Molecular Partners AG (MOLN) Earnings Call Transcript & Summary

Good day, and thank you for standing by. Welcome to the MP0712 update call. [Operator Instructions] Please be advised today's conference is being recorded. I would now like to hand the conference over to your speaker today, Patrick Amstutz, CEO. Please go ahead.

Thanks for opening the call and the kind introduction. My name is Patrick Amstutz, and a warm welcome from my side to this webcast. We are here today to share the first Radio-DARPin human image and talk about the lead program and talk about the study to come. It was roughly 2 years ago when we signed the collaboration agreement with our partner, Orano Med, who will also be named several times in this webcast that we come together and pioneer radiotherapy. And today, we are opening the clinical chapter of this story. I'm joined by Dani Steiner, Head of Radio Strategy; I have Philippe Legenne with me, our Chief Medic; and Michael Stumpp he is the program lead. He will be mostly for the Q&A part of the webcast. Just 2 hours ago, Dani presented this data at the TRP conference in Amsterdam, the story behind the molecule, the mode of action, and he will be recapping that with all of you, hear this firsthand. We will hear Philippe's perspective of the clinical relevance and also the study design and all of us can ask questions to the experts. Before kicking off, I just want to share a few thoughts on why this is a special moment for myself, but also Molecular Partners and the Radiotherapy field. First of all, this is unique to this field that we have the opportunity before we actually start the Phase I to have meaningful clinical imaging data of humans to derisk, to understand and to really speed up the development, and that makes it also very cost effective for us to develop such drugs. MP0712, especially with this mode of action that we will be discussing, capitalizes on the rapid internalization of DLL3, the target I will just come to, to improve the therapeutic index to then help patients, and that will be most the core of this talk. And this target DLL3 is on cancers, mostly lung cancer, where we have a high medical need, and we need very potent approaches to create the therapeutic effect like radiotherapy. So let's kick off and move to the first slide, which is actually the disclaimer. So we will be making forward-looking statements, but also going to now the Slide #3, that is sort of the introduction. And I shared with you that it was only in January '24 that we started and signed the deal with Orano Med. And what you see here is really the combination of 2 cutting-edge technologies on the one side, the DARPin and on the other side, the isotope in this case, lead-212. And together, we create a new modality, and that's what we're talking about today. We have engineered the DARPin to be kidney cells and especially we have optimized the half-life for matching the disease and the target, and Dani will be talking about that. While Orano Med is the leader and the pioneer in targeted alpha therapy, and we like lead and alpha as it deposits high energy in short time. And for us, and this is important, I will come to that, is in short time means high impact. We have a low probability of escape and resistance and a great potential to synergize with IO approaches. And so if I frame the problem we're trying to solve, and Dani will talk about, it's really we have a small cell lung cancer patient in front of us with a very fast-growing tumor, high chemo resistance and a low copy number target. So how did we go about to solve that conundrum to come up with a candidate that actually has the potential to help these patients. So Dani, over to you. How did we try that? And how did we succeed?

Thank you, Patrick. Very happy to present here from Amsterdam just being on the stage on sharing this data 2 hours ago. So if we move to Slide #4, and I'm now fully focusing on the first program coming out of the Orano Med collaboration, the DLL3 and MP0712 lead-based program. So what we see on Slide #4 is preclinical data showing on the left-hand side, nice tumor accumulation at the 4- and 24-hour time points, low kidney values and as per design, as Patrick mentioned before, elevated blood levels needed for the high tumor accumulation. On the right-hand side, you see the molecule is very efficacious at these 2 different dose levels, leading to strong tumor regression and complete tumor control. The key question that was raised here now several times at the conference how did you manage for -- target with such low expression numbers, and that's illustrated on Slide #5. How did you manage to get such high tumor uptake, while only having a couple of hundred of receptors per cell. To understand this better, one from a scientific curiosity perspective, but also to inform us on next programs that are in our pipeline and new programs to be nominated, we investigated this, which is depicted on the next Slide #6. So let me guide you through that data. On the left-hand side, you see a cell internalization assay where you're basically spiking DARPin. And what you can see the cell internalizes -- the cell expressing DLL3 internalizes this DARPin extremely rapidly. So within 20 minutes, you have more than 50% of the cell DARPin internalized. Then, if you move to the middle graph, we track what is happening with the DARPin by immunofluorescence assays. And what you can see, the DARPin nicely co-localizes in the endosome, which is staying here in red by the EEA1 marker. You can't see in the lysosome because the detection of the DARPin is integrated in the lysosome that will not be able, but you can nicely see in the endosome. And then if you move to the right-hand side, and that's probably the most relevant part of that data, if you now do a similar assay, again cell binding, but you measure the total fluorescence taken up by the cell and you expose the cells continuously to DARPin. What we can see is the blue curve where you get a continuous increase in signal of fluorescence inside the cell, which is indicating that the cell can continuously pump in basically this label. The curve would even look more steep by using a radiometal, which is residualizing and staying inside the cell. Here, we're looking at fluorescence-label data. So integrating this data and moving to the next slide, our hypothesis how this molecule, how the mechanism of achieving high tumor uptake despite the very low expression of DLL3 is twofold. So first, from a biology perspective, DLL3 internalizes extremely rapidly and at the same time, is extremely rapidly replenished, basically leading to a high apparent receptor density over time. The second aspect, the DARPin that we generated is able to piggyback on that internalization to allow us to follow that rapid internalization. And at the same time, the half-life extension we introduced allows the continuous refeeding of DARPin, allowing to really continuously reload the tumor with that radioactivity. Finishing all the preclinical package, seeing good efficacy and favorable safety profile, we then decided to move into the clinics that's depicted on the Slide #8, where you say -- we see we took a 2-step approach. So the first step is using lead-203, which is an imaging isotope with the same characteristics as lead-212 and the imaging isotope is used to collect SPECT/CT images, which you basically can use for imaging the patient and for dosimetry calculation, which allows you to inform then the next step, which is the treatment with lead-212 labeled MP0712. Phase I has been submitted -- the IND for the Phase I in the U.S. has been submitted and is under review and pending approval by the authorities, we hope to initiate the Phase I before end of this year. In parallel, we received a request from the team around Mike Sathekge, one of the key leading Nuclear Medical Person in -- at NuMeRI in South Africa to provide MP0712 for imaging and potentially treating patients with small cell lung cancer or other neuroendocrine tumors. Then in South Africa, a series of patients have been imaged using lead-203 and Mike Sathekge and his team will be presenting dosimetry and imaging data of the full series of these patients at the Theranostics World Conference end of January in Cape Town. Based on support from Mike Sathekge, we got approval to use one of these patient cases out of the series and present to you the data from that patient already today. So if you move to Slide #9, quickly going into details of the patient and guiding you through that. If you focus first on the patient characteristic displayed on the left-hand side, it's a 69-year-old smoker, small cell neuroendocrine carcinoma of the lung. At referral, that patient was Stage 3 with a primary tumor located in the upper part of the lung. Treatment history, radiotherapy and chemotherapy. So maybe quickly -- let me quickly pause here. So this profile of that patient with the stage and the pretreatment history is what we believe gets as close as we can get to patients we would potentially need in our Phase I study in the U.S. That patient received 5.1 [ milligram ] of 203 -- lead-203 labeled MP0712. And based on the assessment of those images, that patient was restaged into Stage 4 with additional 4 liver mets detected by that imaging. So let me quickly guide you through the data. I want to start completely on the right-hand side on the colorful image. That's a planar coronal projection. That's how nuclear medics look at these images where you basically see the orange indicates -- the more orange or yellow, the color, the more radioactivity. And what you can nicely see the radioactivity fully located with the primary lesion, which is indicated with an orange arrow and the liver metastases indicated with the blue arrows. If you move then to the left-hand side, the gray images. So here, the more radioactivity you have the darker area. So what you can nicely see, this is like 4 hours, 24 hours and 116 hours post injection, what you can nicely see as per design, we have a high blood pool at the early time point, which decreases over time. And very importantly, we have no uptake or very low uptake in any of the healthy organs such as kidney and liver. Now focus zooming in on this tumor, what you can nicely see at 24-hour post injection, you already nicely see the uptake in the primary lesion as well in the metastasis, which is still obscured by the high blood pool. And once the blood pool is down at 116 hours post injection, you see even higher intensity of the primary lesion and the metastatic lesions. So zooming out and summarizing this, we see initial high blood pool followed by a specific uptake in the primary and the metastatic lesions over time and a limited accumulation in healthy organs in line with the mode of action of 712 and as well in line with the preclinical data. And with this, I'm happy to hand over to Philippe to guide us through the next stages, which are ahead of us with that program.

Thank you very much, Dani. So we are going to spend a minute on that image -- on those images, and I'd like to bring a little clinical facet to them. You already spoke about the blood pool at 4 hours, 24 hour and 116. But it is interesting to note that this is exactly, in fact, what we have predicted per our preclinical work. And we can see that at 24 hours when this blood pool starts to go bit down, then we -- the tumors emerge and we see them most visible at 116. So in fact, this is a very -- from a patient standpoint, it's a pretty interesting image. And when we were discussing this with the experts, Mike Sathekge first, this is a patient where the prediction of that blood pool evolution and the image evolution makes them think that it's a patient that could have been benefiting if treated. okay? So that's one. Then I would also want to emphasize 2 points. One is about the overall value of the SPECT. You mentioned that, Dani, but I want to reemphasize that basically, the patient was presented as Stage 3, but the value of that SPECT helps requalify that patient as a Stage 4. This is important for the patient treatment. This is important for the clinical team to adjust treatments, okay? So that's -- and then the third point I want to emphasize which is important this time for the development and for us developing that product. Basically, it's really the value of those early images that help us inform and derisk to a good extent, the upcoming Phase I, which is now going to start very soon. So I'm going to move to the next slide on Slide 10 and describe a bit the Phase I, which we are planning, which we are close to initiating. This is a Phase I/IIa study for small cell lung cancer and other neck neuroendocrine cancers. That study is a U.S. multicenter study and obviously, dose escalation around 712 monotherapy. On the bottom left screen, some important points. You can see on the blue part, that basically we have 4 dose escalation steps, so pre-compressed dose escalation starting at 75 mg, which is at effective dose already or close to effective dose. And I really want to thank in a way, all the inputs from the Orano experience already on that and also the interaction that we are having with the FDA and also the good quality of the protection, which we had from our preclinical package. So nice, compressed design starting at effective level. Obviously, patients will all get an imaging first and then will be treated alongside 1 to 4 doses and the dose escalation. First, we focus on the small cell lung cancer. And then the green boxes is that at some point, we will branch and open other neuroendocrine cancers in green when we are close to an effective dose on the blue part. So now if I move on the right part, there is still high unmet medical need in small cell lung cancer. That means that if we get the right benefit and risk, the right signal of activity and efficacy, which we hope and anticipate, we should be able to still take advantage of a path for accelerated review and approval through -- in second-line plus small cell lung cancer. So there is an avenue here. And if we drive quickly and right, we should be able to take that one. Then below on the right, you can see that in complement to that, obviously, as soon as we get a confirmed signal, we want to branch and open evaluation of combination with immune checkpoints, which we believe that the mechanism of action of lead and alpha in a way is the optimal complement to immune checkpoint inhibition. And also, we want to open registration with other neuroendocrine cancers, which where there is a high unmet medical need too. So a compressed and let's say, accelerated path across those developments. So that was -- I'm going to move to the next slide, which is Slide 11. So one could think why DLL3, we have heard that, obviously, T-cell engagers are started to be approved, Tarlatamab and their ADCs. But in fact, when we speak to experts, there is high appetite for more modalities and specifically Radiopharma. And why? Because all those 3 modalities first are potent and can act in low expressing tumor, low numbers. So that's -- they have that in common in a way. Then what we can also say is that in the T-cell engager, the Tarlatamab, yes, it's approved. Yes, it's helping patients. It's great. But it still is moderate response rate with a promising duration of response. We should not forget that there are side effects with T-cell engagers and not every patient can benefit from them and not every patient is a candidate from them. And it's still -- it's going to move into first line likely. Then next to it, ADCs are promising antibody drug conjugate candidates and basically, they promise a fairly high response rate. But for every time that we've seen ADCs in development, there is -- the duration of response is up to 6 months. So -- and they likely would move in first line. So it really opens for this additional modality of Radiopharma, which we are part of. We would like to first enter in second line. And then we think that there is optimal mechanistical combination with immune checkpoints that could make us good candidates for maintenance in first line. So that's -- there is space and there is value for this as long as we move quickly. So those would be the main points I wanted to deliver on that slide. And I think I can move to the next one, which in a way is a bit of a conclusion. We heard Patrick and Dani on the preclinical package and on the specificity of DLL3 internalization. But I really want to emphasize this point of images today, which are starting to deliver. And again, let's listen to what Mike Sathekge will present at the end of January. But this is really a very effective manner to inform and there is our Phase I and what we have seen so far is highly encouraging. As also Dani mentioned, we have filed our IND. It's currently in review, and we are expecting an opening of the first sites before the end of the year and initial data to be generated in 2026. And I hope we will be discussing this with you in 2026 on the effect of those first cohorts. So that's more or less what I wanted to say. Let me thank -- I guess, first, I would like to thank our colleagues from Orano and who -- this is because of this partnership that we are there and so quickly. Then the NuMeRI team, which is really working hard on helping those patients and generating some information and precious data. Patrick, maybe you want to complement that.

Sure. And first of all, thank you, Philippe, and thanks, Dani, for presenting today. Also my thanks goes specially to our partners and most and foremost, to Mike Sathekge, who had the trust to do this trial with us to the patients and their families that were in these trials. So we have dosed, I think, roughly 8 patients so far. So big thanks to all of them making that effort and being part of this trial. And I also want to thank really -- yes, you all for joining this call, for being with us, for joining the new chapter of radiotherapy with -- let me summarize my conclusion, let's say, in 3 dimensions. I think first, we have MP0712, unique mode of action and really slated to become the leading alpha therapy in small cell lung cancer. With that, we open the opportunity to build a pipeline on similar targets. So we have a very good understanding how to now work with the low copy number internalizing targets and our technology. We have the capabilities on top of that to run this fast up to, as we now see, clinical data in a very fast, cost-effective way. And the next stop is really Phase I where we want to bring home that value in for the patients in the clinical trial opening in the U.S. With that, thanks, and let's open for questions.

[Operator Instructions] Our first question comes from Jonathan Chang with Leerink Partners.

First question, what is your latest thinking on where 0712 fits the evolving small cell lung cancer treatment landscape? And then second question, what are the key learnings from this presentation as you think about what other targets could be addressed by Radio-DARPin approach?

I can kick off and then maybe I think it's one for Philippe. So where do we think we will fit? So I think at this point in time, we -- as Philippe pointed out, I think in a second and maybe third line setting, sort of last line setting in this case, a fast-to-market strategy as there is still a very high unmet medical need. And when we speak to doctors, especially for T-cell engagers, the side effect profile can be inhibiting, but we expect that also our side effect profile should look superior to that, also allowing more an intervention than a full line. But keep in mind, it's going to be 2, 3, 4, 5, 6 treatment cycles and you're done. So that's just one thing to think about. Then long term, ideally, as Philippe pointed out in a first-line combined with IO, this seems to be quasi-ideal. So we hope that, that's sort of also the most logical setting to run a trial showing the combination of alpha therapy with IO to gain really long-term control over these tumors. So that's where I personally hope this will go. So use the high medical need for a fast-to-market strategy combined with a first-line strategy in combination. And maybe Philippe will talk a bit about branching out into other indications than lung as I have read that DLL3 is the next HER2 where more and more indications are coming up.

Yes. Thank you, Patrick. So just to reemphasize what you said, there is high unmet medical need and no good standard of care in second/third line. That is -- small cell lung cancer has been a bit more up to very recently. There is a good glimmer of hope with the DLL3 coming in and Tarlatamab is helping the proportion of patients. However, it's only a proportion of patients. And it's both, in fact, either Tarlatamab or the potential ADCs in development will be moving in the first line. We also know that there is like a preservation of the expression across lines for DLL3. So it's, in a way, it's inviting and there is that need will still be there in relapse. So we can start there. This is where we should start and there is -- where this is a quick path to approval. Then I think as Patrick was also mentioning, it's a lot about first line and maintenance. And we need to cure those patients or to keep them in a very long status in the maintenance part. And immune checkpoints are well established here. And in fact, likely all the biology points that radiation [indiscernible] immune checkpoint is a great duet. So this is likely where I would like to develop that drug just as we get enough of good signal in relapsed/refractory moving early in. So that's still the small cell lung cancer part. Then if we look at the other neck and the more this area is now being researched and the more we find that the other 3 is relevant. So -- and there is not good standard of care, post first line in other neck. So those are the avenues where we can further develop those, and this is where we have a plan in our phase, in our expansion to start evaluating that signal.

Thanks, Philippe. Maybe I actually do love your second question, which is sort of posing towards pipeline build. So where does this leave us? And I think it actually the DLL3 understanding has really led to a renaissance of us looking at ADC targets. When the radiotherapy field started, everybody was saying, yes, yes, will be -- it's going to be like ADC. And it turns out that the short-lived peptides are very different than full antibodies because of the internalization that we actually presented to you today. So we are in a position like to take the best of both worlds, so to take targets that are rather low copy number and internalizing fast as we did show and build a set of programs around those where we think simple peptides that are fast in, fast out are likely going to be missing part of the therapeutic window. Next to that, we have targets that are just very difficult to reach with peptides like the [ mesofilling ] approach we're doing. And if you want in the third wave, we're also looking into bispecifics. Now I'm not in the room with Dani, but he is our Head of Radio Strategy. And I do want to give him the opportunity to talk about this because he's spending a lot of time on that. We literally have 3, 4 targets already in development lined up to be next. And that's really because we have built the capability to -- after we have a candidate, be able to test it with a compassionate care setting, as we have shown you now in a very fast way. But Dani, maybe you add a few words how you see the next wave, I think you call them waves of targets in our pipeline.

Thanks, Patrick. You summarized it really well. And I think for me, in the context of 712 and DLL3, the learnings we made how to piggyback on this rapid utilization, rapid replenishment of low-density target antigens has been extremely valuable in that sense. And for me, it almost becomes a strategic imperative to consider this for the future pipeline. So that's why we've been starting and have already initiated activities looking at other ADC validated targets where we say the biology risk in that sense is low, but we can exactly try to duplicate what we've been seeing on DLL3. So that will be for us. I say this is wave #1, where I feel like we can execute very fast.

Our next question comes from Charles Zhu with LifeSci Capital.

This is Su on for Charles. How many grades of alpha particle radiation would you expect to have a therapeutically meaningful effect on tumors? And similarly, to what degree are you able to exceed the EBRT radiation dose limits on healthy tissues given the field's experience on renal dosimetry and updated radiopharmaceutical dosing guidance earlier this year?

No, that's a great question, and I will just quickly give the short answer, and then I possibly ask Michael or Dani to answer. And just to sort of -- I can now reference the advanced cell, very beautiful advanced cell data on PSMA. I think they started to see activity when they were dosing around, I think it was 100, 100 plus for even less [ mg ] . And that was in their second lowest dose or even lowest dose, lowest dose in stable disease on the prostate and second dose, it was already leading to very good responses. Now we don't know how much tumor uptake there is at their dose and how -- and what their therapeutic index is because that is just not known. We just know how much they gave. And if we look at our dose, I think their lowest dose was 60, and we're starting at 75. So from that part on, we think we're really on par. Now how much they reach the tumor versus us, we don't know. And the second part is we also are comparing prostate cancer with a lung cancer. We also don't know. But I'll be happy -- and then the healthy organs, I mean, that is part of the equation, we will see. I mean our hypothesis is strongly based on that the blood pool will be not toxic. We'll see a drop in blood cell count, but it will come back hopefully fast, that we can redose fast. That's what you see on the image, while the healthy organs look very, call it, healthy. I mean that's kind of the image we did show today. But maybe Michael or Dani, you're better on post to give the absolute numbers. I don't see if Dani wants to go first or Michael goes first.

No, absolutely. Thanks, Patrick, and I hope you can hear me. So it's very, very difficult to say and to be sure, but obviously, we designed the protocol together with all the experts believing that we reach this range as I say, also second, third dose. It's very important to have a safe dose delivered and hopefully, within the grades we are expecting to get, so the field has a huge range of numbers from, say, double digit, triple digit. So it's very, very difficult to say where we'll end up. But I'm very confident with the protocol we designed, we see what we need to see.

Dani?

Not much to add from my side. And I think one of the key questions will be for small cell lung cancer patients is like at which dose levels do they start to respond. And I think for healthy organs, we have a pretty good understanding in terms of EBRT limits. We can -- we know how much people are -- or other companies are going above these limits for their clinical trials. But tumor uptake and understanding at which level tumor uptake will be sufficient in terms of triggering the desired response. I think that's really something we will need to now explore in the Phase I trial, and we will be guided by the data.

Our next question comes from Mike Nedelcovych from TD Cowen.

I have 3, if you'll allow me. My first question is on the competitive landscape. Can you offer us key points of differentiation between your program and other DLL3 targeted radioligands in clinical development, such as the one from [ Addera ] or that from Novartis? And I know the clinical data for 0712 are limited at this point, mainly illustrative, but are there any early from the empirical data that suggests your program is indeed differentiated? That's my first question. And then my second question is on your isotope of choice, lead-212. It seems like the most compelling image in terms of tumor to normal organ ratios is probably from 116 hours post injection. I think that several lead-212 half-lives later. So I'm just curious whether lead-212 is the right isotope to capture the DLL3 replenishment phenomenon that you described. And I'll stop there if there's time I can ask my third question.

No, thanks. All great questions. Let me quickly start with the differentiation. And let's start with the Mariana peptides. Mariana gets very nice tumor-to-kidney ratios. And I would say the best published data is 15% injected dose. So my guess is that is the max they will get versus our 60. And if you just do the math, a peptide that is not half-life engineered will just be able to load the cell once. So we think for these low copy number peptides, the half-life is not ideal. The idea of fast in, fast out is not the best way to go. You might then dose several times that you could do or you have to half-life engineer the peptide. That is the peptide side. Then you have the [ Adhera ] data. And I think there, the differentiation is that [ Adhera ] as us, takes a longer half-life. We go with HSA binder, which we really hope and we see has a very clean blood distribution. The [ Adhera ] has an FT-type molecule, so it will bind to immune cells. And from the data that is published, you see a much more uptake in the liver. And keep in mind, we did show liver uptake. And this is because we have lesions in the liver. The livers of our non-lesion patients look very clean that I can say. So from that point of view, I think we have a differentiation over the Mariana with half-life. And we have a differentiation of an FT-type approach by our HSA technology, which for us positions us at the, let's say, winning strategy in this approach. I'm not saying you cannot half-life engineer peptides, you can. But as of now, those are the 3 molecules in the clinic. Then your other question is also super interesting. And I mean, we also looked at the images and said, yes, sure, this is -- why not test other isotopes. And in principle, there is nothing to hinder us from doing that. At the same time, don't underestimate the lead approach. As -- and Dani nicely pointed out that the uptake is also there. You just don't see it because the contrast is so strong. And in these images, you always go for a contrast. So if you would just take out the liver and cut off the blood pool, you do see uptake much earlier than what you think you see here. So -- and also Dani presented the fast uptake. We're talking 30 minutes. So within a few cycles, so within 10 hours, we see good uptake. It's just hidden behind the blood pool. At the same time, you're also right, nothing speaks against the long list isotope like actinium that you could also use. What you would not likely want to use is lutetium because our blood pool would be too high and with the long pathway and the broad killing, you would have too much side effect. So you see a clean alpha strategy. You see a very good potential for lead and the upside, if you want, for other isotopes.

[Operator Instructions] Our next question comes from [ Kiara Montorani ] with Bern [indiscernible] Kempen.

Congratulations with the update. So I was wondering if you could provide more color on what to expect from the first Phase I data next year, whether we are going to see some efficacy data points? And also, you have submitted the IND and will start Phase I year-end, pending regulatory clearance. I was wondering whether you foresee any risk there.

Can you repeat the risk question, we just acoustically couldn't hear the second part of your question. What type of risk do we foresee?

Yes. So you just submitted the IND and we start the Phase I year-end, pending the clearance from the regulatory FDA. So do you foresee any risk over here?

Yes. I think Michael speak to like what do we expect in, let's say, the first data set, but also how is, I guess, the question is and it reaches a bit after regulatory shutdown in the U.S. and our interaction with the authorities. I think, Michael, you are in almost a daily exchange. So I think you're best positioned to answer here.

Yes. Thanks, Kiara. And I indeed was in the U.S. last week at the conference. And obviously, logistics is a key challenge right now because not everyone is working. Many things have been piled up. So we are monitoring this very closely. Luckily, our supplies within the U.S., so we don't have to cross the border. Luckily, FDA is really doing a good job in turning around question. So nothing to look out from there. But should anything change, of course, this will have an effect. Also starting up sites, of course, everyone needs to be there, the usual routine. But we are very confident we have a very good collaboration and team size to say this should be possible by year-end. And again, we're very grateful to everyone involved who makes this such a smooth process. Philippe?

What I can add in terms of study dynamics, we are -- again, we learned a lot from our colleagues from [ Morano ] and there is a lot of interest on development in small cell lung cancer. So there is appetite. And what we have selected a team of investigators, it's a combination of, I would say, early starting sites, more on the private side, if I may say, and also academic side. So we have a good mix. And that's why we think that we should be able to have a good throughput. So that's that. And I think you were also asking on when -- what type of data when. So again, every patient gets imaged. So we hope you know that when we start in January, ideally, we would be able to start seeing images fairly quickly and then patients quickly -- in small cell lung cancer, patients get quickly dosed. So I think that should develop fairly quickly in the first part of the year to get some early data.

Our next question is a follow-up question from Mike Nedelcovych with TD Cowen.

This question is on the regulatory path and supply chain. I'm curious if the trial enrollment and data cooperate and you can indeed pursue accelerated approval in the U.S., is it at least conceivable that you could have a registrational package in the next, call it, 18 months? And if so, do you think that the Orano Med supply chain will be sufficient at that time for a reasonable launch?

So I can start, thanks, Michael. So I have high confidence in Orano Med's supply chain ability. So I don't think 18 months is a problem. I'm not sure everything will go through smoothly. But of course, once we have data, we go again to the agency, some review, some learning. None of my programs has gone as fast as the COVID times. So if we had COVID times, I would say, yes, absolutely. Generally, I think it's more in the time frame of a year.

Okay. Well, I'm not showing any further questions at this time. I'd like to turn it back to Patrick for any further remarks.

No. Thanks again for this very good call for all the questions. We are excited to now be moving towards Phase I in the U.S. Obviously, shutdown is hopefully over, and we can progress fast. All questions are going in the right direction and next up will definitely be the Phase I. Again, with the ambition to be the leading alpha therapy in small cell lung cancer and to branch out and build a pipeline building on this unique differentiation now with clinical imaging data showing the value of our platform. So a big day for us. Very pleased with the outcome and looking forward to generate value in lung cancer with 712 and building a pipeline beyond lung cancer. Thanks, and stay tuned, and we'll be in touch.

Ladies and gentlemen, this does conclude today's presentation. You may now disconnect, and have a wonderful day.