I'd like to thank everybody for joining our 2024 R&D Day presentation. Initially, I will give updates across our radiopharmaceutical and non-radiopharmaceutical business segments, and then that will be followed by Christian Cunningham giving an update and overview of innovations around our platform technologies. Initially, slide four represents our two main R&D areas of focus, which we've divided, of course, into our radiopharmaceutical efforts, which largely revolve around the discovery and development of targeted radiotherapies and radiodiagnostics. Then on the right side, of course, is the non-radiopharmaceutical part of the business, which is largely focused around the development of peptide therapeutics and/or other types of peptide drug conjugates or non-RI peptide drug conjugates. We'll discuss both aspects of the business in today's presentation. Proceed to slide six. We've used this slide numerous times previously to describe the concept of targeted radiotherapies and the attractiveness of this area. The modality relies on the conjugation of a radioisotope payload to a cancer-targeting vehicle. In this description, in the upper right, shows a macrocyclic peptide attached to a radioisotope payload, to which the therapeutic peptide then targets, specifically targets the tumor in the patient to deliver the cancer-killing or cell-killing radioisotope payload directly to the tumor cells without going to other areas of the body. This methodology, this targeted radioligand therapy methodology, can utilize both macrocyclic peptides as the targeting vehicle. It can also utilize small molecules in some cases, and it also can rely on other types of biologics. The real benefits of using macrocyclic peptides are listed on the lower right, which is macrocyclic peptides give you extremely high affinity and selectivity for the cancer-related targets, and they offer very, very favorable pharmacokinetic profiles, including fast renal clearance, which is often not seen if you're using a biological targeting vehicle. We also see lower immunogenicity and toxicity, and because they can be chemically made, they're extremely robust and easy to manufacture and produce, so a significant number of advantages for using a macrocyclic peptide to be the targeting portion of these therapeutics and diagnostics. On the next slide, there's an additional power of combining a diagnostic with a therapeutic. This has been coined the concept of theranostics. In this case, you can use the same compound to either label the molecule with a radiodiagnostic radioisotope, such as, as is listed there, 18F is fluorine, or 68Ga, or 64Cu, which many of you have probably heard of, or a therapeutic radioisotope such as 177Lu or 225Ac as examples. Your body sees the exact same type of molecule, whether using the diagnostic radioisotope or the therapeutic radioisotope. This has two strong advantages. One, on the preclinical development side, it allows us to actually very rapidly see in vivo, in animal models, whether our compound directly targets tumor or not, allowing us to very, very to speed up preclinical development efforts since we can very quickly confirm whether it's going to work or not work. And then on the right side is the ability to do de-risk at the human stage by doing phase zero studies. So phase zero studies being small patient populations where you simply use the diagnostic to microdose and determine whether or not in the human cancer setting or in the human cancer patient, whether the compound in fact targets their tumors or not. This allows you, again, to de-risk the asset prior to actually moving into more expensive phase I, phase II clinical development studies. And it further serves to really accelerate not only the de-risking of programs so that once they're fed to the clinic, they have a very, very high chance of commercial or therapeutic approval success, but also allowing us to test the very early stages about what targets would be best for these types of therapies. In part, I think because of these attributes, as we've discussed many times, the radiopharmaceutical field continues to rapidly grow here in 2024. The predicted market size for 2030, all this was predicted about a year and a half ago, is around $30 billion for 2030. I'm going to assume that these numbers will continue to be revised up over the coming years, but the real kind of advantage of the radiopharma space, as I mentioned, is both that it's a very simple and powerful MOA, mechanism of action, and it really is truly precision medicine. You can really see the tumor, see the cancer, and then treat the cancer, and that is for a very effective commercial and development strategy. We have two largely approved targeting therapeutics in LUTATHERA and PLUVICTO, both originally developed by AAA and then Endocyte, but both of those companies have, of course, been acquired by Novartis, and both of these products are currently sold and marketed by Novartis, one of the leaders in the targeted radiopharmaceutical space. On the right side is just a growing kind of map of the radiopharmaceutical community to which PeptiDream has had a core for the last six, seven years, has had a very core position in as one of the largest companies discovering and identifying the peptide carriers for these radioisotope payloads, and again, we have partnerships with Genentech and Bristol Myers Squibb, RayzeBio, Novartis, et cetera, across a number of these areas, but this is a very rapidly growing space with most of the large pharmaceutical companies in the last 18 months now moving into this field. On the next slide, on slide nine, highlights how we are kind of uniquely positioned to drive value creation across our therapeutic pipeline, therapeutic and diagnostic pipeline. As everyone is aware, we acquired the PDRadiopharma Company in 2022. It is one of only two licensed RI companies in Japan, which currently sells 32 different diagnostic and therapeutic products on the Japan market, and Japan has significant high barriers to market entry because of the requirement of radioisotope handling license and the various infrastructure needed to not only develop but also to commercialize radiopharmaceutical, radioisotope-containing compounds, putting us in a very strategic or a very advantageous position within the Japan radiopharmaceutical sector, but also we have a very strong, as I mentioned, global presence in our ability to find the peptide ligands to be used in the development of these targeted therapies. Our model is focused on, at this stage, three efforts. I highlighted on the right side, really the development of our in-house programs. We have already previously announced our CA9 program, which we'll talk on a little bit more today. And of course, today we're announcing our second fully owned internal program targeting Claudin 18.2. In addition to that, we also have a number of programs that are coming from collaborations, such as our collaboration with Novartis and our collaboration with RayzeBio, BMS. And we'll be highlighting some of those programs today. And then the third aspect, of course, is in-licensing compounds, to which we'll touch on both the LinqMed program and also the more recently partnered Curium programs. The goal of these three efforts, of course, is to create a very robust development pipeline expanding the targeted radiodiagnostic and radiopharmaceutical space, both for the Japan market but also for the global market. On slide 10 is the current to-date status of our radiopharmaceutical pipeline. I will touch on all of the therapeutic programs in the subsequent slides. Only the bottom, the diagnostic products, I will not be mentioning, except to say that the Tauvid diagnostic agent or imaging agent that we had partnered with Lilly recently had the NDA filed, and we're expecting actually a decision on that by year-end, so very excited to see that product actually move forward and launch into the Japan market in 2025. Moving forward, on slide 11 is initially highlighting the 64Cu-ATSM program. This program was partnered with LinqMed, which is a small Japanese biotech company, in late 2023. I think we announced this in December of 2023 while they were in a phase I study of this compound. The 64Cu-ATSM is a small molecule drug that is chelated with 64Cu and actually localizes or targets sites of hypoxia in the tumor microenvironment, so they initially have been developing this compound for a variety of gliomas or brain cancers, but potentially it actually could be used in other types of tumors or other types of indications also in the future, but initially, the focus has been on gliomas. On the lower part of this slide is highlighting some of the take homes from their phase I START64 study, which had been run in Japan. They reported this data in early summer of this year in 2024 and have been presenting some of those findings at a variety of different conferences. The goal of that phase I study, of course, was the primary endpoint to assess dose limiting toxicity of the compound. Then there were a number of secondary endpoints that were investigated also. The take homes are kind of highlighted in green, which they had investigated the 30, 60, 99, and 150 megabecquerel per kilogram dosing. And across the dosing scheme or the dose escalations, they had determined that largely the maximum tolerated dose was roughly around 100 megabecquerel per kilogram, which is what they've carried forward into the phase III study. The 64Cu-ATSM was shown to be safe and well tolerated. There was no serious adverse events. There were a few, I think, Grade 3 and a few Grade 3 lymphocytopenias that had come out of the study, but overall, once you remove therapy, those also completely went away. It was determined to be safe and well tolerated. The median OS, they reported that this was a relatively small patient size of only 18 patients, was around 30 months with a one-year OS overall survival rate of 76%. This is quite attractive given the nature of these types of gliomas being Grade 3 and Grade 4, and these are recurrent gliomas. On the next slide, that data was utilized for discussions with the PMDA, and LinqMed moved very quickly into a phase III study, which started in June of this year. As is listed on this slide 12, the upper part is actually the design of the study, which they will be enrolling or have already started enrolling recurrent high-grade glioma patients with glioblastoma or Grade 3, Grade 4 astrocytomas, or Grade 3 oligodendrogliomas into the study, with the overall primary endpoint, of course, around overall survival and then secondary endpoints around progression-free survival, PFS, and other types of response rates. So patient enrollment, again, as is highlighted in green, has already begun. We are at current between LinqMed anticipating potential for product filing in 2020, late 2027 at the earliest. And the intention of the two companies is to potentially apply for SAKIGAKE designation once we have enough phase III data to justify and support such filing, which also potentially could truncate or shorten certain aspects of the approval process for us. Very excited how this program is overall progressing in a wonderful partnership with LinqMed. On slide 13 are two products that we recently announced with Curium on October 1st to bring these two programs into Japan, the 177Lu-PSMA-I&T and also the 64Cu-PSMA-I&T compounds. As is listed on slide 13 on the left, the lutetium version is the therapeutic and the copper version is the diagnostic. Both of these compounds have been in phase III studies in the United States. Just recently here in November, Curium announced the completion of the phase III study for the Lutetium, the therapeutic on the upper portions, has completed the phase III demonstrating a statistically significant and clinically meaningful benefit for patients with PSMA-positive castration-resistant prostate cancer. This is extremely exciting. They haven't released the full study results, but we're expecting those to be released sometime in 2025. But this partnership will allow us to utilize the phase III data generated in the U.S. to rapidly bring both of these compounds into the Japan market as soon as possible. And we've already, with the collaboration kicking off, are putting the various pieces in place to both handle the development aspects and also discussions with the PMDA as far as the development path for both these programs. And I think that's something in 2025, they'll be starting development and we'll be explaining to the public, the market, more about the actual details of both of those efforts. But the I&T, the therapeutic compound, will of course be a competitor to PLUVICTO in Japan. And PLUVICTO is not yet approved in Japan. It is currently in phase III testing here. And also potential to bring a Copper-64 diagnostic to the Japan market, which we think will have significant benefit to patients as far as diagnosing prostate cancer and potential patients for use with the therapeutics. So think about bringing that into the Japan market here. On slide 14 is one of our historical programs. This program was a part of the Fujifilm business when we acquired the PDRadiopharma business when we acquired the company in 2022. It is partnered with Novartis, and it is running. It is a small molecule compound that targets Integrin alpha-v beta-3/ beta-5 for the potential treatment of gliomas. They had partnered this program with Novartis. It is currently being run in a phase I study by Novartis, an associated study by Novartis. This study is still ongoing, so I don't have any specific comments on this today, but we're very hopeful to see this program continue to progress. On slide 15 is our Glypican-3 program. Initially, to highlight, Glypican-3 is actually a member of the Glypican family of cell surface heparan sulfate proteoglycans. It's involved in several critical cellular processes, and its expression is actually very tightly regulated, and abnormal expression can contribute to the progression of cancer. As is highlighted on the right, why Glypican-3? Glypican-3 is, in fact, highly expressed in patients with hepatocellular carcinoma, HCC. Greater than roughly 80% of patients have high expression of Glypican-3. It really shows minimal to no expression in normal tissues, making it an ideal target for these targeted RI therapeutics. As is shown in the lower right panel, is the expression of Glypican-3 in certain tumor types, to which certainly HCC is one of the highest. Very excited for Glypican-3 as a target. On the next slide on slide 16 is we have identified at PeptiDream highly selective and highly potent binders to Glypican-3 in a collaboration with RayzeBio, which of course was acquired by BMS earlier in the year. Those compounds have shown very potent binding, and as is listed on the lower parts of this panel, have shown very clean distribution and targeting to tumors of RYZ801, which is the therapeutic -labeled peptide, and also excellent biodistribution with the gallium- labeled agent. On the right side shows, we had looked at both Actinium-225 and Lutetium-177 as the potential therapeutic radioisotopes, with seeing slightly better activity with Actinium-225 overall, in part because we see wonderful targeting utilizing these peptides. Glypican-3 for hepatocellular carcinoma, this is very much a large need. This is the sixth most common form of cancer worldwide, so there is significant medical need for better therapeutics for HCC. On the next slide, slide 17 is the current status of the program. RayzeBio had gone through one of the most maybe extensive ever phase 0 studies, testing a significant number of patients for both the diagnostic and the therapeutic, which really gave significant confidence in continuing this program forward. In part, these had led to the IND filings, which have happened recently and been accepted. We're now looking forward to both the diagnostic RYZ811 and RYZ801 moving into the phase I human testing very soon here. Expecting that to happen by Q1 of 2025 anytime. Very much looking forward to announcing that as both these products move into the clinic and very excited about seeing this. Just for everyone's reference, as we've discussed, PeptiDream has the Japan rights to both of these compounds, and we are very much looking forward to utilizing the data generated from the global study or from the initial U.S. study to bridge back into Japan and bring these products to market at the same time as they're brought to market in the U.S. On slide 18 is what is listed as our Novartis RI Program #2. This is the first program. It is a macrocyclic peptide conjugated to a chelator. It is the first program that actually originated from our 2019 collaboration with Novartis to discover these types of ligands for this application. Novartis has global development and commercialization rights for this program. We had announced in October of 2023 that this program had initiated IND-enabling studies, which we received a development milestone fee, and since the IND filing, Novartis has proceeded through IND filing, and we're looking forward to actually the initiation of a phase I study for both of these products, both the diagnostic and the therapeutic, in the near term, potentially by end of year or certainly in the early parts of next year at the latest, so very much looking for both these programs also to move into the clinic here shortly. On slide 19 is our wholly owned internal CA9 targeted program. Just for brief overview on CA9 itself, it's referred to as carbonic anhydrase 9. It's a member of a family of carbonic anhydrases that are cell surface transmembrane proteins. They are catalyzed with reversible hydration of carbon dioxide into bicarbonate ions and protons, not proteins, protons. This reaction is essential for various cellular processes, including respiration, pH regulation, and ion transport. And what you see, as is depicted in the lower left, is for cancer cells, you have often a loss of this VHL function, which results in an upregulation of CA9 expression and then translocation of CA9 on the cancer cell surface. So CA9 is listed in the upper right is why CA9. CA9 is highly expressed in renal cell carcinoma patients. About roughly 90% of patients have high expression of CA9. It's also expressed in a variety of other tumor types, such as triple negative breast cancer, head and neck cancer, glioblastoma, and ovarian, and even colorectal cancer at lower percentages. The lower depiction, of course, there shows how high that expression actually is in kidney cancer, but of course, CA9 is actually expressed across a variety of different tumor types. So potentially it has wide use across a variety of different cancer indications. It also shows relatively minimal expression in normal tissues, again, making it an ideal target for these types of therapies. We had announced this program last year, our CA9 program. It was an internally discovered macrocyclic peptide, again, conjugated to a chelator, which could be radio-labeled with either Copper-64 or Gallium-68, and then for the therapeutic, Lutetium-177 or Actinium-225. We've decided, of course, to progress with Actinium-225 as the therapeutic radioisotope and Copper-64 as the diagnostic radioisotope. Renal cell, as is the right panel there, renal cell, clear cell renal cell carcinoma is very much a high unmet medical need. It is the most common type of kidney cancer and does not have a very good overall survival rate. As we looked on the lower left, our compound, our lead program or clinical candidate is considered PD-32766. Shows very strong and selective binding to CA9. Then, as we looked on the lower right, clearly detects ccRCC tumors with rapid renal clearance in the animal mouse studies. Very much giving us confidence to take this program forward, to which we're very excited about. On the next slide, slide 21 is additional animal study data. In the upper left, it shows that both copper-labeled PD-32766 and also lutetium-labeled PD-32766 show very strong accumulation in tumors, significantly over kidney or any other type of organ, so this is just a fantastic looking profile for those who are just seeing this kind of for the first time. Also on the right, it shows very rapid blood clearance and very rapid safety kinetics, which are fantastic. Again, this is really fantastic data for use as both a diagnostic and a therapeutic for these molecules, and then on the lower left, we could show that this resulted in very clean and clear tumor killing that in these mice models of RCC or renal cell carcinoma, we were very effectively able to completely wipe out the tumors after dosing with these compounds, after a single dose, so very excited. These compounds, PD-32766, show an excellent PK and a clean distribution profile. It's shown clean in vivo anti-tumor effect, excellent tolerability in a clinically relevant renal cell carcinoma xenograft mouse model, and has the potential here to be best-in-class. On slide 22 is the current status of this program. As we had mentioned through a variety of press releases since last year, we had initiated a phase zero study in June of 2024, which was conducted here in Japan at the National Cancer Center of Japan. It enrolled a total of five patients with ccRCC, and they were each administered Copper-64- labeled PD-32766, followed by imaging by PET and CT. The study's key objectives were, of course, to evaluate the safety, pharmacokinetics, and exposure of the compound in newly diagnosed relapsers or those suspected to have relapsed RCC. We will be presenting for the study all five patients that enrolled. We now have all the data. It's going through final analysis and final reporting, and we will present the phase zero, what I think is a very exciting phase zero study results at next year's ASCO GU meeting in February, which will be in San Francisco, and we will, of course, begin making that presentation public at that stage. We also have been continuing IND-enabling studies, as is written in the upper portion of this, which will be largely wrapping up here next January or February. We should have the full totality of the IND-enabling studies completed, therefore putting us in the position for IND filing in sometime in 2025 and preparing for initiation of phase I in the second half of 2025. So we feel, again, this is a program that has now been very much de-risked and very excited about taking this program forward into RCC patients. In addition to the CA9 program, which is our lead wholly owned program, today we are announcing our second wholly owned program targeting Claudin 18.2; 18.2 is a member of the Claudin family of proteins involved in the formation of tight junctions between cells. It's essential for maintaining healthy interactions between cells and thus the integrity of tissues and organs. Its expression is tightly regulated, and abnormal expression can contribute to the progression of cancer, as well as the ability of cancer cells to invade surrounding tissue or spread into other organs and/or develop resistance to chemotherapy and other treatments. As is shown in the lower left depiction, 18.2 is, again, a tight junction protein. It's normally between cells and therefore not readily exposed to compounds. But when the cancer cells actually break down the normal architecture and start to grow, you see increased expression of Claudin 18.2, and also it becomes far more accessible to compounds that could bind to it. So in the upper right, why 18.2? It's highly expressed in gastric cancer, roughly 40% or higher. There are variations on the numbers here, somewhere between 40% and 50%, I think, as well as many other types of cancers, including pancreatic cancer. And as is listed at the bottom there, expression table, this is based off of available information that is highly expressed in gastric cancer and also pancreatic cancers as the main two areas we've been going after. So we're very excited about this compound, this target as our second program. On slide 24, the name of the program is PD-29875. Again, it's a very highly potent and selective macrocyclic binder, too. Claudin 18.2, discovered as an internal program, to which we have, of course, full rights to. Gastric cancer is very much a significant medical need with more than 1.1 million new cases per year in 2020, and this is actually potentially predicted to go to almost 1.8 million new cases by 2040, so significant unmet medical need here, and Claudin 18.2 seems to be a very strong target, for it's actually a clinically validated target for the treatment of gastric cancer. As is shown in the lower part here, we show an image of PD-29875 in the same kind of tumor model. We see very high targeting and high accumulation to these gastric tumor models. And then in the middle part of the slide, we also see very strong response to Lutetium -labeled 875 peptide, clearly removing the growth or stopping the growth of these tumors in their tracks with no real effect on the weight gain of these animals, showing that they're not only very targeted, but they show very good tolerability. So our 875 program exhibits very high affinity and selectivity for 18.2. It's shown very high uptake in these mouse models of gastric cancer that have 18.2 expressing tumors with very minimal non-tumor accumulation. So we see almost no accumulation in any other organs besides very, very, very low kidney, which is the common place to see any kind of residual. And it's shown very strong tumor reduction efficacy, supporting our decision to take this into IND-enabling studies and also human imaging phase zero studies. As is listed on slide 25 is the current status of this program. We have elected it, of course, as a clinical candidate. We have already initiated IND-enabling studies of this program, intending to develop it utilizing Actinium-225 as a therapeutic radioisotope with the paired diagnostic imaging agent using Copper-64. In addition to that, we are also actually planning phase zero studies to run concordant with the IND-enabling studies, which also should happen in 2025. We'll be announcing more of those, more details again around this program as it progresses forward into next year. The upcoming milestones are the first in human phase zero imaging studies. And then also we will be presenting the key results of the preclinical study at a medical conference here in, and I think the first half of 2025 to detail more of the preclinical supporting data around this program. So very excited about seeing this program move forward. And going forward, the goal is to launch at least one internal program per year going forward. And so we're two years in a row, CA9 in 2023, Claudin 18.2 here in 2024. And we have a number of programs up for consideration for 2025. So couldn't be more excited about the progress of our internal efforts to develop some really groundbreaking targeted therapeutics here. Lastly, in the radiopharm side of the coin is slide 26. I just want to touch on a few other programs. Our Novartis program, which is being called Program #3 in 2024, also like Program #2, hit the initiation of IND-enabling studies milestone, which we received that milestone in July 2024. In this program, while at this time we're not able to provide significant details around this program, we are very excited about this program. This program is also progressing forward, expecting some impactful news in 2025 for this. So our collaboration with Novartis is going fantastic, and we're expecting a lot of success and a lot of programs to come out of that, a lot of products to come out of that. Also with RayzeBio, our Program #2 is RayzeBio after Glypican-3. The target of this has not been disclosed, and there hasn't been a lot of details in 2024, in part because of BMS's acquisition of RayzeBio. We're looking forward in 2025 to potential next steps around this exciting program also. Then lastly is a program partnered with PPMX, which is a Japan biotech company, which is the antibody targeting cadherin 3. This had originally gone into the clinic using yttrium as the therapeutic radioisotope, and they subsequently decided to change to a stronger alpha radioisotope, Actinium-225, to which they announced in mid-2024 that they saw actually equal and better efficacy when they had switched to Actinium-225. So they seem very excited with this program. PPMX is, we are partners on the program, but they're leading development of the program, and we're excited to see that progress forward, so. Next, on slide 28, we'll start to discuss the non-radiopharmaceutical side of our business. As is listed on the left side is our efforts around peptide therapeutics. We're largely focused on oral and injectable peptides at this stage, peptide therapeutics at this stage. And then on the right side is other types of peptide conjugates or non-RI peptide conjugates, utilizing our macrocyclic peptides to deliver oligonucleotide payloads or deliver small molecule cytotoxic payloads or to do other types of multifunctional peptide conjugates or protein degraders or immune recruiters, etc., as is listed on the right. We have a number of partners, of course, across a variety of these different topic areas, and we think these programs are actually going extremely well. Most of them are, of course, still at the preclinical stage. And so we very much look forward in 2025 to actually announcing hopefully some large events coming out of all of these efforts. So very excited to see the progress move forward there. On slide 29 is the clinical pipeline as it stands today, and I will touch on all of these programs briefly here. So on slide 30 is our most advanced program, is AZP-3813. This is a macrocyclic peptide, a bi-cyclic peptide growth hormone receptor antagonist that was discovered at PeptiDream. We licensed this to Amolyt Pharma, which was a French biotech in 2021, to which they took into a phase I study and then reported on this. Initiated in June of 2023, they reported the phase I results in June of 2024, and they were acquired by AstraZeneca in early, or I think the acquisition closed in the summer of 2024, but the acquisition, the intent to acquire the company was announced in early 2024. So Amolyt is now a part of AstraZeneca, and it actually is fit into the Alexion rare disease unit of AstraZeneca. And so this program has been referred to as AZP-3813. It will be or is being renamed to ALXN2420. Now that will be announced in the coming weeks or in any future press releases going forward. This peptide is being developed as an add-on therapy for the treatment of acromegaly in patients insufficiently controlled currently with somatostatin analogs. As is written on the lower half of this slide is the mechanism of action of this compound. These SSAs or the somatostatin analogs suppress growth hormone production, but they don't do a perfect job actually managing that, and you can still get expression of IGF-1 in cells. And therefore, if you actually combine the somatostatin analog with AZP-3813, which acts through a different mechanism of action, it blocks the GHR receptor or blocks binding of growth hormone to the GHR receptor. And therefore, they have two different mechanisms to actually reduce circulating growth factor or growth hormone and therefore better control the production of IGF-1 in the liver. This is shown on the right side there where you have simply a somatostatin analog in octreotide in the dark purple, and its reduction, its percent change to IGF-1 levels versus AZP-3813. And both of these then, when added together, you actually get the very additive effect here of further decreasing circulating IGF-1 levels. This really gave confidence. This was in rat model data, but this gave strong confidence to actually employing the AZP-3813 in combination with somatostatin analogs for the treatment of these patients. On slide 31 is the phase I data that had been reported. They reported this data at two different conferences at ECE and ENDO in June and July of 2024. This was a phase I randomized double-blind placebo-controlled single ascending dose study with also a multiple ascending dose arm to it conducted to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics. Also, the pharmacokinetics and pharmacodynamics were assessed by measuring serum IGF-1 levels of AZP-3813. They reported extremely good tolerability with no safety concerns at all and no clinically significant abnormalities with respect to safety lab vital signs or ECG. In addition, as is reported in the lower part of this slide, you have the SAD results on the left, and you have the MAD or the multiple ascending dose data on the right. You could see very much a dose-dependent, dose-related decrease in circulating IGF-1 levels upon repeated administration of AZP-3813. The Amolyt conclusion was that this reduction or control of IGF levels was well within the level of reduction expected to result in excellent control of IGF-1 levels in patients with acromegaly and strongly supported its continued development into acromegaly patients. With the acquisition, that probably slowed down development slightly, but this program is now moving into a phase II study, and we expect to hopefully announce that in early 2025. We are very excited about seeing this program also move forward. On slide 32 is just a brief update on two other programs that have been in our pipeline for some time. The PD-L1 program, which was an oral PD-L1 macrocyclic peptide inhibitor. This had been taken into a phase I study in 2022 by Bristol Myers Squibb. We've discussed this previously as we had an explanatory meeting in 2023 that they had announced that they were not continuing the program into a phase II for business reasons and that we were looking into our ability to review the phase I data and determine whether there was any future option regarding this program. It has taken longer, I think, than we expected to receive all of the relevant phase I data, and in fact, there were parts of the data that had not been analyzed that I might consider kind of in the raw form, and so we've had to spend a little bit more time than we had expected, certainly, to review the current data, so we're still, I think, hopefully in 2025, in the first half of 2025, we'll be able to make a definitive decision on what to do in regards to this oral program. The underlying peptide, for everyone's information, the underlying peptide to the oral program has actually also been -labeled with 18F and has been continuing as an imaging agent, so that is still in development. It had completed a phase I study, and we are kind of waiting for a BMS determination to what is next in regards to the imaging agent, but currently, we're certainly free to pursue any therapeutic modalities around PD-L1 as a target, and as many people may be aware, PD-L1 is starting to show up in additional kind of bi-functional and other potential peptide drug conjugate or conjugate-based applications, so we still think there's very much a utility for the compounds that we actually have for this program, so I think this is something we'll talk about more, hopefully in 2025 here. On the right side is the CD38 program. This is a multifunctional peptide. It has two macrocyclic peptides, one binds to CD38, one binds to IgG. This had actually moved into a phase I study in 2021 that was being conducted by Dana-Farber Cancer Institute in partnership with Biohaven. More recently, actually, the clinical trial protocol has been adjusted. This was a physician-led study that, because this is multiple myeloma, had actually very quite stringent inclusion or enrollment criteria. That enrollment criteria was to the point where it was becoming very challenging for the study to actually recruit patients into. So maybe over they were recruiting at a very slow pace of only one or two patients, I think, per year. So they've recently we've had these discussions with Biohaven. They've amended that, and they are potentially the inclusion criteria to allow for potentially the recruitment of more patients. So hopefully, we'll have something to discuss around this program also in 2025, but we don't have more than that to report at this stage. Simply the amendment we hope will fit for or account for the recruitment challenges that program has encountered. On slide 33 is excitingly two programs that originate from Merck with our macrocyclic peptides. On the right side is Program #1 that actually went into a phase I study in July of 2023. Unfortunately, we could not disclose the indication nor the target at this stage. The study is being run in healthy volunteers, so there's no ClinicalTrials.gov identifier for this study. But if this study progresses out of phase I into a phase II, we should be in a position to be able to both get an NCT identifier number and also be able to disclose both the target and indication for this program. Similarly, on the left side is the second program to enter the clinic. This entered in June of 2024. We were able to disclose the indication was for inflammatory disease, but we are still not able to disclose what the actual target of this study is. Similarly to the first program, because this is being run in a phase I investigating safety, tolerability of pharmacodynamics in healthy volunteers, there is no clinical trial identifier for us to disclose. And likewise, we expect if this program progresses into phase II, that we will be in a position to disclose more about these programs. Also, they should both show up in Merck's own pipeline once they enter phase II. Merck does not normally put phase I programs into their disclosed pipeline. Very excited about both of those programs going forward. On slide 34 is PA-001, our partner program with the PeptiDream spinout PeptiAID that many of you may be familiar with. This was a very potent macrocyclic peptide inhibitor of the spike protein for potential use in the treatment of COVID-19. It acts by a very different mechanism of action compared to the other agents, such as Paxlovid, that had been disclosed, and Shionogi's compound, also Shionogi's, Pfizer's, and Merck's compounds, by blocking actual viral entry using this peptide. It binds to an excellent epitope on the stalk portion of this spike protein, which is actually quite conserved across every variant that we've looked at to date, suggesting it's, again, a very attractive potential modality here for the treatment of coronavirus. We had applied or PeptiAID had applied for AMED support, and this program was actually adopted by AMED as part of their research program to promote the development of innovative therapeutics for emerging and re-emerging infectious diseases that we had previously announced, and so this program has actually moved forward into a phase I study in the U.S. in elderly volunteers. We had already made press releases, as is shown on the lower right, in which, in July, the FDA had approved the IND application for the phase I study, and on October 7th of this year, we announced the dosing of the first patient. We're expecting to be able to release those phase I results sometime in the second half of 2025, and then at that time, determine, of course, next steps for this program. Lastly, on slide 35 is an update around our myostatin inhibitor program. Myostatin, along with GDF, which is also known as GDF8, along with GDF11 and activin, are members of the TGF-beta superfamily, and they function in a very complex process that regulates muscle growth and function, and that is depicted in the illustration in the middle part of the slide here. myostatin has both a pro and latent form of it, and it's regulated by a complex network of inhibitory proteins as well as local autocrine and paracrine signaling events that likely play a predominant role in its ability to regulate muscle homeostasis. Recently, as many of you are likely well aware, inhibitors of myostatin, GDF11, activin, this signaling pathway have been investigated across a broad range of disorders, including muscular dystrophy. More recently, there's been very exciting data in the SMA space, but also ALS, cachexia, and also you're starting to see results coming out from obesity studies as well. And the potential to use inhibitors of this pathway in a variety of different muscle-related and/or metabolic diseases is extremely attractive. PeptiDream has developed a series of potent macrocyclic and bridged macrocyclic peptide inhibitors to myostatin. These are extremely potent compounds, and they show varying degrees of selectivity to myostatin over GDF11. So we have compounds that show equal binding to both myostatin and GDF11, and we have compounds that show selectivity for myostatin thousandfold over GDF11. So we have a very nice set of compounds, and all of these have selectivity over activin. So we think it's a very attractive profile for these peptides. They exhibit excellent pharmacokinetics, and including what I would say is very high exposure in muscle tissues, which is potentially a significant differentiating factor between the other biologics being developed in this space, which are largely antibody-based digestics or, sorry, therapeutics, as we'll say. Most excitingly, we've now efficaciously administered these either by subq or orally, making these the first reported orally bioavailable or orally administratable myostatin inhibitors that actually show function. And so we're very excited about that as far as positioning this program. As many are aware, we had originally started off developing this program to DMD, to which those efforts continue. We saw very, very good therapeutic benefit in the mouse models of DMD, which we actually had made a presentation at the World Muscle Symposium a little while back. So the ability to take both these candidates forward for both DMD, potentially SMA, and also obesity gives us a variety of different indications to drive potential growth. Initially, on this slide 36, though, and the point of today's presentation is to focus on the obesity aspect of their use. This slide 36 highlights the current landscape of inhibitors for this myostatin pathway. You have Lilly after their acquisition of Versanis, which has an antibody that actually binds to the receptor, which inhibits the signaling of all three ligands. And then you have Roche2Guy, Biohaven, Regeneron, and Scholar Rock, as all having alternative antibodies that bind to different ligand patterns, right? Myostatin, GDF11, or activin, as depicted here with the arrows. These compounds were initially developed largely for SMA, or at least on the myostatin. So the Roche2Guy program is a phase III for SMA. Biohaven's in a phase III for SMA, and Scholar Rock is in a phase III for SMA. Only more recently has there been a pivot more toward obesity, to which Scholar Rock has been generating both preclinical, and I think is now in a phase I for obesity. Biohaven's also in a phase I for obesity. And so I think Roche2Guy is also in a phase I for obesity. So there's a pivot, of course, to these studies for application in obesity. Our compound is the first compound that is an PO or an orally bioavailable compound and shows very exciting data. So we actually think we're in a very strong position to have the first-in-class oral myostatin inhibitors. On the next slide, I just want to show you a part of the preclinical data that has been generated here recently in 2024. This is the result of the testing of one of our candidates in an obesity mouse model of obesity, which is basically a diet-induced obesity mouse model. This is a very common model used across the industry to judge the efficacy of these types of compounds. When we gave this compound at three different doses, 0.5, 1.5, and 4.5 mg/kg, in combination with the GLP-1 agonist semaglutide, which, of course, classically causes you to lose weight, but you also lose muscle at the same time. So the goal of this study was to determine whether the addition of our oral myostatin inhibitor would, in fact, offset the lean muscle mass loss characteristic to these GLP-1 agonists. What you can see on the left is, so I guess to start in the middle, the middle is the black bar is semaglutide only, and with semaglutide administration, of course, you lose not only do you lose weight or fat mass, as you can see in the lower left, with these patients losing significant% change of fat mass in these animals, but in the middle of the screen, you also lose 8% of the lean body mass in these animals. If you administer increasing doses, daily oral administration of our inhibitor peptide, you can see that you continue to lose the same amount of overall fat mass, but you actually retain or preserve lean body muscle mass, lean body mass in these animals, suggesting, of course, or showing, demonstrating that these compounds are very much preserving the lean muscle mass or lean body mass and offsetting the unintended consequences of giving semaglutide or any of these weight loss compounds. So an excellent verification and demonstration of the efficacy of these compounds in combination with semaglutide. On the next slide, which was even more outstanding, was not only daily oral administration showed this type of effect, but in fact, weekly, once a week, oral administration of our compound also showed very clearly this very strong preservation of lean body mass in these animals. So very exciting, again, these animals continue to have reduced their fat mass, but they're no longer losing the lean muscle mass or lean body mass, which is a key finding. So these compounds, as being the first oral compounds, as everyone is aware, the current weight loss drugs are all injectables. They're all, or the approved ones, are all administered usually daily. And there are a number of efforts, of course, for the pharmaceutical sector to be searching for oral alternatives for this weight loss for semaglutide and the GLP-1 agonists. But this is the first evidence of an actual myostatin pathway inhibitor that could be orally administered and offset any type of oral weight loss drug that is out there. So we think there's a very strong chance of combination therapy with our compounds going forward. We'll continue our preclinical development activities here into 2025, and we've already been having a number of discussions with potential partners in the space, determining kind of what is the best opportunity for us around this exciting program, not just for obesity, but potentially for SMA and DMD. And so I think hopefully there'll be significantly more to come in 2024. So 25, sorry. So with that, I want to pass this over to Christian. I have used up a significant amount of time, but I'm sure 15 minutes we can still handle. Please, Christian. Yep. So it's absolutely my pleasure to present to all of you today. It's been an absolute honor being able to join PeptiDream after getting to work with them for nearly 10 years while I was at Genentech, both in collaboration with PeptiDream, but also in licensing the technology transfer. And it was these experiences that really gave me the firsthand exposure to how powerful PDPS is, as well as a window into the exceptional scientists and strategies really employed to deliver peptide-based therapeutics. And it was that motivation that really brought me over here. And I can firmly say that upon joining, my expectations have truly been exceeded. I'm now very excited to join the PeptiDream leadership team, to continue building upon the amazing work that's already been going on, as witnessed in these last several slides and presentation, and really continue to drive more peptides into the clinic, into patients in need. And so just for a few slides, I really wanted to talk about some of the innovations that we're working on at the earlier stages of our platform in order for us to continue to deliver to our portfolio as well as patients. And as all of you know, the real power of PDPS is the fact that we can incorporate non-canonical amino acids at the start of discovery. And we can build these into combinatorial peptide libraries in massive amounts, where our libraries are on the order of 10 trillion peptides in every library. These are made using in vitro translation technologies. And in this way, we are able to covalently attach the barcoded mRNA DNA that actually made that peptide to the peptide itself. This allows us to leverage the power of next-generation sequencing and other technologies to identify peptides that bind to our targets of interest. But when you start with unprecedented libraries that are 10 trillion in size, we leverage the power of directed evolution in order to identify these. This allows us to not only profile these peptides round over round, where we can translate, bind to our targets of interest, elute that DNA, reamplify, and iteratively permute the discovery, but it also allows us to customize kinetic and thermodynamic parameters, enabling us to build customized discovery pipelines for each of our programs. Over the last several years, we've also developed high-throughput automation to truly maximize the amount of libraries that we can pursue, as well as to maximize our hit discovery rate. Now, this is not a singular technology that isn't developed. This is a constantly evolving technology. We are every year developing novel scaffolds and conjugations to try and increase our probability of success for difficult MOAs. We've been inventing novel reagents such as our proprietary tRNAs, allowing us to drive in even more complex non-canonical amino acids than we've ever been able to incorporate. And one of the most impressive things that I have seen is really the collaboration between our discovery scientists and our medicinal chemistry scientists, such that we can integrate the strategies used in our later stage operations and bring those all the way to the earliest aspects of our discovery to try and minimize that time of optimization and continue to drive forward our programs as fast as possible. As I mentioned earlier, we identify our hits out of these libraries using next-generation sequencing. But what this also enables is our ability to generate massive datasets for every target that we look at internally. With this type of data generation, this now enables us to truly utilize computational methodologies as well as machine learning and AI approaches to not only identify better, more lead-like chemical matter at the start, but also reduce those optimization cycle times, reducing some of the bottlenecks of traditional drug discovery to deliver on our portfolio. On slide 41, I'm going to give one vignette as to some of the optimization as it goes towards the earlier side, which is really, what do we want to put into our libraries at the start? As we've grown from 2006 until today, one of the heavy focuses of the organization has been increasing that chemical diversity of our amino acid libraries, really trying to input those drug-like properties from the start. Instead of becoming a hit identifying engine, we're becoming a lead-like identifying engine. This incorporates ideas such as increasing backbone diversity, side chain diversity, but also probing the properties that make a tool an actual drug, such as solubility, as well as reducing plasma protein binding and stability. As we evolve our libraries, we're now able to implement these across a variety of different MOAs, as well as administration routes in order to further our focus R&D areas, such as peptide drug conjugates and oral injectable peptide therapeutics. This also leverages us a visibility into the five to 10-year horizon in terms of trying to interrogate very difficult targets on the intracellular landscape. Just as a little bit of details and specifics, here are some recent additions to our 2024 that we did in 2024 to our library. What you can see is these are truly diversifying ourselves away from the natural 20 amino acids that are found in nature, really trying to utilize some of the chemistry and properties built into commercialized therapeutics into our peptide-based libraries. If we now move to slide 42, we can look at the other side of our drug discovery pipeline in an area that I think we are only just touching the very, very outer edges of. This is really in terms of the massive amount of data that we can generate here at PeptiDream. When we originally started working, we were doing manual PDPS, which allowed us to do 8-16 selections. With the sequencing technologies at the time, we would be sequencing a little under 2 million sequences. With our onboarding and development of automation, we've now been able to increase the datasets upwards of six million, and now, with other newer NGS technologies, as well as other automation work that we're doing, we're now moving towards a 2025 ambition of sequencing well over 100 million peptides from any one given selection, so this really will start to form the data that we can now start to understand how to marry machine learning and AI approaches into our drug discovery and development operations, and so, as a part of this journey, we have been consistently working on this over the last several years. Currently, at PeptiDream, we have a proprietary non-canonical peptide clustering algorithm. When you are sequencing hundreds of millions of sequences, we need a way for humans to still be able to interpret that kind of data, and so clustering algorithms are absolutely important. We had to build our own because publicly available ones can only handle the 20 canonical amino acids that nature has. We've also been developing machine learning physicochemical property models, such as plasma protein binding, as well as solubility, to help identify peptides, again, with those more drug-like properties at the start, in addition to other peptides that we would normally be identifying. Where do we want to continue to move? Again, it's about reducing optimization cycle times. As we start to think about where our targets exist inside the body and how we are going to administer these, we really want to ensure our peptides are delivered in a stable way. We're really trying to move towards stability prediction models, where we can start to help reduce some of the optimization timelines and really drive more stable peptides at the start. And one of the most exciting areas, and this is an area where we will truly start to see and drive and follow the science as it goes, is how do we incorporate ideas like generative peptide design? We have massive libraries for every single target that we can move, especially as we start moving into 2025. Peptide space is already immediately amenable to large language model predictors. And so, the questions that we're starting to interrogate in 2025 and beyond is how can we use these types of models to not only allow us to identify and design peptides in chemical space that is new that we have not been able to sample from our selections, but also how do we funnel these types of generative models into more library-based design so we can build target-based models with future generation libraries that will be more tailored not only to the target, but also tailored to the application that we're moving forward. And so as you look towards what we are trying to do and some of the inspiration I saw while working with PDPS over the last 10 years, that true power is really how this platform differs from any other types of peptide discovery platforms. In most cases, you're identifying your peptides as hits in selections and moving to medicinal chemistry optimization to get you to the most important question, which is that in vivo efficacy and safety profile as you're trying to deliver candidates into the clinic, into patients. Where PDPS truly separates itself is the fact that not only have we started to move ourselves away from a hit-generating engine into more of a lead-like generating engine, but we also have the entire ability to optimize peptides on platform. This takes us away from looking at hundreds of peptides synthetically in order to drive our programs at a time to now looking at our peptides and optimizing them at the thousands, millions, and even possibly billions. And if you layer this in with some of the innovations that we've been employing in the last several years and into where we're moving in the future with automation, more drug-like amino acids, machine learning and AI technologies, and next-generation synthetic methods, this should enable us to really shorten the optimization timeline as well as reduce the number of cycles so that we can get ourselves to the key critical efficacy and safety questions to make the best decision for each of our programs and the portfolio moving forward.