It's fatty acid synthase, which is an enzyme that is very important for the survival of cancer cells in the brain. Its upregulation of the novel fatty acid synthases enables cancer cells to grow in this brain microenvironment, which is actually lipid deprived. They basically regulate their own lipid production. So by disrupting fatty acid synthase, we can impair the growth and represent both and have this both as a potentially a therapeutic target, but also an imaging agent, obviously. Our own study is the first-in-class Phase IIb study, currently recruiting in the U.S., in patients who have suspected or equivocal data in the MRI after stereotactic radiosurgery. So why do cancer cells activate lipogenesis in the brain? If you look at the left side, there is a pre-activated lipogenic program that enables cancer cells, once they metastasize to the brain, to go there and essentially overcome the limitation of a lipid-derived microenvironment. As I already said, through the metabolic reprogramming of the cancer cells, those cells are able to synthesize their own fats, so their own fuel, if you will, to survive and grow in this actually nutrient-poor microenvironment of the brain. This metabolic adaptation can make brain metastasis more aggressive and also resistant to therapies. Sorry. So we have, of course, a lot of preclinical data. We'll not show this in a whole lot of detail, but I think it's enough to say that when compared to FPIA, RAD-101 to 18F-FDG in several cancer models, breast and prostate, we had a much better uptake and also a better superior tumor-to-brain ratio, tumor-to-background ratio compared with FDG PET. So very positive preclinical data in the mouse models. So when we talk about brain metastases, the majority of the metastasis really come from essentially three or four tumors. So lung cancer, which essentially is non-small cell lung, breast cancer, which can be triple negative, but also HER2- positive breast cancer, as well as hormone receptor positive breast cancer, and then melanoma. So between melanoma, breast cancer, and lung cancer, those are about 90% of all the primary tumors representing patients who develop brain metastases. And as you can see on the right, this is just one example. The survival, overall survival of these patients is particularly poor. So when we talk about imaging and brain metastasis management, we are focusing here and for our study essentially in what's in the Red box. So for screening of brain metastasis, the initial diagnosis, MRI is sufficient. But then when those metastases are being treated, let's say with stereotactic radiosurgery, Gamma Knife, it's very difficult to differentiate between, let's say, recurrence and potentially treatment-related effects following stereotactic radiosurgery. So a pseudoprogression radiation necrosis can appear similar on an MRI compared to active tumor. So we're focusing on patients who have undergone previous stereotactic radiosurgery, Gamma Knife, for example, and trying to understand how our PET imaging agent compares with MRI. So we are in the Phase IIb. The compound was developed initially at Imperial College London. They ran a Phase I dose escalation and a food effect study, a Phase IIa with 22 patients that I will very briefly mention. And we are now in the Phase IIb, the study that we're running here in the U.S., 30 patients. Based on these results, when we are able to analyze the final results and hopefully have a positive outcome, we will go into Phase III, which we anticipate is going to be around 150 patients, and it will, of course, be a global study, so summarizing the Phase II study from Imperial College London, the primary objective was to measure the uptake in patients with brain metastases to understand the impact of stereotactic radiosurgery, and for that, they included patients who were treatment naive as well as pre-treated. And when we look at the results, the uptake of our agent was very high, independent of the origin of primary tumors. There was high tracer uptake in all intracranial disease compared to contralateral white matter, regardless of the tumor of origin. A very interesting finding was that patients with a higher SUV than two showed particularly short overall survival, while contrast-enhanced MRI was actually uninformative for that. Very briefly, the results from the Phase IIa, I'm not going to focus on the left side. These are images that are representing patients at various stages. But on the right side, you can see the different colors are different tumors of origin. And then you can see that the SUV max, which is a measure of uptake, is pretty much the same, whether patient had lung melanoma, breast, or colorectal cancer, as was the tumor-to-background ratio on the lower graph. As already mentioned, a very interesting finding, albeit, of course, in a very small sample size of 22 patients, was that those patients who had a higher SUV than two had a very short survival. In this case, two patients, as an example, this is one patient with a PET SUV of 3.3. That patient had, unfortunately, a survival of only four months, whereas the patient with the lower uptake here of 1.08 had a much longer survival, as you can see, of 34 months. So they did plot the SUVs against PFS and OS, and you can clearly see that compared to the SUV max of two and higher, which is really low, PFS was much better in those with little uptake. So it's a very interesting observation. It does make sense from a biology perspective since a very aggressive tumor with a high uptake would also have consequences for patient progression and survival. So this is the Phase IIa. The existing data clearly demonstrate that the technology works. We do have clinical proof of concept. We have published positive Phase II data. The full dataset was published in January of this year. When looking at comparing pretreated versus not pretreated, there was a better differentiation with RAD-101. As already discussed, there was a correlation between high SUV, short survival. Our own Phase II study is well underway. We're presenting the preplanned interim analysis, and we will have the Phase IIb readout in the first half of 2026. And based on that, of course, we will then have the Phase III in planning to address this huge gap in medical care. And there is no competition right now, so potential approval would give us a unique leadership position in the field. So next, we have a few patients that I would like to discuss with Dr. Kulkarni. Those patients are from our own study, from the Phase IIb study shown here. We had IND approval in the second half of 2024, started recruiting patients this year. We are now at the early interim data, as promised, and we will have the Phase II data readout next year. So this is now one patient who is also from Dr. Kulkarni's side. This is a patient with renal cell cancer who had their first initial diagnosis of brain metastasis and stereotactic radiosurgery in 2015, and then, unfortunately, relapsed 10 years later. And what we're seeing here is the scan at the visit date of our study. On the left side is the MRI, and on the right side is the PET. Dr. Kulkarni, what's your take on these images? I mean. Yeah, certainly. But before that, if I can just give a brief overview about why this study is really so vital, there's definitely an unmet need because, in general, the size criteria for determination of response is always not very reliable because you might also have what we call as pseudoprogression or false progression because of swelling of the metastasis. But that actual viable tissue can be found out by imaging technologies like molecular imaging, and specifically for brain metastasis and after radiation. There's been a long-standing dilemma for many physicians, whether this is radiation necrosis or this is viable recurrent tumor tissue. So this particular case also demonstrates that there is, first of all, the first primary endpoint has to be that you establish that there is a concordance with your standard of care imaging. So in this particular case as well, on the left side, you can see this was a patient of renal cell carcinoma, which metastasizes very commonly to the brain. You can see that after stereotactic radiosurgery, you can see a large region of radiation necrosis, and there was some sort of a discrepancy in terms of the size criteria, and so the neurosurgeon had referred this patient to us to find out what is the significance, so this particular case clearly shows. You can see on the right side in the PET image, there is an overlap of the signal, which is marked by essentially uptake of 18F-pivalate, seen as more white in the same region as the MRI. Dimitris? Yeah, thank you. So this is the same patient. On the left side, again, is the original scan from when the patient was enrolled into the study in October. And then in November, one month later, you see basically a somewhat similar picture, maybe more intratumoral necrosis, but still a white rim, which could indicate radiation necrosis there. And again, remember, so this was a very high uptake here in terms of the PET. And again, that same patient now over a period of time. So this is on the left where it says pre-SRS. This was basically in January of 2025. Then the patient had, as I mentioned earlier, their SRS in August. So the post-SRS is after the stereotactic radiosurgery. Then the study day, we already saw that. And then the longitudinal together with the PET. So you can see that it does change over time, but it's important to realize that, again, by definition, these were all equivocal patients. So it was not 100% clear if and how much active tumor there is, but the PET clearly indicates that there is active tumor. Next patient is also from your side, Dr. Kulkarni. This is a patient with breast cancer, 56-year-old patients with breast cancer. They had their diagnosis of brain metastases in 2022 for the first time, received an SRS then in 2022, again for 24 gray, and then were followed up over a period of time. And on the left is, again, the MRI at the study date compared to the PET on the right side. And radiation necrosis in an MRI does show up pretty much exactly like you would see it here. And then the question, as we already discussed, it's right, I mean, is this necrosis? Is this tumor? The PET seems to indicate really that there's active tumor. Dr. Kulkarni, any comments here? Yeah, yeah, I would just like to add that in MRI as well, you can see that there's a rim of enhancement. But the advantage of PET is also the quantitation. So Dimitris mentioned previously about the prognostic role of maximum standardized uptake value, which is essentially how we quantify the PET. And that is, I think, a single most important kind of characteristic of molecular imaging so that you can actually monitor that particular metastasis over time and are not really relying only on the size criteria, but also on the changes in the SUV max over time or changes in the mean standardized uptake value. So that takes into account the heterogeneity of the tumor as well as how the viable tumor really progresses or diminishes over time. And that can really help guide decisions at very early stage. So if you rely only on the MRI, then you have to do several MRIs before you can reach a particular decision. So that is really a standard of truth here. I just want to add to that. So like you saw in the previous case, we did several MRIs or two MRIs. So that forms as a standard of truth. So potentially, with PET, you can really identify the recurrence. When it is doubtful, you can actually make sure about the viable tumor tissue at an earlier stage. Yeah, it's a good point. I mean, RANO criteria, which are used for brain metastases, RANO-BM, they're really only looking at the size, right? So the functional uptake, the metabolic activity is never part of that yet. Yeah. So next patient is somewhat similar. This is a patient with, again, non-small cell lung cancer, also from your side. This patient was diagnosed with brain metastasis in August of 2024, then received 30 gray to that lesion in October and went into the study in September, obviously, right? Exactly. So right after the SRS, and we also have a longitudinal scan for this patient from October. So this one here is the initial MRI. Again, you see a similar pattern. It's a questionable lesion, I think, from a perspective of the size, but also what's going on with this white rim. The PET really helps us to establish the potential diagnosis or the possible likely diagnosis, actually, of viable tumor cells. Any comments here? Indeed. I would just like to add, and this is, I think you made all the points. Just one other important aspect is when you're planning a treatment for such lesions or such recurrent lesions or residual viable tumor tissue within the brain metastasis, then actually the PET can actually guide your treatment because if you're planning a second treatment, because then you're not really doing it guided based on the MRI, which obviously was doubtful to begin with what is the exact extent of the tumor tissue. So when you're directing a treatment towards such metastasis, the PET component of it, as we've been talking about, it's an unmet clinical need. So it can really help the neurosurgeon and/or the radiation oncologist to direct the treatment to that viable tumor. Very good. The next example of a patient, I think, is very, very interesting and informative. I have to apologize for the small size, but this is a very good example of what the technology can actually do for patients with brain metastasis. So this is a patient with brain metastasis diagnosed in 2021, stereotactic radiosurgery at that point, and then was in constant follow-up after that. And what you see actually here, it's very, very faint. It's a tiny questionable area of the brain, which may or may not be something, right? Radiation necrosis or active tumor. The PET from that same day is very bright, is very clearly showing that there's an indication for tumor. Now, when we then look at that same patient after two months and after four months, you can see that now the MRI lesion does increase. So we go from the first post-study to the second, and clearly you can see here a progression. So we have a patient who, after four months, finally showed an MRI-readable progression, but if we had gone back four months earlier, that was already shown in the PET. So this could have been a patient who could have been treated much earlier with maybe better outcome. Any comments here? I find this really a very, very. Absolutely. Yeah, absolutely agree with you. I think this is really the essence of molecular imaging in which you can easily miss just because of the pattern of the uptake what we see also after radiation, which very easily can be missed as radiation necrosis or in this particular where you're kind of, it's there within the sulci, so to say. And really, just because of the higher tumor-to-background ratio and the nature of the functional imaging, as Dimitris you mentioned, there is a good characterization of that particular lesion as a viable tumor tissue. And in hindsight, that was proven by the couple of MRIs, which clearly showed the increase in size of that particular lesion. So again, at PET-D1, if we had done the intervention, that could have possibly spared the patient the progression, and we could have targeted that particular metastasis early on. That's really a great example for the value of such a method, right? Yep. All right. So two more. So this is a patient who had, this is a non-small cell lung cancer patient, again, who had their brain metastasis diagnosed in 2023, stereotactic radiosurgery. This is a lesion in the cerebellum. And I'm showing this because sometimes the cerebellum is a little difficult to identify to what extent this is active tumor or not. You can see clearly here that there is uptake. And that patient is somebody that, of course, we continue also to follow- up after the study. So we'll have what we call the longitudinal scans to see whether that lesion increases over time. Yeah. And one more point, Dimitris, as you mentioned, cerebellum can be slightly difficult to judge just because you see a lot of gliosis or just because of the nature as against the cerebrum where the MRI findings could be much more conclusive. So there again, just because of the fatty acid metabolism or the fatty acid synthase targeting, you can really confirm or you can be sure about this particular lesion. And I can only just emphasize the role of PET MRI, which could have the best of both worlds kind of combined. That would be really ideal for follow-up of brain metastasis. Exactly. Yeah. Yeah. The combination, I mean, should be really very strong. So this is the last patient who is interesting for a different reason. So this is a patient who has, quite frankly, questionable lesions in the cerebellum. You can see one up here and two smaller ones up here. So they are a little atypical for metastatic disease, but the patient did have metastatic disease, was diagnosed from adenocarcinoma, non-small cell lung cancer, adenocarcinoma of the lung, was diagnosed in 2024, had their stereotactic radiosurgery in January of 2025, and then moved into follow-up and entered the study here with the visit in September. And this is the MRI. And this is really a patient where we did not see a PET uptake, which can easily be because the patient simply does not have active tumor, right? We need and we will have such patients who have nothing more than necrosis, no active disease, and those patients would definitely not show uptake in the PET. This is probably also a concordance, but more in the direction of having no uptake because it's likely that the tumor is actually not even more active. Yeah. So. This is also very. Yeah. Sorry. No, go ahead. No, I was just going to say this is also another important finding, the true negative value. Of course, as far as I know, Dimitris, we are still awaiting the longitudinal follow-up of this particular patient. So early days yet, but it just emphasizes our earlier point about the cerebellum where it could be really anything difficult to image. But PET, just because of the nature of its metabolic/molecular imaging, can really point out the metabolism at the cancer cellular level. So from the first findings, it seems to be a negative scan, whereby the MRI some doubts about it. Yeah. And you're a big believer in molecular imaging, right? Absolutely. Of such approaches. It's really, think about it, the MRI, at the end of the day, it's just an anatomical picture, whereas everything that has to do with tumor growth, metabolism cannot be judged from an MRI. So this is where the PET would come in, right? So this is where we are in terms of our interim analysis. I did not show you all the patients. These are six here, which are very representative. The study is recruiting very well. People are very engaged with this. We have a positive interim analysis at this point with a high degree of positive correlation. And of course, the longitudinal scans are underway to establish what we call the truth standard. And once we have the longitudinal scans from all the patients, we'll be able to provide the final results. So that's what I had as a presentation. Thank you for your attention. Dr. Kulkarni, thanks for the input and the nice conversation here. Thanks for inviting me. Yeah. Looking forward to the questions. Thank you for that. It's time to move on to the Q&A. So once again, these will be based on those sent through via email and live during the session. So as a reminder, if you want to type one in, please do so using the Q&A panel within Zoom. So the first question I have is, could you elaborate on the importance of finding metabolic activity in the equivocal MRI findings? Is this confirmation that the inconclusive MRI result was a false negative? Well, yes. I mean, it's still a little early, right? But that's the whole point, exactly. So we are trying to understand by doing molecular imaging to what extent we can differentiate what is really difficult to differentiate in this case, pseudoprogression or radiation necrosis versus true progression. Exactly. In this case, an MRI with an equivocal finding, which is not then confirmed as a tumor in the longitudinal, would indeed be a false positive. Thank you. The next question is, how many patients would you need for a pivotal? We anticipate around 150. But obviously, this is something where these are subject of discussions that we will have with regulatory agencies, particularly the FDA, who has been very instrumental also for us in the Phase II program. So around 150. Thank you. And when thinking about. So for oncology, I do have to say that for oncology study, this is really not a very big trial at all. Yeah. Great. Thanks. When thinking about registrational trial design, are you planning to seek a similar design for Phase IIb? Oh, sorry. Excuse me. Similar design to the IIB. So we would swap the endpoints. Typical for the endpoints are sensitivity and specificity, which in our case are the first secondary endpoints. We used concordance here, again, based on the input from the FDA, but we would probably swap when it comes to a Phase III and make concordance secondary and sensitivity specificity primary endpoints. Thank you. How would you anticipate RAD-101 could be used in clinical practice? Would it replace MRI or be used in combination? I think initially, at least from our discussion here, ideally, I think it would be a combination. So it's a bit early to say that it would replace it. I mean, if, let's say, the Phase III is positive and we realize that the MRI has so little value, that's a discussion that we will need to have going forward. But right now, we're doing both. The next question is, with the independent economic analysis that found a $500 million market in the U.S., what assumptions were made surrounding pricing? Yeah, I can take this. So the assumption was in line with the imaging agent in prostate cancer that are currently reimbursed and approved by FDA. So we think this is absolutely realistic. The gross price is around $4,800-$5,000 per dose. So we think this is absolutely realistic. Thank you. The next question is, how does your brain imaging agent compare to TLX101-CDx? Yeah, I'm happy to start this and then let the expert answer, but it's completely different. So an amino acid is using a different mechanism of action compared to fatty acid that we are using. So the drugs are really different. They have nothing in common. The second very important element that the FET or amino acid or the products that Telix and other company are having development so far has shown some preliminary activity in primary brain tumor or glioma. What we are doing here with RAD-101 is using for brain metastasis, so secondary tumor. From a prevalence point of view, the patient with glioma are 12,000-15,000 patients per year. That's the addressable market for the Telix products. Our products have an addressable market that is 25 times larger because our addressable market is 300,000 patients that every year in the U.S. are diagnosed with brain metastasis. This is U.S. only. So different mechanism of action, different products, very different prevalence between the two. And I think Dimitris mentioned before, but we are not aware of any other products that are in clinical development as imaging for brain metastasis. So as of today, we don't have competition. And if something new will happen, we probably will keep five- to six-year advantage versus any newcomer. So we think we are in a very good position. I don't know if Dimitris or Harshad like to add anything. Yeah. Well, I would just add, I completely concur with you, Riccardo. There's a lot of data also outside of clinical trials from places like Europe where we have investigated FET, fluoroethyl tyrosine. But the amino acid metabolism has been well studied in glioblastoma and differentiated from the lower grades of gliomas as well as for therapy effect, radiation necrosis versus viable tumor tissue. But for brain metastasis as a niche, this is also not a label or not a potential label for this. And I would also add to that that the lipid metabolism or fatty acid synthase, it's well studied in these secondary brain tumors. And so that is a clear differentiator. Moving forward, if there is an interest at all to also develop this as a primary agent for detection of primary brain cancers like glioblastomas, then we will talk about it. But right now, it's a completely niche indication, as Riccardo said. Completely agree. Yeah. And I'll thank you, Harshad. And it's a fair comment. We do have for RAD-101 additional data for the primary tumors, so for glioma, that sounds promising. So nothing is preventing us in the life cycle management approach to look for a second indication like the primary brain tumor. But for the time being, our focus is on the brain metastasis because it's the largest unmet medical need in terms of patient prevalence. And that's our focus. Thank you. The next question is, can you discuss the market potential for RAD-101 in more detail? Yeah. So we believe, as Dimitris was saying, we believe that in the Phase III, the likely primary endpoint would be sensitivity and specificity. What does it mean? It means that when the patient with brain metastasis receives SRS, they found themselves in the situation that has been described now by the two speakers. So we can expect to conduct a trial where this is the main objective, to differentiate tumor and necrosis with a product that can be combined with MRI. The huge benefit, of course, for the patient has been seen in some of these examples. Some patients can be diagnosed earlier as tumor recurrence post-SRS instead of waiting two or four months. The objective is a better and an improved patient management so the patient can receive a better or the best treatment sooner with more positive outcomes. Based on that one, considering that there are about 300,000 new patients in the U.S. only that every year are diagnosed with brain metastasis, we like to focus on those that receive SRS and then need to continue to be imaged to be sure that they are properly controlled. This is the large patient population that we think we are going after. In our commercial assessment, we have been conservative in the number of RAD-101 doses that are going to be used. We assume only one or 1.1. We do believe that there is the possibility to design a trial where more than one dose is needed because you might want to check with the patient the baseline with RAD-101, but also after six months, how this PET image looks like to have further confirmation. I think we have been quite conservative on that. As I mentioned before, patients post-SRS starting from 300,000 new patients every year in the U.S., around $5,000 price per dose. That is the standard for the current imaging and 1 to 1.1 dose per patient. This is what was driving the assessment that brought more than $500 million every year at peak sales, making RAD-101 potentially the third largest imaging agent available in the market. Thank you. The next question is, could accelerated approval where we can market the drug while conducting a confirmation study in parallel a possible pathway? If so, would a Phase III need to be undertaken before accelerated approval is granted? FDA will drive our decision, our current assessment that after our Phase IIb, a Phase III is needed to get approval. Thank you. Next question is, what is the median time between PET imaging and the last radiation therapy to the brain? Will you set a limit on this time interval when you enroll patients for the Phase III trial? No, we don't plan to set a time limit. We have patients who had, in this study, their stereotactic radiosurgery a few months earlier, and then we had patients who had it a year or two earlier. The point is really to what extent the patients are showing, even if it's equivocal, but potentially signs of progression or radiation necrosis itself. It's not per se a matter of how much time. The follow-on from that, Dimitris, was, is there enough learning about AUC/SUV max for specificity and sensitivity analysis cutoff to be used for the Phase III trial? So at the end of the day, the SUV numbers, the absolute numbers are not the most important thing. We did look, of course, at this correlation, albeit, again, with 22 patients, we have to be very, very careful. But they did, for what it's worth, see that correlation. So we will evaluate. We will measure. As long as you can see the SUV, that's all that you need. At the end of the day, it's less about the absolute value. Dr. Kulkarni, any comments on the SUV? We discussed this with you and Dimitris. Yeah, absolutely, so the Phase IIa study, which was from Imperial College London, already showed that the prognostic value of a particular cutoff. So I'm definitely a firm believer of what is the level of uptake, how does it change over time? Because, again, more aggressive the tumors, more is the metabolic activity within those tumors. But again, just to add on to that, I think once we have all the data and then, of course, we can do additional analysis as the questioner mentioned on, for example, molecular tumor volume or having some sort of a cutoff of the SUV, which can really predict the follow-up of these particular patients. That would be certainly valuable. But I think incorporating these quantitative molecular imaging parameters is definitely reasonable also for the Phase III study. But they don't. I mean, a high SUV does not really per se increase the sensitivity or the specificity, right? Correct. But I mean, when we look at the scans, the SUV is in the low single-digit numbers. But still, there is a good kind of target to background ratio so one can really differentiate. And so these values can, I mean, at the end of the day, just to kind of address that, we need more data and then more follow-up, and then we can see more convincing statements. Yeah. So the answer, to summarize, we obviously are gathering the data, and we will evaluate and see to what extent this is something where we will do more evaluation than in Phase III. Thank you. The next question is, what is the potential here for a therapeutic isotope combined with RAD-101? Yeah, I think I remember this question from some previous conversation. Look, it's interesting. And we are looking into it. So the same partner that we worked together to develop RAD-101 are also working to see if there is a possibility to develop the therapeutic version of RAD-101. This is a very small molecule that needs to cross the blood-brain barrier. So you cannot attach a large isotope and a large chelator. So you need some interesting approach from an isotope and chemistry point of view that is too soon to disclose. But we are working on a therapeutic version. Yes. Thank you. What are the risks of using SRS when it's not needed? I mean, obviously, any interventional treatment has certain risks, so if you have a patient that doesn't really have active disease, obviously, there's some potential here, so Dr. Kulkarni, I don't know how many times you have where SRS is being conducted in patients that are thought to be more or less negative and what the side effects are of that. Yeah. I mean, I would definitely agree that there is risk associated with treatment, especially when there is no viable tissue. And that's why that really underscores the importance of imaging and early accurate imaging to find out if there is viable tissue. I mean, obviously, if you're doing SRS to, let's say, already a region which has radiation necrosis, then A, really, it's a loss of time for the patient, but potentially also other side effects like pressure effects on the brain. So that really underscores that we need to find out the viable tumor tissue where the SRS is actually indicated. Yeah. I mean, Gamma Knife or other stereotactic radiosurgeries, they can induce headache, nausea, vomiting, brain swelling. So you end up potentially with swelling in the brain. If that's severe, you could have seizures or other neurological deficits like numbness, weakness, and also damage to healthy brain tissue that is close to the tumor. And then also things like hemorrhage and bleeding. So it's not. I mean, it's a treatment that does have potential for serious side effects. So you want to be very sure that when you do this, you have a patient that has active tumor. Thank you. In some of the PET scans, it came up with white areas that weren't there on the MRI. I think it was on the third or fourth patient example. Does this mean you need both the PET scan and the MRI? Initially, yes. I mean, we discussed this already from a similar question earlier. So I think it's a bit early to say that it will entirely replace. But I think together with the MRI, it could be a very, very powerful tool to understand what we see as an anatomical lesion, how that corresponds to metabolic activity and functional tracer uptake, and whether that's actually active tumor that should be treated versus simply tumor necrosis or radiation necrosis from the previous treatment that you just leave alone, right? So initially, we would be using both. But of course, we have to see how then this would develop over time. The next question is, are there biological differences between brain metastasis and primary brain tumors that would make uptake of amino acid versus fatty acid preferable? Yeah. I mean, there's. That's actually a. Go ahead. No, no, no. No, go ahead, Dimitris. Please. I mean, they're completely different tumors, right? So I don't know that you can say that for glioma, amino acid target is a better target than fatty acid synthase, right? So let's not forget that the two trials that were using amino acids as a target, Axumin and the Telix compound, they failed, right? Or at least they didn't get it approved. So Telix got a complete response letter. So I don't know how their discussions with the FDA are developing. But I mean, they're different tumors, yeah. Yeah. And then I would just add to that. I mean, we need obviously comparative studies for that. But just that's a really great question, by the way. I mean, you always see invariably in the primary brain tumors and upregulation of the amino acid transport. But in the secondary brain tumors or the brain metastasis, there are certain properties of that particular primary tumor, whether it is in the RCC or the lung, like more angiogenesis, more necrosis, and switch of glycolysis and lipid metabolism. So I think there is certainly things to be investigated further. But having said that, it is quite natural that the first step for anything which is really determining the lipid metabolism, that you start with the secondary brain tumors just because of the characteristics that it would retain from the particular primary tumor within the breast, renal cell carcinoma, etc. Thank you. Thank you. One final one is, Dimitris, in a pivotal study, do you expect the FDA will require the study to include biopsy or longitudinal studies in order to confirm standard of truth? Or would they allow you to determine sensitivity and specificity based on SUV in comparison to MRI only? We expect that they will want to see longitudinal scans for around six months or a biopsy. So one of the two would help us to establish the truth standard. Sorry. It's either. Sorry, I just want to let one come in. Does your agent attach to non-cancerous regions of the brain as well? No. Again, the metabolism or the target is because the brain cancer cells, the brain metastasis cells, the cancer cells in the brain, they upregulate their own lipid production, right? So cancer cells need fatty acids. They need lipids. There's not much of that in the brain. So they produce their own lipid metabolism. Right. Which means that, of course, the non-cancerous doesn't have that. The healthy brain tissue doesn't have that. Great. Thank you, Dimitris and Harshad. There's been a lot of questions, a lot of very good questions from the audience. We've obviously concentrated on RAD-101. But Riccardo, I'll hand it back to you just to wrap up and provide a comment on the pipeline overall. Yeah. No, thank you. Thank you very much, Dimitris. Thank you, Harshad. It's been amazing having you. And Harshad, thanks a lot again for enrolling patients and being such an advisor to us. Really appreciate it. Look, these interim analyses are a major milestone for us. They came on time as the recruitment is going well. And the results are at least as good as we expected. It's not better than expected. 11 out of 12 patients achieving the primary endpoint. It's difficult to wish for better than that. So we are very, very excited. On the rest of the pipeline, we do have trials ongoing that are progressing on track as well. Our two therapeutics, RAD-202 and RAD-204, are now enrolling cohorts of patients with higher doses. And this is also progressing on time. And we are excited to start two new trials, the B7-H3 targeting agent, that also is in the center where Harshad is. So maybe we will have you as well for a webinar about our B7-H3 targeting molecule and also our KLK3 program. Both are tracking on time. It's difficult to say if we will have the first patient in the next week or two because Christmas is coming. But if it's not this week or the next, we are confident that this trial will dose the first patient in the month of January. So everything is going well. And thank you very much for all of you attending this very interesting webinar. And we have the commitment to keep the market informed every time we have any relevant and important information about our trial. And we will keep doing so. So thank you very much, Matt. Thank you very much, everybody, for being here with us and have a good night in the U.S. and a good day in Australia. Thanks, Riccardo. Thanks. Have a great day. Thank you, Harshad. Thanks, Riccardo. All right. Thank you. Bye-bye. Bye.