Moderna, Inc. (MRNA) Earnings Call Transcript & Summary

Fantastic. Hi, everyone. It's great to have you here today. Thank you so much for joining us. I am privileged to be sharing the stage with Rose Loughlin here from Moderna. For those of you who do not know me, my name is Courtney Breen. I cover the U.S. large cap names here at Bernstein. And we're hoping to have a bit of a conversation, particularly into the oncology portfolio at Moderna today. We're going to start first, though, with a bit of a presentation to get some context around this part of the business because I think -- it hasn't necessarily been front and center over the last kind of 5 to 10 years of the Moderna story. And so this will be a great opportunity to perhaps dive into that a little bit better. And then we will shift to Q&A. As a reminder for everyone in the room, please feel free to use the Pigeonhole app. You can put through some questions if there's something that's burning that you really want answered, and I'll work to integrate those into the question set that I already have. So with that, I'll perhaps hand over to you, Rose, to walk us through the presentation and any other opening comments that you have.

Fantastic. Well, thank you very much for having us. We, of course, are incredibly excited about the work that we're doing in oncology and recognize that we want to share that more broadly. So today, we want to share right. Well, we'll start the clicker out. Maybe we can -- but we want to share an overview power an overview of our oncology portfolio. So as we look to establish ourselves in the field of oncology, we are advancing a portfolio that takes multiple different therapeutic approaches and uses multiple parts of our platform technology. And in doing this, it's letting us address multiple different types of cancer as well as different stages of cancer. So we'll walk through the different parts of the portfolio and give you a sense of where we are. So we'll start with Entismeran Autogene, which is also known as INT for individualized neoantigen therapy, or mRNA-4157. Now this is a truly individualized therapy. So for every patient, we take a sample from their blood, which we consider healthy tissue and from their tumor. We sequence those samples and compare them. So we can identify mutations that are present only in their tumor. Now those mutations are specific to that patient. We refer to those as neoantigens. We then use our own proprietary algorithms to select neoantigens and design this therapeutic just for that patient. We then manufacture it and get it back to that patient within weeks so that they can start their therapy. Now we have previously shared last year results from the 3-year follow-up of a Phase II randomized study, where we combined INT with Keytruda and compared that to Keytruda alone. So in that study, the primary endpoint was recurrence-free survival and we'll walk through the 3-year data, but we also want to highlight that we'll have that final 5-year follow-up available in 2026, and we look forward to sharing that as well. So what we saw in our 3-year follow-up has been very encouraging, and I think you'll see it's driven substantial investment in expanding the settings in which we are testing INT. So when we look at recurrence-free survival, what we saw was that by combining INT with Keytruda, we could reduce the risk of a patient having their cancer recur, or death by 49% versus Keytruda alone. When we look at some of our secondary endpoints, such as that risk that a patient might develop a distant metastasis, we see that we can reduce the risk of that by 62% by combining INT versus Keytruda alone. And importantly, for a large portion of our oncology portfolio, we see a safety and tolerability profile that is we believe, differentiating. So when you combine INT with Keytruda, you see a well-tolerated profile, you do not see, we believe, enhanced safety or tolerability events on top of Keytruda alone. And so for patients particularly in these early settings where they're thinking about that risk-benefit equation, we think being able to offer clinical benefit with no additional safety or tolerability issues is particularly differentiating. Now we are currently in a Phase III study in the adjuvant melanoma setting, where we are combining INT with Keytruda, and this study completed its enrollment at the end of 2024. Now the design of the study is again looking at recurrence-free survival. So we actually will need to accrue a certain number of cases before we are able to look at those data. We have gone, of course, as we look at that case accrual and modeled it based on our Phase II study as well as other Keytruda studies. And so we are cautiously optimistic that we'll be able to share data from this study in 2026. Now in addition to this pivotal study in adjuvant melanoma, we've started a development program for INT that expands across multiple different tumor types. So for example, you'll see we have two additional pivotal studies running in non-small cell lung cancer and SCLC. We have studies that are Phase II randomized studies in high-risk muscle-invasive bladder cancer, renal cell cancer and non-muscle invasive bladder cancer. Now as we look through these studies, in addition to testing different cancer types, we have the opportunity to test INT in different combinations. So for example, in the non-muscle invasive bladder cancer setting, we're able to test INT on top of BCG, which is standard of care there as opposed to Keytruda and also as a monotherapy. So we're excited to see those data. And then finally, we most recently announced that we started a study in a late-stage setting. So first-line metastatic melanoma to really understand what INT's potential is in those more advanced patients. So based on the data that we saw in INT, we've been very encouraged about this therapeutic approach for oncology, and we've expanded our pipeline of cancer antigen therapies And as you can see from the small graphic there, where INT is individualized, our other cancer antigen therapies -- our other cancer antigen therapies, we actually refer to them as off the shelf. So they target antigens that are shared among many patients, so they do not need to be individualized. They can be manufactured once and available when that patient appears and their clinician is ready to treat. So there are two flavors of our cancer antigen therapies that we'll talk through. The first is mRNA-4359. So 4359 is designed to encode antigens from the PD-L1 and IDO protein and to train your immune system to kill the cells that overexpress those proteins. Now there are two types of cells that do that. One are cancer cells. So you can imagine, simply to the immune system to kill the tumor. The second are immunosuppressive cells, and we think this is an important aspect of the mechanism of action of 4359. So you can think about T-regulatory cells, myeloid-derived suppressor cells. The types of cells that create that environment that makes it hard for your immune system to recognize and then get activated as it's finding antigens on tumor cells. Do you think about it as taking the brakes off of the immune system? Because this is such a central mechanism in cancer, we believe mRNA-4359 will be applicable in multiple different types of cancer. So we think of it more like the pipeline and a product type of concept. We've previously shared data from the Arm 1A shown here, the dose escalation at ESMO last year, I believe. And that is looking at 4359 as a monotherapy in advanced metastatic patients. We are looking forward in October of this year at ESMO to sharing additional data from the Arm 1B of the study, where we are looking at 4359 in combination with Keytruda, and looking in melanoma and NSCLC patients who are again advanced in metastatic and checkpoint inhibitor refractory. So these are very heavily pretreated patients that we're going into. We're excited to be able to show those data shortly. In addition, we are planning Phase II Arms, we're expanding into different indications, including first-line in NSCLC with PD-L1 high, as well as first-line melanoma. Now as we think again about that mechanism of action, we've been excited to see as we think about some of our translational data that we're seeing those regulatory T cells and those myeloid-derived suppressor cells being depleted from the periphery in our studies. We're actually seeing less T cell exhaustion. So we're starting to see that the therapy is creating that much more permissive immune environment for your body to identify and tackle a cancer. And in doing that, we're still seeing that safety and tolerability profile. It's pretty similar to what we saw with INT. So quite favorable, well tolerated, your adverse events are very low grade. So coming back to our office-shelf therapies, we have another flavor that is specifically tumor targeted. So the antigens that it encode are present in those tumor cells. And our lead program there is mRNA-4106. So for mRNA-4106, this therapy, it encodes for multiple tumor targets. We have designed this therapy such that when you look at an indication within cancer, we expect a broad population to have these antigens present in their tumors. So we do not need to go and sequence their tumors. We do not need to go and look and see if their tumors are expressing these proteins. So in addition to covering a broad set of patients within a type of cancer, if you look at a single patient, we anticipate their tumor will also be expressing multiple antigens within our design for this therapeutic. As it turns out, when you look at the different types of cancer, many of them actually share underlying biology. So even though this is not going after a central immune pathway, it is going after antigens present in cancer cells, they are actually shared across quite a number of different types of cancer. So we do believe that mRNA-1046 and the cancer vaccines we're developing in this space will be broadly applicable as well. So 4106 is currently in a Phase I study, where our primary objective is safety and tolerability. We're looking at it as a monotherapy and in combination with checkpoint inhibitor therapy. So now we'll take a bit of a pivot in the portfolio in terms of the therapeutic approach that we're taking on oncology. So as opposed to our cancer antigen therapies, which we think of as really training the immune system to identify and kill cells, we think those T cell engagers is actually guiding your immune system towards the cells that you want to eliminate. So we have two flavors of T cell engagers that we are developing. The first is focused on targeting what we call surface antigen, so proteins on the surface of cancer cells. So the T cell engager is a secreted protein, and it will bind to CD3 on any T cell, and it will bind to this protein on the surface of a cancer cell, hold those two in proximity, help activate that T cell and help that T cell kill that cancer cell. Now as we think about developing T cell engagers with our mRNA platform, we have two key advantages in this space that we believe are differentiating versus recombinant protein approaches. So the first, is what we refer to as multiplexing. And we specifically use that vocabulary as opposed to combination because from a regulatory perspective, our products are a single product. So within one product, not a combination, we are able to encode for T cell engagers that can identify three different surface antigens. We believe this is important as you're thinking about antigen escape when you're treating different types of cancers. We also believe that this is important to address tumor heterogeneity. Not every cancer cell is identical. They don't all express all of the same targets. So by being able to go for multiple targets at the same time, you have a better chance of getting that deep and durable response. The second differentiating factor for us is that we can also encode for proteins that can provide some of those important co-stimulatory signals which can both increase your T cell activation and increase your specificity. You wouldn't just want to increase T cell activation without giving it that specificity, but we have the ability to do that with our mRNA platform. I'll come back to mRNA-2808 in a second, but to see the second flavor of T cell engagers that we're developing, are in combination with our collaboration partner, Immatics and these rather than targeting proteins on the surface of a cancer cell, actually target intracellular antigens that are presented on that cancer cell. Now what's important for us in this aspect is that it allows us to open up that antigen space. So there are more targets available to us to pursue. And in addition, some of these proteins that only appear inside cancer cells are very, very specific to those cancer cells. They are not appearing. They are not expressed or presented in your healthy tissue. So you're broadening that therapeutic index and being able to offer a potentially, safer and more tolerable therapeutic. So coming to our lead program in this space, mRNA-2808 is in a Phase I study now in relapsed multiple myeloma patients and who have been triple class exposed. So our primary endpoints are safety in this study. And we are quite keen to see the translational and clinical outcomes of this study, for example, looking at impacts on different B cell populations in these patients. So moving to the final portion of our oncology portfolio. We have what we refer to as our cell therapy enhancers and our In vivo cell therapies. So I'll start on the top here, but I'm actually going to do a bit of an aside to talk about ex vivo cell therapy. Now we are not developing Ex vivo cell therapies. However, we do believe that we can improve the performance of them. So for those who are familiar with Ex vivo CAR-T or Ex vivo TCR-T, these have been truly transformative therapies for the hematological malignancies. In solid tumors, they have shown some pretty interesting effect, but they haven't shown the same level of effect as in this malignancies. So what we believe, based on clinical data that you continue to see this correlation between the persistence of those engineered T cells and to the state, the health, if you want to think of it that way, of those engineered T cells in a patient and clinical outcomes. So our cell therapy enhancers are designed to improve those two things in the patient. So in collaboration with Immatics, who's developing an Ex vivo TCR-T, you can imagine Ex vivo cell therapy, what you first do is you take the cells out of the patient, you activate them, you proliferate them, you engineer them. You have to lymphodeplete the patient so killing a bunch of their remaining immune cells, then you infuse those cells back into the patient. So you have the engineered T cells back into the patient is extremely arduous and individualized process. We can then administer our cell therapy enhancer, which is designed to encode the exact antigen that the engineered T cells recognize. So we can actually boost the T cell response of the engineered T cells in the patient's body. And we can do this over time. They only get those cells infused once, but we can boost as often as is needed. So we currently are in a Phase I study, where we are combining our mRNA-4203, which, as I mentioned, was designed explicitly to activate the engineered T cells of our partner, Immatics and their IMA203 therapy. So this is in patients with cutaneous melanoma or synovial sarcoma. And again, our private endpoints are safety with the translational and clinical data from the study that we'll be watching closely. Now I'm going to come back actually to the bottom half of this slide, which is In vivo cell therapy. So as I described, Ex vivo cell therapy, I think you can start to imagine some of the hurdles both that patients go through, that clinicians go through, that your manufacturers go through in providing that drug. And we think if you're able to have cell therapy that uses an mRNA-LNP based approach, you could eliminate many of those barriers. So our first approach is what we refer to as CARM. You can think of the M as standing for monocytes. So using mRNA-LNPs, we transfect monocytes and macrophages within the patient's body and encode a CAR, just like you would imagine, in CAR T. Now with that car expressed on these monocytes, they are going to traffic to the tumor within the tumor, that car finds its antigen, binds to it. That monocyte or macrophage will then get activated. It will start secreting immune stimulatory cytokines around it. It will start phagocytosing and eating those cancer cells around it. But perhaps most importantly, in doing that, what it does is start to present even more antigens from those cancer cells to the rest of your immune system. So it actually broadens the response well beyond the CAR that was originally encoded in the therapy because once it gets into the tumor, it's showing many, many, many different antigens to immune system. In vivo CAR-T similarly uses LNP technology to transfect T cells so that they express a CAR. And again, once they recognize that antigen on the tumor through the CAR, they will directly kill those cancer cells. So thank you again for the opportunity to share some of our oncology portfolio with you. We are really excited about the diversity of therapeutic approaches that we were able to take. We're excited about the different parts of our platform technology that we are able to leverage in this space. And we really like the opportunity that it offers to be able to treat different types of cancer and different stages of cancer to truly have an impact on those patients.

Absolutely. Thank you so much for taking us through that because I think there's a lot there. There's a lot that sits kind of behind the INT, which has been kind of your leading asset in many ways. Can you talk a little bit about kind of how these pieces fit together? It feels like there's a lot of different approaches to come at patients, perhaps kind of shifting from individualized, but it's all built on the backbone of the mRNA. So can you talk about kind of the portfolio strategy?

Yes, absolutely. So as we are thinking about it, we are thinking about this as building a toolkit that can engage with the immune system in different ways based on what's needed in different stages of cancer. So for example, if you were thinking about a patient that is in a preventative or precancerous state, you might only need to prime the immune system such that when one of those cancer cells develops, it quickly recognizes it and eliminates it. If you are thinking about an early-stage cancer patient, perhaps they've had a resection, you might want to train the immune system with a cancer antigen therapy to prevent recurrence after they've had their tumor removed. If you start thinking about some of your more advanced patients that are later line, their immune systems might not be quite as competent, you might want to access a broader population of T cells. You might think there that in order to really, again, have deep and durable responses, you might want to use something like a T cell engager that is multiplex and can handle a complex heterogeneous tumor. You might want to consider a cell therapy where, instead of just guiding your immune system, you're just engineering it to go in and fight that cancer. So we think of it as the different ways to leverage the immune system that will be most relevant in those different stages of cancer.

Absolutely. And I think kind of in a couple of different places, you're doing kind of concept of off-the-shelf versus your own personalized work plus kind of perhaps potentiating other personalized work when it comes to the CAR T space as well. How do you think about kind of the utilization of those opportunities and kind of is there the potential that off-the-shelf can perhaps deliver the same types of durable responses as the personalized or how might you think fit together?

Yes. Ultimately, the data will determine whether an individualized approach or a sort of off-the-shelf approach may be superior as we go forward. We are seeing similar safety profiles from those two, which we think is encouraging. Ultimately, some of the other differentiators might actually be the availability. So when you think about the manufacturing of those individualized therapies, you do need a window to design and manufacture. And when we think about some of the off-the-shelf therapies, they may be available as soon as the patient arrives. And so those may fit really well together in a sort of complementary way.

Absolutely. Because I think it's about a 6-week window or so for your INT study. One thing that I just wanted to ask about because I think it popped up in the presentation, the 4203, which is kind of potentiating the cell therapy interventions. As you look at those, I think the early studies are in solid tumors predominantly where CAR T hasn't necessarily had the kind of full deep durable effects in the same way as we've seen in liquid. Is that the space where you think the most opportunity is? Or could these also be used to help increase the response rate or increase the durability of responses or perhaps even reduce the amount of CAR T that needs to be infused in the heme space as well?

We do think any space where you may not have the same access to antigen or you may be in an immune suppressive environment we do believe a cell therapy enhancer could have a benefit. Those are perhaps exaggerated in the solid tumor settings, but it's not that they are not present in some of those other liquid tumors.

Got it. That's super helpful. As you kind of walk through that, it feels like there's a lot going on as we kind of looked at kind of -- and a lot early as well as kind of some big readouts for the INT program as well. Can you talk about kind of some of the big catalysts we should be looking out for, you mentioned kind of some of the data we're going to get in 2026. Can you talk about kind of expectations on what you might be looking to deliver and kind of the goals there?

Sure. So if we go sort of in a chronological order, as I mentioned at ESMO this year, we are looking forward to sharing Arm 1B data from 4359. And as we roll into 2026, we should be able to share the 5-year follow-up from INT in that Phase II randomized study in adjuvant melanoma. So again, the same setting as the pivotal study that we have ongoing. The pivotal study. We are cautiously optimistic that we will have enough cases to be able to share data over the course of 2026. And when you look through the other indications as they are coming, our study in adjuvant RCC, renal cell carcinoma with INT has also fully enrolled. So that is likely next in line for providing data we may also have some smaller, more opportunistic readouts this year, because we still have Phase I cohorts running with INT in exploratory setting, so spaces like pancreatic and gastric where we're really going into different cancer types that have very different profiles of the tumor microenvironment and tumor mutational burden.

And maybe to that point that you just finished on the different types of tumors that kind of perhaps immune sensitivity of those tumors as well. As I look through your portfolio, in many ways, it's about potentiating enhancing or directing being in system to target -- to target kind of that particular tumor type. Melanoma is kind of a good place to start always highly immune-sensitive cancer. Some might then say non-small cell lung cancer is another place, triple-negative breast is another place that's potentially being very responsive to checkpoint inhibitors as well. How do you think about that strategy and your ability to perhaps kind of double down in a place like melanoma or non-small cell lung versus being able to broaden and go across different tumor types?

I think what you're seeing us do is a very methodical exploration of those different variables because we believe INT has the potential to bring clinical benefit in the different settings. So starting in melanoma, as you pointed out, tends to have high tumor mutational burden, given that many, many years ago when we started INT, thinking about the design, it is required to have sufficient mutations to be able to design it. And so starting in an environment where you have a high tumor mutational burden and sensitivity to checkpoint inhibitors and IO therapies makes a lot of sense. So starting out in early settings in adjuvant melanoma. As we proceeded through, you can think through how you walk down on tumor mutational burden. So in NSCLC often comes next. We then look at things like bladder cancer, renal cell carcinoma as you're working through. We've also been thinking about things like the tumor microenvironment, what sort of T cell infiltration you have there. So how hot is that tumor microenvironment. And you can sort of see us walking down that as well. And then the last variable that we've introduced is truly that stage. So when you think about that early adjuvant setting, many of these patients, they've had a resection. And so you're really looking to stop recurrence, you don't anticipate having a very large tumor bulk as burden. So we're exploring that area first, but we are still looking to see if we have the potential for impact in those later-line patients that may have more tumor burden and potentially metastatic disease who sort of explored those in chronological order.

Fantastic. And I do want to kind of ask, I mean there's a few other players out there, and so we'll get into kind of some of the read across kind of questions. But even within your own portfolio, as you're getting kind of scientific questions, answers for one of these assets or one of these profiles, how much are you able to feel like that derisks the others? Because I think kind of safety is clearly one area where you feel really good and that almost is carried across from COVID, and kind of where you began in terms of a commercial product and the safety that you've been able to carry through. What other markets are you looking for for success in particular indications or with particular assets that give you confidence for the rest of the portfolio as well?

So as we look at the data coming out of INT, I think you've already called out safety as the first piece that we believe translates across our cancer antigen therapies. We also believe, as you look at our ability to drive really strong CD8 and CD4 T cell responses that we're understanding a lot about that in the individualized setting and then reinforcing those learnings with mRNA-4359. And we do believe that, that will pull through into the rest of the portfolio. And I would say there are also quite a few translational endpoints that shouldn't be underestimated. As you start to recognize over the course of multiple studies initially with INT as it's most advanced, what those transitional signatures are that are -- that appear to be correlated with your clinical benefit. So those could be -- you think of things as how broad the T cell response is, not just what did we encode in the vaccine. We believe that, that translational understanding will also inform the rest of the cancer antigen therapies.

Fantastic. And maybe getting to the competitive set, kind of BioNTech is out there doing some similar things in the mRNA space. What are the read across is that you're looking at from data you see out of them? I think IO Biotech is also doing some work on some of the components that you're experimenting with. And so what data do you look to coming from those players as giving you either positive signals or things that you get worried about?

Sure. I would perhaps make the general statement and then go into the more nuanced and the general statement being where we and our competitors are exploring similar biological hypotheses, I think we look forward to that as potential read-through and derisking for us as well. But we -- all three of us utilize slightly different platforms, and that's where some of the nuance does come in for us. As we think about BioNTech's INS to their individualized therapy, there are some differences. We can't necessarily say which one may or may not make a difference, which is why we're sort of looking to those readouts, but they, for example, encode 20 neoantigens, we encode 34. We each have our own proprietary algorithm for selecting those neoepitopes and designing those therapies for patients. They do have an mRNA-based platform, but they actually use a lipoplex that they IV infuse, whereas we use a lipid nanoparticle that we inject intramuscularly. So you may have different antigen presentation within the body. So there are some of those platform differences that we want to keep in mind as we start to see the different results. As we look at IO Biotech, so their lead asset is a peptide-based vaccine for PD-L1 and IDO. So very similar in concept to what we're approaching with 4359. So they recently released actually their Phase III data in first-line melanoma, which, of course, we were watching closely. And as we look at those data and the biological hypothesis that we tested, so is this the right therapeutic approach? Are those targets relevant? Can they have clinical impact? We feel like they did demonstrate that biological hypothesis. As the trial read out, they did narrowly miss on the statistical significance. But from the -- what do we read through to our vaccine for mRNA-4359, we feel like that's helped derisk it as well and encouraged us to continue aggressively developing in that space. From a platform perspective, they are still a peptide-based platform, and we have slightly different antigens that we encode. We've chosen to encode slightly broader antigens for broader coverage. And again, we look to the mRNA platform to drive particularly strong CD8 and CD4 T cell responses, which we think are really critical to that mechanism. So we do believe that there is still some nuance between a result that would be generated with their vaccine and a result we would generate in the same setting.

Absolutely. One other area that I did want to touch on with the T cell engagers and kind of the work -- some of the earliest work that you're doing and kind of trying to bring conformationally these cells close together and ensure that they can have real impact. Why is that the next place to go after kind of presenting antigens. Why is this the next place for Moderna to begin to advance this technology?

Yes, absolutely. So as we mentioned, as you get into some of these other later lines of cancer. You may not have the same immune confidence. You may not be able to take just one T cell population. You may have immune dysfunction. You may not be able to say I'm going to use a cancer antigen therapy approach in that setting. And so in that case, if you use a T cell engager, you can actually access any T cell in that patient's body, and you can administer these repeatedly over time. We also find that the heterogeneity, as you get into those settings is particularly well addressed by our platform. So -- and this has actually been playing out in clinical data in the field. If we think about multiple myeloma, where some of the earliest T cell engagers have shown their promising data. Right now, I believe it's moving to pivotal now. There's data taking to T cell engagers that were developed separately that look very promising and clinically combining those recombinant proteins in patients and when doing that, the results look like an improvement in your overall response rate. And again, durability of response starts to look even better. And you start to see patients that have some of the more complicated disease responding in a perhaps parallel thought experiment, there are protein engineering approaches that others are taking so that they can actually target both of those antigens. So instead of a clinical combination. They're designing it all into one protein, which is pretty complex protein engineering and also seeing similar clinical benefit, remarkably, both of these are not seeing additive toxicity, which is fantastic for patients and developers alike. So when we look at that data, we see a significant opportunity to expand multiplexing. So mRNA-2808, our lead asset in that setting, happens to target three cell surface proteins, but there's no actual reason that we need to necessarily limit to three from a platform perspective.

Wonderful. That's very exciting. This is kind of a journey that Moderna has been on for a while. kind of as I said earlier, it hasn't necessarily been at the front of the conversation or the company story. And so through this, you've also partnered with a number of other companies kind of along the way and Merck being one of the big partners when it comes to INT and combinations with Keytruda. As you look to these newer assets coming through, you've got a couple of partnerships here and there, but -- what are the capabilities that you're looking to bring in from the outside? Is it kind of particular assets that you want to combine with? Is it clinical development capabilities? Is it commercial capabilities? What's going to be important for Moderna to succeed with these assets going forward and building the partnerships and collaborations around the assets?

And just for those who aren't familiar, in INT, we are partnered with Merck. It's a 50-50 cost and profit sharing relationship. So we share our costs, including our CapEx. We make our decisions together. It also means that we and Merck together are able to access some pretty substantial development and commercial capabilities that are already in place that has allowed us to accelerate that development program into so many different settings, which has been fantastic. Now our partnership with Immatics comes from a very different angle. It's in a very early space where they brought deep biological expertise in T cell receptors. And we were able to combine that with the power of our platform to really start these new concepts early in development. So as we think about the rest of our portfolio, we are in a fortunate state where we have many different investment opportunities. So should a partner be able to bring capability to that, that could accelerate a development program or let us explore a broader set of spaces where we believe we may have that type of pipeline and a product opportunity, and we would be open to doing that to create even more value

Fantastic. Often, if is the trade-off of what can I start today? What do we have to wait to start next year and the year after because of those constraints and kind of derisking those opportunities while making sure you're fully investing simultaneously, which can be really, really, really tough. In the last couple of minutes, I do want to hear just a little bit about kind of -- the -- as you think about your oncology strategy and the whole theme of this conference has been leading and disrupting. It feels like kind of you're on a path to disrupt some of the ways that we have traditionally gone after some of these cancer types. Kind of, how will you know that kind of you're on the track before perhaps all these drugs eventually make it to market? How will you know the kind of successes around the corner? And what are those disruptive milestones that kind of will kind of derisk this portfolio for you over time?

Sure. I think for our earlier programs, we are certainly looking at some of those translational data that you can get out of your early clinical studies because as you look across the field, you can start to interpret translational data and translate that into what you would anticipate as clinical effect. I think for INT, as I mentioned, it's sort of a methodical walk through all of the different settings in which it can work. And so we'll be watching that and sort of adjusting and potentially adding to our development program in certain places where we see success and potentially exploring new spaces. Depending on what we see in some of those transitional data.

Fantastic. Very exciting time ahead. Any final comments on kind of what you hope Moderna to look like when it comes to oncology over the next 5 to 10 years?

Well, I'm obviously very excited about the different therapeutic approaches that we've been able to take. It is an incredibly diverse portfolio for a company. And for us, it utilizes different parts of our platform technology that we have invested in and derisked in actually very many different settings from infectious diseases to rare diseases. So for us, this is really fulfilling the mission that we've had to have a really significant impact on patients' lives because it's opening up just such a vast opportunity space to do that.

Fantastic. Thank you so much for your time today, Rose. It's been a pleasure.

Thank you for having me.