Good morning, everyone. Thank you for joining our deep dive today into ABS-201. At Absci, our mission is to use generative AI to create better biologics for patients who don't have good enough options today. We talk a lot about our platform, our lab in the loop, and our ability to create better biologics faster. But today isn't just about the platform in the abstract. Today is about the results: ABS-201, which we believe could be a paradigm-changing therapeutic for androgenetic alopecia. Now, historically, the biopharma industry has dismissed hair loss as just cosmetic. But when you speak to patients, you realize that characterization is deeply flawed. For tens of millions of people, both men and women, this is not about vanity. It's about identity. It's about mental health and a profound loss of confidence that impacts their daily lives. Despite this massive unmet medical need, the standard of care has remained stagnant for decades. We're relying on old mechanisms that often come with difficult trade-offs. This is why we're so excited about ABS-201. By leveraging our AI drug creation platform, we have unlocked the prolactin receptor pathway in a way that we believe offers a differentiated, best-in-class profile. We have an incredible agenda for you today. It follows the journey from the patient to the antibody to the market. First, you'll hear from Dr. Rossi, who will lay the groundwork in the patient reality and the psychosocial impact of hair loss. Then we'll move into the science. Andreas will discuss his long history with the mechanism and why he's so excited to finally see this brought forward in the clinical trials. Professor Ralf Paus, a world expert on hair biology, will walk you through the mechanism of action and the compelling ex vivo data we've generated. Next, Denis and Dr. Sinclair will detail our clinical trial design. Dr. Sinclair's experience with the prolactin receptor mechanism is unparalleled. He will explain why he believes this trial is set up for success. Finally, Dr. Goldberg, Mike Jafar, and Zach Jonasson will define the target product profile necessary to change the treatment landscape. They will walk us through the significant commercial opportunity that lies ahead. We believe ABS-201 is more than just an asset. It is proof of what happens when you combine deep biological insight with the speed and precision of generative AI. But before we get into the data, I want to ensure we start where every drug development journey should start: with the patient. We'll play a short video that captures the reality of living with AGA. After that, I'll hand it over to Dr. Rossi. Thank you for being here. Let's watch. My name is Kelly Caesars. I have three kids, a husband. I'm from Wisconsin, a middle school and high school teacher. I hope they would describe me as kind, funny occasionally, a lover. Yeah, I hold my family really close to the heart. It would have been my junior year because I was living in an apartment, and I just noticed in the shower that a ton of hair was falling out. I already had my thyroid checked, and I had the vitamin deficit, all that stuff checked that they say you should get checked, and it all came out normal, so kind of my last stop was a dermatologist, and she was the one who said I had the female pattern baldness, and they said there were medications available, but they didn't recommend them if I was going to have kids or if I wanted to have kids. I did want kids, so that wasn't an option. I basically kind of left. I literally think I called my now husband, and I was like, "We need to lock down a date because I'm balding, and I need to make sure you're locked in for life because I'm losing my hair. So let's set a date." I have my topper in right now, and this is kind of how I do it every day. I'll take it off so you can kind of see where my hair loss is thinning. My part is kind of starting to widen, and you can see at the top, it's like when you can start seeing the scalp that drives me nuts. The really bad spots are the crown of my head, which is where the hair thinning started from the get-go. It's just slowly getting worse. It's a struggle that I have. I don't always love the way that I look. But again, that doesn't make all of me. That's just one piece of me. And I think that's been the biggest thing. And that is a daily struggle that I have to tell myself. It's exhausting. Yeah, it sucks. And I don't want my daughters and my son to see me as someone that doesn't love themselves because I don't want them to love themselves and never think they're less than. Sorry. So I just will keep faking it till I really believe it. I'm not wrong for feeling this way. There should be a solution, and people should be paying attention. I wish there was actually something that would not just thicken the hair I already have, but regrow the hair that I have lost. That is what I want. If science could eliminate hair loss, that would be the dream. As a kid, I remember very vividly being five and six years old, scoring a goal, feeling the adoration from the parents on the sideline or my teammates. And that translated to being a professional scoring goals and feeling the love and adoration from the crowd. And that was almost an addictive cycle that I wanted to feel more of that, and it propelled me to score more. I'm Landon Donovan. I played soccer for 14 years for the Los Angeles Galaxy and the U.S. Men's National Team. I was fortunate to play in three World Cups. I scored five goals, which is the most all time for the U.S. Men's National Team. I won six MLS Cup championships. I proudly lifted 11 trophies in my career and over 150 games played for the U.S. Men's National Team. I don't know the exact age, probably 22 or 23. I wasn't losing hair, but my hairline was receding. And I would start looking and look back on earlier pictures, and I was like, "Oh, it was here, and now it's here." And in warm-ups or during the game, I would hear people start making comments about my hair. And they would say, "Hey, looks like your hair's falling out, Landon. You're getting bald, Landon." As the internet became the internet, there were so many comments about receding hairline and look how bald Landon is. And then it would happen also in the stadium. So it was just this constant dribble about it all the time. And over time, that starts to impact you. Knowing millions of people or tens of millions or hundreds of millions of people around the world are watching, you feel helpless. There's nothing you can do about it. When you're on TV a lot, it's right in front of people. They're not distracted by the game and what's going on. They're just looking at you and your hair. So it's been exacerbated since I stopped playing. And sadly, unfortunately, so has the receding. It's gotten worse and worse. So I went in at 25, 25 years old, pretty young. The only option that was viable was to get a hair transplant. I've taken oral medication, topical medication. I've tried it all. Now I have a hair system. I've tried everything, and I've been desperate, I think, like many, many, many millions of Americans for something that will solve this problem once and for all. A perfect situation is I have my real hair in my real head. I mean, that I would feel free. I can feel it in my body. That would feel so free. I desperately want that back. I think in the past, people view this as a vanity thing. For me, it's not vanity. It's a disease. I know how this impacts human beings. It's impacting me. I'm really grateful that Absci is putting the resources and the funding into this. Hi, I'm Dr. Rossi. I'm a board-certified dermatologist and dermatologic surgeon. I work at Memorial Sloan Kettering in New York City, and there's not a day that goes by that I don't talk about hair loss with my patients. Hair loss for many patients is not just a cosmetic issue. It's actually a medical problem that affects them psychosocially, emotionally, and then their daily activities of living. We view hair as something cultural, something religious, something that people identify with. Growing up with hairdressing parents and being in a hair salon my whole life, I really know that firsthand, how meticulous people are with their hair, and so hair loss for me is not just something cosmetic. It's a disease that dermatologists want to tackle. They want to treat, and they want to improve their patients' quality of life. It's akin to obesity. For many years, people didn't think obesity was a disease. They thought it was more a cosmetic, basically cosmetic issue, but it's not. We know it's a disease. We know it represents something that's going on inside the body as well. And I view hair loss as that. I try to get to a root cause analysis of why this patient's losing their hair and how we can better treat them holistically. There's different causes of hair loss. There's different types of hair loss. But we do know, above all, that it really affects patients psychosocially. And not only is it something that's going on physically, but emotionally, it can really take a toll on patients, and even young patients and female patients. And we've seen an uptick of female patients coming in for this. And this is driven by awareness. Back in the day, we didn't have so much awareness of female pattern hair loss, and now that more women are talking about it or describing it, it's really helped to bring this to the forefront, especially for women, and hair loss does affect everyone. We know all ages, males, females, as you heard from Landon and Kelly, two different time points in their life, both affected by androgenetic alopecia. What's really amazing is that I'm seeing patients that are highly motivated to tackle their hair loss, and this includes young men who sort of know that they have it coming down the genetic pipeline. They see their parents with hair loss, and they know they really need to address this early, as well as now females, which is amazing because they're talking more about hair loss, even though there's a lack of FDA-approved medications for it. They're talking more about it in the chat rooms, and they're bringing it up in their consultation. They really want to address their hair thinning and their hair loss, especially around the 30s and 40s. It's really critical for them. And this is something that we want to give options to patients. We don't want to just say, "Hey, there's this only medication that you can take." But if we had more medications that we could actually use in these populations that were safe, efficacious, but also durable because we know we will have to be treating them for quite some time. And I'm really excited about the future of hair loss. And for myself to treat hair loss, that's because ABS-201 represents a completely novel mechanism of action that we can use to help actually tackle hair loss and androgenetic alopecia. It comes at hair loss in a completely new perspective than anything we've had before, and to hear more about the science of ABS-201, the prolactin story, the mechanism of blocking the prolactin receptor, we're going to hear from Andreas Busch, who's going to go over all that amazing research. Hi, I'm Andreas Busch. I'm the Chief Innovation Officer at Absci. Previously, I've been for many years in the industry being responsible for research and development at Bayer and at Schering. In these times, we have brought numerous projects towards clinical development and approval. I think I would probably account for more than 10 compounds being approved in my past. And I have to say very few projects present themselves with such an excitement and potential as the prolactin receptor antibody, which we're going to talk today about in our workshop. It was at Bayer where we started work on prolactin. Prolactin, as the name says, was obviously first discovered for its role in lactation. But what was also very obvious is that prolactin plays multiple roles in very different, diverse pathophysiological events in human biology. We identified a role in endometriosis, but it was already at that time known that also prolactin could play a role in hair growth. So we found that prolactin was responsible in a dual manner in endometriosis. On the one hand, it was clearly playing a role in nociception in the way women perceive pain in endometriosis. On the other hand, it was at least also in part responsible for the proliferation of endometrial cells, which is, of course, the cause of the lesions and the lesion size. As a consequence, our thought was that inhibition of prolactin in endometriosis would have a dual mechanism too, which is, of course, reduce the lesion, would therefore be disease modifying, and of course, also reduces the pain, which is the number one problem women really perceive in endometriosis. We obviously then developed an antibody against prolactin to study this antibody in disease models. And not to our surprise, it really nicely affected the proliferation of endometriosis in animal models. But much to our surprise, there was a more striking and obvious result, which we got, which is the shaved animals, which we had to shave for surgery for endometriosis models, had a very rapid and significant hair growth. The hair really grew like hell in those mice treated with the antibody, thereby validating and confirming the previously mentioned observation that prolactin could play a role in hair growth. After the very compelling results in mice, we wanted to take that result one step further. We became aware of a naturally occurring androgenetic alopecia model in stump-tailed macaques. And again, believe me or not, what is a bigger dream of a pharmacologist than a naturally occurring disease model in a non-human primate? So we went into that primate. I commissioned a study, and the result was just striking. Both in male as well as in female non-human primates, we saw a sustained hair growth. And even further, we saw repigmentation of the hair, which at that point in those non-human primates had already turned gray. The experimental design of this macaque study was very well thought through. We treated the animals for six months. We dosed in a way that we assumed that we can see 90% occupancy of the prolactin receptors. And we followed up after six months of dosing these animals for several years. What we saw was, as already mentioned before, significant hair growth. In some regions, we saw doubling the hair. But we didn't just see significant hair growth, but we saw repigmentation of the already gray hair of those macaques. Not only that, we saw that after six months, we saw this in the follow-up period of up to four years in a sustained manner. So that certainly gave us very significant confidence that hair loss is indeed dramatically affected by prolactin and the inhibition of prolactin in this androgenetic alopecia setting can cause hair regrowth. Together with the compelling efficacy results in non-human primates, we, of course, were interested in the safety profile of the prolactin receptor antibody. We did the relevant pre-IND safety studies without any significant findings, which we were, of course, very pleased about. But probably even more important, we meanwhile got aware of genetic studies in females in which a complete knockout of the prolactin receptor was shown. And this complete knockout of the prolactin receptor antibody caused nothing in that woman except a problem with lactation, but no other health concerns, which, of course, gives us again additional confidence in the safety of prolactin receptor antagonism. So despite those compelling results on the efficacy and safety of prolactin receptor antibody in hair loss, we at the time did not further follow up on development in hair loss for numerous reasons. Hair loss was not in our strategic focus. An indication like hair loss was considered not appropriately treated with biologics or injections. That was considered an application which should be reserved to other indications. So similar to other indications, a learning curve had to be taken. This learning curve, which we saw in the industry, was taken by GLP-1 agonists, I believe, where in obesity, the application of injectable peptides resulted in a complete new market situation, in a situation where patients understood the value of peptide injections. They were very much willing to pay out of their pocket for this indication. And therefore, we see that, of course, a safe and efficacious biologic in an indication such as hair loss is something very viable and something very marketable. Besides being convinced about the mechanism being a tangible one for hair loss, we also saw the shortcomings of this original antibody. We saw that the half-life was not the half-life we wanted to see. The solubility was not the solubility we wanted to see for an overall commercially attractive antibody in hair loss. And when I arrived at Absci, Sean and I very quickly discussed whether this would be an attractive mechanism to, A, show that our platform, our AI platform, works for generating an optimized antibody where we can simultaneously optimize several parameters of an antibody and make this prolactin receptor antibody commercially viable. We started this task a little more than two years ago, and we came up with an antibody which now does provide a half-life, which we believe will enable us to apply the antibody maybe every two to three months only. We do think that we have an antibody with a formulation which can be applied subcutaneously, also very important for that indication. Taking all of that together, we do believe that we now have generated with our platform a commercially highly attractive antibody. I was for a very long time a believer in AI and the potential of AI in the entire value chain of R&D processes. Having said that, it is extremely gratifying now to see that we are bringing an AI-optimized antibody into the clinic, that we will see that indeed the power of AI does translate to a clear benefit of the patient. I talked about the multiple roles of prolactin in human biology, both in pathophysiological settings as well as in physiological settings. Of course, one of the pioneers in the role of prolactin in hair growth is Professor Paus. Not only is Professor Paus an expert in hair follicle biology, he will now work together with us to further characterize the effectiveness and mechanism of ABS-201 on hair follicle biology. With this, it's my privilege and honor to hand over to Professor Paus. Over to you. My name is Ralf Paus. I'm a research professor of dermatology at the University of Miami Miller School of Medicine, and I've worked for a long time on hair research. In addition, we have investigated neurohormones of human skin. And in both areas, we have done some pioneering studies. And this is where the hair follicle enters the picture. This tiny but miraculous mini organ that makes hair shafts, for example, on your scalp. This organ is so special because it not only is highly responsive to numerous hormones which control its growth and hair shaft production and hair pigmentation, but it even makes these hormones themselves. And the discovery that we made about 20 years ago is that one of these hormones that is hardly ever talked about in hair research is prolactin. Prolactin is most famous for being the key hormone that controls milk production. That's where the name comes from, prolactin, but we now know that this hormone does multiple other things. It is controlling growth. It has immunoregulatory functions, and about 20 years ago, we found that not only do human scalp hair follicles respond to stimulation with this hormone, in fact, they were inhibited when we microdissected and organ cultured them by prolactin, but they even made prolactin themselves, and this is where ABS-201 comes in, the prolactin receptor blocking antibody developed by Absci. The company had read this old study and thought, well, could we perhaps promote human hair growth by blocking the receptor for this neurohormone in order to keep the hair follicle longer in its growth phase and anagen and thereby reduce the daily hair shaft shedding and get longer-lasting effects than you would get with normal drugs with a short half-life. We used a system that we have been using for many years to study the effects of all sorts of hormones and neurohormones on human scalp hair follicles. What you can do is you can microdissect these little organs, and then you throw them into a culture medium. Crazily enough, they still grow as if they were on the living human scalp. In this assay, as shown here on this slide, you ask the question, is my test substance, in this case, for example, prolactin or the prolactin receptor antibody, is that pushing the growing follicle or the anagen follicle? You start with 100% anagen follicles in your culture. Is that pushing the anagen follicle faster into the regression phase, catagen, or is it retaining it longer in anagen? If it retains it longer in anagen, that means you will have less hair loss. What we are really looking for in this essay is on the right-hand part of the slide, the transition of androgenetic follicles into catagen in this hair cycle. But in this case, we studied it not in isolated microdissected hair follicles, but we took the entire human scalp skin. And specifically, we used so-called temporofrontal scalp skin. That is the scalp skin where androgenetic alopecia first becomes manifest in males. And why did we take the entire scalp skin and not microdissected hair follicles as we had done 20 years before? We did that because we know that many cells in the skin have receptors for prolactin and can respond to it. And we wanted to see how this antibody is impacting on hair follicles that are living in the real tissue environment that they see in the living human body. What you do then is you take photos. You see this on the right-hand side of scalp skin biopsies that you get from volunteers, and you see what is changing in the hair shaft production over six days. Then you take sections of these tissue fragments, and you look at them under the microscope, and you assess first and foremost what is happening with the hair cycle. Are these hair follicles staying longer in anagen, or do they go faster into catagen? That's the key question you have. Then you can look at all sorts of additional markers and give you a better idea of what exactly is happening. The first thing you need, of course, to check in this system is, does this antibody even do what is claimed that it does? And if you want to show that your antibody in this case is blocking signaling through the prolactin receptor, you have to show that phosphorylated STAT5, one of the signals that transmit a signal after stimulation of the receptor by prolactin, is upregulated. And you see this in the green bar on the right-hand side, that that's exactly what happens. If you stimulate scalp skin with prolactin, then you get an upregulation of this signal. And if you do this in the presence of the blocking antibody, this is abrogated. That was good news. So we know this antibody is really active. It does what it's supposed to do at the level of the prolactin receptor. And this perhaps is the most important result that we initially got. So we looked, was there any effect on hair shaft production? As expected from our older studies in microdissected hair follicles, if we stimulated entire scalp skin, male scalp skin with prolactin, hair shaft production over six days was reduced. The follicles, the number of follicles that stayed longer in anagen in the growth phase, you see this by photodocumenting that the hair shaft gets longer, was actually increased not only when you co-cultured prolactin with the prolactin receptor antibody, but even by the prolactin receptor antibody itself. That's the bar on the second bar from the left in the center. That this antibody alone has already hair growth promoting activities suggests that it is actually inhibiting prolactin that is locally made in the hair follicle, just as we had published many years ago. And I was particularly interested to see this result and quite gratified because when we had first published this, there was lots of disbelief in the field that this actually is real. But this is all macroscopic data that we see. So what you can almost see with the naked eye. But the real litmus test is to use histological microscopic markers to prove that these follicles are really longer in anagen and that the antibody against the prolactin receptor can antagonize the push towards catagen that prolactin gives the follicle. That's exactly what you see on this slide. So again, the antibody alone, the second bar from the left, keeps hair follicles longer in its growth stage. If you only give prolactin, they move into catagen. And if you give prolactin and the antibody, you again have an anagen prolonging effect. Then you can look at this more fine-tuned, and you can see what is the effect on cell proliferation and cell death, apoptosis in the actual hair shaft factory, which is the so-called androgen hair bulb, the androgen hair matrix. No surprise, what you see here is a phenomenon that perfectly supports what we had seen in terms of the hair cycle changes. Proliferation in the hair matrix is stimulated by this antibody against the prolactin receptor, and cell death, apoptosis, is reduced. Note on the graph on the right-hand side, the blue bar, the impressive cell death protection effect of just the prolactin antibody, the prolactin receptor antibody itself. When we initially started with this work and we discussed how to set up these experiments, I reminded our colleagues that five years after our initial paper, we had found in female scalp hair follicles. And then if you blocked the prolactin receptor with a drug that may not have been as selective as this new prolactin receptor antibody, the stem cells did not like it and went into apoptosis. Therefore, we were nervous to see what would happen here in male scalp hair follicles in the stem cell compartment, the so-called bulge. Lo and behold, the stem cells loved it. The apoptosis actually went down when they were stimulated with this prolactin receptor blocking antibody. And in the presence of prolactin, the stem cells even proliferated, divided more than in the vehicle control group. That was excellent news and is particularly interesting in a context of androgenetic alopecia because androgenetic alopecia has two driving factors. One probably critical driving factor is that the follicle gets smaller and smaller due to missing inductive signals from the so-called dermal papilla at the base of the hair follicle. But the other contributing factor is that the capacity of hair follicles to generate daughter cells from these stem cells is diminished. So we looked at that too. And interestingly, if you just give prolactin, that's the green bar on the left-hand side of the slide, the number and the expression of these cells that are daughter cells that are directly produced from these stem cells gets reduced. And if you give the prolactin receptor blocking antibody, this can be completely reversed. That is fascinating from an androgenetic alopecia perspective because so far we have no drugs that can really do that. It appears that just blocking signaling through this one neurohormone receptor can restore the capacity of hair follicle stem cells to make daughter cells and thus keep the organ in its desired large size. But that's not all. When I first saw these slides, I said, "What, God? What is this antibody not doing?" It's actually improving the production of the key growth-stimulating growth factors that the hair follicle makes itself. If you dump prolactin on male scalp skin, the green bars, then the production of key growth factor called insulin-like growth factor 1, IGF-1, goes down. And even that of another important growth factor, FGF-7, fibroblast growth factor 7, goes down. And that can be completely counteracted by adding the prolactin receptor antibody. But even better, insulin-like growth factor 1, the one growth factor that in human hair follicles keeps the follicle longest in its growth phase, is stimulated just by the antibody alone. That means that just blocking the prolactin receptor with this antibody increases the capacity of the hair follicle to produce growth factors itself with which it maintains and promotes its own growth. Yeah, and finally, we had shown before that you see this here again on the left-hand side of the slide that hair shaft production is stimulated by adding this antibody. And if you see this microscopically, you would expect that also the production of hair shaft keratins, proteins that make the hair shaft, is upregulated. And that's what you see in the graph on the center in the immunofluorescence microscopy images on the right, that that's exactly what happens. The antibody has the capacity to prolong the growth phase of the hair cycle and thereby reduce the daily hair shaft shedding that dermatologists call telogen effluvium. It moreover also promotes hair follicle stem cells themselves and specifically their capacity to produce new daughter cells and to maintain this. This would antagonize the androgenetic alopecia associated hair follicle miniaturization process. As if this were not enough, the antibody also stimulates the follicle to make more potent growth factors itself and to increase hair shaft production. They're very impressive. I did not expect that when we started this in reality. I was fairly skeptical that any of this would happen, but it did. We repeated this in three donors, and that's about the time point when you feel confident about your own data. So in summary, we are looking here at an antibody that really blocks signaling through the prolactin receptor directly in human scalp hair follicles in intact human scalp. So in the target organ that we want to treat clinically. And it does this on multiple levels. It on the one hand keeps the follicle longer in anagen. On the other hand, it stimulates the production of growth factors that the follicle needs to remain in anagen. And finally, it even stimulates stem cells and their capacity to generate new daughter cells and also promotes hair shaft production. That a single neurohormone receptor antibody could do all of this is highly unusual. I did not expect it, and I'm quite impressed by this. Until now, we discussed our data from organ cultured male scalp skin. But now it's time to talk about clinical trial data. We go from ex vivo to in vivo, and this will be introduced by Denis, followed by Professor Rod Sinclair from Melbourne. Hi, my name is Denis Akkad. I'm VP Research at Absci and Program Lead for ABS-201. Within my role as VP in Research at Absci, I'm ensuring that the antibodies which the talented AI and wet lab scientists create have a seamless transition into the clinical development. Prior to joining Absci, which was an amazing opportunity in my career, I worked for a decade in big pharma across multiple indications, spanning from heart, lung, kidney, and endometriosis in women's health. My background is a trained biochemist with a PhD in neuroscience and also a training as laboratory geneticist. As you have heard from Andreas, the prolactin receptor ABS-201 is one of these rare occasions as a geneticist where you really have these cases where human mutations guide you with regard to the safety profile, but also with the efficacy when we're looking into the mode of action. And I'm very excited to announce that we have dosed our first participant in our headline trial. The phase 1/2a study aims not only to look into safety and tolerability as the main readout, but also we anticipate to have our interim efficacy readout in the second half of 2026. At Absci, we always go big. This is why we have designed the ABS-201 headline trial in a way where we not only combine safety and tolerability, but also efficacy in a really fast way. So how do we do that? So basically, what we have thought about is how can we combine the preclinical readouts which we have from the monkey study and the ex vivo study in a really nice clinical trial design? And I'll walk you through that, how we have outlined it. The headline trial is a double-blinded placebo-controlled trial, which aims to enroll up to 227 participants with and without androgenetic alopecia across single ascending dose and multiple ascending dose cohorts. Within the SAD portion of our clinical trial, where we are looking into up to four single ascending doses in healthy volunteers, we will mostly assess safety and tolerability, but also immunogenicity and what is most important, pharmacokinetic profile. So how long is the half-life of the antibody? We will then transition in the multiple ascending dose portion of the trial, which has been designed in a way to be statistically powered to show hair growth efficacy throughout this treatment duration. What do I mean with that when we're speaking about treatment iteration? What you have heard earlier from Andreas is that within this naturally occurring androgenetic alopecia stump-tailed macaque model, those monkeys were treated for up to six months, and we are aiming to do so for the healthy volunteers. So this means that the healthy participants are dosed over 26 weeks, and we will do a hair regrowth assessment at baseline, at 13 weeks, and then at 26 weeks, and then look at the hair regrowth progression over time. Based on the engineered long half-life of our antibody, we will follow up the participants for nearly a year, and within this follow-up period, we will further interrogate the durability effect of the hair regrowth. The hair regrowth assessment is measured by taking global images from the healthy volunteers, but also what Professor Paus showed you, macroscopic images of the scalp area where target area hair count, target area hair width, and target area hair darkening is measured in order to get from these quantifiable variables regulatory approved measures for efficacy assessment. Aside from these quantifiable measurements, we will also have patient-reported outcome measures, which are very important because it's one thing if you have really a numeric improvement, but it's really most important that the participant themself feels or sees that there is improvement on the hair regrowth in order to have afterwards a quality of life improvement. Of course, the next question is, when are we going to have our interim readout? As mentioned earlier, we are treating our participants with androgenetic alopecia over a period of six months, mimicking not only what we have seen in the stump-tailed macaque study, but also reflecting standard practice in hair regrowth trials. Within this six-month period, we will have a baseline assessment and then an assessment at 13 weeks and then 26 weeks. Now, when are we expecting the first interim readout across all three multiple ascending dose trials? That will be as early as Q3, Q4 in 2026, and the 26th readout as early as beginning of 2027. These readouts are important and will guide us in our registration of trials moving forward down the line. The described phase 1/2a headline trial will take place in Australia within the multi-site setup, and we're super excited that one of the PIs will be Professor Rodney Sinclair, who is a world-renowned expert in androgenetic alopecia and will talk to you more about ABS-201 and the headline trial. Hi, my name is Rod Sinclair. I'm the Professor of Dermatology at the University of Melbourne, and I've held that post for close to 20 years now, and over the years, hair loss has been my passion. I wrote my doctorate thesis on androgenetic alopecia in women. I've written multiple textbooks on hair loss. I've written the chapters on hair loss in Rook's Textbook of Dermatology and Bolognia's Dermatology, which are the key textbooks that are used by dermatologists around the world in their training, and so they've learned a lot about hair loss through those chapters. I've now published over a thousand peer-reviewed articles, and averaged over the last 10 years at about one a week. And we've done a lot of work in androgenetic alopecia. So I was involved in the publication of the first genes for male pattern baldness, which was the androgen receptor, and we did that through gene association studies. We also identified genetic linkage in female pattern hair loss with the aromatase gene and the estrogen receptor gene. We have been involved in understanding the patterning of hair loss through epigenetic silencing of the androgen receptor on the occipital scalp. And we've also developed the main clinical grading scales used for female pattern hair loss, known eponymously as the Sinclair scale. So my clinic here in Melbourne is one of the largest dermatology centers in the southern hemisphere. We have over 20 specialist dermatologists. We see over 70,000 patients per year, but we also integrate clinical research into our clinical practice. So we have one entire floor of our building devoted to clinical trials. We've done, over the past 15 years, over 300 industry-sponsored clinical trials for pretty much all the major pharmaceutical players, and that goes from phase I through to phase IV. And in androgenetic alopecia alone, we've probably done at least six phase III clinical trials developing products for androgenetic alopecia. So I've been interested in prolactin for over 25 years because one of my other roles has been as president of the Australasian Hair and Wool Research Society, which is a group that brings together scientists who do basic fundamental research on all mammals because, of course, the defining feature of mammals is hair, and bring them together with the clinicians, the dermatologists who are treating hair loss. That's the sister society of the American Hair Research Society, which you might be familiar with. The work that I was introduced to through my role in the Australasian Hair and Wool Research Society centered around the way in which prolactin regulates the hair cycle in the possum. The possum, of course, has seasonal molting. They have a winter coat and a summer coat, and that transition from the winter coat to the summer coat is regulated by prolactin. What you've probably just recently seen in the fundamental research data presented by Professor Paus is that prolactin is a hormone that has many more functions than simply inducing lactation. Certainly it's named because of its effect on women at the end of pregnancy in terms of activating their breasts to start to stimulate lactation. It's a prolactin, prolactation hormone. But just because it's named for one thing doesn't mean it doesn't do many other things. And the demonstration that prolactin is manufactured in the hair follicles, the demonstration that prolactin has receptors in the hair follicles is testimony to the fact that this hormone is involved in regulation of the hair cycle, doing things that people who were thinking of it as purely a lactation hormone hadn't previously turned their mind to. And it turns out that it's actually a really important hormone in the regulation of hair growth. I think a lot of people have oversimplified the causation of male pattern baldness. Many people have simplified the causation to be activation of testosterone into dihydrotestosterone, dihydrotestosterone binding to androgen receptors in the hair bulb. That leads to miniaturization of the hair follicle and hey presto, you go bald. What we've been able to show is that the mechanism is actually much more complex. Before you start to miniaturize the hair follicle, you shorten the duration of the hair follicle growth cycle. And that is something that involves the cyclical regeneration of the hair follicles. So what most people are aware of is that if you pluck a hair, new hair grows out of the same follicle. What many people haven't realized is that if you don't pluck a hair, a new hair grows out of that same follicle and just pushes the old one out. And of course, the best example of that is that if you suddenly decided to start shaving your armpits, you'd see that the hairs are growing every day. But if you don't shave your armpits, they only grow so long, and then the next hair starts to grow and it just pushes the old one out, which is, of course, a good thing. Otherwise, we'd have hairs poking out of our sleeves. So that regulation of the hair cycle is the first thing to change in the onset of male pattern baldness, and that precedes the DHT-mediated miniaturization of the hair follicle in the hair bulb. And that shortening of the anagen duration is triggered by events happening at the top of the hair follicle, near where the arrector pili or the goosebump muscle inserts into the hair follicle. And the other thing that we've shown even more recently is that before you get miniaturization, you get disruption of the attachment of the muscle to the hair follicle. So in fact, that miniaturization of the hair bulb through DHT is actually a secondary and a late event in androgenetic alopecia. It's probably permissive, and it probably affects the patterning of the baldness, but it's not. It's It's overstating it to say that that DHT binding to the androgen receptor is the cause. We want to see the upstream events that cause the baldness. We're interested in the hair cycle changes, and that's where the hormones that regulate the hair cycle, such as prolactin, suddenly start to come into play. That's where the focus, where the smart money is starting to look now. What has started in Melbourne this week and will continue over the next 12 months is the headline trial, which is the Absci phase I, phase 2a clinical trial testing their novel monoclonal antibody in healthy volunteers with and without androgenetic alopecia. The initial study is being conducted in a residential phase I clinical trial center, which is about two kilometers down the road to the south. What we'll be involved in, where I'm going to be the principal investigator, is the phase 2a study investigating people with androgenetic alopecia. This is a highly regulated, highly controlled clinical trial. All the endpoints have been clearly established, and the endpoints center around high-quality photography. This is something that we've done before. It's something we've got great experience in. I think I can honestly say we produce the highest quality clinical photographs available for clinical research. The recruitment is always a challenge in any clinical trial, but this is something that we've done before. In fact, we've just closed recruitment on a trial with 140 participants for sublingual minoxidil in an androgenetic alopecia clinical trial. And so we're very confident that we can recruit the lion's share of participants for the next study. But of course, there are multiple sites in a competitive recruitment process, and the aim for everybody involved is to complete the recruitment as rigorously and as fast as possible, with, of course, no compromise on the quality of the participants. So the question on everybody's lips is, what gives me as a dermatologist confidence that this trial can produce a meaningful benefit for our patients? Well, the first step is I think we're moving upstream in the mechanism of baldness. We're moving away from being fixated on the hair bulb and the miniaturization of the follicle to some of the earlier events through the regulation of the hair cycle. We know from the animal models in, first of all, the possum that prolactin is involved in the regulation of the hair cycle. We've seen experimental studies in the macaque monkey, and the macaque monkey is probably the only animal model that reliably predicts treatment effects in androgenetic alopecia, and I think there's some tantalizing interest from the macaque monkey where there was a suggestion that even after the trial finished and the dosing had stopped, that there was some ongoing benefit. Now, whether that happens in humans or not, we'll have to just wait and see, but I think there's a lot of excitement in the patient world around this mechanism of approach to the treatment of androgenetic alopecia. There's a lot of excitement in the medical world to see how we can impact androgenetic alopecia, looking at a variety of different targets beyond the historical target of the 5-alpha reductase, the DHT, where the finasteride and related molecules were focused on. I was the principal investigator in the phase 1b open label study for Hope with their molecule HMI-115. And this was an intravenous study. And for Hope, my impression was that this study was a bit of an afterthought and that their main focus was around endometriosis, and they were interested in androgenetic alopecia as perhaps a secondary market. And based on their phase I dosing, the doses that were selected for the androgenetic alopecia trial were probably a little bit too low. And the reason I say that is that the receptor occupancy with the biologic therapy in the animal studies with the macaque monkey, and of course, as I've said before, the macaque monkey is the most reliable animal model for investigating androgenetic alopecia. But the receptor occupancy in the macaque monkey studies was north of 90%, whereas the receptor occupancy that was achieved in the HMI-115 Hope Medicine study was probably somewhere between about 60%-80%, but probably south of 70%. In contrast, Absci have done some significant modifications directed by AI, and they've led to better tissue distribution, better pharmacokinetics, and specifically a longer half-life, which is going to be attractive to the patients interested in pursuing this treatment. And we anticipate it's going to achieve greater than 90% receptor occupancy in the humans because of the dose they've selected. As a consequence of that dose that achieves higher receptor occupancy in the humans, we anticipate we're going to get more hair growth than Hope achieved. So I will finish off here, and I'm going to pass you over to Professor David Goldberg, who's going to describe to you the significant unmet need for a hair loss treatment that really shifts the dial amongst our patients. This is something that everybody's been waiting for, and David Goldberg's the man to tell you about it. I'm Dr. David Goldberg. I am the director of clinical research and cosmetic dermatology for the Schweiger Dermatology Group. We are somewhat less than 200 offices from coast to coast, Midwest, Eastern Seaboard, Florida. I also run two fellowship programs in cosmetic dermatology through the American Society for Dermatologic Surgery. I practice cosmetic dermatology. We've done a lot of research in the area of hair, going all the way back to the 1980s and '90s with topical minoxidil. We've done some of the studies on platelet-rich plasma for hair. We've done some of the studies on low-level light. We're currently involved in a trial for oral minoxidil through the FDA. I run meetings. I just ran a meeting this past weekend called New Frontiers in Cosmetic Medicine, where we talked about the current prolactin studies, and we do a lot of research as well. So the current standard of care for androgenetic alopecia, frankly, is not very high. As I mentioned, I was involved in the topical minoxidil studies. That's known as Rogaine now. Everybody comes in on that. That's not a prescription. The numbers of people seeking treatment for hair thinning are staggering. If you look at men, by the time they're 35, people are complaining. Women, by the time they're 40, women actually, by the time they're 65%, 80% of them complain of hair loss. And yet, what do we do for them? We have them on topical minoxidil. That doesn't do a lot. We start talking about platelet-rich plasma and low-level light. In order to do that, they have to have their blood drawn from their arms. That's painful. It can lead to black and blue. We then take that blood. We spin it down in a centrifuge, and then we re-inject it into their scalps. That's a painful procedure. They have to come into the office. It's done once a month. And although we do a series of usually four or five treatments, it really is in perpetuity. So they're constantly coming in. On some of the men and some of the women, we give them what's called oral minoxidil now. It's not even FDA approved for hair loss. It's FDA approved for blood pressure. The dosages are really made for blood pressure. They're not made for hair thinning. Some people have problems with dizziness, dropping of blood pressure. Some of the men, we give oral finasteride. That blocks testosterone, the hormone that leads to hair thinning, both in men and women, and the problem with that in men is some of them get erectile dysfunction. There's so much talk now on social media about suicidal thought patterns in men who are taking that drug. You get a sense that the treatment approach right now is just not optimal, and we currently don't have an ideal treatment for hair thinning. I mean, that's just pretty obvious. If you look at surveys out there, less than 10% of people are happy with the current treatments we have. And so what we want in a new hair treatment for hair thinning and hair loss is something that is convenient, doesn't have to be done that often, and it's got to be durable. Durable means they don't have to necessarily have an injection every week. They don't have to come into the office every month. Something that ideally they could do at home, maybe they'll start every week, but ultimately maybe every two months, every three months, something along that line. And we now are on the cusp of a drug that potentially can do that. And this is such an exciting arena right now that I'm going to be discussing this at the end of January, at a meeting called IMCAS Paris. It's the largest cosmetic dermatology plastic surgery meeting in the world. There are some 20,000 people there. They all want to learn about this new product, this new approach, this prolactin receptor inhibition. It's a very exciting area. So ABS-201 clearly is a game changer. One, it's a totally new mechanism. The fact that these hair follicles have these receptors, and then ABS-201 now can block those receptors and convert resting, non-growing, non-pigmented hairs into thick, terminal, growing, darkened hairs is revolutionary. So as I mentioned before, we currently are involved in FDA studies for longer-lasting minoxidil products, allowing the higher dosage to be given, hopefully safer than is what currently available on the market. But in the end, that doesn't work the way ABS-201 works. The way minoxidil works is it dilates blood vessels in the area of the hair. It gives them more nutrition, but it's not a direct impact on the hair. That's number one. Number two, that's going to require compliance. People have to take pills twice a day. What's exciting about ABS-201 is how often people are going to need the drug. We're looking initially at maybe two to three injections over the first six months. But think about it this way. Growing hairs, they're called anagen hairs. They last for a couple of years. And so if we get those injections two to three over six months, and then we're back in that growing hair stage, people are not going to need to do injections very often at all. With the excitement behind ABS-201, I cannot help but think about my own personal practice and where I am with Schweiger Dermatology. I mean, as I mentioned, we're talking about slightly under 200 practices coast to coast. We're the second largest dermatology group in the country. We have over two million patient visits every year. Roughly 10% of people coming in come in for hair thinning. I can only imagine the commercial market we're going to have once ABS-201 comes onto the market. So we recognize what role ABS-201 can play in our huge dermatology practice. But it'd be nice to now hear something about the commercial development of this product. With that, I'll pass it on to Mike and Zach. Good morning, everyone. My name is Mike Jafar. I'm excited to be here and appreciate the Absci team for inviting me. I've built my entire career and been fortunate to be around great people and great brands in this cross-section of medicine and aesthetics. I've had a chance to scale, build from zero to one, acquire, and just be part of an organization at the time called Allergan, now AbbVie, that owned many of these assets like Botox and CoolSculpting and Juvéderm. Also was the chief commercial officer for a public company called Evolus, who had a wonderful product and, frankly, the first product to compete against Botox called Jeuveau, and took that company from zero to a few hundred million in revenue as we scaled the company. At the time that we spent at Allergan developing the Latisse business, we started to learn a lot about hair, right, and hypertrichosis was a thing, and we started to talk to trichologists and dermatologists that really understood hair. What was really hard at the time was to find an asset that impacted so many people in America. And that drove this definition of the last frontier that we were always looking for, at least at my time at Allergan. If you look at just hair loss in general, nearly a third of Americans are impacted by this. And it has a massive psychological impact. Clearly, it has a visible impact. It's one of the few things that impacts both men and women, kind of akin to weight loss. So just the idea to address this from a true scientific standpoint with a novelty product and a novelty target, I think has such mass commercial appeal. The limitation and why this category has been so hard has been driven by the lack of efficacy, frankly, and/or an experience that many don't want to go through. So if you look at just the consumer base today and what they're willing to do, clearly they're willing to be on topical meds for the rest of their life, systemic products. They're interested in surgery. Some are flying to Turkey. I mean, this is such a profound need in the marketplace. But unfortunately, it all comes with massive drawbacks, whether it's systemic side effect or the experience of a hair transplant, the stigma behind surgery. Even despite going to the greatest lengths of surgery, you still have to maintain and be on these topical drugs that many people just don't want to be. So it's just been a high burden for, I'd say, decent or mediocre results at best. And the opportunity here is to reframe this. If you look at what patients and clinicians are seeking for just better treatments, significant hair growth, durability, safety, especially around side effects, and then convenience. The idea of taking daily administration of drugs that may have an impact on sexual dysfunction and may have an impact on a host of things systemically is just not appealing to the masses, which is why I feel like there's a greater cohort sitting on the sidelines looking for something like Absci as a project that we'll discuss today. So if you look at the ABS-201 target product profile, the opportunity to deliver a blockbuster drug, if the following tenets are met, I think is the exciting part. Right now, we sit on oral minoxidil as the gold standard. So ABS-201 has to be greater than oral minoxidil when it comes to hair growth. Durability is critical. The idea of taking something and however it's administered, lasting for a few years, is clearly an unmet need and a driver of growth. Safety and efficacy is non-negotiable, right? And then lastly, a subcutaneous injection once, twice, three times over the course of the year, lasting for two to three years would be ideal. So if you look at the ABS-201 target product profile as it compares to what's out in the marketplace, minoxidil, finasteride, topicals, orals, PRP, it is the only target product profile that exists in the marketplace that allows you a few interactions with long-range durability. Taking a few thousand pills over the course of three years is not that exciting for people, right? Going in for PRP 4x-5x a year, every year, and getting an injection upwards of 30x-40x on your scalp is not terribly appealing, which is why you see a massive drop-off rate when it comes to PRP. So from an efficacy standpoint, here's what the market has come to call it trade-off. You got convenience and comfort on one side, and then you have performance or call it outcomes and growth on the other side. Ideally, you want to be in the top right. Super convenient, extremely comfortable interaction with any product with tremendous duration and/or outcome, right? That is the target product profile design. That's where you want to be. Unfortunately, the only option today for most consumers is either uncomfortable, high-frequency, or minimal outcome. I feel like at my time at Allergan, we always used to say body contouring was the next frontier and then came along CoolSculpting, now Ozempic. But in the background, the last frontier truly was hair. And it's so wonderful to be part of this project with Sean and Zach and the Absci team. So thank you for having me. Hi, I'm Zach Jonasson. I'm the CFO and Chief Business Officer at Absci. Today, I'm excited to share some results from our market research. We started this process by interviewing both clinicians as well as patients and then commissioned a consumer research survey in the fall of this year. This survey included 610 participants, about evenly split between males and females. They were all U.S. adults, 25 years-59 years old, with an income exceeding $75,000 a year, including some disposable income. All of the participants were experiencing and bothered by hair loss or hair thinning. The objectives of this survey were to assess attitudes about hair loss as well as survey the psychosocial impacts of hair loss. We also looked at consumers' sentiments around current standard of care. We explored interest in the ABS-201 target product profile, including willingness to pay premium for such a TPP. We're going to share a few results from this study. To level set, we asked patients about the impacts of their hair loss on their psychological well-being. What we found is 80% of men and 81% of women registered strong negative psychological impacts from their hair loss, principally feeling less confident, feeling like they looked less attractive, and also feeling like they looked older than their actual age, and generally feeling self-conscious in social situations. These results correspond to the patient testimonials you heard earlier today from Kelly and Landon and are a strong motivator for why these patients seek treatment. We also asked respondents about their interest level in the ABS-201 target product profile. And here we see a vast majority of both males and women were highly interested. In fact, 87% of men surveyed said they were extremely or very likely to ask a healthcare professional about procuring the ABS-201 product if it were available. Similarly, 69% of women said that they were extremely or very likely to seek out ABS-201 from a healthcare professional. We also wanted to evaluate the interest level of patients who are currently taking a standard of care therapy in ABS-201. And here the results are even more exciting. Patients that are on a current standard of care therapy were even more interested in contacting a healthcare professional about ABS-201. For example, 90% of men currently taking topical minoxidil said they were extremely or very likely to contact a healthcare professional about ABS-201. 92% of men currently taking oral minoxidil said they were very likely or extremely likely to contact an HCP about ABS-201. And finally, 97% of men undergoing in-office procedures such as PRP or hair transplantation said they were extremely or very likely to contact an HCP about ABS-201. Similarly, with women, we see 76% of women who are currently taking topical minoxidil said that they were extremely or very likely to contact a healthcare professional about ABS-201. That number goes to 89% of women who are taking oral minoxidil. And finally, 88% of women who are undergoing in-office procedures such as PRP or hair transplantation said they were extremely or very likely to contact a healthcare professional about procuring ABS-201. Now, these results underscore two important points. First, the standard of care isn't cutting it. Patients are dissatisfied with current treatment options. And secondly, the strong interest in the TPP that ABS-201 offers. We further asked respondents about their interest in using ABS-201 as first-line therapy. And here, the results are very exciting. 37% of men said they would try ABS-201 as their first course of therapy to treat AGA. And 36% of women said they would try it as a first-line. The key takeaways from our consumer research, including the survey we just discussed, are number one, we confirmed the significant unmet need that exists today, which is driven by the psychological impacts from hair loss. Number two, the overall high level of interest in ABS-201 and the potential for it to become first-line therapy for a significant share of both male and female AGA consumers, and number three, although we did not discuss the results from the questions pertaining to pricing in our survey, we found that there was a significant share of men and women respondents who were willing to pay a premium for the ABS-201 target product profile. Using data from our consumer survey, as well as demographic data, we were able to construct a classic patient treatment funnel. Here at the top of the funnel, we start with the total estimated AGA population in the U.S. of 80 million. We then cut the funnel according to income. Here, we're looking at the AGA population that would have an income greater than $75,000 a year and be within the age bracket 17 years- 69 years old. That brings the funnel to an estimated 39 million. Then we further cut the funnel according to the AGA population that is concerned and motivated about treating their hair loss. That brings the funnel to an estimated 26 million U.S. consumers. The next cut of the funnel considers the interest level in the target product profile of ABS-201 based on our consumer market research survey. This brings the funnel to an estimated 22 million-24 million AGA consumers. The final cut of the funnel is constrained to AGA consumers with the highest interest in the TPP and willing to pay premium pricing based on our survey. This brings the funnel to an estimated 15 million-18 million patients. Now, if we assume two to three years of durability of the ABS-201 treatment, this would imply five million- nine million patients are treated each year. At that level of treatment, we estimate a total available market in the U.S. of greater than $25 billion and a potential TAM of greater than $40 billion globally. We're also pleased to see that the go-to-market channels are already in place. 80% of consumers that seek hair treatments already go to our target market channels, principally dermatologists, med spas, and plastic surgeons. So as we think about a potential FDA approval in 2029 or 2030, we believe we're well-positioned to ramp into this market. There are currently over 30,000 of these locations when you consider dermatologists, med spas, and plastic surgeon offices across the U.S. alone. More broadly, we believe we have a strong strategy to capture and expand the ABS-201 total available market. We're starting from a position of strength. There's a massive motivated patient population with high unmet need and with high interest in the ABS-201 TPP based on our survey results. There's also a robust practitioner market channel already in place, encompassing the derm offices, plastic surgeons, and med spas, and as we think about going forward, once the product is approved, we'll be focused on creating viral awareness and direct patient engagement. We'll also be looking to leverage our first-mover advantage to create an iconic brand to further protect and grow our market share. Finally, longer term, we look to expand the market by going direct to consumer. We're excited to leverage both the strategy and the market infrastructure built by the GLP-1 players. And when we look at that playbook, post-market, we'll be focused on creating viral awareness of ABS-201 that can drive more patients to clinicians, hence driving more demand and more revenue. We will also be looking to build direct patient engagement, which can enable further expansion of the market in a direct-to-consumer fashion. Altogether, we're very excited to advance ABS-201 through clinical development towards approval. We believe this therapy can be category-defining and address the significant unmet need that exists in the AGA population today. And with that, I'm happy to turn it back over to Sean. Thank you, Mike and Zach. And a huge thank you to Dr. Rossi, Professor Paus, Professor Sinclair, and Dr. Goldberg for sharing their time and expertise with us today. I want to close by connecting the dots on what we've heard over the past hour. We started this session grounded in the reality of the patient experience. And I want to sincerely thank Kelly and Landon for being so open with their personal stories. Hearing Landon, an elite athlete and a soccer legend and icon, talk about his hair loss experience and how that's impacted him really drives home the point that Dr. Rossi made earlier today, that this is not just a cosmetic issue. It deeply is tied to identity and our mental well-being, regardless of who you are or what you've achieved. From that foundation, we went deep into the science. We saw the biology with Professor Paus and Professor Sinclair validating the prolactin receptor mechanism as a master switch of hair regrowth. We saw how ABS-201 is uniquely engineered to unlock that pathway. And finally, Dr. Goldberg, Mike, and Zach made the commercial reality clear. The bar for success is defined, and the market opportunity is effectively uncapped for a drug that delivers durable efficacy with a clean safety profile. For Absci, ABS-201 represents exactly what we set out to do as a company. We used our generative AI platform to identify a high-value biological target and designed a best-in-class biologic to address it faster and more precisely than traditional methods allow. We are incredibly excited that we have started the trial this month and already have enrolled our first cohort. With the protocol Dr. Sinclair and Denis outlined, we have a streamlined, efficient path to a proof of concept. We anticipate sharing an interim efficacy readout in the second half of next year. We look forward to updating you as we progress through the clinic and ultimately to sharing the data we believe will transform the standard of care for patients like Kelly and Landon and millions of others. Thank you for joining us today, and thank you for your continued support of Absci. For the Q&A section of today's session, we'll be utilizing the raise hand feature. If you'd like to ask a question, click on the raise hand button at the bottom of the screen. Once prompted, please unmute yourself and begin with your question. As a reminder, we ask that you stick to one question and one follow-up. We'll now pause a moment to assemble the queue. Thank you. Our first question comes from Vamil Divan with Guggenheim. Your line is open. Please feel free to unmute and ask your question. Vamil, please unmute your line. Yeah, sorry. Sorry about that. Can you hear me now? Okay. Yeah, we can hear you fine. Okay, sorry about that. So I just had a couple of questions more on sort of the commercial side of things. And you mentioned this sort of pay-for-performance that people would be willing to pay for it. I'm curious, just given the nature of this product, and I guess you'd be paying upfront and then getting the benefit over time. Are you thinking about some sort of almost like a value-based pricing where people pay upfront and then it's sort of dependent on how they respond is kind of what they're paying? I'm just trying to get a sense because I'm assuming it'd be a relatively large upfront cost that people would be having to put up for that. And then the other question I had was just around some of the market research, which was very helpful. So I appreciate you sharing that. I noticed there was like a little bit of a difference. I think very strong interest from men and women. But for men, it was like 90%. For women, I think the interest in talking to the doctor about it was around 70%. So a little bit of a difference. I'm just curious if anything you saw in the research that's showing differences in how men and women are reacting to the potential target profile here. Thank you. Yeah, thank you, Vamil. I think one of the things that came as no surprise to us as we had talked with KOLs was just the immense impact that this has on both men and women. Men and women look at it slightly differently. One of the things that women really care a lot about is seeing the hair in the drain when they shower. Versus men, it's losing the hair in the front area of the scalp as well as just wanting to be able to regrow that. In regards to the commercial side of things, I'll hand that over to Zach and Mike to get their perspective on that. Zach, you want to start off? Sure. Thanks. Thanks, Sean. So Vamil, one other point. When you dig into the numbers of male versus female in the consumer research study, one thing that's important to point out is if you look at women that are actually already taking a standard care treatment, those numbers are very similar to men with respect to their interest level in ABS-201. And we also see a very similar level of excitement about using ABS-201 if it were available as first-line. So we think the survey data is tremendously strong supporting the TPP and how well we see this is going to be in the marketplace. As to your question about financing plans and how you might structure payment for ABS-201, I think it's too early for us to really go through that. I will say we do believe longer term there will be ways to do financing plans around this and spread out payments for patients. But in our survey, we really didn't test those assumptions and whether that would further expand interest. We really presented it in the pricing portions as an upfront cost. I think patients were able to compare that to what it would cost for other standard of care and also compare what the efficacy and durability would be relative to other standard of care. Okay. Mike, I don't know if you'd like to comment as well. Yeah, happy to complement this. Keep in mind that the consumer today, if they're going in for CO2 and the physicians on the phone can speak to this or body contouring, they're paying for something that has prolonged effect, not immediate effect. And so I think the mindset of the consumer to exchange money for a procedure and then watch the effect happen over time is not a foreign concept in our category. It happens daily. If anything, you would probably ask for a refund after a CO2 treatment because the first three to four weeks, frankly, the experience is not optimal. Same thing with body contouring. When we're managing the body contouring CoolSculpting business, you would take several thousands of dollars and you would tell the consumer that the effect will happen over time. So the mindset of the consumer is already there. Sean, if I can comment at this point? Yes, absolutely. Go for it, Dr. Goldberg. So Vamil, you and I have talked about this a little bit as well before. Two things. One, patients coming in for PRP injections, which is really our standard of care now. Forget about the fact that they have to get the phlebotomy of their arm and injected multiple times in their scalp, and it's a pain in the neck for them. They're paying, I mean, in the Midwest, maybe $1,000 a treatment. I'm in New York and New Jersey. It's $2,000, sometimes $3,000 a treatment. They're paying good, good money right now for a treatment that does very, very little. And so it's not hard to extrapolate from that to figure that they're going to pay for this. The other comment I want to make is I'm listening to some of the data out there. For someone like me who runs a very strong FDA research program on multiple treatments for hair, some 30%, I think the numbers I heard, 37%-38% of people, if offered ABS-201, would jump to it. And I find that number remarkably high because this is a drug that's not on the market at all. We have so much trouble getting people into any of our studies because it's new. And our success rate, some of the other things we do, getting people in the studies is really under 10%. So the fact that 37%-38% of people, if given the option to use ABS-201, would use it, it tells you how difficult this market is right now. Okay. Thanks for those thoughts. Appreciate it. Our next question comes from Brendan Smith with TD Cowen. Please unmute your line and ask your question. Hi, can you hear me? Hi, this is Jackie on for Brendan. Hey. Hey. Hey. As much as I'd love to ask Landon Donovan a question or two, I'll just stick with just one for you guys. I know you've mentioned that there's plenty of room for multiple players within the AGA space and given the size and the unmet need. You've demonstrated that great today. That said, I'd be remiss to not bring up Cosmo Pharmaceuticals' recent phase III data, which demonstrated significant improvements in their hair growth over placebo. Obviously, these are very different MOAs, and you've also spoken to the DHT and androgen receptor targets today as well. But assuming clascoterone does make it to market, could you walk us through what the patient split might be, which patient types are more likely to choose ABS-201 over a topical solution, and sort of what the dynamics may be around that competitive lineup? Yeah, it's a great question. If you look at the Cosmo data, I'll hand it over to both Denis and the KOLs on the line to speak to this. But the percent increase was to baseline. And if you compare that to minoxidil, it's right in line with minoxidil. So it doesn't seem like there is much of a benefit compared to current standard of care. But Denis and Professor Sinclair, Dr. Goldberg, and Dr. Rossi, please feel free to chime in as well. Yeah. Hi, Sean. Happy to do so. As Sean mentioned, it seems to be rather a safer option as soon as there is a tested route for a topical administration. And this 500% or 300% sounds initially very, very significant. But if you average it with a high variability across the trials, approximately three-fold, which compares to minoxidil effect. But basically, we see that, as Sean outlined, also as potential complementary. Does any of the KOLs want to chime in too? I was going to say Dr. Sinclair. I'm going to just add to that. I think what the clascoterone seems to be comparable to is the topical minoxidil rather than the oral minoxidil. So it's still weak from a price comparison point of view. It's not something I would be investing in. It has legs. We'll have to wait and see. The actual hair that I'm describing it as a percentage is a bit large. Yeah. The Cosmo data, I mean, if you look at it, the idea behind this is to have a topical form of finasteride, if you will, without the potential side effects, but it's really looked at as an alternative to topical minoxidil. I look at it as an adjunctive treatment. I think there will be other adjunctive treatments as well, but I don't see this in the same place as ABS-201, and we know from other topicals that compliance is such a limiting factor of daily use and such, and patients are just not great with compliance on topicals, and for most of us, we're treating hair in a multi-modality fashion, so while we have our systemic medications, we also supplement with topicals if the patient is even willing to do topicals. That's super helpful. Thank you so much. Dr. Sinclair, do we have you back online? You were cutting in and out there. Yeah, I think it had jumped on the Wi-Fi, so I think I'm back now. I can hear you. And hopefully. Perfect. Do you maybe just want to repeat what you said? I think you were cutting in and out there. So what I was saying is that my interpretation of the clascoterone data is that it was a comparison to the topical minoxidil, not the oral minoxidil. The way they've presented the data as a percentage increase isn't really comparable to other forms. It should be presented as an absolute hair count change. And so I'm very skeptical that clascoterone is going to be an effective treatment. And it certainly wouldn't be something I would personally invest in. I think it's going to have hairs on it, so to speak. Great. Thank you. Our next question comes from Gil Blum with Needham. Please unmute your line and ask your question. Can you hear me? Yeah, we can hear you, Gil. Okay. So just a couple of quick ones from us. Considering there is this study was conducted in endometriosis, is there any anecdotal evidence from that study of hair regrowth in the women treated? And maybe a more general question as to the study data cadence. Will we have any reports out of the SAD portion of the study ahead of the larger data set in the second half? Thank you. All right. Gil, I can answer that first question. So we do plan to have a safety readout on the SAD prior to the 13-week efficacy readout in the second half. So be on the lookout for that. And with regards to the first question, Denis and Andreas, I'll hand that over to you. Yeah. Happy to take the question. So unfortunately, there is no information on the androgenetic phenotype in women reported in the endometriosis trial. We were also looking forward to see some anecdotal outcome, but we will have to wait for our trials to see an effect. Thank you. Our next question comes from Brian Cheng with JP Morgan. Please unmute your line and ask your question. Hey, guys. Can you hear me? Yep. Loud and clear, Brian. Well, thanks for taking our questions here. A couple from us. Just want to pick your brain a bit on the setup for the phase 1a trial. What do you want to see across the three doses in the MAD portion that you have selected for hair counts and also hair width? We have a quick follow-up. Thank you. Yeah, it's a great question. So the TPP slide that Zach went over, what we're looking to achieve is at the higher end of oral minoxidil, potentially up to what you see in a hair transplant. We see that as ultimately being a win in terms of total area hair count. And Denis, please feel free, and as well as Dr. Sinclair, to give your perspective on this as well. Yeah, absolutely. Maybe also tying it back to the topic, which Rodney touched upon about with receptor occupancy. So the doses have been selected in a way that we can see a dose-response relationship to really then define for the later clinical development the efficacious dose we want to run for the test into the bigger cohorts. Rodney, do you want to add something to that? I suppose as a comparison, oral finasteride grows around about 20 hairs per cm. Minoxidil foam grows about 16 hairs per cm. The lotion's a little bit more than that. The oral Minoxidil is looking to grow around about 30 hairs-40 hairs per cm. Hair transplants, somewhere between about 25 and 30 hairs per cm. You can't pack them much closer than that. So I think we want to be in the range of north of 30, but ideally north of 40 hairs per cm. Then you'd have a very, very strong market comparison. And then the other thing, of course, is there's the hint in the macaque monkey studies of longevity of the response. If you can actually demonstrate that in the studies, and that'll take a little bit longer, of course, if you can actually generate a sustained response after they've completed the dosing, then that's also going to make it attractive for people who want to move away from having to take a daily tablet. And then if I can just add one more, just on the sub-Q versus IV dose formulation here, how should we think of the sub-Q dose range in relationship to the IV doses that you have selected? Thank you. That's a really great question. So the IV dose is mainly to establish really safety and tolerability, where you have really 100% bioavailability. So you really establish this fundamental foundation for your clinical development. With regard to the sub-Q dosing, there, this is also the later intended commercial route of administration, where we will see also the profile of bioavailability after sub-Q administration. Then, together with the PK profile, which we obtain, we can then determine at which dose we see really the best hair growth efficacy in combination also with the dosing and the availability on the line. Yeah. We are currently at 200 mg per ml, and that will be the commercial sub-Q formulation. So that will be tested in the MAD. What we saw in the NHP was greater than 90% bioavailability for that sub-Q formulation. All right. Thank you, guys. Our next question comes from Debanjana Chatterjee at Jones Research. Please unmute your line and ask your question. Hi. Do you guys hear me? Thanks for the exciting presentation. Can you please confirm if the ex vivo experiments were performed on hair follicles from healthy male donors? And if so, how do you think the findings would translate into patients with established AGA? And I have a commercial follow-up. Yeah, absolutely. Professor Paus, do you want to answer that? Yeah. Actually, that's a brilliant question. So when we do these scalp skin organ cultures, they have to be done in an anonymized fashion. And so we are not allowed to know anything about the skin other than where it is from, age, and sex. But it was all from the frontotemporal region. And if you look carefully at the gentlemen here in this Zoom call, they all have androgenetic alopecia in the frontotemporal region. So the likelihood that the three donors we investigated all had that too was extremely high. But you're absolutely right. We can't 100% guarantee this, so in theory, they were healthy because we are not allowed to know whether they had AGA. Does it answer your question? Yes. Thank you. And maybe thinking about the commercial. Sorry, Professor. Professor, I was just going to add one other piece. We didn't share this data, but I think it'd be good for you to speak to it. It's actually in each of those patients what we saw from a prolactin receptor profile and what that looked like. Yeah, so there were also individual differences in the prolactin receptor expression profile, which is to be expected. Basically, every hormone receptor that you look at shows individual variations. And yet, despite these substantial prolactin receptor expression differences between these three donors we looked at, we had significant and reproducible responses throughout these three donors. Now, three donors, there's nothing compared to the hundreds of patients that are now going to clinical trial, right? But that's what you can do at the preclinical level. But since we have run these preclinical trials for a very long time, if we find such reproducible results within three different donors, for us, this is very, very encouraging. And remember that what we are looking at is the human target organ itself. It's not some mouse model, not some monkey. We are looking at real frontotemporal human scalp skin. And to see such reproducible data is actually at the level of preclinical research, highly encouraging. Great. Thanks for those insights. And are there any additional hair loss conditions where you think modulating the prolactin signal could offer therapeutic benefit outside of AGA? Yeah. Yeah. Go for it, Denis. Oh, that's another great question. Of course, we are also exploring the space where this mechanism could hold true. Another area could be, of course, alopecia areata based on what also Professor Paus mentioned, the role of prolactin on immune modulation. So we're conducting preclinical studies, and we'll, of course, explore different indications, but also dermatology areas. Maybe Anthony or Mike want to share some thoughts there too. But I just wanted also to briefly mention that with the donors, even if one of the donors or two of the donors might not have AGA, they are really promising because that also shows you that this mechanism works in healthy skin and will likely most work even better when prolactin is a driver of this phenotype. Very helpful. Thank you. I'll back in the line. Do you want to? Yeah, if I can. Do you want to mention that the skin? Yeah, go. Yeah. So, additional indications in skin. If you remember the stem cell data we showed, so as you know, there are very nasty hair loss disorders, which are actually increasing in incidence and prevalence, particularly frontal fibrosing alopecia. And these hair loss disorders are caused by depletion of hair follicle epithelial stem cells. So if you now have a new antibody that protects these hair follicle epithelial stem cells from cell death and keeps them in a better position to produce daughter cells, as this antibody seems to be doing, you might actually have a new therapy that could be at least used as an adjuvant therapy in this very nasty form of hair loss, frontal fibrosing alopecia, many patients affected, to whom we have fairly little to offer these days. If I might chime in, also another indication is going to be telogen effluvium. Oh, absolutely. Because that's what our data support, right? That anything that prolongs anagen will be a wonderful treatment to suppress telogen effluvium. And if the durability of the effect is as long as initial data seem to suggest, then that would be wonderful news. So with one or two shots of the antibody, you could have a very long-lasting telogen effluvium reduction. And that is often the first symptom that brings the patient to the dermatologist, that they find this increased hair shaft shedding. And increased hair shaft shedding, that is telogen effluvium. If I can extrapolate that one step further, we're seeing so many people now on the GLP-1 agonist coming in also with hair loss. And whether that's a telogen effluvium or what exactly is going on there, I don't think we know. But to me, I know as this drug comes to market, when those people start coming in complaining about volume loss, lax skin, they're often complaining about hair thinning as well. And they're going to go right on this injection. Very true. 10%-20%, actually, of these patients on the drug are complaining about telogen effluvium. Yeah. And like frontal fibrosing, there are other scarring alopecia that really have a paucity of any treatments available. So it would be amazing to actually try this in those. Great. Thanks for all the additional color. Very useful context. Thank you. Our next question comes from Morgan Grieger wi th Morgan Stanley. Please unmute your line and ask your question. Hi, everyone. Thanks. I'm calling in for Sean Laaman. So we've seen in preclinical studies for ABS-201 potential repigmentation effects too. How could that present potential upside for ABS-201 in this market? Yeah, it's a great question. And actually, that's a piece of data that was not shown, but we did generate, which was very promising. Professor Paus, do you want to talk a little bit about the melanin data that we got from the ex vivo? Well, so the verdict on that is still out, what the pigmentation effect in a hair cycle-independent manner is. But there seems to be a stimulation of the hair follicle pigmentary unit. One thing one needs to keep in mind, whenever a gray or white hair follicle gets repigmented, that can only happen in anagen during the growth phase. So it's an absolute prerequisite for any kind of repigmentation of gray hair that the follicle stays longer in anagen and reactivates its pigmentary unit. And the initial data that we have from these preclinical trials would suggest that even that the antibody might be able to do. But we have to shore up this evidence to be more certain about that. Great. Thank you. Our next question comes from Charles Wallace at H.C. Wainwright. Please unmute your line and ask your question. Hi. Thanks for a great presentation. And a little bit of color, if I may, on the headline phase 2a design. Regarding later clinical development, would you need to do an additional or what additional trials would you need to do? Would you go into a phase 2b or directly into a phase III? And then also, is there precedence to keep males and females in separate cohorts or even separate studies? Thanks. Yeah, it's a great question. So in this current study that we're doing, we do have females in the SAD to enable the phase II study that'll start in Q4 in endometriosis. And we do have optional cohorts in the MAD that we're planning on filling. And depending on how the trial goes, our plan would be to have a registrational trial after this. Denis, I don't know if you have anything. Denis or Zach, if you have anything else to add regarding the plan there? Sure. Happy to expand on what you already perfectly alluded to, is that if everything goes well, especially when we're looking at the male participants, the additional pieces which are then missing is a long-term safety database. So you could envision directly proceeding in a combined phase II, III study design to have an accelerated clinical development setting. Great. And then a follow-up, if I may. So on the proof of concept data that's coming out, what differences should we expect to see between the 13 weeks and the 26 weeks? And then also on this, would we get any idea of the potential repigmentation from these readouts? Thanks. Denis and then Dr. Sinclair. Yeah, sure. Happy to give a first stab at it and hand it over to Rod. So basically, when you look at classical hair regrowth trial, each mechanism has a different rate of how the hair grows. Some are steady, some plateau. So of course, we anticipate, as you have seen from the NHP data, that we have a continuous growth. But we are looking forward to see initial differences at 13 weeks, which can then early guide our next clinical steps. But of course, we anticipate that at 26 weeks, the amount of hair has grown, and that it will then even be bigger than compared to placebo. But Rod, maybe you have also an additional perspective to that. Sure. I think that the trajectory of growth is going to be very similar to what we've seen with minoxidil. So with the finasteride, where you work from the bottom up from the hair bulb up the hair follicle, the peak improvement in hair count was about 12 months, whereas with the minoxidil, the peak improvement in hair count was around about 16 weeks. And a lot of the minoxidil trials have been focused on 16 weeks. I know Virodermics recently released their phase II data, and they showed about, I think it was about 30 hairs per centimeter at two months and 40 hairs at four months. That's similar to what we've seen with the sublingual minoxidil data, which is not yet publicly available, and so I think that's the sort of trajectory that we would be hoping to see with the prolactin. With regards to hair color, this is probably the first time that we're looking at hair repigmentation through a clinical trial. We originally did studies in twins in gray hair, and it was very hard to do because when we were just looking at people from a distance, like through the Zoom, the perception of graying of the hair is very much influenced by hair length, and so I know that if I let my hair grow long, it goes a bit dark, and then I get a haircut, it suddenly goes all gray, and so now we're doing the hair color through phototrichogram. So we're going to get a much more accurate reading, and it's going to happen much quicker. And I think this is probably, to my knowledge, one of the first studies we're actually investigating hair color. We've seen with minoxidil some very soft observations that it delays graying, but it's not as significant in terms of reversing graying. And I can say that from personal experience, having been on oral minoxidil for over 12 years, and I've gone very gray. So minoxidil doesn't do it. We'll be interested to see whether the ABS-201 molecule does. Great. Yeah. I know my mom would be one of your first customers if that's the case. Well, the big customer for gray hair is Southeast Asia. So while it's universal among women on this planet that they don't like gray hair, gray hair is very largely tolerated by men in Western societies. But in Southeast Asia, gray hair has got very low acceptability. And so all the men in Southeast Asia, that's a huge marker. And in the Arab countries as well. Maybe it's noteworthy that we're all excited about repigmentation. However, this is not baked into our case. I think we should point that out at this point. Great. Thank you, guys. Our last question will come from Anna Lee with Truist. Please unmute your line and ask your question. Hi. Can you guys hear me? Yep. Hi. This is Anna on for Kripa. Sorry. Thanks for the question. For Dr. Sinclair, one question. Besides the dose selection, could you also talk about any key trial design differences between the HMI-115 Hope trial and the headline trial? And I have a follow-up. So the Hope trial was an intravenous study. This is subcutaneous. This is sort of staged in two phases. The Hope study was an open-label study. So all the patients received active medication. This is a subcutaneous study. There's different dosing cohorts. There's men and women. I suppose the Hope study also had men and women as well. But this is a much larger study. In terms of the primary endpoint of the study, it still centers around target area hair count. Secondary endpoints are target area hair width and global photography and patient-reported outcome measures. But everything really centers around the target area hair count in pretty much all the hair studies. All the others are nice-to-haves rather than must-haves. We really want to see significant improvement in the target hair count of non-vellus hairs. Yeah. And to expand on what Rodney mentioned, also, we have included now target area hair darkening. Although, as rightfully Andreas mentioned, we have not baked it into the case, and we are still looking into this phenomenon too, and then we are exploring way higher doses, for example, in the clinical trial to really address this receptor occupancy and efficacy topic than the Hope Medicine study did. So we really believe that with the current clinical design, we will be able to bring the best out of this mechanism. and any expectations for kind of that safety SAD readout besides kind of looking at half-life? Any potential safety concerns? I know there's some theoretical concerns of prolactin suppression with immune bone loss, anything like that. Yeah. Denis, do you want to speak to that and Dr. Sinclair after that? Yeah. Sure. Happy to do so. So, as you have heard from Andreas initially, this mechanism is really one spectacular where we have the human genetics showing really a favorable safety profile. So the affected individuals are healthy. We also have phenomenal toxicology data so far from a preclinical toxicology, so where you have really to test high doses of the drug in NHPs. And then you also have the precedent of anti-prolactin receptor inhibition in clinical trials where also at very high doses, the participants showed no adverse events. So all taken together, we are pretty confident moving forward. Nevertheless, we have always, of course, the safety of the participant as our highest priority. And we will record any observations throughout the clinical trial. And also, Rodney will have a close eye on the participants here. Yeah. I think that from memory, the molecule doesn't cross the blood-brain barrier, so that you've got no central effects. And that's going to mean that there's going to be less interaction with the natural functioning of prolactin and its regulation. But like any clinical study, there is a whole stratified program going through the phase I, II, and III, where any side effects will be closely monitored. There's no red flags at this stage. But certainly, it's the same with any new molecule that there's a process to go through. And there's no guarantees until you've finished the process. Thank you so much. This concludes the Q&A section of the call. I would now like to turn the call back to the outside team for closing remarks. Well, first off, I just want to thank everyone for joining. I hope that this was educational from both a scientific perspective as well as a commercial perspective. And I want to thank the wonderful KOLs that joined today and gave their perspective for joining. And look forward to sharing the clinical data along the way, both with the SAD and then the upcoming MAD POC 13 week. This concludes the interview. And with that, we will conclude the call. Thank you for joining us. Thanks, everyone.