I will leave the floor to Ulf, who will tell us all about Diamyd and the type 1 diabetes day. This is the purpose probably you have in your life, to fight against type 1 diabetes. Please give an applause to Ulf.
Thank you. Thank you. I won't tell you everything about Diamyd Medical, because then we would be sitting here for a few hours, I think. You will get a glimpse into the company, but probably a bit more about type 1 diabetes, and a bit more about some maybe interesting research findings when it comes to a precision medicine approach. Given this crowd, it's not only trying to convince you to buy our share, which is, I mean, everyone should always consider that, but a bit more of a research perspective, hopefully there are some time for questions as well, that you can ask me afterwards. For us in the company, the purpose, which I agree, regardless of what you do in life, purpose is very important.
I think the purpose for us is our mission to eventually try to cure type 1 diabetes. I think without this purpose, this company wouldn't exist anymore. It was the purpose of the founding of the company a long time ago, around 30 years ago, the company has gone through many very significant challenges, but have survived everything. I think it's big part because of the purpose. It's not only an interesting technology with a big commercial potential, it's actually the founding was the purpose, and then the rest has come thereafter. But briefly about type 1 diabetes and obviously what is the challenge we are trying to solve here? So it's, as you may know, it's an autoimmune disease, and it's a lifelong chronic autoimmune disease.
At the time of the diagnosis, you are put on insulin injections or insulin pump for the rest of your life to manage blood sugar control. It's probably more than a half a million, at least every year, that gets this disease. This number could be double or even more because 10% of type 2 diabetics actually have autoimmune diabetes, they are misdiagnosed as type 2 diabetics, but they actually have an autoimmune disease. It used to be called LADA, latent autoimmune diabetes in adults, but now it's considered that it's adult-onset type 1 diabetes. It's a bit slower progression than the classical type 1, it's still autoimmune. Depending on the country and the clinic where you get your diagnosis as a type 2 diabetic, it might be a misdiagnosis, actually, it's type 1 diabetes.
Type 1 diabetes has a very high risk of complications. Even if you are on standard of care, insulin injections, insulin pumps, continuous glucose monitoring, even these closed-loop systems where you integrate everything, you can't manage your blood sugars as well as the body itself does when you have your own insulin production. That's why we are actually also have this roll up here. There's no insulin like your own. We try to preserve your own insulin production with what we do in the company. These complications, they translate into quite significant, like, 35 years on average, shorter health span, which means a healthy life without complications, and 15 years shorter lifespan. That's based on a Swedish registered study, where they followed individuals for a long time with type 1 diabetes.
If you are a girl who gets the diagnosis before the age of 10, you have an average, almost 18 years shorter lifespan. That's really because of all the complications. Both acute complications, you can die from too much insulin, but then the long-term complications where your body starts to get damage, nerves, blood, and everything else. Like I mentioned, what we try to do is preserve pancreatic function, and specifically, we try to preserve the insulin producing production in the body. You have the beta cells in the islets of Langerhans that are in type 1 diabetes being destroyed by the immune system, and we try to stop this immune attack and thereby preserve the insulin production. By doing that, we can then really improve the glycemic control.
If the body can help assist in regulating the blood sugars, you will have considerably fewer complications and a lower risk of these complications in the future. That's why this is really all companies that are trying to develop immune, like, disease-modifying therapies for type 1 diabetes. This is the purpose, really. How do we preserve the insulin production? How do we stop the autoimmune attack? In best case, we could also then halt it completely. We go in earlier before diagnosis and treat preventively, so we can prevent. We know who has a high risk of getting the disease. You go in before diagnosis to delay or, in the best case, avoid that someone ever gets the clinical diagnosis.
Before we go into a bit more of the, here starts the more research part, but what we do, this is like a simplistic, still a busy slide of our approach. First of all, it's a precision medicine approach. We target a genetic subgroup of type 1 diabetics based on their HLA genetics. The active component in our therapeutic is a protein, so an endogenous protein that we have a recombinant version of. What we try to do is to reprogram the immune system towards this protein. This protein is expressed in the insulin-producing cells in other parts of the body as well, but for some reason, the immune system sees it as something foreign and starts attacking it, and thereby destroys the insulin-producing cells.
We want to reprogram the immune system, basically present the same protein to the body and tell it that this is nothing dangerous, stop attacking it. We don't do any immunosuppression. It's kind of a reverse vaccine, what we are doing. This thing has been developed over the past 30 years. It was in phase III development around 15 years ago and failed. The phase III study didn't show a statistical significant efficacy. We are back now in phase III with the first readout coming up actually towards the end of March. Same exact therapy. The big difference is again that now we go for this genetic subgroup, and that's been the biggest learning over the past, I would say, 10 years in the company, that it doesn't work in everyone.
You need to find the responders, in this case, it's genetic subgroup based on HLA genetics, where HLA is the recipe for these MHC II receptors that bind to the antigen parts and present them to T cells. Depending on which receptor you have, you will bind different antigens with different affinities, and you need to have the right one to get the right immune effect. That's really why HLA is completely central to our approach when you treat with an antigen. The next slides will kind of go back and show what we saw previously and what we have learned over the years and come up to this thing, that this is completely central. Now, hopefully, fingers crossed, in first time, we will have a first phase III readout now in like, one and a half months.
We will see if this works. Type 1 diabetes, as many other common diseases, it's a complex disease, and I think that in itself is important. I don't think there's any complex disease where you have a therapy out there that works 100% in everyone. It usually work in 30%-40%, but you treat everyone, 40% maybe gets the effect, 100% gets the side effects, so it's not really a sustainable approach. In immune oncology, that has really paved the way for more precision medicine approaches, where you characterize the tumors, the expression levels, and target the treatments accordingly. Now other complex diseases are following up on this, and we are the first ones out in type 1 diabetes in the whole world with a precision medicine phase III trial ongoing.
In type 1 diabetes, we know that there's a sex or gender effect. It's a bit more common in, like, in males versus females. Usually, in autoimmune diseases, you have the opposite. It's a bit more common in females versus males. Then age is a factor. You have the highest incidence in the early teen, teenage years. In absolute numbers, more adults get type 1 diabetes than children, only because there are more adults in the world than children. You can get type 1 as a serial at birth, and you can get it when you're 100 years old, but highest incidence is in the teenage years. HLA, that is the most significant genetic risk factor for type 1 and other autoimmune diseases. Then geography, there's a big difference in geography as well.
Like, for example, Finland is number one in the world when it comes to incidence of type 1. Then there's usually a north to south gradient. Then you have some other, like in the Middle East, in some countries, a very high prevalence, for example. In China, it's at low levels, but it's growing quite fast now. Autoantibodies, these are, obviously, when the immune system starts attacking the different components in the beta cells, you get these autoantibodies in blood. By measuring them, you can see which one appears first and how many do you have that actually then also determines the progression of the disease. All of these also somehow are interlinked. They are not like individual isolated risk factors. They are all...
It's a big mix, a complex mix here. That's important, what we have learned. When you try to evaluate the therapeutic response, you need to understand these different factors, that some of them are confounders, some of them are more mediators of disease. You can have hormonal effects, for example, during puberty, that influences the disease progression and stuff like this. It's a, it's a big, big complexity. I think from a therapeutic development perspective, you need to control for these, so you need to remove some of the variation so that you have a more homogeneous population where you evaluate in order to see an effect. Otherwise, all of this complexity might mask the therapeutic effect.
Going back, we were in phase III, like I told you, around 15 years ago, this is the publication then that it didn't show statistical significance. You see on the right-hand side here, the disease progression curves from baseline, you can see that, yes, there's a slight trend or positive trend in the treatment arms, so the 4 and the 2 dose regimen versus placebo, this wasn't statistical significance. The question is why? Because the previous studies had showed that it works, seems to work. This is also from the same publication. You're not meant to be able to read this. Congratulations if you can. My eyes can't handle this anymore.
This is the post hoc analysis from the same New England Journal of Medicine publication for all the different baseline criteria that were then assessed to see how it works in the different subgroups. If you can see, on the right, this is a tree plot. On the right, it shows that the active treatment was more worked versus placebo, if it's trending to the left. Most of the stuff was more to the right here. It really showed again that this there, it's definitely not only a placebo thing here. There is an effect. There were certain subgroups that were very interesting. For example, this one looked at sex at baseline, and here you can see a statistically significant treatment effect in males and not in females.
That was a strange finding and obviously generated a lot of hypotheses that maybe this is exactly because they were mostly teenagers in this study. Maybe there is an hormonal effect, and this, the immune system, works differently in the, in puberty, for example, in girls versus boys. Maybe there's a rationale here. What we have done then, going back into this. On the y-axis here, you have the number of individuals, and then on the x-axis, we have divided the males and females into age groups, so pediatric, adolescents, and adults. These are just the numbers of individuals that were part of the study. You can see here actually that when we look at the specific HLA type that we are now targeting, there was an enrichment in males, in these, adolescents males.
That was the dominant, basically, age group in the trial. This is probably why that post hoc analysis show that it works better in males than in females. It's not because of the gender factor, it's because they just happen to have more of the right HLA type, and there were more males than females, and that's why that statistical analysis became significant in males and not in females. Looking at another interesting subgroup here, it was, we looked at non-Nordic versus Nordic countries, and it shows that there's a significant effect in non-Nordic individuals.
The hypothesis back then was that maybe it could be a seasonality effect, a vitamin D effect, partly, and also there was at that time when this phase III study was run, you had the swine flu epidemic or pandemic ongoing, and all Nordic countries, basically everyone got vaccinated. Even if it's in the clinical trial protocol, it said that you should not get another vaccine during the treatment period, it was impossible to prevent anyone from doing it. Everyone in the Nordics got their whilst in other parts of Europe, it wasn't the same kind of a pressure on getting vaccinated. That was the hypothesis. Maybe that swine flu vaccination kind of destroyed the immune effect of our treatment.
Again, going back into the data, when we look at the, again, the HLA frequency in these different countries, you can see, for some reason, it says zero here now, but you can still see the boxes. I think these are like 60%-65% prevalence of the HLA type here in Southern Europe, that Finland and Sweden, and Finland had, like, 35%, Sweden, maybe 40%. Again, there's an enrichment of our HLA type in Southern Europe compared to Northern Europe, and this is most likely the reason why that statistical analysis showed significance in non-Nordic versus Nordics. We have actually also done the more proper analysis, when you add the HLA type as an interaction variable into the all of these gender effects, geographic effects disappear. It's all about the HLA.
Understanding why, going back to why is HLA central to this treatment. On the left, you can see in this graph, it's actually when you follow children who are at a high risk of getting type 1 diabetes, and then you follow them for a long time, and this is when they get their first autoantibody appears in their blood. On the left, you have the ones that get GAD autoantibodies first, and GAD is the protein that we use in our therapeutic, and they tend to have HLA DR3 DQ2, and then you get GAD is the primary autoimmunity in these individuals. On the right, you have the other, when you get IAA autoantibodies first, and they tend to have the other very common HLA type, DR4 DQ8.
By selecting on the HLA, you can also select individuals based on their kind of what is the dominant antigen behind their disease. That's kind of the scientific rationale. If you treat with a GAD-based therapeutic, you should most likely treat individuals who have a dominant autoimmunity against that protein, not to worry. You shouldn't treat with an insulin-based antigen because it will only then maybe take care of the insulin autoimmunity, but GAD autoimmunity is driving the disease. You won't probably have an effect. This is the reason in the previous phase III, we treated everyone. Half of them most likely had this more insulin-based autoimmunity, half of them had the GAD autoimmunity. We did see effect in these individuals, nothing in this one, and the average wasn't good enough for significance.
Again, going back to what I just said, in these individuals, you would have most likely have the engine behind their autoimmunity is like GAD. That's where the immune system starts. You have this, what's called epitope spreading, that the immune system starts reacting to other beta cell antigens when they appear, and these insulin-producing cells are destroyed. They present more and more antigens, and the immune system starts attacking other, and then it keeps on spreading. Well, the hypothesis is that in this case, you should treat the dominant, the driving autoimmunity. Sort of take care of that one, and it will take care of the rest.
That also means probably that the earlier you treat, potentially you will have a more better and better effect, which our data also could. We have some data from the individuals who are at risk of getting type I diabetes, so we treat very early, and those data look very promising as well. So this could potentially be that the earlier we treat, the better the effect will be as well. Then just a single slide before we can go to questions about, well, what's happening now? This is the pathway for us to, hopefully, to market. We have a single registrational study ongoing in Europe and U.S.
Usually you need 2 studies, phase III studies, but in our case, it's enough with one because we have done in total, like 16 clinical trials with this, with this asset, and this is aligned both with the FDA and EMA. We have a potential for an accelerated approval in the U.S. This readout, interim readout, happening now towards the end of March. If it's statistical significant on C-peptide, which is the marker for insulin production, that can then pave the way for a potential accelerated approval pathway in the U.S. The full readout in the trial will happen towards the end of the second quarter next year. We read out the full trial of 300 patients, 50-month follow-up.
We have Fast Track Designation and Orphan Drug Designation in the U.S., which gives us both, like regulatory advantages with the FDA and also Orphan Drug Designation is important when you go to payers. I mean, it's not enough with approval, you need to get paid as well. As an orphan drug, you usually get a premium pricing as well and better coverage than if you don't have this. That was it. Questions?