Welcome, everybody, to our last webinar of 2024. Today, Dario Neri, our Chief Executive Officer and Chief Scientific Officer, and myself, Emanuele Puca, as Investor Relations, will give an update on scientific developments of the company. The financial developments will be updated after the issue of the financial report of the full year, which will happen around March, April next year. Today, we will give a presentation, as always, which is being recorded and that will last around 30 minutes, and that will be followed by a Q&A session, which is not recorded, and please raise your hands to ask questions, and we'll be able to unmute you, and then, or alternatively, if you don't want to speak, you can just type your question in the chat, and without further ado, I hand over the stage to Dario Neri, who will start off with the presentation. Thanks a lot, Emanuele. And again, we are a Swiss-Italian biotech company. Many of you have followed this kind of webinars in the past. Whenever you see green, we will relate to antibody-based therapeutics developed by Philogen in late-stage clinical trials, but you will see also a blue pipeline which is growing, and this relates to chemistry products of our fully-owned daughter company called Philochem. Everything we do follows a very simple but powerful strategy. We use payloads of proven therapeutic activity, not only cytokines, but also drugs and radionuclides. You will see clinical data for all three examples. And we deliver these payloads to the site of disease thanks to ligands that serve as pharmacodelivery vehicles. In other words, these ligands are very good molecules that concentrate the active payload at the site of disease, helping spare normal tissues. These ligands are discovered in-house from our large encoded combinatorial libraries, so antibody phage display libraries or DNA-encoded chemical libraries that contain billions and billions of library members. At least in cancer, the benefit of targeting tumors with pharmacodelivery vehicles is extremely clear. Here you look at four patients with cancer imaged because they received four representative drugs labeled radioactively, and basically, you see the benefit of targeted delivery. Starting from conventional chemotherapy, in this case, docetaxel labeled with carbon-11 in a patient with mesothelioma, basically, you see how this poison goes everywhere except to the tumor, to the liver, to the spleen, to the intestine, to the urine, but at no moment in time there is a preferential accumulation in the tumor, which is around the lungs. With conventional IgGs, the products reach the tumors, but very slowly. You see colorectal cancer at the metastatic stage with an anti-FAP antibody. We get much better with Philogen's antibody fragments. This is one of our patients, 24 hours, tumor-to-organ ratio of about 10 to 1, liver mets of breast cancer, but the world record of tumor targeting is obtained using small ligands that bind with ultra-high affinity to accessible targets. In this case, you see OncoFAP, and you see a patient with metastatic breast cancer. Every single black dot in this patient is the localization of the product at the site of disease. You see the primary tumor in one breast, the many bone mets, the liver mets. The rest of the body is clean already at 60 minutes. Now, as mentioned, we have a green and a blue pipeline. The green products are antibody cytokine fusions, and together with Emanuele, we will guide you through the latest developments for Nidlegy Fibromun, but we will show you new clinical data also for the blue part of the pipeline, which is growing in number of patients and also, I think, with very significant clinical results. So I will start with Nidlegy, a dermatoncology program partnered with Sun Pharma, Europe, Australia, New Zealand, and I'll tell you about melanoma and also non-melanoma skin cancer programs. We started traditionally working on melanoma, but we then realized that the product is active also against other main types of skin cancers like basal cell carcinoma and squamous cell carcinoma. And in terms of numbers, actually, there are even many more patients in BCC and SCC. These are the new cases per year in the United States. Nidlegy is a combination of two active ingredients, L19 IL2 and L19 TNF. So the L19 moiety in green is the antibody that anchors the cytokine payloads at the site of disease. It's the only product that we give intralesionally because we treat superficial tumors, skin tumors, and we have a combination pack authorization from EMA. Now, earlier this year, we announced the successful completion of our phase III clinical trial in Europe. You see, we treated 256 patients in four European countries in 22 centers. There was a one-to-one randomization in patients who received only surgery within four weeks or Nidlegy once a week in the neoadjuvant setting followed by surgery. Recurrence-free survival was the primary endpoint for the study. The data have been presented at ASCO. They were clearly statistically significant. What has happened is that in Europe, we have filed for a Marketing Authorization Application on June 3rd. In the United States, a similar trial is ongoing. We have treated 108 out of 186 patients, and we have a pre-BLA meeting with the FDA that will be organized shortly to present the European phase III data to the FDA. The ongoing trial has the main purpose to support a full approval in the United States pending the successful outcome for the primary endpoint. I've already mentioned the distribution agreement that we have reached with Sun Pharma. Now, we have made a lot of progress also in non-melanoma skin cancer. For example, in basal cell carcinoma, we have two phase II clinical trials. The most advanced one, DUNCAN, has studied 72 out of the 72 target patients with very impressive benefit for the patients, which is shown in the images. Approximately 50% complete response rate with really very good functional outcome for these patients. And the centers are very happy, and the patients also are very happy. We have examples of patients who had multiple lesions at different moments in time, and they received our drug, or they received, for example, surgery, and you can actually see that it's a very striking difference between the benefit achieved with our drug and other mutilating procedures. And similarly, in squamous cell carcinoma, we have completed the phase II DUNCAN trial. Here, we aimed at studying 22 patients, which we have done, and again, with a good complete response rate. So the summary is that DUNCAN has completed the enrollment both in BCC and SCC. There is a second phase II clinical trial, which is well ongoing in Europe. It started later, but it's recruiting well, and we have already received the first feedback from the FDA, for example, about new studies which are planned with the aim to get pivotal status actually for registration also in these indications, and the study is scheduled to start around mid-2025. Now, I hand over to Emanuele because Emanuele will tell us about substantial progress with FIBROMUN, our second most advanced product partnered with Sun Pharma for a global distribution strategy, and he will tell us about various combinations in soft tissue sarcoma and glioblastoma. Thank you, Dario. For those who are for the first time attending this event, just a recap on what these diseases are. Glioblastoma is the most malignant primary brain tumor. Unfortunately, at present, it is incurable. You see here on the right the incidence, the yearly incidence in the U.S. for 15,000 new cases every year. In Europe, it's even more than this. And unfortunately, virtually all of them succumb to the disease. The most advanced trials that we have ongoing now are in the recurrent setting where the median overall survival is around eight months. In soft tissue sarcomas, so those are tumors arising from muscles, nerves, fats, and other soft tissues. Here, the incidence in the U.S. is about 13,600 new cases every year. In Europe, it is also a bit more. And about 50% of them become metastatic. For those metastatic patients, unfortunately, there is nothing that cures them, and all of them die. You see that basically there are approximately 5,200 deaths every year of the disease. Here, the most advanced trial is in the first line, and the median overall survival for these patients is around 12 months. FIBROMUN is one of the two active ingredients of Nidlegy. There is the L19 antibody fused to the TNF, and the L19 antibody anchors TNF selectively at the site of disease, and TNF is the anti-cancer payload. As said by Dario, we have announced on October 1st a new licensing agreement with Sun Pharma that will take care of the commercialization of the product globally in all oncology indications. Sun Pharma is a healthy and multinational company headquartered in Mumbai. It's growing significantly. Just if you look at the market cap last year, they were at about $27 billion. This year, they are about more than $50 billion. They have a global footprint, revenues of about $6 billion. They have a clear commitment for specialty therapeutics. They want to grow. And you see that the economic terms were quite attractive for us because we will split revenues in a ratio between 45, Philogen, 55, Sun Pharma post-commercial launch. Other terms were not disclosed. With regards to the pivotal developments in glioblastoma, you may remember that the GLIOSUN study is currently running in newly diagnosed patients. We have completed phase I. We're actually cleaning up the data, and we'll be able to present you some efficacy data and safety data also at the next webinars. We're now transitioning to the phase II part of the study. For the GLIOSTAR, we are running the trial, and it's going very fast. Last year, we completed phase 1. We're now already at 123 patients. As of today, in October, we were 104, so it's basically 10 patients per month. We're now almost 35 patients away from the final readout, the final involvement of the full patients foreseen by the protocol. And at that stage, then we just need to wait for the events too much here for the readout of the study. So we expect to complete the enrollment in the first quarter, let's say, of next year. So it's very soon. In the GLIOSTELLA, which is a new study we launched in the U.S., phase 2 disease in patients with first or later progression. Also, now, imagine with only three centers, we already have 23 patients out of the 90 patients we need to enroll. Last October 1st, we were at 12. Now, with opening of new sites, we expect to speed up the enrollment rate. So the objective here is to use the GLIOSTAR study to ask for full approval in Europe and, of course, pending the successful completion of the study, and to use both GLIOSTAR study and GLIOSTELLA study that was requested by FDA to go and submit a biologic license application in the United States. So that is the plan in glioblastoma. In soft tissue sarcoma, we have made substantial progress. For example, in the phase III study we're conducting in Europe in first-line patients, we've completed enrollment. And as you see here, we are at 73 events out of the 92 events that we need for the readout of the study. An event here is progression since the primary endpoint is progression-free survival. We expect, based on the final projection, to reach that goal around early April next year. Of course, we don't have a control on when disease is progressing on a given patient. Also, in the third line, we actually completed enrollment of the patients foreseen by the protocol. Here, we are at 52 events out of the 75 that we need to enroll the study. Since patients with a more advanced setting, so third line, progress faster, we actually foresee a similar readout timeline for the third-line trial as compared to the one in the first line. We'll give you an update also on the next webinar, but I think both studies have completed enrollment, and we just are waiting for the events to mature, so progression before opening the books and knowing if we met the primary endpoint. With this, I hand over again the stage to Dario. The situation is really very nice also for the small molecule therapeutics, which is a new area in which I think we have products with a huge potential, but you will judge for yourself. As mentioned before, here you see two patients with FAP-positive malignancies, but in one case targeted with conventional antibodies, in the other case targeted with our high-affinity small molecules called OncoFAP. It's really a day and night comparison. The small molecule goes to the tumor much more rapidly. It accumulates more selectively, and it has better diffusion into the tumor mass. The strategy is to capitalize on our excellence in DNA-encoded chemical libraries to discover ultra-high-affinity small molecules that we can attach to different types of payloads. For the sake of simplicity, today I will focus on clinical data with radionuclides and with drug conjugates. We have at present five targets for which we have nuclear medicine validation. FAP is the first that I will discuss. I will also comment on striking clinical results with ACP3, but for example, a clinical trial on CAIX has recently been approved, and we are making progress in many other targets. Let's start with fibroblast activation protein. Let's start with radionuclide payloads. The platform is useful for imaging and for therapy. For imaging, we have completed a phase I clinical trial. We have treated more than 200 patients, and the asset for imaging has been partnered with the Bracco Group. So the right and duty of development sits with Blue Earth Diagnostics, which is a company of the Bracco Group. Of course, if a patient has metastatic disease and you can show that the product localizes selectively at the site of disease, typically patients want therapy, and you enable therapy by substituting the radionuclide going from gallium-68 to lutetium-177, our phase I clinical trial has been approved. We have already treated more than three patients. We know that the product, at least in these patients, was tolerated up to 200 mCi. And we are eager to collect more clinical information on the therapeutic outcome. Now, you can also think of delivering a drug rather than a radionuclide. And for this, we launched a phase I clinical trial in animal patients, meaning dogs with spontaneous tumors. These are dogs of owners that have failed all therapeutic activities, and the owners want that we try our product. And you will see that the results are quite promising. FAP, our target, is unique not only because it's a protein which is expressed at the site of disease, so it's a target for localization, but it's also an enzyme. So we have designed a release strategy for our drug that capitalizes on the fact that FAP cleaves after GlyPro sequence, after glycine proline. So if you look at our product, OncoFAP is the molecule that goes to the tumor. The glycine proline linker is the one which is cleaved by FAP at the site of disease. And the payload that we release is monomethyl auristatin E, but we have very nice data also with other payloads. But again, today, I will focus on MMAE, which is a standard drug in the oncology setting. The phase I clinical trial in animal patients had a dose escalation, and we have reached the 10 mg/ sq m dose. We could confirm safety of the approach also with accurate measurements of hematology, and we treat these dogs like human patients, meaning that we look also by CT scan whether we are able to induce tumor regression, and I will show you that we have already the first regressions documented in the clinic, and in particular, I want to show you one story, the story of the first dog that we treated called Coco this is, a collaboration with Professor Stefanello at the University of Milan. You see that this dog who had failed different therapeutic alternatives presented with a tumor. Here you see the caliper measurement. You see by CT scan it's a sarcoma of three centimeters, basically in this direction, and after four injections, you could see how small the tumor had become, and this is also confirmed by CT scan. The protocol did not allow the center to continue treating, so they only gave four injections at three milligrams per square meter. And then they only could wait. And basically, the second treatment was several months later, but the tumor had grown back. And you see that now the tumor was 15 centimeters in diameter. And again, four injections could shrink the tumor substantially, as you can see both with the caliper and also by the CT scan. So if you compare this huge ball that was the tumor at the start of treatment and this was the tumor after four weeks, the difference is very impressive. We have now decided not only to continue offering this treatment modality to animal patients, but also to advance the program to clinical trials in humans with cancer. The last example I want to show is ACP3, a revolution in the field of prostate cancer. Prostate cancer with radiopharmaceuticals is at present dominated by a target which is called PSMA, prostate-specific membrane antigen. PYLARIFY is one of the approved products for imaging. Lantheus sells more than $1 billion per year in 2024. And for therapy, the lutetium-labeled product sold by Novartis, the name is PLUVICTO. And again, the company will sell more than $1.5 billion. So if you sum up the imaging and the therapy data, and there are other products on the market, this is a market at present of $3 billion plus per year growing. Now, this is a product, so at least the PSMA-targeting products for imaging and for therapy have liabilities. For imaging, you see an undesired uptake in lacrimal glands, salivary glands, kidney, certain GI structures which may hide tumors. There are some diagnostic limitations. Also, there are patients like the ones depicted in these slides who have tumor depicted by the black uptake of fluorodeoxyglucose, but which do not express PSMA. This would be patients that you cannot treat. Even the patients that you treat, you cannot go so high with the dose because of this accumulation in healthy organs. The data that I've given, the registration to Novartis, indicate that the blue curve is better than the red curve. You're looking at progression-free survival over time. If you wait about one year and a half, basically all patients progress, and therefore one needs better drugs. We have decided to beat the PSMA by going with a better target called ACP3. You see a side-by-side comparison of the expression of the targets in healthy organs. Wherever you see brown, it means that the target is present, and you don't want it. You don't want expression in healthy organs. But for PSMA, again, the localization in healthy organs is the result of antigen expression in healthy organs. You see how clean ACP3 is. You don't see brown staining. There is expression in prostate, but this doesn't matter because it's intracellular expression. It's a complicated thing, but you will see it doesn't matter in practice when I show you the clinical data. We have contracted out a race, so to say, between ACP3 and PSMA to a pathology group in Pisa. And the center has assessed these targets by immunohistochemistry. And wherever you see brown, it means it's good. It means there is a lot of target. You see that basically ACP3 patients are always positive, whereas there are many patients with PSMA that are negative or only weakly positive. And one more slide. So the center scored the staining intensity from 0 to 3, 3 being the best for tumor targeting application. And to cut a long story short, with ACP3, 34 out of 39 patients were top score. And with PSMA, only nine out of 39. So really 87% against 23%. So based on immunohistochemistry, you would say ACP3 wins. We had the opportunity together with colleagues at the University Hospital in Münster to investigate this competition, so to say, in the clinical setting, both with patients with very advanced prostate cancer, but also in patients with biochemical recurrence, which basically means these patients are supposed not to have tumor, but their levels of PSA rise. There is the suspicion that the tumor may be coming back. You will see that in both settings, we are helping patients. Let's start with the heavily metastatic disease. You see the same patient who had been imaged with a PSMA-targeting agent or with our OncoACP3 labeled with gallium-68. You see that the PSMA targeting has the said liability in salivary glands, in other glands, in GI structures, in the kidney. These numbers indicate the metastasis. All these black numbers correspond to metastasis that we see with ACP3. Please note how clean the background is with our OncoACP3. We see also this metastasis in red, which would have gone lost with the PSMA-targeting agent. The SUV max, which measures the efficiency of uptake, these are values which are very high, up to 54. There is a literature that suggests that if you are above 20, you can basically do effective therapy. So it's useful from a diagnostic perspective, but it's promising also in terms of therapy. One more patient. Again, you see more metastatic disease. You see extensive targeting of healthy structures with PSMA and extremely clean background with ACP3. One more patient. Again, you see PSMA, heavy uptake in normal organs. This is an uptake that you don't want to have. And with ACP3, you see the metastasis, but the background is much cleaner. One more patient. This was imaged at two hours with a PSMA-targeting agent and same story, salivary glands, liver, kidney, GI tract structures. Look how clean the background is with ACP3, imaged at one hour or at three hours and a half. The beautiful information is not only that we reached the tumor, which is good, but also that the SUV, which measures the efficiency of the uptake, continues to grow. This is a good prerequisite for therapy. One last example, a patient who had PSMA-positive tumors, again with a lot of background, but see, for example, this lesion one, clearly visible. The patient was treated with PLUVICTO. Okay, so for therapy, you go from fluorine-18 to lutetium. You can see the normal organs, but you can also see this lesion one. When we gave ACP3, lesion one was weaker, probably because PLUVICTO was working on this lesion. But we could detect other lesions that were not visible with PSMA, again, probably indicating that we have a better coverage of tumor lesions in prostate cancer. Now, when we look at patients with biochemical recurrence, it's a different setting. But again, a good diagnosis can make a difference between life and death. And let me make this example. This was a patient, 58 years old, who had biochemical relapse after primary radiotherapy. And the patient still had the prostate. So the suspicion was simply that the PSA levels went up again in blood. And the doctors and the patients were interested to know if the tumor was coming back. Now, with the PSMA scan, you don't see much. You see the normal organs, but you don't see tumors. With ACP3, very clearly, this dot here below the bladder shows that the tumor was coming back in the prostate. And so the patient could be treated. And this can be a difference that saves the patient. Similar story, patient seven. You see that this patient had biochemical relapse, which means that the PSA levels were rising after prostatectomy and salvage radiotherapy, and again, by PSMA, you see the normal organs, but you cannot tell if the tumor is growing back. Whereas this tiny but very intense dot that you see here, and you see the transaxial projection with this yellow spot, confirms that the tumor was growing back as a bone metastasis that has been irradiated, and hopefully, the tumor will never come back in this patient, so this is my last slide. In summary, I think we are doing well both for green and for blue products. With Nidlegy, the marketing authorization application dialogue with EMA is progressing. And we have a dialogue which has been requested with FDA. We have completed one of the phase 2 clinical trials. We are defining the registration strategy also for BCC and SCC. For Fibromun, Emanuele has shown how we have completed enrollment in the pivotal trials in first and third line. The events are expected for readout very soon. If the readout is delayed, this is not necessarily bad news because it may mean that patients actually stay longer before the disease progresses. Again, in glioblastoma, patient recruitment is on track. For the chemistry, I hope that the images could show very clearly that we have excellent targeting with OncoFAP and we have excellent targeting with OncoACP3 in this latter case. This is a market of more than $3 billion that we can potentially claim by beating PSMA-targeting agents. With this, we have finished the presentation. We have been in the time that we had promised. We will stop the recording now. If there are any questions, we are here to discuss with you. As always, we are available for one-to-one meetings with investors that may ask for a dedicated discussion. I see Clémence and then Francesco. Clémence? Yes, hi. Thank you for taking my question. First, on non-melanoma skin cancer, you mentioned that you received some feedback from the FDA for the next step of development. Is there anything you can share with us on that? Yes. Please go ahead. No, no. I just have two other short ones, but we can talk on them. Yes, we completed a trial that for us is really the trial that has the registration potential. But we wanted to check with the FDA. We requested a meeting. Basically, we got ahead of time feedback from the FDA that they agreed with everything that we had proposed. We canceled the in-person meeting because we had already received in writing confirmation that our strategy was accepted. More in general, there are two clear avenues where I think we are providing a benefit. The first avenue is, of course, to go in patients who are not eligible or have progressed after drug inhibitors and PD-1 blockers. But there are more patients actually that could be addressed. This is a topic of intense discussion with key opinion leaders and also with authorities. Okay. Very clear. Thank you. Second question still on NMSC. When will we see the consolidated results from DUNCAN? Do you plan to present it at a congress or? Yes. The center that has treated most patients is the center in Tübingen. But of course, many other centers have participated at the trial and treated patients. It's usual practice that the center that has treated most patients will be like the presenting group at ASCO. And they have confirmed their commitment to submit an abstract for ASCO and at the same time to submit the manuscript for publication in a major journal. This is the plan that we will follow. We will ask for presentation at ASCO, and we will publish the data after a first publication that has already come out in which we had presented the first patients. Okay. Perfect. And if I can squeeze just one last on ACP3, in your summary, you say the first patient is expected in the coming weeks. Do you mean to be treated as part of a phase 1 study? Yes. We are treating basically two to four patients every week in the context of Article 13(2)(b), which is German legislation that actually facilitates certain experimental treatments to patients. Our phase 1 clinical trial has been authorized for imaging, both for ACP3 and for CAIX, which means we will follow a path which is identical to the one that we have already successfully implemented for FAP. This means that the compassionate treatment will continue. In parallel, now the trial starts, the company-sponsored trial starts. This is the basis to set the dosimetry. Of course, down the road, there are two main opportunities. One is an opportunity for imaging, which we intend to pursue. The other one is an opportunity for therapy that we also intend to pursue. The first centers have already requested the compound for therapy with lutetium-177. And these results will be disclosed soon. So everything is on track to be absolutely transparent. Many companies have expressed interest on this particular product. And we are very diligently talking to companies. And if we see that there is a good opportunity for a partner program, we will do it. And otherwise, we are well capitalized to develop the products ourselves. When you say interest in that product, do you mean OncoACP3 or is it sort of the whole platform of? I think potentially the whole platform is attractive. But I want to be very clear that FAP and ACP3 are the most advanced and I think unique products because we have demonstrated superiority over competition in comparative studies. And so these are products that we are advancing at full speed. There is a big value demonstrated, at least in prostate cancer, by the PSMA products which are already on the market. This is our benchmark that we intend to beat. Okay. Perfect. Very clear. Thank you very much. Thanks a lot. Then Francesco, Francesco. I think you are probably on mute. I can see that you just unmuted yourself. Now you should be able to speak if you try to speak. Now you are on mute. We cannot hear you. Of course, we are available for one-to-one or for phone calls whenever you want, as you know. I think we will also meet soon. If you have any comment that you want to share with the whole group, we are here at your disposal. If this is not the case, let me say that, as mentioned already, after the nine months, we are expected to finish the year with record profits and with a healthy pipeline. I think as of today, all the promises that we made four years ago for the IPO have been delivered much more. Francesco, now we can hear you. Yes. Okay. I can hear you. Francesco? Now we can hear you. Okay. Ciao. Ciao, Dario. Ciao, Emanuele. A couple of questions regarding the last page that you showed us regarding the OncoFAP and the OncoACP3. Maybe I missed something because I do think that this area is the area that today is really unknown by most of the companies. The potential that is linked to these developments. My question is, if you can be a little bit more detailed, what is the phases that we have to respect to have this OncoFAP methodology and the OncoFAP ACP3 fundamentally? So what is the timeline? What is the steps that we have to obtain to have these two products fundamentally? Yes. The audio was not perfect. But I think I understood the question you're asking. What are the steps which are necessary for FAP and for ACP3, both for imaging and for therapy? Yeah, exactly. Correct. Correct. To have the products on the market. So let's go slowly. For imaging and for therapy, nowadays, the registration trials have similar size. Okay? If you look at products that have already reached the market, typically, they are studied first in phase 1 clinical trials to demonstrate the dose and to demonstrate safety. Then you need the registration trial with probably 300-400 patients. This is the size of the registration trial. Now I go one by one. With FAP, as mentioned, we have completed the phase 1 clinical trial. We have treated more than 200 patients. The product for imaging is in the hands of Bracco, of the Bracco Group. It has been licensed exclusively to Blue Earth Diagnostics. We cannot speak on their behalf. Of course, we have constant joint steering committee meetings. The last one was today. We cannot speak on that product because all the communication activities are with Bracco. I think this is a question which has to be addressed to the Bracco Group. For therapy, we have the phase 1 trial which is ongoing. And phase 1 basically aims at determining whether we should give 100-200 or 300 mCi of the product. Once we have completed the phase 1 part, okay, then we can go straight to a registration trial. And all the products that have been approved so far had trials with a few hundred patients. So we have to complete phase 1 before starting a registration trial. For ACP3, it is exactly the same story. We now have the experience coming from compassionate use that we have shown. We have a phase 1 trial which has been authorized and which will be finished in 2025. And the registration program will start in 2026. So this is a long answer only to say that the phase 1 part for radiopharmaceuticals is usually short. It can be finished in less than one year. The registration part, so either phase 2 or phase 3, but with registrational intent, it's typically a trial that requires one year for imaging because imaging is fast. You take the picture and you are done, and it's really between two and three years for therapy because you have to monitor the patient over time, so these are different timelines for imaging registration and for therapy registrations. I've tried to be specific on times. I'll pause here. I don't know if you have additional questions. No, it's good. Thanks. Thanks Thanks a lot. We don't see other questions, and with this, we would like to thank all of you for your support. We are happy with the results that we have achieved, and as always, we remain at your disposal for dedicated one-to-one meetings. Thank you very much. Thanks a lot.