Dear ladies and gentlemen, welcome to the Merck R&D Update Call 2024. As a reminder, all participants will be in listen-only mode. May I now hand you over to Constantin Fuest, Head of Investor Relations, who will lead you through this conference. Please go ahead, sir.
Thank you very much, Nadia. Dear ladies and gentlemen, a very warm welcome to this 2024 Merck R&D Update Call with a focus on early oncology. I'm delighted to have today with me here, Danny Bar-Zohar, Head of Research and Development, Victoria Zazulina, Head of Development Unit Oncology, as well as Paul Lyne, Head of Research Unit Oncology. In the next couple of minutes, we'd be delighted to take all of your questions, but before that, we will guide you through the key slides of this presentation. And with this, I'd like to directly hand over to Danny to kick us off. Over to you, Danny.
Thank you. Thank you so much, Constantin. Good morning, good afternoon, everybody. Warm welcome from me as well, and thanks for taking the time and joining us at this exciting ASCO call. What we'll do today is have a quick sanity check on the progress when it comes to the agenda that we laid out at the very end of 2022. But the focus, as we communicated, will be the early oncology pipeline, which we are very proud of. So Victoria and Paul are here with me today, ready to dive deeper into the progress that we are making with DDR space, ADCs, and more. We would love to get your questions and provide additional color as much as we can. So let's go to slide number 6, and where are we today?
This is what we presented back then, and we stay committed to delivering on the journey, but more importantly on the outcome of a launch every 18 months. Focused leadership, building on areas that we know in biology, technology, and therapeutic areas, but also thoughtfully expanding to adjacencies. Another principle, we cannot do it all by ourselves, so we have been very active in the past year across the entire R&D chain to make sure that we are in the ballpark of roughly 50% of future launches coming from the outside.
Strong emphasis on discipline and execution, being fast in the basics and thoughtful when you need to be, thoughtful and carefully design a trial using AI throughout the value chain, and making sure that we are properly sized, taking organizational structure savings and reinvesting these into medicines, into pipeline, thus keeping the overall R&D spend at the low 20s% of sales to support the profitable growth. Moving to slide 7, we keep on walking the talk when it comes to a focused leadership approach. What do we mean with that? As we said, expanding from areas that we have reasonable stronghold in, whether these are certain tumors, technologies, taking tons of know-how from small molecules and antibodies, to ADCs, to products, to complex bispecifics, or biology when it comes to DNA damage response, for example.
We do that both on the internal and the external innovation fronts. When it comes to the latter, to the external innovation, this is the why we do certain things. We have great ambitions in ADCs, so we need more targets, hence the deal with Caris Life Sciences. DDR, needless to say, PARP1 selective with Hengrui. Colorectal cancer, we are with Erbitux, with M9140, so we go and do an option deal on panaclide. Pimicotinib for TGCT, the deal that we signed several months ago with Abbisko, could be seen as an outlier, but here, strong target validation, de-risked asset, under the radar of maybe other pharmas, modality that we feel comfortable with, with a very high unmet need and interesting markets in China, and also a super exciting option outside of China. Moving to slide eight.
Now, although the focus of this call is on the early oncology pipeline, our frontline phase three assets in oncology make us super excited. First and foremost, the Avelumab currently tested in the curative setting in the Trillium study completed recruitment long ago, event-driven, and we're happy to say that we actually have the number of events required for the interim analysis, and now we let the magic of data lock and IDMC discussions take place. With pimicotinib, on the right-hand side of the slide, this is a new kid in the block, global phase III trial, fully recruited with a primary endpoint of ORR at week 25. So you can do the math, and see that this trial is going to be read out by the end of the year.
Of note, this trial is run by Abbisko, so just to be clear, but we are not just sitting there, we are lining all the troops for the China submission and potentially ex-China as per the option. Moving to slide 9. This is an oncology call, as we said, but we are consciously neglecting NNI here. But to remind you that we have important readouts for enpatoran this year with CLE and SLE later. We're also starting now the myasthenia gravis with cladribine capsules, so there is a lot going on there. In oncology, three phase III trials, phase Ia/Ib programs, which are progressing towards mature POCs in the foreseeable timeframe, and compounds getting into the pipeline from our research lab, as well as from the outside at all stages.
So this is quite dynamic, and we like that optionality. Moving to slide 10. Our philosophy in oncology is quite familiar to you. The team here is keen to strike cancer cells at their core, either with targeted toxic payload, impeding the DNA repair responses, or with sort of convincing the cancer cell to go through the programmed death route. Victoria and Paul will walk you through the first two, and I will hand it over now to Victoria.
Good morning, everyone. I would like to update you on our strategy and plans for clinical DNA damage response and ADC pipeline. Slide 12 starts with a vision for our DDR portfolio. In our hands today, we hold 4 clinical assets, including the most recently licensed PARP-1 selective inhibitor from Hengrui Pharma, as Danny mentioned. All of them are targeting crucial orchestrators of DDR cascade and allow us to leverage synergies not only between and within this portfolio, but also to explore broader space of combinations with standards of care. This slide illustrates the key scientific hypothesis and our approach, how we want to differentiate from other players in this attractive field, as well as the linkage with potential indications and settings where this concept can come to fruition.
Synthetic lethality is concept number one, the one that has been already unlocked through earlier success of first generation PARP inhibitors. We want to go beyond the pair of BRCA mutants equals PARP inhibitor, looking into more complex biomarker spaces associated with resistance to PARP inhibitors. We want to leverage unique combinations within our portfolio, such as ATR, ATM inhibitor, ATR selective PARP inhibitor, and others. And these combinations are taking us to the PARP legacy indications in both PARP pretreated as well as the PARP-naive spaces. Number two is talking about rekindling immune response with ATR inhibitors in patients who had prior immune checkpoint inhibitor failure.
The key to our differentiation here is to move from the unselected approaches, which we have seen with prior PARP combinations or in the ongoing phase 3 Latify trial within ATR, to selecting tumors with ATR sensitizing mutations or with known high replication stress. Hypothesis number 3 is talking about potentiating cytotoxic treatment as we explore improved safety profile of next generation, specifically PARP inhibitors here. The synergy between certain classes of cytotoxics and DDR has been known for a while and has been demonstrated robustly through preclinical data, however, had limited utilization in the clinic due to the narrow therapeutic window, for example, with the first generation PARPs. Of high importance in this context, for us, of course, is to leverage this synergy with our top one inhibitor payload in the growing ADC portfolio.
On the next slide, from high level concepts, let's look a little bit more practically how and where we plan to unlock each of these hypotheses, focusing on the two lead compounds, ATR inhibitor, tuvusertib, and PARP1 inhibitor, M9466, or also known as HRS-1167. This is the nomenclature which you see presented by Hengrui Pharma. Let us start from the center of the Venn diagram, showing the area of synthetic lethality. This one applies to both drugs because they can and will be combined between themselves and with other DDR assets in the PARP legacy spaces. As you can see, we prioritized ovarian and prostate cancer as lead indications, starting from the PARP pretreated space.
Then for ATR, we are focusing on activation of immune response in checkpoint pretreated populations, so you will see combinations of tuvusertib with cemiplimab in lung cancer, with avelumab in urothelial cancer. These have been selected as the first sentinel indications to try hypothesis. And then for PARP-1 inhibitor, we are focusing on the combinations with cytotoxics. Irinotecan, as an example of a topoisomerase 1 inhibitor, as well as subsequently our own ADC portfolio are on the map, and also platinum-based regimens that can lead to a variety of indications. Here we are quoting small cell lung cancer, platinum sensitive ovarian cancer, urothelial cancer, et cetera. But the main prerequisite and the foundation to all of these concepts is a good combinability of both drugs, and this is exactly the lens through which we are assessing them.
On slide 14, we are sharing the monotherapy profile of the ATR inhibitor, tuvusertib, where we can state that, first of all, we can achieve a good target coverage with the recommended dose selected. That's the table on the top left corner, 180 mg. Moving to the right, the dosing regimen, 100 mg per every two weeks on and one week off, is the regimen that demonstrates a favorable safety profile when compared to another contender in the class. Here we use an example of camonsertib. The rates of hematological events, discontinuations, and dose reductions from our monotherapy data appear to be more favorable. Lastly, the dosing regimen is able to demonstrate a biological proof of concept, if you will, with credible rates of reduction in the ctDNA rates and the molecular response, what we declare as a molecular response.
On slide 15, we are talking about now the combination potential. By now, we have combined tuvusertib with a PARP inhibitor, niraparib, with our own ATM inhibitor, lartesertib, and with two checkpoint inhibitors, and we have a dose for all 4 combinations. We're using the example of niraparib here on slide 15, as the key development that we are taking forward and also literally in parallel now, these data are being shared at ASCO session. Recognizing the overlap in toxicities between the PARP inhibitors and ATR inhibitors, one of the key questions is what dose of each can you deliver safely in combination in order to ensure the feasibility of the regimen? This table on the left illustrates the experience and the recommended doses that we were able to achieve and other companies with a similar approach.
In comparison to others, we're able to deliver the highest 75% of the total dose of ATR inhibition in the combination with a PARP at the expense of the reduced amount of PARP inhibitor. And we consider this as an appropriate strategy, given that we are rescuing PARP inhibitor failure with ATR, with the addition of ATR in this case. The regimen yields objective responses in unselected solid tumor populations, as you can see on the right. And of high interest here is the response rate of 38% in a small subset of patients with ovarian cancer. Here, all but one patient have been PARP retreated. This is what we are taking forward into our phase 2 as a signal. Molecular response of 47% in a valuable population also shows enrichment, as would be expected for BRCA status, and shows regardless of the prior use of PARP.
On slide 16, we are talking about a higher level operational plan, what we are planning to do with two research combinations, delivering on the clinical proof of concepts now in phase 2 in the next 2 years. We're in the middle of 2024 with Cemiplimab at the bottom, the combination in lung cancer already ongoing, and two other trials in PARP-pretreated ovarian cancer with DDR, DDR combinations, and in urothelial cancer with Avelumab combination, initiating literally as we speak and being ready to recruit from Q3. With this, I would like to move on to the new kid on the block. On slide 17, we talk about M9466, and I remind you again, HRS-1167 is another name for the same compound, and this is how it has featured at this ASCO.
As we understand the science of PARP inhibition, the enzymatic activity, as well as the ability to trap PARP on the DNA, will contribute to the response to PARP inhibitors. On the table on the left, we are illustrating that M9466 is a highly potent trapping PARP inhibitor with high selectivity towards PARP1, in contrast to olaparib, the first-generation PARP inhibitor. The initial clinical monotherapy data that I'm going to show you in a few moments come from the dose escalation and dose expansion part of this phase 1 trial in China. This scheme is shown on the right, and we are initiating 3 new combination trials in Q3 this year, delivering on the talk, as mentioned here on the slide. On the next slide, we provide the outline of available clinical data from the phase 1 from this PARP-selective, PARP1-selective inhibitor.
Safety across the mixture of the doses looks reassuring, with predictable and manageable adverse events, which are consistent with the therapeutic class. No maximum tolerated dose was reached. No dose-limiting toxicities were reported. Some patients were able to stay on treatment for a long time, deriving clinical benefit. With regards to efficacy in the specifically homologous recombination repair-deficient population expected to be sensitive to PARP inhibition, we see a strong objective response of 40%-50%, which further goes up as we enrich for PARP-naive populations, up to 70% in ovarian cancer. These are encouraging data for a phase 1 patient population. With that, I would like to move to our ADC portfolio. On slide 20, we are talking and introducing again our proprietary ADC technology, and which we talked about during the previous update.
I would only highlight a few elements associated with the first wave of our exatecan-based ADCs, and you will hear more from Paul in the research section. On the antibody side, we are differentiating from other ADCs through the targets that we are pursuing and also through our ability to deliver innovative antibody formats. More to follow later. We are using arguably one of the most potent topoisomerase 1 inhibitor payloads with a strong bystander effect, allowing to kill neighboring cells, which may not be expressed in the target. Our linker has high stability in circulation, and we have a flexibility in constructing ADCs with different drug to antibody ratio, depending on the properties of the target. On the next slide, slide 21, we are presenting our front runner in the clinic, anti-CEACAM5 ADC M9140, for which we have presented phase 1 data at this ASCO.
CEACAM5 is a membrane protein highly expressed in some tumor types, notably colorectal, gastric, pancreatic, lung, which build the core of our development strategy. We started the program with a focused exploration on colorectal cancer, the tumor, which almost universally expresses the target, and the scheme of this study is presented on the slide at the top. With a demonstration of early activity already during the dose escalation phase, we are now expanding the program to other tumor types, also planning for the combinations. Slide 22 summarizes the early clinical data for M9140. In the clinic, we're able to reach the dose that's predicted to be relevant for effect. From the PK curve, we see more than 3 log difference between the ADC and the free payload, which is a reassuring difference.
The safety profile is very much driven and consistent with what we know about the exatecan payload, predominantly hematological adverse events, including some qualifying as dose-limiting toxicities. We observed a milder GI toxicity, mainly grade 1, small number of grade 2s, compared to the agents in this class. And importantly, we saw no ocular events, interstitial lung disease, even at the highest doses, bearing in mind that our trial recruited Japanese population during the dose escalation, the patients who are considered to be at a high risk of reporting an ILD. It's also very reassuring to see what we can achieve at the active doses, 2.4 and above, in terms of tumor responses and progression-free survival.
By now, we have seen 5 responses, of which 3 have been confirmed, and more than 60% of patients are deriving clinical benefit as a minimum with the stabilization of disease, and that is in a highly pretreated population, which has already received 4 or more regimens, prior regimens, and irinotecan pretreatment. In this context, the progression-free survival, reaching 6.6 months at active doses, shows a really reassuring sign because the standard of care in this setting can deliver 2%-6% response rate and also PFS of maximum 5.4 months, and that's third line patient population. And lastly, I would like to spend a few moments talking about the next ADC, which is coming to the clinic, and that is our exatecan ADC against the GD2 target.
As you will see from the table on the left, GD2 is expressed abundantly in some tumors, and in normal tissue, is present in peripheral nerves, CNS, and melanocytes. The target itself has already been clinically validated through GD2 antibodies, such as dinutuximab and naxitamab, which are used in the clinic in pediatric neuroblastoma patients. Both drugs have a box warning for acute pain. We used the same antibody as dinutuximab and modified its region to abrogate its immunological effect on the peripheral nerves, which we believe are responsible for the side effect. And then we linked it with the exatecan payload to create M3554, the anti-GD2 ADC. Here we demonstrate very strong preclinical data in relevant GD2-expressing tumor types, showing complete regressions in some PDX models, including those from neuroblastoma with prior GD2 pretreatment.
In Q3 this year, we are taking this program into the clinic and hope to see a similar effect in patients. With that, I would like to hand over now to look into the even earlier portfolio presented by Paul.
Thanks very much, Victoria. Good morning, good afternoon, everyone. It's a pleasure to share some high-level details of our research efforts with you. Moving to slide 25, I want to take you through the focus of our research efforts and how we are evolving both our transformation to sustainably deliver competitive assets and organically to the development pipeline. Our focus remains in the four areas we've outlined previously: antibody-drug conjugates, DNA damage response, next generation IO, and intrinsic tumor signaling, with the specific execution priorities depicted on the right-hand side, where we are driving internal innovation in the ADC space, having a balanced portfolio of first-in-class and best-in-class opportunities in tumor biology, and concentrating IO efforts on specific populations and mechanisms that can work in post-IO as well as IO-naive settings.
All of this is founded on our core expertise and innovation in small molecule design and protein engineering. With our renewed focus on efficiency in research, we are projecting to consistently deliver on average three new oncology assets to the clinic annually. Moving to slide 26, I'd now like to take you a little deeper into our efforts and strategy in the ADC space. There are four main components underpinning our plans to enhance our position as a major ADC player. Firstly, we want to maximize the opportunity we have with our differentiated internally developed Topo1-Linker platform. Next, we are moving beyond exatecan to newer, biologically distinct payloads, where we are exploring different cytotoxic warheads, as well as immune stimulatory payloads and targeted tumor killing mechanisms, including protein degrader-based payloads.
Finally, we are devoting efforts to identifying novel tumor-associated antigens and have recently completed a deal with Caris to help drive that. The tangible output of our efforts is depicted on the right-hand side of the slide. As shared by Victoria, we have our anti-GD2 asset joining M9140 in clinical studies. Those programs will be quickly followed by 4 assets moving to IND in the next 12 months against the tumor antigens shown. M7437 and M0121 are part of an undisclosed collaboration, and so we can't share the targets currently. But I can add that, like the other assets, they are directed to tumor-associated antigens with first-in-class potential.
Lastly, toward the latter part of the time window, we will start to bring to the clinic ADCs with next generation payloads, moving beyond standard of care cytotoxic mechanisms to exploit core tumor-promoting biology in a tumor-specific way. This will allow us to address some canonical tumor biologies that have previously been hampered by broad systemic toxicity concerns. We're excited about the progress we've made internally and through collaborations toward building a leading ADC portfolio, and we could potentially have 5-6 ADC programs in the clinic in the next 18 months. Moving to slide number 27, I'd like to share our excitement about our next IO asset, M0324, an innovative conditional CD40 agonist that will be filed with regulatory authorities shortly. CD40 agonism is a highly desirable mechanism to boost T-cell responses, but previous therapeutic efforts have been dogged by off-tumor toxicities.
M0324, as shown on the left-hand side, is designed to recognize MUC1 antigens on tumor cells and agonize CD40 on immune cells in the vicinity of the tumor. This conditional agonism, depicted in the central panel, is brought about by CD40 clustering that is mediated by the high density of MUC1 on tumor cells. Receptor clustering is needed to transmit an effective signal through the CD40 signaling cascade. This is in contrast to the case for normal cells, where MUC1 expression is low, and as a consequence, there is no clustering, nor agonism of CD40 outside the tumor tissue. This is illustrated by data shown on the right-hand side that show very robust immune activation by M0324 in the presence of MUC1-expressing tumor cells, and a complete lack of activation in the presence of tumor cells without MUC1 expression....
The exquisite selectivity of the agonism is in contrast to first generation unconditional CD40 agonists, which you can see don't as robustly activate the immune system in tumor cells that express the MUC1, nor do they exhibit any cell activity for tumor cells. The design of M-zero three two four leads to robust T-cell antitumor activity in several preclinical models without immune activation in normal tissues. We look forward to trialing this drug in both IO and in IO-naive patients soon. With that, I'd like to thank you for your attention, and I'll hand it back to Danny to conclude our presentation.
Thank you so much, Paul. Let's switch quickly to slide 29. So to conclude, we are following the R&D principles when it comes to focus leadership, approach, external innovation, mix, and execution. As you heard, beyond our phase 3 front runners, Xevi and pimicotinib, we have made very good progress on DDR and ADCs. In DDR, key pillars are tuvusertib, M9140, M9466, the PARP1 selective with Hengrui, with strong data suggesting potential best-in-class and combination on the way. When it comes to ADCs, our linker payload platform is showing itself clinically, but very encouraging efficacy and safety data from M9140 and another first-in-class ADC, the M3554, is underway, followed by several more, with a clear strategy how to go even further to Paul's point.
We're super excited about that, and I'd like to thank you again for listening, and let's open up for questions.
Thank you very much. Nadia, over to you. We have time for a couple of questions. Thank you.
Thank you. We will now begin the question-and-answer session. If you have a question for our speakers, please press star one one on your telephone keypad to enter the queue. Once your name has been announced, you can ask your question. If you find your question is answered before it's your turn to speak, you can press star one one to cancel your question. One moment, please. And now we're going to take our first question. And it comes to the line of Richard Foster from JP Morgan. Your line is open. Please ask your question.
Hi, thanks for taking my questions. Just a couple on M9140, please. Firstly, just, we've seen the 10% response rate, which I agree looks greater than we've seen with some of the standard of cares in third- and fourth-line. What do you need to see in the dose optimization phase? Do you need a repeat of the 10% to move forward to phase 3? Are you looking for improved response rate in that trial? And, you know, this is a very refractory patient population. How do you get a better handle on the efficacy? Do you need to do the combinations that are planned with bevacizumab?
What would you be looking for from those combinations to continue a broad program of the product in colorectal cancer? Thanks so much.
Thank you very much for your question. So I think your train of thought is exactly like ours. One thing I would add is that 10% response rate at the moment, obviously, that spans across several doses, and you're right, we need to dose optimize to see what's the actual response rate in a less refractory population. Moving forward, not only response rate, as we have seen in this refractory population, even though standards of care had low response rates, they won on PFS. So PFS will be a very important parameter for us with some milestone landmark data, because that's the population where irinotecan pretreatments may already can create certain hurdles if we go to third line plus colorectal cancer. And we have to be careful also not to miss the effect on stabilizing or shrinking the disease under control, that we do not miss that effect.
So PFS will play a role, especially as we see the kinetics of response to our drug is actually evolving over time, and it's very reassuring that the safety profile allows the patients to stay on treatments for a prolonged period of time, several cycles, before we start seeing traditional resistance response. Prior to that, it could be just a stable disease, but important stable disease at that, in that setting. Combinations are on the radar. Depending on the single agent activity that we see in those optimization, yes, we plan to take it in combination, potentially into earlier lines, as well as the other indications where irinotecan pretreatment has not been, is not part of a standard of care, such as gastric cancer, and we are hoping to see what we call competitive response rate or meaningful response rate for different respective populations.
Excellent. Thank you very much.
Thank you. Dear participants, as a reminder, if you wish to ask a question, please press star one one on your telephone keypad. Now we're going to take our next question. It comes from the line of Sachin Jain from Bank of America. Your line is open. Please ask your question.
Hi there, Sachin Jain, Bank of America. Thanks for taking my questions. I've got a few, if I may please. Firstly, just to get a better understanding of the differentiation of your PARP1 and ATR. So thanks for calling out the slides differentiation, but, for, for your PARP1, I wonder if you could comment on differentiation to Astra's follow-on, saruparib, you compare to the marketed Lynparza. And on the ATR inhibitor, I wonder if you could comment versus, ciralasertib, which has phase three data next year. Again, the comparison you draw, I think, is an asset that Roche has already handed back rights to. So just to get a better understanding of, the PARP1 and ATR versus, competition that seems to be further ahead. And then a quick one for Danny on the xevinapant interim.
If you said you're willing to comment, just where are you in the process? There's been a lot of interest in, on relative timelines. Are you past the point of knowing on futility as yet? Thank you.
So thank you. I will start with the PARP and ATR differentiation. Let's start with PARP1. So this is a highly selective, potent, made potential to be best in class. We haven't presented it here. In the assays provided or run by Hengrui themselves in preclinical settings, it appears that this PARP inhibitor can be stronger, can be more potent, compared to AstraZeneca's inhibitor. The jury will be out there clearly in the clinical, what kind of results we see and whether it matters and translates into effect. Now, in terms of the differentiation of ATR with others, I think, and that would apply for PARP1 as well. It's all about the spaces where you would like to play, because some companies are limited for certain considerations for their existing portfolio. Talking about the Olaparib and the context for the next generation PARP here.
We have a different stake on similar indications and might go also to challenge Olaparib in certain settings, not only going after Olaparib or other approved PARP inhibitors. With ATR and with Camonsertib, Camonsertib has been returned by Roche, not to say that this is a bad drug. This still remains a very important contender. Ceralasertib is ahead of all the ATR inhibitors because AstraZeneca took it into phase 3 trials, and that's what I alluded to. The ongoing tuvusertib clinical trial in non-small cell lung cancer is using unselected population. And that's where I try to draw your attention to the fact that we would like to go, even in combination with checkpoint inhibitors and in combination with PARP inhibitors, et cetera, we want to constantly select.
We believe that the field is open to the biomarkers and not to the unselected population.
When it comes to your question regarding the interim analysis of development, so technically, we are... As we said, we are at a stage where we have in our database the required number of events for the event-free survival, which is the primary endpoint. Database is cleaned, it's being locked, and then the DMC will see the data and perform both analysis, the efficacy and the futility. So, that's the sequence. It's not that we passed something and, it's still at the technical stage of locking it.
Very clear. Constantin, do you mind if I take a couple of additional questions? So just on the, on the ATR, where you referenced a slightly different strategy, could you just touch on, and perhaps I missed it in the earlier commentary, what your biomarker strategy is? And I actually had a follow on. You used to list a follow on IE inhibitor, talazinapan. I didn't see it listed today, so I just wanted to check on the status of that, if I could.
Yes. So the biomarkers that we work with ATR, and I was referring to specifically to lung cancer stage, the trial, which is already ongoing with nivolumab, in contrast to the ATR inhibitor that we see going into phase 3, ceralasertib, in combination with durvalumab in AstraZeneca's hands. There they go with unselected. This is a trial called LATIFY. We would like to select the biomarkers, and these are the biomarkers associated with resistance to IO, as well as the ATR sensitizing mutations such as ARID1A, ATM loss, et cetera. So you will see this trial design was presented already at the one of the congresses, the LCC. We have presented the poster about the study design. In terms of the second question was about the IO follower. So that compound is in late-stage preclinical setting.
We are still profiling it and, you know, the further steps will also be linked with the talazinapan success.
Thank you very much.
Thank you very much. I believe with this, all the questions have been answered. And, yeah, to all of you on this call, thank you for joining. Thank you for joining the Merck journey. Goodbye.
Ladies and gentlemen, thank you for your attendance. This call has been concluded. You may now disconnect.