I'm the CEO of the company. Since six years back, I'm going to talk about what we do and where we stand at the moment. We're based in Stockholm. We're focusing on ophthalmology, which is eye diseases. We have some work ongoing in oncology as well, but I will not talk about that today. We're listed since seven years back, almost eight years back. We base the science on things coming from the Karolinska and from Inserm in Paris, but also a lot of our IP is actually built on our internal work, particularly in the CMC region. We're working with Annex V, which is a version of a protein that you all contain, right? An Annexin A5, which protects cells. It's going to be first in class if we reach that stage. We have a disease-modifying potential, which is very important, but that's why we're also very different from the different opportunities available today in ophthalmology. We are hoping to stop chronicity of disease in the eye. Right now, we're in phase 2A data that we're still working on and presenting to potential partners. We're geared towards running a phase 2B trial with the partners, help with the partners' financing, but also expanding a little bit into another field of ophthalmology with diabetic retinopathy, which I will come back to. It's really working with an upstream mechanism. The current therapies are targeting targets which are downstream of our work. If we succeed, those other medicines will not be needed. That's a very blunt way of putting it, but that's potentially the reality. The phase ll data, which tells us very clean on the safety side, we have what we call positive signals of effect in ophthalmology disease called retinal vein occlusion, and it's a rapid and durable effect. To the right in your eyes, we have RVO, retinal vein occlusion. We are going towards multi-billion dollar opportunities, and we do stand out in terms of the proof of concept data that I present to you. This is the eye. When I'm looking at you, or you, or you, you, I make sure that the light from you comes onto my what's called the macula, which is a place inside the retina, which is net hinnan in Swedish. I make sure that that light targets that because that's the spot, very tiny spot about three millimeters wide where you see the best, your most sharp vision. That's what we measure in ophthalmology. We measure sharp vision. You know, looking at the board with the different letters on it, you try to read as many letters as possible. That defines your quality of your visual acuity. Sometimes you use lenses. That's called best corrected visual acuity. If you look at a normal macula, which I hope is what it might look like, it's very clean. It's a spot there in red. Below that spot and elsewhere in the eye, there's the rods and cones, tapper or stavar. You see the light hitting them. They translate the light into an electrical signal, which is brought back to the brain. That's what you see. If you look at retinal vein occlusion up there, you see that's a very different view of the retina looking in the microscope. It looks pretty bad. Also in diabetic retinopathy, which has a later stage of retinopathy, it looks pretty bad too. It doesn't take an eye doctor to tell you that you have a bad vision in these cases. In terms of retinal vein occlusion, it's really a rapid onset to potentially one of those happy people, sudden, painless. You start seeing in a very blurry way up to the right. What basically has happened in your eyes is your veins making the blood leave the eye actually are clogged by red blood cells. That's why you have like a backflow problem. You get swelling, your cells are dying, and it gets worse and worse. The swelling is right in the middle where you see the different layers of the retina become distant from each other. Basically, you get fluid into those spaces. Therefore, you can't see. This is a standard treatment. It looks kind of ugly. These patients, both in retinopathy from diabetes or an RVO, are treated like this. You get injections straight into the eye by anti-VEGF. There's an antibody that reduces the presence of VEGF, the growth factor. They get in real life five treatments in patients with the RVO in the first half year in the US. That's in real life data. They require five first half year, and then they require two or three more. Some are chronic. They would have to receive them monthly or bi-monthly for almost their entire life. In diabetic retinopathy, they started getting one or two, three, four first when they get this kind of worst kinds of retinopathy. Our really differentiating proposal is that we give an IV infusion for three days or maybe five days, and then we probably do not need as many anti-VEGFs, if any. That's really the goal. We attack a small phospholipid on the surface of cells, which is exposed on the surface of cells when they are stressed and when they are dying. This little phospholipid is triggering inflammation, coagulation, and all sorts of bad things in the tissue. Annexin A5, and therefore Annex V, blocks this phospholipid from signaling all these bad things, to put it in a simple word. Why are we so different? Anti-VEGFs and the currently available and actually pipeline type of approaches to treat RVO and diabetes is often triggered towards these factors, VEGF, NH2, PDGF, and so forth. We are claiming that if you because these are triggered by the loss of perfusion of blood into the lower parts of the retina and indicated by the green arrow. That's where the hypoxia, the loss of oxygen supply, is the worst. That starts producing VEGF, and that VEGF drives the swelling and a lot of bad things. That's why anti-VEGF works, because it reduces the swelling, goes back, but it becomes like a Botox of the eye. You have to have repeat injections every month. Those are bad things. What if we can actually stop hypoxia by improving the blood flow in the lower parts of the retina? That will solve the problem and take away the needs for anti-VEGF and other drugs. We did a phase 2A study in the United States, started three years ago, I guess, two and a half years ago, and we finished it. We had 16 patients. They were treated with five injections daily. We followed them for four months. We had different kinds of patients compared to the anti-VEGF studies. We had patients with less problems or with huge problems. We were able to show safety, like I said before. The key thing, I think, is that we reduced the need for anti-VEGFs from expected five injections for six months to maximally one injection for four months. Five of the seven or 12 patients we evaluated along these lines had only needed one anti-VEGF. The other seven did not need any anti-VEGF treatment, which is a bit of a surprise. Again, it is not a controlled study, so we cannot really draw major conclusions from it, but still, it warrants a phase 2B study in our minds, in many opinion leaders' minds. The effects were durable. We have visual gains, meaning reading the board better. They were durable. We have fluid decrease in the eye and so forth. These are very key components in ophthalmology study. This is another Eureka type of data. Focus on the left side of the slide. We actually, key opinion leaders in the U.S. will say, wow, this is a bit of a holy grail. You achieved something and nobody has shown us before. That is very important. The patient had obviously two eyes, the healthy eye and the blood flow in the retina is reflected in the green line, where the blood flow in the unhealthy eye suffered from RVO is in the blue line. You see from the screening of the patient, it is actually straightforward for the healthy eye, but goes down further in the affected eye. After only one Annexin A5 or Annex V treatment, blood flow is up and becomes stable, which makes sense. That is because this patient did not need an anti-VEGF and so on. It was a very stable development for this patient. This is another patient that has been stable for 30 months with only one anti-VEGF. If we look at the patient response again in the blood flow in the deeper parts of the retina in the macula, which is most important, the blood flow goes up dramatically after the Annexin treatment. It is probably not possible to be a placebo effect. You can probably disregard that. It is a very important mechanistic differentiating factor in ophthalmology to be able to show this kind of data. Again, we need a phase 2B controlled placebo trial. Talking about this going forward, phase 2B and phase 3, we assign or assemble this very knowledgeable group of key opinion leaders from the US. They sit on similar panels in 20 different companies and so on. They see everything that gets to the FDA. They see pretty much every project in much detail. They are very enthusiastic about our data as well. We got their advice on the 1st of October, and we were putting together everything they said into a comprehensive phase 2B design. We're very happy to have this group of people on board. Last slide, summary wise, we're addressing these RVO and we're positioned to start phase 2B trial ASAP, pending funding, pending FDA feedback. This is reducing the need for IVT injections, meaning injections straight to the eye. It's a multi-billion dollar market for RVO. It's not a multi-billion dollar market for retinopathy. Seeking regulatory advice said by many is key to the development. This is key to discussions as well. We know they want some regulatory advice to be able to or willing to take a next step. Not all of them, but some of them will say that. The company is positioned to move forward in other diseases of the eye, as well as the embroidered, and that we can do different formulations. With Annexin A5 that we got, Annex V, it's very stable to work with. First and foremost, or maybe last and foremost then, is that we're seeking strategic partnerships with a major player to finance and run the phase 2B on their own or together with us. Thank you. That was my message for today. Thank you, Anders. Someone going straight to the heart of the matter here with the question about what the price is going to be when it goes to the market. We have actually done some price comparison and actually asked payers in the US what they think about the pricing. I can't really go into the detail. I have to give the perspective is that the cost for anti-VEGFs, I think that's well known, is about $13,500 per annum given the multiple injections they need to have. If we can reduce that use of anti-VEGFs in the U.S. alone, we have to discuss the pricing, of course, but I mean, it's a relatively attractive pricing opportunity. You mentioned and you showed your new medical advisory board on a slide there. Can you elaborate a little bit on how you're leveraging their expertise? How are you using them? They are practicing ophthalmology, so they know the patient situation. They know how to run a trial. They know how to work with patients and the team at their sites. What is reasonable? Would they want to treat patients with edema with an Annexin straight away, or would they actually want them to have an anti-VEGF first and then give them Annexin A5 and so on? It is a discussion where they kind of bring us back to reality in the sense that this is actually doable. This is what I think you should do. They meet with FDA. They represent companies with the FDA to have discussions with their expertise in ophthalmology. They are totally invaluable. I mean, they provide us with all kinds of references, and they know the endpoints that are provable by the FDA. It is a very US-centric team so far, but normally you would say that half of the market for these kinds of products will be in the US, and the rest is the rest of the world. Because that was going to be my last question. It was about the market because it is very US-centric, and that's by design then because the US is your main target market. No, it's not. I mean, but it's really for any strategic partnership, they will want to know what the FDA thinks. They want to know what the US market is. The rest of the world, Europe is more complicated. Asia is also complicated, so it comes as a next step for us. Thank you so much, Anders. Thank you very much. Thank you. Thank you.