Regeneron Pharmaceuticals, Inc. (REGN) Earnings Call Transcript & Summary

Good day, and thank you for standing by. Welcome to the Regeneron Oncology Investor Event, ESMO 2021. [Operator Instructions] Please be advised today's conference may be recorded. [Operator Instructions] I'd now like to hand the conference over to Justin Holko, Vice President, Investor Relations.

Thank you, Liz, and welcome to everybody to join this call this morning. Joining me on the call today are Dr. George Yancopoulos, Co-Founder, President and Chief Scientific Officer; and Dr. Israel Lowy, Senior Vice President of Transitional Sciences and Oncology. After our prepared remarks, we'll open the call for Q&A. Before handing the call over to George, however, I would like to remind you that remarks made on today's call include forward-looking statements about Regeneron, including those related to Regeneron's business and research and development programs, anticipated milestones regulatory matters. Each forward-looking statement is subject to risks and uncertainties that could cause actual results and events to differ materially from those projected in that statement. A more complete description of these and other material risks can be found in Regeneron's SEC filings. Regeneron does not take any obligation to update publicly any forward-looking statements, whether as a result of new information, future events or otherwise. With that, let me turn the call over to George.

Thanks, Justin. I hope everybody can see a slide that says Regeneron technologies power our pipeline. I'm here to primarily introduce Izzy Lowy, who will tell you all about our entire work in a second. But first, I want to remind you all that we believe we have a bit different type of company here at Regeneron, most notably reflected by the fact that we have invented what we believe are some of the most powerful biologics discovery and development technologies in history, which create and power our pipeline. And these allow us to create an incredibly diverse pipeline, whether it be our VelocImmune technology that creates our antibodies, our Veloci-Bi technology that creates our bispecifics, or our Regeneron Genetics Center that has sequenced more humans than any other effort and has gotten us into major genetics medicines efforts along with some key collaborators such as Alnylam and Intellia. It's these technologies that have provide our targets and our medicines and allow us to contribute important first-in-class medicines, such as EYLEA for leading causes of vision loss; dupilumab for asthma atopic dermatitis; or monoclonal antibodies for Ebola and COVID-19; or our checkpoint inhibitors and bispecifics for cancer. And the latter are what you're going to hear about today from Izzy. I've known Izzy for over 40 years since we were MD Ph.D. students together at Columbia. And I continually tried to recruit him while I was following his work all the way through the time when he was at Medarex, where he was a pioneer in developing the first checkpoint inhibitors that ultimately became OPDIVO and Yervoy. And it was about this point that I was finally able to convince to come here about 10 years ago because he saw the power of our capabilities and technologies and thus to lead our immuno-oncology efforts. Which I think we both believe have a chance to really make a difference for cancer patients based on our unique platforms that can repeatedly create targeted biologics that are creative clinical scientists can mix and match to attack particular cancers. And one of the first foundational agents in these efforts is having our own PD-1 antibody that can match up with the best-in-class. And led by Izzy, we have been doing this with Libtayo, first in dermato-oncology and now, in lung cancer. And so, without further ado, here's Izzy to tell you all about it. Izzy?

Thank you, George. Thanks for the kind introduction, and it's actually a pleasure to come to work every day because of this great environment and exciting opportunities, not just in oncology, but also in other areas as the team has led. And I would say that when we first came here, the field still hadn't accepted immuno-oncology, but you guys were open to -- with science, and we took a long-term view in mind, and we are executing on it. So if I to go to Slide 6. So we've described our strategy in the past. And I think with today's review of the ESMO data, what we'll be able to do is give you further proof that we are executing on it. Our idea has been to develop a portfolio that can compete with an anti-PD-1 to enhance beyond areas that are already shown to be active and most importantly, for the future, extend our ability by virtue of combinations that are available to us because of the really remarkable Regeneron technology and scientists. Slide 7, just as a reminder that despite what PD-1 has done with a seismic shift and acceptance of immuno-oncology in the field, most patients still need more than just anti-PD-1. And so there's a lot of work to do. And that's why we have built a broad pipeline that we think will work to extend our ability to bring these benefits to more patients. And Slide 8 is a summary of the key aspects of our approach. So we have our VelocImmune antibodies, which is foundationally PD-1 Libtayo, but we have others LAG-3, GITR. Most importantly, we have a very creative and broad bispecific platform using CD3 bispecifics, which have already established proof of concept with CD20 and BCMA immunologic malignancies. We're very excited about our co-stimulatory bispecifics, where we are first in class in this field and have moved multiple such agents into the clinic, and novel types of bispecifics. They use creative approaches to getting a benefit out of bispecifics. And where our portfolio can benefit from complementary expertise from quality collaborators, we've reached out and have multiple collaborations ongoing. From our internal portfolio, Slide 9, you can see what we have cooking. So Libtayo is not our only anti-oncology agent. It's the first. It was developed to be equivalent to any best-in-class agent and to serve as a foundation. You can see here a broad array of studies, which I'm happy to take some questions on later. But let's move to Slide 10, where I can -- let's discuss Libtayo specifically. So we first established Libtayo as a first-in-class agent to be approved in cutaneous squamous cell carcinoma. We -- that data continues to hold up and mature over time with better results with longer follow-up. We have a Phase III adjuvant study underway as well as neoadjuvant studies. In the last year, we received an approval for advanced basal cell carcinoma for patients that had progressed, so were intolerant to hedgehog inhibitors. Again, they had no other agents approved. We recently announced our data of combination of Libtayo with fianlimab, our LAG-3 antibody that look very compelling, and that is on track to begin a Phase III study in early 2022. And we also recently showed in a second line advanced cervical cancer in patients who had progressed after prior platinum therapy, that we were the first immunotherapy to demonstrate an improvement in overall survival compared to standard of care choices that clinicians could pick. And these are -- submissions are underway for that as well. So today, we're going to focus on non-small cell lung cancer. We've been approved as a monotherapy agent for patients with PD-L1 expression on tumor cells and greater than 50% of those cells. And we now have demonstrated the survival benefit in combination with chemotherapy. So we are 5 for 5 on major registration studies and with data that I think are not surpassed by anyone. And we believe, therefore, that we have demonstrated that Libtayo is essentially a best-in-class agent and has proven its merit as a foundational piece for our oncology strategy. So let's get into more detail on what we showed in lung cancer. So Slide 12. Just to remind you that we have already our Libtayo monotherapy approved by both the FDA and EMA in first-line non-small cell lung cancer and high PD-L1 expressors. And just yesterday, we presented our data for our chemo combination study. This was an efficient innovative trial design in which we combine both histologies -- major histologies, squamous and non-squamous in one study, we enrolled patients across PD-L1 spectra, and we have a positive study. And therefore, we are preparing our regulatory submissions. And again, it's 1 of only 2 antibodies in this class that has demonstrated positive Phase III studies, both as a monotherapy and as a combination with chemotherapy in first-line lung cancer of any histology. Next, Slide 13. Just to remind you the quality of our data in our first study of monotherapy, which led to a 32% reduction in the risk of death overall. And when we look specifically at the population that had confirmed PD-L1 greater than 50% enrolled in our study, it went to a 43% reduction in death. Let's talk about today's study. So I'm going to reprise Slide 15, the presentation that was given yesterday by Dr. [indiscernible] who had only 5 minutes to present. So maybe I'll take a few more minutes to just get you through all the details and then give you some additional comments on how we see the data. Slide 16 is the design of the study. This was randomization 2:1 of cemiplimab versus placebo on top of chemotherapy that was appropriate to histology. In the case of non-squamous, patients received amotrexad containing platinum regimen, and all were mandated to receive pemetrexed maintenance. In the case of squamous, patients were generally treated with a platinum and a paclitaxel-containing regimen. Any PD-L1 expression was allowed. We also included patients who were Stage IIIb or c, not just patients with Stage 4. And I remind you that these patients with Stage IIIb or c that were inoperable were patients who were ineligible for radiation. These typically have large masses that cannot be radiated. So in some ways, they're often even more advanced than patients who might have a single lesion in the lung and another lesion in the liver or somewhere else and therefore, be classified as Stage 4. We included patients with ECOG 0 or 1. Turns out most of our patients were ECOG 1, again, reflecting real-world practice. We also allowed for patients who have brain metastases that were clinically stable. We didn't make them wait to have subsequent MRIs or CT scans to demonstrate it. The primary endpoint was survival. Key secondary endpoints, progression-free survival and objective response rate. We enrolled 466 patients. We had prespecified interim analyses that had to hit high bars in order to call the study positive. Who was enrolled? Study -- Slide 17. This gives you again a description of the patients that were enrolled into the study. Again, I highlight here that we were pretty balanced between non-squamous and squamous histologies, PD-L1 expression across the board, 85% had ECOG Stage 1. It also included 15% of patients with these locally advanced group. Next slide tells you the story. Very clear results obtained at a second interim analysis. The data was -- continues to -- we will continue follow-up on these patients. But basically, what we see here is essentially a 22-month median survival, which is what has been seen in the best of agents. And this is overall, not just -- this is the mix, non-squamous and squamous versus a chemotherapy median of about 13 months. The next slide gives you the progression-free survival curves. Again, an unambiguous separation of curves. And in this case, the median of 8.2 months versus 5. And again, this is a relatively more complete data because at the time that we did the interim analysis, most patients had already achieved the PFS events. The third major pillar is the tumor response data. And here, again, we see a compelling superiority of the cemiplimab Libtayo containing arm, including the presence of complete responses, which are typically not seen with chemotherapy alone. And the duration of response tells you also a Kaplan-Meier curve on the right shows that the median duration of response or responders of cemiplimab is close to 16 months basically double what you see with the chemotherapy duration of response of 7.3 months. When we look at the groups -- when we subgroup the patients on Slide 21, what you can see here by OS and PFS, and we have separate data for response rate that also correlates with this. But basically, the benefit extended up and down the line. When there's a question, for example, female patients, well, that was a small number. And remember, this was a study that was powered for the entire population of 466 patients, which is about 40% of what combined studies have been for other groups that have looked at separately squamous and non-squamous histologies. And when you start looking at subgroups, they'll be a little bit more wobbles because the numbers are a little smaller. But I think we were very satisfied seeing this, and we're very pleased with the data. If I could go to the next slide, safety. We had safety data that was -- showed no surprises. We had adverse events expected of immune-related adverse events at the appropriate frequency. And so we did not uncover any new or different safety signals. Interestingly, we also did patient-reported outcomes in this study. And we were pleased to see a very clear delay in the time to definitive meaningful deterioration in global health scores and quality of life. Patients maintained their quality of life. And in fact, there was an improvement in the overall change from baseline. Again, patients on chemotherapy, with the addition of cemiplimab, they actually had an improvement in their change from baseline despite being on chemotherapy. So the conclusions on Slide 23, given that a talk with that patients with advanced non-small cell lung cancer, first-line, the combination of cemiplimab and chemotherapy, provided clinically meaningful and statistically significant improvement in OS, PFS, ORR and duration of response. You have the numbers there. It provided an acceptable benefit risk profile, improved PROs and a safety profile consistent with what we've known before. And we believe, after we file and hopefully with approval, that cemiplimab, or in combination with chemotherapy, will be a new first-line treatment option for patients with advanced lung cancer without driver mutations regardless of histology, regardless of PD-L1 levels. And we believe that it -- combined with this, as well as our monotherapy data, that we have a best-in-class agent. And we can go to the next slide, 24. We know everybody is going to ask the question, well, why -- what about everybody else? So let's be candid. It's only Libtayo and KEYTRUDA that have consistent Phase III results as monotherapy and in combination with chemo in first-line lung cancer. They're the ones in green. And we believe, therefore, that it stands up as a best-in-class agent. No blemishes. Let's look at Slide 25, where we take a harder look again at this comparison. On the top, we have comparisons of our monotherapy data where we have in our labels description of the intent to treat the overall population as well as the confirmed PD-L1 greater than or equal to 50%. And when you look at these corresponding populations in the KEYNOTE studies, our data are, we think, as good and compare favorably to that, which has been shown by other agents in this class. On the bottom is a summary of our subgroup analyses between squamous and non-squamous from this study compared to the much larger studies that were done by KEYTRUDA for these groups. And again, the data are comparable. People will -- may ask questions about plus minus here, plus minus there. We found in our hands, squamous did better than non-squamous. To us, that suggests not that we are mechanistically different but just goes to show the point that with the subgroup analysis, you will have a little bit more wobble in your estimate -- your point estimate. And the precision would improve both with longer follow-up, which we did not have because it was stopped due to a significant statistical result on the overall population as well as with longer follow-up. And again, I remind you, we are not approved with chemo. So I don't want to get in trouble with anybody. But obviously, we hope it will be, and when it is, it will be considered as an option. So the next slide, 26, I've just shown you what we've done with Libtayo. Again, in lung cancer, you've seen some were approved in monotherapy. We believe our data presented yesterday at ESMO are compelling, and we are preparing regulatory submissions. As I mentioned earlier, we are 5 for 5 in registration in 10 studies including CSCC, BCC and cervical cancer. But for lung cancer, it's not just about anti-PD-1 and standard chemotherapy. What else can we bring to the table to help patients with lung cancer because, as I said earlier on, we are not curing everybody. We've made a big difference, and there's a lot more that needs to be done. And what you see here are 3 major prongs of an offensive going on. We have an EGFRxCD28 costim molecule in dose escalation, we have a METxMET novel bispecific in dose expansion, and we have that same METxMET antibody, which is rapidly internalized, conjugated to chemotherapy cytotoxic agent as our first antibody drug conjugate. Let me say a few more words about each of those. Slide 27, our costim bispecifics, remember how they work, they basically press on the gas after you get that initial signal to the TCR. And in combination with anti-PD-1, they lead to augmented activity of T cells against cancer cells. Why EGFRxCD28? Well, EGFR is widely expressed on epithelial tumors, and abnormal activation of EGFR is, in fact, a validated target for multiple tumor types, including lung cancer, head and neck and colorectal cancer. So we believe that if this EGFRxCD28 co-stimulatory molecule proves itself to have activity, it could become a widely useful co-stimulatory bispecific. So the study is currently enrolling, dose escalation. As with all of these bispecifics, the class, we have to be very cautious. Patient safety first, but we're very excited and moving forward with this as well as others in different indications. The next slide is a reminder on METxMET antibody. Remember, many MET antibodies attempted to date, have had difficulty inhibiting the MET receptor without also activating it. Our bispecific holds the dimer components of the homodimeric receptor apart in such a way that they can signal and in such a way that they are rapidly internalized. And we have successfully completed our dose escalation without toxicity, and we are now expanding in a variety of cohorts characterized by different features of activation of the MET pathway. And finally, our METxMET ADC. This is our first ADC to enter the clinic. It is using a proprietary platform that we have developed by our chemists. And we -- this is our first, we've been very picky about which one we will take into the clinic. We like it because of the payload and linker but more importantly, because it's rapidly internalized. And we believe that 1/4 of lung cancer patients may benefit from this if it proves to have activity. And we're expecting to start dosing any day. So if I will conclude with some key upcoming milestones. We have our submissions in preparation for cervical indication for the first-line lung cancer indication with chemotherapy. They should be -- we will announce them when they're under -- they've been accepted for review. We have a LAG-3 combination study with Libtayo, plan to begin in melanoma to complete a triad of efforts in dermato-oncology. Our CD20xCD3 program in lymphoma, and our BCMAxCD3 program in myeloma are both continuing and enrolling into potentially registrational studies. We have solid tumor bispecifics, a MUC16xCD3, primarily in ovarian cancer; a PSMAxCD28 costim for prostate cancer. And for both of those, we have announced we have a corresponding MUC16xCD28 and a PSMAxCD3 that will be entering the clinic. All of these can be in combination with Libtayo. So with that, I'll conclude my presentation, and I'll be happy to take questions. I'll hand it over to Justin to fill them.

Thank you, Izzy. Liz, we're now ready to open the call for Q&A. [Operator Instructions]. Lizzie?

[Operator Instructions] Our first question comes from Kennen MacKay with RBC Capital Markets.

Congrats on the Libtayo update. Maybe just hoping sort of at a high level, thinking about that frontline chemo combo data. What you see as maybe the most competitive advantage over KEYTRUDA and sort of what you think would be the major driver of adoption of Libtayo's combo versus KEYTRUDA's chemo combo?

Thank you for that question. So I would say that there are 2 broad categories of considerations. One is from the study itself and one is for the future. So from the study itself, we did include in this study, a significant number of patients that had an extensive locally advanced disease who would not be eligible for radiation because the size of their tumor would prevent -- would be contraindicated, and yet we saw a benefit there. We also had 85% of our patient population sort of at the edge of the performance boundary. Usually, it's more like 50-50 between ECOG 0 and 1. And we also included patients with brain METs, although they weren't a huge component of this study. So I would say what we had here is a real world -- closer to a real-world spectrum of patients being enrolled. And we believe that these results, combined with our monotherapy established Libtayo, is only 1 of 2 such agents to have these consistent results. And if approved, I think it would be useful for physicians who like options, who like flexibility to try it. I think they will be happy with it, if it's -- when it comes to that. But most importantly, this is just the beginning for us. We had to establish this to be "credible". As an immuno-oncology player, we believe we've done that in spades. As I said, 5 for 5. We didn't take in Libtayo into the clinic until it passed an enormous array of internal checks of many different antibodies, and we put our best foot forward. So it will be a reliable option and it will be a foundation for future therapies to come.

Our next question comes from Robyn Karnauskas with Truist Securities.

And then congrats on the data. I was just not to slice and dice further but I just wanted to ask a quick question about the response you had in the low PD-1 population, so less than 1% with the chemo. I couldn't tell from the hazard ratio whether like you were seeing a response or any impact out there. Can you just talk a little bit about that because I know we've seen with some of the keynote studies that you've seen in response just at least with chemo and potentially in combination with check point a little bit more in that population? And maybe what's going on there?

Sure. So I think what you saw there is, if you look across OS, PFS and ORR. PFS and ORR were unequivocal that you had benefit in that group. For -- remember, this was a study that was sized for an overall population. And when you start to look at subgroups because the OS endpoint was called at an interim analysis based on fewer events. By definition, with further subgroup analysis the precision around those estimates will be a little wobbly. If you actually look at it, they're all consistent. And in fact, the 1% to 49% looked a little better than the greater than 50%. So that doesn't make sense. What we've shown in our previous studies is clearly, there's a gradient that the higher the PD-L1 level, the better the response. So if you imagine that there's going to be a benefit in the PD-L1 less than 1%, it won't be as pronounced as in the greater than 50%. And with the smaller numbers available to us at the time of the interim analysis, there'll be some wiggle room. But for the PFS events, we had all the events then that you would need for a final analysis. And there was unequivocal. So I would say it's an issue of small numbers and follow-up. And I would not -- and we've not seen a loss of activity in other studies with low PD-L1 levels -- or absence of activity, I should say.

Our next question comes from Ronny Gal with Bernstein.

So first, only KEYTRUDA have got NCCN preferred status for PD-1 combination with combo. Do you anticipate also getting it and how critical it is for your commercial projections? And second, just a housekeeping. The METxMET, you are now in dose expansion. Is this first -- set of data going to be available for mid next year for either so ASCO or ESMO? Are we looking at something closer to year-end before we can present some data from that cohort?

Okay. So the first question, I'm not going to speculate on commercial projections, but we obviously do hope that in addition to getting approval, the quality of the data would narrate the same kind of preferred 1a, whatever their classification is, from the NCCN. It's a randomized double-blind, placebo-controlled study with a positive outcome. That's the highest bar for quality of data. Second, with regard to METxMET, we are in dose expansion. We are early in those groups. I don't know if we'll have data by ASCO, but I certainly hope that we'll be in a position to share some of the results from those expansion cohorts in the coming year.

Our next question comes from Yaron Werber with Cowen.

This is Brendan on for, Yaron. Really, just kind of a quick one from us for the kind of the costim and MET bispecifics here. Obviously, a ton of shutdown goal. So I guess, really when you're kind of looking at these different approaches, whether it's MET, MET or CD28 or ADC, I guess what are kind of the driving considerations for you guys in terms of which populations do you think are really best suited for each? And I'm just trying to get a better sense of how they might be used relative to each other.

So we believe that all of these are potentially combinatorial. And there will be something. So we believe -- for example, 25% of patients with lung cancer will have some form of MET overexpression, some that may be potentially benefit particularly from a METxMET ADC. In that regard, it becomes essentially a very targeted chemotherapy, which I don't see why it wouldn't work well with Libtayo. So that's a potential area of combination. With regard to EGFRxCD28, pretty much all lung cancer epithelial cells expressed in EGFR. So remember, we are not targeting EGFR here to inhibit EGFR or to directly kill cells that are EGFR positive by -- but actually use the EGFR as a hitch post, if you will, or a linker so that the tumor cell now behaves as if it's expressing the B7 molecule, which is very important for triggering the CD28 on T cells to sort of push that first signal from the TCR and make it more effective. And we've shown that in combination with PD-1, that that's very effective in multiple preclinical models. So we believe that the EGFRxCD28 could be an applicable companion to Libtayo and a number of epithelial cancers, including cervical cancer, including breast cancer, including potentially colorectal cancer, which has proven quite difficult, particularly in the MSS group. So I think I've answered your questions.

Our next question comes from Alethia Young with Cantor.

Congrats on all the progress with Libtayo. 5 for 5 is notable. I wanted to talk a little bit about what you're kind of solving for with some of the novel classes of bispecifics that go beyond costims?

Well, the novel classes of -- allow us, like the METxMET, allow us to address the target, like MET, in a novel way. So as I said earlier, prior efforts with antibodies targeting that MET were unsuccessful. And the major reason they were unsuccessful was that while they may have blocked the binding of the typical ligand for MET, the hepatocyte growth factor, unfortunately, by virtue of binding to the MET receptor, they triggered the MET receptor. So it didn't really do any good. What this agent does is takes the -- this bispecific, which binds to this homodimer in such a way that it locks them in a configuration that is unable to signal. So it doesn't signal. And moreover, because of this abnormal state, what we think probably triggered by this abnormal state on the cell surface, it is then rapidly internalized as if it's like a defective receptor. And so it can really bring a payload in -- very quickly into the cell. So what we are trying to solve for is we believe the bispecifics are a great way to link between cells of the tumor and separately to engage cells of the immune system, whether they're T cells by virtue of CD3 or by virtue of CD28. We're exploring other ligands also for trying to look at other cells in the immune system that might make sense to try to engage in this way. But the bispecific technology allows us to think about even targeting tumor antigens in a novel way that was previously unavailable.

Our next question comes from Mike King with H.C. Wainwright.

Let's add to the congratulations as well. Just 2 data-related questions. Israel, you said that the PFS analysis is mature. But how -- can we get a time line or any kind of sense of when we might see updated data on overall survival? Or will that pretty much stay the same?

So I'd just point out that what -- when we get the interim analysis and the study is declared a win, the study is technically over. So we are going to attempt to get additional follow-up data, and we hope to be able to present additional follow-up data. But the data as it is, is technically the end of the study. And so it had enough OS event for us to call it a win on the overall population, which was the primary endpoint. As I said, since the OS events take longer to occur than the PFS events, by the time we were able to get these OS events, the PFS events, there were many more of them. And the responses obviously pretty much occur within the first 6 months of treatment. So those data are -- there's -- rather than calling them mature, immature, I would just say that there's more of it. And therefore, as a consequence, the precision around the point estimates for what the number is and the confidence intervals are sharper. But basically, it's a positive study and the subgroup analyses are all consistent.

Okay. So it's unlikely that the OS, even if you did follow up, it would be unlikely that the OS would increase at all. It would just be that the confidence intervals would narrow. That's your point, right?

I don't know what it would do. I would -- we've seen -- I would hope that it actually would improve further. But I don't know that it will, and I don't know that we'll be able to tell you that because of the nature of what will happen to the study.

Operator, we have time for 2 more questions.

Our next question comes from Matthew Luchini with BMO Capital.

Just wanted to ask, given the -- with the subgroups and sort of what's been characterized a little bit of the wobbliness, just wondering if there's any strategy or thoughts around doing additional work to try to shore up some of those groups where the data perhaps are opened up with some of the questions, whether it's women or nonsmokers?

Well, you can ask about the women or the nonsmokers, but there are very few patients. So it's not -- and again, if you look at the PFS data and the ORR data, they're all positive. They're all in line with that. So the -- as I said before, the precision around the subgroup analysis is going to be a little bit less precise than for the overall population, which is what the primary endpoint was. And we believe the study is positive. And where you'll see additional data coming in the future is with our novel combinations.

Our next question comes from Esther Rajavelu with UBS.

Can you talk a little bit about the Libtayo combo strategy with agents other than the bispecifics? I mean you have a number of Phase II trials ongoing with oncolytic viruses. So curious what your thought process is there, and if we should be expecting to see any of those data readouts in the near term?

Thank you for that. So as I said earlier on, we have a robust internal pipeline between all our bispecifics, engaging CD3, CD28, novel. And we have other classical type antibodies. But we are engaged in a number of collaborations. We have a collaboration with Vyriad, which has a novel VSV-based oncolytic virus that can be given intravenously, which we think is a great advantage. We have studies underway with in a collaboration with Replimune that have an HSV-based oncolytic virus. We also have studies underway with a variety of tumor vaccine platforms, one with ISA, which is a peptide vaccine for HPV16 peptides. We have one with RNAi and both -- with BioNTech in both prostate cancer and in melanoma that are underway and we're actively discussing other potential collaborations with them. And we also have -- looking at DNA vaccines where we did a study with Inovio and their DNA vaccine platform in GBM. So these are all in the early stages, exploratory stages. We hope we'll be able to present data at meetings like SITC, AACR as well as ESMO and ASCO. And all I can say there is kind of stay tuned. We're pushing them all forward. And we picked these, and we also have studies that we're looking at in combination with cellular therapy companies like Bluebird and [ Adaset ] because we believe there's opportunities for not just bispecifics. There may be reasons to try cellular therapies. So we have a very broad outlook. We have as a central foundation in our whole approach, have always believed that combination therapy is essential, and we have a very broad approach to that.

Thank you for the question, and thank you all for joining the call this morning after a busy ESMO weekend. This concludes the call and the Q&A. The IR team is available to answer any further questions. Thank you, and be safe, everyone.

Thank you.

This concludes today's conference call. Thank you for participating. You may now disconnect.