Good morning, good afternoon. I am Emmanuel Dulac, CEO of Zealand Pharma, and on behalf of the entire organization, I am glad to welcome you to Zealand Pharma R&D Day. As 2020 monopolized all attention on operations, we are excited today to share the leap we have made in our R&D platform as well as R&D projects. 2021 promised to be a special year for Zealand Pharma, as we are planning to build and to turn into a highly performing commercial organization while remaining a strong R&D-driven organization. So, without waiting, I'm going to cover the agenda for today. Right after me, Adam Steensberg, Head of R&D, will cover with you the R&D strategy going forward. David Kendall, Head of Medical Affairs, will zoom in the metabolic portfolio. Steven Russell, Associate Professor of Medicine at Harvard Medical School, will walk you through in detail on the dasiglucagon bi-hormonal pump program.
After that, Adam Steensberg will come back to cover in detail the gastrointestinal portfolio. And Rie Schultz Hansen, our Head of Discovery and Innovation, will walk you through the improvements we're making on our R&D platform, as well as some of the progress we've made on early research programs. Finally, Adam and I will come back to wrap it up on the corporate strategy, corporate vision, as well as the R&D ambitions. I want to remind you that during this presentation, we will be making forward-looking statements which are only engaging the management of the company and are subject to change. Now, 2020 has been a turbulent year for the society, and while the crisis is not behind us, I think we've spoken enough about it. So now, let's look ahead and plan for going back to normal.
At Zealand Pharma, we are already exploring what changes to keep and what changes to roll back. For example, we've all benefited from an improvement in productivity by cutting on long commutes, by adding flex work and flex time for employees. We've actually adopted and gained a lot of maturity on digital tools such as telemedicine, trial management, or tools which are helping us to remotely engage with customers and/or manage patients. But what really excites me is that not only has Zealand Pharma weathered through a storm, but at the same time, we have the great fundamentals to execute going forward. We have a clear vision. We have a strategy which is embraced by all our employees. We have a rich and well-balanced pipeline. We have an organization with strong values, and we have healthy finances to help us carry us through our ambitions.
Let's look at what 2021 has for us. In January, we successfully executed on the largest capital raise of the company's history, providing us a solid foundation to pursue exciting opportunities. Right around the corner, we have the PDUFA date for the HypoPal dasiglucagon rescue pen, which we are expecting to be a major event for the company, not only because it's the first approval of the company, but as well it will be the first launch. We need to turn our organization, which is creating new challenges, into a high-performing commercial organization. And to that effect, we've invested a lot of time and resources in the past year to build our U.S. capabilities. Today, I'm excited to disclose to you that we have the team to execute on this launch.
2021 is also a very important year for us in terms of activities on the pipeline, as well as milestones in the clinical development pipeline. In a minute, Adam, David, and Rie will come and present to you in more detail these progresses. My vision for 2025 is clear. We need to become a fully integrated biotech company to leverage the full potential of our products in order to benefit our patients and our investors. With the acquisition of V-Go, the potential launch of dasiglucagon HypoPal rescue pen, and the highly advanced late-stage pipeline, we have made a significant step in the ambition of having five commercialized products by 2025. It's a bold vision.
To get there, not only do we need to build an outstanding commercial organization, but we also need to pursue our R&D efforts, keep investing in our platform, and keep advancing our programs for clinical development. We are animated at Zealand Pharma by addressing the challenges and the unmet medical needs of the patients in metabolic and gastrointestinal disease, and we have a moral obligation to all the patients and families joining our clinical studies. With that, let's introduce now Adam Steensberg so that we can carry through the rest of the presentation and talk about the R&D strategy. Thank you very much.
A warm welcome to this Zealand Pharma Research and Development Day. My name is Adam Steensberg. I'm the Chief Medical Officer and Head of Research and Development at Zealand Pharma. I'm truly excited about the opportunity to share the recent progress in our pipeline and in our peptide platform, and also to set direction for the five-year ambition for R&D at Zealand Pharma today. I'm joined by my two good colleagues, Rie Schultz Hansen, who's heading up research and early innovation, and David Kendall, who's our Head of Medical Affairs. This is a very unique moment in Zealand's history. We are approaching our first potential launch of a medicine that has been discovered and fully developed by our team, and at the same time, our product pipeline has never been stronger, and we have a very robust peptide platform.
So for more than 20 years, Zealand has been pioneering the engineering of novel peptide drugs that meet the needs of the patients. Lixisenatide was one of our first inventions. It's a GLP-1 molecule for the treatment of type 2 diabetes. And today, this molecule is marketed globally by Sanofi. Since then, we have continued to pioneer the engineering of novel peptide drugs and taken more than 10 molecules into the clinic, and we have many more in the late preclinical phase. We have several sources of inspiration and use a variety of techniques to achieve the biological effects and other attributes that we want to build into our peptides. And before we get further into the presentations today, I would like to share a short video about what makes us Zealand.
Zealand Pharma's peptide platform. For more than 20 years, our sole focus here at Zealand has been to discover and develop innovative peptide-based medicines. We enhance the effect of native peptides to provide better treatments for people struggling with metabolic and gastrointestinal diseases like severe hypoglycemia, congenital hyperinsulinism, diabetes, and short bowel syndrome. But we're getting ahead of ourselves because what are peptides? Peptides are naturally occurring biological molecules that are produced by all living organisms. Humans, for example, have peptides in every single cell and tissue. The great thing about peptides is that they can function as biological messengers, carrying information between cells or organs, and thereby perform a wide range of essential functions, like regulating appetite and blood glucose and stimulating tissue growth. This makes peptides vital to keeping us functioning and healthy, and it makes them a great starting point for creating highly effective medicines.
Peptides are, however, unstable by nature and vanish after a very short time in the bloodstream. Therefore, to capture their medical effects, peptide analogues must be designed, which is a highly complex task. At Zealand, we have extensive know-how of designing and engineering superior peptide drugs. And since our foundation, we have advanced more than 10 novel peptide analogues into clinical development. Combining this experience with advanced computer modeling has enhanced our innovative capabilities even further in recent years. We are passionate about transforming patients' lives through peptide innovation and novel treatment solutions, and our unique research and development platform enables us to design and engineer peptide analogues with enhanced biological activity, extended duration of action, and increased stability. In other words, we use nature's own inventions to improve human health and quality of life. This is what makes us Zealand.
As you can see, we have broadened our innovation space in recent years beyond endogenous peptides such as GLP-1, GLP-2 , and glucagon, so we now get our source of inspiration from a variety of sources such as toxins, phage display, and in silico design. This allows us to focus on disease targets that are otherwise difficult to reach by other modalities such as antibodies or small molecules, and it really sets us in a situation where we're uniquely positioned to excel our innovation and discovery and be much more productive in the future. We are more than 190 people working in R&D focused on delivering on our commitment to patients. I'm really proud to share that we still have one of our founders, Bjarne Due Larsen, with us, who, by the way, is a brilliant peptide chemist.
It's the experience of people like Bjarne and the many talents that have joined us over the years that makes Zealand unique. I personally believe that our success comes from the fact that we always focus at what we are best at, making peptides into drugs that meet the needs of patients. We have seen a significant evolution in our pipeline over the recent years, and we have a strong commitment to continue to deliver. As we are approaching our first potential launch, we have a number of phase two and three programs. And today, you will also learn much more about the early programs that we are approaching as the next value drivers in research and development. For the year, we have three focus areas. Number one is to deliver on the late-stage assets. Number two is to progress the next value drivers towards the clinic.
Number three is to increase our investments in our peptide platform. By focusing on these three pillars, we believe that we will not only secure a strong pipeline progress over the year, but also secure Zealand's ambitions of building a long-term high-value pipeline. Our ambition is to continue to drive innovation and establish a next-generation peptide therapeutic platform and a high-value product pipeline. With this, we'll continue to expand our leadership in the peptide drug discovery and development by enhanced use of novel technologies, of which we have already started to implement some, which you should learn much more about later today. In order to secure the long-term value creation of Zealand Pharma as we establish our commercial footprint in the U.S. with the potential for five products marketed in 2025, we will also expand the therapeutic focus in R&D.
In the metabolic area, we'll expand towards obesity and associated metabolic diseases. And in GI, we'll expand towards IBD and other chronic inflammatory diseases. And with that, I hope that you will enjoy the next set of presentations, which will give you a much deeper understanding of what we are doing in R&D and our ambition for the company in the next five years. Thank you.
My name is David Kendall, Head of Medical Affairs. Zealand started its history in the metabolic space with the discovery of lixisenatide, a GLP-1 receptor agonist co-developed with and commercialized by Sanofi. This therapeutic area is part of the company's DNA and, as such, one of the main areas of focus for our research and development activities.
In the near future, we're aiming to address a spectrum of hypoglycemic conditions based on our dasiglucagon platform, starting with the approval and launch of our HypoPal rescue pen in the United States. In the medium term, we're working with our partner, Beta Bionics, to make the bi-hormonal bionic pump a reality for people with type 1 diabetes. And in the long term, we expect to advance the development of peptide design and formulations to target obesity. Amylin is a particularly attractive candidate, which we plan to move towards phase one later this year. When one thinks about hypoglycemia, insulin treatment immediately comes to mind, as it is the most common side effect of insulin therapy and one of the most dreaded conditions for people with diabetes.
But while iatrogenic hypoglycemia is the most common manifestation of low blood glucose events, there are other, less known conditions that can lead to serious hypoglycemic attacks in all age groups and in a variety of settings. The analog nature of dasiglucagon allows for a stable AQ formulation, enabling it as the only glucagon to potentially be used across the spectrum of hypoglycemic conditions. In the next few slides, I'll highlight the unmet medical need in each of these four conditions and Zealand's plans to address them. The International Hypoglycemia Study Group defined three levels of hypoglycemia severity. Level one refers to blood glucose levels below 70 milligrams per deciliter and alerts the patient to ingest simple sugars to avoid progressing to level two.
At this level, blood glucose is below 54 milligrams per deciliter, and the patient is at very high risk of losing consciousness, which is defined as level three or severe hypoglycemia. The ADA recommends that glucagon be available to any individual at risk of level two hypoglycemia. Glucagon rescue therapies have been available for more than 30 years as kits for reconstitution. Despite their availability and the seriousness of severe hypoglycemia, patients are not comfortable with glucagon administration due to the cumbersomeness of these kits. As you can see on the slide, in a 2019 survey of primarily highly educated, privately insured adult participants on insulin pumps, i.e., people that can afford these medications, most patients with type 1 diabetes had been prescribed glucagon. However, a third did not have a current prescription for glucagon.
A third did not receive education on glucagon use, and only a third of those that did fill their prescription carried glucagon with them at all times. Moreover, the majority of glucagon prescriptions are in pediatric age groups, as it is parents asking for glucagon to treat hypoglycemia in their kids and to train themselves on reconstituting and administering glucagon. As you can see on the graph, the flat part of the curve, adults experiencing hypoglycemia themselves do not seem to be as aware of the consequences of severe hypoglycemia, be those cardiovascular, be those metabolic or cognitive, or they don't find the available glucagon presentations easy to use or to have a spouse or relative be trained on how to administer it.
The fact remains that even after the introduction of newer formulations of glucagon in the past couple of years, there is still a large unmet need for insulin-treated patients, both type 1 and type 2, to have glucagon available at all times. The next generation glucagon analog, dasiglucagon, would be the first glucagon product to be provided in a ready-to-use, stable aqueous formulation. Like glucagon, dasiglucagon is comprised of 29 amino acids, where seven amino acid substitutions have been introduced to improve physical and chemical stability. This allows it to be stored at room temperature, and it makes it available for immediate use in the event of a hypoglycemic attack. Dasiglucagon was studied in three phase 3 studies versus placebo, two in adults and one in children between the ages of 6 and 18 years of age.
In the first adult trial and the pediatric one, the marketed glucagon kit was used as a reference. Across all three studies, there was a consistent 10-minute response time in plasma glucose, which was measured as an increase of 20 milligrams per deciliter from baseline, and this was defined as plasma glucose recovery, or PGR. To the right of the slide, you can see that two-thirds of all patients in all three studies achieved PGR by 10 minutes, with almost 100% by 20 minutes. The safety and the tolerability of dasiglucagon was in line with that observed for the glucagon kit in the two studies in which it was included as a reference. Now, this data forms the backbone of the FDA submission, and we believe that if approved, it will provide a very attractive alternative for patients and providers alike.
Changing gears a little bit, congenital hyperinsulinism, CHI, is a rare disease affecting mainly newborns and toddlers. It is caused by a defect in pancreatic beta cells, resulting in insulin overproduction and leading to persistently and dangerously low blood sugar levels. CHI develops in one out of 50,000 or fewer children, which corresponds to approximately 300 children diagnosed in the U.S. and Europe every year. The most severely affected children need to have their pancreas surgically removed within a few months of birth in order to prevent hypoglycemia. This invariably results in the development of type 1 diabetes, which will follow them for the rest of their lives, and care and treatment options are insufficient. Less than one-third of newborns and less than two-thirds of older children respond to approved medical therapy.
The burden of disease is significant, not just for the affected children, but for their families and caregivers, and it represents a significant unmet medical need. The aqueous formulation of dasiglucagon provides it with stability, and it makes it very well suited for chronic administration through pump systems. We have designed a comprehensive phase 3 program addressing various clinical situations, endpoints, and children's ages. Trial 17109 evaluated children from three months to 12 years of age with a current incidence of more than three hypoglycemic events per week, despite previous near-total pancreatectomy and/or maximum medical therapy, and it compared dasiglucagon versus standard of care. Based on FDA advice, the primary endpoint of the study was the rate of hypoglycemic events as detected by SMPG, or self-monitored plasma glucose, since the agency at the time deemed continuous glucose monitoring, or CGM, to have poor sensitivity in capturing low glucose values.
However, in accordance with the FDA, we still included CGM as a secondary endpoint using Dexcom G4 Platinum CGM meters. Now, the results of the study show no difference in hypoglycemia rates as measured by SMPG, but almost a halving of rates as measured by CGM. We are conducting additional analyses and consulting with experts to understand the data better. It is very important to remark that 31 out of the 32 patients included in the study chose voluntarily to continue on to the 17106 study, in which all patients received Dasi, and which I will talk about in a couple of seconds. Now, trial 17103 is currently evaluating the use of dasiglucagon in neonates up to 12 months of age. In contrast to the previous study, these children are newly diagnosed with CHI. Dasi, or placebo, is administered for 48 hours, at which time the treatments crossover.
At the end of the crossover, all children are treated with dasiglucagon for 21 days. The primary endpoint is intravenous glucose infusion rate, which, in contrast to SMPG, is much more objective and sensitive and a very good indicator of the effect of continuous infusion of dasiglucagon. Hypoglycemic events will be captured both through CGM and SMPG as part of a wide range of secondary endpoints. And finally, trial 17106 complements the safety gathering data for dasiglucagon by allowing all those children and their families who choose to continue to be treated with dasiglucagon for up to two years from the end of the first study. Finally, in terms of other hypoglycemic conditions, we have the ability, the potential ability to use mini doses of dasiglucagon in other conditions, such as post-bariatric hypoglycemia. This is hypoglycemia that occurs after bariatric surgery, primarily Roux-en-Y gastric bypass.
This is increasingly encountered by clinical endocrinologists. Although the reported prevalence varies between 5% and 15%, the true frequency of this condition remains uncertain due to several factors, including a relative lack of patient and physician awareness and understanding of this condition, since most of these patients don't have diabetes. Post-Bariatric Hypoglycemia can be severe and disabling for some patients with neuroglycopenia, resulting in altered cognition, seizures, loss of consciousness, and all of these lead to falls, motor vehicle accidents, job and income loss. Moreover, repeated episodes of hypoglycemia can result in hypoglycemia unawareness, further impairing safety and requiring the assistance of others to treat hypoglycemia.
As you can see on the left-hand side of the slide, patients with PBH, or post-bariatric hypoglycemia, first occurs approximately a year after surgery, and symptoms usually present after eating, with a marked postprandial glucose peak followed by hypoglycemia one to three hours after. Diet is the cornerstone of therapy aimed at reducing the stimulus for these glycemic spikes and the corresponding insulin secretion, but in many patients, this is not enough to prevent hypoglycemic episodes. An unmet need, therefore, exists to prevent and treat severe hypoglycemia in these patients. On the right, you can see that in a study that was presented at the European Association for the Study of Diabetes last year, dasiglucagon was shown to achieve higher nadir plasma glucose levels in post-surgical Roux-en-Y patients with confirmed symptomatic postprandial hypoglycemia.
This was a double-blind, triple-crossover study that showed that a single dose of dasiglucagon, either 80 or 200 micrograms, effectively ameliorated postprandial hypoglycemia, and all of this provides the basis for an upcoming phase 2b study in an outpatient setting to be started later this year. The other condition that mini doses could potentially address is exercise-induced hypoglycemia. This can occur during, shortly after, or many hours after exercise, and therefore, patients should remain vigilant for its occurrence, including frequent use of SMPG or CGM. Measures to reduce early post-exercise hypoglycemia include carbohydrate ingestion and reducing insulin doses, which can result in weight gain and hypoglycemia, respectively. So a better approach is needed to prevent and to treat this condition. Dasiglucagon was studied in small doses, ranging from 30 micrograms to 600 micrograms or 0.6 milligrams, which, coincidentally, is the dose that will be used in the rescue pen.
This was studied in patients with type 1 diabetes in a hypoglycemic state, as you can see from the Y-axis on the graph. It showed a consistent and dose-dependent increase in blood glucose levels. Another study to be presented at the ADA later this year is comparing dasiglucagon 80 and 120 micrograms to carbohydrate replacement, and it showed a faster and more durable response with dasiglucagon data, which hopefully you'll be able to see at the ADA meeting. All of this data has led us to embark upon another phase 2 study evaluating a low dose of dasiglucagon administered by a pen device scheduled to start later this year. The study will recreate real-life conditions for people with type 1 diabetes to investigate how they would use dasiglucagon as a non-caloric alternative to manage their plasma glucose in everyday life, including exercise.
As a matter of fact, patients are requested to exercise regularly during the study, and they're free to decide when to administer treatment, either before, during, or after the start of aerobic exercise. Let's now talk about what Zealand Pharma is planning to help out with the treatment and the management of persons with type 1 diabetes. It is very well established that maintaining mean blood glucose concentrations near normal range prevents many complications of type 1 diabetes and reduces mortality. However, most people with type 1 diabetes are not able to maintain mean blood glucose in this range, and intensifying treatment to achieve therapeutic goals increases the risk of both symptomatic and life-threatening hypoglycemia. An unmet need exists for better methods to manage glycemia. So I would now like to have Dr.
Steven Russell from Harvard Medical School explains in more detail the gap that remains in achieving normal glycemia, as well as the potential of the bi-hormonal bionic pancreas to help people with type 1 diabetes reach that goal while reducing the need for ongoing physician intervention or user input and monitoring so that the pump operates effectively. Dr. Russell.
Hi. My name is Steven Russell. I'm an associate professor of medicine at Harvard Medical School, and I'm on the staff of the Massachusetts General Hospital Diabetes Center. In addition to my medical practice caring for people with diabetes, I've been doing clinical research on automated insulin delivery for more than 15 years. In the course of doing pre-pivotal feasibility studies of the bionic pancreas, I've received research funding from Beta Bionics and Zealand Pharma, and I am a consultant for Beta Bionics.
I'm also a principal investigator and the clinical study director for the NIH-funded, investigator-initiated insulin-only bionic pancreas pivotal trial, and I will be directing the upcoming bi-hormonal bionic pancreas pivotal trial. From my perspective as a clinician, automated insulin delivery systems are the current state-of-the-art therapies for type one diabetes. But as good as they can be, there's potential for clinically important benefits from adding automated delivery of glucagon. Why is that? One of the important benefits of the automation of insulin is that insulin delivery can be decreased or suspended when glucose is falling towards the hypoglycemic range. However, even rapid-acting insulin formulations are absorbed and cleared fairly slowly after infusion, so suspension of insulin delivery isn't always sufficient to prevent hypoglycemia. Users must always have fast-acting carbohydrates at hand for treatment of lows.
To minimize the number of these episodes, control systems must be conservative with insulin dosing, and this limits how low an average glucose can be achieved. In contrast to insulin-only artificial pancreas systems, the normally functioning pancreatic islets don't rely on insulin alone to regulate blood glucose. Even though the pancreas has the benefit of much faster insulin delivery than can be achieved with subcutaneous infusion, glucagon is an integral part of the way it controls glucose. Glucagon counters the action of insulin on the liver, where it can cause the breakdown of glycogen and release of glucose into the bloodstream. The pancreas releases glucagon during fasting, when glucose returns to the bottom of the normal range after rising from a meal, and during exercise. The iLet bionic pancreas, an investigational device developed by Beta Bionics, can automate delivery of both glucose-regulating hormones used by the pancreas.
If suspension of insulin delivery alone isn't sufficient to prevent hypoglycemia, then microdoses of glucagon can be given automatically. Since insulin delivery was already suspended by this point, these tiny doses are usually sufficient, and there's no need to eat carbohydrates to treat a low. It makes sense that mimicking the approach of the normally functioning pancreatic islets could improve glucose control, and data from small feasibility studies that I've directed suggest this is true. We compared the bi-hormonal configuration of the iLet delivering both insulin and glucagon to the insulin-only configuration of the iLet. In these studies, the insulin-only iLet achieved outcomes similar to those reported for other insulin-only systems, with about 50% of study participants achieving an average glucose at or below the American Diabetes Association goal for therapy, which corresponds to a hemoglobin A1c of 7%.
The amount of time in the hypoglycemic range was low and consistent with the ADA guidelines. This was much better glucose control than is achieved by the population of people with type 1 diabetes at large, but many of the people with diabetes won't meet goals for the therapy with insulin-only systems. Therefore, even if insulin-only systems were used universally, an important unmet need would remain. In contrast, because the bi-hormonal configuration of the iLet can be more aggressive in dosing insulin without an increase in hypoglycemia, it was able to achieve lower average glucose values in these studies, with about 90% of study participants achieving the ADA goal for average glucose. There was less hypoglycemia than with the insulin-only iLet configuration and less need to eat carbohydrates to prevent or treat hypoglycemia.
In my opinion, these are important differences, both in terms of risk of long-term complications and also for quality of life. The participants in the trial seem to agree, rating their experience using the insulin-only iLet highly, but the bi-hormonal iLet even more highly. As compelling as the benefits of glucagon were in our feasibility trials, the use of human glucagon is not practical for widespread use in the Beta Bionics iLet. In order to take advantage of glucagon's potential to take automation of glucose control to the next level, a more chemically stable glucagon formulation was needed, and that is what Zealand has developed. Small feasibility trials that I've directed found that the Zealand glucagon analog, dasiglucagon, works similarly to human glucagon in the bi-hormonal iLet.
With all of this as background, I'm pleased to be moving forward soon with the next step in making these technologies available to people with diabetes. That is, to begin the bi-hormonal bionic pancreas pivotal trial, which will evaluate the safety and efficacy of the iLet and dasiglucagon working together. Various data sets published in recent years show that in spite of newer insulins and better administration systems, the vast majority of people with type 1 diabetes, around 80%, are unable to reach glycemic goals as defined by the American Diabetes Association. The proportion who do meet the ADA therapy goal increases slightly with age, from young adults, which is only one in eight, to mature adults, approximately one in five, to older adults, approximately one in four.
The slide we're looking at basically shows a red line corresponding to the measures of CGM readings, and it shows a histogram for each one of the groups being evaluated that shows the distribution of the A1c values obtained across that population. And you can see, as I said before, that the number of histograms, the number of bars below the ADA target, really correspond to the people that achieve the ADA glucose target. And it is pretty clear that this part of the slide shows that targets are not being achieved. Well, what about other studies where there's more intensified treatment? This is a representative trial, the first one on the middle, targeting more intensive glucose management. And this intensified usual care resulted in around 40% of participants achieving therapy goals.
The last panel, or next to the last panel on the right, shows the bionic pancreas, the iLet device that operated in the insulin-only configuration, and here it was able to achieve therapy goals in around 50% of those same participants. But, as you see on the last panel, with the bi-hormonal configuration where participants received insulin and dasiglucagon based on their individual needs, more than 90% of participants achieved therapy goals across these studies. And what makes these studies, or the results, even more striking is that participants also experienced less hypoglycemia in the bi-hormonal configuration, as the bionic pancreas automatically and proactively corrects both high and low blood sugar levels every five minutes throughout each day. And finally, what you can see as you move from left to right, culminating with the bionic pancreas, there's a striking reduction in inter-subject variability.
With the bionic pancreas, it's noteworthy relative to usual care and the general population, as evidenced by the tight clustering of the histograms in the two bionic pancreas arms compared with the much more spread-out histograms seen from the usual care arm data and the general population data. Zealand is collaborating with Beta Bionics on developing dasiglucagon for use with the Beta Bionics iLet bionic pancreas, which you can see to the right of the slide. This is a purpose-built, pocket-sized, dual-chamber, autonomous glycemic control system. It is designed to mimic a biological pancreas for a person with diabetes by calculating automatically and dosing automatically both insulin and dasiglucagon as needed every five minutes based on data from their body-worn continuous glucose monitor.
Results from a phase two study in people with type 1 diabetes, which you can see on the left, comparing the bi-hormonal iLet configuration using dasiglucagon to the insulin-only iLet configuration, were presented at the ADA and Diabetes Technology Meeting last year. The study enrolled 10 adult participants with type 1 diabetes in a crossover design where each participant used the insulin-only iLet for a week and the bi-hormonal iLet for another week in randomized order. The analysis of the CGM glucose endpoints showed that the bi-hormonal configuration using dasiglucagon provided superior glycemic control over the insulin-only configuration, with mean CGM glucose levels being 10 milligrams per deciliter lower on the bi-hormonal iLet, where 90% of participants on the bi-hormonal iLet had a mean CGM glucose level of less than 154 milligrams per deciliter.
This is a level that corresponds to an A1c level of 7%, which, as I said before, is a therapeutic goal for people with type 1 diabetes recommended by the ADA. In contrast, on the insulin-only arm, only 50% of participants achieved this mean glucose level of less than 154, but despite the much tighter glycemic control, participants spent less time in hypoglycemia when using the bi-hormonal iLet as compared to the insulin-only iLet. Now, the good news is that we've had a very productive end-of-phase two meeting with the FDA, and we expect the pivotal phase three trials to be initiated in the second half of this year, so let me talk a little bit about what we're planning for phase three.
The phase 3 program will consist of one pivotal adult trial, one pivotal trial in adults with type 1 diabetes, and one pivotal trial in children with type 1 diabetes. There's approximately the same number of adults and children, around 350 in each group, and they will be randomized into the studies. The primary outcome measure for both studies is superiority on A1c on the bi-hormonal iLet configuration or the insulin-only iLet configuration at week 26. A usual care arm, which you see at the bottom and top, respectively, of the adult trial and pediatric trial arms, will be included for secondary comparisons on A1c and various CGM outcome measures. Participants in the insulin-only and the bi-hormonal iLet arms will continue treatment until week 52 to establish long-term safety data.
And upon completion of the randomized period at 26 weeks, all usual care participants will be allowed to enter a 26-week extension study for treatment with a bi-hormonal iLet configuration with dasiglucagon. Finally, upon completion of all 52 weeks of treatment with the insulin-only iLet configuration, these participants will be allowed to enter a 13-week extension study for treatment with the bi-hormonal configuration with dasi. Overall, the program has been designed to demonstrate the clinical outcome of utilizing dasiglucagon in the bi-hormonal iLet versus the insulin-only iLet, while also comparing these results to intensified usual care. In this final part of my presentation, I will be describing the plans we have at Zealand Pharma to expand beyond diabetes and hypoglycemia into obesity and associated metabolic diseases.
In 2019, the journal The Lancet commissioned a group on obesity, which advanced the notion that obesity is a pandemic closely related to those of undernutrition and climate change. Subsequently, a New England Journal of Medicine paper published last November highlights that the global prevalence of obesity has tripled since the mid-1970s, with 650 million adults and 124 million children and adolescents suffering from obesity. In the U.S. alone, more than 40% of the population are considered obese. While awareness of obesity has risen based on its increased prevalence, there's an underappreciation by the public health community of the links between obesity and other health outcomes, including type 2 diabetes, non-alcoholic fatty liver disease and NASH, certain types of cancer, and various manifestations of cardiovascular disease, among others.
Medical treatment of obesity will be one of the cornerstones of addressing this pandemic, and Zealand's peptide expertise can contribute with the development of some of these medicines. In treating obesity, the goal of therapy is to prevent, treat, or reverse the complications of obesity and improve quality of life. Health benefits have been reported with weight loss of as little as 5% of body weight, but many patients have a weight loss goal of 30% or more below their current weight, a goal that is often not achievable without bariatric surgery. Medical treatment based on single receptor target pharmacology has been shown to reach up to 10%-15%, but it is clear that to achieve levels of weight loss approaching those of bariatric surgery, dual or even triple pharmacology is needed.
At Zealand, we have the ability of designing single peptides with dual agonists in action, such as the GLP-1 glucagon receptor agonist being developed in collaboration with Boehringer Ingelheim, which I will discuss in a second. We also have the ability of designing monoagonists that can be co-formulated with other peptides targeting other receptors, such as amylin and GIP. As I said before, the concept of targeting more than one receptor in treating obesity is illustrated in this picture. Activation of the GLP-1 and glucagon receptors leads to complementary actions in terms of appetite suppression and increased energy expenditure, respectively. Preclinical models and early human studies show these effects to be additive. Zealand's collaboration with BI is advancing, with BI having completed phase one studies for the dual agonist in which clinically significant weight loss was seen for the dual agonist.
Detailed results of this data will be communicated by BI at upcoming scientific meetings later this year. The phase 2 program for both obesity and type 1 diabetes, type 2 diabetes, is underway, as well as plans for investigating the dual agonist in NASH. Moving on to amylin. Amylin is a very interesting peptide. It is actually derived from beta cells in the pancreas and is co-secreted with insulin. It both regulates blood glucose by delaying gastric emptying after meal ingestion, and it directly modulates satiety signals in the brain. Preclinical studies also suggest that amylin, like glucagon, can increase energy expenditure, contributing to its weight loss effect. However, human amylin tends to aggregate and form amyloid fibrils, which makes administration of the native hormone very difficult.
A long-acting analog of amylin by another company is currently in phase two studies, and the proof of concept has been shown because it's shown both its effect as monotherapy and in combination with a GLP-1 receptor agonist. At Zealand, we developed an amylin analog, which we call ZP8396, that has a half-life allowing for once-weekly administration and unique to this peptide for co-formulation with other anti-obesity peptides, such as GLP-1 receptor agonists, GIP, PYY, etc. As you can see on the slide, in a preclinical model of obesity, one of our other amylin analogs showed marked weight loss compared with liraglutide, the only marketed GLP-1 receptor agonist currently prescribed for the treatment of obesity. We do anticipate starting phase one trials with the ZP8396 analog later this year, and finally, GIP, or glucose-dependent insulinotropic peptide. This is also a particularly interesting peptide to explore in treating obesity.
It is synthesized by K cells, which are found in the proximal intestine, and it circulates as a biologically active 42-amino acid peptide. GIP receptors are expressed in many organs and tissues, including the central nervous system, enabling GIP to influence regulation of appetite and satiety while showing antiemetic effects. Thus, GIP can contribute to the efficacy of other anti-obesity peptides, both by a complementary effect and by providing an improved and wider therapeutic window of the other peptide. This, in fact, was the approach taken by Eli Lilly in designing their GIP GLP-1 dual receptor agonist, which has shown promising weight loss in phase two studies and again shown proof of concept. We do have our own GIP agonist, ZP6590, and it has shown, as you can see on the graph, additive effects when co-administered with a GLP-1 receptor agonist in an obese mouse model.
We expect to bring the analog to phase one next year, and like our amylin analog, this can also be co-formulated with any other peptide targeting obesity. To summarize, metabolism continues to be a pivotal area of focus for Zealand. We're exploring the use of dasiglucagon across the spectrum of hypoglycemic conditions, starting with the rescue pen to be launched this year. We're working closely together with Beta Bionics in getting the phase three program for the bi-hormonal bionic pancreas started before the end of 2021. Finally, we're expanding our focus to obesity, with plans to put our amylin analog in phase one later this year. As illustrated by Robert's testimony, our focus continues to be on addressing unmet medical needs. Our strong commitment towards patients with short bowel syndrome is the foundation for our gastrointestinal franchise. We are making significant progress on this end.
Today, I will also share some new assets and thereby set the direction for where we will take this franchise in the future. We are developing two molecules for short bowel syndrome: glepaglutide, our long-acting GLP-2 analog, and dapiglutide, our long-acting GLP-1 and 2 receptor dual agonist. We have two new assets, a Kv1.3 blocker and alpha-4 beta-7, which targets IBD, and they are progressing towards phase one. We also have a complement C3 inhibitor, and together, these three assets represent our leading assets towards IBD and other chronic inflammatory diseases. The complement C3 inhibitor, we have licensed to Alexion, and we are making very good progress in this collaboration, and Rie will share more of that when we get to her part of the presentation.
Turning to short bowel syndrome, Marianne is living with short bowel syndrome, which is the result of long-standing Crohn's disease and multiple intestinal surgeries. As she has said herself, getting SBS was her worst nightmare. Few of us can imagine how it would be to one day wake up and find out that you could no longer absorb the fluids and energy you need to survive, and that you have now become dependent on parenteral support for the rest of your life. This means that people will be hooked up to IV infusion lines for up to 17 hours every day to survive. Marianne, however, is also lucky, not only because she's one of the strongest persons and has the most positive inspiration around her, but also because she lives next to a center of excellence with healthcare professionals who know how to help her manage her complex condition.
Marianne and the many people who have shared their stories with us at Zealand give us the energy and focus to continue to progress new medicines to help them ease their condition. There are approximately 40,000 people living with short bowel syndrome in the US and Europe. The condition is defined by having less than two meters of small intestines, leaving the patients with too little absorptive capacity to get the nutrition and fluid they need. When people with SBS eat and drink, they will experience diarrhea, and around half of the patients will become dependent on home parenteral support for the rest of their life. We have seen some progress in the management of SBS with the introduction of the short-acting GLP-2 analog, teduglutide.
However, there remains a huge unmet medical need for faster, more effective, and more reliable treatments that can take reductions in parenteral support to a new level and ultimately get patients to regain full enteral autonomy. Glepaglutide is our long-acting GLP-2 analog with an effective half-life of approximately 50 hours that we have in phase 3 development as either a once-weekly or twice-weekly injection. The unique design of this molecule has allowed us to develop it in a stable and aqueous solution and thereby also progressed the development of an autoinjector for easy and simple injections, as you can see down to the left of this picture. If you look to the right, then you can see the main results of our phase 2 study, which demonstrated that the two higher doses of glepaglutide increased intestinal absorption of fluid.
We also observed changes on a number of other effect parameters and concluded glepaglutide to be safe and well tolerated in the study. As a result of the increased intestinal absorption of fluid, we also saw increases in urine production in the phase two study. That's a very important observation because increases in urine production are directly related to the ability to reduce parenteral support in clinical practice, but also in our ongoing phase three study. If you look to the right of this slide, we have applied the algorithm that we used to guide reductions in PS in our phase three study to the data we achieved in our phase two study.
It's striking to see that only following three weeks of treatment with glepaglutide, 71% of the patients would have had a reduction in their parenteral support, and perhaps even more striking, 57% of the patients would actually have met the responder criteria of a more than 20% reduction in PS defined in the study. EASE SBS 1 is our pivotal phase 3 study that is set to enroll 129 patients with SBS. Following six months of treatment, they are then offered to roll over into EASE SBS 2, which is a long-term two-year study where all patients get active treatment. The primary endpoint in EASE SBS 1 is the reduction in parenteral support as measured by the end of the study. As already announced, enrollment of patients into this study has been impaired by COVID-19.
We are, however, happy to see that recruitment is getting back to pre-COVID conditions here over the last few months, likely due to the introductions of vaccinations. Pending a continuous positive development in recruitment, we expect to see results in 2022. While our focus is on securing patient enrollment into EASE SBS 1, I'm also excited about the opportunity to share that we are starting two additional phase three studies. One study called EASE SBS 3 will allow patients who are completing EASE SBS 2 to roll into a further two years of treatment, here actually being dosed via the autoinjector. In EASE SBS 4, we are evaluating 24 weeks' treatment effects on intestinal absorption of fluid and energy, and thereby confirming in a long-term study the data we observed in our phase two study.
We believe the full program that is displayed here is very well set to highlight the benefits of glepaglutide, and we look so much forward to seeing the pivotal phase three data next year. I would now like to turn to dapiglutide, which is our long-acting GLP-1 and GLP-2 analog that we are also progressing for treatment of short bowel syndrome and potentially other GI diseases. The concept of a dual-acting peptide stimulating both the GLP-1 and the GLP-2 receptor has already been demonstrated in short-term clinical studies. While GLP-2 increases the absorption across the intestines, the GLP-1 component is believed to reduce the gastric motility and thereby allowing more time for the nutrients and fluids to be absorbed.
We therefore believe that dapiglutide has the potential to take treatment of SBS to a completely new level and really get many more patients towards that ultimate goal of full enteral autonomy. Last year, we completed a phase 1A study where we concluded dapiglutide to be safe and well tolerated in doses up to 7.5 milligrams. We also observed a plasma half-life of 120 hours. This allowed us to start the phase 1B study, which is ongoing. I'm happy to report that we have completed the second dosing cohort in the phase 1B and expect the full results of the study later this year. At this time, we also expect to announce the next development steps for the molecule. Over the last few years, we have expanded our research activities into IBD and other chronic inflammatory diseases.
Peptide drugs have proven their effectiveness in other therapeutic areas such as diabetes and obesity, and we believe they hold great potential as novel and innovative treatments in chronic inflammatory diseases as well. It's an area that has otherwise been dominated by antibodies for many years. The programs we are progressing towards the clinic represent high-profile targets, with Kv1.3 and complement C3 having proven very difficult to block by small molecules or by antibodies. And the alpha-4 beta-7 goes for a target that has already clinical evidence in that antibodies have been shown to provide benefit to patients living with IBD. One of the first immunomodulatory molecules we are progressing towards phase 1 is our Kv1.3 ion channel blocker. Kv1.3 is a central ion channel to the T effector memory cells, which plays a key role in autoimmunity and chronic inflammation by the release of pro-inflammatory cytokines.
These factors recruit more immune cells to the inflamed area and cause tissue damage, as you can see schematically presented to the left of this slide. The anti-inflammatory effects of blocking Kv1.3 have been demonstrated in numerous preclinical models of autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, psoriasis, and IBD. The illustration to the right shows the engagement of a leukocyte through the activation of the T cell receptor. Depending on the nature of this leukocyte, different ion channels are engaged. Naive and central memory T cells are dependent on KCa3.1 ion channels, whereas the effector memory T cells are dependent on the Kv1.3 ion channel. The efflux of potassium through these channels activates the cells and causes the release of pro-inflammatory cytokines.
The specific and selective location of Kv1.3 through the effector memory T-cells makes it a high-profile target in that it preserves the immune system's other parts, and therefore we are very excited to bring this molecule forward. So our lead candidate is a potent and selective Kv1.3 blocker with the potential to treat a broad range of autoimmune diseases. Currently, we are progressing the molecules into IND toxicity studies and aim to take the molecule into inflammatory bowel disease as the first indication. The graph to the right shows one example of the link between Kv1.3 and pro-inflammatory cytokine production. In the study, we demonstrated that our lead molecule can inhibit the production of IL-2, IL-17, and interferon gamma stimulated from whole human blood cells, and thereby providing a direct link to humans from the preclinical evidence we have for this molecule.
We expect to take the lead molecule into phase 1 next year, and we look very much forward to share additional scientific data over the year on this molecule. On this slide, you can see some of the data we have generated for ZP10000, which is our oral alpha-4 beta-7 inhibitor. Alpha-4 beta-7 is a clinically validated target, and many patients with IBD have already seen improvement in their disease when they were treated with vedolizumab, which is an antibody for either IV infusion or subcutaneous injection. Some of the success of vedolizumab is ascribed to the gut-restrictive nature of the immune suppression with this target. ZP10000 is a peptide inhibitor of that same target with binding kinetics on par with what we see from antibodies.
In preclinical models of inflammation, the compound is effective in decreasing the inflammation after oral administration, as you can see one example of to the right in this slide. And what is striking is that the molecule has been designed to have oral bioavailability from the start, and what we are focused at right now for this molecule is to optimize the clinical formulation of the molecule. This is our first go with an orally available peptide, and as such, it's also leading the way and our ambition to develop many more peptides with oral bioavailability that we hope to progress into the clinic over the next years. This concludes our session on the gastrointestinal and chronic inflammation portfolio. We are committed to progress new assets into this area and have made significant progress getting new both late and early assets forward.
Glepaglutide and dapiglutide represent our opportunity to change the management of people living with short bowel syndrome, and the early assets I shared represent opportunities for totally new innovation in an area of IBD and chronic inflammation. Our long-standing commitment to patients living with short bowel syndrome is the foundation for our efforts, and the new assets open up for completely new value creation by Zealand Pharma, and with that, I would like to hand over to Rie for her to take us through our peptide platform.
My name is Rie Schultz Hansen, and I'm head of discovery and innovation here at Zealand Pharma. I'm very pleased to give you a talk through our expertise in peptide design and engineering, and I'm proud to say that for more than 20 years, we have been the drivers of innovation in designing peptide drugs.
We have established our next-generation peptide platform on our innovative capabilities. For my part of the presentation, I'll give you a walkthrough of the technological solutions that we have applied for selected programs. I'll talk about how we used our rational design approach to dasiglucagon and dapiglutide. I'll talk about how we engineered non-human peptide starting points into selective drug candidates in the Kv1.3 and the C3 programs. And finally, I will talk about how we are taking peptide drug discovery to the next level by advancing potential oral treatment for IBD patients based on the known mode of action of blocking alpha-4 beta-7. But first, I'll give you a short presentation of peptides and our innovative peptide platform. Peptides are made from amino acids, which are kind of nature's building blocks, and peptides are a drug class on its own.
They are more specific in inhibiting protein-protein interactions than small molecules, and they do have superior tissue penetrance when we compare them to antibodies. Peptides can regulate cellular processes by being agonists or antagonists of biological function, and it's even possible to engineer dual pharmacology into peptides. At Zealand Pharma, we see our scientists as an integrated part of our discovery platform because it's really built on a deep understanding of rational peptide design, of how to order the amino acid sequence to enhance certain properties.
We are continuously adding several other relevant technologies to our platform, for example, libraries of venoms or molecular display, which I'll come back to a bit later, our in silico modeling or computational chemistry that we are also using, and very importantly, also novel oral formulation technologies, because we believe that together with designing the peptides made for oral delivery, this holds a very exciting future promise. So during this presentation, I'll use examples of how we have exploited these technologies, starting with our phase three asset, dasiglucagon, where our rational design processes were key. Dasiglucagon is a demonstration of our ability to improve drug properties of peptide. Native glucagon has been a treatment offering for severe hyperglycemia for more than 30 years, but it's a highly unstable peptide that is prone to aggregation, and it needs reconstitution from powder, which really limits its clinical use.
So here, the ambition was to make a ready-to-use product to make an analog of glucagon that is stable in an aqueous solution. But how did we approach that? So we know that creating electrostatic repulsors in a molecule will prevent them from getting close to each other and form aggregates. So we needed to make a more charged molecule that could prevent this aggregation, and we did this by replacing only seven of the 29 amino acids. On the graph to the left, you can see aggregation, which is measured as an increase in the fluorescence signal. On the blue graph, you can see native glucagon that aggregates into fibrils within days, but dasiglucagon, as you can see on the red graph, is not aggregating at all. So we managed with our replacing of the seven amino acids to make a peptide that is not aggregating.
Of course, it's also key to ensure that the potency and specificity for the glucagon receptor is maintained. On the graph to the lower right, you can see the effect of dasiglucagon in an aqueous solution in the hyperglycemic rat model. On the red graph, you can see dasiglucagon that elicits a rapid increase in blood glucose. The same effect is seen with native glucagon, so on the blue graph, but of course, that has to be reconstituted before use. If we use DMSO as a stabilizer, we can also elicit a response with native glucagon, but this has a delayed onset of action. In summary, for dasiglucagon, it's a really good example of how we used our deep understanding of peptides to design a drug with excellent stability while maintaining the desired physiological properties.
Now I'd like to turn to how to make peptides with dual agonism. As you know, we have two dual-acting clinical candidates: a dual GLP-1 glucagon that BI is advancing and a dual GLP-1, GLP-2 analog, dapiglutide, and with dapiglutide, our ambition was to engineer a peptide with dual pharmacology and a long plasma half-life, so native GLP-1 and GLP-2 only share 33% amino acid homology, and we rationally replaced 10 amino acids in the GLP-2 sequence to add GLP-1 activity, so we really obtained here a balanced receptor potency. On the graph to the left, you can see a dual dose-dependent effect in a mouse model, and you can see on the left, the intestinal transit time dose-dependently is decreased. That's a hallmark of GLP-1 effect.
On the right side, you can see the weight of the small intestine is increased, and that's a hallmark of a GLP-2 effect. So really here, we managed to combine the two biological effects in one peptide. Now, as mentioned, the scaffold here is the GLP-2 peptide, and native peptides have short half-lives in plasma, and that needed to be addressed too. Attaching an acylated fatty acid to the peptide makes it able to bind to human plasma albumin, and human plasma albumin has a plasma half-life of 19 days. So with this binding, the peptide is then protected from degradation and from fast renal filtration, and furthermore, it's really gradually released into circulation. On the graph to the right, you can see a bioanalysis study where subcutaneous administration of dapiglutide has been administered to the dog.
What you can see is in the dog, it has a half-life of about 35 hours, and that is the effect of the acylation. This roughly translates into a half-life of about 120 hours in humans. We really designed dapiglutide to be a dual GLP-1, GLP-2 agonist that is suitable for once-weekly administration in the clinical setting. As a first example of a program where no human starting point exists, I would like to discuss the Kv1.3 blocker. Kv1.3 is a potassium ion channel that is upregulated in inflammatory conditions, and no human starting points exist for this channel. When we work with ion channel, we know that selectivity is key. This is really difficult to obtain with small molecules, and antibodies are selective, but they are really difficult in entering the channel pore.
Peptides, they are ideal ion channel blockers, but as mentioned, no human starting point exists. We needed to find a peptide starting point, and we know that venoms are a rich source of bioactive peptides. Animals such as spiders, lizards, and scorpions use their toxic cocktails to engage their prey, and we had access to libraries of these bioactive peptides, and we screened for peptide hits. We found such a peptide hit, and it was optimized by evolution to inhibit the Kv1.3 channel. Now, venom starting points are really complex peptides. They're inherently soluble, but the challenge here is to enhance the selectivity and stability of the peptides while maintaining this soluble three-dimensional structure. But by rational design and in silico modeling, we obtained to increase the Kv1.3 selectivity, we maintained the potency, and we also dialed in the stability and maintained the soluble nature of this peptide.
On the graph to the right, you can see the candidate peptide, and it potently blocks the Kv1.3 in an in vitro setup while maintaining a high selectivity towards other very similar ion channels. Also, this peptide is optimized for large-scale production, and we're really eager to take this venom, the right candidate, through the IND enabling studies to further explore its clinical potential. So we are developing a C3 peptide inhibitor in collaboration with Alexion Pharmaceuticals. Alexion Pharmaceuticals is a company that is specialized in complement diseases. I use this program to illustrate how other sophisticated laboratory technologies can be used to generate peptide drug starting points. Now, the complement system is a part of the innate immune system, and C3 is a very central component. C3's interaction size with its target molecule is too small for antibodies, but it has the just right size for peptides.
But again, here, no natural peptide inhibitor exists. The phage display library technology is really well-suited for this kind of target, and we have implemented this technology at Zealand. Phage display is a powerful molecular biology screening technique that can generate libraries of millions of random peptides, and we can use those libraries to identify ligands to proteins such as C3. In this case, the starting point for phage display, but it was publicly available, and we knew the binding site and the conformation. We used our structural knowledge and in silico model to rationally replace amino acids, and we obtained the optimal balance between potencies, stability, and solubility while keeping the peptide's affinity for C3.
On the graph to the left, you can see surface plasmon resonance data, and we can see the concentration-dependent binding kinetics to C3, and it demonstrates that the candidate is a very potent C3 binder. Our candidate is also half-life extended, and it has the potential to be the best in class. We have now selected the candidate molecule, and we are together with Alexion progressing this into the next stage of development. As a last example, I would like to discuss the alpha-4 beta-7 integrin inhibitor. Alpha-4 beta-7 is located on the surface of T cells, and the inhibition prevents the interaction with MAdCAM-1, which is based on the endothelial cells, and this interaction between alpha-4 beta-7 and MAdCAM plays a very critical role in immune cell recruitment to the intestinal tissue.
This is a mode of action that's clinically validated in inflammatory bowel disease by marketed antibodies, but most IBD patients would really prefer an oral tablet treatment. Due to its size, this interaction surface between alpha-4 beta-7 and MAdCAM-1 is a very attractive target for peptides, but again, here, no natural peptide ligands exist. We know that the MAdCAM-1 mimetic peptide structure is published, and we use this structure to design peptide ligands that selectively bind to the alpha-4 beta-7. This design was guided again by in silico modeling, and we also incorporated properties of oral bioavailability. On the graph to the right, you can see the concentration-dependent properties of our compound ZP10000 that again, here is measured by surface plasmon resonance. What is really remarkable here is that the binding properties are on par with marketed antibodies.
That is something that is really extraordinary to obtain with a peptide this size. We have also demonstrated oral bioavailability in vivo, and currently, we are exploring the optimal oral formulation for this compound while we are progressing the program. So in summary, our peptide platform is founded on more than 20 years of know-how of how to rationally design peptide analogs. The chemistry of several of our newer programs is guided by in silico modeling and computational chemistry, a technology area that is rapidly evolving in the peptide space and that we continue to invest in. Combining this with technologies like venom libraries and molecular display has increased our bandwidth to include targets outside of the traditional peptide receptor area.
Also, with the addition of our first oral program, we are exploring and investing in new formulations that can enhance oral exposure in combination with focused design of smaller peptides that have a built-in propensity for oral bioavailability. I would like to emphasize that we remain determined and committed to design and engineer druggable peptides for any high-value target where peptide drugs can make a difference. We have been pioneers in the peptide world for two decades, and we see a large untapped potential in this class of molecules, and we are dedicated to develop the next-generation peptide drugs that are designed to address unmet medical needs.
I hope you have enjoyed the presentations today and are excited and energized by all the progress we have made across the pipeline and the peptide platform.
We have set a very high ambition for our R&D organization over the next five years, and we are excited about delivering on our promise to the patients. As we enter into 2021, we will focus on three areas. Number one is to deliver on the late-stage assets. Then we'll progress the next value drivers into the clinic, and we'll increase our investments in the peptide platform. So we have some very exciting years ahead of us and can't wait to get going. And with that, I would like to hand over to Emmanuel for his closing remarks.
Thank you, Adam. Zealand has made extraordinary progress over the past two decades, but I believe our next chapter is our best yet. I am thrilled to be leading Zealand Pharma through the next development.
I hope this R&D day brought to you the same excitement that fuels our team daily, and I am honored that we were able to actually bring you all the milestones and information regarding our R&D development. I am thrilled to show you the one-of-a-kind Zealand Pharma is turning into: a company that cares and thrives for the care of patients in metabolic and gastrointestinal disease. Thank you for your attention, and we look forward to having you joining our Q&A session.