Great. I'm Sean McLean, founder and CEO of Abcci. We're a generative AI drug creation company. So when I founded the company 15 years ago, originally we were not focused on AI drug discovery. We were focused on how we can scale technology to look at protein-protein interactions, and we were an early adopter of generative AI in 2018, looking at how we could take this protein-protein interaction data with these transformers and really be able to go after hard-to-drug targets and start to engineer biology to be able to go after hard targets like GPCRs, ion channels. And we're at an exciting inflection point now in the history of AvSci where we're actually starting to see the drugs that we've designed with our AI go into the clinic. And within the next 24 months, we'll have two phase two clinical readouts from ABS-201 for antigenic alopecia, as well as endometriosis. I think it's a very, very differentiated pipeline that we're building out with the prolactin receptor biology. So when we think about drug discovery and utilizing AI, we think about it in the sense of being able to industrialize it, being able to get more shots on goal. And I think if you look at what we've been able to do to date, being able to get drugs into the clinic for, you know, roughly $10 to $15 million of investment, when traditionally that takes, you know, $50-plus million, it's really exciting to be able to see that you can start to fail fast with these investments. And you start to look at China, along with Agentic AI and these foundation models that are being built, you can start to see where you can very, very rapidly get to go from target to a phase two proof of concept readout in a very short amount of time with very low costs. And that's a future that we see and that we're looking to build. And as I mentioned, we've used our pipeline and technology to build a very differentiated asset ABS-201 targeting the prolactin receptor for androgenic alopecia and endometriosis, which I'll talk more about. So as I mentioned, we're using AI to really be able to design the antibodies to have the properties that we want, be able to go after these hard-to-drug targets. Ion channels, GPCRs have been notoriously hard-to-drug. One of our partnerships with Almaral, we've shown that we can go after an Ion channel that had been known for the past 20 years. No one had been able to actually drug this particular Ion channel, and we were able to use our Origin 2 pipeline and technology to actually drug that Ion channel, opening up new opportunities within that particular indication. We came out with an exciting update to our AI platform, an exciting foundation model, Origin1, where we're able to show that we could go after what we call zero prior epitopes. epitopes, so epitopes that have no structural information known to them, so there's no antibody complex to that particular target of interest, really being able to show that we can go after new novel targets and new novel epitopes. We're the first group, to our knowledge, to be able to show this. We recently came out with an updated manuscript on this, and we're excited to, again be utilizing this to create differentiated assets. So in addition to partnerships that we've had in the past with pharma companies like Merck and AstraZeneca, I mentioned Almaril, we're also building out our own internal pipeline. And we have ABS-201 that is in a phase two clinical study right now for androgenic alopecia and the endometriosis study on this program will start at the end of the year. And additionally, we do have exciting new early stage assets that are in development that I would say complement the prolactin receptor pathway and kind of this DTC market that's emerging within these two indications. So, ABS-201. This is an exciting new opportunity in the first indication, which is androgenic alopecia. So, think hair regrowth. This is pattern baldness that you see in both male and females, and it affects 80 million Americans alone. This is a huge on my medical need. There hasn't been a lot of innovation within the space for the last 20 to 30 years. The same two targets are continuously hit, the androgen receptor and finasteride, and then you have minoxidil. Again, these are not giving the patients, the durability that they're looking for, as well as efficacy. And I think that there's a lot of white space to improve on within this category. So what is prolactin doing in the hair follicle and in hair regrowth and just hair biology in general? What we've been able to find is that prolactin stress inflammatory access and from data that we've been able to generate and what's out in the literature is that it is driving this inflammatory process and fibrotic damage within the scalp and it's driving the hair follicle into the catagen state and ultimately driving the miniaturization of the follicle. And what we're seeing is that if you block this receptor, you're able to reverse the miniaturization and rebuild the stem cell niche, which I'll talk about later in these upcoming slides. So how does ABS-201 compare to standard of care? We looked at a hair regrowth model in mice. This is a shaving study. And what we were able to show when comparing ABS-201 to topical minoxidil 5%, we were able to show superior hair regrowth and efficacy when compared to oral minoxidil. Now, what got us really excited about this particular mechanism in the first place was the work that Andreas Bush did, our former chief innovation officer, while he was at Bayer. And what you see in the data up here are stump-tailed macaques. These are a population of monkeys that naturally go bald. and you're looking at the tops of their head. And they were treated for 28 weeks with an antiprolactin receptor antibody. And you can see that by six months, they get their pigmentation back. So you see they go from gray to their jet black hair. Now, it's pretty remarkable to get pigmentation back, regrowth, but what was even more remarkable here was post-treatment, for four years, they continue to regrow their hair. This is a true regenerative effect. Essentially, the body was able to heal itself and to regenerate the necessary machinery for that follicle to continue to grow. And we have a hypothesis as to why this is, And it all comes back to the stem cell. And we were able to elucidate some of this mechanism through a hair regrowth study that we did with Professor Ralph Paus at the University of Miami, a leading hair expert who developed this ex vivo model where we were able to take scalp biopsies. of individuals, in this case, males, and really be able to start to understand the mechanism of prolactin and what's going on. And this was a 72-day culture. And we compared the ABS-201 compared to prolactin. And you can see here from the microscopic hair cycling imaging, that ABS-201 is able to drive the follicle into the antigen state, and proloctin drives it into the catagen. And we have the full data set from this collaboration that we did at our KOL Day in December, so it is online if you'd like to see it. I will just highlight one piece here before moving on to some new exciting data that we are going to announce today. And this is on the stem cells. So what you see here is ABS-201 is able to increase the number of K15 stem cells in the niche. And what you see on the bottom left-hand chart is that prolactin drives the apoptosis of the K15 stem cells. And this is really important because what you see over time is the stem cell population being depleted in those balding regions. And so being able to replenish the stem cells is very key to being able to get that durable effect that you saw in the stump-tail macaques. And another piece of information, which we'll be sharing more later on, is it does look like prolactin does increase collagen 17A, which actually anchors the stem cell to the bulge and to the niche. And what you see with a lot of the literature that's out there is that the collagen 17a decreases over over time and so seeing prolactin or seeing abs 201 increase the collagen 17a in addition to the stem cells is is very encouraging and again what we believe is giving us that durability so one of the new pieces of data that we're presenting today is on the female. So we presented data to date on males. And one piece that we've been asked by investors recently is, how does this work in females? And we had strong confidence that this would work in females. You see it in female mice, You see it in the female stump-tailed macaques. We wanted to take a look at the scalp biopsies in female, and these are premenopausal females. We have postmenopausal females as well that is ongoing. We'll share that data once it's available. But what you see is a very similar effect in females or in males that you do in males. So as you block the receptor with ABS-201, you see an increase in the antigen phase, and when you add prolactin, you see it driving it into the catagen phase. And so, again, this lines up very nicely with what we are seeing in the stump-tailed macaques as well as the mice and what we saw in males. So we are excited to be sharing this with you all today. And just to round this study out, in addition to the stem cells, what we additionally saw from this study was two key growth factors, increased FGF7, IGF1. These are important for driving the follicle into the antigen state. We also see proliferation of the hair matrix with the keratinocytes, and also we see a decrease in TGF beta, again, when you're blocking the prolactin receptor. All of these are critically important for ensuring that all the necessary machinery is there to reverse the miniaturization and regrow the terminal hair follicle. And so we're really excited to be driving this program forward. And a quick update on the clinical study. So we have completed the single ascending dose. Within a very, very short amount of time, we will be releasing the SAD safety, tolerability, and NPK data. So please be on the lookout for that. We're very excited to be announcing that and sharing that data with you. And then additionally, the MAD portion of the study has started, and this is with healthy individuals that do have AGA. And then we'll have a 13-week interim readout on that later this year with the 26th efficacy readout, first part of 27. And again, everything is progressing as planned and very excited for these upcoming readouts. And again, here in June, in just a very short amount of time, we're going to have that SAD data out. So we took the TPP that we got feedback from dermatologists and being able to achieve roughly what oral minoxidil is able to achieve. And we see this being a very large market opportunity. And we took this into a consumer quant study. So assuming that you could have roughly oral minoxidil levels along with durability of two to three years, we estimate the market opportunity for this within the U.S. alone is $25 billion, and globally it's a $40 billion market. And we see this, you know, playing really nicely into this total vitality market that we're seeing evolve where, you know, patients not only want, you know, weight, they want their hair, they want to feel better, they want to look better. And we think that this, you know, fits really nicely into that and excited again for the upcoming data later this year. So now moving on to endometriosis. Same drug, same target, different indication, and very similar to AGA. This is a large market opportunity. The standard of care is really poor, and the need for therapy here is extremely high. The 1 in 10 women have endometriosis. It's a very debilitating disease. And prolactin and being able to shut that pathway off has the opportunity to actually be potentially disease-modifying where you're able to reduce overall lesion pain as well as decrease the lesion size as well. So as I mentioned, prolactin does seem to be driving the lesion formation as well as the pain sensitization. And here's some preclinical data. Data on the left-hand side shows how prolactin does drive lesion formation. And we have data on the right-hand side looking at overall pain. And you do see that by blocking the prolactin receptor in mice, you do see an overall reduction in overall pain seen by how far these mice can walk. We've also done some recent studies showing how prolactin drives pain sensitization as well, and so you have the opportunity to reduce, again, the pain as well as the lesion formation. Again, given the fact that standard of care here is extremely poor, there is no disease-modifying therapy out there. one in 10 women do experience endometriosis and have it, we do see this being a large market opportunity of over $4.5 billion. I'll end with this. We have two very exciting phase two readouts coming up within the next 24 months. We have AGA, second half of this year, 13-week, and then followed up with the 26th week and early 27. We have the endometriosis study starting and we'll have a phase two readout on that next year. And as I mentioned, tune in. Very soon we're going to have the SAD safety, tolerability, and PK data out on ABS-201. And I'd like to thank you all for