AJ, welcome to the Jefferies New York Global Healthcare Conference. It's my pleasure to introduce Sean and Zach from Absci Corporation with you here today.
Great. Thank you. I'm Sean McClain, Founder and CEO at Absci. Absci is a AI drug creation company. We've built a AI native platform at Absci, where we're able to accelerate the time it takes to get new drugs to the clinic and overall reducing the timelines, and we'll talk more about that on later slides, and really creating an exciting differentiated pipeline that's focused on prolactin receptor biology. Two programs, one focused on hair regrowth, androgenetic alopecia, and the other focused on endometriosis.
We see AI drug discovery as being able to really industrialize drug discovery, being able to have a wet lab in the loop to rapidly design molecules. Now we're actually shifting with agentic AI, being able to start to use these models to reason through data, being able to help us select the right targets, and then fully integrate into our design platforms to design the drug. What we've been able to show to date is we've been able to dramatically reduce overall cost and timelines. Traditionally it takes $50 million-$100 million just to get one drug into the clinic. We've been able to show with ABS-101 and ABS-201 that we are able to get these drugs into the clinic with an investment of roughly $10 million-$15 million. Additionally, it takes five to six years, again, just to get one drug into the clinic.
We've been able to show that we can get new drugs into the clinic in roughly 24 months, these timelines are continuing to come down and get cheaper. We see this as being able to fail faster and be able to get the right drugs into the clinic that are ultimately going to impact patients. As I'd mentioned, we have two drugs that have come out of our pipeline, ABS-201 for androgenetic alopecia, which is in a phase I/II-A study right now, as well as endometriosis, which will be starting in a phase II at the end of this year. We're wanting to use AI to create differentiated assets, being able to go after modalities and targets that have been traditionally hard to drug, such as ion channels, GPCRs, where we have known biology, but it's been difficult to drug.
We've been able to show success with this platform, not only on our own pipeline, but also with partners, in particular Almirall. We were able to show that we could actually drug an ion channel that had been known for 30 years, but no one had been able to successfully drug it. We recently released an exciting state-of-the-art model, Origin-1. This is an antibody design model where we were able, for the first time, to show that you could go after what's called zero-prior epitopes. Targets that have no known binders or structural known binders to that epitope. The significance of this is being able to go after hard-to-drug targets where traditional approaches have failed.
If you start to look at it in terms of integrating into an agentic AI workflow that discovers novel antigens and targets, it can then feed directly into this Origin-1 platform to design the molecule and then design the killer experiment to validate that and rapidly be discovering new novel biology really faster than we've seen to date. We see this as a very scalable approach. We see the AI platform not just as a technology, but really putting the value in the assets and making sure that we are investing in the right targets, and ultimately taking those into the clinic, because that's where the value is at. It's not necessarily on the platform, it's what the platform can ultimately achieve, and that's with these particular assets.
We're really excited to be focusing on prolactin biology, and we have, again, as I'd mentioned, two assets, ABS-101, that's going after two indications, androgenetic alopecia, so think hair regrowth, as well as endometriosis. ABS-201. This is a really exciting asset for us. This is targeting the prolactin receptor for androgenetic alopecia. This really hits on a new trend that you're starting to see, this total vitality market. We saw that the GLP-1s were able to provide weight loss and a lot of other benefits. What we're seeing is that patients and the consumer are not just wanting weight loss. They're wanting their hair to be regrown. They want their wrinkles removed. It's this total vitality market. We see just an absolutely massive market here. 80 million men and women in the U.S. suffer from androgenetic alopecia.
Additionally, there is a massive psychological burden that's associated with losing your hair. It's not just men, but women also, especially perimenopausal women that are losing their hair. They have zero solutions out there. They can't take finasteride, and minoxidil gives them hair in unwanted areas, and so there is a wide open space here, a massive market, and we see this being on par with the size of the GLP-1 market. How is prolactin and prolactin receptor involved in hair regrowth? What we've found is, over time, you build up prolactin or you have prolactinemia on the scalp. That is driving the follicle into a miniaturization state, essentially taking it from this active growth state, this anagen state, and driving it into the catagen state. We'll talk more about the mechanism in detail.
Essentially what goes on is you start to lose the stem cells within the hair follicle, and over time, that leads to the miniaturization and ultimately the hair loss that you see. By blocking the prolactin receptor, you're able to have the follicle go back into the anagen state and convert those vellus hairs into robust terminal hair growth. This is a novel mechanism. For the past 30 years, everyone's been going after the same targets. This is a brand new target to hit the androgenetic alopecia space. When you compare this to standard of care, oral minoxidil in mice, we were able to show that ABS-201 was able to provide superior hair regrowth compared to 5% oral minoxidil. You can see the mice. These are shaved mice. You have the control arm, 5% minoxidil, and ABS-201.
You can see the dramatic hair regrowth that these mice experience when compared to oral minoxidil. What got us really excited in the first place about this particular mechanism were these stump-tailed macaques. Our Chief Innovation Officer, Andreas Busch, prior to his time at Absci, was at Bayer. They were studying the prolactin receptor for endometriosis. What they ended up finding was when you shaved the mice, the mice that were on drug regrew their hair faster. They commissioned this stump-tailed macaque study. What you see here are bald stump-tailed macaques. These are stump-tailed macaques that naturally go bald. There's no chemical induction or any modification that go on, which really make this the perfect androgenetic alopecia model. They were on drug for 28 weeks, an anti-prolactin receptor antibody.
After six months of treatment, it was pretty remarkable what ended up happening. They go from their bald gray hair to a full head of hair, jet black. What's even more remarkable is post-treatment, they continued to regrow their hair. There was a regenerative effect that was going on for up to four years. We believe that the regenerative effect is the ability to rebuild the stem cell niche. We know that miniaturization happens slowly over time, so you can almost think of it as we're rebuilding the wall, we're rebuilding the machinery, and that gives that durable effect, that regenerative effect that we have yet to see in this space. We saw efficacy in mice, we saw it in these stump-tailed macaques. The next model we wanted to run was an ex vivo sample from punch biopsies from humans.
We worked with Professor Ralf Paus, a leading hair expert in this space, and performed a 72-hour ex vivo model where we compared hair growth and looked at the mechanism when comparing ABS-201 while adding prolactin. What we saw was really consistent with the stump-tailed macaques. What you see here is a microscopic hair imaging of the various different cycles. As I'd mentioned, anagen is the active growth state. Catagen is where you start to see the miniaturization occur. What you see in a very short amount of time is that ABS-201 alone was able to drive the follicle into the anagen state. When you add prolactin, you can see that it drives the follicle into the catagen state. When you have prolactin as well as ABS-201, you're able to rescue the follicle.
Again, seeing that same mechanism play out in humans, or at least human biopsies. I'd mention that our belief is that ABS-201 is able to rescue the stem cell niche. Once you rescue that stem cell niche, you're able to drive the rest of the machinery that is necessary to drive the follicle into a sustained anagen state. That's exactly what we see is that ABS-201 is able to promote K15 stem cell growth while prolactin drives the apoptosis of K15 stem cells. We're able to preserve and prevent their exhaustion, that's seen.
What's really quite interesting as well is that these stem cells are anchored by collagen XVII, and it looks like in studies that we've followed up on, that prolactin on its own is able to drive the increase of collagen XVII, which is ensuring that these stem cells stayed anchored to the niche and the bulge, again, allowing them to continue to proliferate and give that sustained, durable hair regrowth. Some other pieces that we were excited about from this study was not only the stem cells that we are able to preserve, but additionally, the other growth factors that are important for hair regrowth. That's FGF7, IGF-1, were all upregulated. Again, important for driving the follicle into the anagen state. Additionally, we did see a decrease of TGF-β, which is a known catagen driver. Earlier this year, we started a phase I/II-A study.
We started off with a single ascending dose in non-AGA patients. These were four doses, 150 mg, all the way up to 1,800 mg. Far, everything is looking good with that. We do see a favorable safety and PK profile. In June or later this month, we will be disclosing the initial safety and PK data that's coming out of the single ascending dose. We additionally have started the MAD portion, which is in healthy volunteers that have AGA, and this is sub-Q dosing, and we have 3 different doses here, 300 mg, 600 mg, and 1,200 mg. This is going to be dosed every eight weeks. We'll have a 13-week interim readout and a 26-week interim readout or the final readout at 26 weeks. The 13-week readout will be the second half of this year. The primary endpoint on that is safety and tolerability.
The secondary endpoint is the efficacy, so looking at total area, hair count, thickness, and darkening. For this, we just want to see hair regrowth showing that the mechanism is working. It's a directional readout. It'll be a responder analysis, so it'll stay blinded, looking at the growth of the responders. Again, second half of this year, that data will be available. Then the study will complete early next year, and this will be the 26 readout, unblinded, looking at safety tolerability, total area, hair count, darkness, and hair width. As I'd mentioned, we see this as a large, massive market. The standard of care hasn't changed in the last 20-30 years. It's still minoxidil and finasteride, and additionally, do have hair transplants.
What we've seen from physicians and patients when we've interviewed them is that they are not happy with the current standard of care in terms of efficacy, hair regrowth, and just being able to take a daily pill. We believe that if we are able to achieve efficacy that is around oral minoxidil, call it 30 - 50 hairs per square centimeter, and we're able to have a durable hair regrowth, so think two to three doses over a six-month period, and you have hair regrowth for the next one to two years, we believe that is a home run product from the consumer quant studies that we've done. If we're able to achieve greater than that, we do see the TAM growing much larger.
We did do a consumer quant study looking at those that would be interested in the TPP that I had just laid out. As I'd mentioned, there is a large patient population, 80 million men and women suffer from androgenetic alopecia. If you work your way down the funnel here, we do see an overall TAM within the U.S. of $25 billion and globally being $40 billion. This market is just getting started. Again, standard of care hasn't changed. This is a brand-new novel mechanism and a massive opportunity that we're looking to tap into. The second indication that we're going into with ABS-201 is another underserved patient population, and that is endometriosis in women. One in 10 women suffer from endometriosis. This is a debilitating disease. It's extremely painful for women during menstruation. It's an inflammatory-based disease, and current standard of care is not great.
Far too long there hasn't been a lot of investment here. The diagnostic tests aren't great, which we believe is actually underestimating the overall patient population. Really excited to be pursuing this particular indication just due to standard of care being so low, and just a massive unmet medical need here. How is prolactin involved in endometriosis? What we're seeing is very similar to what we see in the scalp. That you get high levels of prolactin in the endometrial tissue. What that does is it drives inflammation within the endometrial tissue and drives lesion formation, as well as drives pain sensitization. What we've seen from both publicly available data as well as some data we've generated pre-clinically, is that it does look like indeed, at least in mouse studies, that prolactin is driving the lesion formation that women get on the endometrial tissue.
Additionally, prolactin is driving the pain sensitization that women experience during dysmenorrhea. As I'd mentioned, this is a very large patient population. One in 10 women have endometriosis. It is a very debilitating disease, and we see the market opportunity for this being over $4.5 billion. Excited to be pursuing this in an area that has been very much overlooked and underappreciated, and we do believe that we could be bringing forward a treatment that is truly disease modifying. Over the next 24 months, we have exciting readouts that are occurring. First off, June of this year, this month, we'll be having the safety PK readout on the phase I/II-A study for the SAD portion, looking at initial safety tolerability and PK data.
Later this year, in the second half, we'll have the 13-week interim readout on AGA. Then we will be starting the endometriosis study at the end of this year, a phase II study. In the beginning of next year, we will be having the full 26-week readout on AGA. It's a very exciting 24 months for us with multiple readouts and yeah, two phase II readouts. We'll open it up for questions. Thank you. All righty. Well, thank you--