Mention, of course, we're gonna make forward-looking statements, so please refer to our SEC filings for appropriate risk factors. We built Pharvaris around a heritage in a particular mechanism calle d the bradykinin B2 receptor pathway. Our founders worked together at Jerini to find the first molecule that exploited that pathway at icatibant and built on that desire to come up with an improved therapy for that space. We grew out the team with experts in orphan disease, also in HAE, leaders in both in development and commercialization in those spaces. We built our work around the discovery of an innovative new molecule we've called now deucrictibant. This is the first orally available bradykinin B2 receptor antagonist. The real breakthrough here was finding a compound that had potency and actually superior potency at the receptor to icatibant, with the size and the properties that allowed it to be used orally. That opened up for us a new opportunity to address bradykinin-mediated diseases, particularly leading with hereditary angioedema. Hereditary angioedema, or HAE, is a rare genetic disorder. It's characterized by swelling attacks that occur randomly and at various sites around the body. It's unpredictable in its frequency and location. Those attacks are actually quite serious. They're painful. They often lead to hospitalization, and in the case of attacks that occur in the face or in the larynx can be life-threatening as well. There's actually quite a bit of medical need in HAE. Globally, up to about 100,000 people live with HAE. In the case of US and Europe, there are a number of products that have introduced. Outside those areas especially, there's a great deal of underdiagnosis and undertreatment. There's a real opportunity to bring forward into this space a product that can be used in a variety of markets and in a variety of settings, much as we think an oral would be the way to do it. People who live with HAE treat their disease in 2 different ways. They either treat attacks when they happen, that's referred to as on-demand, and you see the segment of that global market here in the upper left of this pie chart. They prevent attacks with prophylactic treatment on the lower right. The prophylactic market currently is more dominant and has grown more, and that largely reflects innovation that's happened in this prophylactic disease space through new products that have introduced improving efficacy, tolerability, and convenience for patients. The market itself, while it looks like there are a lot of products, is actually quite dynamic. There's quite a lot of movement between products as these factors and these qualities improve. As I'd mentioned, this is what patients are seeking. They're seeking products that work, that are safe and tolerable, but then more and more products that fit into their life and fit into how they want to live and control their condition and their disease. Our ambition there is to come forward with products that meet all of those needs. The mechanism that we have our expertise in, shown here on the right, and the pathway that generates and was responsible for the HAE attacks is the production of bradykinin, shown in the yellow box, as it interacts with the B2 receptor. That sends off signals that leads to edema and swelling at various sites. There's a main pathway that we've shown here, which is activated plasma kallikrein generating this bradykinin, but there are other ways to get at this. So our mechanism at the level of the receptor intervenes regardless of how bradykinin is made. That's important because if you look to the left of this graph, hereditary angioedema has some subtypes. The blue we show subtypes caused by missing or non-functional C1 inhibitor. It's a central inhibitor of that plasma kallikrein enzyme. In a whole category known as normal C1 HAE have other types of mutations. The dependency on the C1 may not be there. We believe there's a universal approach by being down here at the receptor, the actual signal that sends off the angioedema. Another advantage that comes to us as a result of this mechanism is our ability to use a surrogate endpoint in humans to assess and predict an efficacious dose. We've used this endpoint. It was validated in the clinical experience with icatibant, the first product acting at the receptor, which is an injectable. Here we have an oral product where we use this endpoint to assess in a healthy volunteer the effects of bradykinin and how we can blunt those effects. We can set a. We set an efficacious dose. Through that, we've used that, for our on-demand study, which read out this past December and saw positive results. We're using that same approach for our prophylactic study, which we'll read out by the end of this year. With all of those factors in play, we have deucrictibant as a molecule with actually very versatile properties that give us the ability to create two different formulations addressing both the on-demand and the prophylactic segments of HAE. We're the only product in this space that can do that. We have on the left PHVS416 is our on-demand product. It's an immediate-release capsule. You see in the cartoon below the release profiles, it's actual PK data. You're taking a softgel capsule, immediate rapid exposure of compound above our target threshold to treat an attack once it's happened. On the right-hand side, PHVS719 is our extended-release tablet, and the aim of that is to have a slower release. Actually, no initial release, but maintain exposure above the threshold to prevent attacks. How we're using these in the clinic, PHVS416 has completed Phase 2 in the on-demand treatment of attacks. We're preparing for Phase 3 there. PHVS719 is in Phase 1, where we're preparing to actually jump that straight to Phase 3 because we've used as a tool the PHVS416 capsule with twice-a-day dosing and food to give us long-term, all-day exposure for a prophylactic experiment. We'll be able to leapfrog PHVS719 from Phase 1 into Phase 3 when we have the efficacy data. I'd like to mention a regulatory update. We are active in trials ongoing right now ex-U.S. In the U.S., we are on a clinical hold as a result of some non-clinical evaluation by FDA. We've met with the FDA. They've requested that we conduct a repeat 26-week rodent study. That study is underway, and we anticipate submitting the data from that study to FDA by the end of this year. They had partially lifted the hold in our on-demand program, where they allowed remaining patients from our repeat one Phase 2 study to finish. Outside the US, there's been no change to our regulatory status. All countries and sites there remain active, and our trials, both Phase 1 and Phase 2 studies continue. As we think about our pipeline and future possibilities, you know, around our mechanism of bradykinin activity, and one of the additional indications we think about is acquired angioedema. There can be multiple causes for acquired angioedema. In the blue sort of most prominently is an illness-related loss of C1 inhibitor. People who have lost C1 function will experience HAE attacks much like HAE. That's an area where we were thinking of expanding. It's about 10% of HAE. There's been a recent investigator-initiated study that's shown activity of deucrictibant on-demand in that setting, and that's an area where we will continue to evaluate and think about moving forward. When we think about our Phase 2 data in on-demand, you know, briefly, the goals here for patients, because patients are seeking in an on-demand treatment something that works quickly, something that works with a single dose, and something that's convenient and an oral. This was our aim with this study. We studied 74 patients in 13 countries. Together, 62 of them had 147 attacks, which built our database for this study. All the primary and then secondary endpoints were met. We showed rapid onset activity, symptom relief, and resolution of HAE attacks. We substantially reduced the use of rescue medication and were well-tolerated. We were very happy with the consistent outcomes we saw in the study across all marks. Very briefly, showing the tolerability here. You see 2 AEs in 2 attacks. 1 was placebo attack, and 1 was a treated attack. Very happy with that profile across that 147 attacks. The PK profile met all of our expectations. You see all 3 doses exceeded our target level very rapidly, we wouldn't expect to see any difference between those doses in the initial. Where you see differences in the long-term exposure, which would come out to reflect on the use of rescue medication. I'll show you that slide in a bit. Here's our primary endpoint, FAST-3 endpoint. It's a patient-reported outcome. As I said, all 3 doses show at 4 hours a significant drop in that score, which is a measure of swelling symptoms, and very strong separation from the placebo-treated attacks. In rescue medication, we saw that most of the attacks treated with placebo required rescue medication. It tells us that those were the attacks that people were experiencing were significant and real. We saw a very large drop in use of rescue for attacks that were treated with active. You see, you know, a hint of a dose response there, which reflects the PK of increasing doses lasting longer for attack resolution. In prophylaxis, we're proceeding with a CHAPTER-1 study. This is a multi-dose study, two different doses controlled against placebo, looking at a 12-week treatment period, running in 30 patients or rolling, I should say, 30 patients running in Canada, Europe, Israel, and the U.K. All those regulators are up to speed on the U.S. clinical hold, as I mentioned, everything is proceeding there. We are expecting that study to read out by the end of this year. Showing you for comparison, this PHVS416 and the PHVS719. You see here in blue, the PHVS416 capsule, the immediate-release. By dosing that twice a day with food is how we get to the exposure that we need. Overlaid here with the PHVS719 is where we aim to go when we go to Phase 3 with the tablet. Here we're showing you single-dose with and without food, exposure over a full-day with a single-dose of the tablet. The AUC that we see on this, with the tablet actually is similar to the AUC we see with a twice-a-day capsule dose. We're very encouraged that we'll be able to translate directly over. Summing up very quickly, you know, in our on-demand program, we've seen successful data in Phase 2. We are moving forward to Phase 3 in that program with the immediate-release capsule. With going diagonally down to the bottom right with PHVS719, we've shown single-dose activity there. We're doing the work to get ready to move that formulation into Phase 3. In the meantime, the proof-of-concept study using the capsule, in the CHAPTER-1 study is ongoing. Enrollment is going well, and we expect to announce that data by the end of the year. Very briefly, that's the story of Pharvaris. Happy to be around to take any questions. Thank you.