Good morning, everyone, and welcome to the Adocia virtual Key Opinion Leader event on the phase III results for BC Lispro in type 2 diabetes. At this time, all attendees are in a listen-only mode, and a question-and-answer session will follow the formal presentations. To ask a question, please use the written Q&A text box at the bottom of the webcast player, and f or our sell-side analysts that are joining us live, we ask that you use the raise hand feature to indicate that you have a question. As a reminder, this call is being recorded, and a replay will be made available on the Adocia website following the conclusion of the event. Our first speaker today will be Steve Daly. With more than 30 years in pharma and biotech, he spent 20 of them in diabetes and metabolism across commercial, operational, and C-suite roles at companies including Amylin Pharmaceuticals and Adocia, where he spent six years as U.S. General Manager during the period of development of BC Lispro. Steve is now Chief Executive Officer at TIXiMED, a clinical stage company developing a first-in-class oral disease modifying therapy for type 1 diabetes. Steve, please go ahead. Thank you very much, Tara. I appreciate the introduction and thank you everyone for joining us today on this exciting day for Adocia. If we could just advance to the agenda slide. Thank you very much. In this hour, we have a lot to cover. I'm doing the opening remarks, and then we'll turn it over to Olivier Soula, the CEO and Co-Founder of Adocia, to give a little background around Adocia, the company itself. You Ping Chan, the R&D Director over at Adocia, will be covering some of the mechanics and details of the BioChaperone technology platform. Then, we'll turn the floor over to Dr. Tim Heise from Profil. Profil is a world-recognized expert center in understanding new therapies, particularly insulins in type 1 and type 2 diabetes. Tim is a well-recognized expert in the space, and I think you'll enjoy his talk and his thorough knowledge in the space. Tim will turn the floor back over to Olivier for a summary of the presentation and next steps for the company, and then we'll open the floor up for some questions from analysts and some questions that come in through the chat. Before we begin, I just wanted to say how excited I am to be here. As Tara mentioned at the kickoff, I was part of the formative work around BC Lispro in the six years in the late teens here, in the century. I've always had a focus on postprandial control and the importance of postprandial glucose in managing type 1 and type 2 diabetes, especially managing postprandial glucose safely. It was a real pleasure to work with the team on BC Lispro, and it's more of a pleasure to see how far it's come, and w e look forward to sharing these results with you today. Next slide, Tara, please. You've heard from me, and Tim Heise, as I mentioned, is a little more bio on Tim here in detail from the Profil Institute, where he leads a team that does exceptional work in understanding PK/PD and beyond in terms of new therapies for type 1 and type 2 diabetes. Olivier Soula, as I mentioned, is the CEO and Co-Founder. You Ping, who you'll be seeing in a few moments, is the R&D Director, and Martin Gaudier is the R&D Director, along with You Ping. Without further delay, why don't I turn the floor over directly to Olivier to take us through the rest of the agenda. Thank you, Steve, for your kind introduction. It was also a pleasure to work with you. I'm glad, ladies and gentlemen, to introduce you to Adocia, a French innovative company dedicated to peptide delivery. We have dedicated our time to diabetes and obesity, and most of it on insulin product. I'm glad to present you today more details about phase III results of our ultra-fast insulin. We, more recently, let's say, the last five years, focused on metabolic peptides. Everybody knows that these diabetes and obesity are pandemics, and they are both related to a peptide dysregulation. The most well-known of them is insulin, but now, everybody knows also GLP-1, amylin, GIP, glucagon. For all these peptides are inspired from normal physiology, t hat's why they are very powerful and very safe. Nevertheless, there is a delivery challenge for these compounds, and it's especially true for metabolic peptides today. There are two critical challenges. One is how to ensure the long-term use of these treatments. As you know, these are replacement therapies. As soon as they are stopped, we lose their effect. The second critical challenge is how to ensure a mass distribution of these obesity treatments. For both challenges, we know that probably around 20%-30% of the users are abandoning the trial-- oh, no, are on the trial, on the treatment, after two years. Only 20%-30%. And according to McKinsey, probably only 15 million- 20 million people are using these drugs, so t hat is not a significant portion of the eligible population. Until we answer to these two critical challenges, we will not deliver the positive health impact that we should expect. We will not close the gap between health span and lifespan. We are convinced that the answers are coming from the peptide delivery forms that we can propose. In fact, we can take the case of insulin. Insulin is a mature market after 100 years, but it took a while after multiple innovations to make it faster and faster, and that's the subject of the day. It's an ultra-fast insulin. It's the last class of mealtime insulin but also making longer and longer for basal insulin and combined fast and long profiles. Also, in parallel to that, how to treat 80 million people daily. That's the situation today. With both these innovations, with all these innovations, I mean, I mean that today, the use of insulin has delivered the positive health impact expected. The life expectancy is as close to the normal population, not suffering from insulin dependency, and health span also is very good. So, we should replicate, and in fact, it has been replicated for GLP-1 and amylin. Since the launch of the first GLP-1, all these products have been proposed with longer and longer release form of action or whole combination of peptides. That will continue with many more players because, of course, the market is much bigger than the insulin market. We intend, at Adocia, to be recognized and to be positioned as a leader to innovate in the space of delivery of these peptides. The next step for us is to reach commercialization with our product BioChaperone Lispro, based on these positive phase III results in type 1D and type 2D, and to leverage on this platform technology for obesity treating hormones because I repeat, these peptides have the same characteristics, the same constraints as an insulin product. There's a real opportunity for us, and our vision is to become a profitable leader in this space of delivery of metabolic hormones, and at some point, when our cash position will be sufficient to develop our own product. This has been developed with the expertise of a team with technology that are relevant, as I said, not only for insulin, but for these peptides of the metabolisms. I leave the floor to You Ping to present you this platform, BioChaperone. Next slide. Okay. Good morning, everybody. I will introduce our BioChaperone technology platform. Next slide. Thank you. Over the past 20 years, we have developed more than 800 BioChaperone compounds for the formulation of peptides and proteins. This number reflects multiple generations of innovation with a continuous structure property optimization to address specific formulation challenges. The compounds are patent protected and have been assessed in over 30 clinical trials from phase I to phase III. Within this portfolio, two advanced BioChaperone excipients are highlighted in the table. The first one, BC 449, was developed to stabilize proteins and peptides and to support the co-formulation of otherwise incompatible peptides. BC 449 has already been tested in three clinical studies and is now produced at large scale with a CMC and safety package that can support development up to phase III. One example is the co-formulation of semaglutide and cagrilintide for diabetes and obesity treatment. I'll come back to this case in a moment. BC 449 addresses a strategic need that has recently emerged, and it is a versatile excipient that can be used for various peptide combinations. To date, we have two feasibility studies with major pharmaceutical companies that have yielded positive results, and a third one is currently underway. The second excipient, BC 222, has been engineered to accelerate insulin absorption. BC 222 has been evaluated in more than 10 clinical studies in combination with insulin lispro, which is the subject of today's event. Commercial scale manufacture is in place, and the BC Lispro product is now ready for NDA submission. Both the BioChaperone polymers have been shown to be safe and well-tolerated in humans across multiple clinical studies. Next slide, please. This is a brief summary of the mode of action of BC 449 for peptide stabilization. BC 449 is an amphiphilic polymer that spontaneously associates with the peptide to form reversible complexes. These complexes represented on the right protect the peptide or protein at the molecular level, ensuring both physical and chemical stability during storage and use. Practically, this means that individual peptides can be stabilized when needed, and importantly, that this technology enables peptide combinations that would otherwise be incompatible, as already demonstrated for several co-formulations developed within this platform at Adocia. Next slide, please. In summary, the technology makes it possible to obtain stable, ready-to-use aqueous solutions, and when required, these formulations can be combined with preservatives for multiple use presentations in injection pen or vial. One current application of BC 449 is the co-formulation of semaglutide and cagrilintide, as shown on this slide. The fixed dose combination is being developed by Novo Nordisk. The product name, CagriSema, could be approved by year-end. Because of the underlying chemical and physical incompatibilities between the two components, Novo is planning to commercialize the product in a dual-chamber device and a dministered as a single dose only, meaning one pen for every injection. In our hands, with BC 449, we have been able to obtain a stable co-formulation that is compatible with preservatives and therefore can support at least four fixed doses in a single pen. The key advantages are reduced manufacturing cost, improved production capacity, and also to have a multiple dose pen that could also enable flexible dosing if, for example, the formulation is filled into an insulin-type pen, meaning that we can control the doses adapted to each patient. Next slide, please. In the case of BC Lispro, the formulation contains insulin lispro, BC 222 citrate together with common excipients, metacresol as a preservative, and zinc to maintain the insulin in its hexameric form, as illustrated on the left of the figure. Most commercial insulins are formulated as hexamers to ensure long-term stability in solution, but f or fast absorption, they have to dissociate into monomers. Only the monomers will cross the vascular blood barrier. Insulin lispro itself was designed to dissociate more rapidly than human insulin, and therefore to be absorbed more quickly after injection. For BC Lispro, once administered in the subcutaneous tissue, now we move to the right of the figure, the hexamers will dissociate more rapidly into monomers, and remarkably, the BC 222 excipient also promotes faster diffusion of the monomer across the vascular blood barrier. To conclude, the key messages are, first, insulin needs to be in its hexameric form for stability, but only the monomer is active. The unique properties of BC 222 are to dissociate faster the insulin hexamer to promote its rapid absorption into the bloodstream. The result of this mechanism, as Dr. Tim will show in a moment, is a faster pharmacokinetic profile of the insulin lispro compared to conventional rapid-acting formulations. Thank you for listening. I will now hand over to Dr. Tim Heise. Thank you, Dr. Chan. It's a pleasure being here and to present on current mealtime insulin treatment paradigm for diabetes and limitations. These are my disclosures, and I should also mention that I have been doing studies together with Adocia, as you will see in the course of my presentation. Before we move into the data, we thought it might be a good idea to give a short introduction into diabetes, its form of treatments, and limitations. I know that many of you are very familiar with that, but some might not, and it's very important to get the basis for understanding the data. Let's start with type 1 diabetes. Type 1 diabetes has nothing to do with type 2 diabetes, which everybody knows. Type 1 diabetes is an autoimmune disease. It is not caused by nutrition or obesity or anything. It really is an autoimmune disease and an autoimmune destruction of beta cells, and that is reflected in the picture over there, histological pictures of the beta cells. You know that in the islets of Langerhans, there are glucagon-producing cells, here in this purple. There are insulin-producing cells in yellow, and i f you look at the left panel, in a usual and normal islet of Langerhans, there are the yellow insulin-producing cells and the glucagon-producing cells. If you move to the right, then you see that people with type 1 diabetes still have glucagon-producing cells, but they don't have any insulin-producing cells left. This is what happens with this disease. Usually, it's a rapid onset of symptoms and then also a rapid progression to a complete loss of endogenous insulin secretion. These people don't have any insulin left within months after onset of disease. Usually, it may vary, but many people really lose all insulin secretion within a few weeks or months. The disease usually occurs in the childhood or early teen years. That's why in former times it was also called juvenile diabetes. Peak ages are four to seven years and 10- 14 years. It can, however, occur also at later age, even in the very old, but this is rare. There are, of course, many attempts to cure type 1 diabetes, but this is difficult because we don't know the causes exactly. We know that causes include genetics. There are a collection of genes, but it's not a single gene. It's many genes that might contribute, and they don't explain everything. Genetics certainly contribute. We know that environmental factors play a role, climate and geography. It's well known that in the Scandinavian countries, for instance, the incidence of type 1 diabetes is higher than anywhere else in the world, but we don't know exactly why. Usually, the disease is triggered by viral infections. It could be all kinds of viral infections. COVID has been discussed. It's not quite clear, but it could just be a common cold or other viral infections that basically then lead to the onset of type 1 diabetes. It is not a very common disease, but it doesn't count as rare disease either. There are some estimates from the Breakthrough Type 1 Diabetes, which formerly was called JDRF. In the U.S., they try to simulate the current prevalence of type 1 diabetes and came up with a pretty low number of close to 10 million people living with type 1 diabetes worldwide. This number has been challenged. Other people think more of 30 million or 40 million people, so this is a very conservative estimate, but y ou see, there are a couple of million people living with type 1 diabetes, but when we progress to type 2 diabetes, type 1 is certainly a minority. It's also quite interesting if you look at the simulation, the blue curve on the right-hand side, that the incidence of type 1 diabetes is rising, and we don't know exactly why. The simulator basically projected that there are about, right now, 4.1 million premature deaths due to type 1 diabetes right now, and t here are 30 years of healthy life lost on average per person with type 1 diabetes. It is a pretty dramatic disease. Although it's treatable, the challenge is that people have to achieve very good glycemic control to prevent microvascular complications, so complications at the kidneys, at the eyes, at the feet, but also macrovascular complications like stroke or myocardial infarction. What is the treatment paradigm? This is easy, of course. If you lose all your insulin, you need to replace this and fortunately, this has been possible since more than 100 years now. In 1922, the first patient was treated with insulin therapy. Insulin was isolated at the end of 1921, then progressed to treatment in 1922, and then there were larger scale manufacturing of animal insulin preparations starting in 1923. These insulin formulations were much different to what we have right now, so l et's say they contained a bit of insulin, but many other things that you didn't want to have, so i t was not a very pure insulin, but it was lifesaving. People complained about having to inject so often, so p eople at that time had to inject four or five times a day. There were lots of research ongoing how you can recharge or prolong the action of insulin, and that has been possible since 1936 and the 1940s, when protamine retarded insulin and the so-called neutral protamine Hagedorn insulin, which is still on the market, became available. There hasn't been a lot of progress for short-acting insulin, and this took quite a while and only the discovery in insulin sequence and insulin structure then made it possible in 1977 to produce human insulin recombinantly, and that also opened the door for producing analogs, so i nsulin formulations that are more rapidly acting, have a shorter duration of action. Finally, in 1996, the first short-acting insulin analogs, lispro and aspart, came to the market. Also, for a while, the focus was more on basal insulin analogs, and many of you will know that we now have several basal analogs on the market. It took till 2018 that the rapid-acting analog, short-acting analogs have been further refined for two ultra-rapid insulin analogs, and that already indicates that people were not happy with the rather slow onset, and the rather long duration of action of human insulin and the first-generation rapid-acting analogs. What we try to achieve with insulin therapy is to mimic the insulin secretion of healthy people. If you look into that, you can basically divide, these are the insulin levels in healthy people, and y ou see that immediately after each meal, breakfast, lunch, and dinner, there is a very rapid rise in insulin formulations then, and then a very or reasonably fast decline to near baseline levels after the meal within four hours or a bit more. This is something we would try to replicate with rapid-acting or ultra rapid-acting insulins. Then, there also is a basal insulin secretion, so r egardless if you eat or not, you always need a little bit of insulin, and this is pretty constant over the day, here visualized in yellow. This should be replaced with a basal insulin. The idea that came up in the 1990s, that you should have basically a basal insulin supplementation. Then, add prandial insulin, usually four to five injections per day, depending if you needed to inject basal insulin once or twice daily. Y ou needed to supplement prandial insulin and still do three times a day or for every meal you take in. You can also see it's pretty hard to get this rapid onset of action. This is something that people have been complaining about, even with modern insulins or insulin pumps. If you look at the treatment guidelines from the American Diabetes Association or the European Association, you can see that what they really recommend is what they call MDI, multiple daily injections, with long-acting analogs and rapid or ultra-rapid analogs in the first line. You see this gives you lots of flexibility, a lower risk of low blood glucose levels, hypoglycemia. It comes at a higher cost though, but t his is what people really need. The alternative nowadays, at least in modern countries, is given in the second box. Insulin pumps or what we call the hybrid closed-loop technology, where you basically couple the pumps to glucose sensors and the pumps react to glucose changes so that patients don't have to adjust pump infusion rates all the time. They still need to announce meals and exercise because the insulins that are available don't react fast enough. That has been one of the major limitations throughout the years. If you look over at this graph, that's a study we did quite some time ago where we compared the rapid-acting analog insulin aspart in green with regular human insulin in red and looked into the time-action profile. You see, particularly at higher doses, so here we chose 24 units, so the straight lines, you see that the duration of action for regular human insulin is about 9-10 hours. It is shorter with insulin aspart, but it's still seven or eight hours at this dose level. You can also see that the maximum of aspart is beyond two hours, so that's far slower than physiological insulin secretion. All key opinion leaders agree that faster prandial rapid insulin are needed, and they really look into what has been available, and these are data that we generated a couple of years ago in people with type 1 diabetes using insulin pumps. If you look at the BC Lispro curve at the left-hand panel, you basically see this is a faster onset and a shorter duration of action versus aspart in gray, but also faster and shorter than the faster-acting insulin aspart, so an ultra-rapid insulin. On the right-hand panel, zooming in on the first two hours, you can see that even better. The onset of action is faster with BC Lispro, and that should enable people to achieve better glycemic control, particularly after meals. I should also say that this is not the only study that we did. Nine studies were done with BC Lispro, and they all confirm that BC Lispro has an ultra-rapid onset and a short duration of action versus available rapid-acting or ultra-rapid insulins. Let's move to type 2 diabetes. Type 2 diabetes is a completely different disease to type 1 diabetes. It is caused by insulin resistance, usually triggered by obesity. Usually, obese people are in danger of being insulin resistance. They need more of their endogenous insulin to cover for this insulin resistance, so their own insulin doesn't work as well as it should be. To compensate for that, the beta cell increases the insulin production. After a while, their beta cell function can't cope with the rising demand of increased insulin resistance, and therefore, as you can see in the black line, the beta cell function starts to decline, and it takes quite a while. You can measure that with rising, fasting, and most importantly, postprandial glucose levels. When you reach type 2 diabetes, then there are basically calculations that tell you that about 50% of the maximum beta cell function is already lost. If there is no treatment, then postprandial and fasting glucose concentrations will occur to rise. Beta cell function will occur to decline, so i t's important to understand that type 2 diabetes is a progressive disease, and most people at the very end of their disease career will be more like type 1 people because then beta cell function will be nearly zero, and that means that despite all the treatments we have, that many people with type 2 diabetes eventually will need insulin treatment. That has been also reflected in treatment guidelines. Type 2 diabetes is a very common disease. These are data from the IDF Diabetes Atlas. As Dr. Soula mentioned, there are about 590 million adults living with diabetes. This includes the type 1, but as I said, type 1 is about 10 million- 40 million, so the vast, vast majority of all people with diabetes are type 2. This is going to rise to perhaps 850 million by 2050. Every eighth person living worldwide will probably suffer from type 2 diabetes. Type 2 diabetes is a deadly disease because of its progressive nature, so if it's not well-treated, there is a high risk of particularly macrovascular complications, myocardial infarction, stroke, leading to death. Good treatment is needed, and you will see that the ADA and EASD treatment guidelines have very sophisticated treatment algorithms. You usually don't start with insulin. You usually start with oral agents. Then, the GLP-1 or SGLT2 inhibitors are very important because they have been shown cardiovascular benefits. As you can see, or it's very difficult to see, but on the left-hand side, you see efficacy for glucose lowering, very high. There, insulin is listed. Insulin basically is the only drug that can be dosed up to indefinitely, so it's really dosed according to the effect. If people are needing very high doses, they will just get very high doses of insulin. As you can see on the right-hand side, eventually, w ell, you start with basal insulin preparations, eventually, people will also need prandial insulin preparations, either in a mixture with basal or alone. These days, we discuss GLP-1s very frequently, and they are wonderful drugs, but we shouldn't forget that because of the progressive nature of type 2 diabetes, we will need insulin in these people. That's why it is so important to get better insulins for type 1, but also for type 2 diabetes. I'm happy to share some data that we just presented last week at the American Diabetes meeting in New Orleans. This was a study in Chinese people with type 2 diabetes, investigating BC Lispro. I won't go through the mechanism of action; Dr. Chan did that very elegantly. The study was done, was a comparison of BioChaperone Lispro versus mealtime insulin lispro in combination with basal insulin glargine and was done in Chinese people with type 2 diabetes. You will see it is a treat to target open trial multicenter done in China. This slide gives you the study design. We included people with type 2 diabetes that were already treated with insulin, either with basal insulin and prandial insulin or on a premix insulin. They had to be pretty poorly controlled. The HbA1c, our marker of glycemic control, ideally, it should be below 7.5, seven, or even lower, b ut here, people were included if they had a baseline HbA1c between 6%, 7%, and 11%. The primary endpoint were changes in HbA1c and also postprandial glucose excursions. At the bottom, you see how the study was done. After screening, people entered an eight-week lead-in period, and that's pretty important because if you want to give good insulins or good prandial insulin treatment relies on having good basal insulin treatment. The idea behind these eight weeks was to optimize the basal insulin, the insulin glargine. In these eight weeks, all people used insulin lispro as prandial insulin, and those who were on metformin already, kept metformin and the other oral agents then were stopped. People were randomized 3:2, so basically, there were 50% more people randomized to BC Lispro than to insulin lispro, and that is to expose more people to the investigational drug. It is a very common randomization scheme. We basically compared BC Lispro in combination with glargine and perhaps metformin, or in the other arm, lispro, glargine, and metformin over 26 weeks. In these 26 weeks, the glargine dose was kept more or less constant unless changes were absolutely necessary. Basically, the prandial insulin, the BC Lispro and lispro were adjusted. The baseline characteristics are given here and so you see, a ltogether, there were more than 600 people on BC Lispro, more than 400 people on lispro, so more than 1,000 people included in this study. You can also see if you look at the BMI, that was close to 26, which is low for European or U.S. standards, but in an Asian population like in China, this fulfills the criteria of overweight and obesity. You can also see that people had very long diabetes for almost 14 years, and at randomization had a HbA1c of 7.7%, so not optimally controlled. If you look at the HbA1c levels in the course of the study, you can see that at baseline, they started even higher, above 8.5%, but due to the optimization of insulin glargine in the eight weeks lead-in period, they improved similarly in both arms to 7.7%, and then further improved when BC Lispro and lispro were added. Basically, at the end of the study, were very similar, so BC Lispro in green, slightly lower, not statistically significant, but non-inferiority was confirmed. What is striking is that there were important subpopulations that reached superiority. People using metformin, about 400 people that used metformin basically had a better outcome with BC Lispro than with lispro, a difference of 0.16% at end of treatment, and that was statistically significant. Similarly, people who had a pretty good, or at least reasonable HbA1c, so below 8.5% at randomization, they also benefited from BC Lispro and had significant improvement, so 0.13%, and that, again, was significant for superiority. This was confirmed by a mixed meal tolerance test that was included in the study. You see that overall, after a test meal, that was a liquid test meal, there were lower postprandial glucose excursions with BC Lispro, about 1 mmol per maximum, so 16-18 mg/dL, and that was statistically significant. That again was confirmed by the self-measured blood glucose profiles. If you look at the profiles here at end of treatment, you see that the BC Lispro arm was always lower over the day. On average, the glucose reduction was 0.44 mmol/L, so close to 0.5 mmol or 9 mg/dL. You can also see that as expected, particularly after the meals, all postprandial values one or two hours after breakfast, lunch, and dinner were significant with the exception of the two-hour post breakfast, which was lower, but not statistically significant. That really confirms the faster onset, and the better postprandial glucose control. Safety, very brief, because there were no differences in the Treatment-Emergent Adverse Events, TEAEs, i njection site reactions, very important in ultra-rapid insulin because [audio distortion], for instance, hasn't been widely used in pumps because people complained about injection site pain. You see that was really very low, five versus two events, so very well-tolerated at the injection site. With regard to low blood glucose levels, hypoglycemia, no difference overall and nocturnal. No differences for level 1, so below 70 mg/dL. No difference in level 2, below 54 mg/dL, and very rare, serious hypoglycemia where people need third-party help. Also postprandially, not a real difference overall over four hours, no difference between two and four hours, but due to the faster onset of action and the better postprandial control, there were slightly more hypoglycemic events within two hours postprandially, but numbers were pretty low. Overall, to sum up, this study with 1,040 Chinese people with type 2 diabetes showed superior HbA1c improvements in people using metformin or with HbA1c below 8.5%. I didn't show it, but more people reached the HbA1c target below 7%, and overall, in the whole population, non-inferiority was achieved. Superior blood glucose control was shown throughout the day, the mean blood glucose control in SMBG and also after each meal with similar safety and tolerability. It was a very pleasant surprise that at ADA, the principal investigator of this study, Professor Li from Shanghai, was able to join us. He was very impressed by the data, and I think it is a great study, and I look forward to discussing that with you a bit later. For now, I just hand over again to Dr. Soula. Thank you, Tim, for this clear presentation and how it is difficult to improve the insulin delivery and how it was pretty cool over 100 years to make it faster and faster. We got with this phase III results very interesting data in type 2D, but also in type 1D that I hope we will be able to present in next conference. About the collaboration with our partner, Tonghua Dongbao, which is a Chinese leader in insulin field with 80% of its revenue on insulin. The next step now is to file our market authorization dossier and we are actively supporting them, but they are under their control. Associated to the first marketing approval, we are intended to receive a $20 million milestone plus double-digit royalties on sales. As you may know, we have also retained the rights for licensing BioChaperone outside the Tonghua Dongbao territories, and for that, there are two cases. The countries that are recognizing the approval in China and which would allow to commercialize the product on their territories with this Chinese dossier. The countries of Middle East and LATAM are generally following the Chinese regulatory authorities. We are already discussing about that with some potential commercial partners but of course, the submission of this dossier will be a critical step to progress. The other case is, of course, Europe and U.S., and these markets, they would require a new phase III program, and that is, of course, a significant expense, and we intend to have a partner, financial at least, but also maybe industrial partner for conducting such studies. That's the case for commercialization of the product and to have additional revenues, additional to the revenues of Tonghua Dongbao. There are also other potential applications of BioChaperone Lispro U100 that has been tested in phase III in pen, as presented my team. There is obviously the application of U100 in pump, and that is not today a very strong market in China, but whereas it's a strong use in Europe and in U.S., and for that, we would require probably pivotal phase III trial in type 1D and eventually in type 2D, even if this population is not so concerned by the use of the pump. The other opportunity with this product is to develop a U200 form, which is twice concentrated compared to the U100 that has been presented, and that could be used also in pump and in pen. This product, BC Lispro U200, has been demonstrated to be bioequivalent to the U100 in a clinical study conducted with Eli Lilly in the past. We have here a straightforward development with just a bioequivalent study and eventually a pivotal phase III, again in pump. Just a bioequivalent study in pen would be sufficient to make it approved. That is, of course, a subject to THDB decision choice or signing a partnership with eventually a partner on these other applications. I'm glad to give the floor back to Tara, and thank you all for these presentations. Great. Thank you, Olivier. Yes, at this time, we'll be conducting a question-and-answer session with our speakers, so please hold for a brief moment while we pull for questions. Our first question comes from Clemence Thiers at Stifel. Please go ahead, Clemence. Hi. Thank you everyone for the presentation. Very interesting. If I can start maybe on the clinical trials, just two question. Regarding the superiority that we saw on the metformin and certain HbA1c patient, is there anything that we can conclude based on that? Should we see some sort of narrowing of the population because those would be the primary target, or does it open new avenues? Yeah, perhaps I can take that. Basically, I think it's a nice confirmation of what we know. There are lots of simulations and that basically prandial insulins in type 2 diabetes matter most in those who are well-controlled, and I think that is confirmed here. Those who had a better baseline HbA1c, and probably the people on metformin also had a better baseline HbA1c, will benefit most, so that the impact on HbA1c of prandial insulins is most pronounced in these people. That doesn't mean that you shouldn't treat the others, but in them, a good basal insulin is even more important than a good prandial insulin. In a way, it's a really nice confirmation and something that hasn't been shown before. With all the other ultra rapid insulins, there were no real changes in HbA1c to first generation analogs. I think that is also a nice confirmation of the faster onset and shorter duration of action. I wouldn't really position this differently. Overall, people needing insulins, type 2 or type 1, should get the best insulin formulations available, and certainly BC Lispro is better even than Lyumjev or Fiasp. Okay. Thank you. Thank you very much. It's clear. Maybe just a second one on the early post-meal hypoglycemia that we observed due to the faster pharmacokinetics. Is that something that can be mitigated by titration or anything? Is that really an area of concern, or it just what it is based on the pharmacokinetics with that not so much of an impact, I'd say? In general, that's, of course, one of the downsides of all insulins, that if you intensify insulin therapy, you also increase the risk of hypoglycemia. I wouldn't see it as a concern here. Our numbers were low. You need to keep in mind that here, hypoglycemia means all kinds of hypoglycemia. Most of these were level 2 hypoglycemia, so below 70 mg/dL. The rates were really, really low, but o f course, people should be aware that if you intensify, you might have a slightly higher risk of postprandial hypoglycemia, so they should pay attention in the first two hours, particularly. In modern countries, most people, even with type 2 diabetes on insulin, are on continuous glucose monitoring, so they will pick it up very quickly. Others, of course, have to be a bit careful, but I don't see it as a concern. Okay. Thank you. If I may, just one last and t hen I'll jump back in the queue and let the other ask the question. More generally, now that you've disclosed the data in more details, you went to Congress, what level of enthusiasm did you feel from physicians there and even outside of China, obviously in markets where ultra-rapid insulins are available? What was the level of enthusiasm? I think there is excitement, particularly in people working on closed loop systems and also certainly more in Asian market than in the European market. The overall attention, as I said, right now is in the diabetes world, is really focused on incretins. Insulins have been put a bit aside. I'm pretty sure that this is going to change. Professor Li, for instance, was very interested in China, premix or multiple daily injections are widely used. I'm sure once we realize that incretins are wonderful drugs but do not provide the overall solutions, there will be even more attention on prandial insulins. All right. Thank you very much for your answers. Great. Thank you, Clemence. That looks like that is it for analyst questions. Steve, I'll turn it back to you for questions that came over the webcast. Great. Thank you, Tara, and thank you, Tim. Tim, I always learn something in your presentation, so thank you for that thorough review. We appreciate it. There are a couple of questions in the chat. One, I think is a logical flow from the question we just had, and I know the answer might be a little nuanced. Tim, another one for you, if you don't mind. How does your ultra-rapid insulin compare with Fiasp and Lyumjev, which are the two ultra-rapids marketed by Novo Nordisk and Eli Lilly, respectively? Tim, maybe I'll turn it over to you to comment on that question. Yeah, certainly. This, of course, is the question that everybody asks. Can we improve further? The answer is yes. I showed you the data. We know that Fiasp and Lyumjev have a very similar time action profile. There are no differences. Basically, the proof that BC Lispro is faster than Fiasp also implies that it is faster than Lyumjev. Indirectly, this is also confirmed with the results of the clinical studies. If you look at the phase III data of both Fiasp and Lyumjev, they showed improved postprandial control. They showed non-inferior HbA1c. They have not shown any improvements, not even in subpopulations in HbA1c. This difference that was observed here in people using metformin and in people with lower baseline HbA1c is something which is new, hasn't been shown before, and shows the unique properties of BC Lispro. That in combination with the safety data, I mentioned that Lyumjev, many people were very excited about Lyumjev, and when they used it, particularly in pumps, they experienced injection site reactions and injection site pain and then switched back to other insulins. Even on Fiasp, there are many users complaining that it doesn't work as fast as it should be. Right now, the ultra-rapid insulins are used, perhaps not as widely as they could. BC Lispro could change that, I'm sure at least it is superior to both the currently available ultra-rapid insulins. Thank you, Tim. There's another question here that's come up a couple of times. Tim, you talked about type 1 in your presentation and also mentioned closed loop a couple of times. Maybe this is a question for the R&D team at Adocia. What about the results of BC Lispro in type 1? Maybe Martin? Yeah. I will take this question. It is our partner, Tonghua Dongbao, that run the clinical trial. Because of the specifics of the Chinese market, they have focused more on the type 2 versus type 1. The type 2 study was bigger, started earlier, and finished earlier. That's why we started by talking about the type 2 result. That said, we have the type 1 results, and w e shared the top line in a press release in October 2025. What we said, and that's still valid, is that the results are very similar from the type 2 to the type 1 in terms of size of effect. What we see is that we have the non-inferiority in HbA1c. We also have the very nice postprandial glycemic control as shown in the SMBG, so self-monitored blood glucose with reduction after each meal, and t hat's something that's very difficult to achieve. We also have the good safety, no difference in terms of safety when compared to Humalog. Basically, those results are the same. We intend to publish them at a further conference. That's why we also have an embargo on those data for the moment. We'll give all the details at a later time. Thank you, Martin. Maybe time for one more question. Tim, maybe this one is another one for you. What has been the trend and evolution in the methodology of insulin delivery in China? Is it still a fixed mix market? Is it moving more towards basal bolus? I know we don't have much time. Why don't I just turn over to you for a quick response? Yeah, I think it's still a very much premix market as far as I know, but i t is changing, so it's more changing to MDI, and I'm sure eventually, it will also change to pumps and hybrid closed-loop. It just may take some time. Premix, I think right now is dominating, but I'm sure, an ultra-rapid insulin will be important in the Chinese market more and more. Thank you, Tim. We're almost out of time, so why don't I turn it back over to Olivier for any closing thoughts? Thank you. Thank you, Steve. Yes, I think you have appreciated how difficult this disease is and the treatment of insulin is. That's why still after 100 years, we are still trying to improve the PK profiles, and this is clearly incremental innovations and every detail count. I would like to thank our Chinese partner for the industrialization, because first, you need to have a product with a very good cost of goods, and the performance, of course, is critical, and thank you for the very nice phase III results. We now intend to apply this platform, BioChaperone, to key hormones for the treatment of diabetes and obesity, and that is our ambition to become a leader in this space, very well connected to the insulin space. Our first priority right now is to get this product approved in China and to continue. And you know what? On insulin, if you observe over 100 years, it's quite a slow market, but a very sustainable market because as Tim really well explained, you cannot really replace insulin soon. We are very proud of these results. I would like to thank you all for your participation and your interest for the company. Thank you.