about?
David Reese
Yes, that’s absolutely part of the development program. In the Phase 2 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, adolescents and adults, different ethnic backgrounds, as well as prior exposure. So whether patients have had no biologics prior Dupixent or prior JAK inhibitors, so we’re going to be taking a look at all of that in the suite to Phase 3 trials.
Umer Raffat
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 and then use that to form the basis of an accelerated approval, because theoretically that should exist?
David Reese
Yes, 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.
Umer Raffat
I see, okay. No, that makes a lot of sense. But I guess on the flipside if the efficacy is still durable, like you can just do one shot or two shots in Dupi refractory and say that’s that, we’re not aiming for more at least not for the early?
David Reese
Yes, so we’re taking a look at some of these questions within the Phase 3 program. We are actually planning to restart Phase 3 study in the very near future. And in addition, you’ll see additional studies starting at that time to start rounding out this suite of about a half dozen studies or so that will constitute —
Umer Raffat
Okay, so that was my next one because I only see one Phase 3 clinical trial. So you have a bunch more coming it sounds like?
David Reese
Yes, I would say stay tuned in the relatively near future and then we will provide more guidance and information on what other studies will look like.
Umer Raffat
Is this one of your highest profile programs on your top three, David, if I may?
David Reese
Yes, I think this is certainly one of the, I would say 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 optimistic based on what we’ve seen so far.
Umer Raffat
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’ve 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?
David Reese
Yes, it’s it seems to be — so fevers and chills, we’re seeing in a number of patients in the Phase 2 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 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.
Umer Raffat
I see, okay. And do you buy into that mechanistic explanation why Sanofi didn’t necessarily see that?
David Reese
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.
Umer Raffat
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 one or two in particular that you find most promising and your expectations on efficacy in those trials?
David Reese
Yes, we’ve got —
Umer Raffat
Knowing that the derm trial was kind of hit or miss.
David Reese
Yes, so chronic rhinosinusitis with nasal polyps on Phase 3 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 two 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 3 trial. We’re planning a Phase 3 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.
Umer Raffat
Got it. And, Dave, maybe just the last one for you and I have a couple quick ones for Arvind as well. But just very quickly, what will be the top three or so programs that you would have put? Like I remember you mentioned OX40. What would be the other ones you would say the commercially most important from your perspective, or the highest priority?
David Reese
Yes, highest priority in the non-marketed, I think we’ve talked about them. In the cardiometabolic portfolio, it’s obviously the Olpasiran trial program in the lead, AMG 133 moving into Phase 2; rocatinlimab in the inflammation portfolio in Phase 3; 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 on in the oncology portfolio.
Umer Raffat
Okay, excellent. Arvind, just two 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?
Arvind Sood
Yes. The fact that we have a broad spectrum of indications that we cannot cover with Otezla when we are at 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. Again, we think we are very well positioned. We do get a lot of questions on [indiscernible] in terms of 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 maybe the niche that [indiscernible] goes 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’re very well positioned in this market.
Umer Raffat
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’ll flag for people?
Arvind Sood
We have been planning. Obviously, we have provided the guidance for the year and we’ll 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, again, I will provide the guidance at that time.
Umer Raffat
Okay, sounds great. Thank you guys so much for making time. Really appreciate you joining us.
Arvind Sood
Sure. Thank you. Thanks for having us.
Umer Raffat
Thank you, guys.
Be the first to comment